PHANTOMS

IN THE
BRAIN
Oter book by Sanda Blaeslee
Second Chances (with Judith Wallerstein, Ph.D.)
Te Good Marriage (with Judith Wallerstein, Ph.D.)
Probing the Mysteries of the Human Mind
V.S. Rmachandran, M.D., Ph.D.,
and Sandra Blaeslee
WLLIA MOROW AND COMPA, INC.
New Yrk
Copyright 1998 by V.S. Rmachandran and Sandra Blakeslee
Foreword copyright 1998 by Oliver Sacks
The names of people and distinctive characteristics referred to in the case histories in
this book have been changed to protect the identities of the individuals concerned.
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Library of Congress Cataloging-in-Publication Data
Ramachandran, V.S.
Phantoms in the brain : probing the mysteries of the human mind /
V.S. Ramachandran, and Sandra Blakeslee.
p. em.
Includes bibliographical references and index.
ISBN 0-688-15247-3
l. Neurology-Popular works. 2. Brain-Popular works.
3. Neurosciences-Popular works. I. Blakeslee, Sandra. II. Title.
RC35l.R24 1998
612.8'2-dc21
Printed in the United States of America
First Edition
2 3 4 5 6 7 8 9 10
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To my mother, Meenakshi
To my father, Subramanian
To my brother, Rvi
To Diane, Mani and Jayakrishna
To all my former teachers in India and England
To Saraswathy, the goddess of learning, music and wisdom
foreword
The great neurologists and psychiatrists of the nineteenth and early twen
tieth centuries were masters of description, and some of their case histories
provided an almost novelistic richness of detail. Silas Weir Mitchell-who
was a novelist as well as a neurologist-provided unforgettable descrip
tions of the phantom limbs ( or "sensory ghosts," as he frst called them) in
soldiers who had been injured on the battefelds of the Civil War. Joseph
Babinski, the great French neurologist, described an even more extraor
dinary syndrome-anosognosia, the inability to perceive that one side of
one' s own body is paralyzed and the ofen-bizarre attribution of the para
lyzed side to another person. ( Such a patient might say of his or her own lef
side, "It's my brother's" or "It's yours . ")
Dr. V. S. Rmachandran, one of the most interesting neuroscientists
of our time, has done seminal work on the nature and treatment of
phantom limbs-those obdurate and sometimes tormentng ghosts of
arms and legs lost years or decades before but not forgotten by the brain.
A phantom may at frst feel like a normal limb, a part of the normal body
image; but, cut of from normal sensation or action, it may assume a
pathological character, becoming intrusive, "paralyzed," deformed, or
excruciatingly painfl-phantom fngers may dig into a phantom palm
with an unspeakable, unstoppable intensity. The fact that the pain and
the phantom are "unreal" is of no help, and may indeed make them
more difcult to treat, for one may be unable to unclench the seemingly
paralyzed phantom. In an attempt to alleviate such phantoms, physicians
and their patients have been driven to extreme and desperate measures:
making the amputation stump shorter and shorter, cutting pain or sen
sory tracts in the spinal cord, destroying pain centers in the brain itself
But all too frequently, none of these work; the phantom, and the phan
tom pain, almost invariably return.
To these seemingly intractable problems, Rmachandran brings a fresh
and diferent approach, which stems fom his inquiries as to what phan
toms are, and how and where they are generated in the nerous system.
It has been classically considered that representations in the brain, in
cluding those of body image and phantoms, are fxed. But Rmachandran
( and now others) has shown that striking reorganizations in body image
occur very rapidly-within forty- eight hours, and possibly much less
following the amputation of a limb. Phantoms, in his view, are
Vll
v i i i I FoREWORD
generated by such reorganizations of body image in the sensory cortex
and may then be maintained by what he terms a "learned" paralysis . But
if there are such rapid changes underlying the genesis of a phantom, if
there is such plasticity in the cortex, can the process be reversed? Can
the brain be tricked into unlearning a phantom?
By using an ingenious "virtual reality" device, a simple box with a
transposing mirror, Rmachandran has found that a patent may be
helped by merely being given the sight of a normal limb-the patient's
own normal right arm, for example, now seen on the lef side of the
body, in place of the phantom. The result of this may be instantaneous
and magical : The normal look of the arm competes with the feel of the
phantom. The frst efect of this is that a deformed phantom may
straighten out, a paralyzed phantom may move; eventually, there may be
no more phantom at all . Rmachandran speaks here, with characteristic
humor, of "the frst successfl amputaton of a phantom limb, " and of
how, if the phantom is extinguished, its pain must also go-for if there
is nothing to embody it, then it can no longer surive. ( Mrs . Gradgrind,
in Hard Times, asked if she had a pain, replied, "There is a pain some
where in the room, but I cannot be sure that I have got it. " But this
was her confsion, or Dickens's joke, for one cannot have a pain except
in oneself)
Can equally simple "tricks" assist patients with anosognosia, patients
who cannot recognize one of their sides as their own? Here too, R
machandran fnds, mirrors may be of great use in enabling such patients
to reclaim the previously denied side as their own; though in other
patients, the loss of "lefness, " the bisection of one' s body and world,
is so profound that mirrors may induce an even deeper, through- the
lookng- glass confsion, a groping to see if there is not someone lurking
"behind" or "in" the mirror. ( Rmachandran is the frst to describe this
"mirror agnosia. ") It is a measure not only of Rmachandran' s tenacity
of mind but of his delicate and supporive relationship with patients that
he has been able to pursue these syndromes to their depths.
The deeply strange business of mirror agnosia, and that of misattri
buting one' s own limbs to others, are ofen dismissed by physicians as
irrational . But these problems are also considered careflly by Rma
chandran, who sees them not as groundless or crazy, but as emergency
defense measures constructed by the unconscious to deal with sudden
overhelming bewilderments about one:s body and the space around it.
They are, he feels, quite normal defense mechanisms ( denial, repression,
projection, confabulation, and so on) such as Freud delineated as uni-
FOREWORD / i x
versal strategies of the unconscious when forced to accommodate the
intolerable or unintelligible. Such an understanding removes such pa
tients from te realm of the mad or freakish and restores them to the
realm of discourse and reason-albeit the discourse and reason of the
unconscious.
Another syndrome of misidentifcation that Rmachandran considers
is Capgras' syndrome, where the patient sees familiar and loved fgures
as impostors. Here too, he is able to delineate a clear neurological basis
for the syndrome-the removal of the usual and crucial afective cues to
recognition, coupled with a not unnatural interpretation of the now af
fectless perceptions ("He can't be my father, because I feel nothing-he
must be a sort of simulacrum").
Dr. Rmachandran has countless other interests too: in the nature of
religious experience and the remarkable "mystical" syndromes associated
with dysfnction in the temporal lobes, in the neurology of laughter and
tickling, and-a vast realm-in the neurology of suggestion and placebos.
Like the perceptual psychologist Rchard Gregory (with whom he has
published fascinating work on a range of subjects, from the flling-in of
the blind spot to visual illusions and protective colorations), Rm a chan
dran has a fair for seeing what is fndamentally important and is pre
pared to turn his hand, his freshness, his inventiveness, to almost
anything. All of these subjects, in his hands, become windows into the
way our nerous systems, our worlds, and our very selves are constituted,
so that his work becomes, as he likes to say, a form of "experimental
epistemology." He is, in this way, a natural philosopher in the eight
eenth-century sense, though with all the knowledge and know-how of
the late twentieth century behind him.
In his Preface, Rmachandran tells us of the nineteenth-century sci
ence books he especially enjoyed as a boy: Michael Faraday's Chemical
Histor of a Candle, works by Charles Darwin, Humphry Davy and Tho
mas Huxley. There was no distinction at this time between academic and
popular writng, but rather the noton that one could be deep and serious
but completely accessible, all at once. Later, Ramachandran tells us, he
enjoyed the books of George Gamow, Lewis Thomas, Peter Medawar,
and then Carl Sagan and Stephen Jay Gould. Rmachandran has now
joined these grand science writers with his closely obsered and deeply
serious but beautflly readable book Phantoms in the Brain. It is one of
the most original and accessible neurology books of our generation.
-Oliver Sacks, M.D.
Preface
In any fld, fnd the strangest thing and then explore it.
-jOHN ARCHIBALD WHEELER
This book has been incubating in my head for many years, but I never
quite got around to writing it. Then, about three years ago, I gave the
Decade of the Brain lecture at the annual meeting of the Society for
Neuroscience to an audience of over four thousand scientists, discussing
many of my fndings, including my studies on phantom limbs, body im
age and the illusory nature of the self. Soon afer the lecture, I was
barraged with questions fom the audience: How does the mind infu
ence the body in health and sickness? How can I stimulate my right brain
to be more creative? Can your mental atttude really help cure asthma
and cancer? Is hypnosis a real phenomenon? Does your work suggest
new ways to treat paralysis afer strokes? I also got a number of requests
from students, colleagues and even a few publishers to undertake writing
a textbook. Textbook writing is not my cup of tea, but I thought a
popular book on the brain dealing mainly with my own experiences
working with neurological patients might be fn to write. During the
last decade or so, I have gleaned many new insights into the workings
of the human brain by studying such cases, and the urge to communicate
these ideas is strong. When you are involved in an enterprise as exciting
as this, it's a natural human tendency to want to share your ideas with
others. Moreover, I feel that I owe it to taxpayers, who ultimately sup
port my work through grants fom the National Institutes of Health.
Popular science books have a rich, venerable tradition going as far
back as Galileo in the seventeenth century. Indeed, this was Galileo's
main method of disseminating his ideas, and in his books he ofen aimed
barbs at an imaginary protagonist, Simplicia-an amalgam of his profes
sors. Almost al of Charles Darwin's famous books, including Te Oriin
of Species, Te Descent of Man, Te Epression of Emotions in Animals
and Men, Te Habits of Insectivorous Plants-but not his two-volume
monograph on barnacles!-were written for the lay reader at the request
of his publisher, John Murray. The same can be said of the many works
of Thomas Huxley, Michael Faraday, Humphry Davy and many other
Victorian scientists. Faraday's Chemical Histor of a Candle, based on
Christmas lectures that he gave to children, remains a classic to this day.
Xl
Xll I P R E F A C E
I must confess that I haven't read all these books, but I do owe a
heavy intellectual debt to popular science books, a sentiment that is ech
oed by many of my colleagues. Dr. Francis Crick of the Salk Institute
tells me that Erwin Schrodinger's popular book Wat Is Lie? contained
a few speculative remarks on how heredity might be based on a chemical
and that this had a profound impact on his intellectual development,
culminating in his unraveling the genetic code together with James Wat
son. Many a Nobel Prize-winning physician embarked on a research ca
reer afer reading Paul de Kuif's Te Microbe Hunters, which was
published in 1926. My own interest in scientifc research dates back to
my early teens, when I read books by George Gamow, Lewis Thomas,
and Peter Medawar, and the flame is being kept alive by a new generaton
of writers-Oliver Sacks, Stephen Jay Gould, Carl Sagan, Dan Dennett,
Richard Gregory, Richard Dawkins, Paul Davies, Colin Blakemore and
Steven Pinker.
About six years ago I received a phone call from Francis Crick, the
codiscoverer of the structure of deoxyribonucleic acid ( DNA) , in which
he said that he was writing a popular book on the brain called Te Aston
ishing Hypothesis. In his crisp British accent, Crick said that he had com
pleted a frst draf and had sent it to his editor, who felt that it was
extremely well written but that the manuscript still contained j argon that
would be intelligible only to a specialist. She suggested that he pass it
around to some lay people. "I say, Rama, " Crick said with exasperation,
"the trouble is, I don't know any lay people. Do you know any lay people
I could show the book to? " At frst I thought he was j oking, but then
realized he was perfectly serious . I can' t personally claim not to know
any lay people, but I could nevertheless sympathize with Crick's plight.
Wen writing a popular book, professional scientists always have to walk
a tightrope between making the book intelligible to the general reader,
on the one hand, and avoiding oversimplifcaton, on the other, so that
experts are not annoyed. My solution has been to make elaborate use of
end notes, which sere three distinct fnctions: First, whenever it was
necessary to simplif an idea, my cowriter, Sandra Blakeslee, and I re
sorted to notes to qualif these remarks, to point out exceptons and to
make it clear that in some cases the results are preliminary or contover
sial . Second, we have used notes to amplif a point that is made only
briefy in the main text-so that the reader can explore a topic in greater
depth. The notes also point the reader to original references and credit
those who have worked on similar topics. I apologize to those whose
works are not cited; my only excuse is that such omission is inevitable in
P R E F A C E I Xlll
a book such as this ( for a while the notes threatened to exceed the main
text in length) . But I 've tried to include as many pertinent references as
possible in the bibliography at the end, even though not all of them are
specifcally mentioned in the text.
This book is based on the true-life stories of many neurological pa
tients. To protect their identity, I have followed the usual traditon of
changing names, circumstances and defning characteristics throughout
each chapter. Some of the "cases" I describe are really composites of
several patients, including classics in the medical literature, as my purpose
has been to illustrate salient aspects of the disorder, such as the neglect
syndrome or temporal lobe epilepsy. Wen I describe classic cases ( like
the man with amnesia known as H. M. ), I refer the reader to original
sources for details . Other stories are based on what are called single-case
studies, which involve individuals who manifest a rare or unusual syn
drome.
A tension exists in neurology between those who believe that the most
valuable lessons about the brain can be learned from statistical analyses
involving large numbers of patients and those who believe that doing
the right kind of experiments on the right patents-even a single pa
tient-can yield much more usefl informaton. This is really a silly de
bate since its resoluton is obvious: It's a good idea to begin with
experments on single cases and then to confrm the fndings through
studies of additional patients. By way of analogy, imagine that I cart a
pig into your living room and tell you that it can talk. You might say,
"Oh, really? Show me. " I then wave my wand and the pig starts talking.
You might respond, "My God! That's amazing! " You are not likely to
say, "A, but that' s just one pig. Show me a few more and then I might
believe you. " Yet this is precisely the attitude of many people in my feld.
I think it's fair to say that, in neurology, most of the major discoveries
that have withstood the test of time were, in fact, based initially on single
case studies and demonstrations. More was learned about memory from
a few days of studying a patent called H. M. than was gleaned from
previous decades of research averaging data on many subj ects. The same
can be said about hemispheric specialization ( the organizaton of the
brain into a lef brain and a right brain, which are specialized for diferent
fnctions ) and the experiments carried out on two patients with so-called
split brains ( in whom the lef and right hemispheres were disconnected
by cutting the fbers between them) . More was learned from these two
individuals than from the previous ffy years of studies on normal people.
In a science still in its infancy ( like neuroscience and psychology)
XIV I P RE F A C E
demonstration- style experiments play an especially important role. A clas
sic example is Galileo's use of early telescopes. People ofen assume that
Galileo invented the telescope, but he did not. Aound 1607, a Dutch
spectacle maker, Hans Lipperhey, placed two lenses in a cardboard tube
and found that this arrangement made distant objects appear closer. The
device was widely used as a child's toy and soon found its way into
country fairs throughout Europe, including France. In 1609, when Ga
lileo heard about this gadget, he immediately recognized its potential .
Instead of spying on people and other terrestrial objects, he simply raised
the tube to the sky-something that nobody else had done. First he
aimed it at the moon and found that it was covered with craters, gullies
and mountains-which told him that the so-called heavenly bodes are,
contrary to conventional wisdom, not so perfect afer all: They are fll
of faws and imperfections, open to scrutiny by mortal eyes just like ob
jects on earth. Next he directed the telescope at the Milky Way and
noticed instantly that far from being a homogeneous cloud ( as people
believed) , it was composed of millions of stars. But his most startling
discovery occurred when he peered at Jupiter, which was known to be a
planet or wandering star. Imagine his astonishment when he saw three
tny dots near Jupiter (which he initially assumed were new stars ) and
witnessed that afer a few days one disappeared. He then waited for a
few more days and gazed once again at Jupiter, only to fnd that not
only had the missing dot reappeared, but there was now an extra dot-a
total of four dots instead of three. He understood in a fash that the four
dots were Jovian satellites-moons just like ours-that orbited the
planet. The implications were immense. In one stroke, Galileo had
proved that not all celestial bodies orbit the earh, for here were four
that orbited another planet, Jupiter. He thereby dethroned the geocen
trc theory of the universe, replacing it with the Copernican view that
the sun, not the earth, was at the center of the known universe. The
clinching evidence came when he directed his telescope at Venus and
found that it looked like a crescent moon going though all the phases,
just like our moon, except that it took a year rather than a month to do
so. Again, Galileo deduced from this that all the planets were orbiting
the sun and that Venus was interposed between the earth and the sun.
All this from a simple cardboard tube with to lenses. No equations, no
graphs, no quantitative measurements: "just" a demonstration.
When I relate this example to medical students, the usual reaction is,
Well, that was easy during Galileo's time, but surely now in the twentieth
century all the major discoveries have already been made and we can't
P R E F ACE I XV
do any new research without expensive equipment and detailed quanti
tative methods. Rubbish! Even now amazing discoveries are staring at
you all the time, right under your nose. The difculty lies in realizing
this. For example, in recent decades all medical students were taught that
ulcers are caused by stress, which leads to excessive acid production that
erodes the mucosal lining of the stomach and duodenum, producing te
characteristic craters or wounds that we call ulcers. And for decades the
treatment was either antacids, histamine receptor blockers, vagotomy
( cutting the acid-secreting nere that innerates the stomach) or even
gastrectomy ( removal of part of the stomach. ) But then a young resident
physician in Australia, Dr. Bill Marshall, looked at a stained section of a
human ulcer under a microscope and noticed that it was teeming with
Helicobacter pylori-a common bacterium that is found in a certain pro
portion of healthy individuals. Since he regularly saw these bacteria in
ulcers, he started wondering whether perhaps they actually caused ulcers.
Wen he mentioned this idea to his professors, he was told, "No way.
That can't be true. We all know ulcers are caused by stress. What you
are seeing is just a secondary infection of an ulcer that was already in
place. "
But Dr. Marshall was not dissuaded and proceeded to challenge the
conventional wisdom. First he carried out an epidemiological study,
which showed a strong correlation between the distribution of Helico
bacter species in patients and the incidence of duodenal ulcers. But this
fnding did not convince his colleagues, so out of sheer desperation,
Marshall swallowed a culture of the bacteria, did an endoscopy on himself
a few weeks later and demonstrated that his gastrointestinal tract was
studded with ulcers! He then conducted a formal clinical trial and
showed that ulcer patients who were treated with a combination of an
tibiotics, bismuth and metronidazole ( Flagyl , a bactericide) recovered at
a much higher rate-and had fewer relapses-than did a control group
given acid-blocking agents alone.
I mention this episode to emphasize that a single medical student or
resident whose mind is open to new ideas and who works without so
phisticated equipment can revolutionize the practice of medicine. It is in
this spirit that we should all undertake our work, because one never
knows what nature is hiding.
I' d also like to say a word about speculation, a term that has acquired
a pejorative connotation among some scientists. Describing someone' s
idea as "mere speculation" is ofen considered insulting. This is unfor
tunate. A the English biologist Peter Medawar has noted, "A imagi-
XVl I P R E F ACE
native conception of what miht be true is the starting point of all great
discoveries in science. " Ironically, this is sometimes true even when the
speculation turns out to be wrong. Listen to Charles Darwin: "False facts
are highly inj urious to the progress of science for they ofen endure long;
but flse hypotheses do little harm, as everyone takes a salutary pleasure
in proving their falseness; and when this is done, one path toward error
is closed and the road to truth is ofen at the same time opened. "
Every scientist knows that the best research emerges from a dialectic
between speculation and healthy skepticism. Ideally the two should co
exist in the same brain, but they don't have to. Since there are people
who represent both extremes, all ideas eventually get tested ruthlessly.
Many are rejected (like cold fsion) and others promise to turn our views
topsy turvy (like the view that ulcers are caused by bacteria) .
Several of the fndings you are going to read about began as hunches
and were later confrmed by other groups (the chapters on phantom
limbs, neglect syndrome, blindsight and Capgras' syndrome) . Other
chapters describe work at an earlier stage, much of which is fankly spec
ulative (the chapter on denial and temporal lobe epilepsy) . Indeed, I will
take you at tmes to the very limits of scientifc inquiry.
I strongly believe, however, that it is always the writer's responsibility
to spell out clearly when he is speculating and when his conclusions are
clearly warranted by his obserations. I've made every efort to presere
this distinction throughout the book, ofen adding qualifcations, dis
claimers and caveats in the text and especially in the notes. In striking
this balance between fact and fancy, I hope to stimulate your intellectual
curiosity and to widen your horizons, rather than to provide you with
hard and fast answers to the questions raised.
The famous saying "May you live in interesting times" has a special
meaning now for those of us who study the brain and human behavior.
On the one hand, despite two hundred years of research, the most basic
questions about the human mind-How do we recognize faces? Wy do
we cry? Wy do we laugh? Wy do we dream? and Why do we enjoy
music and art? -remain unanswered, as does the really big question:
What is consciousness? On the other hand, the advent of novel experi
mental approaches and imaging techniques is sure to transform our un
derstanding of the human brain. What a unique privilege it will be for
our generation-and our children' s-to witness what I believe will be
the greatest revolution in the history of te human race: understanding
ourselves. The prospect of doing so is at once both exhilarating and
disquieting.
P R E F ACE I XVII
There is something distinctly odd about a hairless neotenous primate
that has evolved into a species that can look back over its own shoulder
and ask questions about its origins . And odder still, the brain can not
only discover how other brains work but also ask questions about its own
existence: Wo am I ? Wat happens afer death? Does my mind arise
exclusively from neurons in my brain? And if so, what scope is there for
free will? It is the peculiar recursive quality of these questions-as the
brain struggles to understand itself-that makes neurology fascinating.
Contents
Foreword by Oliver Sacks, M. D. vii
Preface XI
Chapter l: The Phantom Within 1
Chapter 2: "Kowing Were to Scratch" 2 1
Chapter 3: Chasing the Phantom 39
Chapter 4: The Zombie i n the Brain 63
Chapter 5 : The Secret Life of James Thurber 85
Chapter 6: Through the Looking Glass 113
Chapter 7: The Sound of One Hand Clapping 127
Chapter 8: "The Unbearable Likeness of Being" 158
Chapter 9: God and the Limbic System 174
Chapter 10: The Woman Who Died Laughing 199
Chapter 11: "You Forgot to Deliver the Twin" 2 12
Chapter 12: Do Martians See Red? 227
Ackowledgments 259
Notes 263
Bibliography and Suggested Reading 299
Index 3 14
x i x
By the defcits, we may know the talents, by the exceptions, we may
discer the rules, b studying pathology we may construct a model
of health. And-most important-om this model may evolve the
insihts and tool we need to afect our own lives, mold our own
destinies, change ourselves and our societ in ways that, as yet, we
can only imagine.
-LURENCE MILLER
Te world shal perish not for lck of wonders, but for lack of
wonder.
-]B.S. HDANE
PHANTOMS
IN THE
BRAIN
CHAPTER 1
The Phantom Within
For in and out, above, about, below,
'Tis nothing but a Magic Shadow-show
Play'd in a Box whose Candle is the Sun,
Round which we Phantom Fiures come and go.
-The Rubaiyat of Omar Kayyam
I know, my dear Watson, that you share my love
of all that is bizarre and outside the conventions
and humdrum routines of everday life.
-SHERLOCK HOLMES
A man wearing an enormous bej eweled cross dangling on a gold chain
sits in my ofce, telling me about his conversations with God, the "real
meaning" of the cosmos and the deeper truth behind all surface appear
ances. The universe is sufsed with spiritual messages, he says, if you
just allow yourself to tune in. I glance at his medical chart, noting that
he has sufered fom temporal lobe epilepsy since early adolescence, and
that is when "God began talkng" to him. Do his religious experiences
have anything to do with his temporal lobe seizures?
A amateur athlete lost his arm in a motorcycle accident but continues
to feel a "phantom arm" with vivid sensations of movement. He can
wave the missing arm in midair, "touch" things and even reach out and
"grab" a cofee cup. If I pull the cup away fom him suddenly, he yelps
in pain. "Ouch! I can feel it being wrenched from my fngers, " he says,
wmcmg.
l
2 I P HAN T O MS I N T H E B RA I N
A nurse developed a large blind spot in her feld of vision, which is
troubling enough. But to her dismay, she ofen sees cartoon characters
cavorting within the blind spot itself Wen she looks at me seated across
from her, she sees Bugs Bunny in my lap, or Elmer Fudd, or the Road
Runner. Or sometimes she sees cartoon versions of real people she's
always known.
A schoolteacher sufered a stroke that paralyzed the lef side of her
body, but she insists that her lef arm is not paralyzed. Once, when I
asked her whose arm was lying in the bed next to her, she explained that
the limb belonged to her brother.
A librarian from Philadelphia who had a diferent kind of stroke began
to laugh uncontrollably. This went on for a fll day, until she literally
died laughing.
And then there is Arthur, a young man who sustained a terrible head
injury in an automobile crash and soon aferard claimed that his father
and mother had been replaced by duplicates who looked exactly like his
real parents. He recognized their faces but they seemed odd, unfamiliar.
The only way Ahur could make any sense out of the situation was to
assume that his parents were impostors.
None of these people is "crazy"; sending them to psychiatrists would
be a waste of time. Rather, each of them sufers from damage to a specifc
part of the brain that leads to bizarre but highly characteristic changes
in behavior. They hear voices, feel missing limbs, see things that no one
else does, deny the obvious and make wild, extraordinary claims about
other people and the world we all live in. Yet for the most par they are
lucid, rational and no more insane than you or I .
Although enigmatic disorders like these have intrigued and perplexed
physicians throughout history, they are usually chalked up as curiosities
case studies stufed into a drawer labeled "fle and forget. " Most neu
rologists who treat such patients are not particularly interested in ex
plaining these odd behaviors. Their goal is to alleviate symptoms and to
make people well again, not necessarily to dig deeper or to learn how
the brain works . Psychiatrists ofen invent ad hoc theories for curious
syndromes, as if a bizarre condition requires an equally bizarre explana
tion. Odd symptoms are blamed on the patient's upbringing ( bad
thoughts from childhood) or even on the patient's mother (a bad nur
turer) . Phantoms in the Brain takes the opposite viewpoint. These pa
tients, whose stories you will hear in detail, are our guides into the inner
workngs of the human brain-yours and mine. Far from being curiosi
ties, these syndromes illustrate fndamental principles of how the normal
T H E P H A N T O M WI T H I N I 3
human mind and brain work, shedding light on the nature of body im
age, language, laughter, dreams, depression and other hallmarks of hu
man nature. Have you ever wondered why some j okes are fnny and
others are not, why you make an explosive sound when you laugh, why
you are inclined to believe or disbelieve in God, and why you feel erotic
sensations when someone sucks your toes? Surprisingly, we can now be
gin to provide scientifc answers to at least some of these questions.
Indeed, by studying these patients, we can even address lofy "philo
sophical " questions about the nature of the self: Why do you endure as
one person through space and time, and what brings about the seamless
unity of subj ective experience? What does it mean to make a choice or
to will an action? Ad more generally, how does the activity of tiny wisps
of protoplasm in the brain lead to conscious experience?
Philosophers love to debate questions like these, but it's only now
becoming clear that such issues can be tackled experimentally. By moving
these patients out of the clinic and into the laboratory, we can conduct
experiments that help reveal the deep architecture of our brains. Indeed,
we can pick up where Freud lef of, ushering in what might be called
an era of experimental epistemology ( the study of how the brain repre
sents knowledge and belief and cognitive neuropsychiatry ( the interface
between mental and physical disorders of the brain) , and start experi
menting on belief systems, consciousness, mind- body interactions and
other hallmarks of human behavior.
I believe that being a medical scientist is not all that diferent from
being a sleuth. In this book, I've attempted to share the sense of mystery
that lies at the heart of all scientifc pursuits and is especially characteristic
of the forays we make in trying to understand our own minds. Each story
begins with either an account of a patient displaying seemingly inexpli
cable symptoms or a broad question about human nature, such as why
we laugh or why we are so prone to self-deception. We then go step by
step through the same sequence of ideas that I followed in my own mind
as I tied to tackle these cases. In some instances, as with phantom limbs,
I can claim to have genuinely solved the mystery. In others-as in the
chapter on God-the fnal answer remains elusive, even though we come
tantalizingly close. But whether the case is solved or not, I hope to con
vey the spirit of intellectual adventure that accompanies this pursuit and
makes neurology the most fascinating of all disciplines. A Sherlock
Holmes told Watson, "The game is afoot! "
Consider the case of Ahur, who thought his parents were impostors.
Most physicians would be tempted to conclude that he was j ust crazy,
4 I P HAN T O MS I N T H E B RAI N
and, indeed, that is the most common explanation for this type of dis
order, found in many textbooks. But, by simply showing him photo
graphs of diferent people and measuring the extent to which he starts
sweating ( using a device similar to the lie detector test) , I was able to
fgure out exactly what had gone wrong in his brain ( see chapter 9) . This
is a recurring theme in this book: We begin with a set of symptoms that
seem bizarre and incomprehensible and then end up-at least in some
cases-with an intellectually satisfing account in terms of the neural
circuitry in the patient's brai n. And in doing so, we have ofen not only
discovered something new about how the brain works but simultaneously
opened the doors to a whole new direction of research.
But before we begin, I think it's important for you to understand my
personal approach to science and why I am drawn to curious cases. When
I give talks to lay audiences around the country, one queston comes up
again and again: "When are you brain scientists ever going to come up
with a unifed theory for how the mind works? There' s Einstein' s general
theory of relativity and Newton's universal law of gravitation in physics.
Why not one for the brain? "
My answer i s that we are not yet at the stage where we can formulate
grand unifed theories of mind and brain. Every science has to go
through an inital "experiment" or phenomena-driven stage-in which
its practitioners are stll discovering the basic laws-before it reaches a
more sophistcated theory-driven stage. Consider the evolution of ideas
about electricity and magnetsm. Athough people had vague notions
about lodestones and magnets for centuries and used them both for
making compasses, the Victorian physicist Michael Faraday was the frst
to study magnets systematically. He did to very simple experiments with
astonishing results. In one experiment-which any schoolchild can re
peat-he simply placed a bar magnet behind a sheet of paper, sprinkled
powdered iron flings on the surface of the paper and found that they
spontaneously aligned themselves along the magnetic lines of force ( this
was the very frst time anyone had demonstrated the existence of felds
in physics ) . In the second experiment, Faraday moved a bar magnet to
and fro in the center of a coil of wire, and, lo and behold, this action
produced an electrical current in te wire. These informal demonstra
tions-and this book is fll of examples of this sort-had deep implica
tions:1 They linked magnetsm and electricity for the frst time. Faraday's
own interpretation of these efects remained qualitative, but his experi-
T H E P HAN T O M WI T H I N I 5
ments set the stage for James Clerk Maxwell's famous electromagnetic
wave equatons several decades later-the mathematical formalisms that
form the basis of all modern physics.
My point is simply that neuroscience today is in the Faraday stage,
not in the Maxwell stage, and there is no point in trying to j ump ahead.
I would love to be proved wrong, of course, and there is certainly no
harm in trying to construct formal teories about the brain, even if one
fails ( and there is no shortage of people who are trying) . But for me, the
best research strategy might be characterized as "tnkering. " Whenever
I use this word, many people look rather shocked, as if one couldn' t
possibly do sophisticated science by j ust playing around with ideas and
witout an overarching theory to guide one' s hunches. But tat's exactly
what I mean ( although these hunches are far fom random; they are
always guided by intuition) .
I've been interested i n science as long as I can remember. When I was
eight or nine years old, I started collecting fossils and seashells, becoming
obsessed with taxonomy and evoluton. A little later I set up a small
chemistry lab under the stairay in our house and enj oyed watching iron
flings "fzz" in hydrochloric acid and listening to the hydrogen "pop"
when I set fre to it. ( The iron displaced the hydrogen from the hydro
chloric acid to form iron chloride and hydrogen. ) The idea that you
could learn so much from a simple experiment and that eerything in
the universe is based on such interactions was fascinating. I remember
that when a teacher told me about Faraday's simple experments, I was
intrigued by the noton tat you could accomplish so much with so littl e.
These experiences l ef me with a permanent distaste for fancy equipment
and the realizaton that you don't necessarily need complicated machines
to generate scientfc revolutions; all you need are some good hunches. 2
Aother pererse streak of mine is that I've always been drawn to the
exception rather than to the rule in every science that I 've studied. In
high school I wondered why iodine is the only element that turns fom
a solid to a vapor directly when heated, without frst melting and going
trough a liquid stage. Why does Saturn have rings and not the other
planets? Why does water alone expand when it turns to ice, whereas every
other liquid shrinks when it solidifes? Why do some animals not have
sex? Wy can tadpoles regenerate lost limbs tough an adult frog cannot?
Is it because the tadpole is younger, or is it because it's a tadpole? Wat
would happen if you delayed metamorphosis by blocking the acton of
thyroid hormones (you could put a few drops of thiouracil into the
aquarium) so that you ended up with a very old tadpole? Would te
6 I P H A N T O MS I N T H E B RA I N
geriatric tadpole be able to regenerate a missing limb? (A a schoolboy
I made some feeble attempts to answer this, but, to my knowledge, we
don't kow the answer even to this day. ) 3
Of course, looking at such odd cases is not the only way-or even the
best way-of doing science; it's a lot of fn but it's not everyone's cup
of tea. But it's an eccentricity that has remained with me since childhood,
and fortunately I have been able to turn it into an advantage. Clinical
neurology, in particular, is fll of such examples that have been ignored
by the "establishment" because they don't really ft received wisdom. I
have discovered, to my delight, tat many of them are diamonds in the
rough.
For example, those who are suspcious of the claims of mind- body
medicine should consider multiple personality disorders. Some clinicians
say that patients can actually "change" their eye structure when assuming
diferent personas-a nearsighted person becomes farsighted, a blue-eyed
person becomes brown-eyed-or that the patient's blood chemistry
changes along with personality ( high blood glucose level with one and
normal glucose level with another) . There are also case descriptions of
people's hair turning white, literally overnight, afer a severe psycholog
ical shock and of pious nuns' developing stigmata on their palms in ec
static union with Jesus. I fnd it surprising that despite three decades of
research, we are not even sure whether these phenomena are real or
bogus. Given all the hints that there is something interesting going on,
why not examine these claims in greater detail? Are they like alien ab
duction and spoon bending, or are they genuine anomalies-like X rays
or bacterial transformation4-that may someday drive paradigm shifs
and scientifc revolutions?
I was personally drawn into medicine, a discipline fll of ambiguities,
because its Sherlock Holmes style of inquiry greatly appealed to me.
Diagnosing a patient's problem remains as much an art as a science,
calling into play powers of obseration, reason and all the human senses.
I recall one professor, Dr. K. V. Thiruvengadam, instrcting us how to
identit disease by j ust smelling the patient-the unmistakable, sweetish
nail polish breath of diabetic ketosis; the freshly baked bread odor of
typhoid fever; the stale- beer stench of scrofla; the newly plucked chicken
feathers aroma of rubella; the foul smell of a lung abscess; and the am
monialike Windex odor of a patient in liver failure. (And today a pedia
trician might add the grape j uice smell of Pseudomonas infection in
children and the sweaty-feet smell of isovaleric acidemia. ) Inspect the
fngers careflly, Dr. Thiruvengadam told us, because a small change in
T H E P HAN T O M WI T H I N I 7
the angle between the nail bed and the fnger can herald the onset of a
malignant lung cancer long before more ominous clinical signs emerge.
Remarkably, this telltale sign-clubbing-disappears instantly on the op
erating table as the surgeon removes the cancer, but, even to this day,
we have no idea why it occurs. Another teacher of mine, a professor of
neurology, would insist on our diagnosing Parknson' s disease with our
eyes closed-by simply listening to the patients' footsteps ( patients with
this disorder have a characteristic shufing gait) . This detectivelike aspect
of clinical medicine is a dying art in this age of high-tech medicine, but
it planted a seed in my mind. By careflly observing, listening, touching
and, yes, even smelling the patient, one can arrive at a reasonable diag
nosis and merely use laboratory tests to confrm what is already known.
Finally, when studying and treating a patient, it is the physician's duty
always to ask himself, "Wat does it feel like to be in the patient's shoes? "
"Wat i f I were? " I n doing this, I have never ceased to be amazed at
the courage and forttude of many of my patients or by the fact that,
ironically, tragedy itself can sometimes enrich a patient's life and give it
new meaning. For this reason, even though many of the clinical tales
you will hear are tinged wit sadness, equally ofen they are stories of
the triumph of the human spirit over adversity, and there is a strong
undercurrent of optimism. For example, one patient I saw-a neurologist
from New York-suddenly at the age of sixty started experiencing epi
leptic seizures arising from his right temporal lobe. The seizures were
alarming, of course, but to his amazement and delight he found himself
becoming fascinated by poetry, for the frst time in his life. In fact, he
began thinking in verse, producing a voluminous outfow of rhyme. He
said that such a poetic view gave him a new lease on life, a fresh start
just when he was starting to feel a bit j aded. Does it follow from this
example that all of us are unflflled poets, as many new age gurus and
mystics assert? Do we each have an untapped potential for beautifl verse
and rhyme hidden in the recesses of our right hemisphere? If so, is there
any way we can unleash this latent ability, short of having seizures?
Before we meet the patients, crack mysteries and speculate about brain
organization, I'd like to take you on a short guided tour of the human
brain. These anatomical signposts, which I promise to keep simple, will
help you understand the many new explanatons for why neurological
patients act the way they do.
It's almost a cliche these days to say that the human brain is the most
8 I P HAN T O MS I N T H E B RAI N
Fige l.l
complexly organized form of matter in the universe, and there is actually
some truth to this. If you snip away a section of brain, say, from the
convoluted outer layer called the neocortex and peer at it under a mi
croscope, you'll see that it is composed of neurons or nere cells-the
basic fnctional units of the nerous system, where information is ex
changed. At birth, the typical brain probably contains over one hundred
billion neurons, whose number slowly diminishes with age.
Each neuron has a cell body and tens of thousands of tiny branches
called dendrites, which receive information from other neurons. Each
neuron also has a primary axon (a proj ection that can travel long dis
tances in the brain) for sending data out of the cell, and axon terminals
for communication with other cells.
If you look at Figure l.l, you'll notice that neurons make contacts
with other neurons, at points called synapses. Each neuron makes any
where from a thousand to ten thousand synapses with other neurons.
These can be either on or of, excitatory or inhibitory. That is, some
synapses turn on the j uice to fre things up, whereas others release j uices
that calm everything down, in an ongoing dance of staggering complex
ity. A piece of your brain the size of a grain of sand would contain one
hundred thousand neurons, two million axons and one billion synapses,
all "talking to" each other. Given these fgures, it's been calculated that
the number of possible brain states-the number of permutations and
combinations of activity that are theoretically possible-exceeds the
number of elementary particles in the universe. Given this complexity,
Frontl lob
(a)
Motor cortex Central lissure
T H E P HA N T O M WI T H I N I 9
(b)
Fige 1.2 Gross anatomy of the human brain. (a) Shows the left side of the left
hemisphere. Notice the four lobes: fontal, parietal, temporal and occipital. Te
frontal is separated from the parietal by the central or rolandic sulcus ( furrow or
fssure), and the temporal from the parietal by the lateral or slvian fssure. (b)
Shows the inner surface of the left hemisphere. Notice the conspicuous corpus cal
losum (black) and the thalamus (white) in the middle. Te corpus callosum bridges
the to hemispheres. (c) Shows the two hemispheres of the brain viewed down the
top. (a) Rmachandran; (b) and (c) redrawn from Zek, 1993.
how do we begin to understand the fnctions of the brain? Obviously,
understanding the structure of the nervous system is vital to understand
ing its fnctions5-and so I will begin with a brief survey of the anatomy
of the brain, which, for our purposes here, begins at the top of the spinal
cord. This region, called the medulla oblongata, connects the spinal cord
to the brain and contains clusters of cells or nuclei that control critical
fnctions like blood pressure, heart rate and breathing. The medulla con
nects to the pons (a kind of bulge) , which sends fbers into the cerebel
lum, a fst-sized structure at the back of the brain that helps you carry
out coordinated movements . Atop these are the two enormous cerebral
hemispheres-the famous walnut-shaped halves of the brain. Each half
is divided into four lobes-frontal , temporal , parietal and occipital-that
you will learn much more about in coming chapters ( Figure 1. 2) .
Each hemisphere controls the movements of the muscles ( for example,
those in your arm and leg) on the opposite side of your body. Your right
brain makes your lef arm wave and your lef brain allows your right leg
l 0 I P HA N T O MS I N T H E B RA I N
to kick a ball. The two halves of the brain are connected by a band of
fbers called the corpus callosum. Wen this band is cut, the two sides
can no longer communicate; the result is a syndrome that ofers insight
into the role each side plays in cognition. The outer part of each hemi
sphere is composed of cerebral cortex: a thin, convoluted sheet of cells,
six layers thick, that is scrunched into ridges and frrows like a caulifower
and packed densely inside the skull .
Right in the center of the brain is the thalamus. It is thought to be
evolutionarily more primitive than the cerebral cortex and is ofen de
scribed as a "relay station" because all sensory information except smell
passes through it before reaching the outer cortical mantle. Interposed
between the thalamus and the cortex are more nuclei, called basal ganglia
(with names like the putamen and caudate nucleus ) . Finally, on the foor
of the thalamus is the hypothalamus, which seems to be concerned with
regulating metabolic fnctions, hormone production, and various basic
drives such as aggression, fear, and sexuality.
These anatomical facts have been known for a long time, but we still
have no clear idea of how the brain works. 6 Many older theories fall into
two warring camps-modularity and holism-and the pendulum has
swng back and forth between these two extreme points of view for the
last three hundred years. At one end of the spectrum are modularists,
who believe that diferent parts of the brain are highly specialized for
mental capacities. Thus there is a module for language, one for memory,
one for math ability, one for face recognition and maybe even one for
detecting people who cheat. Moreover, they argue, these modules or
regions are largely autonomous. Each does its own job, set of compu
tations, or whatever, and then-like a bucket brigade-passes its output
to the next module in line, not "talking" much to other regions .
At the other end of the spectrum we have "holism, " a theoretical
approach that overlaps with what these days is called "connectionism. "
This school of thought argues that the brain fnctions as a whole and
that any one part is as good as any other part. The holistic view is de
fended by the fact that many areas, especially cortical regions, can be
recruited for multiple tasks. Everything is connected to everything else,
say the holists, and so the search for distinct modules is a waste of time.
My own work with patients suggests that these two points of view are
not mutually exclusive-that the brain is a dynamic structure that em
ploys both "modes" in a marelously complex interplay. The grandeur
of the human potential is visible only when we take all the possibilities
into account, resisting the temptation to fall into polarized camps or to
T H E P HAN T O M WI T H I N I l l
ask whether a given fnction is localized or not localized? As we shall
see, it's much more usefl to tackle each problem as it comes along and
not get hung up taking sides.
Each view in its extreme form is in fact rather absurd. A an analogy,
suppose you are watching the program Bayatch on television. Were is
Bayatch localized? Is it in the phosphor glowing on the T screen or
in the dancing electrons inside the cathode-ray tube? Is it in the electro
magnetic waves being transmitted through air? Or is it on the celluloid
flm or video tape in the studio from which the show is being transmit
ted? Or maybe it's in the camera that's looking at the actors in the scene?
Most people recognize right away that this is a meaningless question.
You might be tempted to conclude therefore that Bayatch is not lo
calized ( there is no Bayatch "module") in any one place-that it per
meates the whole universe-but that, too, is absurd. For we know it is
not localized on the moon or in my pet cat or in the chair I'm sitting
on ( even though some of the electromagnetic waves may reach these
locations ) . Clearly the phosphor, the cathode-ray tube, the electromag
netic waves and the celluloid or tape are all much more directly involved
in this scenario we call Bayatch than is the moon, a chair or my cat.
This example illustrates that once you understand what a television
program really is, the question "Is it localized or not localized? " recedes
into the background, replaced with the question "How does it work? "
But it's also clear that looking at the cathode-ray tube and electron gun
may eventually give you hints about how the television set works and
picks up the Bayatch program as it is aired, whereas examining the
chair you are sittng on never will . So localization is not a bad place to
start, so long as we avoid the pitfall of thinking that it holds all the
answers.
So it is with many of the currently debated issues concerning brain
fnction. Is language localized? Is color vision? Laughter? Once we un
derstand these fnctions better, the question of "where" becomes less
important than te question of "how. " A it now stands, a wealth of
empirical evidence supports the idea that there are indeed specialized
parts or modules of the brain for various mental capacities. But the real
secret to understanding the brain lies not only in unraveling the structure
and fnction of each module but in discovering how they interact with
each other to generate the whole spectrum of abilities that we call human
nature.
Here is where the patients with bizarre neurological conditions come
into the picture. Like the anomalous behavior of the dog that did not
1 2 I P H A N T O MS I N T H E B RA I N
bark when the crime was being committed, providing Sherlock Holmes
with a clue as to who might have entered the house on the night of the
murder, the odd behavior of these patients can help us solve the mystery
of how various parts of the brain create a usefl representation of the
external world and generate the illusion of a "self' that endures in space
and time.
To help you get a feel for this way of doing science, consider these
colorfl cases-and the lessons drawn from them-taken from the older
neurological literature.
More than ffy years ago a middle- aged woman walked into the clinic
of Kurt Goldstein, a world-renowned neurologist with keen diagnostic
skills. The woman appeared normal and conversed fuently; indeed, noth
ing was obviously wrong with her. But she had one extraordinary com
plaint-every now and then her lef hand would fy up to her throat and
try to strangle her. She ofen had to use her right hand to wreste the
lef hand under control, pushing it down to her side-much like Peter
Sellers portraying Dr. Strangelove. She sometimes even had to sit on the
murderous hand, so intent was it on trying to end her life.
Not surprisingly, the woman's primary physician decided she was men
tally disturbed or hysterical and sent her to several psychiatrists for treat
ment. Wen they couldn' t help, she was dispatched to Dr. Goldstein,
who had a reputation for diagnosing difcult cases. Aer Goldstein ex
amined her, he established to his satisfaction that she was not psychotic,
mentally disturbed or hysterical . She had no obvious neurological defcits
such as paralysis or exaggerated reflexes. But he soon came up with an
explanation for her behavior: Like you and me, the woman had two
cerebral hemispheres, each of which is specialized for diferent mental
capacities and controls movements on the opposite side of the body. The
two hemispheres are connected by a band of fbers called the corpus
callosum that allows the two sides to communicate and stay "in sync. "
But unlike most of ours, this woman's right hemisphere (which con
trolled her lef hand) seemed to have some latent suicidal tendencies-a
genuine urge to kill herself. Initially these urges may have been held in
check by "brakes"-inhibitory messages sent across the corpus callosum
from the more rational lef hemisphere. But if she had sufered, as Gold
stein surmised, damage to the corpus callosum as the result of a stroke,
that inhibition would be removed. The right side of her brain and its
murderous lef hand were now free to attempt to strangle her.
T H E P HA N T O M WI T H I N I 1 3
This explanation is not as far-fetched as it seems, since it's been well
known for some time that the right hemisphere tends to be more emo
tionally volatile than the lef. Patients who have a stroke in the lef brain
are ofen anxious, depressed or worried about their prospects for recov
ery. The reason seems to be that with the lef brain injured, their right
brain takes over and frets about everything. In contrast, people who suf
fer damage to the right hemisphere tend to be blissflly indiferent to
their own predicament. The lef hemisphere just doesn't get all that up
set. ( More on this in Chapter 7. )
Wen Goldstein arrived at his diagnosis, i t must have seemed like
science fction. But not long afer that ofce visit, the woman died

ud
denly, probably from a second stroke ( no, not from strangling herself) .
A autopsy confrmed Goldstein's suspicions: Prior to her Strangelovean
behavior, she had sufered a massive stroke in her corpus callosum, so
that the lef side of her brain could not "talk to" nor exert its usual
control over the right side. Goldstein had unmasked the dual nature of
brain fnction, showing that the two hemispheres are indeed specialized
for diferent tasks.
Consider next the simple act of smiling, something we all do every
day in social situations. You see a good friend and you grin. But what
happens when that friend aims a camera at your face and asks you to
smile on command? Instead of a natural expression, you produce a hid
eous grimace. Paradoxically, an act that you perform efortlessly dozens
of times each day becomes extraordinarily difcult to perform when
someone simply asks you to do it. You might think it's because of em
barrassment. But that can't be the answer because if you walk over to
any mirror and try smiling, I assure you that the same grimace will ap
pear.
The reason these two kinds of smiles difer is that diferent brain
regions handle them, and only one of them contains a specialized "smile
circuit. " A spontaneous smile is produced by the basal ganglia, clusters
of cells found between the brain's higher cortex (where thinking and
planning take place) and the evolutionarily older thalamus. When you
encounter a friendly face, the visual message from that face eventually
reaches the brain's emotional center or limbic system and is subsequently
relayed to the basal ganglia, which orchestrate the sequences of facial
muscle activity needed for producing a natural smile. When this circuit
is activated, your smile is genuine. The entire cascade of events, once set
in motion, happens in a faction of a second without the thinking parts
of your cortex ever being involved.
1 4 I P HAN T O MS I N T H E B RAI N
But what happens when someone asks you to smile while takng your
photograph? The verbal instruction from the photographer is received
and understood by the higher thinking centers in the brain, including
the auditory cortex and language centers. From there it is relayed to the
motor cortex in the front of the brain, which specializes in producing
voluntary skilled movements, like playing a piano or combing your hair.
Despite its apparent simplicity, smiling involves the carefl orchestration
of dozens of tiny muscles in the appropriate sequence. As far as the motor
cortex ( which is not specialized for generating natural smiles ) is con
cerned, this is as complex a feat as playing Rchmaninof tough it never
had lessons, and therefore it fails utterly. Your smile is forced, tight,
unnatural .
Evidence for two diferent "smile circuits" comes from brain-damaged
patients. Wen a person sufers a stroke in the right motor cortex-the
specialized brain region that helps orchestrate complex movements on
the lef side of the body-problems crop up on the lef. Asked to smile,
the patient produces that forced, unnatural grin, but now it's even more
hideous; it's a half smile on the right side of the face alone. But when
this same patient sees a beloved friend or relative walk through the door,
her face erupts into a broad, natural smile using both sides of the mouth
and face. The reason is that her basal ganglia have not been damaged by
the stroke, so the special circuit for making symmetrical smiles is intact. 8
Very rarely, one encounters a patient who has apparently had a small
stroke, which neither he nor anyone else notices until he tries to smile.
All of a sudden, his loved ones are astonished to see that only one half
of his face is grinning. Ad yet when the neurologist instructs him to
smile, he produces a symmetrical, albeit unnatural grin-the exact con
verse of the previous patient. This fellow, it turns out, had a tiny stroke
that only afected his basal ganglia selectively on one side of the brai n.
Yawning provides frther proof for specialized circuitry. As noted,
many stroke victims are paralyzed on the right or lef side of their bodies,
depending on where the brain inj ury occurs . Voluntary movements on
the opposite side are permanently gone. And yet when such a patient
yawns, he stretches out both arms spontaneously. Much to his amaze
ment, his paralyzed arm suddenly springs to life! It does so because a
diferent brain pathway controls the arm movement during the yawn
a pathway closely linked to the respiratory centers in the brain stem.
Sometimes a tiny brain lesion-damage to a mere speck of cells among
billions-can produce far-reaching problems that seem grossly out of
proportion to the size of the injur. For example, you may think that
T H E P HA N T O M WI T H I N I 1 5
memory involves the entire brain. Wen I say the word "rose, " it evokes
all sorts of associations: perhaps images of a rose garden, the frst time
someone ever gave you a rose, the smell , the sofness of petals, a person
named Rose and so on. Even the simple concept of "rose" has many
rich associations, suggesting that the whole brain must surely be involved
in laying down every memory trace.
But the unforunate story of a patient kown as H. M. suggests oth
erwise.9 Because H. M. sufered from a particularly intractable form of
epilepsy, his doctors decided to remove "sick" tissue from both sides of
his brain, including two tiny seahorse-shaped structures (one on each
side) called the hippocampus, a structure that controls the laying. down
of new memories. We only know this because afer the surgery, H. M.
could no longer form new memories, yet he could recall everything that
happened before the operation. Doctors now treat the hippocampus with
greater respect and would never knowingly remove it from both sides of
the brain (Figure 1 . 3) .
Although I have never worked directly with H. M. , I have ofen seen
patients with similar forms of amnesia resulting from chronic alcoholism
or hypoxia (oxygen staration in the brain following surgery) . Talking to
them is an uncanny experience. For example, when I greet the patient,
he seems intelligent and articulate, talks normally and may even discuss
philosophy with me. If l ask him to add or subtract, he can do so without
trouble. He's not emotionally or psychologically disturbed and can dis
cuss his family and their various activities with ease.
Then I excuse myself to go to the restroom. When I come back, there
is not a glimmer of recognition, no hint that he's ever seen me before
in his life.
"Do you remember who I am? "
"No. "
I show him a pen. "What i s this? "
"A fountain pen. "
"What color i s it? "
"It's red. "
I put the pen under a pillow on a nearby chair and ask him, "Wat
did I just do? "
He answers promptly, "You put the pen under that pillow. "
Then I chat some more, perhaps askng about his family. One minute
goes by and I ask, "I just showed you something. Do you remember
what it was? "
He looks puzzled. "No. "
1 6 / P H A N T O MS I N T H E B RA I N
Figre 1.3 Artist's rendering of a brain with the outer convoluted cortex rendered
partially transparent to allow inner structures to be seen. Te thalamus (dark) can
be seen in the middle, and interposed between it and the cortex are clusters of cells
caled the basal ganglia (not shown). Embedded in the front part of the temporal
lobe you can see the dark, almond-shaped amygdala, the ((gateway" to the limbic
sstem. In the temporal lobe you can also see the hippocampus (concerned with
memory). In addition to the amygdala, other parts of the limbic sstem such as the
hypothalamus (below the thalamus) can be seen. Te limbic pathways mediate
emotional arousal. The hemispheres are attached to the spinal cord by the brain
stem (consisting of medulla, pons and midbrain), and below the occipital lobes
is the cerebellum, concerned mainly with coordination of movements and timing.
From Brain, Mind and Behavior by Bloom and Laserson ( 1988) by Educa
tional Broadcasting Corporation. Used with permission from W. H. Freeman
and Company.
"Do you remember that I showed you an obj ect? Do you remember
where I put it? "
"No. " He has absolutely no recollection of my hiding the pen sixty
seconds earlier.
Such patients are, in efect, frozen in time in the sense they remember
T H E P HA N T O M WI T H I N I 1 7
only events that took place before the accident that injured them neu
rologically. They may recall their frst baseball game, frst date and college
graduation in elaborate detail , but nothing afer the injury seems to be
recorded. For example, if post accident they come upon last week's news
paper, they read it every day as if it were a brand-new paper each time.
They can read a detective novel again and again, each time enj oying the
plot and the surprise ending. I can tell them the same joke half a dozen
times and each time I come to the punch line, they laugh heartily (ac
tually, my graduate students do this too) .
These patients are telling us something very important-that a tny
brain structure called the hippocampus is absolutely vital for laying down
new memory traces in the brain (even though the actual memory traces
are not stored in the hippocampus ) . They illustrate the power of the
modular approach: In helping to narrow the scope of inquiry, if you want
to understand memory, look at the hippocampus. And yet, as we shall
see, studying the hippocampus alone will never explain all aspects of
memory. To understand how memories are retrieved at a moment's no
tice, how they are edited, pigeonholed (sometimes even censored! ) , we
need to look at how the hippocampus interacts with other brain struc
tures such as the frontal lobes, the limbic system (concerned with emo
tions ) and the structures in the brain stem (which allow you to attend
selectively to specifc memories ) .
The role of the hippocampus i n forming memories i s clearly estab
lished, but are there brain regions specialized in more esoteric abilities
like the "number sense" that is unique to humans? Not long ago I met
a gentleman, Bill Marshall , who had sufered a stroke a week earlier.
Cheerfl and on his way to recovery, he was only too happy to discuss
his life and medical condition. Wen I asked him to tell me about his
family, he named each of his children, listed their occupations and gave
many details about his grandchildren. He was fluent, intelligent and ar
ticulate-and not everyone is so soon afer a stroke.
"What was your occupation? " I asked Bill .
Bill replied, "I used to be an Air Force pilot. "
"What kind of plane did you fly? "
He named the plane and said, "It was the fastest man- made thing on
this planet at that time. " Then he told me how fast it flew and said that
it had been made before the introduction of jet engines.
At one point I said, "Okay, Bill, can you subtract seven from one
hundred? What's one hundred minus seven? "
He said, "Oh. One hundred minus seven? "
1 8 I P HA N T O MS I N T H E B RA I N
"Yeah. "
"Hmmm, one hundred minus seven. "
"Yes, one hundred minus seven. "
"So," said Bill . "One hundred. You want me to take away seven from
one hundred. One hundred minus seven. "
"Yes. "
"Ninety six? "
"No. "
"Oh, " he said.
"Let's try something else. What's seventeen minus three? "
"Seventeen minus three? You know I ' m not very good at this kind of
thing, " said Bill .
"Bill , " I said, "is the answer going to be a smaller number or a bigger
number? "
"Oh, a smaller number," he said, showing that he knew what sub-
traction is.
"Okay, so what's seventeen minus three? "
"Is i t twelve? " he said at last.
I started wondering whether Bill had a problem understanding what
a number is or the nature of numbers. Indeed, the question of numbers
is old and deep, going back to Pythagoras.
I asked him, "What is infnity? "
"Oh, that's the largest number there is. "
"Which number i s bigger: one hundred and one or ninety-seven?
He answered immediately: "One hundred and one is larger. "
"Wy? "
"Because there are more digits. "
This meant that Bill still understood, at least tacitly, sophisticated nu
merical concepts like place value. Also, even though he couldn't subtract
three from seventeen, his answer wasn't completely absurd. He said
"twelve, " not seventy-fve or two hundred, implying that he was still
capable of makng ballpark estimates.
Then I decided to tell him a little story: "The other day a man walked
into the new dinosaur exhibit hall at the American Museum of Natural
History in New York and saw a huge skeleton on display. He wanted to
know how old it was, so he went up to an old curator sitting in the
corner and said, 'I say, old chap, how old are these dinosaur bones? '
"The curator looked at the man and said, ' Oh they're sixty million
and three years old, sir. '
" 'Sixty million and three years old? I didn't know you could get that
T H E P H A N T O M WI T H I N I 1 9
precise with aging dinosaur bones. What do you mean, sixty million and
three years old? '
" ' Oh, well , ' he said, ' they gave me this j ob three years ago and at
that time they told me the bones were sixty million years old. ' "
Bill laughed out loud at the punch line. Obviously he understood far
more about numbers than one might have guessed. It requires a sophis
ticated mind to understand that joke, given that it involves what philos
ophers call the "fallacy of misplaced concreteness. "
I turned t o Bill and asked, "Well, why do you think that' s fnny? "
"Well, you know," he said, "the level of accuracy is inappropriate. "

Bill understands the j oke and the idea of infnity, yet he can' t subtract
three from seventeen. Does this mean that each of us has a number center
in the region of the lef angular gyrus (where Bill's stroke injury was
located) of our brain for adding, subtracting, multiplying and dividing?
I think not. But clearly this region-the angular grus-is somehow nec
essary for numerical computational tasks but is not needed for other
abilities such as short- term memory, language or humor. Nor, paradox
ically, is it needed for understanding the numerical concepts underlying
such computations . We do not yet know how this "arithmetic" circuit
in the angular gyrus works, but at least we now know where to look.
1 0
Many patients, like Bill, with dyscalculia also have an associated brain
disorder called fnger agnosia: They can no longer name which fnger the
neurologist is pointing to or touching. Is it a complete coincidence that
both arithmetic operations and fnger naming occupy adj acent bran
regions, or does it have something to do with the fact that we all learn
to count by using our fngers in early childhood? The obseration that
in some of these patients one fnction can be retained ( naming fngers)
while the other ( adding and subtracting) is gone doesn't negate the ar
gument that these two might be closely linked and occupy the same
anatomical niche in the brain. It's possible, for instance, that the two
fnctions are laid down in close proximity and were dependent on each
other during the learning phase, but in the adult each fnction can sur
vive without the other. In other words, a child may need to wiggle his
or her fngers subconsciously while counting, whereas you and I may not
need to do so.
These historical examples and case studies gleaned from my notes sup
port the view that specialized circuits or modules do exist, and we shall
encounter several additional examples in this book. But other equally
interesting questions remain and we'll explore these as well. How do the
modules actually work and how do they "talk to" each other to generate
2 0 I P H A N T O MS I N T H E B RA I N
conscious experience? To what extent is all this intricate circuitr in the
brain innately specifed by your genes or to what extent is it acquired
gradually as the result of your early experiences, as an infant interacts
with the world? ( This is the ancient "nature versus nurture" debate,
which has been going on for hundreds of years, yet we have barely
scratched the surfce in formulating an answer. ) Even if certain circuits
are hard-wired from birth, does it follow that they cannot be altered?
How much of the adult brain is modifable? To fnd out, let's meet Tom,
one of the frst people who helped me explore these larger questions.
CHAPTER 2
"Knowin
g
Where to Scratch"
My intention is to tell
of bodies changed
to di erent forms.
1e heavens and all below them,
Earth and her creatures,
Al change,
And we, part ofcreation,
Also must sufer change.
-OV
Tom Sorenson vividly recalls the horrifing circumstances that led to the
loss of his arm. He was driving home from soccer practice, tired and
hungry from the exercise, when a car in the opposite lane swered in
front of him. Brakes squealed, Tom' s car spun out of control and he was
thrown from the driver's seat onto the ice plant bordering the freeway.
A he was hurled through the air, Tom looked back and saw that his
hand was still in the car, "gripping" the seat cushion-severed from his
body like a prop in a Freddy Keger horror flm.
A a result of this gruesome mishap, Tom lost his lef arm just above
the elbow. He was seventeen years old, with j ust three months to go
until high school graduation.
In the weeks aferard, even though he knew that his arm was gone,
Tom could still feel its ghostly presence below the elbow. He could
wiggle each "fnger, " "reach out" and "grab" obj ects that were within
2 1
2 2 I P H AN T O MS I N T H E B RA I N
arm's reach. Indeed, his phantom arm seemed to be able to do anything
that the real arm would have done automatically, such as warding of
blows, breaking falls or patting his little brother on the back. Since Tom
had been lef-handed, his phantom would reach for the receiver when
ever the telephone rang.
Tom was not crazy. His impression that his missing arm was still there
is a classic example of a phantom limb-an arm or leg that lingers in
defnitely in the minds of patients long afer it has been lost in an accident
or removed by a surgeon. Some wake up from anesthesia and are in
credulous when told that their arm had to be sacrifced, because they still
vividly feel its presence. 1 Only when they look under the sheets do they
come to the shocking realization that the limb is really gone. Moreover,
some of these patients experience excrciating pain in the phantom arm,
hand or fngers, so much so that they contemplate suicide. The pain is
not only unrelenting, it's also untreatable; no one has the foggiest idea
of how it arises or how to deal with it.
A a physician I was aware that phantom limb pain poses a serious
clinical problem. Chronic pain in a real body part such as the j oint aches
of arthritis or lower backache is difcult enough to treat, but how do
you treat pain in a nonexistent limb? A a scientist, I was also curious
about why the phenomenon occurs in the frst place: Why would an arm
persist in the patient's mind long afer it had been removed? Why doesn't
the mind simply accept the loss and "reshape" the body image? To be
sure, this does happen in a few patients, but it usually takes years or
decades. Why decades-why not just a week or a day? A study of this
phenomenon, I realized, might not only help us understand the question
of how the brain copes with a sudden and massive loss, but also help
address the more fndamental debate over nature versus nurture-the
extent to which our body image, as well as other aspects of our minds,
are laid down by genes and the extent to which they are modifed by
experience.
The persistence of sensation i n limbs long afer amputation had been
noticed as far back as the sixteenth century by the French surgeon A
broise Pare, and, not surprisingly, there is an elaborate folklore surround
ing this phenomenon. Aer Lord Nelson lost his right arm during an
unsuccessfl attack on Santa Cruz de Tenerife, he experienced compel
ling phantom limb pains, including the unmistakable sensation of fngers
digging into his phantom palm. The emergence of these ghostly sensa
tions in his missing limb led the sea lord to proclaim that his phantom
was "direct evidence for the existence of the soul . " For if an arm can
" KN O WI N G WHE R E T O S C RATC H " I 2 3
exist afer it is removed, why can' t the whole person surive physical
annihilation of the body? It is proof, Lord Nelson claimed, for the ex
istence of the spirit long afer it has cast of its attire.
The eminent Philadelphia physician Silas Weir MitchelF frst coined
the phrase "phantom limb" afer the Civil War. In those preantibiotic
days, gangrene was a common result of injuries and surgeons sawed in
fected limbs of thousands of wounded soldiers. They returned home
with the phantoms, setting of new rounds of speculaton about what
might be causing them. Weir Mitchell himself was so surprised by the
phenomenon that he published the frst article on the subj ect under a
pseudonym in a popular magazine called Lippincott's Journal rather than
risk facing the ridicule from his colleagues that might have ensued had
he published in a professional medical j ournal . Phantoms, when you
think about it, are a rather spooky phenomenon.
Since Weir Mitchell's time there have been all kinds of speculations
about phantoms, ranging from the sublime to the ridiculous. A recently
as ffeen years ago, a paper in the Canadian Journal of Pschiatr stated
that phantom limbs are merely the result of wishfl thinking. The authors
argued that the patient desperately wants his arm back and therefore
experiences a phantom-in much the same way that a person may have
recurring dreams or may even see "ghosts" of a recently deceased parent.
This argument, as we shall see, is utter nonsense.
A second, more popular explanation for phantoms is that the frayed
and curled-up nerve endings in the stump ( neuromas) that originally
supplied the hand tend to become infamed and irritated, thereby fooling
higher brain centers into thinking that the missing limb is still there.
Though there are far too many problems with this nere irritation theory,
because it's a simple and convenient explanation, most physicians still
cling to it.
There are literally hundreds of fascinating case studies, which appear
in the older medical journal s. Some of the described phenomena have
been confrmed repeatedly and still cry out for an explanaton, whereas
others seem like far-fetched products of the writer's own imagination.
One of my favorites is about a patient who started experiencing a vivid
phantom arm soon afer amputation-nothing unusual so far-but afer
a few weeks developed a peculiar, gnawing sensation in his phantom.
Naturally he was quite puzzled by the sudden emergence of these new
sensations, but when he asked his physician why this was happening, the
2 4 I P H A N T O MS I N T H E B RA I N
doctor didn't kow and couldn't help. Finally, out of curiosity, the fellow
asked, "Whatever happened to my arm afer you removed it? " "Good
question, " replied the doctor, "you need to ask the surgeon. " So the
fellow called the surgeon, who said, "Oh, we usually send the limbs to
the morgue. " So the man called the morgue and asked, "What do you
do with amputated arms? " They replied, "We send them either to the
incinerator or to pathology. Usually we incinerate them. "
"Well , what did you do with this particular arm? With my arm? " They
looked at their records and said, "You know, it's fnny. We didn' t in
cinerate it. We sent it to pathology. "
The man called the pathology l ab. "Where i s my arm? " he asked again.
They said, "Well , we had too many arms, so we just buried it in the
garden, out behind the hospital . "
They took him t o the garden and showed him where the arm was
buried. Wen he exhumed it, he found it was crawling with maggots
and exclaimed, "Well, maybe that's why I' m feeling these bizarre sen
sations in my arm. " So he took the limb and incinerated it. Ad from
that day on, his phantom pain disappeared.
Such stories are fn to tell, especially around a campfre at night, but
they do very little to dispel the real mystery of phantom limbs. Athough
patients with this syndrome have been studied extensively since the turn
of the century, there's been a tendency among physicians to regard them
as enigmatic, clinical curiosities and almost no experimental work has
been done on them. One reason for this is that clinical neurology his
torically has been a descriptive rather than an experimental science. Neu
rologists of the nineteenth and early twentieth centuries were astute
clinical observers, and many valuable lessons can be learned from reading
their case reports. Oddly enough, however, they did not take the next
obvious step of doing experiments to discover what might be going on
in the brains of these patients; their science was Aristotelian rather than
Galilean. 3 Given how immensely successfl the experimental method has
been in almost every other science, isn't it high time we imported it into
neurology?
Like most physicians, I was intrigued by phantoms the very frst time
I encountered them and have been puzzled by them ever since. In ad
dition to phantom arms and legs-which are common among ampu
tees-! had also encountered women with phantom breasts afer radical
mastectomy and even a patient with a phantom appendix: The charac
teristic spasmodic pain of appendicitis did not abate afer surgical re
moval , so much so that the patient refsed to believe that the surgeon
" KN O WI N G WH E RE T O S C RAT C H " I 2 5
had cut it out! As a medical student, I was just as bafled as the patients
themselves, and the textbooks I consulted only deepened the mystery. I
read about a patient who experienced phantom erections afer his penis
had been amputated, a woman with phantom menstrual cramps follow
ing hysterectomy, and a gentleman who had a phantom nose and face
afer the trigeminal nerve innervating his face had been severed in an
accident.
All these clinical experiences lay tucked away in my brain, dormant,
until about six years ago, when my interest was rekindled by a scientifc
paper published in 1991 by Dr. Tim Pons of the National Institutes of
Health, a paper that propelled me into a whole new direction of research

and eventually brought Tom into my laboratory. But before I continue
with this part of the story, we need to look closely at the anatomy of the
brain-particularly at how various body parts such as limbs are mapped
onto the cerebral cortex, the great convoluted mantle on the surface of
the brain. This will help you understand what Dr. Pons discovered and,
in turn, how phantom limbs emerge.
Of the many strange images that have remained with me from my
medical school days, perhaps none is more vivid than that of the de
formed little man you see in Figure 2. 1 draped across the surface of the
cerebral cortex-the so- called Penfeld homunculus. The homunculus is
the artist's whimsical depiction of the manner in which diferent points
on the body surface are mapped onto the surface of the brain-the gro
tesquely deformed features are an attempt to indicate that certain body
parts such as the lips and tongue are grossly overrepresented.
The map was drawn from information gleaned from real human
brains. During the 1 940s and 1950s, the brilliant Canadian neurosur
geon Wilder Penfeld performed extensive brain surgeries on patients un
der local anesthetic ( there are no pain receptors in the brain, even though
it is a mass of nere tissue) . Ofen, much of the brain was exposed during
the operation and Penfeld seized this opportunity to do experiments that
had never been tried before. He stimulated specifc regions of the pa
tients' brains with an electrode and simply asked them what they felt. All
kinds of sensations, images, and even memories were elicited by the elec
trode and the areas of the brain that were responsible could be mapped.
Among other things, Penfel
d
found a narrow strip running from top
to bottom down both sides of the brain where his electrode produced
sensations localized in various parts of the body. Up at the top of the
brain, in the crevice that separates the two hemispheres, electrical stim
ulation elicited sensations in the genitals. Nearby stimuli evoked sensa-
2 6 I P HA N T O MS I N T H E B RA I N
(a) (b)
Fige 2.1 (a) Te representation of the body surface on the surface of the human
brain (as discovered by Wilder Penfeld) behind the central sulcus. Tere are many
such maps, but for clarit only one is shown here. Te homunculus ( ((little man")
is upside down for the most part, and his feet are tucked onto the medial surface
(inner surface) of the parietal lobe near the very top, whereas the face is down near the
bottom of the outer surface. Te face and hand occup a disproportionately large share
of the map. Notice, also that the face area is below the hand area instead of being
where it should-near the neck-and that the genitals are represented below the foot.
Could this provide an anatomical explanation of foot fetishes ? (b) A whimsical three
dimensional model of the Penfeld homunculus-the little man in the brain-depict
ing the representation of body parts. Notice the gross overrepresentation of mouth and
hands. Reprinted with permission from the British Museum, London.
tions in the feet. A Penfeld followed this strip down from the top of
the brain, he discovered areas that receive sensations from the legs and
trunk, from the hand ( a large region with a very prominent representa
tion of the thumb) , the face, the lips and fnally the thorax and voice box.
This "sensory homunculus, " as it is now called, forms a greatly distorted
representation of the body on the surface of the brain, with the parts
that are particularly important taking up disproportionately large areas.
For example, the area involved with the lips or with the fngers takes up
as much space as the area involved with the entire trunk of the body.
This is presumably because your lips and fngers are highly sensitive to
touch and are capable of very fne discrimination, whereas your trunk is
considerably less sensitive, requiring less cortical space. For the most part,
the map is orderly though upside down: The foot is represented at the
top and the outstretched arms are at the bottom. However, upon close
" KN O WI N G WHE R E T O S C RAT C H " I 2 7
examination, you will see that the map is not entirely continuous . The
face is not near the neck, where it should be, but is below the hand.
The genitals, instead of being beteen the thighs, are located below the
foot. 4
These areas can be mapped out with even greater precision in other
animals, parcularly in monkeys. The researcher inserts a long thin needle
made of steel or tungsten into the monkey' s somatosensory cortex-the
strip of brain tissue described earlier. If the needle tip comes to lie right
next to the cell body of a neuron and if that neuron is active, it will
generate tiny electrical currents that are picked up by the needle electrode
and amplifed. The signal can be displayed on an oscilloscope, maing it
possible to monitor the activity of that neuron.
For example, if you put an electrode into the monkey's somatosensory
cortex and touch the monkey on a specifc part of its body, the cell will
fre. Each cell has its territor on the body surface-its own small patch
of skin, so to speak-to which it responds. We call this the cell' s receptive
feld. A map of the entire body surface exists in the brain, with each half
of the body mapped onto the opposite side of the bran.
While animals are logical experimental subjects in which to examine
the detailed structure and fnction of the brain's sensory regions, they
have one obvious problem: Monkeys can' t talk. Therefore, they cannot
tell the experimenter, as Penfeld's patients could, what they are feeling.
Thus a large and important dimension is lost when animals are used in
such experiments.
But despite this obvious limitation, a great deal can be learned by
doing the right kinds of experments. For instance, as we've noted, one
important question concerns nature versus nurture: Are these body maps
on the surface of the brain fxed, or can they change with experience as
we grow from newborns to infancy, through adolescence and into old
age? And even if the maps are already there at birth, to what extent can
they be modifed in the adult?5
It was these questions that prompted Tim Pons and his colleagues to
embark on their research. Their strategy was to record signals fom the
brains of monkeys who had undergone dorsal rhizotomy-a procedure
in which all the nerve fbers carrying sensory information from one arm
into the spinal cord are completely severed. 6 Eleven years afer the sur
gery, they anesthetized the animals, opened their skulls and recorded
from the somatosensory map. Since the monkey' s paralyzed arm was not
sending messages to the brain, you would not expect to record any sig-
2 8 I P HA N T O MS I N T H E B RA I N
nals when you touch the monkey's useless hand and record from the
"hand area" of the brain. There should be a big patch of silent cortex
corresponding to the afected hand.
Indeed, when the researchers stroked the useless hand, there was no
activity in this region. But to their amazement they found that when
they touched the monkey's face, the cells in the brain corresponding to
the "dead" hand started fring vigorously. ( So did cells corresponding
to the face, but those were expected to fre. ) It appeared that sensory
information from the monkey's face not only went to the face area of
the cortex, as it would in a normal animal , but it had also invaded the
territory of the paralyzed hand!
The implications of this fnding are astonishing: It means that you can
change the map; you can alter the brain circuitry of an adult animal , and
connections can be modifed over distances spanning a centimeter or
more.
Upon reading Pons's paper, I thought, "My God! Might this be an
explanation for phantom limbs? " Wat did the monkey actually "feel"
when its face was being stroked? Since its "hand" cortex was also being
excited, did it perceive sensations as arising from the useless hand as well
as the face? Or would it use higher brain centers to reinterpret the sen
sations correctly as arising from the face alone? The monkey of course
was silent on the subject.
It takes years to train a monkey to carry out even very simple tasks,
let alone signal what part of its body is being touched. Then it occurred
to me that you don't have to use a monkey. Why not answer the same
question by touching the face of a human patient who has lost an arm?
I telephoned my colleagues Dr. Mark Johnson and Dr. Rita Finkelstein
in orthopedic surgery and asked, "Do you have any patients who have
recently lost an arm? "
That i s how I came to meet Tom. I called him up right away and
asked whether he would like to participate in a study. Although initially
shy and reticent in his mannerisms, Tom soon became eager to partici
pate in our ex
p
eriment. I was carefl not to tell him what we hoped to
fnd, so as not to bias his responses . Even though he was distressed by
"itching" and painfl sensations in his phantom fngers, he was cheerfl ,
apparently pleased that he had surived the accident.
With Tom seated comfortably in my basement laborator, I placed a
blindfold over his eyes because I didn't want him to see where I was
touching him. Then I took an ordinary Q- tip and started stroking various
" KN O WI N G WH E RE T O S C RATC H " I 2 9
parts of his body surface, asking him to tell me where he felt the sensa
tions. ( My graduate student, who was watching, thought I was crazy. )
I swabbed his cheek. "Wat do you feel ? "
"You are touching my cheek. "
"Aything else? "
"Hey, you know it's fnny," said Tom. "You're touching my missing
thumb, my phantom thumb. "
I moved the Q-tip to his upper lip. "How about here? "
"You're touching my index fnger. Ad my upper lip. "
"Really? Ae you sure? "
"Yes. I can feel i t both places. "
"How about here? " I stroked his lower j aw with the swab.
"That's my missing pinkie. "
I soon found a complete map of Tom's phantom hand-on his face!
I realized that what I was seeing was perhaps a direct perceptual correlate
of the remapping that Tim Pons had seen in his monkeys . For there is
no other way of explaining why touching an area so far away from the
stump-namely, the face-should generate sensations in the phantom
hand; the secret lies in the peculiar mapping of body parts in the brain,
with the face lying right beside the hand. 7
I continued this procedure until I had explored Tom' s entire body
surface. Wen I touched his chest, right shoulder, right leg or lower
back, he felt sensations only in those places and not in the phantom. But
I also found a second, beautiflly laid out "map" of his missing hand-
tucked onto his lef upper arm a few inches above the line of amputation
( Figure 2. 2) . Stroking the skin surface on this second map also evoked
precisely localized sensations on the individual fngers : Touch here and
he says, "Oh, that's my thumb, " and so on.
Wy were there two maps instead of j ust one? If you look again at
the Penfeld map, you'll see that the hand area in the brain is fanked
below by the face area and above by the upper arm and shoulder area.
Input from Tom's hand area was lost afer the amputation, and conse
quently, the sensor fbers originating from Tom's face-which normally
activate only the face area in his cortex-now invaded the vacated ter
ritory of the hand and began to drive the cells there. Therefore, when I
touched Tom' s face, he also felt sensations in his phantom hand. But if
the invasion of the hand cortex also results from sensory fbers that nor
mally innerate the brain region above the hand cortex ( that is, fbers
that originate in the upper arm and shoulder) , then touching points on
3 0 I P H A N T O MS I N T H E B RA I N
Fige 2.2 Points on the body surface that yielded referred sensations in the phan
tom hand (this patient)s left arm had been amputated ten years prior to our testing
him). Notice that there is a complete map of all the fngers (labeled 1 to 5) on the
face and a second map on the upper arm. Te sensory input from these to patches
of skin is now apparently activating the hand territory of the brain (either in the
thalamus or in the cortex). So when these points are touched, the sensations are felt
to arise fom the missing hand as well.
the upper arm should also evoke sensations in the phantom hand. And
indeed I was able to map out these points on the arm above Tom' s
stump. So, this sort of arrangement is precisely what one would expect:
One cluster of points on the face that evoke sensations in the phantom
and a second cluster on the upper arm, corresponding to the two body
parts that are represented on either side ( above and below) of the hand
representation in the brain. 8
It' s not ofen in science ( especially neurology) that you can make a
simple prediction like this and confrm it with a few minutes of explo
ration using a Q-tip. The existence of two clusters of points suggests
strongly that remapping of the knd seen in Pons' s monkeys also occurs
in the human brain. But there was still a nagging doubt: How can we
" KN O WI N G WH E RE T O S C RAT C H " I 3 1
be sure that such changes are actually taking place-that the map is really
changing in people like Tom? To obtain more direct proof, we took
advantage of a modern neuroimaging technique called magnetoence
phalography ( MEG) , which relies on the principle that if you touch dif
ferent body parts, the localized electrical activity evoked in the Penfeld
map can be measured as changes in magnetic felds on the scalp. The
maj or advantage of the technique is that it is noninvasive; one does not
have to open the patient's scalp to peer inside the brain.
Using MEG, it is relatively easy in just a two- hour session to map out
the entire body surface on the brain surface of any person willing to sit
under the magnet. Not surprisingly, the map that results is quite similar
to the original Penfeld homunculus map, and there is ver little variation
from person to person in the gross layout of the map. Wen we con
ducted MEGs on four arm amputees, however, we found that the maps
had changed over large distances, j ust as we had predicted. For example,
a glance at Figure 2. 3 reveals that the hand area ( hatched) is missing in
the right hemisphere and has been invaded by the sensory input from
the face ( in white) and upper arm ( in gray) . These obserations, which
I made in collaboration with a medical student, Tony Yang, and the
neurologists Chris Gallen and Floyd Bloom, were in fact the frst direct
demonstration that such large-scale changes in the organization of the
brain could occur in adult humans.
The implications are staggering. First and foremost, they suggest that
brain maps can change, sometmes with astonishing rapidity. This fding
flatly contradicts one of the most widely accepted dogmas in neurology
the fxed nature of connections in the adult human brain. It had always
been assumed that once this circuitry, including the Penfeld map, has
been laid down in fetal life or in early infancy, there is very little one can
do to modif it in adulthood. Indeed, this presumed absence of plasticity
in the adult brain is ofen invoked to explain why there is so little re
covery of fnction afer brain inj ury and why neurological ailments are
so notoriously difcult to treat. But the evidence from Tom shows
contrary to what is taught in textbooks-that new, highly precise and
fnctionally efective pathways can emerge in the adult brain as early as
four weeks afer inj ury. It certainly doesn't follow that revolutionary new
treatments for neurological syndromes will emerge from this discovery
right away, but it does provide some grounds for optimism.
Second, the fndings may help explain the very existence of phantom
limbs. The most popular medical explanation, noted earlier, is that neres
that once supplied the hand begin to innervate the stump. Moreover,
3 2 I P HA N T O MS I N T H E B RA I N
Figre 2. 3 Magnetoencephalography (MEG) image superimposed on a magnetic
resonance (MR) image of the brain in a patient whose riht arm was amputated
below the elbow. Te brain is viewed from the top. Te riht hemisphere shows
normal activation of the hand (hatched), face (black) and upper arm (white} areas
of the cortex corresponding to the Penfeld map. In the left hemisphere there is no
activation corresponding to the missing riht hand, but the activity from the face
and upper arm has now ((spread" to this area.
these frayed nerve endings form little clumps of scar tissue called neu
romas, which can be very painfl . Wen neuromas are irritated, the the
ory goes, they send impulses back to the original hand area in the brain
so that the brain is "fooled" into thinking the hand is still there: hence
the phantom limb and the notion that the accompanying pain arises
because the neuromas are painfl .
On the basis of this tenuous reasoning, surgeons have devised various
treatments for phantom limb pain in which they cut and remove neu
romas . Some patients experience temporary relief, but surprisingly, both
the phantom and the associated pain usually return with a vengeance.
To alleviate this problem, sometimes surgeons perform a second or even
a third amputation ( making the stump shorter and shorter), but when
you think about this, it's logically absurd. Wy would a second ampu-
' ' KN O WI N G WHE R E T O S C RAT C H ' ' I 3 3
tation help? You'd simply expect a second phantom, and indeed that's
usually what happens; it's an endless regress problem.
Surgeons even perform dorsal rhizotomies to treat phantom limb pain,
cutting the sensory nerves going into the spinal cord. Sometimes it
works; sometimes it doesn't. Others try the even more drastic procedure
of cutting the back of the spinal cord itself-a cordotomy-to prevent
impulses from reaching the bain, but that, too, is ofen inefective. Or
they will go all the way into the thalamus, a brain relay station that
processes signals before they are sent to the cortex, and again fnd that
they have not helped the patient. They can chase the phantom farther
and farther into the brain, but of course they'll never fnd it.
Why? One reason, surely, is that the phantom doesn't exist in any one
of these areas; it exists in more central parts of the brain, where the
remapping has occurred. To put it crudely, the phantom emerges not
from the stump but from the face and j aw, because every time Tom
smiles or moves his face and lips, the impulses activate the "hand" area
of his cortex, creating the illusion that his hand is s,till there. Stimulated
by all these spurious signals, Tom's brain literally hallucinates his arm,
and perhaps this is the essence of a phantom limb. If so, the only way
to get rid of the phantom would be to remove his j aw. (And if you think
about it, that wouldn't help either. He' d probably end up with a phan
tom j aw. It's that endless regress problem again. )
But remapping can't be the whole story. For one thing, it doesn't
explain why Tom or other patients experience the feeling of being able
to move their phantoms voluntarily or why the phantom can change its
posture. Where do these movement sensations originate? Second, re
mapping doesn't account for what both doctor and patient are most
seriously concerned about-the genesis of phantom pain. We'll explore
these two subj ects in the next chapter.
Wen we think of sensations arising from skin we usually only think
of touch. But, in fact, distinct neural pathways that mediate sensations
of warmth, cold and pain also originate on the skin surface. These sen
sations have their own target areas or maps in the brain, but the paths
used by them may be interlaced with each other in complicated ways. If
so, could such remapping also occur in these evolutionarily older path
ways quite independently of the remapping that occurs for touch? In
other words, is the remapping seen in Tom and in Pons's monkeys pe
culiar to touch, or does it point to a very general principle-would it
occur for sensations like warmth, cold, pain or vibration? And if such
remapping were to occur would there be instances of accidental "cross-
3 4 I P HA N T O MS I N T H E B RA I N
wiring" so that a touch sensation would evoke warmth or pain? Or would
they remain segregated? The question of how millions of neural connec
tions in the brain are hooked up so precisely during development-and
the extent to which this precision is preserved when they are reorganized
afer injury-is of great interest to scientists who are trying to understand
the development of pathways in the brain.
To investigate this, I placed a drop of warm water on Tom's face. He
felt it there immediately but also said that his phantom hand felt distinctly
warm. Once, when the water accidentally trickled down his face, he ex
claimed with considerable surprise that he could actually feel the warm
water trickling down the length of his phantom arm. He demonstrated
this to me by using his normal hand to trace out the path of the water
down his phantom. In all my years in neurology clinics, I had never seen
anything quite so remarkable-a patient systematically mislocalizing a
complex sensation such as a "trickle" from his face to his phantom hand.
These experiments imply that highly precise and organized new con
nections can be formed in the adult brain in a few days. But they don't
tell us how these new pathways actually emerge, what the underlying
mechanisms are at the cellular level .
I can think of two possibilities. First, the reorganization could involve
sprouting-the actual growth of new branches from nere fbers that nor
mally innerate the face area toward cells in the hand area in the cortex. If
this hypothesis were true, this would be quite remarkable since it is difcult
to see how highly organized sprouting could take place over relatively long
distances ( in the brain several millimeters might as well be a mile) and in
such a short period. Moreover, even if sprouting occurs, how would the
new fbers "know" where to go? One can imagine a higgledy-piggledy
jumble of connections, but not precisely organized pathways.
The second possibility is that there is in fact a tremendous redundancy
of connections in the normal adult brain but that most of them are
nonfnctional or have no obvious fnction. Like resere troops, they may
be called into action only when needed. Thus even in healthy normal
adult brains there might be sensory inputs from the face to the brain's
face map and to the hand map area as well . If so, we must assume that
this occult or hidden input is ordinarily inhibited by the sensory fbers
arriving from the real hand. But when the hand is removed, this silent
input originating from the skin on the face is unmasked and allowed to
express itself so that touching the face now activates the hand area and
leads to sensations in the phantom hand. Thus every time Tom whistles,
he might feel a tingling in his phantom arm.
" KN O WI N G WH E RE T O S C RAT C H " I 3 5
We have no way at present of easily distinguishing between these two
theories, although my hunch is that both mechanisms are at work. Aer
all , we had seen the efect in Tom in less than four weeks and this seems
too short a time for sprouting to take place. My colleague at the Massa
chusetts General Hospital Dr. David Borsook9 has seen similar efects in a
patient just twent-four hours afer amputation, and there is no question
of sprouting's occurring in such a short period. The fnal answer to this will
come from simultaneously tracking perceptual changes and brain changes
( using imaging) in a patient over a period of several days. IfBorsook and I
are right, the completely static picture of these maps that you get fom
looking at textbook diagrams is highly misleading and we need to rethink
the meaning of brain maps completely. Far from signaling a specifc loca
tion on the skin, each neuron in the map is in a state of dynamic equilib
rium with other adj acent neurons; its signifcance depends strongly on
what other neurons in the vicinity are doing ( or not doing) .
These fndings raise an obvious question: What i f some body part i s lost
other than the hand? Will the same knd of remapping occur? When my
studies on Tom were frst published, I got many letters and phone calls
from amputees wanting to kow more. Some of them had been told that
phantom sensations are imaginary and were relieved to learn that that isn't
true. ( Patients always fnd it comforting to kow that there is a logical ex
planation for their otherwise inexplicable symptoms; nothing is more in
sulting to a patient than to be told that his pain is "all in the mind. ")
One day I got a call from a young woman i n Boston. "Dr. Rma
chandran, " she said, "I' m a graduate student at Beth Israel Hospital and
for several years I've been studying Parkinson's disease. But recently I
decided to switch to the study of phantom limbs. "
"Wonderfl , " I said. "The subject has been ignored far too long. Tell
me what you are studying. "
"Last year I had a terrible accident on my uncle's farm. I lost my lef leg
below the knee and I've had a phantom limb ever since. But I'm calling to
thank you because your article made me understand what is going on. "
She cleared her throat. "Something really strange happened to me afer
the amputation that didn't make sense. Every time I have sex I experience
these strange sensations in my phantom foot. I didn't dare tell anybody be
cause it's so weird. But when I saw your diagrams, that in the brain the
foot is next to the genitals, it became instantly clear to me. "
She had experienced and understood, as few of us ever will, the re
mapping phenomenon. Recall that in the Penfeld map the foot is beside
the genitals. Therefore, if a person loses a leg and is then stimulated in
3 6 I P HAN T O MS I N T H E B RA I N
the genitals, she will experience sensations in the phantom leg. This is
what you'd expect if input from the genital area were to invade the
territory vacated by the foot.
The next day the phone rang again. This time it was an engineer from
Arkansas.
"Is this Dr. Rmachandran? "
"Yes. "
"You know, I read about your work i n the newspaper, and it's really
exciting. I lost my leg below the knee about two months ago but there's
still something I don't understand. I'd like your advice. "
"What's that? "
"Well, I feel a little embarrassed to tell you this. "
I knew what he was going to say, but unlike the graduate student, he
didn't know about the Penfeld map.
"Doctor, every time I have sexual intercourse, I experience sensations
in my phantom foot. How do you explain that? My doctor said it doesn't
make sense. "
"Look," I said. "One possibility i s that the genitals are right next to
the foot in the body' s brain maps. Don't worry about it. "
He laughed nerously. "Al that's fne, doctor. But you stll don't
understand. You see, I actually experience my orgasm in my foot. And
therefore it's much bigger than it used to be because it's no longer j ust
confned to my genitals. "
Patients don't make up such stories. Ninety-nine percent of the time
they're telling the truth, and if it seems incomprehensible, it's usually
because we are not smart enough to fgure out what's going on in their
brains. This gentleman was telling me that he sometmes enj oyed sex
more afer his amputation. The curious implication is that it's not j ust
the tactile sensation that transferred to his phantom but the erotic sen
sations of sexual pleasure as well. (A colleague suggested I ttle this book
"The Man Who Mistook His Foot for a Penis . ")
This makes me wonder about the basis of foot fetishes i n normal peo
ple, a subj ect that-although not exactly central to our mental life
everyone is curious about. ( Madonna's book, Sex, has a whole chapter
devoted to the foot. ) The traditional explanation for foot fetshes comes,
not surprisingly, from Freud. The penis resembles the foot, he argues,
hence the fetish. But if that's the case, why not some other elongated
body part? Why not a hand fetish or a nose fetsh? I suggest that the
reason is quite simply that in the brain the foot lies right next to the
genitalia. Maybe even many of us so-called normal people have a bit of
" KN O WI N G WH E RE T O S C RATC H " I 3 7
cross-wiring, which would explain why we like to have our toes sucked.
The journeys of science are ofen tortuous with many unexpected twists
and turns, but I never suspected that I would begin seekng an expla
nation for phantom limbs and end up explaining foot fetishes as well.
Given these assumptions, other predictions follow. 1 0 What happens
when the penis is amputated? Carcinoma of the penis is sometimes
treated with amputation, and many of these patients experience a phan
tom penis-sometimes even phantom erections ! In such cases you would
expect that stimulation of the feet would be felt in the phantom penis.
Would such a patient fnd tap dancing especially enjoyable?
What about mastectomy? A Italian neurologist, Dr. Salvatore Aglioti ,
recently found that a certain proportion of women with radical mastec
tomies experience vivid phantom breasts. So, he asked himself, what body
parts are mapped next to the breast? By stimulating adj acent regions on
the chest he found that parts of the sternum and clavicle, when touched,
produce sensations in the phantom nipple. Moreover, this remapping
occurred j ust two days afer surgery.
Aglioti also found to his surprise that one third of the women with
radical mastectomies tested reported tingling, erotic sensations in their
phantom nipples when their earlobes were stimulated. But this happened
only in the phantom breast, not in the real one on the other side. He
speculated that in one of the body maps ( there are others besides the
Penfeld map) the nipple and ear are next to each other. This makes you
wonder why many women report feeling erotic sensations when their
ears are nibbled during sexual foreplay. Is it a coincidence, or does it
have something to do with brain anatomy? ( Even in the original Penfeld
map, the genital area of women is mapped right next to the nipples. )
A less titillating example of remapping also involving the ear came
fom Dr. A. T. Caccace, a neurologist who told me about an extraor
dinary phenomenon called gaze tinnitus.
People with this condition have a weird problem. When they look to
the lef ( or right) , they hear a ringing sound. Wen they look straight
ahead, nothing happens. Physicians have known about this syndrome for
a long time but were stymied by it. Why does it happen when the eyes
deviate? Why does it happen at all ?
Aer reading about Tom, Dr. Caccace was struck by the similarity
between phantom limbs and gaze tinnitus, for he knew that his patients
had sufered damage to the auditory nere-the major conduit connect
ing the inner ear to the brain stem. Once in the brain stem the auditory
nere hooks up with the auditory nucleus, which is right next to another
3 8 I P H A N T O MS I N T H E B RA I N
structure called the oculomotor nerve nucleus. This second, adj acent
structure sends commands to the eyes, instructing them to move. Eu
reka! The mystery is solved. U Because of the patient's damage, the au
ditory nucleus no longer gets input from one ear. Aons from the eye
movement center in the cortex invade the auditory nucleus so that every
time the person's brain sends a command to move the eyes, that com
mand is sent inadvertently to the auditory nere nucleus and translated
into a ringing sound.
The study of phantom limbs ofers fascinating glimpses of the archi
tecture of the brain, its astonishing capacity for growth and renewal 1 2
and may even explain why playing footsie i s so enj oyable. But about half
the people with phantom limbs also experience the most unpleasant man
ifestation of the phenomenon-phantom limb pain. Real pain, such as
the pain of cancer, is hard enough to treat; imagine the challenge of
treating pain in a limb that isn't there! There is very little that can be
done, at the moment, to alleviate such pain, but perhaps the remapping
that we obsered with Tom may help explain why it happens. We know,
for instance, that intractable phantom pain may develop weeks or months
afer the limb is amputated. Perhaps as the brain adj usts and cells slowly
make new connections, there is a slight error in the remapping so that
some of the sensory input from touch receptors is accidentally connected
to the pain areas of the brain. If this were to happen, then every time
the patient smiled or accidentally brushed his cheek, the touch sensations
would be experienced as excruciating pain. This is almost certainly not
the whole explanation for phantom pain ( as we shall see in the next
chapter), but it's a good place to start.
A Tom lef my ofce one day, I couldn't resist asking him an obvious
question. During the last four weeks, had he ever noticed any of these
peculiar referred sensations in his phantom hand when his face had been
touched-when he shaved every morning, for example?
"No, I haven't," he replied, "but you know, my phantom hand some
times itches like crazy and I never know what to do about it. But now, "
he said, tapping his cheek and winkng at me, "I know exactly where to
scratch! "
CHAPTER 3
Chasin
g
the Phantom
You never identi yoursel with the shadow cast by your body,
or with its reflection, or with the body you see in a dream or
in your imagination. Terefore you should not identi
yoursel with this living body, either.
-SHNKR (A. D. 788-820), Viveka Chudamani
(Vedic scriptures)
When a reporter asked the famous biologist J. B. S. Haldane what his
biological studies had taught him about God, Haldane replied, "The
creator, if he exists, must have an inordinate fondness for beetles, " since
there are more species of beetles than any other group ofliving creatures.
By the same token, a neurologist might conclude that God is a cartog
rapher. He must have an inordinate fondness for maps, for everywhere
you look in the brain maps abound. For example, there are over thirty
diferent maps concerned with vision alone. Likewise for tactile or so
matic sensations-touch, j oint and muscle sense-there are several maps,
including, as we saw in the previous chapter, the famous Penfeld ho
munculus, a map draped across a vertical strip of cortex on the sides of
the brain. These maps are largely stable throughout life, thus helping
ensure that perception is usually accurate and reliable. But, as we have
seen, they are also being constantly updated and refned in response to
3 9
4 0 I P HA N T O MS I N T H E B RA I N
vagaries of sensory input. Recall that when Tom's arm was amputated,
the large patch of cortex corresponding to his missing hand was "taken
over" by sensory input from his face. If I touch Tom's face, the sensory
message now goes to two areas-the original face area ( as it should) but
also the original "hand area. " Such brain map alterations may help ex
plain the appearance of Tom's phantom limb soon afer amputation.
Every time he smiles or experiences some spontaneous activity of facial
nerves, the activity stimulates his "hand area," thereby fooling him into
thinking that his hand is still there.
But this cannot be the whole story. First, it doesn't explain why so
many people with phantoms claim that they can move their "imaginary"
limbs voluntarily. Wat is the source of this illusion of movement? Sec
ond, it doesn't explain the fact that these patients sometimes experience
intense agony in the missing limb, the phenomenon called phantom pain.
Third, what about a person who is born without an arm? Does remap
ping also occur in his brain, or does the hand area of the cortex simply
never develop because he never had an arm? Would he experience a
phantom? Can someone be born with phantom limbs?
The idea seems preposterous, but if there' s one thing I've learned over
the years it's that neurology is fll of surprises. A few months afer our
frst report on phantoms had been published, I met Mirabelle Kumar, a
twenty- fve-year-old Indian graduate student, referred to me by Dr. Sath
yajit Sen, who knew about my interest in phantoms . Mirabelle was born
without arms. Al she had were two short stumps dangling from her
shoulders. X rays revealed that these stumps contained the head of the
humerus or upper arm bone, but that there were no signs of a radius or
ulna. Even the tiny bones of her hands were missing, although she did
have a hint of rudimentary fngernails in the stump.
Mirabelle walked into my ofce on a hot summer day, her face fushed
from walking up three flights of stairs . A attractive, cheerfl young lady,
she was also extremely direct with a "don't pity me" attitude writ large
on her face.
As soon as Mirabelle was seated, I began asking simple questions:
where she was from, where she went to school, what she was interested
in and so forth. She quickly lost patience and said, "Look, what do you
really want to know? You want to know if I have phantom limbs, right?
Let's cut the crap. "
I said, "Well, yes, as a matter of fact, we do experiments on phantom
limbs. We're interested in . . . "
She interrupted. "Yes. Absolutely. I've never had arms. All I've ever
CH A S I N G T H E P HA N T O M I 4 1
had are these. " Defly, using her chin to help her in a practiced move,
she took of her prosthetic arms, clattered them onto my desk and held
up her stumps . "And yet I 've always experienced the most vivid phantom
limbs, from as far back in my childhood as I can remember. "
I was skeptical . Could it be that Mirabelle was j ust engaging in wishfl
thinking? Maybe she had a deep-seated desire to conform, to be normal .
I was beginning to sound like Freud. How could I be sure she was not
making it up?
I asked her, "How do you know that you have phantom limbs? "
"Well, because as I' m talking to you, they are gesticulating. They
point to objects when I point to things, just like your arms and hands. "
I leaned forard, captivated.
"Another interesting thing about them, doctor, is that they're not as
long as they should be. They're about six to eight inches too short . "
"How do you know that? "
"Because when I put on my artifcial arms, my phantoms are much
shorter than they should be, " said Mirabelle, looking me squarely in the
eye. "My phantom fngers should ft into the artifcial fngers, like a
glove, but my arm is about six inches too short. I fnd this incredibly
frustrating because it doesn't feel natural . I usually end up asking the
prosthetist to reduce the length of my artifcial arms, but he says that
would look short and fnny. So we compromise. He gives me limbs that
are shorter than most but not so absurdly short that they look strange. "
She pointed to one of her prosthetic arms lying on the desk, s o I could
see. "They're a little bit shorter than normal arms, but most people don' t
notice it. "
To me this was proof that Mirabelle' s phantoms were not wishfl
thinking. If she wanted to be like other people, why would she want
shorter- than-normal arms? There must be something going on inside her
brain that was giving rise to the vivid phantom experience.
Mirabelle had another point. "When I walk, doctor, my phantom arms
don't swing like normal arms, like your arms. They stay frozen on the
side, like this . " She stood up, letting her stumps drop straight down on
both sides. "But when I talk, " she said, "my phantoms gesticulate. In
fact, they're moving now as I speak. "
This i s not as mysterious as i t sounds. The brain region responsible
for smooth, coordinated swinging of the arms when we walk is quite
diferent from the one that controls gesturing. Perhaps the neural cir
cuitry for arm swinging cannot survive very long without continuous
nurturing feedback fom the limbs. It simply drops out or fails to develop
4 2 I P HAN T O MS I N T H E B RA I N
when the arms are missing. But the neural circuitr for gesticulation
activated during spoken language-might be specifed by genes during
development. ( The relevant circuitry probably antedates spoken lan
guage. ) Remarkably, the neural circuitry that generates these commands
in Mirabelle' s brain seems to have surived intact, despite the fact that
she has received no visual or kinesthetic feedback from those "arms" at
any point in her life. Her body keeps telling her, "There are no arms,
there are no arms, " yet she continues to experience gesticulation.
This suggests that the neural circuitry for Mirabelle's body image must
have been laid down at least partly by genes and is not strictly dependent
on motor and tactile experience. Some early medical reports claim that
patients with limbs missing from birth do not experience phantoms.
What I saw in Mirabelle, however, implies that each of us has an inter
nally hard-wired image of the body and limbs at birth-an image that
can survive indefnitely, even in the face of contradictory information
from the senses. 1
In addition to these spontaneous gesticulations, Mirabelle can also
generate voluntary movements in her phantom arms, and this is also true
of patients who lose arms in adulthood. Like Mirabelle, most of these
patients can "reach out" and "grab" obj ects, point, wave good- bye,
shake hands, or perform elaborate skilled maneuvers with the phantom.
They know it sounds crazy since they realize that the arm is gone, but
to them these sensory experiences are very real .
I didn't realize how compelling these felt movements could be until
I met John McGrath, an arm amputee who telephoned me afer he had
seen a television news story on phantom limbs. A accomplished amateur
athlete, John had lost his lef arm j ust below the elbow three years earlier.
"Wen I play tennis," he said, "my phantom will do what it's supposed
to do. It'll want to throw the ball up when I serve or it will try to give
me balance in a hard shot. It's always trying to grab the phone. It even
waves for the check in restaurants, " he said with a laugh.
John had what is kown as a telescoped phantom hand. It felt as if it
were attached directly to his stump with no arm in between. However,
if an object such as a teacup were placed a foot or two away from the
stump, he could try to reach for it. Wen he did this, his phantom no
longer remained attached to the stump but felt as if it were zooming out
to grab the cup.
On a whim I started thinking, Wat if I ask John to reach out and
grab this cup but pull it away from him before he "touches" it with his
phantom? Will the phantom stretch out, like a cartoon character's rub-
C HAS I N G T H E P HA N T O M I 4 3
bery arm, or will it stop at a natural arm' s length? How far can I move
the cup away before John will say he can't reach it? Could he grab the
moon? Or will the physical limitations that apply to a real arm also apply
to the phantom?
I placed a cofee cup in front of John and asked him to grab it. Just
as he said he was reaching out, I yanked away the cup.
"Ow! " he yelled. "Don't do that! "
"Wat's the matter? "
"Don't do that," he repeated. "I had j ust got my fngers around the
cup handle when you pulled it. That really hurts! "
Hold on a minute. I wrench a real cup from phantom fngers and the
person yells, ouch! The fngers were illusory, of course, but the pain was
real-indeed, so intense that I dared not repeat the experiment.
My experience with John started me wondering about the role of
vision in sustaining the phantom limb experience. Wy would merely
"seeing" the cup be pulled away result in pain? But before we answer
this question, we need to consider why anyone would experience move
ments in a phantom limb. If you close your eyes and move your arm,
you can of course feel its position and movement quite vividly partly
because of j oint and muscle receptors. But neither John nor Mirabelle
has such receptors. Indeed, they have no arm. So where do these sen
sations originate?
Ironically, I got the frst clue to this mystery when I realized that many
phantom limb patients-perhaps one third of them-are not able to
move their phantoms. Wen asked, they say, "My arm is cast in cement,
doctor" or "It's immobilized in a block of ice. " "I try to move my
phantom, but I can' t, " said Irene, one of our patients . "It won't obey
my mind. It won't obey my command. " Using her intact arm, Irene
mimicked the position of her phantom arm, showing me how it was
frozen in an odd, twisted position. It had been that way for a whole year.
She always worried that she would "bump" it when entering doorways,
and that it would hurt even more.
How can a phantom-a nonexistent limb-be paralyzed? It sounds
like an oxymoron.
I looked up the case sheets and found that many of these patients had
had preexisting pathology in the nerves entering the arm from the spinal
cord. Their arms really had been paralyzed, held in a sling or cast for a
few months and later been amputated simply because they were con
stantly getting in the way. Some patients were advised to get rid of it,
perhaps in a misguided attempt to eliminate the pain in the arm or to
4 4 I P HA N T O MS I N T H E B RA I N
correct postural abnormalities caused by the paralyzed arm or leg. Not
surprisingly, afer the operations these patients ofen experience a vivid
phantom limb, but to their dismay the phantom remains locked in the
same position as before the amputation, as though a memory of the
paralysis is carried over into the phantom limb.
So here we have a paradox. Mirabelle never had arms i n her entire
life, yet she can move her phantoms. Irene had j ust lost her arm a year
earlier and yet she cannot generate a flicker of movement. What's going
on here?
To answer this question we need to take a closer look at the anatomy
and physiology of the motor and sensory systems in the human brain.
Consider what happens when you or I close our eyes and gesticulate. We
have a vivid sense of our body and of the position of our limbs and their
movements . Two eminent English neurologists, Lord Russell Brain and
Henry Head (yes, these are their real names ) , coined the phrase "body
image" for this vibrant, internally constructed ensemble of experiences
the internal image and memory of one's body in space and time. To
create and maintain this body image at any given instant, your parietal
lobes combine information from many sources : the muscles, j oints, eyes
and motor command centers.
When you decide to move your hand, the chain of events leading to
its movements originates in the frontal lobes-especially in the vertical
strip of cortical tissue called the motor cortex. This strip lies just in front
of the frrow that separates the frontal lobe from the parietal lobe. Like
the sensory homunculus that occupies the region j ust behind this frrow,
the motor cortex contains an upside-down "map" of the whole body
except that it is concerned with sending signals to the muscles rather
than receiving signals from the ski n.
Experiments show that the primary motor cortex is concerned mainly
with simple movements like wiggling your fnger or smacking your lips.
A area immediately in front of it, called the supplementary motor area,
appears to be in charge of more complex skills such as waving good- bye
and grabbing a banister. This supplementary motor area acts like a kind
of master of ceremonies, passing specifc instructions about the proper
sequence of required movements to the motor cortex. Nerve impulses
that will then direct these movements travel from the motor cortex down
the spinal cord to the muscles on the opposite side of the body, allowing
you to wave good- bye or put on lipstick.
Every time a "command" is sent from the supplementar motor area
to the motor cortex, it goes to the muscles and they move. 2 At the same
CH A S I N G T H E P HA N T O M I 4 5
time, identical copies of the command signal are sent to two other major
"processing" areas-the cerebellum and the parietal lobes-informing
them of the intended action.
Once these command signals are sent to the muscles, a feedback loop
is set in motion. Having received a command to move, the muscles ex
ecute the movement. In turn, signals from the muscle spindles and j oints
are sent back up to the brain, via the spinal cord, informing the cere
bellum and parietal lobes that "yes, the command is being performed
correctly. " These two structures help you compare your intention with
your actual performance, behaving like a thermostat in a servo-loop, and
modifing the motor commands as needed ( applying brakes if they are
too fast and increasing the motor outfow if it's too slow) . Thus inten
tions are transformed into smoothly coordinated movements.
Now let's return to our patients to see how all this relates to the
phantom experience. When John decides to move his phantom arm, the
front part of his brain still sends out a command message, since this par
ticular part of John's brain doesn't "know" that his arm is missing
even though John "the person" is unquestionably aware of the fact.
The commands continue to be monitored by the parietal lobe and are
felt as movements . But they are phantom movements carried out by a
phantom arm.
Thus the phantom limb experience seems to depend on signals from
at least two sources. The frst is remapping; recall that sensory input from
the face and upper arm actvates brain areas that correspond to the
"hand. " Second, each time the motor command center sends signals to
the missing arm, information about the commands is also sent to the
parietal lobe containing our body image. The convergence of informa
tion from these two sources results in a dynamic, vibrant image of the
phantom arm at any given instant-an image that is continuously up
dated as the arm "moves . "
I n the case of an actual arm there i s a third source of information,
namely, the impulses from the joints, ligaments and muscle spindles of
that arm. The phantom arm of course lacks these tissues and their signals,
but oddly enough this fact does not seem to prevent the brain from being
fooled into thinking that the limb is moving-at least for the frst few
months or years afer amputation.
This takes us back to an earlier question. How can a phantom limb
be paralyzed1 Why does it remain "frozen" afer amputation1 One pos
sibility is that when the actual limb is paralyzed, lying in a sling or brace,
the brain sends its usual commands-move that arm, shake that leg.
4 6 I P HA N T O MS I N T H E B RA I N
The command is monitored by the parietal lobe, but this time it does
not receive the proper visual feedback. The visual system says, "nope,
this arm is not moving. " The command is sent out again-arm, move.
The visual feedback returns, informing the brain repeatedly that the arm
isn't moving. Eventually the brain learns that the arm does not move
and a knd of "learned paralysis" is stamped onto the brain's circuitry.
Exactly where this occurs is not kown, but it may lie partly in motor
centers and partly in parietal regions concerned with body image. What
ever the physiological explanation turns out to be, when the arm is later
amputated, the person is stuck with that revised body image: a paralyzed
phantom.
If you can learn paralysis, is i t possible that you can unlearn i t? Wat
if Irene were to send a "move now" message to her phantom arm, and
every time she did so she got back a visual signal that it was moving;
that, yes, it was obeying her command? But how can she get visual feed
back when she doesn't have an arm? Can we trick her eyes into actually
seeing a phantom?
I thought about virtual reality. Maybe we could create the visual il
lusion that the arm was restored and was obeying her commands. But
that technology, costing over half a million dollars, would exhaust my
entire research budget with one purchase. Fortunately, I thought of a
way to do the experiment with an ordinary mirror purchased fom a fve
and-dime store.
To enable patients like Irene to perceive real movement in their non
existent arms, we constructed a virtual reality box. The box is made by
placing a vertical mirror inside a cardboard box with its lid removed. The
front of the box has two holes in it, through which the patient inserts
her "good hand" ( say, the right one) and her phantom hand ( the lef
one) . Since the mirror is in the middle of the box, the right hand is now
on the right side of the mirror and the phantom is on the lef side. The
patient is then asked to view the reflection of her normal hand in the
mirror and to move it around slightly until the reflection appears to be
superimposed on the felt position of her phantom hand. She has thus
created the illusion of observing two hands, when in fact she is only
seeing the mirror reflection of her intact hand. If she now sends motor
commands to both arms to make mirror symmetric movements, as if she
were conducting an orchestra or clapping, she of course "sees" her phan
tom moving as well . Her brain receives confrming visual feedback that
the phantom hand is moving correctly in response to her command. Will
this help restore voluntary control over her paralyzed phantom?
CH A S I N G T H E P HA N T O M I 4 7
The frst person to explore this new world was Philip Martinez. In
1984 Philip was hurled of his motorcycle, going at forty-fve miles an
hour down the San Diego freeway. He skidded across the median, landed
at the foot of a concrete bridge and, getting up in a daze, he had the
presence of mind to check himself for inj uries. A helmet and leather
j acket prevented the worst, but Philip's lef arm had been severely torn
near his shoulder. Like Dr. Pons' s monkeys, he had a brachial avulsion
the nerves supplying his arm had been yanked of the spinal column. His
lef arm was completely paralyzed and lay lifeless in a sling for one year.
Finally, doctors advised amputation. The arm was just getting in the way
and would never regain fnction.
Ten years later, Philip walked into my ofce. Now in his midthirties,
he collects a disability beneft and has made a rather impressive reputation
for himself as a pool player, known among his friends as the "one- armed
bandit. "
Philip had heard about my experiments with phantom limbs i n local
press reports. He was desperate. "Dr. Ramachandran, " he said, "I' m
hoping you can help me. " He glanced down at his missing arm. "I lost
it ten years ago. But ever since I've had a terrible pain in my phantom
elbow, wrist and fngers. " Interviewing him frther, I discovered that
during the decade, Philip had never been able to move his phantom arm.
It was always fxed in an awkward position. Was Philip sufering from
learned paralysis? If so, could we use our virtual reality box to resurrect
the phantom visually and restore movements?
I asked Philip to place his right hand on the right side of the mirror
in the box and imagine that his lef hand ( the phantom) was on the lef
side. "I want you to move your right and lef arms simultaneously, " I
instructed.
"Oh, I can' t do that, " said Philip. "I can move my right arm but my
lef arm is frozen. Every morning when I get up, I try to move my
phantom because it's in this fnny position and I feel that moving it
might help relieve the pain. But," he said, looking down at his invisible
arm, "I have never been able to generate a ficker of movement in it. "
"Okay, Philip, but tr anyway. "
Philip rotated his body, shifing his shoulder, t o "insert" his lifeless
phantom into the box. Then he put his right hand on the other side of
the mirror and attempted to make synchronous movements . As he gazed
into the mirror, he gasped and then cried out, "Oh, my God! Oh, my
God, doctor! This is unbelievable. It's mind- boggling! " He was jumping
up and down like a kid. "My lef arm is plugged in again. It's as if I' m
4 8 I P H A N T O MS I N T H E B RA I N
in the past. Al these memories from so many years ago are fooding back
into my mind. I can move my arm again. I can feel my elbow moving,
my wrist moving. It's all moving again. "
Aer he calmed down a little I said, "Okay, Philip, now close your
eyes. "
"Oh, my, " he said, clearly disappointed. "It's frozen again. I feel my
right hand moving, but there's no movement in the phantom. "
"Open your eyes. "
"Oh, yes. Now it's moving again. "
I t was as though Philip had some temporary inhibition or block of
the neural circuits that would ordinarily move the phantom and the visual
feedback had overcome this block. More amazing still , these bodily sen
sations of the arm' s movements were revived instantly,3 even though they
had never been felt in the preceding ten years !
Though Philip' s response was exciting and provided some support for
my hypothesis about learned paralysis, I went home that night and asked
myself, "So what? So we have this guy moving his phantom limb again.
But it's a perfectly useless ability if you think about it-precisely the sort
of arcane thing that many of us medical researchers are sometmes ac
cused of working on. " I wouldn' t win a prize, I realized, for getting
someone to move a phantom limb.
But maybe learned paralysis is a more widespread phenomenon. 4 It
might happen to people with real limbs that are paralyzed, say, from a
stroke. Wy do people lose the use of an arm afer a stroke? Wen a
blood vessel supplying the brain gets clogged, the fbers that extend
from the front part of the brain down to the spinal cord are deprived
of oxygen and sustain damage, leaving the arm paralyzed. But in the
early stages of a stroke, the brain swells, temporarily causing some
neres to die of but leaving others simply stunned and "of-line, " so
to speak. During this time, when the arm is nonfnctional , the brain
receives visual feedback: "Nope, the arm is not moving. " Aer the
swelling subsides, it's possible that the patient's brain is stuck with a
form of learned paralysis. Could the mirror contraption be used to
overcome at least that component of the paralysis that is due to learn
ing? ( Obviously there is nothing one can do with mirrors to restore
paralysis caused by actual destruction of fbers . )
But before we could implement this kind of novel therapy for stroke
patients, we needed to ensure that the efect is more than a mere tem
porary illusion of movement in the phantom. ( Recall that when Philip
closed his eyes, the sense of movement in his phantom disappeared. )
CH A S I N G T H E P HA N T O M I 4 9
What if the patient were to practice with the box in order to receive
continuous visual feedback for several days? Is it conceivable that the
brain would "unlearn" its perception of damage and that movements
would be permanently restored?
I went back the next day and asked Philip, "Ae you willing to take
this device home and practice with it? "
"Sure, " said Philip. "I' d love to take it home. I fnd it very exciting
that I can move my arm again, even if only momentarily. "
So Philip took the mirror home. A week later I telephoned him.
"What's happening? "
"Oh, it's fn, doctor. I use i t for ten minutes every day. I put my
hand inside, wave it around and see how it feels. My girlfriend and I play
with it. It's very enj oyable. But when I close my eyes, it still doesn't
work. And if I don't use the mirror, it doesn't work. I know you want
my phantom to start moving again, but without the mirror it doesn' t. "
Three more weeks passed until one day Philip called me, very excited
and agitated. "Doctor," he exclaimed, "it's gone! "
"What's gone? " ( I thought maybe he had lost the mirror box. )
"My phantom i s gone. "
"What are you talkng about? "
"You know, my phantom arm, which I had for ten years. It doesn't
exist anymore. Al I have is my phantom fngers and palm dangling from
my shoulder! "
My immediate reaction was, Oh, no! I have apparently permanently
altered a person's body image using a mirror. How would this afect his
mental state and well- being? "Philip-does it bother you? "
"No no no no no no, " he said. "On the contrary. You know the
excruciating pain I always had in my elbow? The pain that tortured me
several times a week? Well, now I don't have an elbow and I don' t
have that pain anymore. But I still have my fngers dangling from my
shoulder and they still hurt. " He paused, apparently to let this sink in.
"Unfortunately, " he added, "your mirror box doesn't work anymore
because my fngers are up too high. Can you change the design to
eliminate my fngers? " Philip seemed to think I was some knd of ra
gician.
I wasn't sure I could help Philip with his request, but I realized that
this was probably the frst example in medical history of a successfl
"amputation" of a phantom limb! The experiment suggests that when
Philip's right parietal lobe was presented with conflicting signals-visual
feedback telling him that his arm is moving again while his muscles are
5 0 I P HA N T O MS I N T H E B RA I N
telling him the arm is not there-his mind resorted to a form of denial .
The only way his beleaguered brain could deal with this bizarre sensory
conflict was to say, "To hell with it, there is no arm! " Ad as a huge
bonus, Philip lost the associated pain in his phantom elbow as well, for
it may be impossible to experience a disembodied pain in a nonexistent
phantom. It's not clear why his fngers didn't disappear, but one reason
might be that they are overrepresented-like the huge lips on the Pen
feld map-in the somatosensory cortex and may be more difcult to
deny.
Movements and paralysis of phantom limbs are hard enough to ex
plain, but even more puzzling is the agonizing pain that many patients
experience in the phantom soon afer amputation, and Philip had
brought me face to face with this problem. What confuence of biological
circumstances could cause pain to erupt in a nonexistent limb? There are
several possibilities.
The pain could be caused by scar tissue or neuromas-little curled-up
clusters or clumps of nerve tissue in the stump. Irritation of these clumps
and frayed nere endings could be interpreted by the brain as pain in the
missing limb. When neuromas are removed surgically, phantom pain
sometimes vanishes, at least temporarily, but then insidiously it ofen
returns.
The pain could also result in part from remapping. Keep in mind that
remapping is ordinarily modality-specifc: That simply means that the
sense of touch follows touch pathways, and the feeling of warmth follows
warmth pathways, and so on. (A we noted, when I lightly stroke Tom's
face with a Q-tip, he feels me touching his phantom. When I dribble ice
water on his cheek, he feels cold on his phantom hand and when I warm
up the water he feels heat in the phantom as well as on his face. ) This
probably means that remapping doesn't happen randomly. The fbers
concerned with each sense must "know" where to go to fnd their ap
propriate targets. Thus in most people, including you, me and amputees,
one does not get cross-wiring.
But imagine what might happen if a slight error were to occur during
the remapping process-a tiny glitch in the blueprint-so that some of
the touch input is hooked up accidentally to pain centers. The patient
might experience severe pain every time regions around his face or upper
arm (rather than neuromas ) were brushed, even lightly. Such trivial
C HA S I N G T H E P HA N T O M I 5 1
touches could generate excruciating pain, all because a few fbers are in
the wrong place, doing the wrong thing.
Abnormal remapping could also cause pain two other ways . Wen we
experience pain, special pathways are activated simultaneously both to
carry the sensation and to amplif it or dampen it down as needed. Such
"volume control" ( sometimes called gate control ) is what allows us to
modulate our responses to pain efectively in response to changing de
mands ( which might explain why acupuncture works or why women in
some cultures don't experience pain during labor) . Among amputees, it's
entirely possible that these volume control mechanisms have gone awry
as a result of remapping-resulting in an echolike "wha wha" reverber
ation and amplifcation of pain. Second, remapping is inherently a path
ological or abnormal process, at least when it occurs on a large scale, as
afer the loss of a limb. It's possible that te touch synapses are not quite
correctly rewired and their activity could be chaotic. Higher brain centers
would then interpret the abnormal pattern of input as junk, which is
perceived as pain. In truth, we really don't know how the brain translates
patterns of nere activity into conscious experience, be it pain, pleasure
or color.
Finally, some patients say that the pain they felt in their limbs im
mediately prior to amputation persists as a knd of pain memory. For
example, soldiers who have grenades blow up in their hands ofen report
that their phantom hand is in a fxed position, clenching the grenade,
ready to toss it. The pain in the hand is excruciating-the same they felt
the instant the grenade exploded, seared permanently in their brains. In
London I once met a woman who told me she had experienced chil
blains-a frostbitelike pain due to cold weather-in her thumb for sev
eral months in her childhood. The thumb later became gangrenous and
was amputated. She now has a vivid phantom thumb and experiences
chilblains in it every time the weather turns cold. Another woman de
scribed arthritic pain in her phantom j oints. She'd had the problem be
fore her arm was amputated but it has continued in the absence of real
j oints, with the pain being worse when it gets damp and cold j ust as it
had in the real j oints before amputation.
One of my medical school professors told me a story that he swore
was true, the tale of another physician, an eminent cardiologist, who
developed a pulsating cramp in his leg caused by Buerger's disease-a
malady that produces constriction of arteries and intense, pulsing pain in
the calf muscles.
5 2 I P H A N T O MS I N T H E B RA I N
Despite many attempts at treatment, nothing eased the pain. Out of
sheer despair, the physician decided to have his leg amputated. He simply
couldn't live with the pain any longer. He consulted a surgeon colleague
and scheduled the operation, but to the surgeon's astonishment, he said
he had a special request: "Aer you amputate my leg, could you please
pickle it in a j ar of formaldehyde and give it to me? " This was eccentric,
to say the least, but the surgeon agreed, amputated the leg, put it in a
jar of preserative and gave it to the physician, who then put it in his
ofce and said, "Hah, at last, I can look at this leg and laugh at it and
say, 'I fnally got rid of you! ' "
But the leg had the last laugh. The pulsatile pains returned with a
vengeance in the phantom leg. The good doctor stared at his floating
limb in disbelief while it stared back at him, as if to mock all his eforts
to rid himself of it.
There are many such stories in circulation, illustrating the astonishing
specifcity of pain memories and their tendency to surface when a limb
is amputated. If this is the case, one can imagine being able to reduce
the incidence of pain afer amputation simply by inj ecting the limb with
a local anesthetic before surgery. ( This has been tried with some success . )
Pain is one of the most poorly understood of all sensory experiences.
It is a source of great frustration to patient and physician alike and can
emerge in many diferent guises. One especially enigmatic complaint fre
quently heard from patients is that ever now and then the phantom
hand becomes curled into a tight, white-knucked fst, fngers digging
into palm with all the fry of a prizefghter ready to deliver a knockout
blow.
Robert Townsend is an intelligent, ffy- fve-year-old engineer whose
cancer caused him to lose his lef arm six inches above the elbow. When
I saw him seven months afer the amputation, he was experiencing a
vivid phantom limb that would ofen go into an involuntary clenching
spasm. "It's like my nails are digging into my phantom hand, " said Rob
ert. "The pain is unbearable. " Even if he concentrated all his attention
on it, he could not open his invisible hand to relieve the spasm.
We wondered whether using the mirror box could help Robert elim
inate his spasms . Like Philip, Robert looked into the box, positioned his
good hand to superimpose its reflection over his phantom hand and, afer
making a fst with the normal hand, tried to unclench both hands si
multaneously. The frst time he did this, Robert exclaimed that he could
C H A S I N G T H E P HA N T O M I 5 3
feel the phantom fst open along with his good fst, simply as a result of
the visual feedback. Better yet, the pain disappeared. The phantom then
remained unclenched for several hours until a new spasm occurred spon
taneously. Without the mirror, his phantom would throb in pain for forty
minutes or more. Robert took the box home and tried the same trick
each time that the clenching spasm recurred. If he did not use the box,
he could not unclench his fst despite trying with all his might. If he
used the mirror, the hand opened instantly.
We have tried this treatment in over a dozen patients and it works
for half of them. They take the mirrored box home and whenever a
spasm occurs, they put their good hand into the box and open it and
the spasm is eliminated. But is it a cure? It's difcult to know. Pain is
notoriously susceptible to the placebo efect ( the power of suggestion) .
Perhaps the elaborate laboratory setting or the mere presence of a
charismatic expert on phantom limbs is all you need in order to elim
inate the pain and it has nothing to do with mirrors. We tested this
possibility on one patient by giving him a harmless batter pack that
generates an electric current. Whenever the spasms and abnormal pos
tures occurred, he was asked to rotate the dial on the unit of his
"transcutaneous electrical simulator" until he began to feel a tingling
in his lef arm (which was his good arm) . We told him that this would
immediately restore voluntary movements in the phantom and provide
relief from the spasms. We also told him that the procedure had
worked on other patients in his predicament.
He said, "Really? Wow, I can' t wait to try it. "
Two days later he was back, obviously annoyed. "It's useless, " he
exclaimed. "I tried it fve times and it just doesn't work. I turned it up
to fll strength even though you told me not to. "
When I gave him the mirror t o try that same afernoon, he was able
to open his phantom hand instantly. The spasms were eliminated and so
too was the "digging sensation" of nails biting into his palm. This is a
mind- boggling obseration if you think about it. Here is a man with no
hand and no fngernails. How does one get nonexistent nails digging
into a nonexistent palm, resulting in severe pain? Why would a mirror
eliminate the phantom spasm?
Consider what happens in your brain when motor commands are
sent from the premotor and motor cortex to make a fst. Once your
hand is clenched, feedback signals from muscles and j oints of your
hand are sent back through the spinal cord to your brain saying, Slow
down, enough. Any more pressure and it could hurt. This propriocep-
5 4 I P HA N T O MS I N T H E B RA I N
rive feedback applies brakes, automatically, with astonishing speed and
precision.
If the limb is missing, however, this damping feedback is not possible.
The brain therefore keeps sending the message, Clench more, clench
more. Motor output is amplifed even frther ( to a level that far exceeds
anything you or I would ever experience) and the overfow or "sense of
efort" may itself be experienced as pain. The mirror may work by pro
viding visual feedback to unclench the hand, so that the clenching spasm
is abolished.
But why the sensation of digging fngernails? Just think of the nu
merous occasions when you actually clenched your fst and felt your nails
biting in your pal m. These occasions must have created a memory link
in your brain (psychologists call it a Hebbian link) between the motor
command to clench and the unmistakable sensation of "nails digging,"
so you can readily summon up this image in your mind. Yet even though
you can imagine the image quite vividly, you don't actually feel the sen
sation and say, "Ouch, that hurts. " Wy not? The reason, I believe, is
that you have a real palm and the skin on the palm says there is no pain.
You can imagine it but you don't feel it because you have a normal hand
sending real feedback and in the clash between reality and illusion, reality
usually wins.
But the amputee doesn't have a pal m. There are no countermanding
signals from the palm to forbid the emergence of these stored pain mem
ories. When Robert imagines that his nails are digging into his hand, he
doesn't get contradictory signals from his skn surface saying, "Robert,
you fool, there's no pain down here. " Indeed, if the motor commands
themselves are linked to the sense of nail digging, it's conceivable that
the amplifcation of these commands leads to a corresponding amplif
cation of the associated pain signals. This might explain why the pain is
so brutal .
The implications are radical . Even feeting sensory associations such as
the one between clenching our hands and digging our fngernals into
our palms are laid down as permanent traces in the brain and are only
unmasked under certain circumstances-experienced in this case as phan
tom limb pain. Moreover, these ideas imply that pain is an opinion on
the organism's state of health rather than a mere refexive response to an
injury. There is no direct hotline from pain receptors to "pain centers"
in the brai n. On the contrary, there is so much interaction between dif
ferent brain centers, like those concerned with vision and touch, that
even the mere visual appearance of an opening fst can actually feed all
CH A S I N G T H E P HA N T O M I 5 5
the way back into the patient's motor and touch pathways, allowing him
to feel the fst opening, thereby killing an illusory pain in a nonexistent
hand.
If pain is an illusion, how much influence do senses like vision have
over our subjective experiences? To fnd out, I tried a somewhat diabol
ical experiment on two of my patients. Wen Mary came into the lab, I
asked her to place her phantom right hand, palm down, into the mirror
box. I then asked her to put a gray glove on her good lef hand and
place it in the other side of the box, in a mirror image position. Afer
makng sure she was comfortable I instructed one of my graduate stu
dents to hide under the curtained table and put his gloved lef hand into
the same side of the box where Mary's good hand rested, above hers on
a false platform. When Mary looked into the box she could see not only
the student's gloved lef hand (which looked exactly like her own lef
hand) but also its refection in the mirror, as if she were looking at her
own phantom right hand wearing a glove. Wen the student now made
a fst or used his index fnger pad to touch the ball of his thumb, Mary
felt her phantom moving vividly. A in our previous two patients, vision
was enough to trick her brain into experiencing movements in her phan
tom limb.
Wat would happen if we fooled Mary into thinkng that her fngers
were occupying anatomically impossible positions? The box permitted
this illusion. Again, Mary put her phantom right hand, palm down, in
the box. But the student now did something diferent. Instead of placing
his lef hand into the other side of the box, in an exact mirror image of
the phantom, he inserted his right hand, palm up. Since the hand was
gloved, it looked exactly like her "palm-down" phantom right hand.
Then the student flexed his index fnger to touch his palm. To Mary,
peering into the box, it appeared as if her phantom index fnger were
bending backward to touch the back of her wrist-in the wrong direc
tion! 5 Wat would her reaction be?
When Mary saw her fnger twisted backward, she said, "One would
have thought it should feel peculiar, doctor, but it doesn' t. It feels exactly
like the fnger is bending backward, like it isn't supposed to. But it
doesn' t feel peculiar or painfl or anything like that. "
Another subject, Kren, winced and said that the twisted phantom
fnger hurt. "It felt like somebody was grabbing and pulling my fnger.
I felt a twinge of pain, " she said.
These experiments are important because they fatly contradict the
theory that the brain consists of a number of autonomous modules acting
5 6 I P H A N T O MS I N T H E B RA I N
as a bucket brigade. Popularized by artifcial intelligence researchers, the
idea that the brain behaves like a computer, with each module perform
ing a highly specialized job and sending its output to the next module,
is widely believed. In this view, sensory processing involves a one-way
cascade of information sensory receptors on the skin and other sense
organs to higher brain centers.
But my experiments with these patients have taught me that this is
not how the brain works. Its connections are extraordinarily labile and
dynamic. Perceptions emerge as a result of reverberations of signals be
tween diferent levels of the sensory hierarchy, indeed even across difer
ent senses . The fact that visual input can eliminate the spasm of a
nonexistent arm and then erase the associated memory of pain vividly
illustrates how extensive and profound these interactions can be.
Studying patients with phantom limbs has given me insights into the
inner working of the brain that go far beyond the simple questions I
started with four years ago when Tom frst walked into my ofce. We've
actually witnessed ( directly and indirectly) how new connections emerge
in the adult brain, how information from diferent senses interacts, how
the activity of sensory maps is related to sensory experience and more
generally how the brain is continuously updating its model of reality in
response to novel sensory inputs.
This last observation sheds new light on the so-called nature versus
nurture debate by allowing us to ask the question, Do phantom limbs
arise mainly from nongenetic factors such as remapping or stump neu
romas, or do they represent the ghostly persistence of an inborn, genet
ically specifed "body image"? The answer seems to be that the phantom
emerges from a complex interaction between the two. I'll give you fve
examples to illustrate this.
In the case of below- the-elbow amputees, surgeons will sometimes
cleave the stump into a lobster claw-like appendage, as an alternative to
a standard metal hook. Aer the surgery, people learn to use their pincers
at the stump to grasp obj ects, turn them around and otherise manip
ulate the material world. Intriguingly, their phantom hand ( some inches
away from real fesh) also feels split in two-with one or more phantom
fngers occupying each pincer, vividly mimicking the movements of the
appendage. I know of one instance in which a patient underent am
putation of his pincers only to be lef with a permanently cleaved phan
tom-strikng evidence that a surgeon's scalpel can dissect a phantom.
CH A S I N G T H E P HA N T O M I 5 7
Afer the original surgery in which the stump was split, this patient's
brain must have reshaped his body image to include the two pincers
for why else would he experience phantom pincers?
The other two stories both entertain and inform. A girl who was born
without forearms and who experienced phantom hands six inches below
her stumps frequently used her phantom fngers to calculate and solve
arithmetic problems. A sixteen-year-old girl who was born with her right
leg to inches shorter than her lef leg and who received a below-knee
amputation at age six had the odd sensation of possessing four feet! In
addition to one good foot and the expected phantom foot, she developed
two supernumerary phantom feet, one at the exact level of amputation
and a second one, complete with calf, extending all the way down to the
floor, where it should be had the limb not been congenitally shorter. 6
Although researchers have used this example to illustrate the role of ge
netic factors in determining body image, one could equally use it to
emphasize nongenetic influences, for why would your genes specif three
separate images of one leg?
A fourth example that illustrates the complex interplay between genes
and environment harks back to our observation that many amputees ex
perience vivid phantom movements, both voluntary and involuntary, but
in most the movements disappear eventually. Such movements are ex
perienced at frst because the brain continues sending motor commands
to the missing limb ( and monitors them) afer amputation. But sooner
or later, the lack of visual confrmation ( Gee, there is no arm) causes the
patient's brain to reject these signals and the movements are no longer
experienced. But if this explanation is correct, how can we understand
the continued presence of vivid limb movements in people like Mirabelle,
who was born without arms? I can only guess that a normal adult has
had a lifetime of visual and kinesthetic feedback, a process that leads the
brain to expect such feedback even afer amputation. The brain is "dis
appointed" if the expectation is not flflled-leading eventually to a loss
of voluntary movements or even a complete loss of the phantom itself.
The sensory areas of Mirabelle's brain, however, have never received such
feedback. Consequently, there is no learned dependence on sensory feed
back, and that lack might explain why the sensation of movements had
persisted, unchanged, for twenty-fve years.
The fnal example comes from my own country, India, which I visit
every year. The dreaded disease leprosy is still quite common there and
ofen leads to progressive mutilation and loss of limbs. At the leprosarium
at Vellore, I was told that these patients who lose their arms do not
5 8 I P HA N T O MS I N T H E B RA I N
experience phantoms, and I personally saw several cases and verifed these
claims . The standard explanation is that the patient gradually "learns"
to assimilate the stump into his body image by using visual feedback, but
if this is true, how does it account for the continued presence of phan
toms in amputees? Perhaps the gradual loss of the limb or the simulta
neous presence of progressive nere damage caused by the leprosy
bacterium is somehow critical . This might allow their brains more time
to readj ust their body image to match reality. Odder still, when such a
patient develops gangrene in his stump and the diseased tissue is am
putated, he does develop a phantom. But it's not a phantom of the old
stump; it's a phantom of the entire hand! It's as though the brain has a
dual representation, one of the original body image laid down genetically
and one ongoing, up-to-date image that can incorporate subsequent
changes. For some weird reason, the amputation disturbs the equilibrium
and resurrects the original body image, which has always been competing
for attention?
I mention these bizarre examples because they imply that phantom
limbs emerge from a complex interplay of both genetic and experiental
variables whose relative contributions can be disentangled only by sys
tematic empirical investigations. As with most nature/nurture debates,
asking which is the more important variable is meaningless-despite ex
travagant claims to the contrary in the IQ literature. ( Indeed, the ques
tion is no more meaningfl than asking whether the wetness of water
results mainly from the hydrogen molecules or from the oxygen mole
cules that constitute H
2
0! ) But the good news is that by doing the right
kinds of experiments, you can begin to tease them apart, investigate how
they interact and eventually help develop new treatments for phantom
pain. It seems extraordinary even to contemplate the possibility that you
could use a visual illusion to eliminate pain, but bear in mind that pain
itself is an illusion-constructed entirely in your brain like any other
sensory experience. Using one illusion to erase another doesn' t seem very
surprising afer all .
The experiments I've discussed so far have helped us understand what
is going on in the brains of patients with phantoms and given us hints
as to how we might help alleviate their pain. But there is a deeper mes
sage here: Your own body is a phantom, one that your brain has
temporarily constructed purely for convenience. I know this sounds
astonishing so I will demonstrate to you the malleability of your own
CHA S I N G T H E P HA N T O M I 5 9
body image and how you can alter it profoundly in just a few seconds.
Two of these experiments you can do on yourself right now, but the
third requires a visit to a Halloween supply shop.
To experience the frst illusion, you'll need two helpers. ( I will cal
them Julie and Mina. ) Sit in a chair, blindfolded, and ask Julie to sit on
another chair in front of you, facing the same direction as you are. Have
Mina stand on your right side and give her the following instrctions:
"Take my right hand and guide my index fnger to Julia's nose. Move
my hand in a rhythmic manner so that my index fnger repeatedly stokes
and taps her nose in a random sequence like a Morse code. At the same
time, use your lef hand to stroke my nose with the same rhythm and
timing. The stroking and tapping of my nose and Julia' s nose should be
in perfect synchrony. "
Aer thirty or forty seconds, i f you're lucky, you will develop the
uncanny illusion that you are touching your nose out there or that your
nose has been dislocated and stretched out about three feet in front of
your face. The more random and unpredictable the stroking sequence,
the more stiking the illusion will be. This is an extraordinary illusion;
why does it happen? I suggest that your brain "notices" that the tapping
and stroking sensations from your right index fnger are perfectly syn
chronized with the strokes and taps felt on your nose. It then says, "The
tapping on my nose is identical to the sensations on my right index
fnger; why are the two sequences identical? The likelihood that this is a
coincidence is zero, and therefore the most probable explanation is that
my fnger must be tapping my nose. But I also know that my hand is
two feet away from my face. So it follows that my nose must also be out
there, two feet away. "8
I have tied tis experiment on twenty people and i t works on about
half of them (I hope it will work on you) . But to me, the astonishing
thing is that it works at all-that your cerain knowledge that you have
a normal nose, your image of your body and face constructed over a
lifetime should be negated by just a few seconds of the right kind of
sensory stimulation. This simple experiment not only shows how malle
able your body image is but also illustates the single most important
principle underlying all of perception-that the mechanisms of percep
tion are mainly involved in extracting statistical correlations from the
world to create a model that is temporarily usefl .
The second illusion requires one helper and is even spookier. 9 You'll
need to go to a novelty or Halloween store to buy a dummy rubber
hand. Then constrct a two-foot by two- foot cardboard "wall" and place
6 0 I P HA N T O MS I N T H E B RA I N
it on a table in front of you. Put your right hand behind the cardboard
so that you cannot see it and put the dummy hand in front of the card
board so you can see it clearly. Next have your friend stroke identical
locations on both your hand and the dummy hand synchronously while
you look at the dummy. Within seconds you will experience the strokng
sensation as arising from the dummy hand. The experience is uncanny,
for you know perfectly well that you're looking at a disembodied rubber
hand, but this doesn't prevent your brain from assigning sensation to it.
The illusion illustrates, once again, how ephemeral your body image is
and how easily it can be manipulated.
Proj ecting your sensations on to a dummy hand is surprising
enough, but, more remarkably, my student Rick Stoddard and I dis
covered that you can even experience touch sensations as arising from
tables and chairs that bear no physical resemblance to human body
parts. This experiment is especially easy to do since all you need is a
single friend to assist you. Sit at your writing desk and hide your lef
hand under the table. Ask your friend to tap and stroke the surface of
the table with his right hand ( as you watch) and then use his hand si
multaneously to stroke and tap your lef hand, which is hidden from
view. It is absolutely critical that you not see the movements of his lef
hand as this will ruin the efect ( use a cardboard partition or a curtain
if necessary) . Afer a minute or so, you will start experiencing taps and
strokes as emerging from the table surface even though your conscious
mind knows perfectly well that this is logically absurd. Again, the sheer
statistical improbability of the two sequences of taps and strokes-one
seen on the table surface and one felt on your hand-lead the brain to
conclude that the table is now part of your body. The illusion is so
compelling that on the few occasions when I accidentally made a much
longer stroke on the table surface than on the subject's hidden hand,
the person exclaimed that his hand felt "lengthened" or "stretched"
to absurd proportions.
Both these illusions are much more than amusing party tricks to try
on your friends. The idea that you can actually project your sensations
to external objects is radical and reminds me of phenomena such as
out- of- body experiences or even voodoo ( prick the doll and "feel" the
pain) . But how can we be sure the student volunteer isn' t j ust being
metaphorical when she says "I feel my nose out there" or "The table
feels like my own hand. " Afer all , I ofen have the experience of
"feeling" that my car is part of my extended body image, so much so
that I become infriated if someone makes a small dent on it. But
CH A S I N G T H E P H A N T O M I 6 1
would I want to argue from this that the car had become part of my
body?
These are not easy questions to tackl e, but to fnd out whether the
students really identifed with the table surface, we devised a simple ex
periment that takes advantage of what is called the galvanic skin re
sponse or GSR. If I hit you with a hammer or hold a heavy rock over
your foot and threaten to drop it, your brain's visual areas will dispatch
messages to your limbic system ( the emotional center) to prepare your
body to take emergency measures ( basically telling you to run from
danger) . Your heart starts pumping more blood and you begin sweat
ing to dissipate heat. This alarm response can be monitored by mea
suring the changes in skin resistance-the so-called GSR-caused by
the sweat. If you look at a pig, a newspaper or a pen there is no GSR,
but if you look at something evocative-a Mapplethorpe photo, a
Playboy centerfold or a heavy rock teetering above your foot-you will
register a huge GSR.
So I hooked up the student volunteers to a GSR device while they
stared at the table. I then stroked the hidden hand and the table sur
face simultaneously for several seconds until the student started expe
riencing the table as his own hand. Next I bashed the table surface
with a hammer as the student watched. Instantly, there was a huge
change in GSR as if I had smashed the student's own fngers . (Wen I
tried the control experiment of stroking the table and hand out of
sync, the subject did not experience the illusion and there was no GSR
response. ) It was as though the table had now become coupled to the
student's own limbic system and been assimilated into his body image,
so much so that pain and threat to the dummy are felt as threats to his
own body, as shown by the GSR. If this argument is correct, then per
haps it's not all that silly to ask whether you identif with your car.
Just punch it to see whether your GSR changes. Indeed the technique
may give us a handle on elusive psychological phenomena such as the
empathy and love that you feel for a child or spouse. If you are deeply
in love with someone, is it possible that you have actually become part
of that person? Perhaps your souls-and not merely your bodies-have
become intertwined.
Now j ust think about what all this means. For your entire life, you've
been walking around assuming that your "selr' is anchored to a single
body that remains stable and permanent at least until death. Indeed, the
"loyalty" of your self to your own body is so axiomatic that you never
even pause to think about it, let alone question it. Yet these experiments
6 2 I P H AN T O MS I N T H E B RA I N
suggest the exact opposite-that your body image, despite all its ap
pearance of durability, is an entirely transitory internal construct that can
be profoundly modifed with just a few simple tricks. It is merely a shell
that you've temporarily created for successflly passing on your genes to
your ofspring.
CHAPTER 4
The Zombie
.
tn Brain
He refused to associate himsel with any investiation
which did not tend towards the unusual, and even
the fantastic.
-DR. jAMES WATSON
David Milner, a neuropsychologist at the University of St. Adrews in
Fife, Scotland, was so eager to get to the hospital to test his newly arved
patient that he almost forgot to take along the case notes descrbing her
condition. He had to rush back to his house through a cold winter ran
to fetch the folder describing Diane Fletcher. The facts were simple but
tragic: Diane had recently moved to northern Italy to work as a fee
lance commercial translator. She and her husband had found one of those
lovely old apartments near the medieval town center, with fresh pant,
new ktchen appliances and a refrbished bathroom-a place nearly as
luxurious as their permanent home back in Canada. But their adventure
was short-lived. When Diane stepped into the shower one morning, she
had no warning that the hot water heater was improperly vented. Wen
the propane gas ignited to heat a steady fow of water fowing past red
hot burners, carbon monoxide built up in the small bathroom. Diane
6 3
6 4 I P H A N T O MS I N T H E B RA I N
was washing her hair when the odorless fmes gradually overhelmed
her, causing her to lose consciousness and fall to the tile floor, her face
a bright pink from the irreversible binding of carbon monoxide to he
moglobin in her blood. She had lain there for perhaps twenty minutes
with water cascading over her limp body, when her husband returned to
retrieve something he had forgotten. Had he not gone home, she would
have died within the hour. But even though Diane surived and made
an amazing recovery, her loved ones soon realized that parts of her had
forever vanished, lost in patches of permanently atrophied brain tissue.
When Diane woke from the coma, she was completely blind. Within
a couple of days she could recognize colors and textures, but not shapes
of objects or faces-not even her husband's face or her own refection
in a handheld mirror. At the same time, she had no difculty identifing
people from their voices and could tell what objects were if they were
placed in her hands.
Dr. Milner was consulted because of his long-standing interest in vi
sual problems following strokes and other brain inj uries. He was told
that Diane had come to Scotland, where her parents live, to see whether
something could be done to help her. When Dr. Milner began his rou
tine visual tests, it was obvious that Diane was blind i n ever traditional
sense of the word. She could not read the largest letters on an eye chart
and when he showed her two or three fngers, she couldn' t identif how
many fngers he held up.
At one point, Dr. Milner held up a pencil . "What's this? " he asked.
A usual, Diane looked puzzled. Then she did something unexpected.
"Here, let me see it," she said, reaching out and defly taking the pencil
from his hand. Dr. Milner was stunned, not by her ability to identif the
object by feeling it but by her dexterity in taking it from his hand. A
Diane reached for the pencil , her fngers moved swifly and accurately
toward it, grasped it and carried it back to her lap in one fuid motion.
You' d never have guessed that she was blind. It was as if some other
person-an unconscious zombie inside her-had guided her actions.
(When I say zombie I mean a completely nonconscious being, but it's
clear that the zombie is not asleep. It's perfectly alert and capable of
makng complex, skilled movements, like creatures in the cult movie
Niht of the Living Dead. )
Intrigued, Dr. Milner decided to do some experiments on Diane' s
covert ability. He showed her a straight line and asked, "Diane, is this
line vertical , horizontal or slanted? "
"I don't kow," she replied.
T H E Z O M B I E I N T H E B RA I N I 6 5
Then he showed her a vertical slit ( actually a mail slot) and asked her
to describe its orientation. Again she said, "I don't know. "
Wen he handed her a letter and asked her to mail i t through the slot,
she protested, "Oh, I can' t do that. "
"Oh, come on, give i t a try," he said. "Pretend that you're posting a
letter. "
Diane was reluctant. "Tr it, " he urged.
Diane took the letter from the doctor and moved it toward the slot,
rotating her hand in such a way that the letter was perfectly aligned with
the orientation of the slot. In yet another sklled maneuver, Diane
popped the letter into the opening even though she could not tell you
whether it was vertical , horizontal or slanted. She carried out this instruc
tion without any conscious awareness, as if that ver same zombie had
taken charge of the task and efortlessly steered her hand toward the
goaJ . l
Diane's actions are amazing because we usually think of vision as a
single process. Wen someone who is obviously blind can reach out and
grab a letter, rotate the letter into the correct position and mail it
through an opening she cannot "see, " the ability seems almost paranor
mal .
To understand what Diane i s experiencing, we need to abandon all
our commonsense notions about what seeing really is. In the next few
pages, you will discover that there is a great deal more to perception than
meets the eye.
Like most people, you probably take vision for granted. You wake up
in the morning, open your eyes and, voila, it's all out there in front of
you. Seeing seems so efortless, so automatic, that we simply fail to rec
ognize that vision is an incredibly complex-and still deeply mysterious
process. But consider, for a moment, what happens each time you glance
at even the simplest scene. A my colleague Richard Gregory has pointed
out, all you're given are two tiny upside-down two- dimensional images
inside your eyeballs, but what you perceive is a single panoramic, right
side-up, three-dimensional world. How does this miraculous transfor
mation come about? 2
Many people cling to the misconception that seeing simply involves
scanning an internal mental picture of some kind. For example, not long
ago I was at a cocktail party and a young fellow asked me what I did for
a living. When I told him that I was interested in how people see things
and how the brain is involved in perception-he looked perplexed.
"Wat's there to study? " he asked.
6 6 I P H AN T O M S I N T H E B RA I N
"Well," I said, "what do you think happens in the brain when you
look at an object? "
He glanced down at the glass of champagne in his hand. "Well , there
is an upside-down image of this glass falling in my eyeball . The play of
light and dark images activates photoreceptors on my retina, and the
patterns are transmitted pixel by pixel through a cable-my optic nere
and displayed on a screen in my brain. Isn't that how I see this glass of
champagne? Of course, my brain would need to make the image upright
again. "
Though his knowledge of photoreceptors and and optics was impres
sive, his explanation-that there' s a screen somewhere inside the brain
where images are displayed-embodies a serious logical fallacy. For if
you were to display an image of a champagne glass on an internal neural
screen, you' d need another little person inside the brain to see that im
age. Ad that won't solve the problem either because you'd then need
yet another, even tinier person inside his head to view that image, and
so on and so forth, ad infnitum. You'd end up with an endless regress
of eyes, images and little people without really solving the problem of
perception.
So the frst step in understanding perception is to get rid of the idea
of images in the brain and to begin thinking about symbolic descriptions
of objects and events in the external world. A good example of a symbolic
description is a written paragraph like the ones on this page. If you had
to convey to a friend in China what your apartment looks like, you
wouldn't have to teletransport it to China. All you'd have to do would
be to write a letter describing your apartment. Yet the actual squiggles
of ink-the words and paragraphs in the letter-bear no physical resem
blance to your bedroom. The letter i s a symbolic description of your
bedroom.
What is meant by a symbolic description in the brain? Not squiggles
of ink, of course, but the language of nere impulses. The human brain
contains multiple areas for processing images, each of which is composed
of an intricate network of neurons that is specialized for extracting certain
tyes of information from the image. Ay object evokes a pattern of
activity-unique for each object-among a subset of these areas. For
example, when you look at a pencil, a book or a face, a diferent pattern
of nere activity is elicited in each case, "informing" higher brain centers
about what you are looking at. The patterns of activity symbolize or
represent visual objects in much the same way that the squiggles of ink
on the paper symbolize or represent your bedroom. As scientists trying
T H E Z O M B I E I N T H E B RA I N I 6 7
Fige 4. 1 A Necker cube. Notice that this skeleton drawing of a cube can be
seen in one oftwo di erent ways-either pointing upward and to the lef or down
ward and to the riht. Te perception can change even when the image on your
retina is constant.
to understand visual processes, our goal is to decipher the code used by
the brain to create these symbolic descriptions, much as a cryptographer
tries to crack an alien script.
Thus perception involves much more than replicating an image in your
brain. If vision were simply a faithfl copy of reality in the same way that
a photograph captures a scene, then your perception should always re
main constant if the retinal image is held constant. But this is not the
case. Your perceptions can change radically even when the image on your
retina stays the same. A striking example was discovered in 1 832 by the
Swiss crystallographer L. A. Necker. One day he was looking through a
microscope at a cuboid crystal and suddenly the thing fipped on him.
Each time he looked, it seemed to change the way it was facing-a phys
ical impossibility. Necker was puzzled and wondered whether something
inside his own head was fipping rather than the crystal itself. To test this
strange notion, he made a simple line drawing of the crystal, and lo and
behold, it, too, fipped ( Figure 4. 1 ) . You can see it pointing up or down,
depending on how your brain interprets the image, even though the
image remains constant on your retina, not changing at all . Thus every
act of perception, even something as simple as viewing a drawing of a
cube, involves an act of j udgment by the brai n.
6 8 I P HA N T O MS I N T H E B RA I N
In making these judgments, the brain takes advantage of the fact that
the world we live in is not chaotic and amorphous; it has stable physical
properties. During evolution-and partly during childhood as a result of
learning-these stable properties became incorporated into the visual ar
eas of the brain as certain "assumptions" or hidden kowledge about
the world that can be used to eliminate ambiguity in perception. For
example, when a set of dots moves in unison-like the spots on a leop
ard-they usually belong to a single object. So, any time you see a set
of dots moving together, your visual system makes the reasonable infer
ence that they're not moving like this j ust by coincidence-that they
probably are a single obj ect. Ad, therefore, that's what you see. No
wonder the German physicist Hermann von Helmholtz ( the founding
father of visual science) called perception an "unconscious inference. "3
Take a look at the shaded images in Figure 4. 2. These are just fat
shaded disks, but you will notice that about half of them look like eggs
bulging out at you, and the other half, randomly interspersed, look like
hollow cavities. If you inspect them careflly, you'll notice that the ones
that are light on top appear to bulge out at you, whereas the ones that
are dark on top look like cavities. If you turn the page upside down,
you'll see that they all reverse. The bulges become cavities and vice versa.
The reason is that, in interpreting the shapes of shaded images, your
visual system has a built-in assumption that the sun is shining from above,
and that, in the real world, a convex object bulging toward you would
be illuminated on the top whereas a cavity would receive light at the
bottom. Given that we evolved on a planet with a single sun that usually
shines from on high, this is a reasonable assumption. 4 Sure, it's some
times on the horizon, but statistically speaking the sunlight usually comes
from above and certainly never from below.
Not long ago, I was pleasantly surprised to fnd that Charles Darwin
had been aware of this principle. The tail feathers of the argus pheasant
have striking gray disk-shaped markings that look very much like those
you see in Figure 4. 3; they are, however, shaded lef to right instead of
up and down. Darin realized that the bird might be using this as a
sexual "come hither" in its courtship ritual, the striking metallic-lookng
disks on the feathers being the avian equivalent of jewelry. But if so, why
was the shading lef to right instead of up and down? Darin conj ectured
correctly that perhaps during courship the feathers stick up, and indeed
this is precisely what happens, illustrating a striking harmony in the birds'
visual system between its courtship ritual and the direction of sunlight.
Even more compelling evidence of the existence of all these extraor-
T H E Z O M B I E I N T H E B RA I N I 6 9
Fige 4.2 A mixture of egs and cavities. Te shaded disks are all identical
except that hal of them are liht on top and the rest are dark on top. Te ones
that are liht on top are always seen as egs buling out from the paper, whereas
the ones that are dark on top are seen as cavities. Tis is because the visual areas
in your brain have a built-in sense that the sun is shining fom above. If that were
true, then only bules (egs) would be liht on top and concavities would be liht
below.
If you turn the page upside down the egs will transorm themselves into cavities
and cavities into egs. Adapted from Ramachandran, l988a.
dinarily sophisticated processes i n vision comes from neurology-from
patients like Diane and others like her who have sufered highly selective
visual defcits . If vision simply involves displaying an image on a neural
screen, then in the case of neural damage, you would expect bits and
pieces of the scene-or the whole scene-to be missing, depending on
the extent of damage. But the defects are usually far more subtle than
that. To understand what is really going on in the brains of these patients
and why they sufer such peculiar problems, we need to look more closely
at the anatomical pathways concerned with vision.
7 0 I P HA N T O MS I N T H E B RA I N
Fige 4.3 Te tail feathers of the argus pheasant have prominent disklike mark
ings ordinarily shaded lef to riht instead of top to bottom. Charles Darin pointed
out that when the bird goes through its courtship ritual, the tail points up. Te disks
then are liht on top-making them bule out prominently like the egs in Fiure
4.2. Tis may be the closest thing to the avian equivalent of jewelr. From Te
Descent of Man by Charles Darin ( 1 871 ) , John Murray, London.
Wen I was a student, I was taught that messages from my eyeballs
go through the optic nerve to the visual cortex at the back of my brain
( to an area called the primary visual cortex) and that this is where seeing
takes place. There is a point-to-point map of the retina in this part of
the brain-each point in space seen by the eye has a corresponding point
in this map. This mapping process was originally deduced from the fact
that when people sustain damage to the primary visual cortex-say, a
bullet passes through one small area-they get a corresponding hole or
blind spot in their visual feld. Moreover, because of some quirk in our
evolutionary history, each side of your brain sees the opposite half of the
world ( Figure 4. 4) . If you look straight ahead, the entire world on your
lef is mapped onto your right visual cortex and the world to the right
of your center of gaze is mapped onto your lef visual cortex. 5
But the mere existence of this map does not explain seeing, for as I
noted earlier, there is no little man inside watching what is displayed on
Ri ght
Optic nerve
Opic tract
Primary visual corex
Lef
Lateral
geniculate
nucl eus
( LGN)
LEF HEMI SPHERE
Fige 4.4 Bottom of the human brain viewed from below. Notice the curious
arrangement of fbers going fom the retina to the visual cortex. A visual image
in the lef visual feld (dark gray) falls on the riht side of the riht eye's retina as
well as the riht side of the lef eye's retina. Te outer (temporal) fbers fom the
riht eye (dark gray) go then to the same riht (visual) cortex without crossing at
the optic chiasm. Te inner (nasal) fbers of the left eye (dark gray) cross at the
chiasm and go to the riht visual cortex as well. So the riht visual cortex asees''
the left side of the world.
Because there is a systematic map of the retina in the visual cortex, a ahole" in
the visual cortex will cause a corresponding blind spot (or scotoma) in the visual
feld. If the riht visual cortex is completely removed, the patient will be completely
blind in the left side of the world. Redrawn from S. Zeki, A Vision of the Brain,
1993. Reproduced with permission from Blackwell (Oxford) .
7 2 I P H A N T O MS I N T H E B RA I N
the primary visual cortex. Instead, this frst map serves as a sorting and
editorial ofce where redundant or useless information is discarded
wholesale and certain defning attributes of the visual image-such as
edges-are strongly emphasized. ( This is why a cartoonist can convey
such a vivid picture with j ust a few pen strokes depicting the outlines or
edge alone; he' s mimickng what your visual system is specialized to do. )
This edited information is then relayed to an estimated thirty distinct
visual areas in the human brain, each of which thus receives a complete
or partial map of the visual world. ( The phrases "sorting ofce" and
"relay" are not entirely appropriate since these early areas perform fairly
sophisticated image analyses and contain massive feedback proj ections
from higher visual areas. We'll take these up later. )
This raises an interesting question. Why do we need thirty areas? 6 We
really don't know the answer, but they appear to be highly specialized
for extracting diferent attributes from the visual scene-color, depth,
motion and the like. Wen one or more areas are selectively damaged,
you are confronted with paradoxical mental states of the kind seen in a
number of neurological patients. One of the most famous examples in
neurology is the case of a Swiss woman (whom I shall call Ingrid) who
sufered from "motion blindness. " Ingrid had bilateral damage to an area
of her brain called the middle temporal ( MT) area. In most respects, her
eyesight was normal; she could name shapes of objects, recognize people
and read books with no trouble. But if she looked at a person running
or a car moving on the highway, she saw a succession of static, strobelike
snapshots instead of the smooth impression of continuous motion. She
was terrifed to cross the street because she couldn't estimate the velocity
of oncoming cars, though she could identif the make, color and even
the license plate of any vehicle. She said that talking to someone in per
son felt like talkng on the phone because she couldn't see the changing
facial expressions associated with normal conversation. Even pouring a
cup of cofee was an ordeal because the liquid would inevitably overfow
and spill onto the foor. She never knew when to slow down, changing
the angle of the cofeepot, because she couldn't estimate how fast the
liquid was rising in the cup. Al of these abilities ordinarily seem so ef
fortless to you and me that we take them for granted. It's only when
something goes wrong, as when this motion area is damaged, that we
begin to realize how sophisticated vision really is.
Another example involves color vision. When patients sufer bilateral
damage to an area called V4, they become completely color- blind ( this
is diferent from the more common from of congenital color blindness
T H E Z O M B I E I N T H E B RA I N I 7 3
that arises because color-sensitive pigments in the eye are defcient) . In
his book An Anthropologist on Mars, Oliver Sacks describes an artist who
went home one evening afer sufering a stroke so small he didn't notice
it at the time. But when he walked into his house, all his color paintings
suddenly looked as if they had been done in black and white. In fact,
the whole world was black and white and soon he realized that the paint
ings had not changed, but rather something had happened to him. Wen
he looked at his wife, her face was a muddy gray color-he claimed she
looked like a rat.
So that covers two of the thiry areas-MT and V4-but what about
all the rest? Undoubtedly they're doing something equally important,
but we have no clear ideas yet of what their fnctions might be. Yet
despite the bewildering complexity of all these areas, the visual system
appears to have a relatively simple overall organization. Messages from
the eyeballs go through the optic nere and immediately bifrcate along
two pathways-one phylogenetcally old and a second, newer pathway
that is most highly developed in primates, including humans. Moreover,
there appears to be a clear division of labor between these two systems.
The "older" pathway goes from the eye straight down to a structure
called the superior colliculus in the brain stem, and from there it even
tually gets to higher cortical areas especially in the parietal lobes. The
"newer" pathway, on the other hand, travels from the eyes to a cluster
of cells called the lateral geniculate nucleus, which is a relay station en
route to the primary visual cortex ( Figure 4. 5 ). From there, visual infor
mation is transmitted to the thirty or so other visual areas for frher
processing.
Wy do we have an old pathway and a new pathway?
One possibility is that the older pathway has been presered as a sort
of early warning system and is concerned with what is sometimes called
"orienting behavior. " For example, if a large looming object comes at
me from the lef, this older pathway tells me where the object is, enabling
me to swivel my eyeballs and turn my head and body to look at it. This
is a primitive reflex that brings potentially important events into my fo
vea, the high- acuity central region of my eyes.
At this stage I begin to deploy the phylogenetically newer sytem to
determine what the object is, for only then can I decide how to respond
to it. Should I grab it, dodge it, fee from it, eat it, fght it or make love
to it? Damage to this second pathway-particularly in the primary visual
cortex-leads to blindness in the conventional sense. It is most com
monly brought on by a stroke-a leakage or blood clot in one of the
7 4 I P H A N T O MS I N T H E B RA I N
Fige 4. 5 Te anatomical organization ofthe visual pathways. Schematic dia
gram ofthe lef hemisphere viewed fom the lef side.
Te fbers fom the eyeball diverge in to parallel ((streams": a new pathway
that goes to the lateral geniculate nucleus (shown here on the surace for clarit,
though it is actually inside the thalamus, not the temporal lobe) and an old pathway
that goes to the superior coliculus in the brain stem.
Te anew" pathway then goes to the visual cortex and diverges again (afer a
couple ofrelays) into to pathways (white arrows)-a ahow" pathway in the pa
rietal lobes that is concered with grasping, naviation and other spatial functions,
and the second, ((what" pathway in the temporal lobes concered with recognizing
objects. Tese to pathways were discovered by Leslie Ungerleider and Mortimer
Mischkin ofthe National Institutes ofHealth. Te to pathways are shown by white
arrows.
T H E Z O M B I E I N T H E B RA I N I 7 5
main blood vessels supplying the brain. If the vessel happens to be a
cerebral artery in the back of the brain, damage can occur in either the
lef or the right side of the primary visual cortex. Wen the right primary
cortex is damaged, the person is blind in the lef visual feld, and if the
lef primary cortex is damaged, the right visual feld is obliterated. This
kind of blindness, called hemianopia, has been known about for a long
time.
But i t, too, holds surprises. Dr. Larry Weiskrantz, a scientist working
at Oxford University in England, did a very simple experiment that
stunned experts on vision. 7 His patient ( known as D. B. , whom I will call
Drew) had an abnormal clump of blood vessels surgically removed from
his brain along with some normal brain tissue in the same vicinity. Since
the malformed clump was located in the right primary visual corex, the
procedure rendered Drew completely blind to the lef half of the world.
It did not matter whether he used his lef eye or right eye-if he looked
straight ahead, he could not see anything on the lef side of the world.
In other words, although he could see out of both eyes, neither eye could
see its own lef visual feld.
Aer the surgery Drew's ophthalmologist, Dr. Mike Sanders, asked
him to gaze straight ahead at a small fxation spot mounted in the center
of a device that looks like an enormous translucent Ping- Pong ball .
Drew's entire visual feld was flled with a homogeneous background.
Next, Dr. Sanders fashed spots of light onto diferent parts of the cured
screen mounted on the inside of a ball and asked Drew whether he could
see them. Each time a spot fell into his good visual feld, he'd say, "Yes,
yes, yes, " but when the spot fell into his blind region he would say
nothing. He didn' t see it.
So far so good. Dr. Sanders and Dr. Weiskrantz then noticed some
thing very odd. Drew was obviously blind in the lef visual feld, but if
the experimenter put his hand in that region Drew reached out for it
accurately! The two researchers asked Drew to stare straight ahead and
put movable markers on the wall to the lef of where he was looking,
and again he was able to point to the markers, although he insisted that
he did not actually "see" them. They held up a stick, in either a vertical
or a horizontal position, in his blind feld and asked him to guess which
way the stick was oriented. Drew had no problem with this task, although
he said again that he could not see the stick. Aer one such long series
of "guesses, " when he made virtually no errors, he was asked, "Do you
know how well you have done? "
7 6 I P H A N T O MS I N T H E B RA I N
"No, " he replied, "I didn't-because I couldn't see anything; I
couldn't see a darn thing. "
"Can you say how you guessed-what i t was that allowed you t o say
whether it was vertical or horizontal ? "
"No, I could not because I did not see anything; I just don't kow. "
Finally, he was asked, "So you really did not know you were getting
them right? "
"No, " Drew replied, with an air of incredulity.
Dr. Weiskrantz and his colleagues gave this phenomenon an oxymo
ronic name-"blindsight"-and went on to document it in other pa
tients. The discovery is so surprising, however, that many people still
don't accept that the phenomenon is possible.
Dr. Weiskantz questioned Drew repeatedly about his "vision" in his
blind lef feld, and most of the time Drew said that he saw nothing at
all . If pressed, he might occasionally say that he had a "feeling" that a
stimulus was approaching or receding or was "smooth" or "j agged. "
But Drew always stressed that he saw nothing i n the sense of "seeing";
that he was typically guessing and that he was at a loss for words to
describe any conscious perception. The researchers were convinced that
Drew was a reliable and honest reporter, and when test objects fell near
the cusp of his good visual feld, he always said so promptly.
Without invoking extrasensory perception, how do you account for
blindsight-a person' s pointing to or correctly guessing the presence of
an obj ect that he cannot consciously perceive? Dr. Weiskantz suggested
that the paradox is resolved when you consider the division of labor
between the two visual pathways that we considered earlier. In particular,
even though Drew had lost his primary visual cortex-rendering him
blind-his phylogenetically primitive "orienting" pathway was still in
tact, and perhaps it mediates blindsight. In other words, the spot of light
in the blind region-even though it fails to activate the newer pathway,
which is damaged-gets transmitted through the superior colliculus to
higher brain centers such as the parietal lobes, guiding Drew's arm
toward the "invisible" spot. This daring interpretation carries with it an
extraordinary implication-that only the new pathway is capable of con
scious awareness ( "I see this") , whereas the old pathway can use visual
input for all kinds of behavior, even though the person is completely
unaware of what is going on. Does it follow, then, that consciousness is
a special property of the evolutionarily more recent visual cortex pathway?
If so, why does this pathway have privileged access to the mind? These
are questions we'll consider in the last chapter.
T H E Z O M B I E I N T H E B RA I N I 7 7
What we have considered so far is the simple version of the percep
tion story, but in fact the picture is a bit more complicated. It turns out
that information in the "new" pathway-the one containing the pri
mary visual cortex that purportedly leads to conscious experience ( and i s
completely damaged i n Drew)-once again diverges into two distinct
streams . One is the "where" pathway, which terminates in the parietal
lobe ( on the sides of your brain above the ears ) ; the other, sometimes
called the "what" pathway, goes to the temporal lobe ( underlying the
temples ) . And it looks as though each of these two systems is also spe
cialized for a distinct subset of visual fnctions.
Actually the term "where" pathway is a little misleading because this
system specializes in not just "where" -in assigning spatial location to
objects-but in all aspects of spatial vision: the ability of organisms to
walk around the world, negotiate uneven terrain and avoid bumping into
obj ects or falling into black pits. It probably enables an animal to deter
mine the direction of a moving target, to judge the distance of approach
ing or receding objects and to dodge a missile. If you are a primate, it
helps you reach out and grab an object with your fngers and thumb.
Indeed, the Canadian psychologist Mel Goodale has suggested that this
system should really be called the "vision for action pathway" or the
"how pathway" since it seems to be mainly concerned with visually
guided movements. ( From here on I will call it the "how" patway. )
Now you may scratch your head and say, My God, what' s lef? Wat
remains is your ability to identif the object; hence the second pathway
is called the "what" pathway. The fact that the majority of your thirty
visual areas are in fact located in this system gives you some idea of its
importance. Is this thing you are looking at a fox, a pear or a rose? Is
this face an enemy, friend or mate? Is it Drew or Diane? What are the
semantic and emotional attributes of this thing? Do I care about it? A
I afraid of it? Three researchers, Ed Rolls, Charlie Gross and David Per
rett, have found that if you put an electrode into a monkey's brain to
monitor the activity of cells in this system, there is a particular region
where you fnd so-called face cells-each neuron fres only in response
to the photograph of a particular face. Thus one cell may respond to the
dominant male in the monkey troop, another to the monkey's mate,
another to the surrogate alpha male-that is, to the human experimenter.
This does not mean that a single cell is somehow responsible for the
complete process of recognizing faces; the recognition probably relies on
7 8 I P H A N T O MS I N T H E B RA I N
a network involving thousands of synapses. Nevertheless, face cells exist
as a critical part of the network of cells involved in the recognition of
faces and other objects. Once these cells are activated, their message is
somehow relayed to higher areas in the temporal lobes concerned with
"semantics"-all your memories and knowledge of that person. Where
did we meet before? What is his name? When is the last time I saw this
person? What was he doing? Added to this, fnally, are all the emotions
that the person's face evokes .
To illustrate frther what these two streams-the what and how path
ways-are doing in the brain, I'd like you to consider a thought exper
iment. In real life, people have strokes, head injuries or other brain
accidents and may lose various chunks of the how and what streams. But
nature is messy and rarely are losses confned exclusively to one stream
and not the other. So let's assume that one day you wake up and your
what pathway has been selectively obliterated ( perhaps a malicious doctor
entered in the night, knocked you out and removed both your temporal
lobes ) . I' d venture to predict that when you woke up the entire world
would look like a gallery of abstract sculpture, a Martian art gallery per
haps. No object you looked at would be recognizable or evoke emotions
or associations with anything else. You' d "see" these obj ects, their
boundaries and shapes, and you could reach out and grab them, trace
them with your fnger and catch one if l threw it at you. In other words,
your how pathway would be fnctional . But you'd have no inkling as to
what these obj ects were. It's a moot point as to whether you'd be "con
scious" of any of them, for one could argue that the term consciousness
doesn't mean anything unless you recognize the emotional signifcance
and semantic associations of what you are lookng at.
Two scientists, Heinrich Kliver and Paul Bucy at the University of
Chicago, have actually carried out an experiment like this on monkeys
by surgically removing their temporal lobes containing the what pathway.
The animals can walk around and avoid bumping into cage walls-be
cause their how pathway is intact-but if they are presented with a lit
cigarette or razor blade, they will likely stuf it into their mouths and
start chewing. Male monkeys will mount any other animal including
chickens, cats or even human experimenters. They are not hypersexual ,
j ust indiscriminate. They have great difculty in knowing what prey is,
what a mate is, what food is and in general what the signifcance of any
object might be.
Are there any human patients who have similar defcits? On rare oc
casions a person will sustain widespread damage to both temporal lobes
T H E Z O M B I E I N T H E B RA I N I 7 9
and develop a cluster of symptoms similar to what we now call the
Kliver- Bucy syndrome. Like the monkeys, they may put anything and
everything into their mouths ( much as babies do) and display indiscrim
inate sexual behavior, such as making lewd overtures to physicians or to
patients in adj acent wheelchairs.
Such extremes of behavior have been known for a long time and lend
credibility to the idea that there is a clear division of labor between these
two systems-and that brings us back to Diane. Though her defcit is
not quite so extreme, Diane also had dissociation between her what and
how vision systems. She couldn't tell the diference between a horizontal
and a vertical pencil or a slit because her what pathway had been selec
tively obliterated. But since her how pathway was still intact ( as indeed
was her evolutionarily older "orienting behavior" pathway) , she was able
to reach out and grab a pencil accurately or rotate a letter by the correct
angle to post it into a slot that she could not see.
To make this distinction even more clear, Dr. Milner performed an
other ingenious experiment. Afer all, posting letters is a relatively easy,
habitual act and he wanted to see how sophisticated the zombie's ma
nipulative abilities really were. Placing two blocks of wood in front of
Diane, a large and a small one, Dr. Milner asked her which was bigger.
He found, not surprisingly, that she performed at chance level. But when
he asked her to reach out and grab the object, once again her arm went
unerringly toward it with thumb and index fnger moving apart by the
exact distance appropriate for that object. All this was verifed by vide
otaping the approaching arm and conducting a frame- by-frame analysis
of the tape. Again, it was as though there were an unconscious "zombie"
inside Diane carrying out complicated computations that allowed her to
move her hand and fngers correctly, whether she was posting a letter or
simply grabbing objects of diferent sizes. The "zombie" corresponded
to the how pathway, which was still largely intact, and the "person"
corresponded to the what pathway, which was badly damaged. Diane can
interact with the world spatially, but she is not consciously aware of the
shapes, locations and sizes of most objects around her. She now lives in
a country home, where she keeps a large herb garden, entertains friends
and carries on an active, though protected, life.
But there's another twist to the tale, for even Diane' s what pathway
was not completely damaged. Although she couldn't recognize the
shapes of objects-a line drawing of a banana would not look diferent
from a drawing of a pumpkin-as I noted at the beginning of this chap
ter, she had no problem distinguishing colors or visual textures. She was
8 0 I P HA N T O MS I N T H E B RA I N
good at "stuf' rather than "things" and knew a banana from a yellow
zucchini by their visual textures .The reason for this might be that even
within the areas constituting the what pathway, there are fner subdivi
sions concerned with color, texture and form, and the "color" and "tex
ture" cells might be more resistant to carbon monoxide poisoning than
the "form" cells. The evidence for the existence of such cells in the
primate brain is still fercely debated by physiologists, but the highly
selective defcits and presered abilities of Diane give us additional clues
that exquisitely specialized regions of this sort do indeed exist in the
human brain. If you're looking for evidence of modularity in the brain
( and ammunition against the holist view) , the visual areas are the best
place to look.
Now let's go back to the thought experiment I mentioned earlier and
turn it around. Wat might happen if the evil doctor removed your how
pathway ( the one that guides your actions ) and lef your what system
intact? You' d expect to see a person who couldn' t get her bearings, who
would have great difculty looking toward objects of interest, reaching
out and grabbing things or pointing to interesting targets in her visual
feld. Something like this does happen in a curious disorder called Balint's
syndrome, in which there is bilateral damage to the parietal lobes. In a
knd of tunnel vision, the patient's eyes stay focused on any small object
that happens to be in her foveal vision ( the high- acuity region of the
eye) , but she completely ignores all other objects in the vicinity. If you
ask her to point to a small target in her visual feld, she'll very likely miss
the mark by a wide margin-sometimes by a foot or more. But once she
captures the target with her two foveas, she can recognize it efortlessly
because her intact what pathway is engaged in fll gear.
The discovery of multiple visual areas and the division of labor be
tween the two pathways is a landmark achievement in neuroscience, but
it barely begins to scratch the surface of the problem of understanding
vision. If I toss a red ball at you, several far- fung visual areas in your
brain are activated simultaneously, but what you see is a single unifed
picture of the ball . Does this unifcation come about because there is
some later place in the brain where all this information is put together
what the philosopher Dan Dennett pejoratively calls a "Cartesian thea
tre"? 8 Or are there connections between these areas so that their simul
taneous activation leads directly to a sort of synchronized fring pattern
that in turn creates perceptual unity? This question, the so- called binding
T H E Z O M B I E I N T H E B RA I N I 8 1
problem, is one of the many unsolved riddles in neuroscience. Indeed,
the problem is so mysterious that there are philosophers who argue it is
not even a legitmate scientifc question. The problem arises, they argue,
from peculiarities in our use of language or from logically flawed as
sumptions about the visual process.
Despite this reseration, the discovery of the how and what pathways
and of multiple visual areas has generated a great deal of excitement,
especially among young researchers entering the feld. 9 It's now possible
not only to record the activity of individual cells but also to watch many
of these areas light up in the living human brain as a person views a
scene-whether it's something simple like a white square on a black
background or something more complex like a smiling face. Further
more, the existence of regions that are highly specialized for a specifc
task gives us an experimental lever for approaching the question posed
at the beginning of this chapter: How does the activity of neurons give
rise to perceptual experience? For instance, we now know that cones in
the retina frst send their outputs to clusters of color- sensitive cells in the
primary visual cortex fanciflly called blobs and thin stripes ( in the ad
j acent area 1 8 ) and from there to V4 ( recall the man who mistook his
wife for a hat) and that the processing of color becomes increasingly
sophisticated as you go along this sequence. Taking advantage of the
sequence and of all this detailed anatomical knowledge, we can ask, How
does this specifc chain of events result in our experience of color? Or,
recalling Ingrid, who was motion blind, we can ask, How does the cir
cuitry in the middle temporal area enable us to see motion?
A the British immunologist Peter Medawar has noted, science is the
"art of the soluble, " and one could argue that the discovery of multiple
specialized areas in vision makes the problem of vision soluble, at least
in the foreseeable fture. To his famous dictum, I would add that in
science one is ofen forced to choose between providing precise answers
to pifing questions ( how many cones are there in a human eye ) or vague
answers to big questions ( what is the self, but every now and then you
come up with a precise answer to a big question ( such as the link between
deoxyribonucleic acid [ DNA] and heredity) and you hit the j ackpot. It
appears that vision is one of the areas in neuroscience where sooner or
later we will have precise answers to big questions, but only time will
tell .
In the meantime, we've learned a great deal about the structure and
fnction of the visual pathways from patients like Diane, Drew and In
grid. For example, even though Diane's symptoms initially seemed out-
8 2 I P HA N T O M S I N T H E B RA I N
Fige 4.6 Te size-contrast illusion. Te to central medium-sized disks are phys
ically identical in size. Yet the one surrounded by the large disks looks smaller than
the one surrounded by the little ones. Wen a normal person reaches out to grab
the central disk, his/her fngers move exactly the same distance apart for either of
them-even though they look di erent in size. Te zombie-or the how" pathway
in the parietal lobes-is apparently not fooled by the illusion.
landish, we can now begin to explain them in terms of what we learned
about the two visual pathways-the what pathway and the how pathway.
It's important to keep reminding ourselves, though, that the zombie
exists not only in Diane but in all of us. Indeed, the purpose of our
whole enterprise is not simply to explain Diane's defcits but to under
stand how your brain and my brain work. Since these two pathways
normally work in unison, in a smooth coordinated fashion, it's hard to
discern their separate contributions. But it's possible to devise experi
ments to show that they do exist and work to some extent independently
even in you and me. To illustrate this, I' ll describe one last experiment.
The experiment was carried out by Dr. Salvatore Aglioti, 1 0 who took
advantage of a well -kown visual illusion ( Figure 4. 6) involving two cir
cular disks side by side, identical in size. One of them is surrounded by
six tiny disks and the other by six giant disks. To most eyes, the two
central disks do not look the same size. The one surrounded by big disks
looks about 30 percent smaller than the one with small disks-an illusion
called size contrast. It is one of many illusions used by Gestalt psychol
ogists to show that perception is always relative-never absolute-always
dependent on the surrounding context.
Instead of using a line drawing to get this efect, Dr. Aglioti set two
medium- sized dominoes on a table. One was surrounded with larger
T H E z 0 M B I E I N T H E B RA I N I 8 3
dominoes and the second with smaller dominoes-j ust like the disks. A
with the disks, when a student looked at the two central dominoes, one
looked obviously smaller than the other. But the astonishing thing is that
when he was asked to reach out and pick up one of the two central
dominoes, his fngers moved the right distance apart as his hand ap
proached the domino. A frame- by-frame analysis of his hand revealed
that the fngers moved apart exactly the same amount for each of the
two central dominoes, even though to his eyes ( and to yours) one looks
30 percent bigger. Obviously, his hands knew something that his eyes
did not, and this implies that the illusion is only "seen" by the obj ect
stream in his brain. The how stream-the zombie-is not fooled for a
second, and so "it" ( or he) was able to reach out and correctly grasp
the domino.
This little experiment may have interesting implications for day-to-day
activities and athletics. Marksmen say that if you focus too much on a
rifle target, you will not hit the bull 's-eye; you need to "let go" before
you shoot. Most sports rely heavily on spatial orientation. A quarterback
throws the ball toward an empty spot on the feld, calculating where the
receiver will be if he is not tackled. An outfelder starts running the
moment he hears the crack of a baseball coming into contact with a bat,
as his how pathway in the parietal lobe calculates the expected destination
of the ball given this auditory input. Basketball players can even close
their eyes and toss a ball into the basket if they stand on the same spot
on the court each time. Indeed, in sports as in many aspects of life, it
may pay to "release your zombie" and let it do its thing. There's no
direct evidence that all of this mainly involves your zombie-the how
pathway-but the idea can be tested with brain imaging techniques.
My eight-year-old son, Mani, once asked me whether maybe the zom
bie is smarter than we think, a fact that is celebrated in both ancient
martial arts and modern movies like Star Wars. When young Luke Sky
walker is struggling with his conscious awareness, Yoda advises, "Use the
force. Feel it. Yes, " and "No. Try not! Do or do not. There is no try. "
Was he referring to a zombie?
I answered, "No, " but later began to have second thoughts. For in
tuth, we kow so little about the brain that even a child's questions
should be seriously entertained.
The most obvious fact about existence is your sense of being a single,
unifed self "in charge" of your destiny; so obvious, in fact, that you
rarely pause to think about it. Ad yet Dr. Aglioti 's experiment and
observations on patients like Diane suggest that there is in fact another
8 4 I P H A N T O MS I N T H E B RA I N
being inside you that goes about his or her business without your knowl
edge or awareness. Ad, as it turns out, there is not just one such zombie
but a multitude of them inhabiting your brain. If so, your concept of a
single "I" or "self" inhabiting your brain may be simply an illusion1 1 -
albeit one that allows you to organize your life more efciently, gives
you a sense of purpose and helps you interact with others. This idea will
be a recurring theme in the rest of this book.
CHAPTER s
The Secret Life of
James Thurber
Is this a dager which I see before me,
Te handle toward my hand?
Come, let me clutch
thee:
I have thee not, and yet I see thee still.
Art thou not fatal vision, sensible
To feeling as to siht? or art thou but
A dager ofthe mind, a false creation,
Proceeding fom the heat oppressed brain?
-WILLIAM SHSPEARE
When James Thurber was six years old, a toy arrow shot accidentally at
him by his brother impaled his right eye and he never saw out of that
eye again. Though the loss was tragic, it was not devastating; like most
one- eyed people he was able to navigate the world successflly. But much
to his distress, in the years afer the accident his lef eye also started
progressively deteriorating so that by the time he was thirty-fve he had
become completely blind. Yet ironically, far from being an impediment,
Thurber's blindness somehow stimulated his imagination so that his vi
sual feld, instead of being dark and dreary, was flled with hallucinations,
creating for him a fantastic world of surrealistic images. Thurber fans
adore "The Secret Life of Walter Mitty, " wherein Mitty, a milquetoast
of a man, bounces back and forth between fights of fantasy and reality
as if to mimic Thurber's own curious predicament. Even the whimsical
8 5
8 6 I P HA N T O MS I N T H E B RA I N
"You said a moment ago that everybody you look
at seems to be a rabbit. Now just what do you mean
by that, Mrs. Sprgue?"
Fige 5. 1 One of James Turber)s well-known cartoons that appeared in The
New Yorker. Could his visual hallucinations have been a source of inspiration for
some of these cartoons ? By James Thurber, 1937, from Te New Yorker Collection.
Al rights resered.
cartoons for which he was so famous were probably provoked by his
visual handicap ( Figure 5 . l ) . 1
Thus James Thurber was not blind in the sense that you or I might
think of blindness-a falling darkess like the blackest night sky, entirely
devoid of moonlight and stars, or even a complete absence of vision
an unbearable void. For Thurber, blindness was brilliant, star-studded
and sprinked with pixie dust. He once wrote to his ophthalmologist:
Years ago you told me about a nun of the middle centuries who confsed her
retinal disturbances with holy visitation, although she saw only about one tenth
of the holy symbols I see. Mine have included a blue Hoover, golden sparks,
melting purple blobs, a skein of spit, a dancing brown spot, snowflakes, safron
and light blue waves, and two eight balls, to say nothing of the corona, which
used to halo street lamps and is now brilliantly discernible when a shaf oflight
breaks against a crystal bowl or a bright metal edge. This corona, usually triple,
is like a chrysanthemum composed of thousands of radiating petals, each ten
T H E S E C RE T L I F E O F ] A ME S T H U R B E R I 8 7
times as slender and each containing in order the colors of the prism. Man has
devised no spectacle of light in any way similar to this sublime arrangement of
colors or holy visitation.
Once, afer Thurber's glasses shattered, he said, "I saw a Cuban fag
fying over a national bank, I saw a gay old lady with a gray parasol walk
right through the side of a truck, I saw a cat roll across a street in a small
striped barrel . I saw bridges rise lazily into the air, like balloons. "
Thurber knew how to use his visions creatively. "The daydreamer,"
he said, "must visualize the dream so vividly and insistently that it be
comes, in efect, an actuality. "
Upon seeing his whimsical cartoons and reading his prose, I realized
that Thurber probably sufered from an extraordinary neurological con
dition called Charles Bonnet syndrome. Patients with this curious dis
order usually have damage somewhere in their visual pathway-in the
eye or in the brain-causing them to be either completely or partially
blind. Yet paradoxically, like Thurber, they start experiencing the most
vivid visual hallucinations as if to "replace" the reality that is missing
from their lives. Unlike many other disorders you will encounter in this
book, Charles Bonnet syndrome is extremely common worldwide and
afects millions of people whose vision has become compromised by glau
coma, cataracts, macular degeneration or diabetic retinopathy. Many
such patients develop Thurberesque hallucinations-yet oddly enough
most physicians have never heard about the disorder. 2 One reason may
be simply that people who have these symptoms are reluctant to mention
them to anyone for fear of being labeled crazy. Wo would believe that
a blind person was seeing clowns and circus animals cavorting in her
bedroom? Wen Grandma, sitting in her wheelchair in the nursing home,
says, "Wat are all those water lilies doing on the floor? " her family is
likely to think she's lost her mind.
If my diagnosis of Thurber's condition is correct, we must conclude
that he wasn't just being metaphorical when he spoke of enhancing his
creativity with his dreams and hallucinations; he really did experience all
those haunting visions-a cat in a striped barrel did indeed cross his
visual feld, snowflakes danced and a lady walked through the side of the
truck.
But the images that Thurber and other Charles Bonnet patients ex
perience are very diferent from those that you or I could conjure up in
our minds. If I asked you to describe the American fag or to tell me
how many sides a cube has, you'd maybe shut your eyes to avoid dis-
8 8 I P H A N T O MS I N T H E B RA I N
traction and conjure up a faint internal mental picture, which you'd then
proceed to scan and describe. ( People vary greatly in this ability; many
undergraduates say that they can only visualize four sides on a cube. )
But the Charles Bonnet hallucinations are much more vivid and the pa
tient has no conscious control over them-they emerge completely un
bidden, although like real objects they may disappear when the eyes are
closed.
I was intrigued by these hallucinations because of the internal contra
diction they represent. They seem so extraordinarily real to the patient
indeed some tell me that the images are more "real than reality" or that
the colors are "superivid"-and yet we know they are mere fgments
of the imagination. The study of this syndrome may thus allow us to
explore that mysterious no- man' s-land between seeing and knowing and
to discover how the lamp of our imagination illuminates the prosaic im
ages of the world. Or it may even help us investigate the more basic
question of how and where in the brain we actually "see" things-how
the complex cascade of events in the thirty- odd visual areas in my cortex
enables me to perceive and comprehend the world.
Wat is visual imagination? Are the same parts of your brain active
when you imagine an object-say, a cat-as when you look at it actually
sitting in front of you? A decade ago, these might have been considered
philosophical questions, but recently cognitive scientists have begun to
probe these processes at the level of the brain itself and have come up
with some surprising answers. It turns out that the human visual system
has an astonishing ability to make educated guesses based on the frag
mentary and evanescent images dancing in the eyeballs. Indeed, in the
last chapter, I showed you many examples to illustrate that vision involves
a great deal more than simply transmitting an image to a screen in the
brain and that it is an active, constructive process. A specifc manifestation
of this is the brain's remarkable capacity for dealing with inexplicable
gaps in the visual image-a process that is sometimes loosely referred to
as "flling in. " A rabbit viewed behind a picket fence, for instance, is not
seen as a series of rabbit slices but as a single rabbit standing behind the
vertical bars of the fence; your mind apparently flls in the missing rabbit
segments. Even a glimpse of your eat's tail sticking out from underneath
the sofa evokes the image of the whole cat; you certainly don't see a
disembodied tail, gasp and panic or, like Lwis Carroll's Alice, wonder
where the rest of the cat is. Actually, "flling in" occurs at several difer-
T H E S E C RE T L I F E O F J A ME S T H U RB E R I 8 9
ent stages of the visual process, and it's somewhat misleading to lump
all of them together in one phrase. Even so, it's clear that the mind, like
nature, abhors a vacuum and will apparently supply whatever information
is required to complete the scene.
Migraine suferers are well aware of this extraordinary phenomenon.
When a blood vessel goes into a spasm, they temporarily lose a patch of
visual cortex and this causes a corresponding blind region-a scotoma
in the visual feld. ( Recall there is a point-to-point map of the visual
world in the visual feld. ) If a person having a migraine attack glances
around the room and his scotoma happens to "fall" on a large clock or
painting on the wall, the object will disappear completely. But instead of
seeing an enormous void in its place, he sees a normal -looking wall with
paint or wallpaper. The region corresponding to the missing object is
simply covered with the same color of paint or wallpaper.
Wat does it actually feel like to have a scotoma? With most brain
disorders you have to remain content with a clinical description, but you
can get a clear sense of what is going on in migraine suferers by simply
examining your own blind spot. The existence of this natural blind spot
of the eye was actually predicted by the seventeenth-century French sci
entist Edme Mariotte. While dissecting a human eye, Mariotte noticed
the optic disk-the area of the retina where the optic nerve exits the
eyeball . He realized that unlike other parts of the retina, the optic disk
is not sensitive to light. Applying his kowledge of optics and eye anat
omy, he deduced that every eye should be blind in a small portion of its
visual feld.
You can easily confrm Mariotte's conclusion by examining the illus
tration of a hatched disk on a light gray background ( Figure 5 . 2 ) . Close
your right eye and hold this book about a foot away from your face and
fxate your gaze on the little black dot on the page. Concentrate on the
dot as you slowly move the page toward your lef eye. At some critical
distance, the hatched disk should fall within your natural blind spot and
disappear completely! 3 However, notice that when the disk disappears,
you do not experience a big black hole or void in its place. You simply
see this region as being "colored" by the same light gray background as
the rest of the page-another striking example of flling in. 4
You may be wondering why you've never noticed your blind spot
before now. One reason is related to binocular vision, which you can test
for yourself. Afer the hatched disk has disappeared, try opening the other
eye and you will see that the disk pops back instantly into view. This
happens because when both eyes are open the two blind spots don't
9 0 I P HA NT OMS I N T HE B RA I N

Fige 5. 2 Blind spot demonstation. Shut your riht eye and look at the black
dot on the right with your lef eye. From about one and a hal feet away, move the
book slowly toward you. At a critical distance the circular hatched disk on the lef
will fal entirely on your blind sot and disappear completely. Ifyou move the book
closer stil, the disk wil reappear. You may need to ((hunt" for the blind spot by
moving the book to and fo several times until the disk disappears.
Notice that when the disk disappears you don't see a dark void or hole in its
place. Te region is seen as being covered with the same liht gray color as the
background. Tis phenomenon is loosely referred to as ('ling in. "
overlap; the normal vision of your lef eye compensates for the right eye's
blind spot and vice versa. But the surprising thing is that even if you
close one eye and glance around the room, you are still not aware of the
blind spot unless you careflly look for it. Again, you don't notice the
gap because your visual system obligingly fls in the missing informa
tion. 5
But how sophisticated is this flling-in process? Are there clear limits
as to what can be fled in and what cannot? And would answering this
question give us hints about what type of neural brain machinery may
be involved in allowing it to happen?
Bear in mind that the fling in is not just some odd quirk of the visual
system that has evolved for the sole purpose of dealing with the blind
spot. Rather, it appears to be a manifestation of a very general ability to
construct surfaces and bridge gaps that might be otherwise distracting in
an image-the same ability, in fact, that allows you to see a rabbit behind
T H E S E C RE T L I F E O F J A M E S T H U RB E R I 9 1
a picket fence as a complete rabbit, not a sliced-up one. In our natural
blind spot we have an especially obvious example of flling in-one that
provides us with a valuable experimental opportunity to examine the
"laws" that govern the process. Indeed, you can actually discover these
laws and explore the limits of flling in by playing with your own blind
spot. ( To me, this is one reason the study of vision is so exciting. It
allows anyone armed with a sheet of paper, a pencil and some curiosity
to peer into the inner workings of his own brain. )
First, you can decapitate your friends and enemies, using your natural
blind spot. Standing about ten feet away from the person, close your
right eye and look at his head with your lef eye. Now, slowly start
moving your lef eye horizontally toward the right, away from the per
son's head, until your blind spot falls directly on his head. At this critical
distance, his head should disappear. When Kng Charles II, the "science
king" who founded the Royal Society, heard about the blind spot, he
took great delight in walking around in his court decapitating his ladies
in waiting or beheading criminals with his blind spot before they were
actually guillotined. I must confess I sometimes sit in faculty meetings
and enjoy decapitating our departmental chairman.
Next we can ask what will happen if you run a vertical black line through
your blind spot. Again, close your right eye and stare at the black spot to
the right of the picture ( Figure 5 . 3 ) with your lef eye. Then move the
page gradually to and fro until the small hatched square on the center of
the vertical line falls exactly inside your lef eye' s blind spot. ( The hatched
square should now disappear. ) Since no information about this central
portion of the line-falling on the blind spot-is available to the eye or the
brain, do you perceive two short vertical lines with a gap in the middle, or
do you "fll in" and see one continuous line? The answer is clear. You will
always see a continuous vertical line. Perhaps neurons in your visual system
are making a statistical estimate; they "realize" that it is extremely unlikely
that two diferent lines are precisely lined up on either side of the blind
spot in this manner simply by chance. So they "signal" to higher brain
centers that this is probably a single continuous line. Everything that the
visual system does is based on such educated guesswork.
But what if you try to confound the visual system by presenting in
ternally contradictory evidence-for instance, by making the two line
segments difer in some way? What if one line is black and the other is
white ( shown on a gray background) ? Does your visual system still regard
these two dissimilar segments as being parts of a single line and proceed
to complete it? Surprisingly, the answer is again yes. You will see a con-
9 2 I P HANT OMS I N T H E B RA I N

Fige 5. 3 A vertical black line running through the blind spot. Repeat the pro
cedure described for Fiure 5.2. Shut your riht eye, look at the smal black dot on
the riht with your lef eye and move the page to and fo until the hatched square
on the lef falls on your blind spot and disappears. Does the vertical line look con
tinuous, or does it have a gap in the middle ? Tere is a lot of variation fom person
to person, but most people ((complete)) the line. I the ilusion doesn't work for you,
tr aiming your blind spot at a single black-white edge (such as the edge of a black
book on a white background) and you will see it complete.
THE S E C RE T LI F E O F J AME S THU RB E R I 9 3

Fige 5.4 Te upper hal ofthe line is white and the lower hal black. Does your
brain complete the vertical line in spite ofthis interaly contradictor evidence ?
tinuous single straight line, black on top and white below, but smeared
in the middle into a lustrous metallic gray (Figure 5.4). This is the com
promise solution that the visual system seems to prefer.
People ofen assume that science is serious business, that it is always
"theor driven, " that you generate lof conjectures based on what you
already know and then proceed to design experiments specifcally to test
9 4 I P HA NT O MS I N T H E B RA I N
these conjectures. Actually real science is more like a fshing expedition
than most of my colleagues would care to admit. ( Of course, I would
never say this in a National Institutes of Health [ NIH] grant proposal ,
for most fnding agencies still cling to the naive belief that science is all
about hypothesis testing and then careflly dotting the "i' s" and crossing
the "t's . " God forbid that you should j ust try to do something entirely
new that's just based on a hunch! )
So let's continue our experiments on your blind spot, just for fn.
What if you challenged your visual system by deliberately misaligning the
two half lines-shifing the top line segment to the lef and the bottom
line segment to the right? Would you then see a complete line anyway
with a kink in the middle? Would you connect the two lines with a
diagonal line running through the blind spot? Or would you see a big
gap ( Figure 5. 5 W
Most people do complete the missing line segment, but the astonish
ing thing is that the two segments now appear collinear-they get per
fectly lined up to form a vertical straight line ! Yet if you try the same
experiment using two horizontal lines-one on either side of the blind
spot-you don't get this "lining-up" efect. You either see a gap or a
big kink-the two lines don't fse to form a horizontal straight line. The
reason for the diference-lining up vertical lines but not horizontal
lines-is not clear, but I suspect that it has something to do with ster
eoscopic vision: our ability to extract the tiny diferences between the
image of the two eyes to see depth?
How "clever" is the mechanism that completes images across the
blind spot? We have already seen that if you aim your blind spot at
some body's head ( so that it vanishes ) , your brain doesn't replace the
missing head; it remains chopped of until you look of to one side so
that the head falls on the normal retina once again. But what if you used
much simpler shapes than heads? For example, you could try "aiming"
your blind spot at the corner of a square ( Figure 5 . 6 ). Noticing the other
three corners, does your visual system fll in the missing corner? If you
try this experiment, you will notice that in fact the corner disappears or
looks "bitten of or smudged. Clearly the neural machinery that allows
completion across the blind spot cannot deal with corners; there's a limit
to what can and what cannot be flled in. 8
Completing a corner is obviously too big a challenge for the visual
system; perhaps it can cope only with very simple patterns such as ho
mogeneous colors and straight lines. But you're in for a surprise. Try
aiming your blind spot at the center of a bicycle wheel with radiating
T H E S E C R E T L I F E O F J A M E S T H U RB E R I 9 5

Fige 5. 5 Repeat the experiment, ((aiming" your blind spot at a patern that
resembles a sastika-an ancient Indo-European peace smbol. Te lines are de
liberately misalined, one on either side of the blind spot.
Many people fnd that when the central hatched disk disappears, the to verical
lines get cclined up" and become collinear, whereas the two horizontal lines are not
lined up-there is a sliht bend or kink in the middle.
spokes ( Figure 5. 7) . Notice that when you do this, unlike what you
observed with the corner of the square, you do not see a gap or smudge.
You do indeed "complete" the gap-you actually see the spokes con
verging into a vortex at the center of your blind spot.
So it appears that there are some things you can complete across the
blind spot and other things you cannot, and it's relatively easy to discover
these principles by simply experimenting with your own blind spot or a
friend' s.
Some years ago, Jonathan Piel, the former editor of Scientic Amer
ican, invited me to write an article on the blind spot for that j ournal .
9 6 I P HANT OMS I N T HE B RA I N

Fige 5. 6 Move the page toward you until the hatched disk fall on the blind
spot. Does the corner ofthe square get completed? Te anser is that most people
see the corer <<missing)) or ccsmudged)J; it does not get flled in. Ti simple dem
onsation shows that fling in is not based on guessork; it is not a hih-level
cognitive process.
Soon afer the article appeared, I received hundreds of letters fom read
ers who tried the various experiments I had described or had devised new
ones of their own. These letters made me realize how intensely curious
people are about the inner workings of their visual pathways. One chap
even embarked on a whole new style of a and had a show of his own
paintings at an a gallery. He had created various complex geometric
designs, which you have to view with one eye, aiming your blind spot at
a specifc section of the painting. Like James Thurber, he had used his
blind spot creatively to inspire his a.
I hope these examples have given you a feel for what it is like to "fl
in" missing portions of the visual feld. You have to bear in mind,
though, that you have had a blind spot all your life and you might be
especially skilled at this process. But what if you lost a patch of visual
cortex as a result of disease or accident? Wat if a much larger hole in
your visual feld-a scotoma-suddenly appeared? Such patients do exist
T H E S E C R E T L I F E O F J A ME S T H U R B E R I 9 7
Fige 5. 7 Amazingly, when the blind spot is aimed at the center of a bicycle
wheel, no gap is seen. People usually report that the spokes converge toward a vortex.
and they present a valuable opportunity to study how far the brain can
go in supplying the "missing information" when needed. Migraine pa
tients have transient scotomas, but I decided it would be best to study
someone who had a large permanent blind spot in his visual feld, and
that is how I met Josh. 9
Josh was a large man with Brezhnev- like eyebrows, a barrel chest and
meaty hands . Yet he exuded a natural twinkle and sense of humor that
infsed what would otherwise be a rather menacing body type with the
burly sweetness of a teddy bear. Whenever Josh laughed, everyone in the
room chucked with him. Now in his early thirties, some years earlier he
had sufered an industrial accident in which a steel rod penetrated the
back of his skull , punching a hole in his right occipital pole in the primary
9 8 I P HA N T O MS I N T H E B RA J N
visual cortex. When Josh looks straight ahead, he has a blind spot about
te size of my palm to the lef of where he's lookng. No other part of
his brain was damaged. Wen Josh came to see me, he said that he was
well aware that he had a large blind spot.
"How do you kow? " I asked.
"Well, one problem is that I ofen walk into the women's room. "
"Wy i s that? "
"Because when I look at the sign WOMEN straight on, I don't see the
'w' and the
'
o
'
to the lef. I just see 'MEN. ' " Josh insisted, however,
tat oter than these occasional hints that something was wrong, his
vsion seemed surprisingly normal . In fact, given his defcit, he was sur
prsed by the unitary nature of his visual world. "When I look at you, "
he said, "I don' t see anything missing. No pieces are l ef out. " He
paused, kitted hi s eyebrows, studied my face and then broke into a huge
smil e. "If I pay carefl attention, Dr. Rmachandran, I notice that one
of your eyes and an ear are missing! Ae you feeling okay? "
Unless he scrtinized his visual feld, Josh seemed to fll in the missing
information with no trouble. Athough researchers have known for a long
tme that patients like Josh exist ( and live quite normally except when
frghtening women in ladies' rooms ) , many psychologists and physicians
have remained skeptical of the flling-in phenomenon. For example, the
Canadian psychologist Justine Sergent claimed that patients like Josh are
confabulating or engaging in a kind of unconscious guesswork when they
say they can see normally. ( He guesses that there is wallpaper in his
scotoma because there is wallpaper everywhere else. ) This tpe of guess
work, she said, would be very diferent from the tpes of true perceptual
completion that you experienced when you had a line passing through
your blind spot. 1 0 But I realized that Josh gave us the opportunity to
fnd out what is really going on inside a scotoma. Wy try to second
guess the mechanisms of vision from scratch when we could ask Josh?
Josh swept into the laboratory one drizzly, cold afernoon, propped an
umbrella in one corner and lit up the room with his cheerflness. He was
dressed in a plaid shirt, loose jeans and beat-up running shoes, damp with
mud from the walk into our building. We were going to have some fn to
day. Our strategy was simply to repeat on Josh all the experiments you just
did on your own blind spot. First, we decided to see what would happen if
we ran a line through his scotoma, where a big piece of the visual feld was
missing. Would he see the line as having a gap, or would he fll it in?
But before we did the experiment, we realized we had a minor tech
nical problem. If we gave Josh an actual line, asked him to look straight
T H E S E C R E T L I F E O F J AM E S T H U RB E R I 9 9
ahead and tell us whether he saw a complete line or piece missing, he
might "cheat" inadvertently. He might accidentally move his eyes a tiny
amount, and the slight motion would bring the line into his normal visual
feld and would tell him that the line is complete. We wanted to avoid
that so we simply presented Josh with two half lines on either side of his
scotoma and asked him what he saw. Would he see a continuous line or
two half lines? Recall that when you tried this little experiment using
your own blind spot, you saw the lines as complete.
He considered for a moment and said, "Well, I see two lines, one
above, one below and there's a big gap in the middle. "
"Okay," I said. This was not going anywhere.
"Wait! " said Josh, squinting. "Wait a minute. You know what?
They're growing toward each other. "
"Wat? "
He held up his right index fnger vertically, pointing upward, to mimic
the bottom line and his lef index fnger pointing downward to mimic
the top line. At frst the two fngertips were two inches apart, and then
Josh started moving them toward each other. "Okay," he said excitedly.
"They're growing, growing, growing, growing together, and now there' s
one complete line. " A he said this, his index fngers touched.
Not only i s Josh flling i n, but the flling i n i s happening i n real time.
He could watch it and describe it, contrary to claims that the phenom
enon doesn't exist in people with scotomas.
Clearly some nerve circuits in Josh's brain were taking two half lines,
lying on either side of the scotoma, as sufcient evidence that there is a
complete line there, and these circuits are sending this message to higher
centers in Josh's brain. So his brain could complete information across
the huge, gaping hole right near his center of gaze in much the same
way that you did across your natural blind spot.
Next we wondered what would happen when we deliberately misa
ligned the two lines. Would he complete it with a diagonal line? Or
would his visual system simply give up? Presented with this display, Josh
said, "No dice. They're not completed. I see a gap. Sorry. "
"I know that; just tell me what happens. "
A couple of seconds later Josh exclaimed, "Oh, my God, look what's
happening! "
"What? "
"Hey, they started like this and now they're moving toward each other
like this. " He again held up his fngers to show the two lines moving
sideways. "Now they're completely lined up, and now they're flling in
1 0 0 I P H A N T O MS I N T H E B RA I N
like that. Okay, now it's complete. " The whole process lasted fve sec
onds, an eternity as far as the visual system is concerned. We repeated
the experiment several times with identical results.
So it seemed fairly clear we are dealing with genuine perceptual com
pletion here, for why else would it take so many seconds? If Josh were
guessing, he should guess immediately. But how far could we push this?
How sophisticated is the visual system' s capacity to "insert" the missing
information? Wat if we used a vertical column of "X's" instead of a
plain line? Would he actually hallucinate the missing "X' s"? What if we
used a column of smiling faces? Would he fll in the scotoma with smiling
faces?
So we put the vertical column "X's" on the computer screen and
asked Josh to look to the immediate right of this column so that the
middle three "X's" fell on the scotoma.
"What do you see? " I asked.
"I see 'X's' on top, 'X's' on the bottom, and there's a big gap in the
middle. "
I told him to keep looking at i t since we had already established that
flling in takes time.
"Look, doctor, I' m staring at it and I kow you want me to see an
'X' there, but I don't see it. No 'X's. ' Sorry. " He stared at it for three
minutes, four minutes, fve minutes, and then we both gave up.
Then I tried a long vertical row of tiny ' x' s, ' one set above and one
below the scotoma. "Now what do you see? "
"Oh, yeah, it's a continuous column of ' x' s, ' little ' x's . ' " Josh turned
to me and said, "I know you're really tricking me. There are no 'x's'
really there. Are there? "
"I' m not going to tell you. But I want to know one more thing. Do
the ' x's' on the lef side of where you're looking (which I knew were i n
his scotoma) appear any diferent from the ones above and below? "
Josh replied, "It looks like a continuous column of 'x's. ' I don' t see
any diference. "
Josh was flling i n the little "x's" but not the big "X's. " This difer
ence is important for two reasons. First it rules out the possibility of
confabulation. Ofen in neurology tests, patients will make up a story,
putting on a show for the physician' s beneft. Knowing there were "x's"
above and below, Josh could have guessed that he "saw" them in be
tween without really doing so. But why would he only engage in such
guesswork for the little "x' s" and not the big ones? Since he did not fll
in the missing large "X's," we can assume that in the case of the little
T H E S E C RE T L I F E O F J AM E S T H U RB E R I 1 0 1
"x's" we' re dealing with a genuine perceptual completion process, not
with guesswork or confabulation.
Why did the genuine perceptual completion occur only for the little
"x's" and not the large ones? Perhaps the brain treats the tiny "x's" as
forming a continuous texture and therefore completes it, but when con
fronted with large "x's" it switches to a diferent mode of operation and
"sees" that some of the "X's" were missing. My hunch is that the tiny
letters activated a diferent part of Josh's visual pathway, one that deals
with continuity of textures and surfaces, whereas the large letters would
be processed in the pathway in his temporal lobes that is concerned with
objects ( discussed in the last chapter) rather than surfaces. It makes sense
that the brain should be especially skilled at completing gaps when deal
ing with continuous surface textures and colors but not when dealing
with objects. The reason is that surfaces in the real world are usually
composed of uniform "stuf' or surface texture-like a block of grainy
wood or a sandstone clif-but there is no such thing as a natural surface
made up of large alphabetical letters or faces. ( Of course man- made sur
faces like wallpaper can be made of smiling faces, but the brain didn't
originally evolve in a man - made world. )
To test the notion that completion of textures and "stuf' across a
gap can occur much more easily than completion of objects or letters, I
was tempted to try something a bit outlandish. I put up the numerals 1 ,
2 and 3 above the scotoma and 7, 8 and 9 below. Would Josh percep
tually complete the sequence? What would he see in the middle? Of
course, I used tiny numerals to ensure that the brain would treat them
as a "texture. "
"Hmmm, " said Josh, "I see a continuous column of numbers, ver-
tically aligned numbers. "
"Can you see a gap i n the middle? "
"No. "
"Can you read them out loud for me? "
"Ur, one, two, three, ur, seven, eight, nine. Hey, that's very strange.
I can see the numbers in the middle, but I can't read them. They look
like numbers, but I don't kow what they are. "
"Do they look blurred? "
"No, they don't look blurred. They kind of look strange. I can't tell
what they are-like hieroglyphics or something. "
We had induced a curious form of temporary dyslexia i n Josh. Those
middle numbers did not exist, were not fashed before his eyes, yet his
brain was making up the textural attributes of the number string and
1 0 2 I P H A N T O MS I N T H E B RA I N
completing it. This is another strikng demonstration of division of labor
in the visual pathways. The system in his brain that deals with surfaces
and edges is saying, "There is numberlike stuf in this region-that's
what you should see in the middle, " but since there are no actual num
bers, his object pathway remains silent and the net result is illegible "hi
eroglyphics"!
I t has been known for over two decades now that what we call the
visual system is actually several systems; that there are multiple specialized
cortical areas concerned with diferent visual attributes such as motion,
color and other dimensions. Does flling in occur separately in each of
these areas, or does it occur all at once in just one single area? To fnd
out, we asked Josh to look at the center of a blank screen on the com
puter monitor, and then we suddenly switched on a pattern of twinkling
black dots on a red background.
Josh whistled, apparently taking as much delight in all this as I was.
"My God, doctor," he said, "I can actually see my scotoma for the frst
time. " He yanked a felt pen from my hand and much to my dismay
proceeded to start drawing on the monitor, producing what appeared to
be an outline of the irregular margins of the scotoma ( Josh's ophthal
mologist, Dr. Lilian Lvinson, had earlier mapped out his scotoma using
a sophisticated technique called perimetry and I could therefore compare
his drawing with hers; they were identical ) .
"But Josh, what do you see inside the scotoma? " I asked.
"Well , it's very strange, doctor. For the frst few seconds, I saw only
the red color bleeding into this part of the screen, but the twinking
black dots did not fll in. Then afer a few seconds, the dots flled in, but
they weren't twinking. And last, the actual twinke-the motion sensa
tion-flled in as well . " He turned around, rubbed his eye, looked at me
and said, "Wat does all this mean? "1 1
The answer is that flling in seems to occur at diferent speeds for
diferent perceptual attributes like color, motion ( twinkle) and texture.
Motion takes longer to fll in than color, and so on. Indeed, such dif
ferential flling in provides additional evidence that such specialized areas
do exist in the human brain. For if perception were j ust one process
happening in a single location in the brain, it should happen all at once,
not in stages.
Finally, we tested Josh's ability to fll in more sophisticated shapes,
like the corners of squares . Remember when you tried aiming your blind
spot on a corner, it was chopped of-your brain apparently couldn't fll
it in. Wen we tried the same experiment on Josh, we got the opposite
T H E S E C RE T L I F E O F J AM E S T H U RB E R I 1 0 3
result. He had no difculty in seeing the missing corner, proving that
very sophisticated types of completion were taking place in his brain.
By now, Josh was feeling tired, but we had succeeded in making him
as intensely curious about the flling-in process as we were. Having heard
the King Charles story from me, he decided to try to aim his scotoma
at my graduate student's head. Would his brain prefer to complete her
head ( contrary to what happened in your blind spot) to prevent such a
horrendous spectacle? The answer is no. Josh always saw this person with
a head missing. Thus he could fll in parts of simple geometric shapes
but not complex obj ects like faces or things of that nature. This experi
ment again shows that flling i n is not simply a matter of guesswork, for
there is no reason Josh shouldn't have been able to "guess" that my
student's head was still there.
A important distinction must be made between perceptual and con
ceptual completion. To understand the diference, just think of the space
behind your head now as you are sitting on your chair reading this book.
You can let your mind wander, thinking about the kinds of obj ects that
might be behind your head or body. Is there a window? A Martian? A
gaggle of geese? With your imagination, you can "fll in" this missing
space with just about anything, but sinc you can change your mind
about the content, I call this process conceptual flling in.
Perceptual flling in is very diferent. Wen you fll in your blind spot
with a carpet design, you don' t have such choices about what flls that
spot; you can't change your mind about it. Perceptual flling in is carried
out by visual neurons . Their decisions, once made, are irreversible: Once
they signal to higher brain centers "Yes, this is a repetitive texture" or
"yes, this is a straight line, " what you perceive is irrevocable. We will
return to this distinction between perceptual and conceptual flling in,
which philosophers are very interested in, later when we talk about con
sciousness and whether Martians see red in Chapter 1 2. For now, it
sufces to emphasize that we're dealing with true perceptual completion
across the scotomas, not just guesswork or deduction.
This phenomenon is far more important that one might imagine from
the parlor games I've just described. Decapitating department chairmen
is amusing, but why should the brain engage in perceptual completion?
The answer lies in a Darwinian explanation of how the visual system
evolved. One of the most important principles in vision is that it tries to
get away with as little processing as it can to get the job done. To econ
omize on visual processing, the brain takes advantage of statistical reg
ularities in the world-such as the fact that contours are generally
1 0 4 I P HA N T O MS I N T H E B RA I N
continuous or that table surfaces are uniform-and these regularities are
captured and wired into the machinery of the visual pathways early in
visual processing. Wen you look at your desk, for instance, it seems
likely that the visual system extracts information about its edges and
creates a mental representation that resembles a cartoon sketch of the
table ( again, this initial extraction of edges occurs because your brain is
mainly interested in regions of change, of abrupt discontinuity, at the
edge of desk, which is where the information is ) . The visual system might
then apply surface interpolation to "fll in" the color and texture of the
table, saying in efect, "Well, there's this grainy stuf here; it must be the
same grainy stuf all over. " This act of interpolation saves an enormous
amount of computation; your brain can avoid the burden of scrutinizing
every little section of the desk and can simply employ loose guesswork
instead ( bearing in mind the distinction between conceptual guesswork
and perceptual guesswork) .
What has all of this got to do with James Thurber and other patients
with Charles Bonnet syndrome? Might the fndings that we have dis
cussed so far about the brain' s capacity for "flling in" blind spots and
scotomas also help us understand the extraordinary visual hallucinations
they experience?
Medical syndromes are named afer their discoverers, not the patients
who sufer from them, and this one was named afer a Swiss naturalist,
Charles Bonnet, who lived from 1 720 to 1 773. Even though he sufered
from precarious health and was always on the brink of losing his own
eyesight and hearing, Bonnet was a shrewd obserer of the natural world.
He was the frst person to observe parthenogenesis-the production of
ofspring by an unfertilized female-and that led him to propose an ab
surd theory known as preformationism, the idea that each egg carried by
a female must contain an entire preformed individual , presumably with
miniature eggs of its own, each of which in turn contains even tinier
individuals with eggs, and so on, ad infnitum. A luck would have it,
many physicians remember Charles Bonnet as the gullible chap who hal
lucinated little people in eggs and not as the insightfl biologist who
discovered parthenogenesis.
Fortunately, Bonnet was more perceptive when he obsered and re
ported on an unusual medical situation in his own family. His maternal
grandfather, Charles Lullin, had successflly undergone what in those
days was dangerous and traumatic surgery-the removal of cataracts at
T H E S E C RE T L I F E O F J AM E S T H U R B E R I 1 0 5
age seventy-seven. Eleven years afer the operation, the grandfather be
gan sufering vivid hallucinations. People and obj ects would appear and
disappear without warning, grow in size and then recede. Wen he stared
at the tapestries in his apartment, he saw bizarre transformations involv
ing people with strange gazes and animals that were, he realized, fowing
from his brain and not the weaver's loom.
This phenomenon, as I mentioned earlier, is fairly common in elderly
people with visual handicaps like macular degeneration, diabetic retinop
athy, corneal damage and cataracts. A recent study in the Lancet, a British
medical journal , reported that many older men and women with poor
vision hide the fact that they "see things which aren't really there. " Out
of fve hundred visually handicapped people, sixty admitted that they
hallucinated, sometimes only once or twice a year, but others experienced
visual fantasies at least twice a day. For the most part the content of their
imaginary world is mundane, perhaps involving an unfamiliar person, a
bottle or a hat, but the hallucinations can also be quite fnny. One
woman saw two miniature policemen guiding a midget villain to a tiny
prison van. Others saw ghostly translucent fgures foating in the hallway,
dragons, people wearing flowers on their heads and even beautifl shin
ing angels, little circus animals, clowns and elves. A surprising number
of them report seeing children. Peter Halligan, John Marshall and I once
saw a patient at Oxford who not only "saw" children in her lef visual
feld but could actually hear their laughter, only to turn her head and
realize no one was there. The images can be in black and white or color,
stationary or in motion, and just as clear as, less clear than or more clear
than reality. At times the objects blend into actual surroundings so that
an imaginary person sits in a real chair, ready to speak. The images are
rarely threatening-no slavering monsters or scenes of brutal carnage.
Patients were always easily corrected by others while hallucinating. A
woman said that she once sat at her window watching cows in a neigh
boring meadow. It was actually very cold and the middle of winter, and
she complained to her maid about the cruelty of the farmer. The aston
ished maid looked, saw no cows and said, "Wat are you talking about?
Wat cows? " The woman flushed with embarrassment. "My eyes are
trickng me. I can't trust them anymore. "
Another woman said, "In my dreams I experience things which afect
me, which are related to my life. These hallucinations, however, have
nothing to do with me. " Others are not so sure. A elderly childless
man was intrigued by recurrent hallucinations of a little girl and boy and
wondered whether these hallucinations reflected his unflflled wish to
l 0 6 I P H A N T O MS I N T H E B RA I N
become a father. There' s even a report of a woman who saw her recently
deceased husband three times a week.
Given how common this syndrome is, I am tempted to wonder
whether the occasional reports of "true" sightings of ghosts, UFOs and
angels by otherise sane intelligent people may merely be examples of
Charles Bonnet hallucinations. Is it any surprise that roughly one third
of Americans claim to have seen angels? I' m not asserting that angels
don' t exist ( I have no idea whether they do or not) but simply that many
of the sightings may be due to ocular pathology.
Poor lighting and the changing tones at dusk favor such hallucina
tions. If the patients blink, nod their heads or turn on a light, the visions
ofen cease. Nevertheless, they have no voluntary control over the ap
paritions, which usually appear without warning. Most of us can imagine
the scenes these people describe-a miniature police van with miniature
criminals running about-but we exert conscious control over such
imaginations. With Charles Bonnet syndrome, on the other hand, the
images appear completely unbidden as if they are real objects.
This sudden appearance of intrusive images was apparent in the case
of Larry MacDonald, a twenty- seven-year- old agronomist who sufered
a terrible automobile accident. Larry's head smashed into the windshield,
fracturing the frontal bones above his eyes and the orbital plates that
protected his optic nerves . Comatose for two weeks, he could neither
walk nor talk when he regained consciousness. But that wasn't the worst
of his problems. A Larry recalls, "The world was flled with hallucina
tions, both visual and auditory. I couldn' t distinguish what was real from
what was fake. Doctors and nurses standing next to my bed were sur
rounded by football players and Hawaiian dancers. Voices came at me
from everywhere and I couldn't tell who was talking. " Larry felt panic
and confsion.
Gradually, however, his condition improved as his brain struggled to
repair itself afer the trauma. He regained control over his bodily fnc
tions and learned to walk. He could talk, with difculty, and learned to
distinguish real voices from imagined ones-a feat that helped him sup
press the auditory hallucinations.
I met Larry fve years afer his accident because he had heard about
my interest in visual hallucinations. He talked slowly, with efort, but was
otherwise intelligent and perceptive. His life was normal except for one
T H E S E C RE T L I F E O F J A ME S T H U RB E R I 1 0 7
astonishing problem. His visual hallucinations, which used to occur any
where and everywhere in his visual feld with brilliant colors and spinning
motions, had retreated into the lower half of his feld of vision, where
he was completely blind. That is, he would only see imaginary objects
below a center line extending from his nose outward. Everything above
the line was completely normal ; he would always see what was really out
there. Below the line, he had intermittent recurrent hallucinations.
"Back in the hospital , colors used to be a lot more vivid, " Larry said.
"Wat did you see? " I asked.
"I saw animals and cars and boats, you know. I saw dogs and elephants
and all kinds of things. "
"You can still see them? "
"Oh, yeah, I see them right now here i n the room. "
"You are seeing them now as we speak? "
"Oh, yeah! " said Larry.
I was intrigued. "Larry, you said that when you see them ordinarily,
they tend to cover other objects in the room. But right now you' re
looking straight at me. It's not like you see something covering me right
now, right? "
"A I look at you, there i s a monkey sitting on your lap, " Larry an-
nounced.
"A monkey? "
"Yes, right there on your lap. "
I thought he was j oking. "Tell me how you know you're hallucinat
ing. "
"I don' t know. But it's unlikely there would be a professor here with
a monkey sitting in his lap so I think there probably isn't one. " He smiled
cheerflly. "But it looks extremely vivid and real . " I must have looked
shocked, for Larry continued, "For one thing they fade afer a few sec
onds or minutes, so I know they're not real . And even though the image
sometimes blends quite well into the rest of the scene around it, like the
monkey on your lap," he continued, "I realize that it is highly improb
able and usually don't tell people about it. " Speechless, I glanced down
at my lap while Larry j ust smiled. "Also, there is something odd about
the images-they ofen look too good to be true. The colors are vibrant,
extraordinarily vivid, and the images actually look more real than real
objects, if you see what I mean. "
I was not sure. Wat does he mean by "more real than real "? There
is a school of art called superrealism in which the paintings of things like
l 0 8 I P H A N T O MS I N T H E B RA I N
Campbell 's soup cans are created with the kind of fne detail you only
get through a magnifing glass. These objects are strange to look at, but
maybe that was how Larry saw images in his scotoma.
"Does this bother you, Larry? "
"Well, it kind of does because it makes me curious about why I ex
perience them, but it really doesn't get in my way. I'm much more wor
ried about the fact that I' m blind than about the fact that I see
hallucinations. In fact, sometimes they are fn to watch because I never
know what I'm going to see next. "
"Are the images you see, like this monkey in my lap, things you've
seen before in your life or can the hallucinations be completely new? "
Larry thought a moment and said, "I think they can be completely
new images, but how can that be? I always thought that hallucinations
were limited to things you've already seen elsewhere in your life. But
then lots of times the images are rather ordinary. Sometimes, when I' m
lookng for my shoes i n the morning, the whole foor suddenly is covered
with shoes. It's hard to fnd my own shoes ! More ofen the visions come
and go, as if they have a life of their own, even though they are uncon
nected to what I' m doing or thinking about at the time. "
Not long afer my conversations with Larry, I met another Charles
Bonnet patient, whose world was stranger yet. She was plagued by car
toons! Nancy was a nurse from Colorado who had an arteriovenous mal
formation or AVM-basically a cluster of swollen and fsed arteries and
veins in the back of her brain. If it were to rupture, she could die from
a brain hemorrhage, so her doctors zapped te AVM with a laser to
reduce it in size and "seal it of. " In so doing they lef scar tissue on
parts of her visual cortex. Like Josh, she had a small scotoma and hers
was immediately to the lef of where she was looking, covering about
ten degrees of space. ( If she stretched her arm out in front of her and
looked at her hand, the scotoma would be about twice the size of her
palm. )
"Well, the most extaordinary thing i s that I see images inside this
scotoma," Nancy said, sitting in the same chair tat Larry had occupied
earlier. "I see them dozens of times a day, not continuously, but at
diferent times lasting several seconds each time. "
"What do you see? "
"Cartoons . "
"What? "
"Cartoons. "
"Wat do you mean by cartoons? You mean Mickey Mouse? "
T H E S E C RE T L I F E O F J AM E S T H U RB E R I 1 0 9
"On some occasions I see Disney cartoons. But most commonly not.
Mostly what I see is just people and animals and objects . But these are
always line drawings, flled in with uniform color like comic books. It's
most amusing. They remind me of Roy Lichtenstein drawings. "
"Wat else can you tell me? Do they move? "
"No. They are absolutely stationary. The other thing i s that my car
toons have no depth, no shading, no curvature. "
So that's what she meant when she said they were like comic books.
"Are they familiar people or are they people you've never seen? " I asked.
"They can be either," Nancy said. "I never know what's coming
next. "
Here i s a woman whose brain creates Walt Disney cartoons i n defance
of copyright. Wat is going on? And how could any sane person see a
monkey on my lap and accept it as normal ?
To understand these bizarre symptoms, we are going to have to revise
our models of how the visual system and perception operate from day
to day. In the not too distant past, physiologists drew diagrams of visual
areas with arrows pointing up. An image would be processed at one level,
sent on up to the next level and so on, until the "gestalt" eventually
emerged in some mysterious manner. This is the so- called bottom-up
view of vision, championed by artifcial intelligence researchers over the
last three decades, even though many anatomists have long emphasized
that there are massive feedback pathways proj ecting from the so- called
higher areas to lower visual areas. To pacif these anatomists, textbook
diagrams usually also included arrows pointing backward, but, by and
large, the notion of back proj ections was given more lip service than
fnctional meaning.
A newer view of perception-championed by Dr. Gerald Edelman of
the Neurosciences Institute in La Jolla, California-suggests that the
brain's information fow resembles the images in a fnhouse fll of mir
rors, continually refected back and forth, and continually changed by
the process of refection. 1 2 Like separate light beams in a fnhouse, visual
information can take many diferent paths, sometimes diverging, some
times reinforcing itself, sometimes traveling in opposite directions .
If this sounds confsing, let's return to the distinction I made earlier
between seeing a cat and imagining a cat. Wen we see a cat, its shape,
color, texture and other visible attributes will impinge upon our retina
and travel through the thalamus ( a relay station in the middle of the
brai n) and up into the primary visual cortex for processing into two
streams or pathways. As discussed in the previous chapter, one pathway
1 1 0 I P HA N T O MS I N T H E B RA I N
goes to regions dealing with depth and motion-allowing you to grab
or dodge obj ects and to move around the world-and the other to
regions dealing with shape, color and object recognition ( these are the
how and what vision pathways ) . Eventually, all the information is com
bined to tell us that this is a cat-say, Felix-and to enable us to recall
everything we've ever learned or felt about cats in general and Felix in
particular. Or at least that's what the textbooks tell us .
Now think of what's going on in your brain when you imagine a cat. 1 3
There' s good evidence t o suggest that we are actually running our visual
machinery in reverse! Our memories of all cats and of this particular cat
fow from top to bottom-from higher regions to the primary visual
cortex-and the combined activities of all these areas lead to the percep
tion of an imaginary cat by the mind's eye. Indeed, the activity in the
primary visual cortex may be almost as strong as if you really did see a
cat, but in fact the cat is not there. This means that the primary visual
cortex, far from being a mere sorting ofce for information coming in
from the retina, is more like a war room where information is constantly
being sent back from scouts, enacting all sorts of scenarios, and then
information is sent back up again to those same higher areas where the
scouts are working. There' s a dynamic interplay between the brain' s so
called early visual areas and the higher visual centers, culminating in a
sort of virtual reality simulation of the cat. (All this was discovered mainly
from animal experiments and neuroimaging studies in humans. )
It's not yet clear exactly how this "interplay" occurs or what its fnc
tion might be. But it may explain what is happening in the Charles Bon
net patients like Larry and Nancy or the senior citizens sitting in a
darkened room at the nursing home. I suggest that they are flling in
missing information in much the same way that Josh did except that they
are using high-level stored memories. 1 4 So, in Bonnet syndrome, the
images are based on a sort of "conceptual completion" rather than per
ceptual completion; the images being "flled in" are coming from mem
ory ( top down)-not from the outside ( bottom up) . Clowns, water lilies,
monkeys and cartoons populate the blind region rather than j ust the
information immediately surrounding the scotoma such as lines and small
"x's. " Of course, when Larry sees a monkey in my lap he isn't duped;
he knows perfectly well it's not real because he realizes it's highly im
probable that there should be a monkey in my ofce.
But if this argument is correct-if the early visual areas are activated
each time you imagine something-then why don't you and I hallucinate
all the time or at least occasionally confse our internally generated im-
T H E S E C RE T L I F E O F } A ME S T H U RB E R I I l l
ages with real objects? Wy don't you see a monkey in the chair when
you simply think of one? The reason is that even if you close your eyes,
cells in your retina and in early sensory pathways are constantly active
producing a flat, baseline signal . This baseline signal informs your higher
visual centers that there is no object ( monkey) hitting the retina
thereby vetoing the activity evoked by top-down imagery. But if the early
visual pathways are damaged, this baseline signal is removed and so you
hallucinate. 1 5
I t makes good evolutionary sense that even though your internal im
ages can be ver realistic, tey can never actually substitute for the real
thing. You cannot, as Shakespeare said, "cloy the hungry edge of appetite
by bare imagination of a feast. " A good thing, too, because if you could
satisf your hunger by thinking about a feast, you wouldn't bother to
eat and would quickly become extinct. Likewise, any creature that could
imagine orgasms is unlikely to transmit its genes to the next generation.
( Of course, we can do so to a limited extent as when our hearts pound
when imagining an amorous encounter-the basis of what is sometimes
called visualization therapy. )
Additional support for this interaction between top-down imagery and
bottom-up sensory signals in perception comes from what we saw in
phantom limb patients who have vivid impressions of clenching their
nonexistent fngers and digging imaginary fngernails into their phantom
palms, generating unbearable pain. Wy do these patients actually feel
clenching, "nails digging" and pain, whereas you or I can imagine the
same fnger position but feel nothing? The answer is that you and I have
real input coming in from our hands telling us that there is no pain, even
though we have memory traces in our brain linking the act of clenching
with nails digging ( especially if you don't ofen cut your nails ) . But in
an amputee, these feeting associations and preexisting pain memories
can now emerge without contradiction from ongoing sensory input. The
same sort of thing might be happening in Charles Bonnet syndrome.
But why did Nancy always see cartoons in her scotoma? One possi
bility is that in her brain the feedback comes mainly from the what path
way in the temporal lobe, which, you will recall , has cells specialized for
color and shapes but not for motion and depth, which are handled by
the how pathway. Therefore, her scotoma is flled with images that lack
depth and motion, having only outlines and shapes, as do cartoons.
If I' m right, all these bizarre visual hallucinations are simply an ex
aggerated version of the processes that occur in your brain and mine
every time we let our imagination run free. Somewhere in the confsed
1 1 2 I P H A N T O MS I N T H E B RA I N
welter of interconnecting forard and backward pathways is the interface
between vision and imagination We don't have clear ideas yet about
where this interface is or how it works ( or even whether there is a single
interface ) , but these patients provide some tantalizing clues about what
might be going on. The evidence from them suggests that what we call
perception is really the end result of a dynamic interplay between sensory
signals and high-level stored information about visual images from the
past. Each time any one of us encounters an obj ect, the visual system
begins a constant questioning process. Fragmentary evidence comes in
and the higher centers say, "Hmmmmm, maybe this is an animal . " Our
brains then pose a series of visual questions: as in a twenty- questions
game. Is it a mammal ? A cat? What kind of cat? Tame? Wild? Big? Small ?
Black or white or tabby? The higher visual centers then proj ect partial
"best ft" answers back to lower visual areas including the primary visual
cortex. In this manner, the impoverished image is progressively worked
on and refned (with bits "flled in," when appropriate ) . I think that
these massive feed forward and feedback proj ections are in the business
of conducting successive iterations that enable us to home in on the
closest approximation to the truth. 1 6 To overstate the argument delib
erately, perhaps we are hallucinating all the time and what we call per
ception is arrived at by simply determining which hallucination best
conforms to the current sensory input. But if, as happens in Charles
Bonnet syndrome, the brain does not receive confrming visual stimuli ,
it is free simply to make up its own reality. And, as James Thurber was
well aware, there is apparently no limit to its creativity.
CHAPTER 6
Throu
g
h the Lookin
g
Glass
Te world is not only queerer than we imagine;
it is queerer than we can imagine.
-]B. S. HLDANE
Wo was this rolling out of the bedroom in a wheelchair? Sam couldn't
believe his eyes. His mother, Ellen, had just returned home the night
before, having spent two weeks at the Kiser Permanente hospital re
cuperating from a stroke. Mom had always been fastidious about her
looks. Clothes and makeup were Marha Stewart perfect, with beautiflly
coifed hair and fngernails painted in tastefl shades of pink or red. But
today something was seriously wrong. The naturally curly hair on the
lef side of Ellen's head was uncombed, so that it stuck out in little
nestlike clumps, whereas the rest of her hair was neatly styled. Her green
shawl was hanging entirely over her right shoulder and dragging on the
floor. She had applied rather bright red lipstick to her upper right and
lower right lips, leaving the rest of her mouth bare. Likewise, there was
a trace of eyeliner and mascara on her right eye but the lef eye was
unadorned. The fnal touch was a spot of rouge on her right cheek-
1 1 3
1 1 4 I P H A N T O MS I N T H E B RA I N
very careflly applied so as not to appear as if she were trying to hide
her ill health but enough to demonstrate that she still cared about her
looks. It was almost as though someone had used a wet towel to erase
all the makeup on the lef side of his mother's face!
"Good grief" cried Sam. "\at did you do to your makeup "
Ellen raised her eyebrow i n surprise. \at was her son talking about
She had spent half an hour getting ready this morning and felt she looked
as good as she possibly could, given the circumstances.
Ten minutes later, as they sat eating breakfast, Ellen ignored all the
food on the lef side of her plate, including the fresh-squeezed orange
juice she so loved.
Sam raced for the phone and called me, as one of the physicians who
had spent time with his mother at the hospital . Sam and I had gotten
to know one another while I had been seeing a stroke patient who shared
a room with his mother. "It's all right, " I said, "don' t be alarmed. Your
mother is sufering from a common neurological syndrome called hemi
neglect, a condition that ofen follows strokes in the right brain, espe
cially in the right parietal lobe. Neglect patients are profoundly
indiferent to objects and events in the lef side of the world, sometimes
including the lef side of their own bodies. "
"You mean she's blind on the lef side "
"No, not blind. She just doesn't pay attention to what's on her lef.
That's why we call it neglect. "
The next day I was able to demonstrate this t o Sam's satisfaction by
doing a simple clinical test on Ellen. I sat directly in front of her and
said, "Fixate steadily on my nose and try not to move your eyes . " \en
her gaze was fxed, I held my index fnger up near her face, just to the
lef of her nose, and wiggled it vigorously.
"Ellen, what do you see "
"I see a fnger wiggling, " she replied.
"Okay," I said. "Keep your eyes fxed on the same spot on my nose. "
Then, very slowly and casually, I raised the same fnger t o the same
position, just lef of her nose. But this time I was carefl not to move it
abruptly. "Now what do you see "
Ellen looked blank. Without having her attention drawn to the fn
ger-via motion or other strong cues-she was oblivious. Sam began to
understand the nature of his mother's problem, the important distinction
between blindness and neglect. His mother would ignore him completely
if he stood on her lef side and did nothing. But if he jumped up and
down and waved his arms, she would sometimes turn around and look.
T H RO U G H T H E L O O K I N G G LA S S I 1 1 5
For the same reason, Ellen fails to notice the lef side of her face in a
mirror, forgets to apply makeup on the lef side of her face, and doesn't
comb her hair or brush her teeth on that side. And, not surprisingly, she
even ignores all the food on the lef side of her plate. But when her son
points to things in the neglected area, forcing her to pay attention, Ellen
might say, "A, how nice. Fresh-squeezed orange juice! " or "How em
barrassing. My lipstick is crooked and my hair unkempt. "
Sam was bafed. Would he have to assist Ellen for the rest of her life
with simple day-to-day chores like applying makeup? Would his mother
remain like this forever, or could I do something to help her?
I assured Sam that I'd try to help. Neglect is a fairly common problem1
and I 've always been intrigued by it. Beyond its immediate relevance to
a patient's ability to care for herself, it has profound implications for
understanding how the brain creates a spatial representation of the world,
how it deals with lef and right and how we are able-at a moment's
notice-to pay attention to diferent portions of the visual scene. The
great German philosopher Immanuel Knt became so obsessed with our
"innate" concepts of space and time that he spent thirty years pacing up
and down his veranda thinking about this problem. ( Some of his ideas
later inspired Mach and Einstein. ) If we could somehow transport Ellen
back in a time machine to visit him, I'm sure he'd be j ust as fascinated
by her symptoms as you or I and would wonder whether we modern
scientists had any inking of what causes this strange condition.
When you glance at any visual scene, the image excites receptors in
your retina and sets in motion a complex cascade of events that culminate
in your perception of the world. A we noted in earlier chapters, the
message from the eye is frst mapped onto an area in the back of brain
called the primary visual cortex. From there it is relayed along two path
ways, the how pathway to the parietal lobe and the what pathway to the
temporal lobe ( see Figure 4. 5, Chapter 4) . The temporal lobes are con
cerned with recognizing and naming individual obj ects and responding
to them with the appropriate emotions. The parietal lobes, on the other
hand, are concerned with discerning the spatial layout of the external
world, allowing you to navigate through space, reach out for objects,
dodge missiles and otherise kow where you are. This division of labor
between temporal and parietal lobes can explain almost all of the peculiar
constellation of symptoms one sees in neglect patients in whom one
parietal lobe-especially the right-is damaged, as is the case with Ellen.
If you let her wander around by herself, she will not pay attention to the
lef side of space and anything that happens in it. She will even bump
1 1 6 I P H A N T O MS I N T H E B RA I N
into objects on her lef side or stub her lef toe on a raised pavement.
( I 'll later explain why this doesn't happen with lef parietal damage. )
However, because Ellen's temporal lobes are still intact, she has no dif
fculty recognizing objects and events as long as her attention is drawn
to them.
But "attention" is a loaded word, and we know even less about it
than we do about neglect. So the statement that the neglect arises from
a "failure to pay attention" doesn't really tell us very much unless we
have a clear notion of what the underlying neural mechanisms might be.
( It's a bit like saying that illness results from a failure of health. ) In
particular, one would like to know how a normal person-you or l-is
able to attend selectively to a single sensory input, whether you are trying
to listen to a single voice amid the background din of voices at a cocktail
party or j ust trying to spot a familiar face in a baseball stadium. Wy do
we have this vivid sense of having an internal searchlight, one that we
can direct at diferent objects and events around us? 2
We now know that even so basic a skill as attention requires the par
ticipation of many far-flung regions of the brain. We've already talked
about the visual , auditory and somatosensory systems, but other special
brain regions carry out equally important tasks . The reticular activating
system-a tangle of neurons in the brain stem that proj ects widely to
vast regions of the brain-activates the entire cerebral cortex, leading to
arousal and wakeflness, or-when needed-a small portion of the cor
tex, leading to selective attention. The limbic system is concerned with
emotional behavior and evaluation of the emotional signifcance and po
tential value of events in the external world. The frontal lobes are con
cerned with more abstract processes like judgment, foresight and
planning. All of these areas are interconnected in a positive feedback
loop-a recursive, echolike reverberation-that takes a stimulus from the
outside world, extracts its salient features and then bounces it from re
gion to region, before eventually fguring out what it is and how to
respond to it. 3 Should I fght, flee, eat or kiss? The simultaneous de
ployment of all these mechanisms culminates in perception.
When a large, threatening stimulus-say, an image of a menacing fg
ure, perhaps a mugger looming toward me on the street in Boston
frst comes into my brain, I haven't the slightest idea of what it is . Before
I can determine, aha, perhaps that's a dangerous person, the visual in
formation is evaluated by both the frontal lobes and the limbic system
for relevance and sent on to a small portion of the parietal cortex, which,
in conjunction with appropriate neural connections in the reticular for-
T H RO U G H T H E L O O K I N G GL A S S I 1 1 7
marion, enables me to direct my attention to the looming fgure. It forces
my brain to swivel my eyeballs toward something important out there in
the visual scene, pay selective attention to it and say, "Aha! "
But imagine what would happen if any part of this positive feedback
loop were interrupted so that the whole process was compromised. You
would then no longer notice what was happening on one side of the
world. You would be a neglect patient.
But we still have to explain why neglect occurs primarily afer injury
to the right parietal lobe and not to the lef. Why the asymmetry?
Though the real reason continues to elude us, Marcel Mesulam of Har
vard University has proposed an ingenious theory. We know that the lef
hemisphere is specialized for many aspects of language and the right
hemisphere for emotions and "global" or holistic aspects of sensory
processing. But Mesulam suggests there is another fndamental difer
ence. Given its role in holistic aspects of vision, the right hemisphere has
a broad "searchlight" of attention that encompasses both the entire lef
and entire right visual felds . The lef hemisphere, on the other hand, has
a much smaller searchlight, which is confned entirely to the right side
of the world (perhaps because it is so busy with other things, such as
language) . A a result of this rather odd arrangement, if the lef hemi
sphere is damaged, it loses its searchlight, but the right can compensate
because it casts a searchlight on the entire world. Wen the right hem
isphere is damaged, on the other hand, the global searchlight is gone
but the lef hemisphere cannot flly compensate for the loss because its
searchlight is confned only to the right side. This would explain why
neglect is only seen in patients whose right hemisphere is damaged.
So neglect is not blindness, but rather a general indiference to objects
and events on the lef. But how profound is this indiference? Aer all ,
even you and I, when driving home from work ignoring familiar terrain,
will perk up immediately if we see an accident. This suggests that at some
level the unattended visual information from the road must have been
getting through. Is Ellen's indiference an extreme version of the same
phenomenon? Is it possible that even though she doesn't notice things
consciously, some of the information "leaks" through? Do these patients
at some level "see" what they don't see? This is not an easy question to
answer, but in 1988 two Oxford researchers, Peter Haligan and John
Marshall,4 took up the challenge. They devised a clever way to demon
strate that neglect patients are subconsciously aware of some of the things
that are going on on their lef side, even though they appear not to be.
They showed patients drawings of two houses, one below the other, that
1 1 8 I P HA N T O MS I N T H E B RA I N
were completely identical except for one salient feature-the house on
the top had flames and smoke spewing fom windows on the lef. They
ten asked the patient whether the houses looked the same or diferent.
The frst neglect patient whom they studied said, not surprisingly, that
the houses looked identical, since he did not pay attention to the lef
side of either drawing. But when forced to choose-"Come on, now,
which house would you rather live in? "-he picked the bottom house,
the one not on fre. For reasons he could not express, he said that he
"preferred" that house. A form of blindsight, perhaps? Could it be that
even though he is not paying attention to the lef side of the house,
some of the information about the fames and smoke leaks through to
his right hemisphere through some alternate pathway and alerts him to
danger? The experiment implies once again that there is no blindness in
the lef visual feld, for if there were, how could he process this level of
detail about the lef side of the house under any circumstances?
Neglect stories are very popular with medical students. Oliver Sacks5
tells the strange tale of a woman who, like many lef hemineglect pa
tients, ate food only from the right side of her plate. But she knew what
was up and realized that if she wanted all her dinner, she had to shif
her head, so as to see the food on the lef. But given her general indif
ference to the lef and reluctance even to look to the lef she adopted a
comically ingenious solution. She rolled her wheelchair in a huge circle
to the right, traveling 340 degrees or so until fnally her eyes would fall
on the uneaten food. That consumed, she'd make another rotation, to
eat the remaining half of the food on her plate, and so on, round and
round, until it was gone. It never occurred to her that she could just
turn lef because-for her-the lef simply didn' t exist.
One morning not long ago while I was fxing the sprinkler system in
our yard, my wife brought me an interesting-lookng letter. I receive
many letters each week, but this one was postmarked from Panama and
had an exotic stamp and curious lettering. I wiped my hands on a towel
and started to read a rather eloquent description of what it feels like to
sufer from hemineglect.
"Wen I came to, other than having a severe headache, I perceived
absolutely no adverse efects of my mishap, " wrote Steve, a former Navy
captain who had heard about my interest in neglect and wanted to see
me in San Diego for a consultation. "In fact, other than a headache, I
felt good. Not wanting to worry my wife-knowing fll well I' d had a
T H RO U G H T H E L O O K I N G G LA S S I 1 1 9
heart attack and that the head pain was subsiding-! told her that she
should not worry; I was fne.
"She responded, 'No, you' re not, Steve. You've had a stroke! '
"A stroke? This statement lef me both surprised and slightly amused.
I' d seen stroke victims on television and in real life, people who either
stared into nothingness or showed clear signs of paralysis in a limb or in
the face. Since I perceived none of these symptoms, I could not believe
my wife was anywhere near correct.
"Actually, I was completely paralyzed on the lef side of my body.
Both my lef arm and lef leg were afected as well as my face. Thus
began my odyssey into a strange warped world.
"To my mind, I was flly aware of all parts of my body on the right
side. The lef side simply did not exist! You might feel I' m exaggerating.
Someone looking at me would see a person with limbs that, though
paralyzed, obviously exist and are just as obviously connected to my
body.
"When I shaved, I neglected the lef side of my face. When I dressed,
I would incessantly leave te lef arm outside its sleeve. I would incor
rectly button the right button side of my clothing to the lef buttonholes,
even though I had to complete this operaton with my right hand.
"There is no way, " Steve concluded, "that you can have any idea of
what happens in Wonderland unless a denizen describes it to you. "
Neglect i s clinically important for two reasons. First, although a ma
jority of patients recover completely afer a few weeks, there is a subset
in whom the disorder can persist indefnitely. For them, neglect remains
a genuine nuisance even though it may not be a life- threatening disorder.
Second, even those patents who seem to recover from neglect quickly
can be seriously handicapped because their indiference to the lef during
the frst few days hinders rehabilitation. Wen a physical therapist urges
them to exercise the lef arm, they don't see te point in doing so be
cause tey don' t notice that it is not performing well . This is a problem
because in stroke rehabilitation most recovery from paralysis occurs in
the frst few weeks and afer this "window of plasticity," the lef hand
tends not to regain fnction. Physicians, therefore, do their utmost to
coax people into using their lef hands and legs in the frst few weeks-a
task frustrated by the neglect syndrome.
Is there some trick you could use to make the patient accept the lef
side of the world and start noticing that her arm was not moving? Wat
would happen if you put a mirror on the patent's right side at right
angles to her shoulder? ( If she were sitting in a phone booth, this would
1 2 0 I P HA N T O MS I N T H E B RA I N
correspond to the right wall of the booth. ) If she now looks in the
mirror, she will see the refection of everything on her lef side, including
people, events and objects, as well as her own lef arm. But since the
reflection itself is on the right-in her nonneglected feld-would she
suddenly start paying attention to these things? Would she realize that
these people, events and objects were on her lef even though the re
flection of them is on the right? If it worked, a trick of this kind would
be nothing short of a miracle. Eforts to treat neglect have frustrated
patients and physicians alike ever since the condition was frst clinically
described more than sixty years ago.
I telephoned Sam and asked whether his mother, Ellen, might be
interested in trying out the mirror idea. It might help Ellen recover more
quickly and it was easy enough to try.
The manner in which the brain deals with mirror reflections has long
fascinated psychologists, philosophers and magicians alike. Many a child
has asked the question "Wy does a mirror reverse things lef to right
but not reverse them upside down? How does te mirror 'know' which
way it should reverse? "-a question that most parents fnd embarrass
ingly difcult to answer. The correct answer to this question comes from
the physicist Richard Feynman ( as quoted by Richard Gregory, who has
written a delightfl book on this topic) . 6
Normal adults rarely confse a mirror reflection for a real object. When
you spot a car fast approaching you in your reariew mirror, you don't
j am on your brakes. You accelerate forard even though it appears that
the image of the car is approaching rapidly from the front. Likewise, if
a burglar opened the door behind you as you were shaving in the bath
room, you'd spin around to confront him-not attack the reflection in
the mirror. Some part of your brain must be making the needed correc
tion: The real obj ect is behind me even though the image is in front
of me. 7
But like Alice i n Wonderland, patients like Ellen and Steve seem to
inhabit a strange no-man's-land between illusion and reality-a "warped
world," as Steve called it, and there is no easy way to predict how they
will react to a mirror. Even though all of us, neglect patients and normal
people alike, are familiar with mirrors and take them for granted, there
is something inherently surrealistic about mirror images. The optics are
simple enough, but no one has any inking of what brain mechanisms
are activated when we look at a mirror reflection, of what brain processes
are involved in our special ability to comprehend the paradoxical juxta
position of a real object and its optical "twin. " Given te right parietal
T H R O U G H T H E L O O K I N G G LA S S I 1 2 1
lobe's important role in dealing with spatial relationships and "holistic"
aspects of vision, would a neglect patient have special problems dealing
with mirror reflections?
Wen Ellen came to my lab, I frst conducted a series of simple clinical
tests to confrm the diagnosis of hemineglect. She funked every one of
them. First, I asked her to sit on a chair facing me and to look at my
nose. I then took a pen, held it up to her right ear and began to move
it slowly, in a sweeping arc, all the way to her lef ear. I asked Ellen to
follow the pen with her eyes, and she did so with no trouble until I
reached her nose. At that point her eyes began to wander of, and soon
she was looking at me, having "lost sight of" the pen near her nose.
Paradoxically, a person who is really blind in her lef visual feld wouldn't
display this behavior. If anything, she would try to move her eyes ahead
of the pen in an efort to compensate for her blindness .
Next, I showed Ellen a horizontal line drawn on a sheet of paper and
asked her to bisect it with a vertical mark. Ellen pursed her lips, took the
pen and confdently placed a mark to the far right of the line because
for her only half a line existed-the right half-and she was presumably
marking the center of that half
When I asked her to draw a clock, Ellen made a fll circle instead of
just a half circle. This is a fairly common response because circle drawing
is a highly overlearned motor response and the stroke did not compro
mise it. But when it came time for Ellen to fll in the numbers, she
stopped, stared hard at the circle and then proceeded to write the num
bers 1 to 1 2, cramped entirely on the right side of the circle!
Finally, I took a sheet of paper, put it in front of Ellen and asked her
to draw a fower.
"What kind of flower? " she said.
"Any kind. Just an ordinary fower. "
Again, Ellen paused, as if the task were difcult, and fnally drew an
other circle. So far so good. Then she painstakingly drew a series of little
petals-it was a daisy-all scrunched on the right side of the fower ( Fig
ure 6. 1 ) .
"That's fne, Ellen, " I said. "Now I want you to do something dif
ferent. I want you to close your eyes and draw a fower. "
Ellen's inability to draw the lef half of objects was to be expected,
since she ignores the lef when her eyes are open. But what would happen
with them closed? Would the mental representation of a fower-the
daisy in her mind' s eye-be a whole fower or just half of one? In other
words, how deep does the neglect reverberate into her brain?
1 2 2 I P HA N T O MS I N T H E B RA I N
Fige 6. 1 Drawing made by a neglect patient. Notice that the lef hal of the
fower is missing.
Many neglect patients will also draw only hal the fower when drawing fom
memor-even with their eyes closed. Tis implies that the patient has also lost the
abilit to as can)) the lef side of the internal mental picture of the fower.
Ellen closed her eyes and drew another circle. Then, frrowing her
brow in concentration, she daintily drew fve petals-all on the right side
of the daisy! It was as though the internal template she used to produce
the drawing was only half presered and therefore the lef side of the
flower simply drops out, even when she' s just imagining it.
Aer a half-hour break, we returned to the lab to try out the mirror.
She sat in her wheelchair, flufng up her hair with her good hand, and
smiled sweetly. I stood on her right holding a mirror on my chest so
that when Ellen faced straight forard in the chair, the mirror was parallel
to the right arm of the wheelchair ( and her profle) and about two feet
away from her nose. I then asked her to turn her head about sixty degrees
and look into the mirror.
From this vantage point Ellen can clearly see the neglected side of the
world reflected in the mirror. She is looking to her right, into her good
side, so to speak, and she knows perfectly well what a mirror is, so she
knows that it is refecting objects on her lef side. Since the information
T H RO U G H T H E LO O KI N G G LA S S I 1 2 3
about the lef side of the world is now coming from the right side-the
nonneglected side-would the mirror help her "overcome" her neglect
so that she correctly reached for the objects on the lef, j ust as a normal
person might? Or would she say to herself, "Oops, that object is really
in my neglected feld, so let me ignore it. " The answer, as so ofen
happens in science, was that she did neither. In fact, she did something
completely outlandish.
Ellen looked in the mirror and blinked, curious about what we were
up to. It ought to have been obvious to her that it was a mirror since it
had a wooden frame and dust on its surface, but to be absolutely sure,
I asked, "What is this I am holding? " ( Remember I was behind the
mirror, holding it. )
She replied without hesitating, "A mirror. "
I asked her to describe her eyeglasses, lipstick and clothing while look
ing straight into the mirror. She did so with no trouble. On receiving a
cue, one of my students standing on Ellen's lef side held out a pen so
that it was well within the reach of her good right hand but entirely
within the neglected lef visual feld. ( This turned out to be about eight
inches below and to the lef of her nose. ) Ellen could see my student's
arm as well as the pen clearly in the mirror, as there was no intent to
deceive her about the presence of a mirror.
"Do you see the pen? "
"Yes . "
"Okay, please reach out and grab i t and write your name on this pad
of paper I've placed in your lap. "
Imagine my astonishment when Ellen lifed her right hand and with
out hesitation went straight for the mirror and began banging on it
repeatedly. She literally clawed at it for about twenty seconds and said,
obviously frustrated, "It's not in my reach. "
When I repeated the same process ten minutes later, she said, "It's
behind the mirror," and reached around and began groping with my
belt buckl e.
A little later she even tried peeking over the edge of the mirror to
look for the pen.
So Ellen was behaving as though the refection were a real object that
she could reach out and grab. In my ffeen-year career, I 'd never seen
anything like this-a perfectly intelligent, levelheaded adult making the
absurd blunder of thinking that an object was actually inside the mirror.
We wanted to make sure that Ellen's behavior did not arise from some
clumsiness of her arm movements or a failure to understand what mirrors
1 2 4 I P H A N T O MS I N T H E B RA I N
are. So we simply tried placing the mirror at arm's length in front of her,
just like a bathroom mirror at home. This time the pen appeared j ust
behind and above her right shoulder ( but just outside her visual feld) .
She saw it i n the mirror and her hand went straight back behind her to
grab it. So her failure in the earlier task could not be explained by claim
ing that she was disoriented, clumsy or confsed as a result of her stroke.
We decided to give a name to Ellen's condition-"mirror agnosia"
or "the looking glass syndrome" in honor of Lewis Carroll. Indeed,
Lewis Carroll is known to have sufered from migraine attacks caused by
arterial spasms. If they afected his right parietal lobe, he may have suf
fered momentary confsion with mirrors that might not only have in
spired him to write Trough the Looking Glass but may help explain his
general obsession with mirrors, mirror writing and lef- right reversal . One
wonders whether Leonardo da Vinci's preoccupation with lef-right re
versed writing had a similar origin.
The looking glass syndrome was intriguing to watch, but it was also
frustrating because I had initially hoped for the exact opposite reaction
that the mirror would make Ellen more aware of the lef side of the
world and help with rehabilitation.
The next step was to fnd out how widespread this syndrome is. Do
all neglect patients behave like Ellen? In testing another twenty patients,
I found that many had the same kind of mirror agnosia. They would
reach into the mirror for the pen or a piece of candy when it was held
in the neglected feld. They knew perfectly well they were looking into
a mirror and yet they made the same mistake as Ellen.
Not all of the patients made this error, however. Some of them initially
looked perplexed, but upon seeing the refection of the pen or candy in
the mirror, they chuckled, and-with a conspiratorial air-reached cor
rectly for the object on the lef j ust as you or I might. One patient even
turned his head to the lef-something he was ordinarily reluctant to
do-and beamed triumphantly as he snatched the reward. These few
patients were clearly paying attention to obj ects they had previously ig
nored, raising a fascinating therapeutic possibility. Will repeated exposure
to the mirror help some people overcome neglect, gradually becoming
more aware of the lef side of the world?9 We are hoping to try this
someday in the clinic.
Therapy aside, the scientist in me is equally intrigued by mirror ag
nosia-the patient's failure to reach correctly for the real object. Even
my two-year-old son, when shown candy only visible in the mirror, gig-
T H RO U G H T H E L O O K I N G G L A S S I 1 2 5
gled, turned around and snatched the sweet. Yet the much older and
wiser Ellen could not do this.
I can think of at least two interpretations of why she might lack this
ability. First, it's possible that the syndrome is caused by her neglect. It's
as though the patient was saying to herself, unconsciously, "Since the
refection is in the mirror, the object must be on my lef. But the lef
does not exist on my planet-therefore, the object must be inside the
mirror. " However absurd this interpretation may seem to us with our
intact brains, it's the only one that would make any sense to Ellen, given
her "reality. "
Second, the looking glass syndrome may not be a direct consequence
of neglect, even though it is usually accompanied by neglect. We know
that when the right parietal lobe is damaged, patients have all kinds of
difculties with spatial tasks, and the looking glass syndrome may simply
be an especially forid manifestation of such defcits. Responding correctly
to a mirror image requires you simultaneously to hold in your mind the
refection as well as the object that is producing it and then perform the
required mental gymnastics to locate correctly the object that produced
the refection. This very subtle ability may be compromised by lesions in
the right parietal lobe, given the important role of that structure in deal
ing with spatial attibutes of the world. If so, mirror agnosia might pro
vide a new bedside test for detecting right parietal lesions . 1 0 In an age
of escalating costs of brain imaging, any simple new test would be a
usefl addition to the neurologist's diagnostic kt.
The strangest aspect of the lookng glass syndrome, however, is lis-
tening to patients' reactions.
"Doctor, why can' t I reach the pen? "
"The darn mirror is in the way. "
"The pen i s inside the mirror and I can' t reach it! "
"Ellen, I want you to grab the real object, not the refection. Where
is the real object? " She replied, "The real object is out there behind the
mirror, doctor. "
It's astonishing that the mere confrontation with a mirror fips these
patients into the twilight zone so that they are unable-or reluctant
to draw the simple logical inference that since the refection is on the
right, the object producing it must be on the lef. It's as though for these
patients even the laws of optics have changed, at least for this smal corner
of their universe. We ordinarily think of our intellect and "high-level"
knowledge-such as laws concerning geometrical optics-as being im-
1 2 6 I P H A N T O M S I N T H E B RA I N
mune to the vagaries of sensory input. But these patients teach us that
this is not always true. Indeed, for them it's the other way around. Not
only is their sensory world warped, but their knowledge base is twisted
to accommodate the strange new world they inhabit. 1 1 Their attention
defcits seem to permeate their whole outlook, rendering them unable
to tell whether a mirror reflection is a real object or not, even though
they can carry on normal conversations on other topics-politics, sports
or chess-j ust as well as you or I. Asking these patients what is the "true
location" of the obj ect they see in the mirror is like asking a normal
person what is north of the North Pole. Or whether an irrational number
( like the square root of 2 or 1 with a never-ending string of decimal s)
realy exists or not. This raises profound philosophical questions about
how sure we can be that our own grasp on reality is all that secure. A
alien four-dimensional creature watching us fom his four-dimensional
world might regard our behavior to be just as pererse, inept and ab
surdly comical as we regard the bumblings of neglect patients trapped in
their strange looking- glass world.
CHAPTER 7
The Sound of One Hand
Clapping
Man is made by his belief A he believes, so he is.
-Bhagavad Gita, 500 B. C.
Te social scientists have a long way to go to catch up,
but they may be up to the most important scientic
business ofall, i and when they fnally get to the riht
questions. Our behavior toward each other is the
strangest, most unpredictable, and almost entirely
unaccountable ofthe phenomena with which we are
oblied to live.
-LEWS THOMS
Mrs. Dodds was beginning to lose patience. Why was everyone around
her-doctors, therapists, even her son-insisting that her lef arm was
paralyzed when she knew perfecty well it was working fne? Wy, j ust
ten minutes ago she had used it to wash her face.
She knew, of course, that she had had a stroke two weeks ago and
that was why she was here, at the University of California Medical Center
in Hillcrest. Except for a small headache, she was feeling better now and
wished she could go home to clip her rose bushes and resume her daily
morning walks along the beach near Point Lora, where she lived. She
had seen her granddaughter Becky j ust yesterday and was thinking how
nice it would be to show of to her the garden now that it was in fll
bloom.
Mrs . Dodds was in fact completely paralyzed on the lef side of her
body afer a stroke that damaged the right hemisphere of her brai n. I
1 2 7
1 2 8 I P H A N T O MS I N T H E B RA I N
see many such patients every month. Usually they have many questions
about their paralysis. Wen will I walk again, doctor? Will I be able to
wiggle my fngers again? Wen I yawned this morning, my lef arm
started to move a little-does that mean I' m starting to recover?
But there is a small subset of patients with right hemisphere damage
who, like Mrs. Dodds, seem blissflly indiferent to their predicament
apparenty unaware of the fact that the entire lef side of their body is
paralyzed-even though they are quite mentally lucid in all other re
spects . This curious disorder-the tendency to ignore or sometimes even
to deny the fact that one's lef arm or leg is paralyzed-was termed
anosognosia ( "unaware of illness") by the French neurologist Joseph
Franois Babinsk who frst obsered it clinically in 1 908.
"Mrs. Dodds, how are you feeling today? "
"Well, doctor, I have a headache. You know they brought me to the
hospital . "
"Why did you come t o the hospital , Mrs. Dodds ? "
"Oh, well , " she said, "I had a stroke. "
"How do you know? "
"I fell down in the batroom two weeks ago and my daughter
brought me here. They did some brain scans and took X rays and told
me I had a stroke. " Obviously Mrs. Dodds knew what had occurred and
was aware of her surroundings.
"Okay, " I said. "And how are you feeling now? "
"Fine. "
"Can you walk? "
"Sure I can walk. " Mrs. Dodds had been lying in her bed or sitting
propped up in a wheelchair for the past two weeks. She had not taken a
single step since her fall in the bathroom.
"Wat about your hands? Hold out your hands. Can you move
them? "
Mrs. Dodds seemed mildly annoyed by my questions. "Of course I
can use my hands, " she said.
"Can you use your right hand? "
"Yes . "
"Can you use your lef hand? "
"Yes, I can use my lef hand. "
"Ae both hands equally strong? "
"Yes, they are both equally strong. "
Now this raises an interesting question: How far can you push this
line of questioning in these patients? Physicians are generally reluctant to
T H E S O U N D O F ON E HA N D C LA P P I N G I 1 2 9
keep on prodding for fear of precipitating what the neurologist Kurt
Goldstein called a "catastrophic reaction," which is simply medical j ar
gon for "the patient starts sobbing" because her defenses crumble. But
I thought, if I took her gently, one step at a time, before actually con
fronting her with her paralysis, perhaps I could prevent such a reaction. 1
"Mrs. Dodds, can you touch my nose with your right hand? "
She did so with no trouble.
"Can you touch my nose with your lef hand? "
Her hand lay paralyzed i n front of her.
"Mrs . Dodds, are you touching my nose? "
"Yes, of course I ' m touching your nose. "
"Can you actually see yourself touching my nose? "
"Yes, I can see it. It's less than an inch from your face. "
At this point Mrs. Dodds produced a frank confabulation, almost a
hallucination, that her fnger was nearly touching my nose. Her vision
was fne. She could see her arm perfectly clearly, yet she was insisting
that she could see the arm move.
I decided to ask just one more question. "Mrs. Dodds, can you clap? "
With resigned patience she said, "Of course I can clap. "
"Will you clap for me? "
Mrs . Dodds glanced up at me and proceeded to make clapping move
ments with her right hand, as if clapping with an imaginary hand near
the midline.
"Are you clapping? "
"Yes, I' m clapping," she replied.
I didn' t have the heart to ask her whether she actually heard herself
clapping, but, had I done so, we might have found the answer to the
Zen master's eternal koan or riddle-what is the sound of one hand
clapping?
One doesn't need to invoke Zen koans, however, to realize that Mrs.
Dodds presents us with a puzzle every bit as enigmatic as the struggle
to understand the nondual nature of reality. Why does this woman, who
is apparently sane, intelligent and articulate, deny that she's paralyzed?
Afer all , she' s been confned to a wheelchair for nearly two weeks. There
must have been scores of occasions when she tried to grab something or
just reach out with her lef hand, yet all the while it lay lifeless in her
lap. How can she possibly insist that she "sees" herself touching my
nose?
Actually, Mrs. Dodd's confabulation is on the extreme end of the
scale. Denial patients more commonly concoct inane excuses or ration-
1 3 0 I P HA N T O MS I N T H E B RA I N
alizations why their lef arms do not move when asked to demonstrate
the use of that arm. Most don't claim that they can actually see the limp
arm moving.
For example, when I asked a woman named Cecilia why she was not
touching my nose, she replied with a hint of exasperation, "Well, doctor,
I mean these medical students, they've been prodding and poking at me
all day. I'm sick of it. I don't want to move my arm. "
Another patient, Esmerelda, took a diferent strategy.
"Esmerelda, how are you doing? "
"I' m fne. "
"Can you walk? "
"Yes. "
"Can you use your arms? "
"Yes. "
"Can you use your right arm? "
"Yes. "
"Can you use your lef arm? "
"Yes, I can use my lef arm. "
"Can you point to me with your right hand? "
She pointed straight at me with her good right hand.
"Can you point to me with your lef? "
Her lef hand lay motionless in front of her.
"Esmerelda, are you pointing? "
"I have severe arthritis i n my shoulder; you know that, doctor. It
hurts. I can't move my arm now. "
On other occasions she employed other excuses: "Well , I've never
been ver ambidextrous, doctor. "
Watching these patients is like obsering human nature through a
magnifing lens; I' m reminded of all aspects of human folly and of how
prone to self-deception we all are. For here, embodied in one elderly
woman in a wheelchair, is a comically exaggerated version of all those
psychological defense mechanisms that Sigmund and Anna Freud talked
about at the beginning of the twentieth century-mechanisms used by
you, me and everyone else when we are confronted with disturbing facts
about ourselves . Freud claimed that our minds use these various psycho
logical tricks to "defend the ego. " Hi s ideas have such intuitive appeal
that many of the words he used have infltrated popular parlance, al
though no one thinks of them as science because he never did any ex
periments. (We shall return to Freud later in this chapter to see how
T H E S O U N D O F O N E HA N D C LA P P I N G I 1 3 1
anosognosia may give us an experimental handle on these elusive aspects
of the mind. )
I n the most extreme cases, a patient will not only deny that the arm
( or leg) is paralyzed, but assert that the arm lying in the bed next to
him, his own paralyzed arm, doesn't belong to him! There' s an unbridled
willingness to accept absurd ideas.
Not long ago, at the Rivermead Rehabilitation Center in Oxford, En
gland, I gripped a woman' s lifeless lef hand and, raising it, held it in
front of her eyes. "Whose arm is this? "
She looked me in the eye and hufed, "What's that arm doing in my
bed? "
"Well, whose arm i s it? "
"That's my brother's arm, " she said fatly. But her brother was no
where in the hospital . He lives somewhere in Texas. The woman dis
played what we call somatoparaphrenia-the denial of ownership of one's
own body parts-which is occasionally seen in conjunction with anosog
nosia. Needless to say, both conditions are quite rare.
"Why do you think it's your brother's arm? "
"Because it's big and hairy, doctor, and I don' t have hairy arms. "
Aosognosia i s an extraordinary syndrome about which almost noth
ing is known. The patient is obviously sane in most respects yet claims
to see her lifeless limb springing into action-clapping or touching my
nose-and fails to realize the absurdity of it all . What causes this curious
disorder? Not surprisingly, there have been dozens oftheories2 to explain
anosognosia. Most can be classifed into two main categories. One is a
Freudian view, tat the patient simply doesn't want to confront the un
pleasantness of his or her paralysis. The second is a neurological view,
that denial is a direct consequence of the neglect syndrome, discussed in
the previous chapter-the general indiference to everything on the lef
side of the world. Bot categories of explanation have many problems,
but they also contain nuggets of insight that we can use to build a new
theory of denial .
One problem with the Freudian view is that it doesn't explain the
diference in magnitude of psychological defense mechanisms between
patients with anosognosia and what is seen in normal people-why they
are generally subtle in you and me and wildly exaggerated in denial pa
tients. For example, if I were to fracture my lef arm and damage certain
1 3 2 I P H A N T O MS I N T H E B RA I N
nerves and you asked me whether I could beat you in a game of tennis,
I might tend to play down my injury a little, asserting, "Oh, yes, I can
beat you. My arm is getting much better now, you know. " But I certainly
wouldn't take a bet that I could arm wrestle you. Or if my arm were
completely paralyzed, hanging limp at my side, I would not say, "Oh, I
can see it touching your nose" or "It belongs to my brother. "
The second problem with the Freudian view is that it doesn't explain
the asymmetry of this syndrome. The kind of denial seen in Mrs. Dodds
and others is almost always associated with damage to the right hemi
sphere of the brain, resulting in paralysis of the body's lef side. Wen
people sufer damage to the lef brain hemisphere, with paralysis on the
body's right side, they almost never experience denial . Wy not? They
are as disabled and frustrated as people with right hemisphere damage,
and presumably there is j ust as much "need" for psychological defense,
but in fact they are not only aware of the paralysis, but constantly talk
about it. Such asymmetry implies that we must look not to psychology
but to neurology for an answer, particularly in the details of how the
brain's two hemispheres are specialized for diferent tasks. Indeed, the
syndrome seems to straddle the border between the two disciplines, one
reason it is so fascinating.
Neurological theories of denial rej ect the Freudian view completely.
They argue instead that denial is a direct consequence of neglect, which
also occurs afer right hemisphere damage and leaves patients profoundly
indiferent to everything that goes on within the lef side of the world,
including the lef side of their own bodies. Perhaps the patient with
anosognosia simply doesn't notice that her lef arm is not moving in
response to her commands, and hence the delusion.
I fnd two main problems with this approach. One is that neglect and
denial can occur independently-some patients with neglect do not ex
perience denial and vice versa. Second, neglect does not account for why
denial usually persists even when te patient's attention is drawn to the
paralysis. For instance, if I were to force a patient to turn his head and
focus on his lef arm, to demonstrate to him that it's not obeying his
command, he may adamantly continue to deny that it's paralyzed-or
even that it belongs to him. It is this vehemence of the denial-not a
mere indiference to paralysis-that cries out for an explanation. Indeed,
the reason anosognosia is so puzzling is that we have come to regard the
"intellect" as primarily propositional in character-that is, certain con
clusions follow incontrovertibly from certain premises-and one ordi
narily expects propositional logic to be internally consistent. To listen to
T H E S O U N D O F ON E HA N D CL A P P I N G I 1 3 3
a patient deny ownership of her arm and yet, in the same breath, admit
that it is attached to her shoulder is one of the most perplexing phenom
ena that one can encounter as a neurologist.
So neither the Freudian view nor the neglect theory provides an ad
equate explanation for the spectrum of defcits that one sees in anosog
nosia. The correct way to approach the problem, I realized, is to ask two
questions : First, why do normal people engage in all these psychological
defense mechanisms? Second, why are the same mechanisms so exagger
ated in these patients? Psychological defenses in normal people are es
pecially puzzling because at frst glance they seem detrimental to
survival . 3 Why would it enhance my surival to cling tenaciously to false
beliefs about myself and the world? If I were a puny weakling who be
lieved that I was as strong as Hercules, I'd soon get into serious trouble
with the "alpha male" in my social group-my chairman, the president
of my company or even my next-door neighbor. But, as Charles Darin
pointed out, if one sees something apparently maladaptive in biology,
then look more deeply, because there is ofen a hidden agenda.
The key to the whole puzzle, I suggest, lies in the division of labor
between our two cerebral hemispheres and in our need to create a sense
of coherence and continuity in our lives. Most people are familiar with
the fact that the human brain consists of two mirror image halves-like
the two halves of a walnut-with each half, or cerebral hemisphere, con
trolling movements on the opposite side of the body. A century of clinical
neurology has shown clearly that the two hemispheres are specialized for
diferent mental capacities and that the most striking asymmetry involves
language. The lef hemisphere is specialized not only for the actual pro
duction of speech sounds but also for the imposition of syntactic struc
ture on speech and for much of what is called semantics-comprehension
of meaning. The right hemisphere, on the other hand, doesn't govern
spoken words but seems to be concerned with more subtle aspects of
language such as nuances of metaphor, allegory and ambiguity-skills
that are inadequately emphasized in our elementary schools but that are
vital for the advance of civilizations through poetry, myth and drama.
We tend to call the l ef hemisphere the major or "dominant" hemisphere
because it, like a chauvinist, does all the talking ( and maybe much of the
internal thinkng as well ) , claiming to be the repository of humanity's
highest attribute, language. Unfortunately, the mute right hemisphere
can do nothing to protest.
Other obvious specializations involve vision and emotion. The right
hemisphere is concerned with holistic aspects of vision such as seeing the
1 3 4 I P H A N T O MS I N T H E B RA I N
forest for the trees, reading facial expressions and responding with the
appropriate emotion to evocative situations. Consequently, afer right
hemisphere strokes, patients tend to be blissflly unconcerned about
their predicament, even mildly euphoric, because without the "emotional
right hemisphere" they simply don't comprehend the magnitude of their
loss. ( This is true even of those patients who are aware of their paralysis . )
I n addition to these obvious divisions of labor, I want to suggest an
even more fndamental diference between the cognitive styles of the
two hemispheres,4 one that not only helps explain the amplifed defense
mechanisms of anosognosia but may also help account for the more
mundane forms of denial that people use in daily life-such as when an
alcoholic refses to acknowledge his drinking problem or when you deny
your forbidden attraction to a married colleague.
At any given moment in our waking lives, our brains are fooded with
a bewildering array of sensory inputs, all of which must be incorporated
into a coherent perspective that' s based on what stored memories already
tell us is true about ourselves and the world. In order to generate co
herent actions, the brain must have some way of sifing through this
superabundance of detail and of ordering it into a stable and internally
consistent "belief system"-a story that makes sense of the available ev
idence. Each time a new item of information comes in we fold it seam
lessly into our preexisting worldview. I suggest that this is mainly done
by the lef hemisphere.
But now suppose something comes along that does not quite ft the
plot. Wat do you do? One option is to tear up the entire script and
start from scratch: completely revise your story to create a new model
about the world and about yourself. The problem is that if you did this
for every little piece of threatening information, your behavior would
soon become chaotic and unstable; you would go mad.
Wat your lef hemisphere does instead is either ignore the anomaly
completely or distort it to squeeze it into your preexisting framework,
to preserve stability. Ad this, I suggest, is the essential rationale behind
all the so-called Freudian defenses-the denials, repressions, confabula
tions and other forms of self-delusion that govern our daily lives. Far
from being maladaptive, such everyday defense mechanisms prevent the
brain from being hounded into directionless indecision by the "combi
natorial explosion" of possible stories that might be written from the
material available to the senses. The penalty, of course, is that you are
T H E S O U N D O F ON E HA N D CL A P P I N G I 1 3 5
"lying" to yourself, but it's a small price to pay for the coherence and
stability conferred on the system as a whole.
Imagine, for example, a military general about to wage war on the
enemy. It is late at night and he is in the war room planning strategies
for the next day. Scouts keep coming into the room to give him infor
mation about the lay of the land, terrain, light level and so forth. They
also tell him that the enemy has fve hundred tanks and that he has six
hundred tanks, a fact that prompts the general to decide to wage war.
He positions all of his troops in strategic locations and decides to launch
battle exactly at 6: 00 A. M. with sunrise.
Imagine frther that at 5 : 5 5 A. M. one little scout comes rnning into
the war room and says, "General ! I have bad news . " With minutes to
go until battle, the general asks, "What is that? " and the scout replies,
"I j ust looked through binoculars and saw that the enemy has seven
hundred tanks, not fve hundred! "
Wat does the general-the lef hemisphere-do? Time is of the es
sence and he simply can't aford the luxury of revising all his battle plans.
So he orders the scout to shut up and tell no one about what he saw.
Denial ! Indeed, he may even shoot the scout and hide the report in a
drawer labeled "top secret" ( repression) . In doing so, he relies on the
high probability that the majority opinion-the previous information by
all the scouts-was correct and that this single new item of information
coming from one source is probably wrong. So the general sticks to his
original position. Not only that, but for fear of mutiny, he might order
the scout actually to lie to the other generals and tell them that he only
saw fve hundred tanks ( confabulation) . The purpose of all of this is to
impose stability on behavior and to prevent vacillation because indeci
siveness doesn't sere any purpose. Any decision, so long as it is probably
correct, is better than no decision at all . A perpetually fckle general will
never win a war!
In this analogy, the general is the lef hemisphere5 ( Freud's "ego, "
perhaps? ) , and his behavior i s analogous to the kinds of denials and re
pressions you see in both healthy people and patients with anosognosia.
But why are these defense mechanisms so grossly exaggerated in the
patients? Enter the right hemisphere, which I like to call the Devil' s
Advocate. To see how this works, we need to push the analogy a step
frther. Supposing the single scout comes running in, and instead of
saying the enemy has more tanks, he declares, "General , I j ust looked
through my telescope and the enemy has nuclear weapons. " The general
would be very foolish indeed to adhere to his original plan. He must
1 3 6 I P H A N T O MS I N T H E B RA I N
quickly formulate a new one, for if the scout were correct, the conse
quences would be devastating.
Thus the coping strategies of the two hemispheres are fndamentally
diferent. The lef hemisphere' s job is to create a belief system or model
and to fold new experiences into that belief system. If confronted with
some new information that doesn' t ft the model, it relies on Freudian
defense mechanisms to deny, repress or confabulate-anything to pre
sere the status quo. The right hemisphere' s strategy, on the other hand,
is to play "Devil 's Advocate, " to question the status quo and look for
global inconsistencies. When the anomalous information reaches a certain
threshold, the right hemisphere decides that it is time to force a complete
revision of the entire model and start from scratch. The right hemisphere
thus forces a "Kuhnian paradigm shif" in response to anomalies,
whereas the lef hemisphere always tries to cling tenaciously to the way
things were.
Now consider what happens if the right hemisphere is damaged. 6 The
lef hemisphere is then given free rein to pursue its denials, confabula
tions and other strategies, as it normally does. It says, "I am Mrs. Dodds,
a person with two normal arms that I have commanded to move. " But
her brain is insensitive to the contrary visual feedback that would ordi
narily tell her that her arm is paralyzed and that she's in a wheelchair.
Thus Mrs. Dodds is caught in a delusional cul-de-sac. She cannot revise
her model of reality because her right hemisphere, with its mechanisms
for detecting discrepancies, is out of order. Ad in the absence of the
counterbalance or "reality check" provided by the right hemisphere,
there is literally no limit to how far she will wander along the delusional
path. Patients will say, "Yes, I' m touching your nose, Dr. Rmachan
dran, " or "Al of the medical students have been prodding me and that's
why I don't want to move my arm. " Or even, "Wat is my brother's
hand doing in my bed, doctor? "
The idea that the right hemisphere i s a lef-wing revolutionary that
generates paradigm shifs, whereas the lef hemisphere is a die-hard con
servative that clings to the status quo, is almost certainly a gross over
simplifcation, but, even if it turns out to be wrong, it does suggest new
ways of doing experiments and goads us into asking novel questions
about the denial syndrome. How deep is the denial ? Does the patient
really believe he's not paralyzed? What if you were to confront patients
directly: Could you then force them to admit the paralysis? Would they
deny only their paralysis, or would they deny other aspects of their illness
as well? Given that people ofen think of their car as part of their ex-
T H E S O U N D O F O N E HA N D CLA P P I N G I 1 3 7
tended "body image"( especially here in California) , what would happen
if the font lef fender of their car were damaged? Would they deny that?
Anosognosia has been known for almost a century, yet there have been
very few attempts to answer these questions. Any light we could shed on
this strange syndrome would be clinically important, of course, because
the patients' indiference to their predicament not only is an impediment
to rehabilitation of the weak arm or leg, but ofen leads them to un
realistic fture goals. ( For example, when I asked one man whether he
could go back to his old occupation of repairing telephone lines-a job
that requires two hands for climbing poles and splicing wires-he said,
"Oh, yes, I don't see a problem there. ") Wat I didn' t realize, though,
when I began these experiments, was that they would take me right into
the heart of human nature. For denial is something we do all our lives,
whether we are temporarily ignoring the bills accumulating in our "to
do" tray or defantly denying the fnality and humiliation of death.
Talking to denial patients can be an uncanny experience. They bring
us face to face with some of the most fndamental questions one can ask
as a conscious human being: Wat is the self What brings about the
unity of my conscious experience? What does it mean to will an action?
Neuroscientists tend to shy away from such questions, but anosognosia
patients aford a unique opportunity for experimentally approaching
these seemingly intractable philosophical riddles.
Relatives are ofen bewildered by their loved ones' behavior. "Does
Mom really believe she' s not paralyzed? " asked one young man. "Surely,
there must be some recess of her mind that knows what's happened. Or
has she gone totally bonkers? "
Our frst and most obvious question, therefore, is, How deeply does
the patient believe his own denials or confabulations? Could it be some
sort of surface facade or even an attempt at malingering? To answer this
question, I devised a simple experiment. Instead of directly confronting
the patient by asking him to respond verbally ( can you touch my nose
with your lef hand? ) , what if I were to "trick" him by asking him to
perform a spontaneous motor task that requires two hands-before he
has had a chance to think about it. How would he respond?
To fnd out, I placed a large cocktail tray supporting six plastic glasses
half flled with water in front of patients with denial syndrome. Now if
I asked you to reach out and grab such a tray, you would place one hand
under either side of the tray and proceed to raise it. But if you had one
1 3 8 I P HA N T O MS I N T H E B RA I N
hand tied behind your back, you would naturally go for the middle of
the tay-its center of gravity-and lif from there. When I tested stroke
patients who were paralyzed on one side of their body but did not sufer
from denial, their nonparalyzed hand went straight for the middle of the
tray, as expected.
When I tried the same experiment on denial patients, their right hands
went straight to the right side of the tray while the lef side of the tray
remained unsupported. Naturally, when the right hand lifed only the
right side of the tray, the glasses toppled, but the patients ofen attributed
this to momentary clumsiness rather than a failure to lif the lef side of
the tray ( "Ooops ! How silly of me! ") . One woman even denied that she
had failed to lif the tray. When I asked her whether she had lifed the
tray successflly, she was surprised. "Yes, of course, " she replied, her lap
all soggy.
The logic of a second experiment was somewhat diferent. What if one
were actually to reward the patient for honesty? To investigate this, I
gave our patients a choice between a simple task that can be done with
one hand and an equally simple task that requires the use of two hands .
Specifcally, patients were told that they could earn fve dollars if they
threaded a light bulb into a bare socket on a heavy table lamp or ten
dollars if they could tie a pair of shoelaces. You or I would naturally go
for the shoelaces, but most paralyzed stroke patients-who do not sufer
from denial-choose the light bulb, knowing their limitations. Obviously
fve dollars is better than nothing. Remarkably, when we tested four
stroke patients who had denial , they opted for the shoelace task every
time and spent minutes fddling with the laces without showing any signs
of frustration. Even when the patients were given the same choice ten
minutes later they unhesitatingly went for the bimanual task. One woman
repeated this bumbling behavior fve times in a row, as though she had
no memory of her previous failed attempts. A Freudian repression per
haps?
On one occasion, Mrs. Dodds kept on fmbling with the shoelaces
using one hand, oblivious to her predicament, until fnally I had to pull
the shoe away. The next day my student asked her, "Do you remember
Dr. Ramachandran? "
She was very pleasant. "Oh, yes, I remember. He's that Indian doc
tor. "
"What did he do? "
"He gave me a child's shoe with blue dots on it and asked me to tie
the shoelaces. "
T H E S o u N D o F O N E HA N D C L A P P I N G 1 1 3 9
"Did you do it? "
"Oh, yes, I tied it successflly with both my hands, " she replied.
Something odd was afoot. Wat normal person would say, "I tied the
shoelace with both my hands' ? It was almost as though inside Mrs. Dodds
there lurked another human being-a phantom within-who knows per
fectly well that she' s paralyzed, and her strange remark was an attempt
to mask this knowledge. Another intriguing example was a patient who
volunteered, while I was examining him, "I can' t wait to get back to
two-fsted beer drinking. " These peculiar remarks are striking examples
of what Freud called a "reaction formation"-a subconscious attempt
to disguise something that is threatening to your self- esteem by assertng
the opposite. The classic illustration of a reaction formation, of course,
comes from Hamlet) "Methinks the lady doth protest too much. " Is not
the ver vehemence of her protest itself a betrayal of guilt?
Let us return now to the most widely accepted neurological expla
nation of denial-the idea that it has something to do with neglect, the
general indiference that patients ofen display toward events and objects
on the lef side of the world. Perhaps when asked to perform an action
with her lef hand, Mrs. Dodds sends motor commands to the paralyzed
arm and copies of these commands are simultaneously sent to her body
image centers ( in the parietal lobes) , where they are monitored and ex
perienced as felt movements. The parietal lobes are thus tipped of about
what the intended actions are, but since she's ignoring events on the lef
side of her body, she also fails to notice that the arm did not obey her
command. Although, as I argued earlier, this account is implausible, we
did two simple experiments to test the neglect theory of denial directly. 7
In the frst experiment, I tested the idea that the patient i s simply
monitoring motor signals that are being sent to the arm. Larry Cooper
is an intelligent ffy-six-year-old denial patient who had sufered a stroke
one week before I went to visit him in the hospital . He lay under a blue
and purple quilt his wife had brought to the room, with his arms fopped
outside the covers-one paralyzed, one normal . We chatted for ten
minutes and then I lef the room, only to return fve minutes later. "Mr.
Cooper! " I exclaimed, approaching his bed. "Why did you just now
move your lef arm? " Both arms were dead still, in the same position as
when I had lef the room. I 've tried this on normal people and the usual
response is utter bewilderment. "What do you mean? I wasn't doing
anything with my lef arm" or "I don't understand; did I move my lef
1 4 0 I P H A N T O MS I N T H E B RA I N
arm? " Mr. Cooper looked at me calmly and said, "I was gesticulating to
make a point! " When I repeated the experiment the next day, he said,
"It hurts, so I moved it to relieve the pain. "
Since there is no possibility that Mr. Cooper could have sent a motor
command to his lef arm at the exact moment I questioned him, the
result suggests that denial stems not merely from a sensory motor defcit.
On the contrary, his whole system of beliefs about himself is so pro
foundly deranged that there' s apparently no limit to what he will do to
protect these beliefs. Instead of acting befddled, as a normal person
might, he happily goes along with my deception because it makes perfect
sense to him, given his worldview.
The second experiment was almost diabolical . What would happen, I
wondered, if one were temporarily to "paralyze" the right arm of a denial
patient whose lef arm, of course, really is paralyzed. Would the denial
now encompass his right arm as well? The neglect theory makes a very
specifc prediction-because he only neglects the lef side of his body
and not the right side, he should notice that the right arm isn't moving
and say, "That's very odd, doctor; my arm isn't moving. " ( My theory,
on the other hand, makes the opposite prediction: He should be insen
sitive to this "anomaly" since the discrepancy detector in his right hem
isphere is damaged. )
To "paralyze" a denial patient's right arm, I devised a new version of
the virtual reality box we had used in our phantom limb experiments.
Again, it was a simple cardboard box with holes and mirrors, but they
were positioned very diferently. Our frst subject was Betty Ward, a
seventy-one-year-old retired schoolteacher who was mentally alert and
happy to cooperate in the experiment. When Betty was comfortably
seated, I asked her to put a long gray glove on her right hand ( her good
one) and insert it through a hole in front of the box. I then asked her
to lean forward and peek into the box through a hole in the top to look
at her gloved hand.
Next, I started a metronome and asked Betty to move her hand up
and down in time with the ticking sounds.
"Can you see your hand moving, Betty? "
"Yes, sure, " she said. "It's got the right rhythm. "
Then I asked Betty to close her eyes . Without her knowledge, a mirror
in the box fipped into position and an undergraduate stooge, who was
hiding under the table, slipped his gray gloved hand into the box from
a hole in the back. I asked Betty to open her eyes and look back into
the box. She thought she was looking at her own right hand again, but,
T H E S O U N D O F ON E HA N D C L A P P I N G I 1 4 1
because of the mirror, she actually saw the student's hand. Previously I
had told the stooge to keep his hand absolutely still.
"Okay, Betty. Keep looking. I' m going to start the metronome again
and I want you to move your hand in time with it. "
Tick, tack, tick, tack. Betty moved her hand but what she saw i n the
box was a perectly still hand, a "paralyzed" hand. Now when you do
this experiment with normal people, they jump out of their seat: "Hey,
what's going on here? " Never in their wildest dreams would they imagine
that an undergraduate was hiding under the table.
"Betty, what do you see? "
"Why, I see my right hand moving up and down, just like before, "
she replied. 8
This suggests to me that Betty's denial crossed over to the right side
of her body-the normal side with no neglect-for why else would she
say that she could see a motionless hand in motion? This simple exper
iment demolishes the neglect theory of anosognosia and also gives us a
clue for understanding what really causes the syndrome. What is damaged
in these patients is the manner in which the brain deals with a discrepancy
in sensory inputs concerning the body image; it's not critical whether
the discrepancy arises fom the lef or right side of the body.
What we observed in Betty and in the other patients we've discussed
so far supports the idea that the lef hemisphere is a conformist, largely
indiferent to discrepancies, whereas the right hemisphere is the opposite:
highly sensitive to perturbation. But our experiments only provide cir
cumstantial evidence for this theory. We needed direct proof.
Even a decade ago, an idea of this kind would have been impossible
to test, but the advent of modern imaging techniques such as fnctional
magnetic resonance ( fR) and positron emission tomography ( PET) has
tremendously accelerated the pace of research by allowing us to watch
the living brain in action. Very recently, Ry Dolan, Chris Frith and their
colleagues at the Queen Square Neurological Hospital for Neurological
Diseases in London performed a beautifl experiment using the virtual
reality box that we had used on our phantom limb patients. ( Recall this
is simply a vertical mirror propped in a box, perpendicular to the person's
chest. ) Each person inserted his lef arm into the box and looked into
the lef side of the mirror at the refection of his lef arm so that it was
optically superimposed on the felt location of his right arm. He was then
asked to move both hands synchronously up and down, so that there
was no discrepancy between the visual appearance of his moving right
hand ( actually the refection of his lef) and the kinesthetic movement
1 4 2 I P H A N T O MS I N T H E B RA I N
sensations-from j oints and muscles-emerging from his right hand. But
if he now moved the two hands out of sync-as when doing the dog
paddle-then there was a profound dscrepancy between what the right
hand appeared to be doing visually and what it felt it was doing. By
doing a PET scan during this procedure, Dr. Frith was able to locate the
center in the brain that monitors discrepancies; it is a small region of the
right hemisphere that receives information from the right parietal lobe.
Dr. Frith then did a second PET scan with the subject looking into the
right side of the mirror at the refection of his right hand ( and moving
his lef hand out of sync) so the discrepancy in his body image now
appeared to come fom his left side rather than the right. Imagine my
delight when I heard from Dr. Frith that once again the right hemisphere
"lit up" in the scanner. It didn't seem to matter which side of the body
the discrepancy arose from-right or lef-it always activated the right
hemisphere. This is welcome proof that my "speculative" ideas on hem
ispheric specialization are on te right track.
Wen I conduct clinical Grand Rounds-presenting a denial patient
to medical students-one of the most common questons I am asked is
"Do the patients only deny paralysis of body parts or do they deny other
disabilities as well? If the patient stubbed her toe, would she deny the
pain and swelling in that toe? Do they deny that they are seriously ill ? If
they suddenly had a migraine attack would tey deny it? " Many neu
rologists have explored this in their patients, and the usual answer is that
they don' t deny other problems-like my patent Grace who, when I
ofered her candy if she could tie shoelaces, shot back at me, "You know
I' m diabetic, doctor. I can't eat candy! "9
Amost all te patients I have tested are well aware of te fact tat
they've had a stroke and none of them sufers from what you might call
"global denial . " Yet there are gradations in their belief systems-and
accompanying denials-that correlate wit the location of their brain
lesions. Wen the inj ury is confned to the right parietal lobe, confabu
lations and denials tend to be confned to body image. But when the
damage occurs closer to the front of the right hemisphere ( a part called
the ventromedial frontal lobe) , the denial is broader, more varied and
oddly self-protective. I remember an especially strikng example of this
a patient named Bill who came to see me six months afer he had been
diagnosed with a malignant brain tumor. The tumor had been growing
T H E S O U N D O F ON E HA N D CL A P P I N G I 1 4 3
rapidly and compressing his right frontal lobe, until it was eventually
excised by the neurosurgeon. Unfortunately, by then it had already
spread and Bill was told that he probably had less than a year to live.
Now, Bill was a highly educated man and ought to have grasped the
gravity of his situation, yet he seemed nonchalant about it and kept
drawing my attention to a little blister on his cheek instead. He bitterly
complained that the other doctors hadn't done anything about the
blister and asked whether I could help him get rid of it. When I would
return to the topic of the brain tumor, he avoided talking about it, saying
things like "Well, you know how these doctors sometimes incorrectly
diagnose things. " So here was an intelligent person flatly contradicting
the evidence provided by his physicians and glibly playing down the fact
that he had terminal brain cancer. To avoid being hounded by a free
floating anxiety, he adopted the convenient strategy of attributing it to
something tangible-and the blister was the most convenient target. In
deed, his obsession with the blister is what Freud would call a displace
ment mechanism-a disguised attempt to deflect his own attention from
his impending death. Curiously, it is sometimes easier to defect than to
deny. 1 0
The most extreme delusion I've ever heard of i s one described by
Oliver Sacks, about a man who kept falling out of bed at night. Each
time he crashed to the floor, the ward staf would hoist him back up,
only to hear a resounding thud a few moments later. Aer this happened
several times, Dr. Sacks asked the man why he kept toppling out of bed.
He looked frightened. "Doctor, " he said, "these medical students have
been putting a cadaver's arm in my bed and I 've been trying to get rid
of it all night! " Not admitting ownership of his paralyzed limb, the man
was dragged to the foor each time he tried to push it away.
The experiments we discussed earlier suggest that a denial patient
is not just trying to save face; the denial is anchored deep in her
psyche. 1 1 But does this imply that the information about her paralysis is
locked away somewhere-repressed? Or does it imply that the informa
tion doesn't exist anywhere in her brain? The latter view seems unlikely.
If the knowledge doesn't exist, why does the patient say things like "I
tied my shoelaces with both my hands' ' or "I can't wait to get back to
two-fsted beer drinking"? And why evasive remarks like "I' m not am
bidextrous"? Comments like these imply that "somebody" in there
1 4 4 I P HA N T O MS I N T H E B RA I N
knows she is paralyzed, but that the information is not available to the
conscious mind. If so, is there some way to access that forbidden knowl
edge?
To fnd out, we took advantage of an ingenious experiment performed
in 1987 by an Italian neurologist, Eduardo Bisiach, on a patient with
neglect and denial . Bisiach took a syringe flled with ice-cold water and
irrigated the patient's lef ear canal-a procedure that tests vestibular
nere fnction. Within a few seconds the patient's eyes started to move
vigorously in a process called nystagmus. The cold water sets up a con
vection current in the ear canals, thereby fooling the brain into thinkng
te head is moving and into making involuntary correctional eye move
ments that we call nystagmus. Wen Bisiach then asked the denial patient
whether she could use her arms, she calmly replied that she had no use
of her lef arm! Amazingly, the cold water irrigation of the lef ear had
brought about a complete ( though temporar) remission from the ano
sognosia.
When I read about this experiment, I j umped out of my seat. Here
was a neurological syndrome produced by a right parietal lesion that had
been reversed by the simple act of squirtng water into the ear. Why
hadn't this amazing experiment made headlines in Te New York Times?
Indeed, I discovered that most of my professional colleagues had not
even heard of the experiment. I therefore decided to try the same pro
cedure on the next patient I saw with anosognosia.
This turned out to be Mrs. Macken, an elderly woman who three
weeks earlier had sufered a right parietal stroke that resulted in lef side
paralysis. My purpose was not only to confrm Bisiach's obseration but
also to ask questions specifcally to test her memory-something that
hadn't been done systematically. If the patient suddenly started admitting
that she was paralyzed, what would she say about her earlier denials?
Would she deny her denials? If she admitted them, how would she ac
count for them? Could she possibly tell us why she had been denying
them, or is that an absurd question?
I had been seeing Mrs. Macken every three or four days for two weeks,
and each time we had gone through the same rigmarole.
"Mrs. Macken, can you walk? "
"Yes, I can walk. "
"Can you use both arms? "
"Yes. "
"Ae they equally strong? "
T H E S O U N D O F O N E HA N D CL AP P I N G I 1 4 5
"Yes. "
"Can you move your lef hand? "
"Yes. "
"Can you move your right hand? "
"Yes. "
"Ae they equally strong? "
"Yes. "
Aer going through the questions, I flled a syringe with ice-cold water
and squirted it into her ear canal . A expected, her eyes started moving in
the characteristic way. Aer about a minute, I began to question her.
"How are you feeling, Mrs. Macken? "
"Well, my ear hurts. It's cold. "
"Aything else? What about your arms? Can you move your arms? "
"Sure, " she said.
"Can you walk? "
"Yes, I can walk. "
"Can you use both your arms? Are they equally strong? "
"Yes, they are equally strong. "
I wondered what these Italian scientists were talking about. But as I
was driving home, I realized that I had squirted the water into the wrong
ear! ( Cold water in the lef ear or warm water in the right ear causes the
eyes to drif repetitively to the lef and jump to the right. And the op
posite is true. It's one of those things that many physicians get confsed
about, or at least I do. So I had inadvertently done the control experi
ment frst! )
The next day we repeated the experiment on the other ear.
"Mrs. Macken, how are you doing? "
"Fine. "
"Can you walk? "
"Sure. "
"Can you use your right hand? "
"Yes. "
"Can you use your lef hand? "
"Yes. "
"Ae they equally strong? "
"Yes. "
Aer the nystagmus, I asked again, "How are you feeling? "
"My ear's cold. "
"Wat about your arms? Can you use your arms? "
1 4 6 I P HA N T O MS I N T H E B RA I N
"No," she replied, "my lef arm is paralyzed. "
That was the frst time she had used that word i n the three weeks
since her stroke.
"Mrs. Macken, how long have you been paralyzed? "
She said, "Oh, continuously, all these days . "
This was an extraordinary remark, for i t implies that even though she
had been denying her paralysis each time I had seen her over these last
few weeks, the memories of her failed attempts had been registering
somewhere in her brain, yet access to them had been blocked. The cold
water acted as a "truth serum" that brought her repressed memories
about her paralysis to the surface.
Half an hour later I went back to her and asked, "Can you use your
arms? "
"No, my lef arm i s paralyzed. " Even though the nystagmus had long
since ceased, she still admitted she was paralyzed.
Twelve hours later, a student of mine visited her and asked, "Do you
remember Dr. Rmachandran? "
"Oh, yes, he was that Indian doctor. "
"And what did he do? "
"He took some ice-cold water and he put i t into my lef ear and it
hurt. "
"Anything else? "
"Well, he was wearing that tie with a brain scan on it. " True, I was
wearing a tie with a PET scan on it. Her memory for details was fne.
"What did he ask you? "
"He asked me i f I could use both my arms. "
"And what did you tell him? "
"I told him I was fne. "
So now she was denying her earlier admission of paralysis, as though
she were completely rewriting her "script. " Indeed, it was almost as if
we had created two separate conscious human beings who were mutually
amnesic: the "cold water" Mrs. Macken, who is intellectually honest,
who acknowledges her paralysis, and the Mrs. Macken without the cold
water, who has the denial syndrome and adamantly denies her paralysis!
Watching the two Mrs. Mackens reminded me of the controversial
clinical syndrome known as multiple personalites immoralized in fction
as Dr. Jekyll and Mr. Hyde. I say contoversial because most of my more
hard-nosed colleagues refse to believe that the syndrome even exists
and would probably argue that it is simply an elaborate form of "play
acting. " What we have seen in Mrs. Macken, however, implies that such
T H E S O U N D O F O N E HA N D CL A P P I N G I 1 4 7
partial insulation of one personality from the other can indeed occur,
even though they occupy a single body.
To understand what is going on here, let us return to our general in
the war room. I used this analogy to illustrate that there is a sort of
coherence-producing mechanism in the lef hemisphere-the general
that prohibits anomalies, allows the emergence of a unifed belief system
and is largely responsible for the integrity and stability of self But what
if a person were confronted by several anomalies that were not consistent
with his original belief system but were nonetheless consistent with each
other? Like soap bubbles, they might coalesce into a new belief system
insulated from the previous story line, creating multiple personalities.
Perhaps balkanization is better than civil war. I fnd the reluctance of
cognitive psychologists to accept the reality of this phenomenon some
what puzzling, given that even normal individuals have such experiences
from time to time. I am reminded of a dream I once had in which
someone had just been telling me a very fnny j oke that made me laugh
heartily-implying that there must have been at least two mutually am
nesic personalities inside me during the dream. To my mind, this is an
"existence proof' for the plausibility of multiple personalities.
12
The question remains: How did the cold water produce such appar
ently miraculous efects on Mrs. Macken? One possibility is that it
"arouses" the right hemisphere. There are connections from the vestib
ular nere projecting to the vestibular cortex in the right parietal lobe as
well as to other parts of the right hemisphere. Activation of these circuits
in the right hemisphere makes the patient pay attention to the lef side
and notice that her lef arm is lying lifeless. She then recognizes, for the
frst time, that she is paralyzed.
This interpretation i s probably at least partially correct, but I would
like to consider a more speculative alternative hypothesis: the idea that
this phenomenon is somehow related to rapid eye movement ( RM) or
dream sleep. People spend a third of their lives sleeping, and 25 percent
of that time their eyes are moving as they experience vivid, emotional
dreams. During these dreams we are ofen confronted with unpleasant,
disturbing facts about ourselves. Thus in both the cold-water state and
RM sleep there are noticeable eye movements and unpleasant, forbid
den memories come to the surface, and this may not be a coincidence.
Freud believed that in dreams we dredge up material that is ordinarily
censored, and one wonders whether the same sort of thing may be hap
pening during "ice water in the ear" stimulation. At the risk of pushing
the analogy too far, let's refer to our general , who is now sitting in his
1 4 8 I P H A N T O MS I N T H E B RA I N
bedroom late the next night, sipping a glass of cognac. He now has time
to engage in a leisurely inspection of the report given to him by that one
scout at 5 : 5 5 A. M. and perhaps this mulling over and interpretation cor
respond to what we call dreaming. If the material makes sense, he may
decide to incorporate it into his battle plan for the next day. If it doesn't
make sense or if it is too disturbing for him, he will put it into his desk
drawer and try to forget about it; that is probably why we cannot re
member most of our dreams. I suggest that the vestibular stimulation
caused by the cold water partially activates the same circuitry that gen
erates RM sleep. This allows the patient to uncover unpleasant, dis
turbing facts about herself-including her paralysis-that are usually
repressed when she is awake.
This is obviously a highly speculative conjecture, and I would give it
only a 1 0 percent chance of being correct. ( My colleagues would prob
ably give it 1 percent! ) But it does lead to a simple, testable prediction.
Patients with denial should dream that they are paralyzed. Indeed, if they
are awakened during a RM episode, they may continue to admit their
paralysis for several minutes before reverting to denial again. Recall that
the efects of calorically induced nystagmus-Mrs. Macken's confession
of paralysis-lasted for at least thirty minutes afer the nystagmus had
ceasedY
Canst thou not minister to a mind diseased,
Pluck fom the memor a rooted sorrow,
Raze out the written troubles of the brain,
And with some seet oblivious antidote
Cleanse the stufed bosom ofthat perilous stuf
Which weihs upon the heart?
-WILLIA SHKESPEAR
Memory has legitimately been called the Holy Grail of neuroscience.
Athough many a weighty tome has been written on this topic, in truth
we know little about it. Most of the work carried out in recent decades
has fallen into two categories. One is the formation of the memory trace
itself, sought in the nature of physical changes between synapses and in
chemical cascades within nere cells. The second is based on the study
of patients like H. M. ( briefly described in Chapter 1 ), whose hippocam
pus was removed surgically for epilepsy and who was no longer able to
make new memories afer the surgery, though he can remember most
things that happened before surgery.
T H E S O U N D O F ON E HA N D CL A P P I N G I 1 4 9
Experiments on cells and on patients like H. M. have given us some
insights about how new memory traces are formed, but they completely
fail to explore equally important narrative or constructive aspects of
memory. How is each new item edited and censored ( when necessary)
before being pigeonholed according to when and where it occurred?
How are these memories progressively assimilated into our "autobio
graphic self," becoming par of who we are? These subtle aspects of
memory are notoriously difcult to study in normal people, but I realized
that one could explore them in patients like Mrs. Macken who "repress"
what happened just a few minutes earlier.
You don't even need ice water to chart this new territory. I found that
I could gently prod some patients into eventually admitting that the lef
arm is "not working" or "weak" or sometimes even "paralyzed" ( al
though they seemed unperturbed by this admission) . If I managed to
elicit such a statement, lef the room and returned ten minutes later, the
patient would have no recollection of the "confession, " having a sort of
selective amnesia for matters concerning his lef arm. One woman, who
cried for a fll ten minutes when she realized that she was paralyzed ( a
"catastrophic reaction") , couldn't remember this event a few hours later,
even though it must have been an emotionally charged and salient ex
perience. This is about as close as one can get to a Freudian repression.
The natural course of the denial syndrome provides us with another
means of exploring memory fnctions. For reasons not understood, most
patients tend to recover completely from the denial syndrome afer two
or three weeks, though their limbs are almost always still paralyzed or
extremely weak. (Wouldn't it be wonderfl if alcoholics or anorexics who
reject the awfl truth about their drinking or their body image were able
to recover from denial so quickly? I wonder whether ice water in the lef
ear canal will do the trick! ) What if I were to go to a patient afer he is
"over" the denial of his paralysis and ask, "When I saw you last week
and asked you about your lef arm, what did you tell me? " Would he
admit that he had been in denial?
The frst patient whom I asked about this was Mumtaz Shah, who had
been denying her paralysis for almost a month afer her stroke and then re
covered completely from the denial ( although not from the paralysis ) . I
began with the obvious question: "Mrs. Shah, do you remember me? "
"Yes, you came to see me at Mercy Hospital . You were always show
ing up with those two student nurses, Becky and Susan. " (Al this was
true; so far she was right on target. )
"Do you remember I asked you about your arms? What did you say? "
1 5 0 I P HA N T O MS I N T H E B RA I N
" I told you my lef arm was paralyzed. "
"Do you remember I saw you several times? Wat did you say each
time? "
"Several times, several times-yes, I said the same thing, that I was
paralyzed. "
(Actually she had told me each time that her arm was fne. )
"Mumtaz. Think clearly. Do you remember telling me that your lef
arm was fne, that it wasn't paralyzed? "
"Well, doctor, if I said that, then i t implies that I was lying. And I
am not a liar. "
Mumtaz had apparently repressed the dozens of episodes of denial
that she had engaged in during my numerous visits to the hospital .
The same thing happened with another patient, Jean, whom I visited
at the San Diego Rehabilitation Center. We went through the usual
questions.
"Can you use your right arm? "
"Oh, yes. "
"Can you use your lef arm? "
"Yes. "
But when I came to the question "Ae they equally strong? " Jean
said, "No, my lef arm is stronger. "
Trying to hide my surprise, I pointed to a mahogany table at the end
of the hall and asked her whether she could lif that with her right hand.
"I guess I could, " she said.
"How high could you lif it? "
She assessed the table, which must have weighed eighty pounds,
pursed her lips and said, "Oh, I suppose I could lif it about an inch. "
"Can you lif a table with your lef hand? "
"Oh, sure, " Jean replied. "I could lif i t an inch and a half"
She held up her right hand and showed me with her thumb and index
fnger how high she could hoist a table with her lifeless lef hand. Again,
this is a "reaction formation. "
But the next day, afer she had recovered from her denial, Jean re
pudiated these same words .
"Jean, do you remember I asked you a question yesterday? "
"Yes, " she said, removing her eyeglasses with her right hand. "You
asked me if I could lif a table with my right hand and I said I could lif
it about an inch. "
"What did you say about your lef hand? "
"I said I couldn't use my l ef hand. " She gave me a puzzled look. 1 4
T H E S O U N D O F ON E HA N D CLA P P I N G I 1 5 1
The "model" of denial that we considered earlier provides a partial
explanation for both the subtle forms of denial that we all engage in, as
well as the vehement protests of denial patients. It rests on the notion
that the lef hemisphere attempts to presere a coherent worldview at all
costs, and, to do that well, it has to sometimes shut out information that
is potentially "threatening" to the stability of self
But what if we could somehow make this "unpleasant" fact more
acceptable-more nonthreatening to a patient' s belief system? Would he
then be willing to accept that his lef arm is paralyzed? In other words,
can you "cure" his denial by simply tampering with the structure of his
beliefs?
I began by conducting an informal neurological workup on the pa
tient, in this instance, a woman named Nancy. I then showed her a
syringe fll of saline solution and said, "A part of your neurological
exam, I would like to inject your lef arm with this anesthetic, and as
soon as I do it, your lef arm will be temporarily paralyzed for a few
minutes. " Aer making sure that Nancy understood this, I proceeded to
"inject" her arm with the salt water. My question was, Would she sud
denly admit that she was paralyzed, now that it had been made more
acceptable to her, or would she say, "Your injection doesn't work; I can
move my lef arm j ust fne? " This is a lovely example of an experiment
on a person' s belief system, a feld of inquiry I have christened experi
mental epistemology, j ust to annoy philosophers.
Nancy sat quietly for a few moments waiting for the "injection" to
"take efect" while her eyes darted around lookng at various antique
microscopes in my ofce. I then asked her, "Well, can you move your
lef arm? " "No, " she replied, "it doesn't seem to want to do anything.
It's not moving. " Apparently my mock injection had worked, for she
was now able to accept the fact that her lef arm was indeed paralyzed.
But how could I be sure that this was not simply the result of my
persuasive charm? Maybe I was just "hypnotizing" Nancy into accepting
that her arm was paralyzed. So I did the obvious control : I repeated the
same procedure with her right arm. Aer ten minutes, I went back into
the room and, afer chatting briefy about various topics, said, "A part
of the neurological exam, I' m going to inject your right arm with this
local anesthetic, and afer I give you the shot, your right arm will be
paralyzed for a few minutes . " I then gave her the inj ection, with the
same syringe containing saline solution, waited a bit and asked, "Can
1 5 2 I P H A N T O MS I N T H E B RA I N
you move your right arm? " Nancy looked down, lifed her right hand
to her chin and said, "Yes, it's moving. See for yourself. " I feigned
surprise. "How could that be possible? I j ust injected you with the same
anesthetic that we used on your lef arm! " She shook her head with
disbelief and replied, "Well , I don' t kow, doctor. I guess it's mind over
matter. I have always believed that . "1 5
What we cal rational grounds for our belief are ofen
extremely irrational atempts to justi our instincts.
-TOMS HENRY HUXLEY
When I began this research about fve years ago, I had no interest
whatsoever in Sigmund Freud. ( He might have said I was in denial . ) And
like most of my colleagues I was very skeptical of his ideas. The entire
neuroscience community is deeply suspicious of him because he touted
elusive aspects of human nature that ring true but that cannot be em
pirically tested. But afer I had worked with these patients, it soon be
came clear to me that even though Freud wrote a great deal of nonsense,
there is no denying that he was a genius, especially when you consider
the social and intellectual climate of Vienna at the turn of the century.
Freud was one of the frst people to emphasize that human nature could
be subj ected to systematic scientifc scrutiny, that one could actually look
for laws of mental life in much the same way that a cardiologist might
study the heart or an astronomer study planetary motion. We take all
this for granted now, but at that time it was a revolutionary insight. No
wonder his name became a household word.
Freud's most valuable contribution was his discovery that your con
scious mind is simply a facade and that you are completely unaware of
90 percent of what really goes on in your brain. (A striking example is
the zombie in Chapter 4. ) And with regard to psychological defenses,
Freud was right on the mark. Can anyone doubt the reality of the "ner
vous laugh" or "rationalizations"? Remarkably, altough you are engag
ing in these mental tricks all the time, you are completely unaware of
doing so and you'd probably deny it if it were pointed out to you. Yet
when you watch someone else doing it, it is comically conspicuous
ofen embarrassingly so. Of course, all this is quite well known to any
good playwright or novelist ( try reading Shakespeare or Jane Austen) ,
but Freud surely deseres credit for pointing out the pivotal role of psy-
T H E S O U N D O F ON E HA N D CL A P P I N G I 1 5 3
chological defenses in helping us organize our mental life. Unfortunately,
the theoretical schemes he constructed to explain them were nebulous
and untestable. He relied all too ofen on an obscure terminology and
on an obsession with sex to explain the human condition. Furthermore,
he never did any experiments to validate his theories.
But in denial patients you can witness these mechanisms evolving be
fore your very eyes, caught in fagrante delicto. One can make a list of
the many kinds of self- deception that Sigmund and Ana Freud de
scribed and see clear- cut, amplifed examples of each of them in our
patients. It was seeing this list that convinced me for the frst time of the
reality of psychological defenses and the central role that they play in
human nature.
Denial: The most obvious one, of course, is outright denial . "My
arm is working fne. " "I can move my lef arm-it's not paralyzed. "
Repression: A we have seen, the patient will sometimes admit with
repeated questioning that she is in fact paralyzed, only to revert soon
aferard to denial-apparently "repressing" the memory of the
confession she made just a few minutes earlier. Many cognitive psy
chologists argue that repressed memories, such as sudden recol
lections of child abuse, are inherently bogus-the harest of
psychological seeds implanted by the therapist and brought to fower
by the patient. But here we have proof that something like repression
is going on, albeit on a smaller time scale, with no possibility that the
patient' s behavior was unduly infuenced by the experimenter.
Reaction formation: This is the propensity to assert the exact op
posite of what one suspects to be true of oneself. For example, a
latent homosexual may drink his beer, strut around in cowboy boots
and engage in macho behavior, in an unconscious attempt to assert
his presumed masculinity. There is even a recent study showing that,
when viewing X-rated flm clips of male pornography, men who are
overt gay bashers paradoxically get bigger erections than men who
are not prej udiced. ( If you're wondering how the erections were
measured, the researchers used a device called a penile plethysmo
graph. )
I am reminded of Jean-the woman who said she could lif a
large table an inch of the ground with her right hand and then
added, when questioned, that her paralyzed lef hand was actually
stronger than the right; that she could use it to lif the table an inch
1 5 4 I P H A N T O MS I N T H E B RA I N
and a half. Aso recall Mrs. Dodds, who when asked whether she
tied her shoelaces, replied, "Yes, I did it with both my hands . " These
are striking examples of reaction formation.
o Rationalization: We have seen many examples of this in this chap
ter. "Oh, doctor, I didn't move my arm because I have arthritis in
my shoulder and it hurts. " Or this from another patient: "Oh, the
medical students have been prodding me all day and I don't really
feel like moving my arm j ust now. "
When asked to raise both hands, one man raised his right hand
high into the air and said, when he detected my gaze locked onto
his motionless lef hand, "Ur, as you can see, I' m steadying myself
with my lef hand in order to raise my right. "
More rarely, we see frank confabulation:
"I am touching your nose with my lef hand. "
"Yes, of course I' m clapping. "
o Humor: Even humor can come t o the rescue-not just i n these
patients but in all of us-as Freud well knew. Just think of the so
called nerous laugh or of all those times when you've used humor
to defate a tense situation. Can it be a coincidence, moreover, that
so many j okes deal wit potentially threatening topics like death or
sex? Indeed, afer seeing these patients, I am convinced that the
most efective antidote to the absurdity of te human condition may
be humor rather than art.
I remember asking a patient who was a professor of English lit
erature to move his paralyzed lef arm. "Mr. Sinclair, can you touch
my nose with your lef hand? "
"Yes. "
"Okay, show me. Please go ahead and touch it. "
"I ' m not accustomed to taking orders, doctor. "
Taken aback, I asked him whether he was being humorous or
sarcastic.
"No, I' m perfectly serious. I' m not being humorous. Wy do
you ask? "
So it would seem that although the patient's remarks are ofen
tinged with a pererse sense of humor, they themselves are unaware
that they're being fnny.
Another example: "Mrs. Franco, can you touch my nose with
your lef hand? "
"Yes, but watch out. I might poke your eye out. "
o Projection: This i s a tactic used when, wanting to avoid confronting
T H E S O U N D O F ON E HA N D CLA P P I N G I 1 5 5
a malady or disability, we conveniently attribute it to someone else.
"This paralyzed arm belongs to my brother, for I know perfectly
well that my own arm is fne. " I leave it for psychoanalysts to decide
whether this is a true case of projection. But as far as I'm concerned,
it's close enough.
So here we have patients engaging in precisely the same types of
Freudian defense mechanisms-denial, rationalization, confabulation, re
pression, reaction formation and so forth-that all of us use every day of
our lives. I 've come to realize that they present us with a fantastic op
portunity to test Freudian theories scientifcally for the frst time. The
patients are a microcosm of you and me but "better, " in that their de
fense mechanisms occur on a compressed time scale and are amplifed
tenfold. Thus we can carry out experiments that Freudian analysts have
only dreamed of. For example, what determines which particular defense
you use in a given situation? Why would you use an outright denial in
one case and a rationalization or reaction formation in another? Is it your
( or the patient's ) personality type that determines which defense mech
anisms you use? Or does the social context determine which one you
muster? Do you use one strategy with a superior and another with social
inferiors? In other words, what are the "laws" of psychological defense
mechanisms? We still have a long way to go before we can address these
questions, 16 but, for me, it's exciting to contemplate that we scientists
can begin encroaching on territor that until now was reserved for nov
elists and philosophers.
Meanwhile, is it possible that some of these discoveries may have prac
tical implications in the clinic? Using cold water to correct someone's
delusion about body image is fascinating to watch, but could it also be
usefl to the patients? Would repeated irrigation permanently "cure"
Mrs. Macken of denial and make her willing to participate in rehabili
tation? I also started wondering about anorexia nervosa. These patients
have disturbances in appetite but are also delusional about their body
image-claiming actually to "see" that they are fat when looking in a
mirror, even though they are grotesquely thin. Is the disorder of appetite
( linked to feeding and satiety centers in the hypothalamus ) primary, or
does the body image distortion cause the appetite problem? We saw in
the last chapter that some neglect patients actually start believing that
the object in the mirror is "real "-their sensory disturbances actually
cause changes in their belief system. And in denial or anosognosia pa-
1 5 6 I P H A N T O MS I N T H E B RA I N
tients, you ofen notice a similar warping of their beliefs to accom
modate their distorted body image. Could some such mechanisms be
involved in anorexia? We know that certain parts of the limbic system
such as the insular cortex are connected to the hypothalamic "appetite"
centers and also to parts of the parietal lobes concerned with body im
age. Is it conceivable that how much you eat over a long period of time,
your intellectual beliefs about whether you are too fat or thin, your per
ception of your body image and your appetite are all more closely linked
in your brain than you realize-so that a distortion of one of these sys
tems can lead to a perasive disturbance in the others as well? This idea
can be tested directly by doing the cold-water irrigation on a patient
with anorexia ( to see whether it would temporarily correct her delusion
about her body image) . This is a far-fetched possibility but it's still
worth trying, given the ease of the procedure and the lack of an efec
tive treatment for anorexia. Indeed, the disorder is fatal in about l 0 per
cent of cases.
Freud bashing is a popular intellectual pastime these days ( although
he still has his fans in New York and London) . But, as we have seen in
this chapter, he did have some valuable insights into the human condi
tion, and, when talking about psychological defenses, he was right on
target, although he had no idea why they evolved or what neural mech
anisms might mediate them. A less well known, but equally interesting
idea put forard by Freud was his claim that he had discerned the single
common denominator of all great scientifc revolutions: Rther surpris
ingly, all of them humiliate or dethrone "man" as the central fgure in
the cosmos .
The frst of these, he said, was the Copernican revolution, in which a
geocentric or earth-centered view of the universe was replaced with the
idea that earth is just a speck of dust in the cosmos .
The second was the Darinian revolution, which holds that we are
puny, hairless neotenous apes that accidentally evolved certain character
istcs that have made us successfl , at least temporarily.
The third great scientifc revolution, he claimed ( modestly) , was his
own discovery of the unconscious and the corollary notion that the hu
man sense of "being in charge" is illusory. He claimed that everything
we do in life is governed by a cauldron of unconscious emotions, drives
and motives and that what we call consciousness is just the tip of the
iceberg, an elaborate post hoc rationalization of all our actions.
T H E S O U N D O F O N E HA N D CL AP P I N G I 1 5 7
I believe Freud correctly identifed the common denominator of great
scientifc revolutions. But he doesn' t explain why this is so-why would
human beings actually enjoy being "humiliated" or dethroned? Wat do
they get in return for accepting the new worldview that belittles human
knd?
Here we can turn things around and provide a Freudian interpretation
of why cosmology, evolution and brain science are so appealing, not just
to specialists but to everone. Unlike other animals, humans are acutely
aware of their own mortality and are terrifed of death. But the study of
cosmology gives us a sense of timelessness, of being part of something
much larger. The fact that your own personal life is fnite is less fright
ening when you know you are part of an evolving universe-an ever
unfolding drama. This is probably the closest a scientist can come to
having a religious experience.
The same goes for the study of evolution, for it gives you a sense of
time and place, allowing you to see yourself as part of a great j ourney.
Ad likewise for the brain sciences. In this revolution, we have given up
the idea that there is a soul separate from our minds and bodies. Far
from being terrifing, this idea is very liberating. If you think you're
someting special in this world, engaging in a lofy inspection of the
cosmos from a unique vantage point, your annihilation becomes unac
ceptable. But if you're really part of the great cosmic dance of Shiva,
rather than a mere spectator, then your inevitable death should be seen
as a joyous reunion with nature rather than as a tragedy.
Brahman is all. From Brahman come appearances,
sensations, desires, deeds. But all these are merely name
and form. To know Brahman one must experience the
identit between him and the Sel or Brahman dweling
within the lotus of the heart. Only by so doing can man
escape fom sorrow and death and become one with the
subtle essence beyond al knowledge.
-Upanishads, 500 B. C.
CHAPTER s
"The Unbearabl e Likeness
of Bein
g
"
"One can't believe impossible things. "
"I daresay you haven't had much practice, " said the
Qeen. "Wen I was your age I always did it for hal
an hour a day. Wy, sometimes I've believed as many as
six impossible things before breakfast. "
-LEWIS CAROLL, Through the Lookng Glass
"Aa rule, " said Holmes, "the more bizarre a thing is
the less mysterious it proves to be. It is your commonplace,
featureless crimes which are really puzzling, just as a
commonplace face is the most difcult to identi. "
-SHEROCK HOLMES
I'll never forget the frustration and despair in the voice at the other end
of the telephone. The call came early one afernoon as I stood over my
desk, rifing through papers looking for a misplaced letter, and it took
me a few seconds to register what this man was saying. He introduced
himself as a former diplomat from Venezuela whose son was sufering
from a terrible, cruel delusion. Could I help?
"What sort of delusion? " I asked.
His reply and the emotional strain in his voice caught me by surprise.
"My thirty-year-old son thinks that I am not his father, that I am an
impostor. He says the same thing about his mother, that we are not his
real parents . " He paused to let this sink in. "We j ust don't know what
to do or where to go for help. Your name was given to us by a psychiatrist
in Boston. So far no one has been able to help us, to fnd a way to make
1 5 8
" T H E UN B E A RA B L E L I KE N E S S O F B E I N G " I 1 5 9
Arthur better. " He was almost in tears. "Dr. Rmachandran, we love
our son and would go to the ends of the earth to help him. Is there any
way you could see him? "
"Of course, I'll see him, " I said. "Wen can you bring him in? "
Two days later, Arthur came to our laboratory for the frst tme i n what
would turn into a yearlong study of his condition. He was a good-looking
fellow, dressed in jeans, a white T- shirt and moccasins. In his mannerisms,
he was shy and almost childlike, ofen whispering his answers to questions
or looking wide-eyed at us. Sometimes I could scarcely hear his voice over
the background whir of air conditioners and computers.
The parents explained that Arthur had been in a near-fatal automobile
accident while he was attending school in Santa Barbara. His head hit
the windshield with such crushing force that he lay in a coma for three
weeks, his survival by no means assured. But when he fnally awoke and
began intensive rehabilitative therapy, everyone's hopes soared. Arthur
gradually learned to talk and walk, recalled the past and seemed, to all
outward appearances, to be back to normal . He just had this one in
credible delusion about his parents-that they were impostors-and
nothing could convince him otherise.
Aer a brief conversaton to warm things up and put Athur at ease,
I asked, "Ahur, who brought you to the hospital ? "
"That guy i n the waiting room, " Arthur replied. "He' s the old gen
tleman who' s been taking care of me. "
"You mean your father? "
"No, no, doctor. That guy isn' t my father. He j ust looks like him.
He's-what do you call it? -an impostor, I guess . But I don't think he
means any harm. "
"Arthur, why do you think he's an impostor? Wat gives you that
impression? "
He gave me a patient look-as i f to say, how could I not see the
obvious-and said, "Yes, he looks exactly like my father but he realy
isn' t. He's a nice guy, doctor, but he certainly isn't my father! "
"But, Arthur, why is this man pretending to be your father? "
Arthur seemed sad and resigned when he said, "That is what is so
surprising, doctor. Wy should anyone want to pretend to be my father? "
He looked confsed as he searched for a plausible explanation. "Maybe
my real father employed him to take care of me, paid him some money
so that he could pay my bills. "
Later, i n my ofce, Arthur's parents added another twist to the mys
tery. Apparently their son did not treat either of them as impostors when
1 6 0 I P H A N T O MS I N T H E B RA I N
they spoke to him over the telephone. He only claimed they were im
postors when they met and spoke face-to- face. This implied that Aur
did not have amnesia with regard to his parents and that he was not
simply "crazy. " For, if that were true, why would he be normal when
listening to them on the telephone and delusional regarding his parents'
identities only when he looked at them?
"It's so upsetting," Arthur's father said. "He recognizes all sorts of peo
ple he kew in the past, including his college roommates, his best friend
from childhood and his former girlfriends. He doesn't say that any of them
is an impostor. He seems to have some gripe against his mother and me. "
I felt deeply sorry for Arthur's parents. We could probe their son's
brain and try to shed light on his condition-and perhaps comfort them
with a logical explanation for his curious behavior-but there was scant
hope for an efective treatment. This sort of neurological condition is
usually permanent. But I was pleasantly surprised one Saturday morning
when Arthur's father called me, excited about an idea he'd gotten from
watching a television program on phantom limbs in which I demon
strated that the brain can be tricked by simply using a mirror. "Dr.
Rmachandran, " he said, "if you can trick a person into thinking that
his paralyzed phantom can move again, why can't we use a similar trick
to help Arthur get rid of his delusion? "
Indeed, why not? The next day, Athur's father entered his son's bed
room and announced cheerflly, "Arthur, guess what! That man you've
been living with all these days is an impostor. He really isn't your father.
You were right all along. So I have sent him away to China. I am your
real father. " He moved over to Arthur's side and clapped him on the
shoulder. "It's good to see you, son! "
Arthur blinked hard at the news but seemed t o accept i t at face value.
When he came to our laboratory the next day I said, "Who's that man
who brought you in today? "
"That's my real father. "
"Wo was taking care of you last week? "
"Oh, " said Arthur, "that guy has gone back to China. He looks sim
ilar to my father, but he's gone now. "
When I spoke to Arthur's father on the phone later that afernoon,
he confrmed that Arthur now called him "Father," but that Arthur still
seemed to feel that something was amiss. "I think he accepts me intel
lectually, doctor, but not emotionally, " he said. "When I hug him,
there' s no warmth. "
' ' T H E UN B E A RA B L E L I K E N E S S O F B E I N G ' ' I 1 6 1
Aas, even this intellectual acceptance of his parents did not last. One
week later Athur reverted to his original delusion, claiming that the
impostor had returned.
Arthur was sufering from Capgras' delusion, one of the rarest and
most colorfl syndromes in neurology. 1 The patient, who is ofen men
tally quite lucid, comes to regard close acquaintances-usually his par
ents, children, spouse or siblings-as impostors. A Athur said over and
over, "That man looks identical to my father but he really isn't my father.
That woman who claims to be my mother? She's lying. She looks just
like my mom but it isn't her. " Athough such bizarre delusions can crop
up in psychotic states, over a third of the documented cases of Capgras'
syndrome have occurred in conjunction with traumatic brain lesions, like
the head injury that Arthur sufered in his automobile accident. This
suggests to me that the syndrome has an organic basis. But because a
majority of Capgras' patients appear to develop this delusion "sponta
neously," they are usually dispatched to psychiatrists, who tend to favor
a Freudian explanation of the disorder.
In this view, all of us so-called normal people as children are sexually
attracted to our parents. Thus every male wants to make love to his
mother and comes to regard his father as a sexual rival ( Oedipus led the
way) , and every female has lifelong deep-seated sexual obsessions over
her father ( the Electra complex) . Although these forbidden feelings be
come flly repressed by adulthood, they remain dormant, like deeply
buried embers afer a fre has been extinguished. Then, many psychiatrists
argue, along comes a blow to the head ( or some other unrecognized
release mechanism) and the repressed sexuality toward a mother or father
comes faming to the surface. The patient fnds himself suddenly and
inexplicably sexually attracted to his parents and therefore says to himself,
"My God! If this is my mother, how come I' m attracted to her? " Perhaps
the only way he can presere some semblance of sanity is to say to him
self, "This must be some other, strange woman. " Likewise, "I could
never feel this kind of sexual jealousy toward my real dad, so this man
must be an impostor. "
This explanation i s ingenious, as indeed most Freudian explanations
are, but then I came across a Capgras' patient who had similar delusions
about his pet poodle: The Fif before him was an impostor; the real Fif
was living in Brooklyn. In my view that case demolished the Freudian
1 6 2 I P H A N T O MS I N T H E B RA I N
explanation for Capgras' syndrome. There may be some latent bestiality
in all of us, but I suspect this is not Ahur's problem.
A better approach for studying Capgras' syndrome involves taking a
closer look at neuroanatomy, specifcally at pathways concerned with vi
sual recognition and emotions in the brain. Recall that the temporal lobes
contain regions that specialize in face and object recognition ( the what
pathway described in Chapter 4) . We know this because when specifc
porions of the what pathway are damaged, patients lose the ability to
recognize faces,2 even those of close friends and relatives-as immortal
ized by Oliver Sacks in his book Te Man Who Mistook His Wi for a
Hat. In a normal brain, these face recognition areas ( found on both sides
of the brain) relay information to the limbic system, found deep in the
middle of the brain, which then helps generate emotional responses to par
ticular faces ( Figure 8 . 1 ) . I may feel love when I see my mother's face, an
ger when I see the face of a boss or a sexual rival or deliberate indiference
upon seeing the visage of a friend who has betrayed me and has not yet
earned my forgiveness. In each instance, when I look at the face, my tem
poral cortex recognizes the image-mother, boss, friend-and passes on
the information to my amygdala (a gateway to the limbic system) to dis
cern the emotional signifcance of that face. When this activation is then
relayed to the rest of my limbic system, I start experiencing the nuances of
emotion-love, anger, disappointment-appropriate to that particular
face. The actual sequence of events is undoubtedly much more complex,
but this caricature captures the gist of it.
Aer thinking about Ahur's symptoms, it occurred to me that his
strange behavior might have resulted from a disconnection between these
two areas ( one concerned with recognition and the other with emotions ) .
Maybe Arthur's face recognition pathway was still completely normal,
and that was why he could identif everyone, including his mother and
father, but the connections between this "face region" and his amygdala
had been selectively damaged. If that were the case, Athur would rec
ognize his parents but would not experience any emotions when looking
at their faces. He would not feel a "warm glow" when lookng at his
beloved mother, so when he sees her he says to himself, "If this is my
mother, why doesn't her presence make me fel like I' m with my
mother? " Perhaps his only escape from this dilemma-the only sensible
interpretation he could make given the peculiar disconnection between
the two regions of his brain-is to assume that this woman merely re
sembles Mom. She must be an impostor. 3
"THE UN B E ARA B L E L I KE N E S S O F B E I N G " I 1 6 3
Fige 8. 1 Te limbic sstem is concerned with emotions. It consists ofa number
of nuclei (cell clusters) interconnected b long C-shaped fber tracts. Te amyg
dala-in the font pole ofthe temporal lobe-receives input fom the sensor areas
and sends messages to the rest of the limbic sstem to produce emotional arousal.
Eventualy, this activit cascades into the hypothalamus and fom there to the au
tonomic nerous sstem, preparing the animal (or person) for action.
Now, this is an intriguing idea, but how does one go about testing
it? A complex as the challenge seems, psychologists have found a rather
simple way to measure emotional responses to faces, obj ects, scenes and
events encountered in daily life. To understand how this works, you need
to know something about the autonomic nerous system-a part of your
brain that controls the involuntary, seemingly automatic activities of or
gans, blood vessels, glands and many other tissues in your body. Wen
you are emotionally aroused-say, by a menacing or sexually alluring
1 6 4 I P H A N T O MS I N T H E B RA I N
face-the information travels from your face recognition region to your
limbic system and then to a tiny cluster of cells in the hypothalamus, a
knd of command center for the autonomic nerous system. Nere fbers
extend from the hypothalamus to the heart, muscles and even other parts
of the brain, helping to prepare your body to take appropriate action in
response to that particular face. Wether you are going to fght, flee or
mate, your blood pressure will rise and your heart will start beating faster
to deliver more oxygen to your tissues. At the same time, you start sweat
ing, not only to dissipate the heat building up in your muscles but to
give your sweaty palms a better grip on a tree branch, a weapon or an
enemy's throat.
From the experimenter's point of view, your sweaty palms are the most
important aspect of your emotional response to the threatening face. The
dampness of your hands is a sure giveaway of how you feel toward that
person. Moreover, we can measure this reaction very easily by placing
electrodes on your palm and recording changes in the electrical resistance
of your skin. ( Called the galvanic skin response or GSR this simple little
procedure forms the basis of the famous lie detector test. When you tell
a fb, your palms sweat ever so slightly. Because damp skin has lower
electrical resistance than dry skin, the electrodes respond and you are
caught in the lie. ) For our purposes, every time you look at your mother
or father, believe it or not, your body begins to sweat imperceptibly and
your galvanic skin response shoots up as expected.
So, what happens when Arthur looks at his mother or father? My
hypothesis predicts that even though he sees them as resembling his
parents ( remember, the face recognition area of his brain is normal ) , he
should not register a change in skin conductance. The disconnection in
his brain will prevent his palms from sweating.
With the family's permission, we began testing Arthur on a rainy win
ter day in our basement laboratory on campus . Arthur sat in a comfort
able chair, joking about the weather and how he expected his father's
car to float away before we fnished the morning's experiments . Sipping
hot tea to take the chill fom his bones, Aur gazed at a video screen
saver while we afxed two electrodes to his lef index fnger. Ay tiny
increase in sweat on his fnger would change his skin resistance and show
up as a blip on the screen.
Next I showed him a sequence of photos of his mother, father and
grandfather interleaved with pictures of strangers, and I compared his
galvanic skin responses to that of six college undergraduates who were
" T H E UN B E A RA B L E L I KE N E S S O F B E I N G " I 1 6 5
shown an identical sequence of photos and who sered as controls for
comparison. Before the experiment, subjects were told that they would
be shown pictures of faces, some of which would be familiar and some
unfamiliar. Aer the electrodes were attached, they were shown each
photograph for two seconds with a ffeen- to twenty-fve- second delay
between pictures so skin conductance could return to baseline.
In the undergraduates, I found that there was a big jolt in the GSR
in response to photos of their parents-as expected-but not to pho
tos of strangers. In Arthur, on the other hand, the skn response was
uniformly low. There was no increased response to his parents, or at
times there would be a tiny blip on the screen afer a long delay, as if
he were doing a double take. This result provided direct proof that our
theory was correct. Clearly Ahur was not responding emotionally to
his parents, and this may be what led to the loss of his galvanic skin
response.
But how could we be sure that Ahur was even seeing the faces?
Maybe his head injury had damaged the cells in the temporal lobes that
would help him distinguish between faces, resulting in a fat GSR
whether he looks at his mother or at a stranger. This seemed unlikely,
however, since he readily acknowledged that the people who took him
to the hospital-his mother and father-looked like his parents. He also
had no difculty in recognizing the faces of famous people like Bill Clio
ton and Abert Einstein. Still, we needed to test his recognition abilities
more directly.
To obtain direct proof, I did the obvious thing. I showed Arthur
sixteen pairs of photographs of strangers, each pair consisting of either
two slightly diferent pictures of the same person or snapshots of two
diferent people. We asked him, Do the photographs depict the same
person or not? Putting his nose close to each photo and gazing hard at
the details, Arthur got fourteen out of sixteen trials correct.
We were now sure that Arthur had no problem in recognizing faces
and telling them apart. But could his failure to produce a strong galvanic
skin response to his parents be part of a more global disturbance in his
emotional abilities? How could we be certain that the head injury had not
also damaged his limbic system? Maybe he had no emotions, period.
This seemed improbable because throughout the months I spent with
Ahur, he showed a fll range of human emotions. He laughed at my
jokes and ofered his own fnny stories in return. He expressed frustra
tion, fear and anger, and on rare occasions I saw him cry. Watever the
1 6 6 I P H A N T O MS I N T H E B RA I N
situation, his emotions were appropriate. Arthur's problem, then, was
neither his ability to recognize faces nor his ability to experience emo
tions; what was lost was his ability to link the two.
So far so good, but why is the phenomenon specifc to close rela
tives? Wy not call the mailman an impostor, since his, too, is a famil
iar face?
It may be that when any normal person ( including Athur, prior to
his accident) encounters someone who is emotionally very close to him
a parent, spouse or sibling-he expects an emotional "glow, " a warm
fzzy feeling, to arise even though it may sometimes be experienced only
very dimly. The absence of this glow is therefore surprising and Athur's
only recourse then is to generate an absurd delusion-to rationalize it
or to explain it away. On the other hand, when one sees the mailman,
one doesn't expect a warm glow and consequently there is no incentive
for Arthur to generate a delusion to explain his lack of "warm fzzy"
response. A mailman is simply a mailman ( unless the relationship has
taken an amorous turn) .
Although the most common delusion among Capgras' patients i s the
assertion that a parent is an impostor, even more bizarre examples can
be found in the older medical literature. Indeed, in a case on record the
patient was convinced that his stepfather was a robot, proceeded to de
capitate him and opened his skull to look for microchips. Perhaps in this
patient, te dissociation from emotions was so extreme that he was forced
into an even more absurd delusion than Arthur' s: that his stepfather was
not even a human being, but was a mindless android! 4
About a year ago, when I gave a lecture on Athur at the Veterans
Administration Hospital in La Jolla, a neurology resident raised a astute
objection to my theory. Wat about people who are born with a disease
in which their amygdalas ( the gateway to the limbic system) calcif and
atrophy or those who lose their amygdalas (we each have two of them)
completely in surgery or through an accident? Such people do exist, but
they do not develop Capgras' syndrome, even though their GSR are fat
to all emotionally evocative stimuli. Likewise, patients with damage to
their frontal lobes (which receive and process information from the limbic
system for making elaborate fture plans ) also ofen lack a GSR. Yet they,
too, do not display Capgras' syndrome.
Wy not? The answer may be that these patents experience a general
blunting of all their emotional responses and therefore do not have a
baseline for comparison. Like a purebred Vulcan or Data on Star Trek,
one could legitimately argue, they don't even know what an emotion is,
" T H E UN B E A RA B L E L I KE N E S S O F B E I N G " I 1 6 7
whereas Capgras' patients like Athur enjoy a normal emotional life in
all other respects.
This idea teaches us an important principle about brain fnction,
namely, that all our perceptions-indeed, maybe all aspects of our
minds-are governed by comparisons and not by absolute values. This
appears to be true whether you are talkng about something as obvious
as judging the brightness of print in a newspaper or something as subtle
as detecting a blip in your internal emotonal landscape. This is a far
reaching conclusion, and it also helps illustrate the power of our ap
proach-indeed of the whole discipline that now goes by the name
cognitive neuroscience. You can discover important general principles
about how the brain works and begin to address deep philosophical ques
tions by doing relatively simple experiments on the right patients. We
started with a bizarre condition, proposed an outlandish theory, tested
it in the lab and-in meeting obj ections to it-learned more about how
the healthy brain actually works.
Taking these speculations even frther, consider the extraordinary dis
order called Cotard's syndrome, in which a patient will assert that he is
dead, claiming to smell rotten fesh or worms crawling all over his skin.
Again, most people, even neurologists, would j ump to the conclusion that
the patient was insane. But that wouldn't explain why the delusion takes
this highly specifc form. I would argue instead that Cotard's is simply an
exaggerated form of Capgras' syndrome and probably has a similar origin.
In Capgras' , the face recognition area alone is disconnected from the
amygdala, whereas in Cotard's perhaps all the sensory areas are discon
nected from the limbic system, leading to a complete lack of emotional
contact with the world. Here is another instance in which an outlandish
brain disorder that most people regard as a psychiatric problem can be ex
plained in terms of known brain circuitry. Ad once again, these ideas can
be tested in the laboratory. I would predict that Cotard' s syndrome pa
tients will have a complete loss of GSR for all external stimuli-not just
faces-and this leaves them stranded on an island of emotional desolation,
as close as anyone can come to experiencing death.
Arthur seemed to enj oy his visits to our laboratory. His parents were
pleased that there was a logical explanation for his predicament, that he
wasn't just "crazy. " I never revealed the details to Ahur because I
wasn't sure how he'd react.
Arthur's father was an intelligent man, and at one point, when Ahur
wasn't around, he asked me, "If your theory is correct, doctor-if the
information doesn't get to his amygdala-then how do you explain how
1 6 8 I P H A N T O MS I N T H E B RA I N
he has no problems recognizing us over the phone? Does that make sense
to you? "
"Well, " I replied, "there is a separate pathway from the auditory cor
tex, the hearing area of the temporal lobes, to the amygdala. One pos
sibility is that this hearing route has not been afected by the accident
only the visual centers have been disconnected from Arthur's amygdala. "
This conversation got me wondering about the other well- known
fnctions of the amygdala and the visual centers that proj ect to it. In
particular, scientists recording cell responses in the amygdala found that,
in addition to responding to facial expression and emotions, the cells also
respond to the directon of eye gaze. For instance, one cell might fre if
another person is looking directly at you, whereas a neighboring cell will
fre only if that person's gaze is averted by a fraction of an inch. Still
other cells fre when the gaze is way of to the lef or the right.
This phenomenon is not surprising, given the important role that gaze
direction5 plays in primate social communications-the averted gaze of
guilt, shame or embarrassment; the intense, direct gaze of a lover or the
threatening stare of an enemy. We tend to forget that emotions, even
though they are privately experienced, ofen involve interactions with
other people and that one way we interact is through eye contact. Given
the links among gaze direction, familiarity and emotions, I wondered
whether Arthur's ability to judge the direction of gaze, say, by looking
at photographs of faces, would be impaired.
To fnd out, I prepared a series of images, each showing the same
model looking either directly at the camera lens or at a point an inch or
two to the right or lef of the lens. Arthur's task was simply to let us
know whether the model was looking straight at him or not. Whereas
you or I can detect tiny shifs in gaze with uncanny accuracy, Athur was
hopeless at the task. Only when the model's eyes were looking way of
to one side was he able to discern correctly that she wasn't looking at
him.
This fnding in itself is interesting but not altogether unexpected,
given the kown role of amygdala and temporal lobes in detecting gaze
direction. But on the eighth trial of looking at these photos, Arthur did
something completely unexpected. In his sof, almost apologetic voice,
he exclaimed that the model 's identity had changed. He was now looking
at a new person!
This meant that a mere change in direction of gaze had been sufcient
to provoke Capgras' delusion. For Arthur, the "second" model was ap
parently a new person who merely resembled the "frst. "
" T H E UN B E ARA B L E L I K E N E S S O F B E I N G " I 1 6 9
"This one is older," Aur said frmly. He stared hard at both images.
"This is a lady; the other one is a girl . " Later in the sequence, Arthur
made another duplication-one model was old, one young and a third
even younger. At the end of the test session he continued to insist that
he had seen three diferent people. Two weeks later he did it again on a
retest using images of a completely new face.
How could Aur look at the face of what was obviously one person
and claim that she was actually three diferent people? Wy did simply
changing the direction of gaze lead to this profound inability to link
successive images?
Answers lie in the mechanics of how we form memories, in particular
our ability to create enduring representations of faces. For example, sup
pose you go to the grocery store one day and a friend introduces you to
a new person-Joe. You form a memory of that episode and tuck it away
in your brain. Two weeks go by and you run into Joe in the library. He
tells you a story about your mutual friend, you share a laugh and your
brain fles a memory about this second episode. Another few weeks pass
and you meet Joe again in his ofce-he' s a medical researcher and he's
wearing a white lab coat-but you recognize him instantly from earlier
encounters. More memories of Joe are created during this time so that
you now have in your mind a "category" called Joe. This mental picture
becomes progressively refned and enriched each time you meet Joe,
aided by an increasing sense of familiarity tat creates an incentive to link
the images and the episodes. Eventually you develop a robust concept
of Joe-he tells great stories, works in a lab, makes you laugh, knows a
lot about gardening, and so forth.
Now consider what happens to someone with a rare and specifc form
of amnesia, caused by damage to the hippocampus ( another important
brain structure in the temporal lobes) . These patients have a complete
inability to form new memories, even though they have perfect recollec
tion of all events in their lives that took place before the hippocampus
was inj ured. The logical conclusion to be drawn from the syndrome is
not that memories are actually stored in the hippocampus ( hence the
preservation of old memories ) , but that the hippocampus is vital for the
acquisition of new memory traces in the brai n. Wen such a patient
meets a new person ( Joe) on three consecutive occasions-in the super
market, the library and the ofce-he will not remember ever having
met Joe before. He will simply not recognize him. He will insist each
time that Joe is a complete stranger, no matter how many times they
have interacted, talked, exchanged stories and so forth.
1 7 0 I P H A N T O MS I N T H E B RA I N
But is Joe really a complete stranger? Rther surprisingly, experiments
show that such amnesia patients actually retain the ability to form new
categories that transcend successive Joe episodes. If our patient met Joe
ten times and each time Joe made him laugh, he'd tend to feel vaguely
jovial or happy on the next encounter but still would not know who Joe
is. There would be no sense of familiarity whatsoever-no memory of
each Joe episode-and yet the patient would acknowledge that Joe
makes him happy. This means that the amnesia patient, unlike Arthur,
can link successive episodes to create a new concept ( an unconscious
expectation of joy) even though he forgets each episode, whereas Athur
remembers each episode but fails to link them.
Thus Arthur is in some respects the mirror image of our amnesia pa
tent. Wen he meets a total stranger like Joe, his brain creates a fle
for Joe and the associated experiences he has with Joe. But if Joe
leaves the room for thirty minutes and returns, Arthur's brain-instead
of retrieving the old fle and adding to it-sometimes creates a com
pletely new one.
Wy does this happen in Capgras' syndrome? It may be that to link
successive episodes the brain relies on signals from the limbic system
the "glow" or sense of familiarity associated with a known face and set
of memories-and if this activation is missing, the brain cannot form an
enduring category through time. In the absence of this glow, the brain
simply sets up separate categories each time; that is why Arthur asserts
that he is meeting a new person who simply resembles the person he met
thirty minutes ago. Cognitive psychologists and philosophers ofen make
a distinction between tokens and types-that all our experiences can be
classifed into general categories or tokens ( people or cars ) versus specifc
exemplars or types ( Joe or my car) . Our experiments with Arthur suggest
that this distinction is not merely academic; it is embedded deep in the
architecture of the brain.
A we continued testing Athur, we noticed that he had certain other
quirks and eccentricities . For instance, Arthur sometimes seemed to
have a general problem with visual categories. All of us make mental
taxonomies or groupings of events and obj ects: Ducks and geese are
birds but rabbits are not. Our brains set up these categories even with
out formal education in zoology, presumably to facilitate memory stor
age and to enhance our ability to access these memories at a moment's
notice.
Athur, on the other hand, ofen made remarks hinting that he was
" T H E UN B E ARA B L E L I K E N E S S O F B E I N G " I 1 7 1
confsed about categories. For example, he had an almost obsessive pre
occupation with Jews and Catholics, and he tended to label a dispro
portionate number of recently encountered people as Jews. This
propensity reminded me of another rare syndrome called Fregoli, in
which a patient keeps seeing the same person everwhere. In walking
down the street, nearly every woman's face might look like his mother's
or every young man might resemble his brother. (I would predict that
instead of having severed connections fom face recognition areas to the
amygdala, the Fregoli patient may have an excess of such connections.
Every face would be imbued with familiarity and "glow," causing him
to see the same face over and over again. )
Might such Fregoli-like confsion occur in otherise normal brains?
Could this be a basis for forming racist stereotypes? Racism is so ofen
directed at a single physical type ( Blacks, Asians, Wites and so forth) .
Perhaps a single unpleasant episode with one member of a visual cate
gory sets up a limbic connection that is inappropriately generalized to
include all members of that class and is notoriously imperious to "in
tellectual correction" based on information stored in higher brain cen
ters . Indeed one' s intellectual views may be colored ( no pun intended)
by this emotional knee-jerk reaction; hence te notorious tenacity of
raCism.
We began our journey with Ahur ting to explain his strange
delusions about impostors and uncovered some new insights into how
memories are stored and retrieved in the human brain. His story ofers
insights into how each of us constructs narratives about our life and the
people who inhabit it. In a sense your life-your autobiography-is a
long sequence of highly personal episodic memories about your frst
kiss, prom night, wedding, birth of a child, fshing trips and so on. But
it is also much more than that. Clearly, there is a personal identity, a
sense of a unifed "self' that runs like a golden thread through the
whole fabric of our existence. The Scottish philosopher David Hume
drew an analogy between the human personality and a river-the water
in the river is ever-changing and yet the river itself remains constant.
Wat would happen, he asked, if a person were to dip his foot into a
river and then dip it in again afer half an hour-would it be the same
river or a diferent one? If you think this is a silly semantic riddle, you' re
right, for the answer depends on your defnition of "same" and "river. "
1 7 2 I P HA N T O MS I N T H E B RA I N
But silly or not, one point is clear. For Arthur, given his difculty with
linking successive episodic memories, there may indeed be two rivers !
To be sure, this tendency to make copies of events and obj ects was most
pronounced when he encountered faces-Arthur did not ofen dupli
cate objects. Yet there were occasions when he would run his fngers
through his hair and call it a "wig," party because his scalp felt unfa
miliar as a result of scars from the neurosurgery he had undergone. On
rare occasions, Arthur even duplicated countries, claiming at one point
that there were two Panamas ( he had recently visited that country dur
ing a family reunion) .
Most remarkable of all, Athur sometimes duplicated himself! The frst
time this happened, I was showing Arthur pictures of himself from a
family photo album and I pointed to a snapshot of him taken two years
before the accident.
"Wose picture is this? " I asked.
"That's another Arthur," he replied. "He looks just like me but it
isn't me. " I couldn't believe my ears . Arthur may have detected my
surprise since he then reinforced his point by saying, "You see? He has
a mustache. I don't. "
This delusion, however, did not occur when Athur looked at himself
in a mirror. Perhaps he was sensible enough to realize that the face in
the mirror could not be anyone else' s. But Ahur's tendency to "dupli
cate" himself-to regard himself as a distinct person from a former A
thur-also sometimes emerged spontaneously during conversation. To
my surprise, he once volunteered, "Yes, my parents sent a check, but
they sent it to the other Arthur. "
Athur's most serious problem, however, was his inability t o make
emotional contact with people who matter to him most-his parents
and this caused him great anguish. I can imagine a voice inside his
head saying, "The reason I don't experience warmth must be because
I' m not the real Athur. " One day Athur turned to his mother and
said, "Mom, if the real Athur ever returns, do you promise that you
will still treat me as a friend and love me? " How can a sane human
being who is perfectly intelligent in other respects come to regard
himself as two people? There seems to be something inherently con
tradictory about splitting the Self, which by its very nature is unitary.
If I started to regard myself as several people, which one would I
plan for? Which one is the "real" me? This is a real and painfl di
lemma for Arthur.
" T H E UN B E ARA B L E L I KE N E S S OF B E I N G " I 1 7 3
Philosophers have argued for centuries that if there is any one thing
about our existence that is completely beyond question, it is the simple
fact that "I" exist as a single human being who endures in space and
time. But even this basic axiomatic foundation of human existence is
called into question by Athur.
CHAPTER 9
God and the Limbic System
It is ver dicult to elucidate this [cosmic reliious}
feeling to anyone who is entirely without it .... Te
reliious geniuses of all ages have been distinguished by
this kind of reliious feeling, which knows no dogma ....
In my view, it is the most important function of art and
science to awaken this feeling and keep it alive in those
who are receptive to it.
-ABERT EINSTEIN
[God} is the greatest democrat the world knows, for He
leaves us "unfettered" to make our own choice between
evil and good. He is the greatest trant ever known, for
He ofen dashes the cup fom our lips and under cover of
fee will leaves us a margin so wholly inadequate as to
provide only mirth for Himsel at our expense. Terefore
it is that Hinduism calls it al His sport (Lila), or call
it all an illusion (Maya) .... Let us dance to the tune of
his bansi (ute), and all would be well.
-MOHNDAS K. GANDHI
Imagine you had a machine, a helmet of sorts that you could simply put
on your head and stimulate any small region of your brain without caus
ing permanent damage. What would you use the device for?
This is not science fction. Such a device, called a transcranial magnetic
stimulator, already exists and is relatively easy to construct. When applied
to the scalp, it shoots a rapidly fuctuating and extremely powerfl mag
netic feld onto a small patch of brain tissue, thereby activating it and
providing hints about its fnction. For example, if you were to stimulate
certain parts of your motor cortex, diferent muscles would contract.
Your fnger might twitch or you'd feel a sudden involuntary, puppetlike
shrugging of one shoulder.
1 7 4
GO D A N D T H E LIM BIC S Y S T E M I 1 7 5
So, if you had access to this device, what part of your brain would
you stimulate? If you happened to be familiar with reports from the early
days of neurosurgery about the septum-a cluster of cells located near
the front of the talamus in the middle of your brain-you might be
tempted to apply the magnet there. 1 Patients "zapped" in this region
claim to experience intense pleasure, "like a thousand orgasms rolled into
one. " If you were blind from birth and the visual areas in your brain had
not degenerated, you might stimulate bits of your own visual cortex to
fnd out what people mean by color or "seeing. " Or, given the well
known clinical obseration that the lef frontal lobe seems to be involved
in feeling "good, " maybe you'd want to stimulate a region over your
lef eye to see whether you could induce a natural high.
When the Canadian psychologist Dr. Michael Persinger got hold of a
similar device a few years ago, he chose instead to stimulate parts of his
temporal lobes . Ad he found to his amazement that he experienced
God for the frst time in his life.
I frst heard about Dr. Persinger's strange experiment from my col
league, Patricia Churchland, who spotted an account of it in a popular
Canadian science magazine. She phoned me right away. "Rma, you're
not going to believe this. There's a man in Canada who stimulated his
temporal lobe and experienced God. What do you make of it? "
"Does he have temporal lobe seizures? " I asked.
"No, not at all . He' s a normal guy. "
"But he stimulated his own temporal lobes? "
"That's what the article said. "
"Hmmmm, I wonder what would happen i f you tried stimulating an
atheist's brain. Would he experience God? " I smiled to myself and said,
"Hey, maybe we should try the device on Francis Crick. "
Dr. Persinger's obseration was not a complete surprise as I 've always
suspected that the temporal lobes, especially the lef lobe, are somehow
involved in religious experience. Every medical student is taught that
patients with epileptic seizures originating in this part of the brain can
have intense, spiritual experiences during the seizures and sometimes be
come preoccupied with religious and moral issues even during the
seizure-free or interictal periods.
But does this syndrome imply that our brains contain some sort of
circuitry that is actually specialized for religious experience? Is there a
"God module" in our heads? And if such a circuit exists, where did it
come from? Could it be a product of natural selection, a human trait as
natural in the biological sense as language or stereoscopic vision? Or is
1 7 6 I P H A N T O MS I N T H E B RA I N
there a deeper mystery at play, as a philosopher, epistemologist or the
ologian might argue?
Many traits make us uniquely human, but none is more enigmatic
than religion-our propensity to believe in God or in some higher power
that transcends mere appearances. It seems very unlikely that any creature
other than humans can ponder the infnite or wonder about "the mean
ing of it all . " Listen to John Milton in Paradise Lost:
For who would lose, though ful of pain
Tis intellectual being
Tose thoughts that wander through eternit to be sallowed up
and lost
In the wide womb of uncreated niht.
But where do such feelings come fom? It may be that any intelligent
sentient being that can look into its own fture and confront its own
mortality will sooner or later begin to engage in such disquieting rumi
nations. Does my little life have any real signifcance in the grand scheme
of things? If my father's sperm had not fertilized that particular egg on
that fatefl night, would I not have existed, and in what real sense then
would the universe have existed? Would it not then, as Erin Schr6-
dinger said, have been a mere "play before empty benches"? Wat if my
dad had coughed at that critical moment so that a diferent sperm had
fertilized the ovum? Our minds start reeling when pondering such pos
sibilities. We are bedeviled by paradox: On the one hand our lives seem
so important-with all those cherished highly personal memories-and
yet we kow that in the cosmic scheme of things, our brief existence
amounts to nothing at all . So how do people make sense of this dilemma?
For many the answer is straightforard: They seek solace in religion.
But surely there's more to it than that. If religious beliefs are merely
the combined result of wishfl thinking and a longing for immortality,
how do you explain the flights of intense religious ecstasy experienced
by patients with temporal lobe seizures or their claim that God speaks
directly to them? Many a patient has told me of a "divine light that
illuminates all things, " or of an "ultimate truth that lies completely be
yond the reach of ordinary minds who are too immersed in the hustle
and bustle of daily life to notice the beauty and grandeur of it all . " Of
course, they might simply be sufering from hallucinations and delusions
of the kind that a schizophrenic might experience, but if that's the case,
why do such hallucinations occur mainly when the temporal lobes are
Go D A N D T H E L I M B I C S Y S T E M I 1 7 7
involved? Even more puzzling, why do they take this particular form?
Wy don't these patients hallucinate pigs or donkeys?
In 1 935, the anatomist James Papez noticed that patients who died
of rabies ofen experienced fts of extreme rage and terror in the hours
before death. He kew that the disease was transmitted by dog bites and
reasoned that something in the dog's saliva-the rabies virus-traveled
along the victim's peripheral neres located next to the bite, up the spinal
cord and into the brain. Upon dissecting victims' brains, Papez found
the destination of the virus-clusters of nere cells or nuclei connected
by large C-shaped fber tracts deep in the brain ( Figure 9. 1 ) . A century
earlier, the famous French neurologist Pierre Paul Broca had named this
structure the limbic system. Because rabies patients sufered violent emo
tional fts, Papez reasoned that these limbic structures must be intimately
involved in human emotional behavior. 2
The limbic system gets its input from al l sensory systems-vision,
touch, hearing, taste and smell . The latter sense is in fact directly wired
to the limbic system, going straight to the amygdala ( an almond-shaped
structure that serves as a gateway into the limbic system) . This is hardly
surprising given that in lower mammals, smell is intimately linked with
emotion, territorial behavior, aggression and sexuality.
The limbic system' s output, as Papez realized, is geared mainly toward
the experience and expression of emotions . The experience of emotions
is mediated by back-and-forth connections with the frontal lobes, and
much of the richness of your inner emotional life probably depends on
these interactions. The outward expression of these emotions, on the
other hand, requires the participaton of a small cluster of densely packed
cells called the hypothalamus, a control center with three maj or outputs
of its own. First, hypothalamic nuclei send hormonal and neural signals
to the pituitary gland, which is ofen described as the "conductor" of
the endocrine orchestra. Hormones released through this system influ
ence almost every part of the human body, a biological tour de force we
shall consider in the analysis of mind- body interactions ( Chapter ll).
Second, the hypothalamus sends commands to the autonomic nerous
system, which controls various vegetative or bodily fnctions, including
the production of tears, saliva and sweat and the control of blood pres
sure, heart rate, body temperature, respiration, bladder fnction, defe
cation and so on. The hypothalamus can be regarded, then, as the
"brain" of this archaic, ancillary nerous system. The third output drives
1 7 8 I P HA N T O MS I N T H E B RA I N
Mammillary
by
Tabmu
Fige 9.1 Another view of the limbic sstem. Te limbic sstem is made up of a
series of interconnected structures surrounding a central fuid-led ventricle of the
forebrain and forming an inner border of the cerebral cortex. Te structures in
clude the hippocampus, amygdala, septum, anterior thalamic nuclei, mammillar
bodies and cingulate cortex. Te fornix is a long fber bundle joining the hippo
campus to the mammillar bodies. Pictured also are the corpus callosum, a fber
tract joining riht and lef neocortex, the cerebellum, a structure involved in mod
ulating movement, and the brain stem. Te limbic system is neither directly sensor
nor motor but constitutes a central core processing sstem of the brain that deal
with information derived fom events, memories of events and emotional associa
tions to these events. Tis processing is essential i experience is to guide future
behavior (Winson, 1985). Reprinted from Brain, Mind and Behavior by Bloom
and Laserson (1988) by Educational Broadcasting Corporation. Used with per
mission from W. H. Freeman and Company.
actual behaviors, ofen remembered by the mnemonic the "four F' s"
fghting, fleeing, feeding and sexual behavior. In short, the hypothalamus
is the body's "surival center," preparing the body for dire emergencies
or, sometimes, for the passing on of its genes.
Goo A N D T H E LI M B I C S Y S T E M I 1 7 9
Much of our knowledge about the fnctions of the limbic system
comes from patients who have epileptic seizures originating in this part
of the brain. When you hear the word "epilepsy, " you usually think of
someone having fts or a seizure-the powerl involuntary contraction
of all muscles of the body-and falling to the ground. Indeed, these
symptoms characterize the most well - known form of epilepsy, called a
grand mal seizure. Such seizures usually arise because a tiny cluster of
neurons somewhere in the brain is misbehaving, fring chaotically until
activity spreads like wildfre to engulf the entire brain. But seizures can
also be "focal "; that is, they can remain confned lagely to a single
small patch of the brain. If such focal seizures are mainly in the motor
cortex, the result is a sequential march of muscle titching-or the so
called j acksonian seizures. But if they happen to be in the limbic system,
then the most striking symptoms are emotional . Patients say that their
"feelings are on fre, " ranging from intense ecstasy to profound despair,
a sense of impending doom or even fts of extreme rage and terror.
Women sometimes experience orgasms during seizures, although for
some obscure reason men never do. But most remarkable of all are
those patients who have deeply moving spiritual experiences, including a
feeling of divine presence and the sense that they are in direct commu
nion with God. Everything around them is imbued with cosmic signif
cance. They may say, "I fnally understand what it's all about. This is
the moment I've been waiting for all my life. Suddenly it all makes
sense. " Or, "Finally I have insight into the true nature of the cosmos. "
I fnd i t ironic that this sense of enlightenment, this absolute conviction
that Truth is revealed at last, should derive from limbic structures con
cerned with emotions rather than from the thinking, rational parts of
the brain that take so much pride in their ability to discern truth and
falsehood.
God has vouchsafed for us "normal " people only occasional glimpses
of a deeper truth ( for me they can occur when listening to some especially
moving passage of music or when I look at Jupiter's moon through a
telescope) , but these patients enj oy the unique privilege of gazing directly
into God's eyes ever time they have a seizure. Wo is to say whether
such experiences are "genuine" (whatever that might mean) or "path
ological "? Would you, the physician, really want to medicate such a pa
tient and deny visitation rights to the Amighty?
The seizures-and visitations-last usually only for a few seconds each
time. But these brief temporal lobe storms can sometimes permanently
alter the patient' s personality so that even between seizures he is diferent
1 8 0 I P HA N T O MS I N T H E B RA I N
from other people. 3 No one knows why this happens, but it's as though
the repeated electrical bursts inside the patient's brain ( the frequent pas
sage of massive volleys of nere impulses within the limbic system) per
manently "facilitate" certain pathways or may even open new channels,
much as water from a storm might pour downhill, opening new rivulets,
frrows and passages along the hillside. This process, called kindling,
might permanently alter-and sometimes enrich-the patient's inner
emotional life.
These changes give rise to what some neurologists have called "tem
poral lobe personality. " Patients have heightened emotions and see cos
mic signifcance in trivial events. It is claimed that they tend to be
humorless, fll of self-importance, and to maintain elaborate diaries that
record quotidian events in elaborate detail-a trait called hypergraphia.
Patients have on occasion given me hundreds of pages of written text
flled with mystical symbols and notations. Some of these patients are
sticky in conversation, argumentative, pedantic and egocentric ( although
less so than many of my scientifc colleagues) , and they are obsessively
preoccupied with philosophical and theological issues.
Every medical student is taught that he shouldn't ever expect to see
a "textbook case" in the wards, for these are merely composites con
cocted by the authors of medical tomes. But when Paul , the thirty-two
year-old assistant manager of a local Goodwill store, walked into our lab
not long ago, I felt that he had strolled straight out of Brain1s Textbook
of Neurolog
y
the Bible of all practicing neurologists. Dressed in a green
Nehru shirt and white duck trousers, he held himself in a regal posture
and wore a magnifcent j eweled cross at his neck.
There is a sof armchair in our laboratory, but Paul seemed unwilling
to relax. Many patients I interiew are initially uneasy, but Paul was not
nerous in that sense-rather, he seemed to see himself as an exper
witness called to ofer testimony about himself and his relationship with
God. He was intense and self- absorbed and had the arrogance of a be
liever but none of the humility of the deeply religious . With very litte
prompting, he launched into his tale.
"I had my frst seizure when I was eight years old, " he began. "I
remember seeing a bright light before I fell on the ground and wonder
ing where it came from. " A few years later, he had several additional
seizures that transformed his whole life. "Suddenly, it was all crystal clear
to me, doctor," he continued. "There was no longer any doubt any
more. " He experienced a rapture beside which everything else paled. In
the rapture was a clarity, an apprehension of the divine-no categories,
Go D A N D T H E LI M B I C S Y S T E M I 181
no boundaries, j ust a Oneness with the Creator. All of this he recounted
in elaborate detail and with great persistence, apparently determined to
leave nothing out.
Intrigued by all this, I asked him to continue. "Can you be a little
more specifc? "
"Well , it's not easy, doctor. It's like trying to explain the rapture of
sex to a child who has not yet reached puberty. Does that make any
sense to you? "
I nodded. "Wat do you think of the rapture of sex? "
"Well , to be honest," he said, "I' m not interested i n i t anymore. It
doesn't mean much to me. It pales completely beside the divine light
that I have seen. " But later that afernoon, Paul firted shamelessly with
two of my female graduate students and tried to get their home tele
phone numbers. This paradoxical combination of loss of libido and a
preoccupation with sexual rituals is not unusual in patients with temporal
lobe epilepsy.
The next day Paul returned to my ofce carrying an enormous man
uscript bound in an ornate green dust j acket-a project he had been
workng on for several months. It set out his views on philosophy, mys
ticism and religion; the nature of the trinity; the iconography of the Star
of David; elaborate drawings depicting spiritual themes, strange mystical
symbols and maps. I was fascinated, but bafled. This was not the kind
of material I usually referee.
When I fnally looked up, there was a strange light in Paul's eyes. He
clasped his hands and stroked his chin with his index fngers. "There's
one other thing I should mention," he said. "I have these amazing fash
backs . "
"What kind of flashbacks? "
"Well , the other day, during a seizure, I could remember every little
detail from a book I read many years ago. Line afer line, page afer page
word for word. "
"Are you sure of this? Did you get the book and compare your mem
ories with the original ? "
"No, I lost the book. But this sort of thing happens to me a lot. It's
not j ust that one book. "
I was fascinated by Paul ' s claim. It corroborated similar assertions I
had heard many times before from other patients and physicians. One of
these days I plan to conduct an "objective test" of Paul 's astonishing
mnemonic abilities. Does he simply imagine he's reliving every minute
detail? Or, when he has a seizure, does he lack the censoring or editing
18 2 I P HA N T O MS I N T H E B RA I N
that occurs in normal memory so that he is forced to record every trivial
detail-resulting in a paradoxical improvement in his memory? The only
way to be sure would be to retrieve the original book or passage that he
was talking about and test him on it. The results could ofer important
insights about how memory traces are formed in the brain.
Once, when Paul was reminiscing about his fashbacks, I interected,
"Paul, do you believe in God? "
He looked puzzled. "But what else is there? " he said.
But why do patients like Paul have religious experiences? I can think
of four possibilities. One is that God really does visit these people. If that
is tre, so be it. Wo are we to question God's infnite wisdom? Unfor
tunately, this can be neither proved nor ruled out on empirical grounds.
The second possibility is that because these patients experience asorts
of odd, inexplicable emotions, as if a cauldron had boiled over, perhaps
their only recourse is to seek ablution in the calm waters of religious
tranquility. Or the emotional hodgepodge may be misinterpreted as mys
tical messages from another world.
I fnd the latter explanation unlikely for two reasons. First, there are
other neurological and psychiatric disorders such as frontal lobe syn
drome, schizophrenia, manic depressive illness or j ust depression in which
the emotions are disturbed, but one rarely sees religious preoccupations
in such patients to the same degree. Even though schizophrenics may
occasionally talk about God, the feelings are usually fleeting; they don't
have the same intense feror or the obsessive and stereotyped quality that
one sees in temporal lobe epileptics. Hence emotional changes alone
cannot provide a complete explanation for religious preoccupation. 4
The third explanation invokes connections between sensory centers
(vision and hearing) and the amygdala, that part of the limbic system
specialized in recognizing the emotional signifcance of events in the
external world. Obviously, not every person or event you encounter
throughout a typical day sets of alarm bells; that would be maladaptive
and you'd soon go mad. To cope with the world's uncertainties, you
need a way of gauging the salience of events before you relay a message
to the rest of the limbic system and to the hypothalamus telling them to
assist you in fghting or feeing.
But consider what might happen if spurious signals stemming from
limbic seizure activity were to travel these pathways . You' d get the sort
of kindling I described earlier. These "salience" pathways would become
Go D A N D T H E L I MB I C S Y S T E M 1 1 8 3
strengthened, increasing communication between brain structures. Sen
sory brain areas that see people and events and hear voices and noises
would become more closely linked to emotional centers. The result?
Ever object and event-not just salient ones-would become imbued
with deep signifcance, so that the patient would see "the universe in a
grain of sand" and "hold[s] infnity in the palm of his hand. " He would
foat on an ocean of religious ecstasy, carried by a universal tide to the
shores of Nirana.
The fourth hypothesis is even more speculative. Could it be that hu
man beings have actually evolved specialized neural circuitry for the sole
purpose of mediating religious experience? The human belief in the su
pernatural is so widespread in all societies all over the world that it's
tempting to ask whether the propensity for such beliefs might have a
biological basis. 5 If so, you'd have to answer a key question: What sorts
of Darwinian selection pressures could lead to such a mechanism? Ad
if there is such a mechanism, is there a gene or set of genes concerned
mainly with religiosity and spiritual leanings-a gene that atheists might
lack or have learned to circumvent (just kidding! ) ?
These kinds of arguments are popular within a relatively new discipline
called evolutionary psychology. ( It used to be called sociobiology, a term
that fell into disrepute for political reasons. ) According to its central
tenets, many human traits and propensities, even ones we might ordi
narily be tempted to attribute to "culture, " may in fact have been spe
cifcally chosen by the guiding hand of natural selection because of their
adaptive value.
One good example is the tendency for men to be polygamous and
promiscuous whereas women tend to be more monogamous. Of the
hundreds of human cultures throughout the world, only one, the Thodas
of South India, have ofcially endorsed polyandry ( the practice of having
more than one husband or male mate) . Indeed, the old adage "Biga
mous hogamous, women are monogamous; hogaous higamous, men
are polygamous" refects this state of afairs. It all makes good evolu
tionary sense, since a woman invests a good deal more time and efort-a
nine-month-long, risky, arduous pregnancy-in each ofspring, so that
she has to be very discerning in her choice of sexual partners. For a man,
the optimal evolutionary strategy is to disseminate his genes as widely as
possible, given his few minutes ( or, alas, seconds ) of investment in each
encounter. These behavioral propensities are unlikely to be cultural . If
anything, culture tends to forbid or minimize them rather than encour
age them, as we all know.
18 4 I P HA N T O MS I N T H E B RA I N
On the other hand, we must be carefl not to carry these "evolution
ary psychology" arguments too far. Just because a trait is universal
present in all cultures including cultures that have never been in con
tact-it doesn't follow that the trait is genetically specifed. For instance,
almost every culture that we know of has some form of cooking, however
primitve. (Yes, even the English. ) Yet one would never argue from this
that there is a cooking module in the brain specifed by cooking genes
that were honed by natural selection. The ability to cook is almost cer
tainly an ofshoot of a number of other unrelated skills such as a good
sense of smell and taste and the ability to follow a recipe step- by- step,
as well as a generous dose of patience.
So is religion ( or at least the belief in God and spirituality) like cook
ing-with culture playing by far the dominant role-or is it more like
polygamy, for which there appears to be a strong genetic basis? How
would an evolutionary psychologist account for the origin of religion?
One possibility is that the universal human tendency to seek authority
fgures-giving rise to an organized priesthood, the participation in rit
uals, chanting and dancing, sacrifcial rites and adherence to a moral
code-encourages conformist behavior and contributes to the stability
of one' s own social group-or "kin"-who share the same genes . Genes
that encourage the cultivation of such conformist traits would therefore
tend to fourish and multiply, and people who lacked them would be
ostracized and punished for their socially deviant behavior. Perhaps the
easiest way to ensure such stability and conformity is to believe in some
transcendent higher power that controls our destiny. No wonder tem
poral lobe epilepsy patients experience a sense of omnipotence and gran
deur, as if to say, "I am the chosen one. It is my duty and privilege to
transmit God's work to you lesser beings. "
This i s admittedly a speculative argument even by the rather lax stan
dards of evolutionary psychology. But whether or not one believes in
religious conformity "genes, " it's clear that certain parts of the temporal
lobe play a more direct role in the genesis of such experiences than any
other part of the brai n. And if the personal experiences of Dr. Persinger
are anything to go by, then this must be true not j ust of epileptics but
also of you and me.
I hasten to add that as far as the patient is concerned, whatever
changes have occurred are authentic-sometimes even desirable-and
the physician has no right, really, to attribute a value label to such esoteric
embellishments of personality. On what basis does one decide whether
a mystical experience is normal or abnormal ? There is a common ten-
Go D A N D T H E LI M B I C S Y S T E M 1 18 5
dency to equate "unusual" or "rare" with abnormal , but this is a logical
fallacy. Genius is a rare but highly valued trait, whereas tooth decay is
common but obviously undesirable. Wich one of these categories does
mystical experience fall into? Why is the revealed truth of such transcen
dent experiences in any way "inferior" to the more mundane truths that
we scientists dabble in? Indeed, if you are ever tempted to j ump to this
conclusion, j ust bear in mind that one could use exactly the same evi
dence-the involvement of the temporal lobes in religion-to argue for,
rather than against, the existence of God. By way of analogy, consider
the fact that most animals don't have the receptors or neural machinery
for color vision. Only a privileged few do, yet would you want to con
clude from this that color wasn't real ? Obviously not, but if not, then
why doesn' t the same argument apply to God? Perhaps only the "cho
sen" ones have the required neural connectons. (Aer all, "God works
in mysterious ways . ") My goal as a scientist, in other words, is to discover
how and why religious sentiments originate in the brain, but this has no
bearing one way or the other on whether God really exists or not.
So we now have several competing hypotheses of why temporal lobe
epileptics have such experiences. Even though all these theories invoke
the same neural structures, they postulate very diferent mechanisms and
it would be nice to fnd a way to distinguish among them. One of the
ideas-the notion that kindling has indiscriminately strengthened all con
nections from the temporal cortex to the amygdala-can be addressed
directly by studying the patient's galvanic skin response. Ordinarily an
obj ect is recognized by the visual areas of the temporal lobes. Its emo
tional salience-is it a fendly face or a ferce lion?-is signaled by the
amygdala and transmitted to the limbic system so that you become emo
tionally aroused and start sweating. But if the kindling has strengthened
al the connections within these pathways, then everything becomes sa
lient. No matter what you look at-a nondescript stranger, a chair or a
table-it should activate the limbic system strongly and make you per
spire. So unlike you and me, who should display a heightened GSR re
sponse only for our moms, dads, spouses or lions, or even a loud thud
or bang, the patient with temporal lobe epilepsy should show an in
creased galvanic skin response to everything under the sun.
To test this possibility, I contacted two of my colleagues who spe
cialize in the diagnosis and treatment of epilepsy-Dr. Vincent Iragui
and Dr. Evelyn Tecoma. Given the highly controversial nature of the
whole concept of "temporal lobe personality" ( not everyone agrees that
these personality traits are seen more frequently in epileptics ) , they were
18 6 I P H A N T O MS I N T H E B RA I N
quite intrigued by my ideas. A few days later, they recruited two of their
patients who manifested obvious "symptoms" of this syndrome-hyper
graphia, spiritual leanings and an obsessive need to talk about their feel
ings and about religious and metaphysical topics. Would they want to
volunteer in a research study?
Both were eager to paricipate. In what may turn out to be the very
frst scientifc experiment ever done on religion directly, I sat them in
comfortable chairs and attached harmless electrodes to their hands . Once
settled in front of a computer screen, they were shown random samples
of several types of words and images-for example, words for ordinary
inanimate objects (a shoe, vase, table and the like) , familiar faces (parents,
siblings ) , unfamiliar faces, sexually arousing words and pictures ( erotic
magazine pinups) , four-letter words involving sex, extreme violence and
horror ( an alligator eating a person alive, a man setting himself afre) and
religious words and icons ( such as the word "God") .
I f you and I were to undergo this exercise, we would show huge GSR
responses to the scenes of violence and to the sexually explicit words and
pictures, a fairly large response to familiar faces and usually nothing at
all to other categories ( unless you have a shoe fetish, in which case you'd
respond to one) .
What about the patients? The kindling hypothesis would predict a
uniform high response to all categories. But to our amazement what we
found in the two patients tested was a heightened response mainly to
religious words and icons. Their responses to the other categories, in
cluding the sexual words and images, which ordinarily evoke a powerfl
response, was strangely diminished compared to what is seen in normal
individuals. 6
Thus the results show that there has been no general enhancement of
all the connections-indeed, if anything, there has been a decrement.
But rather surprisingly, there' s been a selective amplifcation of response
to religious words. One wonders whether this technique could be usefl
as a sort of "piety index" to distinguish religious dabblers or frauds
( "closet atheists") from true believers. The absolute zero on the scale
could be set by measuring Francis Crick's galvanic skin response.
I want to emphasize that not every temporal lobe epilepsy patient
becomes religious. There are many parallel neural connections between
the temporal cortex and the amygdala. Depending on which particular
ones are involved, some patients may have their personalities skewed in
other directions, becoming obsessed with writing, drawing, arguing phi
losophy or, rarely, being preoccupied with sex. It's likely that their GSR
Go D A N D THE LIMBIC SYSTEM 1 18 7
responses would shoot upward in response to these stimuli rather than
to religious icons, a possibility that is being studied in our laboratory and
others.
Was God talking to us directly through the GSR machine? Did we
now have a direct hotline to heaven? Whatever one makes of the selective
amplifcation of responses to religious words and icons, the fnding elim
inates one of the proposed explanations for these experiences-that these
people become spiritual simply because everthing around them becomes
so salient and deeply meaningfl . On the contrary, the fnding suggests
that there has been a selective enhancement of responses to some cate
gories of stimuli-such as religious words and images-and an actual
reduction in response to other categories such as sexually loaded ones
( as is consistent with the diminished libido that some of these patients
report) .
So do these fndings imply that there are neural structures i n the tem
poral lobes that are specialized for religion or spirituality, that are selec
tively enhanced by the epileptic process? This is a seductive hypothesis,
but other interpretations are possible. For all we know, the changes that
have triggered these patients' religious feror could be occurring any
where, not necessarily in the temporal lobes. Such activity would still
eventually cascade into the limbic system and give you exactly the same
result-an enhanced GSR for religious images. So strong GSR itself is
no guarantee that the temporal lobes are directly involved in religion. 7
There i s, however, another experiment that could be done to resolve
this issue once and for a. The experiment takes advantage of the fact that
when seizures become seriously disabling, life- threatening and unrespon
sive to medication, portions of the temporal lobe are ofen surgically re
moved. So we can ask, What would happen to the patient's personality
especially his spiritual leanings-if we removed a chunk of his temporal
lobe? Would some of his acquired personality changes be "reversed"?
Would he suddenly stop having mystical experiences and become an athe
ist or an agnostic? Would we have performed a "Godectomy"?
We have yet to conduct such a study, but meanwhile we have already
learned something from our GSR studies-that the seizures have per
manently altered the patients' inner mental life, ofen producing inter
esting and highly selective distortions of their personality. Aer all , one
rarely sees such profound emotional upheavals or religious preoccupa
tions in other neurological disorders. The simplest explanation for what
happens in the epileptics is that there have been permanent changes in
temporal lobe circuitry caused by selective enhancement of some con-
1 8 8 I P H ANTO MS I I T H E B RA I N
nections and efacement of others-leading to new peaks and valleys in
the patients' emotional landscape.
So what' s the bottom line? The one clear conclusion that emerges
from all this is that there are circuits in the human brain that are involved
in religious experience and these become hyperactive in some epileptics.
We still don't know whether these circuits evolved specifcally for religion
( as evolutionary psychologists might argue) or whether they generate
other emotions that are merely conducive to such beliefs ( although that
cannot explain the feror with which the beliefs are held by many pa
tients ) . We are therefore still a long way from showing that there is a
"God module" in the brain that might be genetically specifed, but to
me the exciting idea is that one can even begin to address questions
about God and spirituality scientifcally.
Ten to the rolling Heav'n itsel I cried,
Aking, awhat Lamp had Destiny to guide
Her little Children stumbling in the Dark?"
And-aA blind Understanding!" Heav'n replied.
-The Rubaiyat of Omar Kayyam
For many of the topics we've discussed in earlier chapters-phantom
limbs, neglect syndrome and Capgras' syndrome-we now have reason
able interpretations as a result of our experiments. But in seeking brain
centers concerned with religious experience and God, I realized that I
had entered the "twilight zone" of neurology. There are some questions
about the brain that are so mysterious, so deeply enigmatic, that most
serious scientists simply shy away from them, as if to say, "That would
be premature to study" and "I' d be a fool if I embarked on such a
quest. " And yet these are the very issues that fascinate us most of all .
The most obvious one, of course, is religion, a quintessentially human
trait, but it is only one unsolved mystery of human nature. What about
other uniquely human traits-such as our capacity for music, math, hu
mor and poetry? What allowed Mozart to compose an entire symphony
in his head or mathematicians like Fermat or Rmanujan to "discover"
flawless conj ectures and theorems without ever going through step- by
step formal proofs? And what goes on in the brain of a person like Dylan
Thomas that allowed him to write such evocative poetry? Is the creative
spark simply an expression of the divine spark that exists in all of us?
Ironically clues come from a bizarre condition called "idiot savant syn
drome" ( or, to use the more politically correct phrase, the savant syn-
Go D A N D T H E L I MB I C S Y S T E M 1 18 9
drome) . These individuals ( retarded and yet highly talented) can give us
valuable insights about the evolution of human nature-a topic that be
came an obsession for some of the greatest scientifc minds of the last
century.
The Victorian era witnessed a vigorous intellectual debate between
two brilliant biologists-Charles Darwin and Alfred Russel Wallace. Dar
win, of course, is a household name. Everyone associates him with the
discovery of natural selection as the main driving force of organic evo
lution. It is a pity that Wallace is almost completely unknown except
among biologists and historians of science, since he was an equally bril
liant scholar and independently came up with the same idea. In fact, the
very frst scientfc paper on evolution by natural selection was presented
j ointly by Darwin and Wallace and communicated to the Linnean Society
by Joseph Hooker in 1850. Instead of feuding endlessly over priority, as
many of today's scientists do, they cheerflly acknowledged each other's
contributions and Wallace even wrote a book called Darinism, cham
pioning what he referred to as "Darwin's" theory of natural selection.
Upon hearing of this book, Darin responded, "You should not speak
of Darinism for it can as well be called Wallacism. "
Wat does the theory state? There are three components: 8
1. Since ofspring vastly outnumber the available resources, there
must be a constant struggle for existence in the natural world.
2. No two individuals of a species are exactly identical ( except in the
rare case of identical twins ) . Indeed, there are always random var
iations, however minute, in body type that arise from the random
shufing of genes that takes place during cell division-a shufing
that ensures that ofspring difer from each other and from their
parents, thereby increasing their candidature for evolutionary
change.
3. Those fortuitous combinations of genes that cause individuals to
be slightly better adapted to a given local environment tend to
multiply and propagate within a population since they increase the
surival and reproduction of those individuals.
Darwin believed that his principle of natural selection could account
not only for the emergence of morphological traits like fngers or noses,
but also for the structure of the brain and therefore our mental capacities.
In other words, natural selection could explain our talents for music, art,
literature and other human intellectual achievements. Wallace disagreed.
He conceded that Darwin's principle might explain fngers and toes and
19 0 I P HA N T O MS I N T H E B RA I N
maybe even some simple mental traits, but that certain quintessentially
human abilities like mathematical and musical talent could not possibly
have arisen through the blind workings of chance.
Why not? According to Wallace, as the human brain evolved, it en
countered a new and equally powerfl force called culture. Once culture,
language and writing emerged, he argued, human evolution became La
marckian-that is, you could pass on the accumulated wisdom of a life
time to your ofspring. These progeny will be much wiser than the
ofspring of illiterates not because your genes have changed but simply
because this knowledge-in the form of culture-has been transferred
from your brain to your child's brain. In this way, the brain is symbiotic
with culture; the two are as interdependent as the naked hermit crab and
its shell or the nucleated cell and its mitochondria. For Wallace, culture
propels human evolution, making us absolutely unique in the animal
kingdom. Isn't it extraordinary, he said, that we are the only animal in
which the mind is vastly more important than any bodily organ, assuming
a tremendous signifcance because of what we call "culture. " Moreover,
our brain actually helps us avoid the need for frther specialization. 9
Most organisms evolve to become more and more specialized as they
take up new environmental niches, be it a longer neck for the girafe or
sonar for the bat. Humans, on the other hand, have evolved an organ,
a brain, that gives us the capacity to evade specialization. We can colonize
the Arctic without evolving a fr coat over millions of years like the polar
bear because we can go kill one, take its coat and drape it on ourselves.
And then we can give it to our children and grandchildren.
Wallace's second argument against "blind chance giving rise to the
talents of a Mozart" involves what might be called potential intelligence
(a phrase used by Richard Gregory) . Say, you take a barely literate young
tribesman from a contemporary aboriginal society ( or even use a time
machine to garner a Cro-Magnon man) and give him a modern public
school education in Ro or New York or Tokyo. He will, of course, be
no diferent from any other child reared in those cities. According to
Wallace, this means that the aborigine or Cro-Magnon possesses a po
tential intelligence that vastly exceeds anything that he might need for
coping with his natural environment. This kind of potential intelligence
can be contrasted with kinetic intelligence, which is realized through
formal education. But why the devil did this potential intelligence evolve?
It couldn't have arisen for learning Latin in English schools. It couldn' t
have evolved for learning the calculus, even though almost anyone who
tries hard enough can master it. What was the selection pressure for the
Go D A N D T H E L I MB I C S Y S T E M I 191
emergence of these latent abilities? Natural selection can only explain the
emergence of actual abilities that are expressed by the organism-never
potential ones. Wen they are usefl and promote surival , they are
passed on to the next generation. But what to make of a gene for latent
mathematical ability? What beneft does that confer on a nonliterate per
son? It seems like overkll .
Wallace wrote, "The lowest savages with the least copious vocabularies
[have] the capacity of uttering a variety of distinct articulate sounds and
of applying them to an almost infnite amount of modulation and in
flection [which] is not in any way inferior to that of the higher [Euro
pean] races. An instrument has been developed in advance of the needs
of its possessor. " Ad the argument holds, with even greater force, for
other esoteric human abilities such as mathematics or musical talent.
There' s the rub. An instrument has been developed in advance ofthe
needs of its possessor, but we know that evolution has no foresight! Here
is an instance in which evolution appears to have foreknowledge. How
is this possible?
Wallace wrestled mightily with this paradox. How can improvement
in esoteric mathematical skills-in latent form-afect the surival of one
race that has this latent ability and the extinction of another that doesn' t ?
"It is a somewhat curious fact," he wrote, "that when all modern writers
admit the great antiquity of man, most of them maintain the very recent
development of intellect, and will hardly contemplate the possibility of
men, equal in mental capacity to ourselves, having existed in prehistoric
times. "
But we know they did. Both the Neanderthal and Cro-Magnon cranial
capacities were actually larger than ours, and it's not inconceivable that
their latent potential intelligence may have been equal to or even greater
than that of Homo sapiens.
So how is it possible that these astonishing, latent abilities emerged in
the prehistoric brain but have only been realized in the last one thousand
years? Wallace's answer: It was done by God! "Some higher intelligence
must have directed the process by which the human nature was devel
oped. " Thus human grace is an earthly expression of "divine grace. "
This is where Wallace parted company with Darin, who resolutely
maintained that natural selection was the prime force in evolution and
could account for the emergence of even the most esoteric mental traits,
without the helping hand of a Supreme Being.
How would a modern biologist resolve Wallace' s paradox? She would
probably argue that esoteric and "advanced" human traits like musical
19 2 I P H A N T O MS I N T H E B RA I N
and mathematical ability are specifc manifestations of what is usually
called "general intelligence"-itself the culmination of a "runaway"
brain that exploded in size and complexity within the last three million
years . 10 General intelligence evolved, the argument goes, so that one can
communicate, hunt game, hoard food in granaries, engage in elaborate
social rituals and do the myriad things that humans enj oy and that help
them surive. But once this intelligence was in place, you could use it
for all sorts of other things, like the calculus, music and the design of
scientifc instruments to extend the reach of our senses. By way of anal
ogy, consider the human hand: Even though it evolved its amazing ver
satility for grasping at tree branches, it can now be used to count, write
poetry, rock the cradle, wield a scepter and make shadow puppets.
But with respect to the mind, this argument doesn' t make much sense
to me. I'm not saying it's wrong, but the idea that the ability to spear
antelope was then somehow used for the calculus is a bit dubious. I' d
like to suggest another explanation, one that takes us back not only to
the savant syndrome that I mentioned earlier but also to the more general
question of the sporadic emergence of talent and genius in the normal
population.
"Savants" are persons whose mental capacity or general intelligence
is abysmally low, yet who have islands of astonishing talent. For example,
there are savants on record with an IQ of less than 50, barely able to
fnction in normal society, yet they could with ease generate an eight
digit prime number, a feat that most tenured mathematics professors
cannot match. One savant could come up with the cube root of a six
fgure number in seconds and could double 8, 388,628 twenty-four times
to obtain 140,737,488, 355, 328 in several seconds. Such individuals are
a living reftation of the argument that specialized talents are merely
clever deployments of general intelligence.
11
The realms of art and music are punctuated with savants whose talents
have amazed and delighted audiences through the ages. Oliver Sacks
describes Tom, a thirteen-year-old boy who was blind and incapable of
tying his own shoes . Although he had never been instructed in music or
educated in any way, he learned to play the piano simply by hearing
others play. He absorbed arias and tunes from hearing them sung and
could play any piece of music on the frst try as well as the most accom
plished performer. One of his most remarkable feats was to perform three
pieces of music all at once. With one hand he played "Fisher's Horn
Pipe, " with the other he played "Yankee Doodle Dandy" and simulta-
Go D A N D T H E LI M B I C S Y S T E M I 19 3
neously he sang "Dixie. " He could also play the piano with his back to
the keyboard, his inverted hands racing up and down the ivories. Tom
composed his own music, and yet, as a contemporary obserer pointed
out, "He seems to be an unconscious agent acting as he is acted on and
his mind [is] a vacant receptor where nature stores her jewels to recall
them at her pleasure. "
Nadia, whose IQ measured between 60 and 70, was an artistic genius.
At age six, she showed all the signs of severe autism-ritualistic behavior,
inabilit to relate to others and limited language. She could barely put two
words together. Yet from this early age, Nadia could draw lifelike pictures
of people around her, of horses and even of complex visual scenes unlike
the "tadpolelike" drawings of other children her age. Her sketches were so
animated that they seemed to leap out from the canvas and were good
enough to hang in any Madison Avenue gallery ( Figure 9. 2 ) .
Other savants have incredibly specifc talents. One boy can tell you
the time of day, to the exact second, without referring to any timepiece.
He can do this even in his sleep, sometimes mumbling the exact time
while dreaming. The "clock" inside his head is as accurate as any Rolex.
Another can estimate the exact width of an object seen from twenty feet
away. You or I would give a ballpark fgure. She would say, "That rock
is exactly two feet, eleven and three- quarter inches wide. " And she' d be
right.
These examples show that specialized esoteric talents do not emerge
spontaneously fom general intelligence, for if that were true, how can
an "idiot" display them?
Nor do we have to invoke the extreme pathological example of savants
to make this point, for there is an element of this syndrome in every
talented person or indeed in every genius. "Genius, " contrary to popular
misconception, is not synonymous with superhuman intelligence. Most
of the geniuses whom I have had the privilege of knowing are more like
idiot savants than they would care to admit-extraordinarily talented in
a few domains but quite ordinary in other respects.
Consider the of-told story of the Indian mathematical genius R
manujan, who at the turn of the century worked as a clerk in the Madras
seaport, a few miles from where I was born. He had matriculated to the
early part of high school , where he performed badly in all his subjects,
and he had no formal education in advanced mathematics. Yet he was
astonishingly gifed in math and was obsessed by it. So poor that he
couldn't aford paper, he would use discarded envelopes to scribble his
19 4 I P HA N T O MS I N T H E B RA I N
(a) (b)
Fige 9.2 (a) A drawing of a horse made b Nadia, the autistic savant, when
she was fve years old. (b) A horse drawn by Leonardo da Vinci. (c) A drawing of
a horse by a normal eiht-year-old. Notice that Nadia's drawing is vastly superior
to that of the normal eiht-year-old and almost as good as (or perhaps better than!)
da Vinci's horse. (a) and (c) reprinted from Nadia, by Lorna Selfe, with permis
sion from Academic Press (New York).
mathematical equations, discovering several new theorems before the age
of twenty-two. Since he was not acquainted with any number theorists
in India, he decided to communicate his discoveries to several mathe
maticians in other parts of the world, including Cambridge, England.
One of the world's top number theorists of that time, G. H. Hardy,
received his scribbles and immediately thought Rmanujan was a crack
pot. Having glanced at them, he went out to play tennis. As the game
wore on, Rmanuj an's equations kept haunting him. He kept seeing the
numbers in his mind. "I had never seen anything in the least like them
before, " Hardy later wrote. "They must be true because no one would
have had the imagination to invent them. " So he promptly went back
and checked the validity of the elaborate equations on backs of envelopes,
saw that most of them were correct and immediately sent a note to his
colleague J. E. Littlewood, who also went over the manuscripts. Both
luminaries quickly realized that Rmanujan was probably a genius of the
highest caliber. They invited him to Cambridge, where he worked for
many years, eventually surpassing them in the originality and importance
of his contributions.
I mention this story because if you were to go out to dinner with
Rmanuj an you wouldn' t think there was anything unusual about him.
He was j ust like any other person except for the fact that his mathematical
skills were way of scale-almost supernatural , some have said. Again, if
GO D A N D T H E L I M B I C S Y S T E M I 19 5
mathematical ability is simply a fnction of general intelligence, a result
of the brain's getting bigger and better overall , then more intelligent
people should be better at math, and vice versa. But if you met Rma
nuj an, you' d know that that j ust isn't true.
Wat is the solution? Rmanuj an's own "explanation"-that the flly
formed equations were whispered to him in dreams by the presiding
village deity, Goddess Namagiri-doesn't really help us very much. But
I can think of two other possibilities.
The frst, more parsimonious, view is that general intelligence is really
a number of diferent mental traits-with both the genes and the traits
themselves influencing each other's expression. Since genes combine ran
domly in the population, every now and then you will get a fortuitous
combination of traits-such as vivid visual imagery combined with ex
cellent numerical skills-and such shufing can throw up all sorts of
unexpected interactions. Thus is born that extraordinary flowering of
talent we call genius-the gifs of an Abert Einstein who could "visu
alize" his equations or a Mozart who saw, and did not merely hear, his
musical compositions unfold in his mind's eye. Such genius is rare only
because the lucky genetic combinations are rare.
But there's a problem with this argument. If genius results from ser
endipitous genetic combinations, how does one explain the talents of
Nadia and Tom, whose general intelligence is abysmal ? ( Indeed, an au
tistic savant's social skills may be less than those of a Bonobo ape. ) It's
difcult, moreover, to see why such unique talent should actually be more
common among savants than it is among the general population, who,
if anything, have a larger number of healthy traits to shufle around in
each generation. (As many as 10 percent of autistic children have perfect
pitch, compared with only 1 or 2 percent of the general population. )
Furthermore, the traits in that individual would have to "interlock" pre
cisely and interact i n such a way that the outcome i s something elegant
rather than nonsensical , a scenario that is as unlikely as a confederacy of
dunces producing a work of artistic or scientifc genius.
This brings me to the second explanation for the savant syndrome in
particular and for genius in general . How can someone who can' t tie
shoelaces or carry on a normal conversaton calculate prime numbers?
The answer might lie in a region of the lef hemisphere called the angular
gyrus, which, when damaged, leaves some people ( like Bill, the Ar Force
pilot in Chapter 1 who couldn't subtract) with an inability to do simple
calculations, such as subtract 7 from 100. This does not mean that the
lef angular gyrus is the brain's math module, but it's fair to say that this
1 9 6 I P HA N T O MS I N T H E B RA I N
structure is doing something crucial for mathematical computation and
is not essential for language, working memory or vision. But you do seem
to need the lef angular gyrus for math.
Consider the possibility that savants sufer early brain damage before
or shortly afer birth. Is it possible that their brains undergo some form
of remapping as seen in phantom limb patients? Does the prenatal or
neonatal injury lead to unusual rewiring? In savants, one part of the brain
may for some obscure reason receive a greater than average input or some
other equivalent impetus to become denser and larger-a huge angular
gyrus, for example. What would be the consequence for mathematical
ability? Would this produce a child who can generate eight-digit prime
numbers? In truth, we know so little about how neurons perform such
abstract operations that it's difcult to predict what the efect of such a
change might be. A angular gyrus doubled in size could lead not to a
mere doubling of mathematical ability but to a logarithmic or hundred
fold increase. You can imagine an explosion of talent resulting from this
simple but "anomalous" increase in brain volume. The same argument
might hold for drawing, music, language, indeed any human trait. 1 2
This argument is zany and unashamedly speculative, but at least it's
testable. A math savant should have a large or hypertrophied lef angular
gyrus, whereas an artistic savant may have a hypertrophied right angular
gyrus. Such experiments have not been done, to my knowledge, although
we do know that damage to the riht parietal cortex, where the angular
gyrus is located, can profoundly disrupt artstic skills (j ust as damage to
the lef disrupts calculation) .
A similar argument can be put forth to explain the occasional emer
gence of genius or extraordinary talent in the normal population, or to
answer the especially vexing question of how such abilities cropped up
in evolution in the frst place. Maybe when the brain reaches a critical
mass, new and unforeseen traits, propertes that were not specifcally cho
sen by natural selection, emerge. Maybe the brain had to become big
for some other more obviously adaptive reason-throwing spears, talk
ing or navigation-and the simplest way to achieve this was to increase
one or two growth-related hormones or morphogens ( genes that alter
size and shape in developing organisms ) . But since such a hormone- or
morphogen- based growth spurt cannot selectively increase the size of
some parts while sparing others, the bonus might be an altogether bigger
brain, including an enormous angular gyrus and the accompanying ten
fold or hundredfold enhancement in mathematical ability. Notice that
this argument is very diferent from the widely held belief that you de-
Go D A N D T H E LI M B I C S Y S T E M I 1 9 7
velop some very "general" ability that is then deployed for a specialized
skill .
Taking this speculation even frther, is it possible that humans fnd
such esoteric talents-be it music, poetry, drawing or math-to be sex
ually attractive mainly because they serve as an externally visible signature
of a giant brain? Just as the peacock's large, iridescent tail or the size of
a majestic bull elephant's tusks constitutes "truth in advertising" for the
animal 's health, so the human ability to croon a tune or pen a sonnet
might be a marker for a superior brain. ( "Truth in advertising" may play
an important role in mate selection. Indeed, Richard Dawkins has sug
gested, half seriously, that the size and strength of a human male's erec
tion may be markers for general health. )
This line of reasoning raises some fascinating possibilities. For instance,
you could inj ect hormones or morphogens into a fetal human brain or
infant to try to increase brain size artifcially. Would this result in a race
of geniuses with superhuman talents? Needless to say, the experiment
would be unethical to do in humans, but an evil genius might be tempted
to try it on the great apes. Is so, would you see a sudden eforescence
of extraordinary mental talents in these apes? Could you accelerate the
pace of simian evolution through a combination of genetic engineering,
hormonal interention and artifcial selection?
My basic argument about savants-that some specialized brain regions
may have become enlarged at the expense of others-may or may not
turn out to be correct. But even if it's valid, bear in mind that no savant
is going to be a Picasso or an Einstein. To be a true genius, you need
other abilities, not just isolated islands of talent. Most savants are not
truly creative. If you look at a drawing by Nadia, you do see creative
artistic ability/3 but among mathematical and musical savants, there are
no such examples. Wat seems to be missing is an inefable quality called
creativity, which brings us face to face with the very essence of what it
is to be human. There are those who asser that creativity is simply the
ability to randomly link seemingly unrelated ideas, but surely that is not
enough. The proverbial monkey with a typewriter will eventually produce
a Shakespeare play, but it would need a billion lifetimes before it could
generate a single intelligible sentence-let alone a sonnet or a play.
Not long ago when I told a colleague about my interest in creativity,
he repeated the well-worn argument that we simply toss ideas around in
our heads, producing random combinations until we hit on aesthetically
pleasing ones. So I challenged him to "toss around" some words and
ideas by coming up with a single evocative metaphor for "taking things
19 8 I P HA N T O MS I N T H E B RA I N
to ridiculous extremes" or "overdoing things . " He scratched his head
and afer half an hour confessed that he couldn't think of anything all
that original ( despite his very high verbal I Q, I might add) . I pointed
out to him that Shakespeare had crammed fve such metaphors in a single
sentence:
To gild refned gold, to paint the lily, to throw a perfme on the violet, to
smooth the ice, or add another hue unto the rainbow . . . is wastefl and
ridiculous excess.
It sounds so simple. But how come Shakespeare thought of it and
nobody else? Each of us has the same words at our command. There' s
nothing complicated or esoteric about the idea that's being conveyed.
In fact, i t' s crystal clear once it is explained and has that universal "why
didn't I think of that? " quality that characterizes the most beautifl and
creative insights . Yet you and I would never come up with an equally
elegant set of metaphors by simply dredging up and randomly shufing
words in our minds. Wat's missing is the creative spark of genius, a trait
that remains as mysterious to us now as it did to Wallace. No wonder
he felt impelled to invoke divine interention.
CHAPTER 1o
The Woman Who Died
Laughing
God is a comedian performing before an audience that is
afaid to laugh.
-FRIEDRCH NIETZSCHE
God is a hacker.
-FRNCIS CRICK
On the morning of his mother's fneral in 193 1 , Willy Anderson-a
twenty-fve-year-old plumber from Lndon-donned a new black suit,
clean white shirt and nice shoes borrowed from his brother. He had loved
his mother very much and his grief was palpable. The family gathered
amid tearfl hugs and sat silently through an hour-long fneral serice
in a church that was much too hot and stuf. Willy was relieved fnally
to get outdoors into the chilly open air of the cemetery and bow his
head with the rest of the family and friends. But j ust as the gravediggers
began lowering his mother's roped casket into the earth, Willy began to
laugh. It started as a mufled snorting sound that evolved into a pro
longed giggle. Willy bowed his head farther down, dug his chin into his
shirt collar and drew his right hand up to his mouth, trying to stifle the
unbidden mirth. It was no use. Against his will and to his profound
embarrassment, he began to laugh out loud, the sounds exploding rhyth-
1 9 9
2 0 0 I P HA N T O MS I N T H E B RA I N
mically until he doubled over. Everyone at the fneral stared, mouth
agape, as the young man staggered backward, desperately looking for
retreat. He walked bent at the waist, as if in supplication for forgiveness
for the laughter that would not subside. The mourners could hear him
at the far end of the cemetery, his laughter echoing amid the gravestones.
That evening, Willy' s cousin took him to the hospital . The laughter
had subsided afer some hours, but it was so inexplicable, so stunning in
its inappropriateness, that everyone in the family felt it should be treated
as a medical emergency. Dr. Astley Clark, the physician on duty, exam
ined Willy's pupils and checked his vital signs. Two days later, a nurse
found Willy lying unconscious in his bed, having sufered a severe sub
arachnoid hemorrhage, and he died without regaining consciousness.
The postmortem showed a large ruptured aneurysm in an artery at the
base of his brain that had compressed part of his hypothalamus, mam
millary bodies and other structures on the floor of his brain.
And then there was Ruth Greenough, a ffy-eight-year-old librarian
from Philadelphia. Although she had sufered a mild stroke, she was able
to keep her small branch library running smoothly. But one morning in
1936, Ruth had a sudden violent headache, and within seconds her eyes
turned up and she was seized with a laughing ft. She began shaking with
laughter and couldn't stop. Short expirations followed each other in such
rapid succession that Ruth' s brain grew oxygen- stared and she broke
into a sweat, at times holding her hand to her throat as if she were
choking. Nothing she did would stop the convulsions of laughter, and
even an injection of morphine given by the doctor had no efect. The
laughter went on for an hour and a half. All the while, Ruth' s eyes re
mained turned upward and wide open. She was conscious and could
follow her doctor's instructions but was not able to utter a single word.
At the end of an hour and a half, Ruth lay down completely exhausted.
The laughter persisted but was noiseless-little more than a grimace.
Suddenly she collapsed and became comatose, and afer twenty-four
hours Ruth died. I can say that she literally died laughing. The post
morem revealed that a cavity in the middle of her brain ( called the third
ventricle ) was flled with blood. A hemorrhage had occurred, involving
the foor of her thalamus and compressing several adj acent structures .
The English neurologist Dr. Purdon Martin, who described Ruth's case,
said, "The laughter is a mock or sham and it mocks the laughter at the
time, but this is the greatest mockery of all , that the patient should be
forced to laugh as a portent of his own doom. "1
More recently, the British j ournal Nature reported a modern case of
T H E WOMA N WH O DI E D LAU G H I N G I 2 0 l
laughter elicited by direct electrical stimulation of the brain during surgery.
The patient was a ffeen-year-old girl named Susan who was being treated
for intractable epilepsy. Doctors hoped to excise the tissue at the focal point
of her seizures and were exploring nearby areas to make sure they did not re
move any critically important fnctions. When the surgeon stimulated Su
san's supplementary motor cortex ( close to a region in the frontal lobes that
receives input from the brain's emotional centers) , he got an unexpected re
sponse. Susan started laughing uncontrollably, right on the operating table
( she was awake for the procedure) . Oddly enough, she ascribed her merri
ment to everything she saw around her, including a picture of a horse,
and added that the people standing near her looked incredibly fnny. To
the doctors, she said: "You guys are just so funny standing around. "2
The kind of pathological laughter seen in Willy and Ruth is rare; only
a couple of dozen such cases have been described in the medical litera
ture. But when you gather them together, a striking fact j umps out at
you. The abnormal activity or damage that sets people giggling is almost
always located in portions of the limbic system, a set of structures in
cluding the hypothalamus, mammillary bodies and cingulate gyrus that
are involved in emotions ( see Figure 8 . 1 ) . Given the complexity oflaugh
ter and its infnite cultural overtones, I fnd it intriguing that a relatively
small cluster of brain structures is behind the phenomenon-a sort of
"laughter circuit. "
But identifing the location of such a circuit doesn' t tell us why laugh
ter exists or what its biological fnction might be. (You can' t say it
evolved because it feels good. That would be a circular argument, like
saying sex exists because it feels good instead of saying it feels good
because it motivates you to spread your genes. ) Asking why a given trait
evolved ( be it yawning, laughing, crying or dancing) is absolutely vital
for understanding its biological fnction, and yet this question is rarely
raised by neurologists who study patients with brain lesions. This is
astonishing given that the brain was shaped by natural selection j ust as
any other organ in the body, such as the kidney, liver or pancreas, was.
Fortunately, the picture is changing, thanks in part to "evolutionary
psychology, " the new discipline that I mentioned in the last chapter. 3
The central tenet of this controversial feld is that many salient aspects
of human behavior are mediated by specialized modules ( mental organs )
that were specifcally shaped by natural selection. As our Pleistocene an
cestors romped across ancient savannas in small probands, their brains
2 0 2 I P HA N T O MS I N T H E B RA I N
evolved solutions to their everyday problems-things like recognizing
kin, seeking healthy sexual partners or eschewing foul-smelling food.
For example, evolutionary psychologists would argue that your disgust
for feces-far from being taught to you by your parents-is probably
hard-wired in your brain. Since feces might contain infectious bacteria,
eggs and parasites, those ancestral hominids who had "disgust for feces"
genes surived and passed on those genes, whereas those who didn' t were
wiped out ( unlike dung beetles, who probably fnd the bouquet of feces
irresistible) . This idea may even explain why feces infected with cholera,
salmonellosis or shigella are especially foul smelling. 4
Evolutionary psychology is one of those disciplines that tend to po
larize scientists . You are either for it or vehemently against it with much
arm waving and trading of raspberries behind backs, much as people are
nativists ( genes specif everything) or empiricists ( the brain is a blank
slate whose wiring is subsequently specifed by the environment, includ
ing culture) . The real brain, it turns out, is far messier than what's im
plied by these simple-minded dichotomies. For some traits-and I' m
going to argue that laughter i s one of them-the evolutionary perspec
tive is essential and helps explain why a specialized laughter circuit exists.
For other traits this way of thinking is a waste of time ( as we noted in
Chapter 9, the notion that there might be genes or mental organs for
cooking is silly, even though cooking is a universal human trait) .
The distinction between fact and fction gets more easily blurred in
evolutionary psychology than in any other discipline, a problem that is
exacerbated by the fact that most "ev-psych" explanations are completely
untestable: You can't run experiments to prove or disprove them. Some
of the proposed theories-that we have genetically specifed mechanisms
to help us detect fertile mates or that women sufer from morning sick
ness to protect the fetus from poisons in foods-are ingenious. Others
are ridiculously far-fetched. One afernoon, in a whimsical mood, I sat
down and wrote a spoof of evolutionary psychology j ust to annoy my
colleagues in that feld. I wanted to see how far one could go in conjuring
up completely arbitrary, ad hoc, untestable evolutionary explanations for
aspects of human behavior that most people would regard as "cultural "
in origin. The result was a satire titled "Wy Do Gentlemen Prefer
Blondes? " To my amazement, when I submitted my tongue-in-cheek
essay to a medical journal , it was promptly accepted. And to my even
greater surprise, many of my colleagues did not fnd it amusing; to them
it was a perfectly plausible argument, not a spoof5 (I describe it in the
endnotes in case you are curious . )
T H E WOMA N WH O DI E D LAU G H I N G I 2 0 3
Wat about laughter? Can we come up with a reasonable evolutionary
explanation, or will the true meaning of laughter remain forever elusive?
If an alien ethologist were to land on earth and watch us humans, he
would be mystifed by many aspects of our behavior, but I'll wager that
laughter would be very near the top of the list. A he watches people
interacting, he notices that every now and then we suddenly stop what
we're doing, grimace and make a loud repetitive sound in response to a
wide variety of situations. What fnction could this mysterious behavior
possibly sere? Cultural factors undoubtedly infuence humor and what
people fnd fnny-the English are thought to have a sophisticated sense
of humor, whereas Germans or Swiss, it is said, rarely fnd anything amus
ing. But even if this is true, might there still be some sort of "deep
structure" underlying all humor? The details of the phenomenon vary
from culture to culture and are influenced by the way people are raised,
but this doesn't mean there' s no genetically specifed mechanism for
laughter-a common denominator underlying all types of humor. In
deed, many people have suggested that such a mechanism does exist, and
theories on the biological origins of humor and laughter have a long
history, going all the way to Schopenhauer and Knt, two singularly
humorless German philosophers.
Consider the following two jokes. ( Not surpisingly, it was difcult to
fnd examples that are not racist, sexist or ethnic. Aer a diligent search
I found one that was and one that wasn't . )
A fellow i s sitting i n a truck stop cafe i n California, having lunch, when
suddenly a giant panda bear walks in and orders a burger with fries and
a chocolate milkshake. The bear sits down, eats the food, then stands
up, shoots several of the other customers and runs out the door. The
fellow is astonished, but the waiter seems completely undisturbed. "What
the hell is going on? " the customer asks. "Oh, well, there' s nothing
surprising about that," says the waiter. "Just go look in the dictionary
under 'panda. ' " So the guy goes to the library, takes out a dictionary
and looks up "panda"-a big frry, black and white animal that lives in
the rain forest of China. It eats shoots and leaves.
A guy carrying a brown paper bag goes into a bar and orders a drink.
The bartender smiles, pours the drink and then, unable to contain his
curiosity, says, "So, what's in the bag? " The man gives a little laugh and
says, "You wanna see? Sure, you can see what's in the bag," and he
reaches in and pulls out a tiny piano, no more than six inches tall.
2 0 4 I P HA N T O MS I N T H E B RA I N
"Wat's that? " asks the bartender. The man doesn't say anything; he
just reaches into the bag a second time and pulls out a tiny man, about
a foot tall , and sits him down next to the piano. "Wow," says the bar
tender, absolutely astonished. "I've never in my life seen anything like
that. " The little man begins to play Chopin. "Holy cow, " says the bar
tender, "where did you ever get him? " The man sighs and says, "Well,
you see, I found this magic lamp and it has a genie in it. He can grant
you anything you want but only gives one wish. " The bartender scowls,
"Oh, yeah, sure you do. Who are you trying to kd? " "You don' t believe
me? " says the man, somewhat ofended. He reaches into his coat pocket
and pulls out a silver lamp with an ornate cured handle. "Here it is.
Here' s the lamp with the genie in it. Go ahead and rub it if you don't
believe me. " So the bartender pulls the lamp over to his side of the
counter and, looking at the man skeptically, rubs the lamp. And then
POOP, a genie appears over the bar, bows to the bartender and says,
"Sire, your wish is my command. I shall grant thee one wish and one
wish only. " The bartender gasps but quickly gains his composure and
says, "Okay, okay, give me a million bucks ! " The genie waves his wand
and all of a sudden the room is flled with tens of thousands of quacking
ducks. They' re all over the place, making a terrible noise: Quack, quack,
quack! The bartender turns to the man and says, "Hey! What's the mat
ter with this genie? I asked for a million bucks and I get a million ducks.
Is he deaf or something? " The man looks at him and replies, " Well, do
you really think I asked for a twelve-inch pianist? "
Why are these stories fnny? Ad what do they have in common with
other j okes? Despite all their surface diversity, most j okes and fnny in
cidents have the following logical structure: Typically you lead the lis
tener along a garden path of expectation, slowly building up tension. At
the very end, you introduce an unexpected twist that entails a complete
reinterpretation of all the preceding data, and moreover, it's critical that
the new interpretation, though wholly unexpected, makes as much
"sense" of the entire set of facts as did the originally "expected" inter
pretation. In this regard, j okes have much in common with scientifc
creativity, with what Thomas Kuhn calls a "paradigm shif" in response
to a single "anomaly. " ( It's probably not coincidence that many of the
most creative scientists have a great sense of humor. ) Of course, the
anomaly in the j oke is the traditional punch line and the j oke is "fnny"
only if the listener gets the punch line by seeing in a flash of insight how
a completely new interpretation of the same set of facts can incorporate
the anomalous ending. The longer and more tortuous the garden path
T H E WOMA N WHO DI E D LAU G H I N G I 2 0 5
of expectation, the "fnnier" the punch line when fnally delivered.
Good comedians make use of this principle by taking their time to build
up the tension of the stor line, for nothing kills humor more surely than
a premature punch line.
But although the introduction of a sudden twist at the end is necessary
for the genesis of humor, it is certainly not sufcient. Suppose my plane
is about to land in San Diego and I fasten my seat belt and get ready
for touchdown. The pilot suddenly announces that the "bumps" that he
( and I ) had earlier dismissed as air turbulence are really due to engine
failure and that we need to empty fel before landing. A paradigm shif
has occurred in my mind, but this certainly does not make me laugh.
Rther, it makes me orient toward the anomaly and prepare for action
to cope with the anomaly. Or consider the time I was staying at some
friends' house in Iowa City. They were away and I was alone in unfamiliar
surroundings. It was late at night and j ust as I was about to doze of, I
heard a thump downstairs. "Probably the wind," I thought. Afer a few
minutes there was another thud, louder than the one before. Again I
"rationalized" it away and went back to sleep. Twenty minutes later I
heard an extremely loud, resounding "bang" and leapt out of bed. Wat
was happening? A burglar perhaps? Naturally, with my limbic system
activated, I "oriented, " grabbed a fashlight and ran down the stairs.
Nothing fnny so far. Then, suddenly I noticed a large fower vase in
pieces on the foor and a large tabby cat right next to it-the obvious
culprit! In contrast to the airplane incident, this time I started laughing
because I realized that the "anomaly" I had detected and the subsequent
paradigm shif were of trivial consequence. Al of the facts could now be
explained in terms of the cat theory rather than the ominous burglar
theory.
On the basis of this example, we can sharpen our defnition of humor
and laughter. Wen a person strolls along a garden path of expectation
and there is a sudden twist at the end that entails a complete reinterpre
tation of the same facts and the new interpretation has trivial rather than
terrifing implications, laughter ensues .
But why laughter? Wy this explosive, repetitive sound? Freud's view
that laughter discharges pent-up internal tension does not make much
sense without recourse to an elaborate and far-fetched hydraulic meta
phor. He argued that water building up in a system of pipes will fnd its
way out of the path of least resistance ( the way a safety valve opens when
too much pressure builds up in a system) , and laughter might provide a
similar safety valve to allow the escape of psychic energy ( whatever that
2 0 6 I P HA N T O MS I N T H E B RA I N
might mean) . This "explanation" really doesn't work for me; it belongs
to a class of explanations that Peter Medawar has called "analgesics" that
"dull the ache of incomprehension without removing the cause. "
To an ethologist, on the other hand, any stereotyped vocalization al
most always implies that the organism is trying to communicate some
thing to others in the social group. Now what might this be in the case
of laughter? I suggest that the main purpose of laughter might be to
allow the individual to alert others in the social group ( usually kin) that
the detected anomaly is trivial , nothing to worry about. The laughing
person in efect announces her discovery that there has been a false alarm;
that the rest of you chaps need not waste your precious energy and
resources responding to a spurious threat. 6 This also explains why laugh
ter is so notoriously contagious, for the value of any such signal would
be amplifed as it spread through the social group.
This "false alarm theory" of humor may also explain slapstick. You
watch a man-preferably one who is portly and self-important-walk
down the street when suddenly he slips on a banana peel and falls down.
If his head hit the pavement and his skull split open, you would not
laugh as you saw blood spill out; you would rush to his aid or to the
nearest telephone to call an ambulance. But if he got up casually, wiped
the remains of the fuit from his face and continued walking, you would
probably burst out laughing, tereby letting others standing nearby know
that they need not rush to his aid. Of course, when watching Laurel and
Hardy or Mr. Bean, we are more willing to tolerate "real" harm or injury
to the hapless victim because we are flly aware that it's only a movie.
Athough this model accounts for the evolutionary origin of laughter,
it by no means explains all the fnctions of humor among modern hu
mans. Once the mechanism was in place, however, it could easily be
exploited for other purposes. ( This is common in evolution. Feathers
evolved in birds originally to provide insulation but were later adapted
for flying. ) The ability to reinterpret events in the light of new infor
mation may have been refned through the generations to help people
playflly j uxtapose larger ideas or concepts-that is, to be creative. This
capacity for seeing familiar ideas from novel vantage points ( an essential
element of humor) could be an antidote to conserative thinking and a
catalyst to creativity. Laughter and humor may be a dress rehearsal for
creativity, and if so, perhaps j okes, puns and other forms of humor should
be introduced ver early into our elementary schools as part of the formal
curriculum?
Athough these suggestions may help explain the logical structure of
T H E WOMA N WHO DI E D LAU G H I N G I 2 0 7
humor, they do not explain why humor itself is sometimes used as a
psychological defense mechanism. Is it a coincidence, for example, that
a disproportionate number of j okes deal with potentially disturbing top
ics, such as death or sex? One possibility is that j okes are an attempt to
trivialize genuinely disturbing anomalies by pretending they are of no
consequence; you distract yourself from your anxiety by setting of your
own false alarm mechanism. Thus a trait that evolved to appease others
in a social group now becomes internalized to deal with truly stressfl
situations and may emerge as so-called nervous laughter. Thus even as
mysterious a phenomenon as "nerous laughter" begins to make sense
in the light of some of the evolutionary ideas discussed here.
The smile, too, may have similar evolutionary origins, as a "weaker"
form of laughter. Wen one of your ancestral primates encountered an
other individual coming toward him from a distance, he may have initially
bared his canines in a threatening grimace on the fair assumption that
most strangers are potential enemies. Upon recognizing the individual
as "friend" or "ki n, " however, he might abort the grimace halfay,
thereby producing a smile, which in turn may have evolved into a ritu
alized human greeting: "I know you pose no threat and I reciprocate. "8
Thus in my scheme, a smile is an aborted orienting response in the same
way that laughter is.
The ideas we have explored so far help explain the biological fnctions
and possible evolutionary origin of humor, laughter and smiling, but they
still leave open the question of what the underlying neural mechanisms
of laughter might be. Wat about Willy, who started giggling at his
mother's fneral , and Ruth, who literally died laughing? Their strange
behavior implies the existence of a laughter circuit found mainly in por
tions of the limbic system and its targets in the frontal lobes. Given the
well - known role of the limbic system in producing an orienting response
to a potenial threat or alarm, it is not altogether surprising, perhaps, that
it is also involved in the aborted orienting reaction in response to a false
alarm-laughter. Some parts of this circuit handle emotions-the feeling
of merriment that accompanies laughter-whereas other parts are in
volved in the physical act itself, but at present we do not know which
parts are doing what.
There is, however, another curious neurological disorder, called pain
asymbolia, which ofers additional hints about the neurological structures
underlying laughter. Patients with this condition do not register pain
2 0 8 I P HA N T O MS I N T H E B RA I N
when they are deliberately j abbed in the fnger with a sharp needle. In
stead of saying, "Ouch! " they say, "Doctor, I can feel the pain but it
doesn't hurt. " Apparently they do not experience the aversive emotional
impact of pain. And, mysteriously, I have noticed that many of them
actually start giggling, as if they were being tickled and not stabbed. For
instance, in a hospital in Madras, India, I recently examined a school
teacher who told me that a pinprick I administered as part of a routine
neurology workup felt incredibly fnny-although she couldn't explain
why.
I became interested in pain asymbolia mainly because it provides ad
ditional support for the evolutionary theory of laughter that I've pro
posed in this chapter. The syndrome is ofen seen when there is damage
to a structure called the insular cortex-buried in the fold between the
parietal and temporal lobes ( and closely linked to the structures that were
damaged in Willy and Ruth) . This structure receives sensory input, in
cluding pain from the skin and internal organs, and sends its output to
parts of the limbic system ( such as the cingulate gyrus) so that one begins
to experience the strong aversive reaction-the agony-of pain. Now
imagine what would happen if the damage were to disconnect the insular
cortex from the cingulate gyrus. One part of the person's brain ( the
insular cortex) tells him, "Here is something painfl , a potential threat,"
while another part ( the cingulate gyrus of the limbic system) says a frac
tion of a second later, "Oh, don't worry; this is no threat afer all . " Thus
the two key ingredients-threat followed by deflation-are present, and
the only way for the patient to resolve the paradox is to laugh, j ust as
my theory would predict.
The same line of reasoning may help explain why people laugh when
tickled. 9 You approach a child, hand stretched out menacingly. The child
wonders, "Will he hurt me or shake me or poke me? " But no, your
fngers make light, intermittent contact with her belly. Again, the rec
ipe-threat followed by defation-is present and the child laughs, as if
to inform other children, "He doesn't mean harm. He's only playing! "
This, by the way, may help children practice the knd of mental play
required for adult humor. In other words, what we call "sophisticated
cognitive" humor has the same logical form as tickling and therefore
piggybacks on the same neural circuits-the "threatening but harmless"
detector that involves the insular cortex, cingulate gyrus and other parts
of the limbic system. Such co- opting of mechanisms is the rule rather
than the exception in the evolution of mental and physical traits ( al -
T H E WOMA N WH O D I E D LAU G H I N G I 2 0 9
though in this case, the co- opting occurs for a related, higher-level fnc
tion rather than for a completely diferent fnction) .
These ideas have some bearing on a heated debate that has been going
on among evolutionary biologists in general and evolutionary psychol
ogists in particular during the last ten years. I get the impression that
there are two warring camps. One camp implies (with disclaimers) that
every one of our mental traits-or at least 99 percent of them-is spe
cifcally selected for by natural selection. The other camp, represented by
Stephen Jay Gould, calls members of the frst camp "ultra- Darinists"
and argues that other factors must be kept in mind. ( Some of the factors
pertain to the actual selection process itself and others to the raw material
that natural selection can act on. They complement rather than contra
dict the idea of natural selection. ) Every biologist I kow has strong views
on what these factors might be. Here are some of my favorite examples:
Wat you now obsere may be a bonus or usefl by-product of
something else that was selected for a completely diferent purpose.
For example, a nose evolved for smelling and warming and mois
tening air but can also be used for wearing spectacles. Hands
evolved for grasping branches but can now be used for counting as
well .
A trait may represent a frther refnement ( through natural selec
tion) of another trait that was originally selected for a completely
diferent purpose. Feathers evolved from reptilian scales to keep
birds warm but have since been co-opted and transformed into wing
feathers for flying; this is called preadaptation.
Natural selection can only select from what is available, and what is
available is ofen a very limited repertoire, constrained by the or
ganism's previous evolutionary history as well as certain develop
mental pathways that either are permanently closed or remain open.
I' d be very surprised if these three statements were not true to some
extent regarding the many mental traits that constitute human nature.
Indeed, there are many other principles of this sort ( including plain old
Lady Luck or contingency) that are not covered by the phrase "natural
selection. "1 0 Yet ultra- Darwinists steadfastly adhere to the view that al
most all traits, other than those obviously learned, are specifc products
of natural selection. For them, preadaptation, contingency and the like
play only a minor role in evolution; they are "exceptions that prove the
rule. " Moreover, they believe that you can in principle reverse engineer
2 1 0 I P HA N T O MS I N T H E B RA I N
various human mental traits by looking at environmental and social con
straints . ( "Reverse engineering" is the idea that you can best understand
how something works by askng what environmental challenge it evolved
for. Ad then, workng backward, you consider plausible solutions to
that challenge. It is an idea that is popular, not surprisingly, with engi
neers and computer programmers. ) A a biologist, I am inclined to go
with Gould; I believe that natural selecton is certainly the single most
important driving force of evolution, but I also believe that each case
needs to be examined individually. In other words, it is an empirical
question whether some mental or physical trait that you obsere in an
animal or person was selected for by natural selection. Furthermore, there
are dozens of ways to solve an environmental problem, and unless you
know the evolutionary history, taxonomy and paleontology of the animal
you are looking at, you cannot fgure out the exact route taken by a
particular trait ( like feathers, laughter or hearing) as it evolved into its
present form. This is technically referred to as the "traj ectory" taken by
the trait "through the ftness landscape. "
My favorite example of this phenomenon involves the three little
bones in our middle ear-the malleus, incus and stapes. Now used for
hearing, two of these bones ( the malleus and incus ) were originally part
of the lower jaw of our reptilian ancestors, who used them for chewing.
Reptiles needed fexible, multelement, multihinged j aws so they could
swallow giant prey, whereas mammals preferred a single strong bone ( the
dentary) for cracking nuts and chewing tough substances like grains. So
as reptiles evolved into mammals, two of the j awbones were co-opted
into the middle ear and used for amplifing sounds ( partly because early
mammals were nocturnal and relied largely on hearing for surival ) . This
is such an ad hoc, bizarre solution tat unless you know your comparative
anatomy well or discovered fossil intermediates, you never could have
deduced it from simply considering the fnctional needs of the organism.
Contrary to the ultra- Darwinist view, reverse engineering doesn't always
work in biology for the simple reason tat God is not an engineer; he' s
a hacker.
Wat has all this got to do with human traits like smiling? Everything.
If my argument concerning the smile is correct, then even though it
evolved through natural selection, not ever feature of a smile is adaptive
for its current demand. That is, te smile takes the particular form that
it does not because of natural selection alone but because it evolved from
the ver opposite-te threat grimace! There is no way you could deduce
this through reverse engineering ( or fgure out its particular trajectory
T H E WOMA N WH O D I E D LAU G H I N G I 211
through the ftness landscape) unless you also know about the existence
of canine teeth, knew that nonhuman primates bare their canines as a
mock threat or knew that mock threats in turn evolved from real threat
displays. ( Big canines are genuinely dangerous. )
I fnd great irony in the fact that every time someone smiles at you
she is in fact producing a half threat by fashing her canines. Wen Dar
win published On the Oriin of Species he delicately hinted in his last
chapter that we too may have evolved fom apelike ancestors. The En
glish statesman Benj amin Disraeli was outraged by this and at a meeting
held in Oxford he asked a famous rhetorical question: "Is man a beast
or an angel ? " To answer this, he need only have looked at his wife' s
canines as she smiled at him, and he'd have realized that in this simple
universal human gesture of friendliness lies concealed a grim reminder
of our savage past.
A Darin himself concluded in Te Descent ofMan:
But we are not here concerned with hopes and fears, only with truth. We
must acknowledge, as it seems to me, that man with all his noble qualities,
with sympathy which he feels for the most debased, with benevolence which
extends not only to other men but to the humblest creature, with his God
like intellect which has penetrated into the movements and constitution of the
solar system-with all these exalted powers-man still bears in his bodily frame
the indelible stamp of his lowly origin.
CHAPTER 11
"You forgot to Del iver
the Twin"
It is an old maxim ofmine that when you have excluded
the impossible, whatever remains, however improbable,
must be the truth.
-SHERLOCK HOLMES
Mary Knight, age thirty-two, bright red hair pinned neatly in a bun,
walked into Dr. Monroe's ofce, sat down and grinned. She was nine
months pregnant and so far everything seemed to be going well . This
was a long- awaited, much desired pregnancy, but it was also her frst visit
to Dr. Monroe. The year was 1932 and money was tight. Mary's hus
band did not have steady work, and so Mary had only talked to a midwife
down the street, on an informal basis .
But today was diferent. Mary had felt the baby kicking for some time
and suspected that labor was about to begin. She wanted Dr. Monroe
to check her over, to make sure that the baby was in the right position
to coach her through this last stage of pregnancy. It was time to prepare
for birth.
Dr. Monroe examined the young woman. Her abdomen was vastly
2 1 2
"Y o u F o RG O T T O DE L I V E R T H E Twi N " 1 2 1 3
enlarged and low, suggesting that the fetus had dropped. Her breasts
were swollen, the nipples mottled.
But something was not right. The stethoscope was not picking up a
clear fetal heartbeat. Maybe the baby was turned in a fnny way, or
perhaps it was in trouble, but, no, that wasn't it. Mary Kight's navel
was all wrong. One sure sign of pregnancy is an everted or pushed-out
belly button. Mary's was inverted, in the normal fashion. She had an
"innie" rather than an "outie. "
Dr. Monroe whistled sofly. He' d learned about pseudocyesis or false
pregnancy in medical school . Some women who desperately want to be
pregnant-and occasionally some who deeply dread pregnancy-develop
all the signs and symptoms of true pregnancy. Their abdomens swell to
enormous proportions, aided by a sway back posture and the mysterious
deposition of abdominal fat. Their nipples become pigmented, as hap
pens in pregnant women. They stop menstruating, lactate, have morning
sickness and sense fetal movements. Everything seems normal except for
one thing: There is no baby.
Dr. Monroe knew that Mary Kight was sufering from pseudocyesis,
but how would he tell her? How could he explain that it was all in her
head, that the dramatic change in her body was caused by a delusion?
"Mary, " he said sofly, "the baby is coming now. It will be born this
afernoon. I' m going to give you ether so that you won't be in pain.
But labor has begun and we can proceed. "
Mar was elated and submitted to the anesthesia. Ether was given
routinely during labor and she'd expected it.
A little later, as Mary woke up, Dr. Monroe took her hand and stroked
it gently. He gave her a few minutes to compose herself and then said,
"Mar, I'm so sorry to have to tell you this. It's terrible news. The baby
was stillborn. I did everything I could but it was no use. I' m so, so
sorry. "
Mary broke down crying, but she accepted Dr. Monroe's news . Right
there, on the table, her abdomen began to subside. The baby was gone
and she was devastated. She'd have to go home and tell her husband and
mother. What a terrible disappointment this would be for the entire
family.
A week passed. And then, to Dr. Monroe's astonishment, Mary burst
into his ofce with her belly protruding, as huge as ever. "Doctor! " she
shouted. "I've come back! You forgot to deliver the twin! I can feel him
kicking in there! "1
2 1 4 I P HA N T O MS I N T H E B RA I N
About three years ago, I came across Mary Kight's story in a crum
bling 1930s medical monograph. The report was by Dr. Silas Weir
Mtchell, the same Philadelphia physician who coined the term "phan
tom limb. " Not surprisingly, he referred to Mary's condition as phantom
pregnancy and coined the term "pseudocyesis" ( false swelling) . Had the
story come from almost any other person I might have dismissed it as
rubbish, but Weir Mitchell was an astute clinical obserer, and over the
years I have learned to pay carefl attention to his writings. I was struck
especially by the relevance of his report to contemporary debates on how
the mind infuences the body, and vice versa.
Because I was born and raised in India, people ofen ask me whether
I believe there are connections between the mind and body that Western
cultures don't comprehend. How do yogis exert control over their blood
pressure, heart rate and respiration? Is it true that the most skilled among
them can reverse their peristalsis ( leaving aside the question of why any
one would ever want to) ? Does illness result from chronic stress? Will
meditation make you live longer?
If you' d asked me those questions fve years ago, I 'd have conceded
grudgingly, "Sure, obviously the mind can afect the body. A cheerfl
attitude might help accelerate your recovery from an illness by enhancing
your immune system. There' s also the so- called placebo efect we don't
understand completely-merely believing in a therapy seems to improve
one' s well - being, if not actual physical health. "
But as t o notions of the mind curing the incurable, I've tended to be
deeply skeptical . It's not j ust my training in Western medicine; I also fnd
many of the empirical claims unconvincing. So what if breast cancer pa
tients with more positive attitudes live, on average, two months longer
than patients who deny their illness? To be sure, two months is better
than nothing, but compared to the efects of an antibiotic like penicillin
in improving the survival rates of pneumonia patients, this is hardly any
thing to boast about. (I know it's not fashionable to praise antibiotics
these days, but one only has to see a single child saved from pneumonia
or diphtheria by a few shots of penicillin to be convinced that antibiotics
really are wonder drugs. )
But as a student I was also taught that a certain proportion of incur
able cancers-a very tiny fraction, to be sure-disappear mysteriously
without any treatment and that "many a patient with a tumor pro
nounced malignant has outlived his physician. " I still remember my skep-
"Yo u F o RG O T T O DE L I V E R T H E Twr N " 1 2 1 5
ticism when my professor explained to me that such occurrences were
known as "spontaneous remissions . " For how can any phenomenon in
science, which is all about cause and efect, occur spontaneous!Jespe
cially something as dramatic as the dissolution of a malignant cancer?
When I raised this obj ection, I was reminded of the basic fact of "bi
ological variability"-that cumulative efects of small individual difer
ences can account for myriad, unexpected responses. But saying that
tumor regression arises from variability is not saying a hell of a lot; it's
hardly an explanation. Even if it is due to variability, surely we must ask
the question, What is the critical variable that causes the regression in
any particular patient? For if we could solve that, then we would have
ipso facto discovered a cure for cancer! Of course, it may turn out that
the remission is the result of a fortuitous combination of several variables,
but that doesn't make the problem insoluble; it merely makes it more
difcult. So why isn't much more attention being paid by the cancer
establishment to these very cases, instead of regarding them as curiosities?
Couldn't one study these rare surivors in detail, looking for clues that
confer resistance to virulent agents or reapply the brakes to renegade
tumor suppressor genes? This strategy has been applied successflly to
acquired immunodefciency syndrome (ADS) research. The fnding that
some long-term surivors carry a gene mutation that prevents the virus
from invading their immune cells is now being exploited in the clinic.
But now let us return to mind- body medicine. The obseration that
some cancers occasionally regress spontaneously doesn't necessarily prove
that hypnosis or a positive attitude can induce such remissions. We must
not commit the blunder of lumping all mysterious phenomena together
simply because they are mysterious, for that may be all they have in
common. Wat I need to be convinced is a single proven example of
one's mind's directly infuencing one' s bodily processes, an example that
is clear-cut and repeatable.
Wen I stumbled across the case of Mar Knight, it occurred to me
that pseudocyesis or phantom pregnancy might be an example of the
kind of connection I was looking for. If the human mind can conjure
up something as complex as pregnancy, what else can the brain do to or
for the body? What are the limits to mind- body interactions and what
pathways mediate these strange phenomena?
Remarkably, the delusion of phantom pregnancy is associated with a
whole gamut of physiological changes associated with pregnancy-ces
sation of menstruation, breast enlargement, nipple pigmentation, pica
( the desire for strange foods ) , morning sickness and most remarkable of
2 1 6 I P HA N T O MS I N T H E B RA I N
all-progressive abdominal enlargement and "quickening" culminating
in actual labor pains! Sometimes, but not always, there is enlargement of
the uterus and cerix, but the radiological signs are negative. A a medical
student I learned that even experienced obstetricians can be fooled2 by
the clinical picture unless they are carefl and that in the past many a C
section was performed on a patient with pseudocyesis. A Dr. Monroe
detected in Mary, the telltale diagnostic sign lies in the belly button.
Modern physicians who are familiar with pseudocyesis assume it results
from a pituitary or ovarian tumor that causes hormones to be released,
mimicking the signs of pregnancy. Tiny, clinically undetectable prolactin
secreting tumors ( adenomas ) of the pituitary could suppress ovulation
and menstruation and lead to the other symptoms. But if that were true,
why is the condition sometimes reversible? What kind of tumor could
explain what happened to Mary Knight? She goes into "labor" and her
abdomen shrinks. Then her abdomen gets big again because of the
"twin. " If a tumor could do all that, it would present an even greater
myster than pseudocyesis.
So what causes pseudocyesis? Cultural factors undoubtedly play a ma
jor role3 and may explain the decline of pseudocyesis from an incidence
of one in two hundred in the late 1 700s to about one in ten thousand
pregnancies today. In the past, many women felt extreme social pressure
to have a baby, and when they felt they were pregnant, there was no
ultrasound to disprove the diagnosis. No one could say with certainty,
"Look here, there's no fetus. " Conversely, pregnant women today sub
mit to round afer round of evaluations leaving little room for ambiguity;
confrontng the patient with physical evidence of an ultrasound is usually
sufcient to dispel the delusion and associated physical changes.
The infuence of culture on the incidence of pseudocyesis cannot be
denied, but what causes the actual physical changes? According to the
few studies carried out on this curious afiction of mind and body, the
abdominal swelling itself is usually caused by a combination of fve fac
tors: an accumulation of intestinal gas, a lowering of the diaphragm, a
pushing forard of the pelvic portion of the spine, a dramatic growth of
the greater omentum-a pendulous apron of fat that hangs loose in front
of the intestines-and in rare cases an actual uterine enlargement. The
hypothalamus-a part of the brain that regulates endocrine secretions
may also go awry, producing profound hormonal shifs that mimic nearly
all the signs of pregnancy. Furthermore, it's a two-way street: The body's
efects on the mind are j ust as profound as those of the mind on the
"Y o u F o RG O T T O DE L I V E R T H E Twi N " 1 2 1 7
body, giving rise to complex feedback loops involved in generating and
maintaining false pregnancy. For instance, the abdominal distension pro
duced by gas and the woman's "pregnant body posture" might be ex
plained, in part, by classic operant conditioning. Wen Mary, who wants
to be pregnant, sees her abdomen enlarge and feels her diaphragm fall,
she learns unconsciously that the lower it falls, the more pregnant she
looks. Likewise, a combination of air swallowing ( aerophagia) and au
tonomic constriction of the gastrointestinal sphincters that would in
crease gas retention could also probably be learned unconsciously. In this
manner, Mary's "baby" and its "missing twin" are literally conj ured out
of thin air through a process of unconscious learning.
So much for the abdominal swelling. But what about the breast, nipple
and other changes? The most parsimonious explanation for the whole
spectrum of clinical signs you see in pseudocyesis would be that the
intense longing for a child and associated depression might reduce levels
of dopamine and norepinephrine-the "joy transmitters" in the brain.
This in turn could reduce the production of both follicle- stimulating
hormone ( FSH) , which causes ovulation, and a substance called
prolactin-inhibition factor. 4 Low levels of these hormones would lead to
a cessation of ovulation and menstruation and an elevation of the level
of prolactin ( the maternal hormone) , which causes breast enlargement
and lactation, nipple tingling and maternal behavior ( although this has
yet to be proved in humans ) , along with an increased production of
estrogen and progesterone by the ovaries, contributing to the overall
impression of pregnancy. This notion is consistent with the well-known
clinical obseration that severe depression can stop menstruation-an ev
olutionary strategy for avoiding a waste of precious resources on ovula
tion and pregnancy when you are disabled and depressed.
But the cessation of menstruation during depression i s common,
whereas pseudocyesis is very rare. Perhaps there' s something special
about the depression of being childless in a child-obsessed culture. If the
syndrome occurs only when the depression is associated with fantasies
about pregnancy, it raises a fascinating question: How does a highly spe
cifc wish or delusion originating in the neocortex get translated by the
hypothalamus to induce FSH reduction and prolactin elevation-if that
is indeed the cause? And even more puzzling, how do you explain the
observation that some patients with pseudocyesis do not have an elevated
prolactin level or that in many patients labor pains begin at exactly nine
months? What triggers the labor contractions if there is no growing fetus?
2 1 8 I P HA N T O MS I N T H E B RA I N
Watever the ultimate answer to these questions, pseudocyesis provides
a valuable opportunity for exploring the mysterious no-man's-land be
tween mind and body.
False pregnancy and labor in women are surprising enough, but there
are even a few recorded instances of pseudocyesis in men! The whole
gamut of changes-including abdominal swelling, lactation, craving for
strange foods, nausea, even labor pains-can occur as an isolated syn
drome in some men. But more commonly it is seen in men who em
pathize deeply with their pregnant spouse, producing the so-called
sympathetic pregnancy or couvade syndrome. I have ofen wondered
whether the man's emotional empathy with the pregnant woman ( or
perhaps pheromones from her) somehow releases prolactin-a key preg
nancy hormone-in her husband's brain, causing some of these changes
to emerge. ( This hypothesis is not as outlandish as it seems; male tamarin
marmosets develop an elevated prolactin level when in close proximity
to nursing mothers, and this may encourage paternal or flial afection
and reduce infanticide. ) I am tempted to interiew men participating in
Lamaze classes and to measure prolactin levels in those who experience
some of these couvadelike signs.
Pseudocyesis is dramatic. But is it an isolated, exceptional example of
mind-body medicine? I think not. Other stories come to mind, including
one I frst heard in medical school . A friend said, "Did you know that
according to Lewis Thomas you can hypnotize someone and eliminate
their warts? "
"Rubbish, " I scofed.
"No, it' s true, " she said. "There are documented cases. 5 You get
hypnotized and the warts disappear in a few days or sometimes over
night. "
Now on the face of i t this sounds very silly, but i f it's true, i t would
have far- reaching implications for modern science. A wart is essentially a
tumor ( a benign cancer) produced by the papilloma virus. If that can be
eliminated by hypnotic suggestion, why not cancer of the cerix, which
is also produced by the papilloma virus ( albeit a diferent strain) ? I am
not claiming that this will work-perhaps nerve pathways infuenced by
hypnosis reach the skn but not the lining of the cerix-but unless we
do the relevant experiment, we will never know.
Assuming, for the sake of argument, that warts can be eliminated by
hypnosis, the question arises, How can a person simply "think away" a
"Yo u F o RG O T T O DE L I V E R T H E Twi N " 1 2 1 9
tumor? There are at least two possibilities. One involves the autonomic
nerous system-the pathways of neres that help control blood pressure,
sweating, heart rate, urine output, erections and other physiological phe
nomena not under direct control of conscious thought. These neres
form specialized circuits that serice distinct fnctions in various body
segments . Thus some nerves control hair standing on end, others cause
sweating and some generate the local constriction of blood vessels. Is it
possible that the mind, acting through the autonomic nervous system,
could literally asphyxiate the wart by constricting blood vessels in its
immediate vicinity, making it shrivel up and wither away? This explana
tion implies an unexpected degree of precise control by the autonomic
nerous system and also implies that the hypnotic suggestion can be
"understood" by the autonomic nerous system and transferred to the
region of the wart.
The second possibility is that the hypnotic suggestion somehow kick
starts the immune system, thereby eliminating the virus. But this would
not explain at least one recorded case involving a hypnotized person
whose warts vanished on just one side of his body. Wy or how the
immune system could selectively eliminate warts on one side over another
is a mystery that invites frther fights of speculation.
A more common example of mind- body interaction involves the in
terplay between the immune system and perceptual cues from the world
around us. Over three decades ago, medical students were ofen told that
an asthmatic attack could be provoked not only by inhaling pollen from
a rose but sometimes by merely seeing a rose, even a plastic rose, prompt
ing a so-called conditioned allergic response. In other words, exposure
to a real rose and pollen sets up a "learned" association in the brain
between the mere visual appearance of a rose and bronchial constriction.
How exactly does this conditioning work? How does the message get
from the brain's visual areas all the way down to the mast cells lining the
bronchi of the lungs? Wat are the actual pathways involved? Despite
three decades of mind- body medicine, we still have no clear answers.
Wen I was a medical student in the late 1960s, I asked a visiting
professor of physiology from Oxford about this conditioning process and
whether the conditioned association could be put to clinical use. "If it's
possible to provoke an asthmatic attack through conditioning merely by
showing a plastic rose to a patient, then theoretically it ought to be
possible to abort or neutralize te attack through conditioning as well.
2 2 0 I P H A N T O MS I N T H E B RA I N
For example, say you sufer from asthma and I give you a bronchodilator
such as norepinephrine ( or perhaps an antihistamine or a steroid) every
time I show you a plastic sunfower. You might begin associating the
sunflower image with relief from asthma. Afer some time you could
simply carry around a sunfower in your pocket and pull it out to look
at when you felt an attack coming on. "
At the time, this professor (who later became my mentor) thought
this was an ingenious but silly idea, and we both had a good laugh. It
seemed far- fetched and whimsical . Thus chastised, I kept my thoughts
to myself, wondering privately whether you really could condition an
immune response and, if so, how selective this conditioning process
could be. For instance, we know that if you inject a person with dena
tured tetanus bacilli he will soon develop immunity to tetanus, but to
keep the immunity "alive" the person needs booster shots every few
years. But what would happen if you rang a bell or fashed a green light
every time these booster shots were administered? Would the brain learn
the association? Could you eventually dispense with the boosters and
simply ring a bell and fash a light to stimulate the selective proliferation
of immunologically competent cells, thereby reviving a person's immu
nity to tetanus? The implications of such a fnding for clinical medicine
would be enormous.
To this day I curse myself for not trying this experiment. The ideas
remained tucked away in my mind until a few years ago, when, as hap
pens so ofen in science, someone made an accidental discovery, proving
that I had missed the boat. Dr. Rlph Ader of McMaster University was
exploring food aversion in mice. To induce nausea in the animals, he
gave them a nausea-inducing drug, cyclophosphamide, along with sac
charin, wondering whether they would display signs of nausea the next
time he gave them the saccharin alone. It worked. A expected, the an
imals did show food aversion, in this case an aversion to saccharin. But
surprisingly, the mice also fell seriously ill , developing all sorts of infec
tions. It is known that the drug cyclophosphamide, in addition to pro
ducing nausea, profoundly suppresses the immune system, but why
should saccharin alone have this efect? Ader reasoned correctly that the
mere pairing of the innocuous saccharin with the immunosuppressive
drug caused the mouse immune system to "learn" the association. Once
this association is established, every time the mouse encounters the sugar
substitute, its immune system will nose- dive, making it vulnerable to
infections. Here again is a powerfl example of mind afecting body, one
that is hailed as a landmark in the history of medicine and immunology. 6
"Y o u F o RG O T T O DE L I V E R T H E Twi N " 1 2 2 1
I mention these examples for three reasons. First, don't listen to your
professors-even if they are from Oxford ( or as my colleague Semir Zek
would say, especialy if they are from Oxford) . Second, they illustrate our
ignorance and illuminate the need for conducting experiments on topics
that most people have ignored for no obvious reason; patients who man
ifest odd clinical phenomena are only one example. Third, perhaps it's
time to recognize that the division between mind and body may be no
more than a pedagogic device for instructing medical students-and not
a usefl construct for understanding human health, disease and behavior.
Contrary to what many of my colleagues believe, the message preached
by physicians like Deepak Chopra and Andrew Weil is not j ust New Age
psychobabble. It contains important insights into the human organism
ones that desere serious scientifc scrutiny.
People have become increasingly impatient with Western medicine's
sterility and lack of compassion, and this would explain the current re
surgence of "alternative medicine. " But unfortunately, even though the
remedies touted by New Age gurus have a ring of plausibility, they are
rarely subjected to rigorous tests? We have no idea which ones ( if any)
work and which ones do not, although even the hardened skeptic would
agree that there is probably something interesting going on. If we are to
make any headway, we need to test these claims careflly and explore
the brain mechanisms that underlie such efects. The general principle of
immune conditioning has been clearly established, but can you pair dif
ferent sensory stimuli with diferent types of immune responses ( for ex
ample, a bell with a response to typhoid and a whistle to cholera) , or is
the phenomenon more difse-involving only a general boosting of all
your immune fnctions? Does the conditioning afect the immunity itself
or only the subsequent infammatory response to the provokng agent?
Does hypnosis tap into the same pathway as placebos? 8 Until we have
clear answers to these questions, Western medicine and alternative med
icine will always remain parallel enterprises with no points of contact
between them.
So with all this evidence staring them in the face, why do practitioners
of Western medicine continue to ignore the many striking examples of
direct links between mind and body?
To understand why, it helps to have a feel for how scientifc knowledge
progresses. Most of the day-to-day progress of science depends on simply
adding another brick to the great edifce-a rather humdrum activity that
2 2 2 I P HA N T O MS I N T H E B RA I N
the late historian Thomas Kuhn called "normal science. " This corpus of
knowledge, incorporating a number of widely accepted beliefs, is, in each
instance, called a "paradigm. " Year afer year new obserations come
along and are assimilated into an existing standard model . Most scientists
are bricklayers, not architects; they are happy simply adding another
stone to the cathedral .
But sometimes the new obseration simply doesn't ft. It is an "anom
aly, " inconsistent with the existing structure. The scientist can then do
one of three things. First, he can ignore the anomaly, sweeping it under
the carpet-a form of psychological "denial " that is surprisingly common
even among eminent researchers.
Second, scientists can make minor adj ustments to the paradigm, trying
to ft the anomaly into their worldview, and this would still be a form of
normal science. Or they can generate ad hoc auxiliary hypotheses that
sprout like so many branches from a single tree. But soon these branches
become so thick and numerous that they threaten to topple the tree itself.
Finally, they can tear down the edifce and create a completely new
one that bears very little resemblance to the original . This is what Kuhn
called a "paradigm shif" or scientifc revolution.
Now, there are many examples in the histor of science of anomalies
that were originally ignored as being trivial or even fraudulent but later
turned out to be of fndamental importance. This is because the vast
majority of scientists are conserative by temperament and when a new
fact emerges that threatens to topple the great edifce, the initial reaction
is to ignore or deny it. This is not as silly as it seems. Since most anom
alies turn out to be false alarms, it is not a bad strategy to play it safe
and ignore them. If we tried to accommodate every report of alien ab
duction or spoon bending into our framework, science would not have
evolved into the immensely successfl and internally consistent body of
beliefs that it is today. Skepticism is as much a vital part of the whole
enterprise as the revolutions that make newspaper headlines.
Consider the periodic table of elements, for example. Wen Mende
leyev arranged elements sequentially according to their atomic weights
to create the periodic table, he found that some elements didn't quite
"ft" -their atomic weights seemed wrong. But instead of discarding his
model , he chose to ignore the anomalous weights, concluding instead
that perhaps they had been measured incorrectly to begin with. And sure
enough, it was later discovered that the accepted atomic weights were
wrong because the presence of certain isotopes distorted the measure
ments . There is much truth to Sir Athur Eddington' s famously para-
"Yo u F o RG O T T O DE L I V E R T H E Twr N " 1 2 2 3
doxical remark "Don' t believe the results of experiments until they're
confrmed by theory. "
But we must not ignore every anomaly, since some of them have the
potential for driving paradigm shifs. Our wisdom lies in being able to
tell which anomaly is trivial and which one is a potential gold mine.
Unfortunately, there' s no simple formula for distinguishing trivia from
gold, but as a rule of thumb, if an odd, inconsistent observation has been
lying around for ages and has not been empiricaly confrmed despite
repeated honest attempts, then it is probably a trivial one. (I regard te
lepathy and repeated Elvis sightings as belonging to this category. ) On
the other hand, if the obseration in question has resisted several at
tempts at disproof and is regarded as an oddity solely because it resists
explanation in terms of our current conceptual scheme, then you are
probably looking at a genuine anomaly.
One famous example is continental drif. Around the turn of this cen
tury ( 191 2) , the German meteorologist Afed Wegener noticed that the
east coast of South America and the west coast of Mrica "ft" neatly
together like the pieces of a giant jigsaw puzzle. He also noticed that
fossils of a small freshwater reptile "mesosaurus" were found in only two
parts of the earth-in Brazil and in West Mrica. How could a freshwater
lizard swim across the Atlantic, he wondered? Is it conceivable that in
the distant past these two continents were in fact parts of a single large
landmass that had subsequently split and drifed apart? Obsessed with
this idea, he sought additional evidence and found it in the form of
dinosaur fossils scattered in identical rock strata, again in the west coast
of Mrica and the east coast of Brazil . This was compelling evidence in
deed, but surprisingly it was rej ected by the entire geological establish
ment, who argued that the dinosaurs must have walked across an ancient
and now submerged land bridge connecting the two continents. A re
cently as 1974, at St. John's College in Cambridge, England, a professor
of geology shook his head when I mentioned Wegener. "A lot of rot, "
he said with exasperation i n his voice.
Yet we now know that Wegener was right. His idea was rej ected
simply because there was no mechanism that people could conceive of
that would cause whole continents to drif. If there' s one thing we all
regard as axiomatic, it is the stability of terra frma. But once plate tec
tonics-the study of rigid plates moving about on a hot gooey mantle
below-was discovered, Wegener's idea became credible and won
universal acceptance.
The moral of this tale is that you should not rej ect an idea as out-
2 2 4 I P HA N T O MS I N T H E B RA I N
landish simply because you can't think of a mechanism that explains it.
And this argument is valid whether you are talking about continents,
heredity, warts or pseudocyesis. Afer all , Darin's theory of evolution
was proposed and widely accepted long before the mechanisms of
heredity were clearly understood.
A second example of a genuine anomaly is multiple personality dis
order or MPD, which in my view may turn out to be j ust as important
for medicine as continental drif was for geology. To this day MPD con
tinues to be ignored by the medical community even though it provides
a valuable testing ground for the claims of mind- body medicine. In this
syndrome-immortalized by Robert Louis Stevenson in Dr. Jekyl and
Mr. Hyde-a person can assume two or more distinct personalities, each
of which is completely unaware, or only dimly aware, of the others.
Again, there have been occasional reports in the clinical literature that
one personality can be diabetic while the other is not, or that various
vital signs and hormone profles can be diferent in the two personalities.
There is even a claim that one personality can be allergic to a substance
while the other is not and that one might be myopic-or nearsighted
whereas the other has 20/20 vision. 9
MPD defes common sense. How can two personalities dwell in one
body? In Chapter 7, we learned that the mind is constantly struggling
to create a coherent belief system from a multiplicity of life experiences.
Wen there are minor discrepancies, you usually readjust your beliefs or
engage in the kinds of denials and rationalizations that Sigmund Freud
talked about. But consider what might happen if you held two sets of
beliefs-each internally consistent and rational-but these two sets were
completely in confict with one another? The best solution might be to
balkanize the beliefs, to wall them of from each other by creating two
personalities.
There is of course an element of this "syndrome" in all of us. We talk
about whore/madonna fantasies and say things like "I was of two
minds, " "I' m not feeling myself today" or "He' s a diferent person when
you're around. " But in some rare instances, it's possible that this schism
becomes literal so that you end up with two "separate minds. " Assume
that one set of beliefs says, "I am Sue, the sexy woman who lives on 1 23
Elm Street i n Boston, goes to bars at night to pick up studs, drinks
straight shots of Wild Turkey and has never bothered to get an ADS
test . " Another says, "I am Peggy, the bored housewife who lives on 1 23
Elm Street i n Boston, watches T at night, drinks nothing stronger than
herbal tea and goes to the doctor for every minor ailment. " These two
" Y o u F o RG O T T O D E L I V E R T H E Twi N " 1 2 2 5
stories are so diferent that they obviously refer to two diferent people.
But Peggy Sue has a problem: She is both of these people. She occupies
one body, indeed one brain! Perhaps the only way for her to avoid in
ternal civil war is to "split" her beliefs into two clusters, like soap bub
bles, resulting in the strange phenomenon of multiple personalities.
According to many psychiatrists, some cases of MPD are a conse
quence of childhood sexual or physical abuse. The child, growing up,
fnds the abuse so emotionally intolerable that she gradually walls it of
into Sue's world, not Peggy' s. What is truly remarkable, though, is that
to keep the illusion going, she actually invests each personality with dif
ferent voices, intonations, motivations, mannerisms and even diferent
immune systems-almost two bodies, one is tempted to say. Perhaps she
needs such elaborate devices to keep these minds separate and avoid the
ever-present danger of having them coalesce and create unbearable in
ternal strife.
I would like t o carry out experiments on people like Peggy Sue but
have thus far been thwarted by the lack of what I would call a clear-cut
case of MPD. When I telephone friends in psychiatry, asking for names
of patients, they tell me that they have seen such patients but most of
them have several personalities rather than j ust two. One apparently had
nineteen "alters" inside him. Claims of this sort have made me deeply
suspicious of the whole phenomenon. Given limited time and resources,
a scientist always has to strike a balance between wasting time on tenuous
and unrepeatable "efects" ( such as cold fsion, poly-water or Krlian
photography) and being open-minded (keeping in mind the lessons from
continental drif or asteroid impacts ) . Perhaps the best strategy is to focus
only on claims that are relatively easy to prove or disprove.
If I ever locate an MPD patient with j ust two personalities, I intend
to eliminate doubt by sending the person two bills. If he pays both, I'll
kow he's for real . If he doesn' t, I 'll know he's a fake. In either case I
can' t lose.
On a more serious note, it would be interesting to carry out systematic
studies on immune fnction when the patient is in the two diferent
states by measuring specifc aspects of the immune response ( such as
cytokne production by lymphocytes and monocytes and interleukin pro
duction by T cells provoked by mitogens-factors that stimulate cell
division) . Such experiments may seem tedious and esoteric, but only by
doing them can we achieve the right blend of East and West and create
a new revolution in medicine. Most of my professors scofed at ancient
"touchy-feely" Hindu practices such as Ayurvedic medicine, Tantra and
2 2 6 I P HA N T O MS I N T H E B RA I N
meditation. Yet ironically, some of the most potent drugs we now use
can trace their ancestry to ancient folk remedies such as willow bark
( aspirin) , digitalis and reserpine. Indeed, it has been estimated that over
30 percent of drugs used in Western medicine are derived from plant
products. ( If you think of molds-antibiotics-as "herbs, " the percent
age is even higher. In ancient Chinese medicine, mold was ofen rubbed
into wounds. )
The moral of all this is not that we should have blind faith in the
"wisdom of the East" but that there are sure to be many nuggets of
insight in these ancient practices. However, unless we conduct systematic
"Wester-style" experiments, we'll never kow which ones really work
( hypnosis and meditation) and which ones don't ( crystal healing) . Several
laboratories throughout the world are poised to launch such experiments,
and the frst half of the next century will, in my view, be remembered as
a golden age of neurology and mind- body medicine. It will be a time of
great euphoria and celebration for novice researchers entering the feld.
CHAPTER 12
Do Martians See Red?
Al ofmodern philosophy consists ofunlocking, exhuming
and recanting what has been said before.
-V.S. RCHANDRAN
Wy is thought, being a secretion ofthe brain, more
wonderul than gravit, a propert ofmatter?
-CHARLES DARWIN
In the frst half of the next century, science will confront its greatest
challenge in trying to answer a question that has been steeped in mys
ticism and metaphysics for millennia: Wat is the nature of the self? A
someone who was born in India and raised in the Hindu tradition, I was
taught that the concept of the self-the "I" within me that is aloof from
the universe and engages in a lof inspection of the world around me-is
an illusion, a veil called maya. The search for enlightenment, I was told,
consists of lifing this veil and realizing that you are really "One with the
cosmos. " Ironically, afer extensive training in Western medicine and
more than ffeen years of research on neurological patients and visual
illusions, I have come to realize that there is much truth to this view
that the notion of a single unifed self "inhabiting" the brain may indeed
be an illusion. Everthing I have learned from the intensive study of both
normal people and patients who have sustained damage to various parts
2 2 7
2 2 8 I P H A N T O MS I N T H E B RA I N
of their brains points to an unsettling notion: that you create your own
"reality" from mere fragments of information, that what you "see" is a
reliable-but not always accurate-representation of what exists in the
world, that you are completely unaware of the vast majority of events
going on in your brain. Indeed, most of your actions are carried out by
a host of unconscious zombies who exist in peacefl harmony along with
you ( the "person") inside your body! I hope that the stories you have
heard so far have helped convince you that the problem of self-far from
being a metaphysical riddle-is now ripe for scientifc inquiry.
Nevertheless, many people fnd it disturbing tat all the richness of
our mental life-all our thoughts, feelings, emotions, even what we re
gard as our intimate selves-arises entrely from the activity oflittle wisps
of protoplasm in the brain. How is this possible? How could something
as deeply mysterious as consciousness emerge from a chunk of meat in
side the skull? The problem of mind and matter, substance and spirit,
illusion and reality, has been a major preoccupation of bot Eastern and
Western philosophy for millennia, but very little of lastng value has
emerged. As the British psychologist Stuart Sutherland has said, "Con
sciousness is a fascinating but elusive phenomenon: it is impossible to
specif what it is, what it does, or why it evolved. Nothing worth reading
has been written on it. "
I won't pretend to have solved these mysteries/ but I do think there's
a new way to study consciousness by treatng it not as a philosophical,
logical or conceptual issue, but rather as an empirical problem.
Except for a few eccentrics ( called panpsychists ) who believe every
thing in the universe is conscious, including things like anthills, thermo
stats, and Formica tabletops, most people now agree that consciousness
arises in brains and not in spleens, livers, pancreases or any other organ.
This is already a good start. But I will narrow the scope of inquiry even
frther and suggest that consciousness arises not from the whole brain
but rather from certain specialized brain circuits that carry out a partcular
style of computation. To illustrate the nature of tese circuits and the
special computations they perform, I 'll draw from the many examples in
perceptual psychology and neurology that we have already considered in
this book. These examples will show that the circuitry that embodies the
vivid subjective quality of consciousness resides mainly in parts of the
temporal lobes ( such as the amygdala, septum, hypothalamus and insular
cortex) and a single projection zone in the frontal lobes-the cingulate
gyrus. And the activity of these structures must flfll three important
criteria, which I call (with apologies to Isaac Newton, who described the
D o MART I A N S S E E RE D 1 I 2 2 9
three basic laws of physics ) the "three laws of qualia" ( "qualia" simply
means the raw feel of sensations such as the subjective quality of "pain"
or "red" or "gnocchi with trufes") . My goal in identifing these three
laws and the specialized structures embodying them is to stimulate fr
ther inquiry into the biological origin of consciousness.
The central mystery of the cosmos, as far as I' m concerned, is the
following: Wy are there always two parallel descriptions of the uni
verse-the frst-person account ( "I see red") and the third-person
account ( "He says that he sees red when certain pathways in his brain
encounter a wavelength of six hundred nanometers") 1 How can these
two accounts be so utterly diferent yet complementary1 Wy isn't there
only a third-person account, for according to the objective worldview of
the physicist and neuroscientist, that's the only one that really exists1
( Scientists who hold this view are called behaviorists . ) Indeed, in their
scheme of "objective science, " the need for a frst-person account
doesn't even arise-implying that consciousness simply doesn't exist. But
we all know perfectly well that can't be right. I' m reminded of the old
quip about the behaviorist who, j ust having made passionate love, looks
at his lover and says, "Obviously that was good for you, dear, but was
it good for me1 " This need to reconcile the frst-person and third-person
accounts of the universe (the "I" view versus the "he" or "it" view) is
the single most important unsolved problem in science. Dissolve this
barrier, say the Indian mystics and sages, and you will see that the sep
aration between self and nonself is an illusion-that you are really One
with the cosmos.
Philosophers call this conundrum the riddle of qualia or subjective
sensation. How can the fux of ions and electrical currents in little specks
of j elly-the neurons in my brain-generate the whole subj ective world
of sensations like red, warmth, cold or pain1 By what magic is matter
transmuted into the invisible fabric of feelings and sensations1 This prob
lem is so puzzling that not everyone agrees it is even a problem. I will
illustrate this so-called qualia riddle with two simple thought experiments
of the kind that philosophers love to make up. Such whimsical pretend
experiments are virtually impossible to carry out in real life. My colleague
Dr. Francis Crick is deeply suspicious of thought experiments, and I
agree with him that they can be very misleading because they ofen con
tain hidden question- begging assumptions. But they can be used to clar
it logical points, and I will use them here to introduce the problem of
qualia in a colorl way.
First, imagine that you are a fture superscientist with a complete
2 3 0 I P HA N T O MS I N T H E B RA I N
knowledge of the workings of the human brain. Unfortunately you are
also completely color- blind. You don't have any cone receptors ( the
structures in your retina that allow your eyes to discriminate the diferent
colors) , but you do have rods ( for seeing black and white) , and you also
have the correct machinery for processing colors higher up inside your
brain. If your eyes could distinguish colors, so could your brain.
Now suppose that you, the superscientist, study my brain. I am a
normal color perceiver-! can see that the sky is blue, the grass is green
and a banana is yellow-and you want to know what I mean by these
color terms . Wen I look at objects and describe them as turquoise,
chartreuse or vermilion, you don't have any idea what I 'm talking about.
To you, they all look like shades of gray.
But you are intensely curious about the phenomenon, so you point a
spectrometer at the surface of a ripe red apple. It indicates that light with
a wavelength of six hundred nanometers is emanating from the fruit. But
you still have no idea what color this might correspond to because you
can' t experience it. Intrigued, you study the light-sensitive pigments of
my eye and the color pathways in my brain until you eventually come
up with a complete description of the laws of wavelength processing.
Your theory allows you to trace the entire sequence of color perception,
starting from the receptors in my eye and passing all the way into my
brain, where you monitor the neural activity that generates the word
"red. " In short, you completely understand the laws of color vision ( or
more strictly, the laws of wavelength processing) , and you can tell me in
advance which word I will use to describe the color of an apple, orange
or lemon. A a superscientist, you have no reason to doubt the completeness
of your account.
Satisfed, you approach me with your fow diagram and say, "Rma
chandran, this is what's going on in your brain! "
But I must protest. "Sure, that' s what's going on. But I also see red.
Were i s the red i n this diagram? "
"Wat is that? " you ask.
"That's part of the actual , inefable experience of the color, which I
can never seem to convey to you because you're totally color- blind. "
This example leads to a defnition of "qualia": they are aspects of my
brain state that seem to make the scientifc description incomplete-from
my point of view.
As a second example, imagine a species of Amazonian electric fsh that
is very intelligent, in fact, as intelligent and sophisticated as you or I. But
it has something we lack-namely, the ability to sense electrical felds
Do MA RT I A N S S E E RE D ? I 2 3 1
using special organs in its skin. Like the superscientist in the previous
example, you can study the neurophysiology of this fsh and fgure out
how the electrical organs on the sides of its body transduce electrical
current, how this information is conveyed to the brain, what part of the
brain analyzes this information and how the fsh uses this information to
dodge predators, fnd prey and so on. If the fsh could talk, however, it
would say, "Fine, but you'll never know what it feels like to sense elec
tricit. "
These examples clearly state the problem of why qualia are thought
to be essentially private. They also illustrate why the problem of qualia
is not necessarily a scientifc problem. Recall that your scientic descrip
tion is complete. It's just that the your account is incomplete episte
mologically because the actual experience of electric felds or redness is
something you never will know. For you, it will forever remain a "third
person" account.
For centuries philosophers have assumed that this gap between brain
and mind poses a deep epistemological problem-a barrier that simply
cannot be crossed. But is this really true? I agree that the barrier hasn't
yet been crossed, but does it follow that it can never be crossed? I' d like
to argue that there is in fact no such barrier, no great vertical divide in
nature between mind and matter, substance and spirit. Indeed, I believe
that this barrier is only apparent and that it arises as a result of language.
This sort of obstacle emerges when there is any translation from one
language to another. 2
How does this idea apply to the brain and the study of consciousness?
I submit that we are dealing here with two mutually unintelligible lan
guages. One is the language of nere impulses-the spatial and temporal
patterns of neuronal activity that allow us to see red, for example. The
second language, the one that allows us to communicate what we are
seeing to others, is a natural spoken tongue like English or German or
Japanese-rarefed, compressed waves of air traveling between you and
the listener. Both are languages in the strict technical sense, that is, they
are information-rich messages that are intended to convey meaning,
across synapses between diferent brain parts in one case and across the
air between two people in the other.
The problem is that I can tell you, the color- blind superscientist, about
my qualia ( my experience of seeing red) only by using a spoken language.
But the inefable "experience" itself is lost in the translation. The actual
"redness" of red will remain forever unavailable to you.
But what i f I were to skip spoken language as a medium of commu-
2 3 2 I P HA N T O MS I N T H E B RA I N
nication and instead hook a cable of neural pathways (taken from tissue
culture or from another person) from the color-processing areas in my
brain directly into the color-processing regions of your brain ( remember
that your brain has the machinery to see color even though your eyes
cannot discriminate wavelengths because they have no color receptors ) ?
The cable allows the color informaton to go straight from my brain to
neurons in your brain without intermediate translation. This is a far
fetched scenario, but there is nothing logically impossible about it.
Earlier when I said "red, " it didn't make any sense to you because
the mere use of the word "red" already involves a translation. But if
you skip the translation and use a cable, so that the nere impulses them
selves go directly to the color area, then perhaps you'll say, "Oh, my
God, I see exactly what you mean. I' m having this wonderfl new
experience. "3
This scenario demolishes the philosophers' argument that there is an
insurmountable logical barrier to understanding qualia. In principle, you
can experience another creature' s qualia, even the electric fsh' s. If you
could fnd out what the electroceptive part of the fsh brain is doing and
if you could somehow graf it onto the relevant parts of your brain with
all the proper associated connections, then you would start experiencing
the fsh's electrical qualia. Now, we could get into a philosophical debate
over whether you need to be a fsh to experience it or whether as a human
being you could experience it, but the debate is not relevant to my ar
gument. The logical point I am making here pertains only to the elec
trical qualia-not to the whole experience of being a fsh.
The key idea here is that the qualia problem is not unique to the mind
body problem. It is no diferent in kind from problems that arise from
any translation, and thus there is no need to invoke a great division in
nature between the world of qualia and the material world. There is only
one world with lots of translation barriers. If you can overcome them,
the problems vanish.
This may sound like an esoteric, theoretical debate, but let me give
you a more realistic example-an experiment we are actually planning to
do. In the seventeenth century the English astronomer William Moly
neux posed a challenge ( another thought experiment) . Wat would hap
pen, he asked, if a child were raised in complete darkness from birth to
age twenty-one and were then suddenly allowed to see a cube? Would
he recognize the cube? Indeed, what would happen if the child were
suddenly allowed to see ordinary daylight? Would he experience the light,
D o MA RT I A N S S E E RE D 1 1 2 3 3
saying, "Aha! I now see what people mean by light! " or would he act
utterly bewildered and continue to be blind1 ( For the sake of argument,
the philosopher assumes that the child's visual pathways have not degen
erated from the deprivation and that he has an intellectual concept of
seeing, just as our superscientist had an intellectual concept of color be
fore we used the cable. )
This turns out to be a thought experiment that can actually be an
swered empirically. Some unfortunate individuals are born with such se
rious damage to their eyes that they have never seen the world and are
curious about what "seeing" really is: To them it's as puzzling as the
fsh' s electroception is to you. It's now possible to stimulate small parts
of their brains directly with a device called a transcranial magnetic stim
ulator-an extremely powerfl, fuctuating magnet that activates neural
tissue with some degree of precision. Wat if one were to stimulate the
visual cortex of such a person with magnetic pulses, thereby bypassing
the nonfnctional optics of the eye1 I can imagine two possible out
comes. He might say, "Hey, I feel something fnny zapping the back
of my head, " but nothing else. Or he might say, "Oh, my God, this is
extraordinary! I now understand what all of you folks are talking about.
I am fnally experiencing this abstract thing called vision. So this is light,
this is color, this is seeing! "
This experiment is logically equivalent to the neuron cable experiment
we did on the superscientist because we are bypassing spoken language
and directly hitting the blind person' s brain. Now you may ask, If he
does experience totally novel sensations (what you and I call seeing) ,
how can we be sure that i t i s i n fact true vision? One way would be to
look for evidence of topography in his brain. I could stimulate diferent
parts of his visual cortex and ask him to point to various regions of the
outside world where he experiences these strange new sensations. This
is akin to the way you might see stars "out there" in the world when I
hit you on the head with a hammer; you don't experience the stars as
being inside your skull. This exercise would provide convincing evidence
that he was indeed experiencing for the frst time something very close
to our experience of seeing, although it might not be as discriminating
or sophisticated as normal seeing. 4
Why did qualia-subj ective sensation-emerge in evolution? Wy
did some brain events come to have qualia? Is there a particular sle of
2 3 4 I P HA N T O MS I N T H E B RA I N
information processing that produces qualia, or are there some tpes of
neurons exclusively associated with qualia? ( The Spanish neurologist
Rmon y Caj al calls these neurons the "psychic neurons. ") Just as we
know that only a tiny part of the cell, namely, the deoxyribonucleic
acid ( DNA) molecule, is directy involved in heredity and other parts
such as proteins are not, could it be that only some neural circuits are
involved in qualia and others aren't? Francis Crick and Christof Koch
have made the ingenious suggestion that qualia arise from a set of neu
rons in the lower layers of the primary sensory areas, because these are
the ones that proj ect to the frontal lobes where many so- called higher
fnctions are carried out. Their theory has galvanized the entire scien
tifc community and sered as a catalyst for those seeking biological ex
planations for qualia. Others have suggested that the actual patterns of
nere impulses ( spikes) from widely separated brain regions become
"synchronized" when you pay attention to something and become
aware of it. 5 In other words, it is the synchronization itself that leads
to conscious awareness. There's no direct evidence for this yet, but it's
encouraging to see that people are at least trying to explore the ques
tion experimentally.
These approaches are attractive for one main reason, namely, the fact
that reductionism has been the single most successfl strategy in science.
A the English biologist Peter Medawar defnes it, "Reductionism is the
belief that a whole may be represented as a fnction ( in the mathematical
sense) of its constituent parts, the fnctions having to do with the spatial
and temporal ordering of the parts and with the precise way in which
they interact. " Unfortunately, as I stated at the beginning of this book,
it's not always easy to know a priori what the appropriate level of reduc
tionism is for any given scientifc problem. For understanding conscious
ness and qualia there wouldn't be much point in looking at ion channels
that conduct nere impulses, at the brain stem reflex that mediates sneez
ing or at the spinal cord refex arc that controls the bladder, even though
these are interesting problems in themselves ( at least to some people) .
They would be no more usefl i n understanding higher brain fnctions
like qualia than lookng at silicon chips in a microscope in an attempt to
understand the logic of a computer program. And yet this is precisely
the strategy most neuroscientists use in trying to understand the higher
fnctions of the brain. They argue either that the problem doesn't exist
or that it will be solved some fne day as we plod along looking at the
activity of individual neurons. 6
Philosophers ofer another solution to this dilemma when they say
Do MART I A N S S E E RE D 1 I 2 3 5
that consciousness and qualia are "epiphenomena. " According to this
view, consciousness is like the whistling sound that a train makes or
the shadow of a horse as it runs: It plays no causal role in the real
work done by the brain. Afer all , you can imagine a "zombie" uncon
sciously doing everything in exactly the same manner that a conscious
being does. A sharp tap on the tendon near your knee j oint sets in
motion a cascade of neural and chemical events that causes a refex
knee jerk ( stretch receptors in the knee connect to neres in the spinal
cord, which in turn send messages to the muscles) . Consciousness
doesn' t enter into this picture; a paraplegic has an excellent knee jerk
even though he can' t feel the tap. Now imagine a much more complex
cascade of events starting with long-wavelength light striking your ret
ina and various relays, leading to your saying "red. " Since you can
imagine this more complex cascade happening without conscious
awareness, doesn't it follow that consciousness is irrelevant to the
whole schemd Afer all , God ( or natural selection) could have created
an unconscious being that does and says all the things you do, even
though "it" is not conscious.
This argument sounds reasonable but in fact it is based on the fallacy
that because you can imagine something to be logically possible,
therefore it is actually possible. But consider the same argument applied
to a problem in physics. We can all imagine something traveling faster
than the speed of light. But as Einstein tells us, this "commonsense"
view is wrong. Simply being able to imagine that something is logically
possible does not guarantee its possibility in the real world, even in prin
ciple. Likewise, even though you can imagine an unconscious zombie
doing everything you can do, there may be some deep natural cause that
prevents the existence of such a being! Notice that this argument does
not prove that consciousness must have a causal role; it simply proves
that you cannot use statements that begin, "Afer all , I can imagine" to
draw conclusions about any natural phenomenon.
I would like to try a somewhat diferent approach to understanding
qualia, which I will introduce by askng you to play some games with your
eyes. First, recall the discussion in Chapter 5 concerning the so-called
blind spot-the place where your optic nere exits the back of your eye
ball . Again, if you close your right eye, fx your gaze on the black spot in
Figure 5 . 2 and slowly move the page toward or away from your eye, you
will see that the hatched disk disappears. It has fallen into your natural
blind spot. Now close your right eye again, hold up the index fnger of
your right hand and aim your lef eye' s blind spot at the middle of your ex-
2 3 6 I P H A N T O MS I N T H E B RA I N
Figre 12. 1 A feld of yellow doughnuts (shmvn in white here) . Shut your riht
eye and look at the small white dot near the middle of the illustration with your
left eye. When the page is about six to nine inches from your face, one ofthe dough
nuts will fall exactly around your left eye's blind spot. Since the black hole in the
center of the doughnut is slihtly smaller than your blind spot, it should disappear
and the blind spot then is "flled in" with yellow (white) qualia from the ring so
that you see a yellow disk rather than a ring. Notice that the disk ''ops out"
conspicuously against the background of rings. Paradoxically, you have made a
target more conspicuous by virtue ofyour blind spot. If the illusion doesn't work,
try using an enlarged photocopy and shifting the white dot horizontally.
tended fnger. The middle of the fnger should disappear, just as the
hatched disk does, and yet it doesn' t; it looks continuous. In other words,
the qualia are such that you do not merely deduce intellectually that the fn
ger is continuous-"Afer all, my blind spot is there"-you literally see the
"missing piece" of your fnger. Psychologists call this phenomenon "fll
ing i n, " a usefl if somewhat misleading phrase that simply means that you
see something in a region of space where nothing exists .
This phenomenon can be demonstrated even more dramatically if you
look at Figure 1 2. 1 . Again, with your right eye shut look at the small
white dot on the right with your lef eye and gradually move the book
toward you until one of the "doughnuts" falls on your blind spot. Since
the inner diameter of the doughnut-the small black disk-is slightly
Do MA RT I A N S S E E RE D ? 1 2 3 7
smaller than your blind spot, it should disappear and the white ring
should encompass the blind spot. Say the doughnut ( the ring) is yellow.
Wat you will see if your vision is normal is a complete yellow homo
geneous disk, which will indicate that your brain "flled in" your blind
spot with yellow qualia ( or white in Figure 1 2. 1 ) . I emphasize this be
cause some people have argued that we all simply ignore the blind spot
and don't notice what' s going on, meaning that there really is no flling
in. But this can't be right. If you show someone several rings, one of
which is concentric with the blind spot, that concentric one will look like
a homogeneous disk and will actually "pop out" perceptually against a
background of rings. How can something you are ignoring pop out at
you? This means that the blind spot does have qualia associated with it
and, moreover, that the qualia can provide actual "sensory support. " In
other words, you don't merely deduce that the center of the doughnut
is yellow; you literally see it as yellow?
Now consider a related example. Suppose I put one fnger crosswise
in front of another fnger ( as in a plus sign) and look at the two fngers.
Of course, I see the fnger in the back as being continuous. I kow it's
continuous. I sort of see it as continuous . But if you asked me whether
I literally see the missing piece of fnger, I would say no-for all I know,
someone could have actually sliced two pieces of fnger and put them on
either side of the fnger in front to fool me. I cannot be certain that I
really see that missing part.
Compare these two cases, which are similar in that the brain supplies
the missing information both times. Wat's the diference? What does it
matter to you, the conscious person, that the yellow doughnut now has
qualia in the middle and that the occluded part of your fnger does not?
The diference is that you cannot change your mind about the yellow in
the middle of the doughnut. You can' t think, "Maybe it's yellow, but
maybe it's pink, or maybe it's blue. " No, it's shouting at you, "I am
yellow," with an explicit representation of yellowness in its center. In
other words, the flled-in yellow is not revocable, not changeable by you.
In the case of the occluded fnger, however, you can think, "There's
a high probability that there is a fnger there, but some malicious scientist
could have pasted two half fngers on either side of it. " This scenario is
highly improbable, but not inconceivable.
In other words, I can choose to assume that there might be something
else behind the occluding fnger, but I cannot do so with the flled-in
yellow of the blind spot. Thus the crucial diference between a qualia
laden perception and one that doesn't have qualia is that the qualia-laden
2 3 8 I p H A NT 0 M s I N T H E B RA I N
perception is irrevocable by higher brain centers and is therefore
"tamper-resistant," whereas the one that lacks qualia is fexible; you can
choose any one of a number of diferent "pretend" inputs using your
imagination. Once a qualia-laden perception has been created, you're
stuck with it. (A good example of this is the dalmatian dog in Figure
12. 2. Initially, as you look, it's all fragments. Then suddenly everything
clicks and you see the dog. Loosely speaking, you've now got the dog
qualia. The next time you see it, there' s no way you can avoid seeing
the dog. Indeed, we have recently shown that neurons in the brain have
permanently altered their connections once you have seen the dog. )8
These examples demonstrate an important feature of qualia-it must
be irrevocable. But although this feature is necessary, it's not sufcient
to explain the presence of qualia. Wy? Well, imagine that you are in a
coma and I shine a light into your eye. If the coma is not too deep, your
pupil will constrict, even though you will have no subjective awareness
of any qualia caused by the light. The entire refex arc is irrevocable, and
yet there are no qualia associated with it. You can' t change your mind
about it. You can't do anything about it, j ust as you couldn't do anything
about the yellow flling in your blind spot in the doughnut example. So
why does only the latter have qualia? The key diference is that in the
case of the pupil ' s constriction, there is only one output-one fnal out
come-available and hence no qualia. In the case of the yellow disk, even
though the representation that was created is irrevocable, you have the
luxury of a choice; what you can do with the representation is open
ended. For instance, when you experienced yellow qualia, you could say
yellow, or you could think of yellow bananas, yellow teeth, the yellow
skin of j aundice and so on. And when you fnally saw the dalmatian, your
mind would be poised to conjure up any one of an infnite set of dog
related associations-the word "dog," the dog's bark, dog food or even
fre engines. And there is apparently no limit to what you can choose.
This is the second important feature of qualia: Sensations that are qualia
laden aford the luxury of choice. So now we have identifed to fnc
tional features of qualia: irrevocability on the input side and fexibility on
the output side.
There is a third important feature of qualia. In order to make decisions
on the basis of a qualia-laden representation, the representation needs to
exist long enough for you to work with it. Your brain needs to hold the
representation in an intermediate bufer or in so-called immediate mem
ory. ( For example, you hold the phone number you get from the infor
mation operator j ust long enough to dial it with your fngers. ) Again this
Do MA RT I A N S S E E RE D 1 1 2 3 9
,
-
- .

I

. "
'
.
--
. -
Figre 1 2. 2 Random jumble ofsplotches. Gaze at this picture for a few seconds
(or minutes) and you will eventually see a dalmatian dog snifng the ground
mottled with shadows of leaves (hint: the dog,s face is at the left toward the middle
ofthe picture; you can see its collar and left ear) . Once the dog has been seen, it is
impossible to get rid ofit.
Using similar pictures, we showed recently that neurons in the temporal lobes
become altered permanently after the initial brief exposure-once you have ((seen,,
the dog ( Tovee, Rolls and Ramachandran, 1 996) . Dalmatian dog photographed
by Ron James .
condition is not enough in itself to generate qualia. A biological system
can have other reasons, besides making a choice, for holding information
in a bufer. For example, Venus' s- flytrap snaps shut only if its trigger
hairs inside the trap are stimulated twice in succession, apparently retai n
i ng a memory of the frst stimulus and comparing it with the second to
2 4 0 I P HA N T O MS I N T H E B RA I N
"infer" that something has moved. ( Darin suggested that this evolved
to help the plant avoid inadvertently shutting te trap if hit by a dust
particle rather than a bug. ) Typically in these sorts of cases, there is only
one output possible: Venus' s-flytrap invariably closes shut. There' s noth
ing else it can do. The second important feature of qualia-choice-is
missing. I think we can safely conclude, contrary to the panpsychists, that
the plant does not have qualia linked to bug detection.
In Chapter 4, we saw how qualia and memory are connected in the
story of Denise, the young woman living in Italy who sufered carbon
monoxide poisoning and developed an unusual knd of "blindsight. " Re
call that she could correctly rotate an envelope to post it in a horizontal or
a vertical slot, even though she could not consciously perceive the slot's
orientation. But if someone asked Denise frst to look at the slot and then
turned of the lights before asking her to post the letter, she could no
longer do so. "She" seemed to forget the orientation of the slot almost
immediately and was unable to insert the letter. This suggests that the part
of Denise's visual system that discerned orientation and controlled her arm
movements-what we call the zombie or the how pathway in Chapter 4-
not only was devoid of qualia, but also lacked short- term memor. But the
part of her visual system-the what pathway-that would normally enable
her to recognize the slot and perceive its orientation is not only conscious,
it also has memory. ( But "she" cannot use the what pathway because it is
damaged; all that's available is the unconscious zombie and "it" doesn't
have memor. ) Ad I don't think this link between short-term memor
and conscious awareness is coincidental .
Wy does one part of the visual stream have memory and another not
have it? It may be that the qualia-laden what system has memory because
it is involved in making choices based on perceptual representations
and choice requires time. The how system without qualia, on the other
hand, engages in continuous real - time processing running in a tighty
closed loop-like the thermostat in your house. It does not need mem
ory because it is not involved in making real choices. Thus simply posting
the letter does not require memory, but choosing which letter to post
and deciding where to mail it do require memor.
This idea can be tested in a patient like Denise. If you set up a situation
in which she was forced to make a choice, the zombie system ( still intact
in her) should go hayire. For example, if you asked Denise to mail a
letter and you showed her two slots ( one vertical , one horizontal ) si
multaneously, she should fail, for how could the zombie system choose
between the two? Indeed, the very idea of an unconscious zombie mak-
Do MA RT I A N S S E E RE D ? 1 2 4 1
ing choices seems oxymoronic-for doesn't the very existence of free will
imply consciousness?
To summarize thus far-for qualia to exist, you need potentially in
fnite implications ( bananas, j aundice, teeth) but a stable, fnite, irrevo
cable representation in your short-term memory as a starting point
(yellow) . But if the starting point is revocable, then the representation
will not have strong, vivid qualia. Good examples of the latter are a cat
that you "infer" under the sofa when you only see its tail sticking out,
or your ability to imagine that there is a monkey sitting on that chair.
These do not have strong qualia, for good reason, because if they did
you would confse them with real objects and wouldn't be able to sur
vive long, given the way your cognitive system is structured. I repeat
what Shakespeare said: "You cannot cloy the hungry edge of appetite by
bare imagination of a feast. " Very fortunate, for otherise you wouldn't
eat; you would j ust generate the qualia associated with satiety in your
head. In a similar vein, any creature that simply imagines having orgasms
is unlikely to pass on its genes to the next generation.
Wy don't these faint, internally generated images ( the cat under the
couch, the monkey in the chair) or beliefs, for that matter, have strong
qualia? Imagine how confsing the world would be if they did. Actual
perceptions need to have vivid, subjective qualia because they are driving
decisions and you cannot aford to hesitate. Beliefs and internal images,
on the other hand, should not be qualia-laden because they need to be
tentative and revocable. So you believe-and you can imagine-that un
der the table there is a cat because you see a tail stickng out. But there
could be a pig under the table with a transplanted eat's tail . You must
be willing to entertain that hypothesis, however implausible, because
every now and then you might be surprised.
Wat is the fnctional or computational advantage to making qualia
irrevocable? One answer is stability. If you constantly changed your mind
about qualia, the number of potential outcomes ( or "outputs") would
be infnite; nothing would constrain your behavior. At some point you
need to say "this is it" and plant a flag on it, and it's the planting of the
flag that we call qualia. The perceptual system follows a rationale some
thing like this: Given the available information, it is 90 percent certain
that what you are seeing is yellow ( or dog or pain or whatever) .
Therefore, for the sake of argument, I 'll assume that it is yellow and act
accordingly, because if I keep saying, "Maybe it's not yellow, " I won't
be able to take the next step of choosing an appropriate course of action
or thought. In other words, if I treated perceptions as beliefs, I would
2 4 2 I P HA N T O MS I N T H E B RA I N
be blind ( as well as being paralyzed with indecision) . Qualia are irrevo
cable in order to eliminate hesitation and to confer certaint to decisions. 9
Ad this, in turn, may depend on which particular neurons are fring,
how strongly they're fring and what stuctures they project to.
Wen I see the eat's tail sticking out from under the table, I "guess"
or "know" there is a cat under the table, presumably attached to the
tail . But I don' t literally see the cat, even though I literally see the tail .
And this raises another fascinating question: Are seeing and knowing
the qualitative distinction between perception and conception-com
pletely diferent, mediated by diferent types of brain circuitry perhaps,
or is there a gray area in between? Lt's go back to the region corre
sponding to the blind spot in my eye, where I can' t see anything. A we
saw in the Chapter 5 discussion on Charles Bonnet syndrome, there is
another kind of blind spot-the enormous region behind my head
where I also can't see anything ( although people don't generally use the
term "blind spot" for this region) . Of course, ordinarily you don't walk
around experiencing a huge gap behind your head, and therefore you
might be tempted to jump to the conclusion that you are in some sense
flling in the gap in the same way that you fll in the blind spot. But you
don' t. You can' t. There is no visual neural representation in the brain
corresponding to this area behind your head. You fll it in only in the
trivial sense that if you are standing in a bathroom with wallpaper in
front of you, you assume that the wallpaper continues behind your head.
But even though you assume that there is wallpaper behind your head,
you don' t literally see it. In other words, this sort of "flling in" is purely
metaphorical and does not flfll our criterion of being irrevocable. In
the case of the "real" blind spot, as we saw earlier, you can't change
your mind about the area that has been flled in. But regarding the region
behind your head, you are free to think, "In all likelihood there is wall
paper there, but who knows, maybe there is an elephant there. "
Filling i n of the blind spot i s therefore fndamentally diferent from
your failure to notice the gap behind your head. But the question re
mains, Is the distinction between what is going on behind your head
and the blind spot qualitative or quantitative? Is the dividing line between
"flling in" ( of the kind seen in the blind spot) and mere guesswork ( for
things that might be behind your head) completely arbitrar? To answer
this, consider another thought experiment. Imagine we continue evolv
ing in such a way that our eyes migrate toward the sides of our heads,
D o MART I A N S S E E RE D ? 1 2 4 3
while presering the binocular visual feld. The felds of view of the two
eyes encroach farther and farther behind our heads until they are almost
touching. At that point let's assume you have a blind spot behind your
head ( between your eyes ) that is identica in size to the blind spot that
is in front of you. The question then arises, Would the completion of
objects across the blind spot behind your head be true flling in of qualia,
as with the real blind spot, or would it still be conceptual, revocable
imagery or guesswork of the kind that you and I experience behind our
heads? I think that there will be a defnite point when the images become
irrevocable, and when robust perceptual representations are created, per
haps even re-created and fed back to the early visual areas . At that point
the blind region behind your head becomes fnctionally equivalent to
the normal blind spot in front of you. The brain will then suddenly
switch to a completely novel mode of representing the information; it
will use neurons in the sensory areas to signal the events behind your
head irrevocably ( instead of neurons in the thinking areas to make edu
cated but tentative guesses as to what might be lurking there) .
Thus even though blind -spot completion and completion behind your
head can be logically regarded as two ends of a continuum, evolution
has seen ft to separate them. In the case of your eye' s blind spot, the
chance that something signifcant is lurking there is small enough that it
pays simply to treat the chance as zero. In the case of the blind area
behind your head, however, the odds of something important being
there ( like a burglar holding a gun) are high enough that it would be
dangerous to fll in this area irrevocably with wallpaper or whatever pat
tern is in front of your eyes.
So far we have talked about three laws of qualia-three logical criteria
for determining whether a system is conscious or not-and we have con
sidered examples from the blind spot and from neurological patients. But
you may ask, How general is this principle? Can we apply it to other
specifc instances when there is a debate or doubt about whether con
sciousness is involved? Here are some examples:
It's known that bees engage in very elaborate forms of communication
including the so- called bee waggle dance. A scout bee, having located a
source of pollen, will travel back to the hive and perform an elaborate
dance to designate the location of the pollen to the rest of the hive. The
question arises, Is the bee conscious when it's doing this? 1 0 Since the
bee's behavior, once set in motion, is irrevocable and since the bee is
2 4 4 I P H A N T OMS I N T H E B RA I N
obviously acting on some short-term memory representation of the pol
len's location, at least two of the three criteria for consciousness are met.
You might then jump to the conclusion that the bee is conscious when
it engages in this elaborate communication ritual . But since the bee lacks
the third criterion-flexible output-! would argue that it is a zombie.
In other words, even though the information is very elaborate, is irrev
ocable and held in short-term memor, the bee can only do one thing
with that information; only one output is possible-the waggle dance.
This argument is important, for it implies that mere complexity or elab
orateness of information processing is no guarantee that there is con
sciousness involved.
One advantage my scheme has over other theories of consciousness is
that it allows us unambiguously to answer such questions as, Is a bee
conscious when it performs a waggle dance? Is a sleepwalker conscious?
Is the spinal cord of a paraplegic conscious-does it have its own sexual
qualia-when he (it) has an erection? Is an ant conscious when it detects
pheromones? In each of these cases, instead of the vague assertion that
one is dealing with various degrees of consciousness-which is the stan
dard answer-one should simply apply the three criteria specifed. For
example, can a sleepwalker (while he's sleepwalking) take the "Pepsi
test"-that is, choose between a Pepsi Cola and a Coca Cola? Does he
have short-term memory? If you showed him the Pepsi, put it in a box,
switched of the room lights for thirty seconds and then switched them
on again, would he reach for the Pepsi ( or utterly fail like the zombie in
Denise ) ? Does a partially comatose patient with akinetic mutism ( seem
ingly awake and able to follow you with his eyes but unable to move or
talk) have short- term memory? We can now answer these questions and
avoid endless semantic quibbles over the exact meaning of the word
"consciousness. "
Now you might ask, "Does any of this yield clues as to where i n the
brain qualia might be? " It is surprising that many people think that the
seat of consciousness is the frontal lobes, because nothing dramatic hap
pens to qualia and consciousness per se if you damage the frontal lobes
even though the patient's personality can be profoundly altered ( and he
may have difculty switching attention) . I would suggest instead that
most of the action is in the temporal lobes because lesions and hyper
activity in these structures are what most ofen produce striking distur
bances in consciousness. For instance, you need the amygdala and other
Do MA RT I A N S S E E RE D 1 1 2 4 5
parts of the temporal lobes for seeing the signifcance of things, and
surely this is a vital part of conscious experience. Without this structure
you are a zombie ( like the fellow in the famous Chinese room thought
experiment proposed by the philosopher John Searle1 1 ) capable only of
giving a single correct output in response to a demand, but with no
ability to sense the meaning of what you are doing or saying.
Everyone would agree that qualia and consciousness are not associated
with the early stages of perceptual processing as at the level of the retina.
Nor are they associated with the fnal stages of planning motor acts when
behavior is actually carried out. They are associated, instead, with the
intermediate stages of processing1 2-a stage where stable perceptual rep
resentations are created (yellow, dog, monkey) and that have meaning
( the infnite implications and possibilities for action from which you can
choose the best one) . This happens mainly in the temporal lobe and
associated limbic structures, and, in this sense, the temporal lobes are the
interface between perception and action.
The evidence for this comes from neurology; brain lesions that pro
duce the most profound disturbances in consciousness are those that
generate temporal lobe seizures, whereas lesions in other parts of the
brain only produce minor disturbances in consciousness. When surgeons
electrically stimulate the temporal lobes of epileptics, the patients have
vivid conscious experiences. Stimulating the amygdala is the surest way
to "replay" a fll experience, such as an autobiographical memory or a
vivid hallucination. Temporal lobe seizures are ofen associated not only
with alterations in consciousness in the sense of personal identity, per
sonal destiny and personality, but also with vivid qualia-hallucinations
such as smells and sounds . If these are mere memories, as some claim,
why would the person say, "I literally feel like I' m reliving it"1 These
seizures are characterized by the vividness of the qualia they produce.
The smells, pains, tastes and emotiona feelings-all generated in the
temporal lobes-suggest that this brain region is intimately involved in
qualia and conscious awareness.
Another reason for choosing the temporal lobes-especially the lef
one-is that this is where much of language is represented. If I see an
apple, temporal lobe activity allows me to apprehend all its implications
almost simultaneously. Recognition of it as a fruit of a certain type occurs
in the inferotemporal cortex, the amygdala gauges the apple's signifcance
for my well - being and Wernicke's and oter areas alert me to all the
nuances of meaning that the mental image-including the word "ap
ple"-evokes; I can eat the apple, I can smell it; I can bake a pie, remove
2 4 6 I P H A N T O MS I N T H E B RA I N
its pith, plant its seeds; use it to "keep the doctor away, " tempt Eve and
on and on. If one enumerates all of the attributes that we usually asso
ciate with the words "consciousness" and "awareness, " each of them,
you will notice, has a correlate in temporal lobe seizures, including vivid
visual and auditory hallucinations, "out of body" experiences and an
absolute sense of omnipotence or omniscience. 1 3 Any one of this long
list of disturbances in conscious experience can occur individually when
other parts of the brain are damaged ( for instance, disturbances of body
image and attention in parietal lobe syndrome), but it's only when the
temporal lobes are involved that they occur simultaneously or in diferent
combinations; that again suggests that these structures play a central role
in human consciousness.
Until now we have discussed what philosophers call the "qualia"
problem-the essential privacy and noncommunicability of mental
states-and I've tried to transform it from a philosophical problem into
a scientifc one. But in addition to qualia ( the "raw feel" of sensations) ,
we also have to consider the self-the "I" inside you who actually ex
periences these qualia. Qualia and self are really two sides of the same
coin; obviously there is no such thing as free- floating qualia not experi
enced by anyone and it' s hard to imagine a self devoid of al l qualia.
But what exactly is the self Unfortunately, the word "self" is like
the word "happiness" or "love"; we all know what it is and know that
it's real , but it's very hard to defne it or even to pinpoint its character
istics. A with quicksilver, the more you try to grasp it the more it tends
to slip away. Wen you think of the word "self, " what pops into your
mind? Wen I think about "myself," it seems to be something that
unites all my diverse sensory impressions and memories ( unity) , claims
to be "in charge" of my life, makes choices ( has free will) and seems to
endure as a single entity in space and time. It also sees itself as embed
ded in a social context, balancing its checkbook and maybe even plan
ning its own fneral . Actually we can make a list of all the characteristics
of the "self'-j ust as we can for happiness-and then look for brain
structures that are involved in each of these aspects. Doing this will
someday enable us to develop a clearer understanding of self and con
sciousness-although I doubt that there will be a single, grand, climac
tic "solution" to the problem of the self in the way that DNA is the
solution to the riddle of heredity.
Do MA RT I A N S S E E RE D ? 1 2 4 7
What are these characteristics that defne the self William Hirstein, a
postdoctoral fellow in my lab, and I came up with the following list:
Te embodied sel My Self is anchored within a single body. If ! close
my eyes, I have a vivid sense of diferent body parts occupying space
( some parts more felt than others)-the so- called body image. If you
pinch my toe, it is "I" who experiences the pain, not "it. " And yet the
body image, as we have seen, is extremely malleable, despite all its ap
pearance of stability. With a few seconds of the right type of sensory
stimulation, you can make your nose three feet long or project your hand
onto a table ( Chapter 3) ! And we know that circuits in the parietal lobes,
and the regions of the frontal lobes to which they project, are very much
involved in constructing this image. Partial damage to these structures
can cause gross distortions in body image; the patient may say that her
lef arm belongs to her mother or ( as in the case of the patient I saw
with Dr. Rita Hari in Helsinki ) claim that the lef half of her body is
still sitting in the chair when she gets up and walks! If these examples
don't convince you that your "ownership" of your body is an illusion,
then nothing will.
Te passionate sel It is difcult to imagine the self without emo
tions-or what such a state could even mean. If you don't see the mean
ing or signifcance of something-if you cannot apprehend all its
implications-in what sense are you really aware of it consciously? Thus
your emotions-mediated by the limbic system and amygdala-are an
essential aspect of self, not just a "bonus. " ( It is a moot point whether
a purebred Vulcan, like Spack's father in the original Star Trek, is really
conscious or whether he is j ust a zombie-unless he is also tainted by a
few human genes as Spock is. ) Recall that the "zombie" in the "how"
pathway is unconscious, whereas the "what" pathway is conscious, and
I suggest that the diference arises because only the latter is linked to the
amygdala and other limbic structures ( Chapter 5 ) .
The amygdala and the rest of the limbic system ( in the temporal lobes )
ensures that the cortex-indeed, the entire brain-seres the organism' s
basic evolutionary goals. The amygdala monitors the highest level of per
ceptual representations and "has its fngers on the keyboard of the au
tonomic nerous system"; it determines whether or not to respond
emotionally to something and what kinds of emotions are appropriate
( fear in response to a snake or rage to your boss and afection to your
child) . It also receives information from the insular cortex, which in turn
2 4 8 I P H A N T O MS I N T H E B RA I N
is driven partially by sensory input not only from the skin but also from
the viscera-heart, lung, liver, stomach-so that one can also speak of a
"visceral , vegetative self' or of a "gut reaction" to something. ( It is this
"gut reaction, " of course, that one monitors with the GSR machine, as
we showed in Chapter 9, so that you could argue that the visceral self
isn' t, strictly speaking, part of the conscious self at all . But it can nev
ertheless profoundly intrude on your conscious self; j ust think of the last
time you felt nauseous and threw up. )
Pathologies of the emotional self include temporal lobe epilepsy, Cap
gras' syndrome and Kliver- Bucy syndrome. In the frst, there may be a
heightened sense of self that may arise partly through a process that Paul
Fedio and D. Bear call "hyperconnectivity"-a strengthening of con
nections between the sensory areas of the temporal cortex and the amyg
dala. Such hyperconnectivity may result from repeated seizures that cause
a permanent enhancement ( kndling) of these pathways, leading the pa
tient to ascribe deep signifcance to evering around him ( including
himself! ) . Conversely, people with Capgras' syndrome have reduced
emotional response to certain categories of objects ( faces ) and people
with Kliver- Bucy or Cotard's syndrome have more perasive problems
with emotions ( Chapter 8) . A Cotard's patient feels so emotionally re
mote from the world and from himself that he will actually make the
absurd claim that he is dead or that he can smell his flesh rotting.
Interestingly, what we call "personality"-a vital aspect of your self
that endures for life and is notoriously imperious to "correction" by
other people or even by common sense-probably also involves the very
same limbic structures and their connections with the ventromedial fron
tal lobes. Damage to the frontal lobes produces no obvious, immediate
disturbance in consciousness, but it can profoundly alter your personality.
When a crowbar pierced the frontal lobes of a railway worker named
Phineas Gage, his close friends and relatives remarked, "Gage wasn't
Gage anymore. " In this famous example of frontal lobe damage, Gage
was transformed from a stable, polite, hardworkng young man into a
lying, cheating vagabond who could not hold down a job. 1 4
Temporal lobe epilepsy patients like Paul in Chapter 9 also show
striking personality changes, so much so that some neurologists speak of
a "temporal lobe epilepsy personality. " Some of them ( the patients, not
the neurologists ) tend to be pedantic, argumentative, egocentric and
garrulous. They also tend to be obsessed with "abstract thoughts. " If
these traits are a result of hyperfnctioning of certain parts of the tem
poral lobe, what exactly is the normal fnction of these areas? If the
Do MA RT I A N s S E E RE D 1 1 2 4 9
limbic system is concerned mainly with emotions, why would seizures
in these areas cause a tendency to generate abstract thought1 Ae there
areas in our brains whose role is to produce and manipulate abstract
thoughts1 This is one of the many unsolved problems of temporal lobe
epilepsy. 1 5
Te executive sel Classical physics and modern neuroscience tell us
that you ( including your mind and brain) inhabit a deterministic billiard
ball universe. But you don't ordinarily experience yourself as a puppet
on a string; you feel that you are in charge. Yet paradoxically, it is always
obvious to you that there are some things you can do and others you
cannot given the constraints of your body and of the external world.
(You know you can't lif a truck; you kow you can' t give your boss a
black eye, even if you'd like to. ) Somewhere in your brain there are
representations of all these possibilities, and the systems that plan com
mands ( the cingulate and supplementary motor areas in the frontal lobes )
need to be aware of this distinction between things they can and cannot
command you to do. Indeed, a "self' that sees itself as completely pas
sive, as a helpless spectator, is no self at all , and a self that is hopelessly
driven to action by its impulses and urgings is equally efete. A self needs
free will-what Deepak Chopra calls "the universal feld of infnite pos
sibilities"-even to exist. More technically, conscious awareness has been
described as a "conditional readiness to act. "
To achieve all this, I need to have i n my brain not only a represen
tation of the world and various objects in it but also a representation of
myself, including my own body within that representation-and it is this
peculiar recursive aspect of the self that makes it so puzzling. In addition,
the representation of the external object has to interact with my self
representation ( including the motor command systems ) in order to allow
me to make a choice. ( He' s your boss; don' t sock him. It's a cookie; it's
within your reach to grab it. ) Derangements in this mechanism can lead
to syndromes like anosognosia or somatoparaphrenia ( Chapter 7) in
which a patient will with a perfectly straight face claim that her lef arm
belongs to her brother or to the physician.
Wat neural structure is involved in representing these "embodied"
and "executive" aspects of the self Damage to the anterior cingulate
gyrus results in a bizarre condition called "akinetic mutism"-the patient
simply lies in bed unwilling to do or incapable of doing anything even
though he appears to be flly aware of his surroundings. If there's such
a thing as absence of free will, this is it.
2 5 0 I P H A N T O MS I N T H E B RA I N
Sometimes when there is partial damage to the anterior cingulate, the
ver opposite happens: The patient's hand is uncoupled from her con
scious thoughts and intentions and attempts to grab things or even per
form relatively complex actions without her permission. For example, Dr.
Peter Halligan and I saw a patient at Rivermead Hospital in Oxford
whose lef hand would seize the banister as she walked down the steps
and she would have to use her other hand forcibly to unclench the fngers
one by one, so she could continue walkng. Is the alien lef hand con
trolled by an unconscious zombie, or is it controlled by parts of her brain
that have qualia and consciousness? We can now answer this by applying
our three criteria. Does the system in her brain that moves her arm create
an irrevocable representation? Does it have short-term memor? Can it
make a choice?
Both the executive self and the embodied self are deployed while you
are playing chess and assume you're the queen as you plan "her" next
move. Wen you do this, you can almost feel momentarily that you are
inhabiting the queen. Now one could argue that you're j ust using a
fgure of speech here, that you' re not literally assimilating the chess piece
into your body image. But can you really be all that sure that the loyalty
of your mind to your own body is not equally a "fgure of speech"? What
would happen to your GSR if I suddenly punched the queen? Would it
shoot up as though I were punching your own body? If so, what is the
justifcation for a hard-and-fast distinction between her body and yours?
Could it be that your tendency normally to identif with your "own"
body rather than with the chess piece is also a matter of convention,
albeit an enduring one? Might such a mechanism also underlie the em
pathy and love you feel for a close friend, a spouse or a child who is
literally made from your own body?
Te mnemonic sel Your sense of personal identity-as a single person
who endures through space and time-depends on a long string of
highly personal recollections: your autobiography. Organizing these
memories into a coherent story is obviously vital to the construction of
self.
We know that the hippocampus is required for acquiring and consol
idating new memory traces. If you lost your hippocampi ten years ago,
then you will not have any memories of events that occurred afer that
date. You are still flly conscious, of course, because you have all the
memories prior to that loss, but in a very real sense your existence was
frozen at that time.
D o MA RT I A N S S E E RE D ? 1 2 5 1
Profound derangement to the mnemonic self can lead to multiple
personality disorder or MPD. This disorder is best regarded as a mal
fnction of the same coherencing principle I alluded to in the discussion
of denial in Chapter 7. A we saw, if you have two sets of mutually
incompatible beliefs and memories about yourself, the only way to pre
vent anarchy and endless strife may be to create two personalities within
one body-the so-called multiple personality disorder. Given the obvious
relevance of this syndrome to understanding the nature of self, it is aston
ishing how little attention it has received from mainstream neurology.
Even the mysterious trait called hypergraphia-the tendency of tem
poral lobe epilepsy patients to maintain elaborate diaries-may be an
exaggeration of the same general tendency: the need to create and sustain
a coherent worldview or autobiography. Perhaps kindling in the amyg
dala causes every external event and internal belief to acquire deep sig
nifcance for the patient, so there is an enormous proliferation of
spuriously self-relevant beliefs and memories in his brain. Add to this the
compelling need we all have from time to time to take stock of our lives,
see where we stand; to review the signifcant episodes of our lives peri
odically-and you have hypergraphia, an exaggeration of this natural ten
dency. We all have random thoughts during our day-to- day musings, but
if these were sometimes accompanied by miniseizures-producing eu
phoria-then the musings themselves might evolve into obsessions and
entrenched beliefs that the patient would keep returning to whether in
his speech or in his writing. Could similar phenomena provide a neural
basis for zealotry and fanatacism?
Te unied sel-imposing coherence on consciousness, flling in and con
fabulation: Another important attribute of self is its unity-the internal
coherence of its diferent attributes. One way to approach the question
of how our account of qualia relates to the question of the self is to ask
why something like flling in of the blind spot with qualia occurs. The
original motive many philosophers had for arguing that the blind spot is
not flled in was that there is no person in the brain to fll it in for-that
no little homunculus is watching.
Since there's no little man, they argued, the antecedent is also false:
Qualia are not flled in, and thinking so is a logical fallacy. Since I argue
that qualia are in fact flled in, does this mean that I believe they are
flled in for a homunculus? Of course not. The philosopher's argument
is really a straw man. The line of reasoning should rr, If qualia are flled
in, they are flled in for something and what is that "something"? There
2 5 2 I P HA N T O MS I N T H E B RA I N
exists in certain branches of psychology the notion of an executive, or a
control process, which is generally thought to be located in the prefontal
and frontal parts of the brain. I would like to suggest that the "some
thing" that qualia are flled in for is not a "thing" but simply another
brain process, namely, executive processes associated with the limbic sys
tem including parts of the anterior cingulate gyrus. This process connects
your perceptual qualia with specifc emotions and goals, enabling you to
make choices-very much the sort of thing that te self was traditionally
supposed to do. ( For example, afer having lots of tea, I have the sen
sation or urge-the qualia-to urinate but I'm giving a lecture so I
choose to delay action until the talk is fnished but also choose to excuse
myself at the end instead of taking questions. ) A executive process is
not something that has all the properties of a fll human being, of course.
It is not a homunculus. Rther, it is a process whereby some brain areas
such as those concerned with perception and motivation infuence the
activities of other brain areas such as ones dealing with the planning of
motor output.
Seen this way, flling in is a kind of treating and "preparing" of qualia
to enable them to interact properly with limbic executive structures. Qua
lia may need to be flled in because gaps interfere with te proper work
ing of these executive structures, reducing their efciency and their ability
to select an appropriate response. Like our general who ignores gaps in
data given to him by scouts to avoid making a wrong decision, the con
trol structure also fnds a way to avoid gaps-by flling them in. 1 5
Were i n the limbic system are these control processes? I t might be a
system involving the amygdala and the anterior cingulate gyrus, given
the amygdala's central role in emotion and the anterior cingulate's ap
parent executive role. We know that when tese structures are discon
nected, disorders of "free will" occur, such as akinetic mutism1 6 and alien
hand syndrome. It is not difcult to see how such processes could give
rise to the mythology of a self as an active presence in the brain-a
"ghost in the machine. "
Te viilant sel A vital clue to the neural circuitry underlying qualia
and consciousness comes from to other neurological disorders-pen
duncular hallucinosis and "vigilant coma" or akinetic mutism.
The anterior cingulate and other limbic structures also receive projec
tions from the intralaminar thalamic nuclei ( cells in the thalamus) , which
in turn are driven by clusters of cells in te brain stem ( including the
cholinergic lateral tegmental cells and the pendunculopontine cells ) . Hy-
Do MA RT I A N S S E E RE D 1 I 2 5 3
peractivity of these cells can lead to visual hallucinations ( penduncular
hallucinosis ) , and we also know that schizophrenics have a doubling of
cell number in these very same brain stem nuclei-which may contribute
to their hallucinations.
Conversely, damage to the intralaminar nucleus or to the anterior cin
gulate results in coma vigilance or akinetic mutism. Patients with this
curious disorder are immobile and mute and react sluggishly, if at all, to
painfl stimuli . Yet they are apparently awake and alert, moving their
eyes around and tracking objects. Wen the patient comes out of this
state, he may say, "No words or thoughts would come to my mind. I
j ust didn't want to do or think or say anything. " ( This raises a fascinating
question: Can a brain stripped of all motivation record any memories at
am If so, how much detail does the patient remember/ Does he recall
the neurologist's pinprick/ Or the cassette tape that his girlfriend played
for him1 ) Clearly these brain stem and thalamic circuits play an important
role in consciousness and qualia. But it remains to be seen whether they
merely play a "supportive" role for qualia ( as indeed the liver and heart
do! ) or whether they are an integral part of the circuitry that embodies
qualia and consciousness. Are they analogous to the power supply of a
VCR or T set or to the actual magnetic recording head and the electron
gun in the cathode- ray tube1
Te conceptual sel and the social sel In a sense, our concept of self is
not fndamentally diferent fom any other abstract concept we have
such as "happiness" or "love. " Therefore, a carefl examination of the df
ferent ways in which we use the word "I" in ordinary social discourse can
provide some clues as to what the self is and what its fnction might be.
For instance, it is clear that the abstact self- concept also needs to have
access to the "lower" parts of the system, so that the person can ac
kowledge or claim responsibility for diferent self- related facts: states of
the body, body movements and so on (j ust as you claim to "control"
your thumb when hitching a ride but not your knee when I tap the
tendon with my rubber hammer) . Information in autobiographical mem
ory and information about one's body image need to be accessible to
the self- concept, so that thought and talk about self are possible. In the
normal brain there are specialized pathways that allow such access to
occur, but when one or more of these pathways is damaged, the system
tries to do it anyay, and confabulation results. For instance, in the
denial syndrome discussed in Chapter 7, there is no access channel be
tween information about the lef side of the body and the patient's self-
2 5 4 I P HA N T O MS I N T H E B RA I N
concept. But the self- concept is set up to try automatically to include
that information. The net result of this is anosognosia or denial syn
drome; the self "assumes" that the arm is okay and "flls in" the move
ments of that arm.
One of the attributes of the self- representation system is that the per
son will confabulate to try to cover up defcits in it. The main purposes
of doing this, as we saw in Chapter 7, are to prevent constant indeci
siveness and to confer stability on behavior. But another important fnc
ton may be to support the sort of created or narrative self that the
philosopher Dan Dennett talks about-that we present ourselves as uni
fed in order to achieve social goals and to be understandable to others.
We also present ourselves as acknowledging our past and fture identity,
enabling us to be seen as part of society. Acknowledging and taking
credit or blame for things we did in the past help society ( usually kin
who share our genes ) incorporate us efectively in its plans, thereby en
hancing the surival and perpetuation of our genes. 1 7
I f you doubt the reality of the social self, ask yourself the following
question: Imagine that there is some act you've committed about which
you are extremely embarrassed ( love letters and Polaroid photographs
from an illicit afair) . Assume frther that you now have a fatal illness
and will be dead in two months. If you kow that people rummaging
through your belongings will discover your secrets, will you do your
utmost to cover your tracks? If the answer is yes, the question arises,
Wy bother? Aer all , you know you won't be around, so what does it
matter what people think of you afer you're gone? This simple thought
experiment suggests that the idea of the social self and its reputation is
not just an abstract yarn. On the contrary, it is so deeply ingrained in us
that we want to protect it even afer death. Many a scientist has spent
his enti re life yearning obsessively for posthumous fame-sacrifcing
everything else just to leave a tiny scratchmark on the edifce.
So here is the greatest irony of all : that the self that almost by def
nition is entirely private is to a signifcant extent a social construct-a
story you make up for others. In our discussion on denial , I suggested
tat confabulation and self-deception evolved mainly as by-products of
the need to impose stability, internal consistency and coherence on be
havior. But an added important fnction might stem from the need to
conceal the truth from other people.
The evolutionary biologist Robert Trivers1 8 has proposed the ingen
ious argument that self- deception evolved mainly to allow you to lie with
Do MA RT I A N S S E E RE D ? I 2 5 5
complete conviction, as a car salesman can. Aer all , in many social sit
uations it might be usefl to lie-in a job interiew or during courtship
( "I' m not married") . But the problem is that your limbic system ofen
gives the game away and your facial muscles leak traces of guilt. One way
to prevent this, Trivers suggests, may be to deceive yourself frst. If you
actually believe your lies, there's no danger your face will give you away.
And this need to lie efcienty provided the selection pressure for the
emergence of self-deception.
I don't fnd Trivers's idea convincing as a general theory of self
deception, but there is one particular class of lies for which the argument
carries special force: lying about your abilities or boasting. Through
boasting about your assets you may enhance the likelihood of getting
more dates, thereby disseminating your genes more efectively. The pen
alt you pay for self-deception, of course, is that you may become de
lusional . For example, telling your girlfriend that you're a millionaire is
one thing; actually believing it is a diferent thing altogether, for you may
start spending money you don't have! On the other hand, the advantages
of boasting successflly ( reciprocation of courtship gestures ) may out
weigh the disadvantage of delusion-at least up to a point. Evolutionary
strategies are always a matter of compromsie.
So can we do experiments to prove that self- deception evolved in a so
cial context? Unfortunately, these are not easy ideas to test ( as with all ev
olutionary arguments ) , but again our patients with denial syndrome whose
defenses are grossly amplifed may come to our rescue. Wen questioned
by the physician, the patient denies that he is paralyzed, but would he deny
his paralysis to himsel as well? Would he do it when nobody was watching?
My experiments suggest that he probably would, but I wonder whether
the delusion is amplifed when others are present. Would his skin register a
galvanic response as he confdently asserted that he could arm wrestle?
What if we showed him the word "paralysis"? Even though he denies the
paralysis, would he be disturbed by the word and register a strong GSR
Would a normal child show a skin change when confabulating ( children
are notoriously prone to such behavior) ? Wat if a neurologist were to de
velop anosognosia ( the denial syndrome) as the result of a stroke? Would
he continue to lecture on this topic to his students-blissflly unaware
that he himself was sufering from denial ? Indeed, how do I know that I
am not such a person? It's only through raising questions such as these that
we can begin to approach the greatest scientifc and philosophical riddle of
all-the nature of the self.
2 5 6 I P HA N T O MS I N T H E B RA I N
Our revel now are ended. Tese our actors,
A I foretold you, were all spirits and
Are melted into air, into thin air . .. .
We are such stuf
A dreams are made on,
And our little life
Is rounded with a sleep.
-WILLIA SHSPEAE
During the last three decades, neuroscientists throughout the world
have probed the nerous system in fascinating detail and have learned a
great deal about the laws of mental life and about how these laws emerge
from the brain. The pace of progress has been exhiliarating, but-at the
same time-the fndings make many people uncomfortable. It seems
somehow disconcerting to be told that your life, all your hopes, triumphs
and aspirations simply arise from the activity of neurons in your brain.
But far from being humiliating, this idea is ennobling, I think. Science
cosmology, evolution and especially the brain sciences-is telling us that
we have no privileged position in the universe and that our sense of
having a private nonmaterial soul "watching the world" is really an il
lusion ( as has long been emphasized by Eastern mystical taditions like
Hinduism and Zen Buddhism) . Once you realize that far fom being a
spectator, you are in fact part of the eternal ebb and flow of events in
the cosmos, this realization is very liberating. Ultimately this idea also
allows you to cultivate a certain humility-the essence of all authentic
religious experience. It is not an idea that' s easy to translate into words
but comes very close to that of the cosmologist Paul Davies, who sai d:
Through science, we human beings are able to grasp at least some of
nature's secrets. We have cracked part of the cosmic code. Why this should be,
j ust why Homo sapiens should carry the spark of rationality that provides te
key to te universe, is a deep enigma. We, who are children of the universe
animated stardust-can nevertheless reflect on the nature of that same universe,
even to the extent of glimpsing te rles on which it rns. How we have
become linked into this cosmic dimension is a myster. Yet the linkage cannot
be denied.
Wat does it mean? What is Man that we might be party to such privilege?
I cannot believe that our existence in this universe is a mere quirk of fate, an
accident of history, an incidental blip in the great cosmic drama. Our
involvement is too intimate. The physical species Homo may count for nothing,
but the existence of mind in some organism on some planet in the universe is
surely a fact of fndamental signifcance. Through conscious beings the
D o MA RT I A N s S E E RE n r 1 2 5 7
universe has generated self-awareness. This can be no trivial detail, no minor
by-product of mindless, purposeless forces. We are truly meant to be here.
Ae wer I don't tink brain science alone, despite all its triumphs, will
ever answer that question. But that we can ask the question at all is, to
me, the most puzzling aspect of our existence.
Acknowledgments
My sojourns into neurology during the last ten years have been fasci
nating, fll of all sorts of unexpected twists and turns as each plot un
folded. My companions during this j ourney have been my numerous
students and colleagues, the many books from which I have drawn in
spiration and the images of my old teachers from Cambridge and India
still fresh in my mind. In particular I would like to thank the following
individuals:
First and foremost, my parents-Vilayanur Subramanian and Vilayanur
Meenakshi-who strongly encouraged my early interest in science. ( My
dad bought me a Zeiss research microscope when I was ten years old,
and my mother whetted my appetite for chemistry by giving me Par
tington's textbook of inorganic chemistry and helping me set up a small
lab under our staircase. ) My brother, Vilayanur Rvi, got me interested
in poetry and literature, which have more in common with science than
many people realize. My wife, Diane, has been my collaborator in ex
ploring the brain and helped me think through many of the chapters.
Two of my uncles, Parameswara Hariharan and Alladi Rmakrishnan,
feled my latent interest in vision and brain science (when I was still in
my teens, Dr. Rmakrishman urged me to submit to Nature a paper that
was accepted and published) . I also owe an enormous debt to former
teachers John Pettigrew, Oliver Braddick, Colin Blakemore, David Whit
teridge, Horace Barlow, Fergus Campbell, Richard Gregory, Donald
MacKy, K.V. Thiruvengadam and P. K. Krishnan Kutty, and to various
colleagues, fiends and students, Reid Abraham, Tom Albright, Krish
naswami Alladi , John Allman, Stuart Anstis, Carrie Amel , Rchard At
tiyeh, Elizabeth Bates, Floyd Bloom, Mark Bode, Patrick Cavanagh,
Steve Cobb, Diana Deutsch, Paul Drake, Sally Duensing, Rosetta Ellis,
Martha Farah, David Galin, Sir Aan Gilchrist, Chris Gillin, Rick Grush,
Ishwar Hariharan, Laxmi Hariharan, Steve Hillyer, David Hubel , Mum
taz Jahan, Jonathan Khazi, Julie Kindy, Ranjit Kumar, Margaret Living
stone, Donald MacLeod, Jonathan Miller, Ken Nakayama, Kumpati
Narenda, David Pearlmutter, Dan Plummer, Mike Posner, Alladi Prab
hakar, David Presti, Mark Raichle, Chandramani Rmachandran, William
Rosar, Vivian Roum, Krish Sathian, Nick Schif, Terry Sej nowski , Mar
garet Sereno, Marty Sereno, Aan Snyder, Subramanian Sriram, Arnie
Starr, Gene Stoner, R. Sudarshan, Christopher Tyler, Claude Valenti,
2 5 9
2 6 0 I AC K NOWL E D G ME N T S
T. R. Vidyasagar, Ben Williams and Tony Yang. And special thanks to
Miriam Alaboudi , Eric Altschuler, Gerald Acilla, Roger Bingham, Joe
Bogen, Pat Churchland, Paul Churchland, Francis Crick, Odile Crick,
Hanna Damasio, Tony Damasio, A Flippin, Harold Forney, William
Hirstein, Bela Julesz, Leah Levi, Charlie Robbins, Irvin Rock, Oliver
Sacks, Elsie Schwartz, Nithya Shiva, John Smythies and Christopher
Wills.
I also thank the University of California, San Diego, and the Center
for Brain and Cognition ( Center for Human Information Processing:
CHIP) for providing a superb academic environment; in a recent surey
by the National Research Council, the UCSD campus was ranked num
ber one in the country in neuroscience. The university is also fortunate
in having a symbiotic relationship with many neighbors, including the
Salk Institute, the Scripps Clinic and the Neuroscience Institute, making
La Jolla a mecca for neuroscientists from all over the worl d.
Many of the investigatons I describe in this book were carried out in
La Jolla, but I also conduct studies on patients in India during my annual
visits there. I thank the Institute ofNeurology, Madras General Hospital ,
and the Tata Institute of Fundamental Research in Bangalore for their
hospitality.
Some of the ideas discussed in the book emerged from discussions I
had with students and colleagues-Eric Altschuler (experiments on pla
cebos and somatoparaphrenia ), Roger Bingham ( evolutionary psychol
ogy) , Francis Crick ( consciousness and qualia; the term "zombie" for
the how pathway in the parietal lobe) , Anthony Deutsch ( analogy with
talking pig) , Ilya Farber ( arm movement sensations in a denial patient) ,
Stephen Jay Gould ( alerting me to Freud's idea on scientifc revolutions ) ,
Rchard Gregory ( qualia, flling i n and mirrors ) , Laxmi Hariharan (pe
diatric diagnosis ) , Mark Hauser ( consciousness of bees ) , William Hirstein
(with whom an early draf of Chapter 12 was written) , Ardon Lyon
( blind spots ) , John Pettigrew ( talent as a marker of brain size) , Bob
Rafael ( somatoparaphrenia) , Diane Rogers- Rmachandran ( the mock in
jection experiment) , Alan Snyder ( similarities between Nadia's horses and
those of da Vinci in the section on savant syndrome) and Christopher
Wills (who helped with an early draf of Chapter 5 ) .
I am also gratefl to my agent, John Brockman, president of the
EDGE Foundation, not only for urging me to write this book but also
for doing everything he has to help bridge the "two cultures. " Like the
Earl of Bridgewater, who commissioned many popular science books in
Victorian England, Brockman has been a potent force in the dissemi-
AC K NOWL E D GME N T S I 2 6 1
nation of science in the latter part of this century. Thanks also to Sandra
Blakeslee and Toni Sciarra, who kept goading me to fnish this project
and helped make the book accessible to a wider readership.
Finally, I owe a very important debt to my patients, who ofen sat
through long hours of tedious testing, many of them as intensely curious
about their predicament as I was. I have sometimes learned more from
chatting with them or reading their letters than I have from my medical
colleagues at conferences.
Notes
Chapter 1, The Phantom Wi thi n
1 . I am of course talking about style here, not content. Modesty aside, I doubt
whether any obseration in this book is as important as one of Faraday's dis
coveries, but I do think that all experimental scientists should strive to emulate
his style.
2. Of course, one doesn't want to make a fetish out of low- tech science. My point
is simply that poverty and crude equipment can sometimes, paradoxically, ac
tually serve as a catalyst rather than a handicap, for they force you to be inventive.
There is no denying, though, that innovative technology drives science j ust
as surely as ideas do. The advent of new imaging techniques like PET, fR
and MEG is likely to revolutionize brain science in the next millennium by
allowing us to watch living brains in action, as people engage in various mental
tasks. ( See Posner and Richle, 1 997, and Phelps and Mazziotta, 1 98 1 . )
Unfortunately, there is currently a lot of gee whiz going on ( almost a repeat
of nineteenth-century phrenology) . But if used intelligently, these toys can be
immensely helpfl . The best experiments are ones in which imaging is combined
with clear, testable hypotheses of how the mind actually works. There are many
instances where tracing the flow of events is vital for understanding what is
happening in the brain and we will encounter some examples in this book.
3. This question can be answered more easily using insects, which have specifc
stages, each with a fxed life span. ( For instance, the cicada species Magicicada
septendecim spends seventeen years as an immature nymph and just a few weeks
as an adult! ) Using the metamorphosis hormone ecdysone or an antibody to it
or mutant insects, which lack the gene for the hormone, one could theoretically
manipulate the duration of each stage separately to see how it contributes to the
total life span. For example, would blocking ecdysone allow the caterpillar to
enjoy an indefnitely long life, and conversely would changing it into a butterfy
allow it to enjoy a longer life as a butterfy?
4. Long before the role of deoxyribonucleic acid ( DNA) in heredity was explained
by James Watson and Francis Crick, Fred Grifths proved in 1 928 that when a
chemical substance obtained from a heat-killed bacterium of one species-called
strain S pneumococcus-was injected simultaneously into mice along with an
other strain ( strain R) , the latter actually became "transformed" into strain S!
I t was clear that something was present i n S bacteria that was causing the R
form to become S. Then, in the 1 940s, Oswald Avery, Colin Macleod and Ma
clyn McCarty showed that this reaction is caused by a chemical substance, DNA.
The implication-that DNA contains the genetic code-should have sent shock
waves through the world of biology but caused only a small stir.
5. Historically there have been many diferent ways of studying the brain. One
method, popular with psychologists, is the so-called black box approach: You
systematically vary the input to the system to see how the output changes and
2 6 3
2 6 4 I NO T E S
construct models of what is going on in between. If you think this sounds boring,
it is. Nevertheless, the approach has had some spectacular successes, such as the
discovery of trichromacy as the mechanism of color vision. Researchers found that
all the colors that you can see could be made by simply combining diferent pro
portions of three primary ones-red, green and blue. From this they deduced
that we have only three receptors in the eye, each of which responds maximally
to one wavelength but also reacts to a lesser extent to other wavelengths.
One problem with the black box approach is that, sooner or later, one ends
up with multiple competing models and the only way to discover which one is
correct is to open up the black box-that is, do physiological experiments on
humans and animals. For example, I doubt very much whether anyone could
have fgured out how the digestive system works by simply looking at its output.
Using this strategy alone, no one could have deduced the existence of mastica
tion, peristalsis, saliva, gastric juices, pancreatic enzymes or bile nor realized that
the liver alone has over a dozen fnctions to help assist the digestive process.
Yet a vast majority of psychologists-called fnctionalists-cling to the view that
we can understand mental processes from a strictly computational, behaviorist
or "reverse engineering perspective"-without bothering with the messy stuf
in the head.
Wen dealing with biological systems, understanding structure is crucial to
understanding fnction-a view that is completely antithetical to the fnction
alist or black box approach to brain fnction. For example, consider how our
understanding of the anatomy of the DNA molecule-its double- helical struc
ture-completely transformed our understanding of heredity and genetics, which
until then had remained a black box subject. Indeed, once the double helix was
discovered, it became obvious that the structural logic of this DNA molecule
dictates the fnctional logic of heredity.
6. For over half a centur, modern neuroscience has been on a reductionist path,
breaking things down into ever smaller parts with the hope that understanding all
the little pieces will eventually explain the whole. Unfortunately, many people
think that because reductionism is so ofen usefl in solving problems, it is
therefore also sufcient for solving them, and generations of neuroscientists have
been raised on this dogma. This misapplication of reductionism leads to the per
verse and tenacious belief that somehow reductionism itself will tell us how the
brain works, when what is really needed are attempts to bridge diferent levels of
discourse. The Cambridge physiologist Horace Barlow recently pointed out at a
scientifc meeting that we have spent fve decades studying the cerebral cortex in
excruciating detail, but we still don't have te foggiest idea of how it works or
what it does. He shocked the audience by suggesting that we are all like asexual
Martians visiting earth who spend fi fy years examining the detailed cellular mech
anisms and biochemistry of the testicles without knowing anything at all about sex.
7. The doctine of modularity was carried to its most ludicrous extremes by Franz
Gall, an eighteenth- century psychologist who founded the fashionable pseudo
science of phrenology. One day while giving a lecture, Gall noted that one par
ticular student, who was very bright, had prominent eyeballs. Gall started
thinking, Wy does he have prominent eyeballs? Maybe the frontal lobes have
something to do with intelligence. Maybe they are especially large in this boy,
NO T E S I 2 6 5
pushing his eyeballs forard. On the basis of this tenuous reasoning, Gall em
barked on a series of experiments that involved measuring the bumps and de
pressions on people's skulls. Finding diferences, Gall began to correlate the
shapes with various mental fnctions. Phrenologists soon "discovered" bumps
for such esoteric traits as veneration, cautiousness, sublimity, acquisitiveness and
secretiveness. In an antique shop in Boston, a colleague of mine recently saw a
phrenology bust that depicted a bump for the "Republican spirit"! Phrenology
was still popular in the late nineteenth and early twentieth centuries.
Phrenologists were also interested in how brain size is related to mental ca
pacity, asserting that heavier brains are more intelligent than lighter ones . They
claimed that, on average, the brains of black people are smaller than white peo
ple's and tat women's brains are smaller than men's and argued that the dif
ference "explained" diferences in average intelligence between these groups.
The crowning irony is that when Gall died, people actually weighed his brain
and found that it was a few grams lighter than the average female brai n. ( For
an eloquent description of the pitfalls of phrenology, see Stephen Jay Gould's
Te Mismeasure ofMan. )
8. These two examples were great favorites of the Harard neurologist Norman
Geschwind when he gave lectures to lay audiences.
9. Hints about the role of medial temporal lobe structures, including the hippo
campus, in memory formation go all the way back to the Russian psychiatrist
Sergei Korsakov. Patient H. M. and other amnesics like him have been studied
elegantly by Brenda Milner, Larry Weiskrantz, Elizabeth Warrington and Larr
Squire.
The actual cellular changes that strengthen connections between neurons
have been explored by several researchers, most notably Eric Kandel, Dan Akon,
Gary Lynch and Terry Sejnowski .
1 0. Our ability to engage in numerical computations ( add, subtract, multiply and
divide) seems so efortless that it's easy to j ump to the conclusion that it is "hard
wired. " But, in fact, it became efortless only afer the introduction of two basic
concepts-place value and zero-in India during the third century A. D. These
two notions and the idea of negative numbers and of decimals ( also introduced
in Indi a) laid the foundation of modern mathematics.
It has even been claimed that the brain contains a "number line, " a sort of
graphical, scalar representation of numbers with each point in the graph being
a cluster of neurons signaling a particular numerical value. The abstract mathe
matical concept of a number line goes all the way back to the Persian poet and
mathematician Omar Khayyam, in the ninth century, but is there any evidence
that such a line exists in the brain? When normal people are asked which of two
numbers is larger, it takes them longer to make the decision if the numbers are
closer together than if they are wider apart. In Bill, the number line seems un
afected because he is okay at making crude quantitative estimates-which num
ber is bigger or smaller or why it seems inappropriate to say the dinosaur bones
are sixty million and three years old. But there is a separate mechanism for
numerical computation, for juggling numbers about in your head, and for this
you need the angular gyrus in the lef hemisphere. For a very readable account
of dyscalculias, see Dehaene, 1 997.
2 6 6 I NO T E S
My colleague here at UCSD Dr. Tim Rickard has shown by using fnctional
magnetic resonance imaging ( fR) that the "numerical calculation area" ac
tually lies not entirely in the classical lef angular gyrus itself but slightly in front
of it, but this doesn't afect my main argument and it's only a matter of time
before someone also demonstrates the "number line" using modern imaging
techniques.
Chapter , " Knowi ng Where to Scratch"
l . Throughout this book I use fctitious names for patients. The place, time and
circumstances have also been altered substantially, but the clinical details are
presented as accurately as possible. For more detailed clinical information, the
reader should consult the original scientifc articles.
In one or two instances when I describe a classic syndrome ( such as the
neglect syndrome in Chapter 6) I use several patients to create composites of
the kind used in neurology textbooks in order to emphasize salient aspects of
the disorder, even though no single patient may display all the symptoms and
signs described.
2. Silas Weir Mitchell, 1 872; Sunderland, 1972.
3. Aristotle was an astute obserer of natural phenomena, but i t never occurred to
him that you could do experiments; that you could generate conjectures and
proceed to test them systematically. For instance, he believed that women had
fewer teeth than men; all he needed to do to verif or refte the theory was to
ask a number of men and women to open their mouths so he could count their
teeth. Modern experimental science really began with Galileo. It astonishes me
when I sometimes hear developmental psychologists assert that babies are "born
scientists," because it is perfectly clear to me that even adults are not. If the
experimental method is completely natural to the human mind-as they assert
why did we have to wait so many thousands of years for Galileo and the birth
of the experimental method? Everyone believed that big, heavy objects fall much
faster than light ones, and all it took was a fve- minute experiment to disprove
it. ( In fact, the experimental method is so alien to the human mind that many of
Galileo's colleagues dismissed his experiments on falling bodies even afer seeing
them with their own eyes ! ) And even to this day, three hundred years afer the sci
entifc revolution began, people have great difculty in understanding the need for
a "control experiment" or "double-blind" studies. (A common fallacy is, I got
better afer I took pill A, therefore I got better because I took pill A. )
4. Penfeld and Rasmussen, 1950.
The reason for this peculiar arrangement is unclear and probably lost i n our
phylogenetic past. Martha Farah of the University of Pennsylvania has proposed
a hypothesis that is consistent with my view ( and Merzenich' s) that brain maps
are highly malleable. She points out that in the curled-up fetus, the arms are
usually bent at the elbow with the hands touching the cheek and the legs are
bent with the feet touching the genitals. The repeated coactivation of these body
parts and the synchronous fring of corresponding neurons in the fetus may have
resulted in their being laid down close to each other in the brain. Her idea is
ingenious, but it doesn't explain why in other brain areas (S2 in the cortex) the
NO T E S I 2 6 7
foot ( not just the hand) lies next to the face as wel l . My own bias is to think
that even though the maps are modifable by experience, the basic blueprint for
them is geneti c.
5. The frst clear experimental demonstration of "plasticity" in the central nerous
system was provided by Patrick Wall of the University College, London, 1977,
and by Mike Merzenich, a distinguished neuroscientist at the University of Cal
ifornia in San Francisco, 1984.
The demonstration that sensory input fom the hand can activate the "face
area" of the cortex in adult monkeys comes from Tim Pons and his colleagues,
1 99 1 .
6 . Wen people are pitched from a motorcycle at high speed, one arm is ofen
partially wrenched from the shoulder, producing a kind of naturally occurring
rhizotomy. A the arm is pulled, both the sensory ( dorsal ) and motor ( ventral )
nere roots going fom the arm into the spine are yanked of the spinal cord so
that the arm becomes completely paralyzed and devoid of sensation even though
it remains attached to the body. The question is, How much fnction-if any
can people recover in the arm during rehabilitation? To explore this, physiolo
gists cut the sensory neres going from the arm into the spinal cord in a group
of monkeys. Their goal was to try to reeducate the monkeys to use the arm, and
a great deal of valuable information was obtained fom studying these animals
(Taub et a! . , 1993 ). Eleven years afer this study was done these monkeys became
a cause c{lebre when animal rights activists complained that the experiment was
needlessly cruel . The so- called Silver Spring monkeys were soon sent to the
equivalent of an old age home for primates and, because they were said to be
sufering, scheduled to be killed.
Dr. Pons and his collaborators agreed to the euthanasia but decided frst to
record from their brains to see whether anything had changed. The monkeys
were anesthetized before the recordings were made, so that they would not feel
any pain during the procedure.
7. Rmachandran et a! . , l 992a, b; 1993; 1994; 1996.
Rmachandran, Hirstein and Rogers- Rmachandran, 1 998 .
8. It had been noticed by many previous researchers (Weir Mitchell, 1 871 ) that
stimulating certain trigger points on the stump ofen elicits sensations from miss
ing fngers. William James ( 1 887) once wrote, "A breeze on the stump is felt
as a breeze on the phantom" ( see also an important monograph by Cronholm,
195 1 ) . Unfortunately, neither Penfeld's map nor the results of Pons and his
collaborators were available at the time, and these early obserations were
therefore open to several interpretations. For example, the severed nerves in the
stump would be expected to reinnerate the stump; if they did, that might ex
plain why sensations from this region are referred to the fngers. Even when
points remote from the stump elicited referred sensations, the efect was ofen
attributed to difse connections in a "neuromatrix" ( Melzack, 1 990) . What
was novel about our obserations is that we discovered an actual topographically
organized map on the face and also found that relatively complex sensations
such as "trickling," "metal" and "rubbing" ( as well as warmth, cold and vibra
tion) were referred from the face to the phantom hand in a modality-specifc
manner. Obviously, this cannot be attributed to accidental stimulation of nere
2 6 8 I NO T E S
endings on the stump or to "difse" connections. Our observations imply in
stead that highly precise and organized new connections can be formed in the
adult brain with extreme rapidity, at least in some patients.
Furthermore, we have tried to relate our fndings in a systematic way to
physiological results, especially the "remapping" experiments of Pons et al . ,
199 1 . We have suggested, for example, that the reason we ofen see two clusters
of points-one on the lower face region and a second set near or around the
amputation line-is that the map of the hand on the sensory homunculus in the
cortex and the thalamus is flanked on one side by the face and the other side
by the upper arm, shoulder and axilla. If the sensory input from the face and
from the upper arm above the stump were to "invade" the cortical territory of
the hand, one would expect precisely this sort of clustering of points. This prin
ciple allows one to dissociate proximit of points on the body surface from prox
imity of points in brain maps, an idea that we refer to as the remapping
hypothesis of referred sensations . If the hypothesis is correct, then one would
also expect to see referral from the genitals to the foot afer leg amputation, since
these two body parts are adjacent on the Penfeld map. ( See Rmachandran,
1993b; Aglioti et al . , 1994. ) But one would never see referral fom the face to a
phantom foot or from the genitals to a phantom arm. Aso see note 1 0.
9. Recently David Borsook, Hans Breiter and their colleagues at the Massachusetts
General Hospital ( MGH) have shown that in some patients sensations such as
touch, paintbrush, rubbing and pinpricks are referred (i n a modality-specifc
manner) from the face to the phantom j ust a few hours afer amputation ( Bor
sook et al . , 1998) . This makes it clear that disinhibition or "masking" of pre
existing connections must at least contribute to the efect, although some
sprouting of new connections probably occurs as well .
1 0. If the remapping hypothesis is correct, then cutting the trigeminal nere ( sup
plying half the face) should result in the exact opposite of what we noticed in
Tom. In such a patient, touching the hand should cause sensatons to emerge
in the face ( Rmachandran, 1994) . Stephanie Clark and her colleagues recently
tested this prediction in an elegant and meticulous series of experiments. Their
patent had the trigeminal nere ganglion cut because a tumor had to be re
moved in its vicinity, and two weeks later they found that when the hand was
touched, the patient felt the sensations emerging from the face-even though
the nerves from the face were cut. In her brain, the sensory input from the skin
of the hand had invaded territory vacated by the sensory input from her face.
Intriguingly, in this patient the sensations were felt only on the face-not on
the hand-when the hand was touched. One possibilit is that during the initial
remapping there is a sort of "overshoot"-the new sensory input from hand
skin to the face area of the cortex is actually stronger than the original connec
tions and as a result the sensations are felt predominanty on the face, masking
the weaker hand sensations .
1 1 . Caccace et al . , 1994.
1 2. Referred sensations provide an opportunity for studying changing corical maps
in the adult human brain, but the question remains, What is the function of
remapping? Is it an epiphenomenon-residual plasticity lef over fom infancy
or does it continue to have a fnction in the adult brain? For example, would
No T E S I 2 6 9
the larger cortical area devoted to the face afer arm amputation lead to improved
sensory discrimination-measured by two-point discrimination-or tactile hy
peracuity on the face? Would such improvement, if it occurred at all, be seen
only afer the abnormal referred sensations have disappeared, or would it be seen
immediately? Such experiments would settle, once and for all, the question of
whether or not remapping is actually usefl for the organism.
Chapter 3, Chasi ng the Phantom
1 . Mary An Simmel ( 1962) originally claimed that very young children do not
experience phantoms afer amputation and that children born with limbs missing
also do not experience phantoms, but this idea has been challenged by others.
(A lovely series of studies was conducted recently by Ron Melzack and his col
leagues at McGill University; Melzack et a! . , 1997. )
2. The importance of frontal brain structures in planning and executing movements
has been discussed in fascinating detail by Fuster, 1980; G. Goldberg, 1987;
Pribram et a! . , 1967; Shallice, 1988; E. Goldberg et a! . , 1987; Benson, 1997;
and Goldman- Rkic, 1987.
3. Next I asked Philip to move his index fnger and thumb of both hands and
simultaneously look in the mirror but this tme the phantom thumb and fnger
remained paralyzed; they were not revived. This is an important observation, for
it rules out the possi bility that the previous result was simply a confabulation in
response to the peculiar circumstances surrounding our experiment. If it was
confabulatory, why is it he was able to move his whole hand and elbow but not
individual fngers?
Our experiments of the use of mirrors to revive movements in phantom limbs
were originally reported in Nature and Proceedings ofthe Royal Societ ofLondon
B ( Rmachandran, Rogers- Rmachandran and Cobb, 1 995; Rmachandran and
Rogers-Rmachandran, 1 996a and b) .
4. The notion of learned paralysis i s provocative and may have implications beyond
treating paralyzed phantom limbs.
As an example, take writer's cramp ( focal dystonia) . The patient can wiggle
his fngers, scratch his nose or tie his necktie with no problem, but all of a sudden
his hand is incapable of writing. Theories about what causes the condition range
all the way from muscle cramps to a form of "hysterical paralysis . " But could it
be another example of learned paralysis? If so, would as simple a trick as using
a mirror help these patients as well ?
The same argument might also apply to other syndromes that straddle the
boundary between overt paralysis and a reluctance to move a limb-a sort of
mental block. Ideomotor apraxia-the inability to perform skilled movements
on command ( the patient can wrte a letter independently but not pretend to
wave good- bye or to stir a cup of tea when asked to do so )-is certainly not
"learned" in the sense that a paralyzed phantom might be learned. But could
it also be based on some sort of temporary neural inhibition or block? Ad if
so, can visual feedback help overcome the block?
Finally, there is Parkinson's disease, which causes rigidity, tremor and poverty
of movements ( akinesia) involving the entire body including the face (a masklike
2 7 0 I NO T E S
expression) . Early in this disease, the rigidity and tremor afect only one hand,
so, in principle, one could try the mirror technique, using the reflection of the
good hand for feedback. Since it is known that visual feedback can indeed influ
ence Parkinson's disease ( for example, the patient ordinarily can't walk, but if
the foor has alternate black and white tiles, he can) , perhaps the mirror tech
nique will help them as wel l .
5. Aother fascinating obseration on Mary deseres comment. In the previous ten
years she had never felt a phantom elbow or wrist; her phantom fngers were
dangling from the stump above the elbow, but upon lookng into the mirror,
she gasped, exclaiming that she could now actually feel-not merely see-her
long-lost el bow and wrist. This raises the fascinating possibility that even for an
arm lost a long time ago, a dormant ghost still survives somewhere in the brain
and can be resurrected instantly by the visual input. If so, this technique may
have application for amputees contemplating the use of a prosthetic arm or leg,
since they ofen feel the need to animate the prosthesis with a phantom and
complain that the prosthesis feels "unnatural" once the phantom is gone.
Perhaps transsexual women contemplating becoming men can try out a dress
rehearsal and revive a dormant brain image of a penis ( assuming something like
this even exists in a female brai n) using a trick similar to the mirror device used
on Mary.
6. Forked phantoms were described by Kallio, 1950. Multiple phantoms in a child
were described by La Croix et a! . , 1992.
7. These are highly speculatve explanations, although at least some of them can
be tested with the help of imaging procedures such as MEG and fnctional
magnetic resonance imaging ( fR) . These devices allow us to see diferent parts
of the living brain light up as a patient performs diferent tasks. ( In the child
with three separate phantom feet, would tere be three separate representations
in her brain that could be visualized using these techniques? )
8. Our phantom nose efect ( Rmachandran and Hirstein, 1 997) i s quite similar
to one reported by Lackner ( 1988) except that the underlying principle is dif
ferent. In Lackner's experiment, the subject sits blindfolded at a table, with his
arm fexed at the el bow, holding the tip of his own nose. If the experimenter
now applies a vibrator to the tendon of the biceps, the subject feels not only
that his arm is extended-because of spurious signals from muscle stretch re
ceptors-but also that his nose has actually lengthened. Lackner invokes
Helmholtzian "unconscious inference" as an explanation for this efect (I am
holding my nose; my arm is extended; therefore, my nose must be long) . The
illusion we have described, on the other hand, does not require a vibrator and
seems to depend entirely on a Bayesian principle-the sheer statistical improb
ability of two tactile sequences being identical . ( Indeed, our illusion cannot be
produced if the subj ect simply holds the accomplice's nose. ) Not all subjects
experience this efect, but that it happens at all-that a lifetime's evidence
concerning your nose can be negated by just a few seconds of intermittent
tactile input-is astonishing.
Our GSR experiments are mentioned in Rmachandran and Hirstein, 1997
and Rmachandran, Hirstein and Rogers- Rmachandran, 1998.
9. Botinik and Cohen, 1 998.
NO T E S I 2 7 1
Chapter 4, The Zombi e i n the Brai n
l. Milner and Goodale, 1995.
2. For lively introductons t o the study of vision, see Gregor, 1 966; Hochberg,
1964; Crick, 1993; Marr, 1 98 1 ; and Rock, 1985.
3. Another line of evidence i s the exact converse: Your perception can remain con
stant even though the image changes. For example, every time you swivel your
eyeballs while obsering everyday scenes, the image on each retina races across
your photoreceptors at tremendous speed-much like the blur you see when
you pan your video camera across the room. But when you move your eyes
around, you don't see objects darting all over the place or the world zooming
past you at warp speed. The world seems perfectly stable-it doesn't seem to
move around even though the image is moving on your retina. The reason is
that your brain's visual centers have been "tipped of' in advance by motor
centers controlling your eye movements. Each time a motor area sends a com
mand to your eyeball muscles, causing them to move, it also sends a command
to visual centers saying, "Ignore this motion; it's not real . " Of course, all this
takes place without conscious thought. The computation is built into the visual
modules of your brain to prevent you from being distracted by spurious motion
signals each time you glance around the room.
4. Ramachandran, 1988a and b, 1989a and b; Klefner and Rmachandran, 1992.
Ask a friend to hold the page (with the pictures of shaded disks ) upright while you
bend down and look at the page with your head hanging upside down between
your legs. The page will then be upside down with respect to your retina. You will
fnd once again that the eggs and cavities have switched places ( Ramachandran,
1988a) . This is quite astonishing because it implies that in judging shape from
shading, the brain now assumes that the sun is shining from below: That is, your
brain is making the assumption that the sun is stuck to your head when you
rotate your head! Even though the world still looks upright because of correction
from the balance organ in the ear, your visual system is unable to use this knowl
edge to interpret shape from shading ( Ramachandran, 1988b) .
Why does the visual system incorporate such a foolish assumption? Why not
correct for head tilt when interpreting the shaded images? The answer is that as
we walk around the world, most of the time we keep our heads upright, not
tilted or upside down. So the visual system can take advantage of this to avoid
the additional computational burden of sending the vestibular information all
the way back to the shape from shading module. You can get away with this
"shortcut" because, statistically speaking, your head is usually upright. Evolution
doesn't strive for perfection; your genes will get passed down on to your of
spring so long as you surive long enough to leave babies.
5 . The architecture of this brain region has been studied in fascinating detail by
David Hubel and Torsten Weisel at Harard University; their research culmi
nated in a Nobel Prize. During the two decades 1960-1980 more was learned
about the visual pathways as a result of their work than during the preceding
two hundred years, and they are rightly regarded as the founding fathers of
modern visual science.
2 7 2 I NO T E S
6. The evidence that these extrastriate cortical areas are exquisitely specialized for
diferent fnctions comes mainly from six physiologists-Semir Zek, John Al
man, John Kas and David Van Essen, Margaret Livingstone and David Hubel .
These researchers frst mapped out these cortical areas systematically in monkeys
and recorded from individual nere cells; it quickly became clear that the cells
had very diferent properties. For example, any given cell in the area called MT,
the middle temporal area, will respond best to targets in the visual feld moving
in one particular direction but not other directions, but the cell isn't particularly
fssy about what color or shape te target is. Conversely, cells in an area called
V4 (in the temporal lobes) are very sensitive to color but don't care much about
direction of motion. These physiological experiments strongly hint that these
two areas are specialized for extracting diferent aspects of visual information
motion and color. But overall, the physiological evidence is still a bit messy, and
the most compelling evidence for this division of labor comes, once again, from
patients in whom one of these two areas has been selectively damaged.
A description of the celebrated case of the motion blind patient can be found
in Zihl, von Cramon and Mai , 1983.
7. For a description of the original blindsight syndrome, see Weiskrantz, 1986. For
an up-to-date discussion of the controversies surrounding blindsight see Weis
krantz, 1997.
8. For a very stimulating account of many aspects of cognitive science, see Dennett,
1 99 1 . The book also has a brief account of "flling in. "
9. See especially the elegant work of William Newsome, Nikos Logotethis, John
Maunsell , Ted DeYoe, and Margaret Livingstone and David Hubel .
1 0. Aglioti , DeSouza and Goodale, 1 995.
1 1 . Here and elsewhere, when I say that the self i s an "illusion," I simply mean that
there is probably no single entity corresponding to it in the brai n. But in truth
we know so little about the brain that it is best to keep an open mind. I see at
least two possibilities ( see Chapter 1 2) . First, when we achieve a more mature
understanding of the diferent aspects of our mental life and the neural processes
that mediate them, the word "self" may disappear from our vocabulary. ( For
instance, now that we understand DNA, the Krebs cycle and other biochemical
mechanisms that characterize living things, people no longer worry about the
question "What is life? ") Second, the self may indeed be a usefl biological
construct based on specifc brain mechanisms-a sort of organizing principle that
allows us to fnction more efectively by imposing coherence, continuity and
stability on the personality. Indeed many authors, including Oliver Sacks, have
spoken eloquently of the remarkable endurance of self-whether in health or
disease-amid the vicissitudes of life.
l. For an excellent biography of Thurber, see Kinney, 1995. This book also has a
bibliography of Thurber's works.
2. Bonnet, 1 760.
NO T E S I 2 7 3
3. My blind-spot experiments were originally described in Scientic American
( 1992) . For the claim that genuine completion does not occur in scotomas, see
Sergent, 1988. For the demonstration that it does occur, see Rmachandran,
1993b, and Rmachandran and Gregory, 1991 .
4. The famous Victorian physicist Sir David Brewster was s o impressed by this
flling-in phenomenon that he concluded, as Lord Nelson did for phantom
limbs, that it was proof for the existence of God. In 1 832 he wrote, "We should
expect, whether we use one eye or both eyes, to see a black or dark spot on
every landscape within ffeen degrees of the point which most particularly at
tracts our notice. The Divine Afcer, however, has not lef his work thus im
perfect . . . the spot, in place of being black, has always the same color as the
ground. " Curiously, Sir David was apparently not troubled by the question of
why the Divine Afcer would have created an imperfect eye to begin with.
5 . In modern terminology, "flling in" is a convenient phrase that some scientists
use when referring to this completion phenomenon-the tendency to see the
same color in the blind region as in the surround or background. But we must
be carefl not to fall into the trap of assuming that the brain recreates a pixel
by-pixel rendering of the visual image in this region, for that would defeat the
whole purpose of vision. There is, afer all, no homunculus-that little man
inside the brain-watching an internal mental screen who would beneft from
such flling in. ( For instance, you don' t say the brain "flls in" the tiny spaces
between retinal receptors . ) I like to use the term simply as a shorthand to indicate
that the person quite literally sees something in a region of visual space from
which no light or other information is reaching the eye. The advantage of this
"theory-neutral" defnition is that it keeps open a door to doing experiments,
allowing us to search for neural mechanisms of vision and perception.
6. Jerome Lettvin of Rutgers University ( 1976) performed this clever experiment.
The explanation of this efect-as having something to do with stereoscopic
vision-is my own ( see note 7) .
I have also seen the same efect i n patients with scotomas of cortical origin:
the lining up of horizontally misaligned vertcal bars ( Ramachandran, 1993b) .
7. Since you look at the world from two slightly diferent vantage points correspond
ing to the two eyes, there are diferences between the retinal images of the two
eyes that are proportional to the relative distances of objects in the worl d. The
brain therefore compares the two images, measures the horizontal separations and
"fses" the images so that you see a single unifed picture of the world-not two.
In other words, you already have in place in your visual pathway a neural mecha
nism for "lining up" horizontally separated vertical edges. But since your eyes are
separated hori zontally and not vertically, you have no such mechanism for lining
up horizontal edges that are vertically misaligned. In my view you are tapping the
very same mechanism when you are trying to deal with edges that are "mis
aligned" across a blind spot. This would explain why the vertical lines get "fsed"
into a continuous line, whereas your visual system fails to cope with the horizontal
lines. The fact that you are using only one eye in the blind spot experiment doesn't
negate this argument because you may ver well be unconsciously deploying the
same neural circuits even when you close the other eye.
2 7 4 I No T E S
8 . These exercises are amusing for those of us with normal vision and natural blind
spots, but what would life be like with a damaged retina, so that you developed
an artifcial blind spot? Would the brain compensate by "flling in" the blind
regions of the visual feld? Or might there be remapping; do adjacent parts of
the visual feld now map onto the region that's no longer getting any input?
Wat would be the consequence of the remapping? Would the patient ex
perience double vision? Imagine I hold up a pencil next to his scotoma. He's
lookng straight ahead and obviously sees the original pencil, but since it now
also stimulates the patch of cortex corresponding to the scotoma, he should see
a second, "ghost" image of the pencil in his scotoma. He should therefore see
two pencils instead of one, just as Tom felt sensations on both his face and hand.
To explore this possibility, we tested several patients who had a hole in one
retina, but not one person saw double. My immediate conclusion was, Oh, well ,
who knows, maybe vision is diferent. And then suddenly I realized that although
one eye has a scotoma, the patient has to eyes, and the corresponding patch
in the other eye is still sending information to the primary visual cortex. The
cells are stimulated by the good eye, so perhaps remapping does not occur. To
get the double vision efect, you'd have to remove the good eye.
A few months later I saw a patient who had a scotoma in the lower lef quadrant
of her lef eye and had completely lost her right eye. Wen I presented spots of
light in the normal visual feld, she did not see a doubling, but to my amazement
ifl jickered the spot at about ten hertz ( ten cycles per second) , she saw two spots
one where it actually was and a ghostlike double inside her scotoma.
I can't yet explain why Joan only sees double when the stimulus is fickering.
She ofen has the experience while driving, amid sunlight, foliage and constant
movement. It may be that a fickering stimulus preferentially activates the mag
nocellular pathway-a visual system involved in motion perception-and that
this pathway is more prone to remapping than others.
9. Rmachandran, 1992.
1 0. Sergent, 1988.
1 1 . I subsequently verifed that this happened every time I tested Josh and also
obsered the same phenomenon in one of Dr. Hanna Damasio's patients ( R
machandran, 1 993b) .
12. A early draf of this chapter, based on my clinical notes, was written in collab
oration with Christopher Wills, but the text has been completely rewritten for
this work. I have, however, retained one or two of his more colorfl metaphors,
including this one about the fn house.
1 3 . Kosslyn, 1 996; Farah, 1991 .
14. Evidence for this comes from the fact that even though most Charles Bonnet pa
tients don't remember having seen the same images before (perhaps they are from
the distant past) , in some patients the images are either objects that they saw j ust a
few seconds or minutes ago or things that might be logically associated with ob
jects near the scotoma. For example, Larry ofen saw multiple copies of his own
shoe ( one that he had seen a few seconds earlier) and had difculty reaching out
for the "real " one. Others have told me that when they're driving a car, a vivid
scene that they had passed several minutes ago suddenly reemerges in the scotoma.
Thus the Charles Bonnet syndrome blends into another well-known visual
NO T E S I 2 7 5
syndrome, called palinopsia (which neurologists ofen encounter afer a patient's
head injury or brain disease that has damaged the visual pathways) , in which
patients report that when an object moves, it leaves behind multiple copies of
itself Although ordinarily conceived of as a motion detection problem, palinop
sia may have more in common with Charles Bonnet syndrome than ophthal
mologists realize. The deeper implication of both syndromes is that we may all
be subconsciously rehearsing recently encountered visual images for minutes or
even hours ( afer they have been seen) and this rernning emerges to the surface,
becoming more obviously manifest, when there is no real input coming from
the retina ( as can happen afer injury to the visual pathway) .
Humphrey ( 1992) has also suggested the idea that the deaferentation i s some
how critical for visual hallucinations and that such hallucinations may be based on
back-projections. Any claim to novelty by me derives from the obseration that in
both my patients the hallucination was confned entirely to the inside of the sco
toma, never spilling across the margins. This obseration gave me the clue that this
phenomenon can only be explained by back-proj ections ( since back-projections
are topographically organized) and that no other hypothesis is viable.
1 5 . If this theory is correct, why don't we all hallucinate when we close our eyes or
walk into a darkoom? Aer all, there's no visual input coming in. For one thing,
when people are completely deprived of sensory input ( as when they float in a sen
sory isolation tank) , they do indeed hallucinate. The more important reason, how
ever, is that even when you close your eyes, the neurons in your retina and the early
stages of your visual pathways are continuously sending baseline activity (we call it
spontaneous activity) to higher centers, and this might sufce to veto the top
down induced activity. But when the pathways ( retina, primary visual cortex and
optic nere) are damaged or lost, producing a scotoma, even this little spontane
ous activity is gone, thereby permitting the internal images-the hallucinations
to emerge. Indeed, one could argue that spontaneous activity in the early visual
pathways, which has always been a puzzle, evolved mainly to provide such a "null"
signal . The strongest evidence for this comes from our two patients in whom the
hallucinations were sharply confned within the margins of their scotoma.
1 6. This somewhat radical view of perception, I suggest, holds mainly for recogniz
ing specifc objects in the ventral stream-a shoe, a kettle a fiend's face-where
it makes good computational sense to use your high-level semantic knowledge
base to help resolve ambiguity. Indeed, it could hardly be otherwise, given how
underconstrained this aspect of perception-object perception-really is.
For the other more "primitive" or "early" visual processes-such as motion,
stereopsis and color-such interactions may occur on a more limited scale since
you can get away with just using generic kowledge of surfaces, contours, tex
tures, and so on, which can be incorporated into the neural architecture of early
vision ( as emphasized by David Marr, although Marr did not make the particular
distinction that I am making here) . Yet even with these low-level visual modules,
the evidence suggests that the interactions across modules and with "high-level"
knowledge are much greater than generally assumed ( see Churchland, Rma
chandran and Sej nowsk. , 1 994) .
The general rule seems t o be that interactions occur whenever i t would be
usefl for them to occur and do not ( and cannot) occur when it isn' t. Discov-
2 7 6 I NO T E S
ering which interactions are weak and which are strong is one of the goals of
visual psychophysics and neuroscience.
Chapter 6, Through the Looki ng Gl ass
l . For descriptions of neglect, see Critchley, 1 966; Brain, 1 941 ; Halligan and Mar
shall, 1994.
2. No one has described the selective fnction of consciousness more eloquently than
the eminent psychologist William James ( 1 890) in his famous essay "The Stream
of Thought. " He wrote, "We see that the mind is at every stage a theatre of si
multaneous possibiliti es. Consciousness consists in the comparison of these with
each other, the selection of some, and the suppression of the rest by the reinforcing
and inhibiting agency of attention. The highest and most elaborated mental prod
ucts are fltered from the data chosen by the faculty next beneath, out of the mass
ofered by the faculty below that, which mass in turn was sifed from a still larger
amount of yet simpler material , and so on. The mind, in short, works on the data
it receives very much as a sculptor works on his block of stone. In a sense the statue
stood there from eternity. But there were a thousand diferent ones beside it, and
the sculptor alone is to thank for having extricated this one from the rest. We may,
if we like, by our reasonings unwind things back to that black and jointless conti
nuity of space and moving clouds of swarming atoms which science calls the only
real worl d. But all the while the world we feel and live in will be that which our an
cestors and we, by slowly cumulative strokes of choice, have extricated out of this,
like sculptors, by simply rej ecting certain portons of the given stuf. Other sculp
tors, other statues, from the same stone! Other minds, other worlds from the same
monotonous and inexpressive chaos ! My world is but one in a million alike em
bedded, alike real to those who may abstract them. How diferent must be the
world in the consciousness of ant, cuttlefsh or crab! "
3. This positive feedback loop involved i n orienting has been described by Heilman,
199 1 .
4. Marshall and Halligan, 1988.
5 . Sacks, 1985.
6. Gregory, 1997.
7. What would happen if I were to throw a brick at you from the backseat so that
you saw the brick coming at you in the mirror? Would you duck forard ( as
you shoul d), or would you be fooled by the expanding image in the mirror and
duck backward? Perhaps the intellectual correction for the mirror reflection, de
ducing accurately where the real object is located, is performed by the conscious
what pathway ( obj ect pathway) in the temporal lobes, whereas ducking to avoid
a missile is done by the how pathway ( spatial stream) in the parietal lobe. If so,
you might get confsed and duck incorrectly-it's your zombie that's ducking!
8. Edoardo Bisiach added a brilliant twist to this line- bisection test that suggests
that this interpretation can't be the whole story, although it's a reasonable frst
pass explanation. Instead of having the patient bisect a predrawn horzontal line,
he simply gave him a sheet of paper with a tiny vertical line in te middle and
said, "Pretend that this vertical mark is the bisector of a horizontal line and draw
NO T E S I 2 7 7
the horizontal line. " The patient confdently drew the line, but once again the
portion of the line on the right side was about half the size of the portion on
the lef. This suggests that more than simple inattention is going on. Bisiach
argues that the whole representation of space is squished to enlarge the healthy
right visual feld and shrink the lef. So the patient has to make the lef side of
the line longer than the right to make them appear equal to his own eyes.
9. The good news is that many patients with neglect syndrome-caused by damage
to the right parietal lobe-recover spontaneously in a few weeks. This is impor
tant, for it implies that many of the neurological syndromes that we've come to
regard as permanent-involving destroyed neural tissue-may in fact be "fnc
tional defcits, " involving a temporary imbalance of transmitters. The popular
analogy between brains and digital computers is highly misleadi ng, but in this
particular instance I am tempted to use it. A fnctional defi cit is akin to a sof
ware malfnction, a bug in a program rather than a problem with the hardware.
If so, there may be hope yet for the millions of people who sufer from disorders
that have traditionally been deemed "incurable" because up to now we have not
known how to debug their brain's sofare.
To illustrate this more directly, let me mention another patient, who, as a
result of damage to parts of his lef hemisphere, had a striking problem called
dyscalculia. Like many patients with this syndrome, he was intelligent, articulate
and lucid in most respects but when it came to arithmetic he was hopelessly
inept. He could discuss the weather, what happened in the hospital that day and
who had visited him. Ad yet if you asked him to subtract 7 from 1 00, he was
stymied. But surprisingly, he didn't merely fail to solve the arithmetic problem.
My student Eric Altschuler and I noticed that every time he even attempted to
do so, he confdently produced incomprehensible gibberish-what Lewis Carroll
would call j abberocky-and he seemed unaware that it was gibberish. The
"words" were flly formed but devoid of any meaning-the sort of thing you
see in language disorders such as Wernicke's aphasia (i ndeed even the words
were largely neologisms) . It was as if the mere confrontation with a math prob
lem caused him to insert a "language floppy disk" with a bug in it.
Why does he produce gibberish instead of remaining silent? We are so used
to thinking about autonomous brain modules-one for math, one for language,
one for faces-that we forget the complexity and magnitude of the interactions
among the modules. His condition, in particular, makes sense only if you assume
that the very deployment of a module depends on the current demands placed
on the organism. The ability to sequence bits of information rapidly is a vital
part of mathematical operations as well as the generation of language. Perhaps
his brain has a "sequencing bug. " There may be a requirement of a certain
special type of sequencing that is common to both math and language that is
deranged. He can carry on ordinary conversation because he has so many more
clues-so many backup options-to go by that he doesn't need the sequencing
mechanism in fll gear. But when presented with a math problem, he is forced
to rely on it to a much larger extent and is therefore thrown of completely.
Needless to say, all this is pure speculation, but it provides food for thought.
1 0. Some sort of conversation between the what system in the temporal lobe and
the how pathway in the parietal lobe must obviously occur in normal people,
2 7 8 I NO T E S
and this communication is perhaps compromised in patients with the looking
glass syndrome. Released fom the influence of the what pathway, the zombie
reaches straight into the mirror.
1 1 . Some patients with right parietal disease actually deny that their lef arm belongs
to them-a disorder called somatoparaphrenia; we consider such patients in
Chapter 7. If you grab the patient's lifeless lef arm, raise it and move it into
the patient's right visual feld, he will insist that the arm belongs to you, the
physician, or to his mother, brother or spouse. The frst time I saw a patient
with this disorder, I remember saying to myself, "This must be the strangest
phenomenon in all of neurology-if not in all of science! " How could a perfectly
sane, intelligent person assert that his arm belongs to his mother?
Robert Rfael, Eric Altschuler and I recently tested two patients with this
disorder and found that when they looked at their lef arm in a mirror ( placed
on the right to elicit the lookng glass syndrome), they suddenly started agreeing
that it was indeed their arm! Could a mirror "cure" this disorder?
Chapter 7, The Sound of One Hand Cl appi ng
l . This may seem harsh, but it's frustrating for the physical therapist to begin re
habilitating patients when they're in denial, so overcoming the delusion is of
great practical importance in the clinic.
2. For descriptions of anosognosia see Critchley, 1966; Cuttng, 1978; Damasio,
1 994; Edelman, 1989; Galin, 1992; Levine, 1 990; McGlynn and Schacter, 1989;
Feinberg and Farah, 1997.
3. The distinguished evolutionary psychologist Robert Trivers at the University of
California in Santa Cruz has proposed a clever explanation for the evolution of
self-deception ( Trivers, 1985 ) . According to Trivers, there are many occasions
in daily life when we need to lie-say, during a tax audit or an adulterous afair
or in an efort to protect someone's feelings. Other research has shown that liars,
unless they are very practiced, almost always give the game away by producing
an unnatural smile, a slightly flawed expression or a false tone of voice that others
can detect ( Ekman, 1992) . The reason is that the limbic system ( i nvoluntary,
prone to truth telling) controls spontaneous expressions, whereas the cortex ( re
sponsible for voluntar control, also the location where the l i es are concocted)
controls the facial expressions displayed when we are fbbing. Consequently,
when we lie with a smile, it's a fake smile, and even if we try to keep a straight
face, the limbic system invariably leaks traces of deceit.
There is a solution to this problem, argues Trivers. To lie efectively to another
person, all you have to do is frst lie to yourself. If you believe it's true, your ex
pressions will be genuine, without a trace of guile. So by adopting this strategy,
you can come up with some very convincing lies-and sell a lot of snake oil .
But it seems to me there is an internal contradiction in this scenario. Suppose
you' re a chimp who has hidden some bananas under a tree branch. Along comes
the alpha male chimp, who knows you have bananas and demands you give them
to him. Wat do you do? You lie to your superior and say that the bananas are
across the river, but you also run the risk of his detecting your lie by the expression
on your face. So then what do you do? According to Trivers, you adopt the simple
NO T E S I 2 7 9
device of frst convincing yourself that the bananas really are on the other side of the
river, and you say that to the alpha male, who is fooled, and you are of the hook.
But there's a problem. What if you later got hungry and went looking for the ba
nanas? Since you now believe that the food is across the river, that's where you'd
go look for it. In other words, the strategy proposed by Trivers defeats the whole
purpose of lying, for the very defnition of a lie is that you must contnue to have
access to the truth-otherwise there'd be no point to the evolutionar strategy.
One escape from this dilemma would be to suggest that a "belief" is not
necessarily a unitary thing. Perhaps self- deception is mainly a fnction of the lef
hemisphere-as it tries to communicate its kowledge to others-whereas the
right hemisphere continues to "know" the truth. One way to approach this
experimentally would be to obtain galvanic skin responses in anosognosics and,
indeed, in normal people ( for example, children) when they are confabulating.
When a normal person generates a false memory-or when a child confabu
lates-would he/she nevertheless register a strong galvanic skin response ( as he
would if he were lying) ?
Finally, there i s another type of lie for which Trivers's argument may indeed
be valid, and that concerns lying about one's own abilities-boasting. Of course,
a false belief about your abilities can also get you into trouble ( "I am a big
strong fellow, not puny and weak") if it leads you to strive for unrealistic goals.
But this disadvantage may be outweighed in many instances by the fact that a
convincing boaster may get the best dates on Saturday night and may therefore
disseminate his genes more widely and more frequently so that the "successfl
boasting through self-deception" genes quickly become part of the gene pool .
One prediction for this would be that men should be more prone to both boast
ing and self-deception than women. To my knowledge this prediction has never
been tested in a systematic way, although various colleagues assure me that it is
true. Women, on the other hand, should be better at detecting lies since they
have a great deal more at stake-an arduous nine- month pregnancy, a risky labor
and a long period of caring for a child whose "maternity" is in no doubt.
4. Kinsbourne, 1989; Bogen, 1 975; and Galin, 1976, have all warned us repeatedly
of the dangers of "dichotomania," of ascribing cognitive fnctions entirely to
one hemisphere versus the other. We must bear in mind that the specialization
in most instances is likely to be relative rather than absolute and that the brain
has a front and a back and a top and a bottom, and not j ust lef and right. To
make matters worse, an elaborate pop culture and countless self-help manuals
are based on the notion of hemispheric specialization. A Robert Ornstein
( 1997) has noted, "It's a cliche in general advice to managers, bankers and
artists, it's in cartoons. It's an advertisement. United Arlines ofers reasons to
fly both sides of you coast to coast. The music for one side and the good value
for the other. The Saab automobile company ofered their Turbo charged sedan
as 'a car for both sides of your brain. ' A fiend of mine, unable to remember a
name, excused this by describing herself as a 'right atmosphere sort of person. ' "
But the existence of such a pop culture shouldn't cloud the main issue-the
notion that two hemispheres may indeed be specialized for diferent fnctions.
The tendency to ascribe mysterious powers to the right hemisphere isn't new-it
goes all the way back to the nineteenth-century French neurologist Charles
Brown-Sequard, who started a fashionable right hemisphere aerobics movement.
2 8 0 I NO T E S
For an up- to-date review of ideas on hemispheric specialization, see Springer
and Deutsch, 1 998.
5 . Much of our knowledge of hemispheric specialization comes fom the ground
breaking work of Gazzaniga, Bogen and Sperry, 1 962, whose research on split
brain patients is well known. When the corpus callosum bridging the two hem
ispheres is cut, the cognitive capacities of each hemisphere can be studied sep
arately in the laboratory.
What I'm calling "the general " is not unlike what Gazzaniga, 1 992, calls
"the interpreter" in the lef hemisphere. However, Gazzaniga does not consider
the evolutionar origin or biological rationale for having an interpreter ( as I
attempt to do here) , nor does he postulate an antagonistic mechanism in the
right hemisphere.
Ideas on hemispheric specialization similar to mine have also been proposed
by Kinsbourne, 1989, not to explain anosognosia, but to explain laterality efects
seen in depression following stroke. Athough he does not discuss Freudian de
fenses or "paradigm shifs, " he has made the ingenious proposal that the lef
hemisphere may be needed for maintaining ongoing behavior, whereas right
hemisphere activation may be required for interrupting behavior and producing
an orienting response.
6. I would like to emphasize that the specifc theor of hemispheric specialization
that I am proposing certainly doesn't explain al forms of anosognosia. For ex
ample, the anosognosia of Wernicke's aphasics probably arises because the very
part of the brain that would ordinarily represent beliefs about language is itself
damaged. Aton's syndrome ( denial of cortical blindness) , on the other hand,
may require the simultaneous presence of a right hemisphere lesion. (I have seen
a single "two-lesion" case like this, with Dr. Leah Levi, but additional research
is needed to settle the matter. ) Would a Wernicke's aphasic become more aware
of his defcit if his ear were irrigated with cold water?
7. Ramachandran, 1 994, 1 995a, 1 996.
8. We are still a long way from understanding the neural basis of such delusions,
but the important recent work of Graziano, Yap and Gross, 1 994, may be rel
evant. They found single neurons in the monkey supplementary motor area that
had visual receptive felds "superimposed" on somatosensory felds of the mon
key's hand. Curiously, when the monkey moved its hand, the visual receptive
feld moved with the hand, but eye movements had no efect on the receptive
feld. These hand -centered visual receptive felds ( "monkey see, monkey do cells")
may provide a neural substrate for the kinds of delusions I see in my patients.
9. The notion that there is a mechanism in the right hemisphere not only for
detecting and orienting to discrepancies of body image ( as suggested by our
virtual reality box and by Ray Dolan and Chris Frith's experiment) but also for
other kinds of anomalies receives support fom three other studies that have been
reported in the literature. First, it has been known for some time that patients
with lef hemisphere damage tend to be more depressed and pessimistic than
those with right hemisphere strokes ( Gainotti , 1 972; Robinson et al . , 1983) , a
diference that is usually attributed to the fact that the right hemisphere is more
"emotional . " I would argue instead that because of damage to the lef hemi
sphere, the patient does not have even the minimal "defense mechanisms" that
NO T E S I 2 8 1
you and I would use for coping with the minor discrepancies of day-to-day life,
so that every trifling anomaly becomes potentially destabilizing.
Indeed, I have argued ( Ramachandran, 1996) that even idiopathic depression
seen in a psychiatric setting may arise fom a failure by the lef hemisphere to
deploy Freudian defense mechanisms-perhaps as a result of transmitter imbal
ances or clinically undetectable damage to the lef fontal region of the brai n.
The ol d experimental obseration that depressed people are actually more sen
sitive to subtle inconsistencies ( such as a briefly presented red ace of spades) than
normal people is consistent with this line of speculation. I am currently admin
istering similar tests to patients with anosognosia.
A second set of experiments supporting this i dea comes from the important
obseration ( Gardner, 1993) that afer damage to the right ( but not lef) hem
isphere patients have trouble recognizing the absurdity of "garden path sen
tences" in which there is an unexpected twist at the ending that contradicts the
beginning. I interpret this fnding as a failure of the anomaly detector.
1 0. Bill's denials would seem comical if they were not tragic. But his behavior
"makes sense" in that he is doing his utmost to protect his "ego" or self When
one is faced with a death sentence, what's wrong with denial ? But even though
Bill's denial may be a healthy response to a hopeless situation, its magnitude is
surprising and it raises another interesting question. Do patients like him who
have been delusional as a result of ventromedial frontal lobe involvement con
fabulate mainly to protect the integrity of "self," or can they be provoked to
confabulate about other abstract matters as wel l ? If you were to ask such a
patient, "How many hairs does Clinton have on his head? " would he confab
ulate or would he admit ignorance?
In other words, would the very act of questioning by an authority fgure be suf
fcient to make him confabulate? There have been no systematic studies to address
these issues, but unless a patient has dementia ( loosely speaking, mental retarda
tion due to difse cortcal damage) he is usually quite "honest" in admitting ig
norance of matters that don't pose any immediate threat to his well - being.
1 1 . Clearly denial runs very deep. But even though it's fascinating to watch, it's also
a source of great frustration and practical concern for the patient's relatives ( al
though by defnition not for the patient! ) . For instance, given that patents tend
to deny the immediate consequences of the paralysis ( having no inkling that the
cocktail tray will surely topple or that they can't tie laces) , do they also deny its
remote consequences-what's going to happen next week, next month, next
year? Or are they dimly aware in the back of their minds that something is amiss,
that they are disabled? Would the denial stop them from writing a wil l ?
I have not explored this question on a systematic basis, but on the few oc
casions when I raised thi s question, patients responded as if they were completely
unaware of how deeply the paralysis would afect their fture lives. For example,
the patient may confdently assert that he intends to drive back home from the
hospital or that he would like to resume golf or tennis. So it is clear that he is
not merely sufering fom a mere sensory/motor distortion-a failure to update
his current body image ( although that is certainly a major component of this
illness) . Rather, his whole range of beliefs about himself and his means of surival
have been radically altered to accommodate his present denial . Merciflly such
2 8 2 1 No T E S
delusions can ofen be a considerable solace and comfort to these patients, even
though their attitude comes into direct conflict with one of the goals of reha
bilitation-restoring the patient's insight into his predicament.
Another way to approach the domain specifi city and depth of denial would
be to fash the word "paralysis" on the screen and obtain a galvanic skn re
sponse. Would the patient fnd the word threatening-and register a big GSR
even though she is unaware of her paralysis? How would she rate the word for
unpleasantness on a scale of 1 to 10, if asked to do so? Would her rating be
higher (or indeed lower) than that of a normal person?
1 2. There are even patients with right frontal lobe stroke who manifest symptoms that
are halfay between anosognosia and multiple personality disorder syndrome. Dr.
Rita Hari and I saw one such patient recently in Helsinki . A a result of two le
sions-one in the right frontal region and one in the cingulate-the patient's brain
was apparently unable to "update" her body image in the way that normal brains
do. When she sat on a chair for a minute and then got up to start walking, she
would experience her body as splitting into two halves-the lef half still sitting in
the chair and the right half walking. And she would look back in horror to ensure
that she hadn't abandoned the lef half of her body.
1 3 . Recall that when we are awake, the lef hemisphere processes incoming sensory
data, imposing consistency, coherence and temporal ordering on our everyday ex
periences. In doing so it rationalizes, denies, represses and otherise censors much
of this incoming information.
Now consider what happens during dreams and RM sleep. There are at least
two possibilities that are not mutually exclusive. First, RM may have an impor
tant "vegetative" fnction related to wet-ware ( for example, maintenance and
"uploading" of neurotransmitter supplies) , and dreams may j ust be epiphenom
enal-irrelevant by-products. Second, dreams themselves may have an important
cognitive/emotional fnction, and RM may simply be a vehicle for bringing
this about. For example, they may enable you to try out various hypothetical sce
narios that would be potentially destabilizing if rehearsed durng wakeflness. In
other words, dreams may allow a sort of "virtual reality" stimulation using vari
ous forbidden thoughts that are ordinarily eclipsed by the conscious mind; such
thoughts might be brought out tentatively to see whether they can be assimilated
into the stor line. If they can' t be, then they are repressed and once again for
gotten.
Why we cannot carry out these rehearsals in our imagination, while flly
awake, is not obvious, but two ideas come to mind. First, for the rehearsals to
be efective, they must look and feel like the real thing, and this may not be
possible when we are awake, since we know that the images are internally gen
erated. A we noted earlier, Shakespeare said, "You cannot cloy the hungry edge
of appetite with bare imagination of a feast . " It makes good evolutionary sense
that imagery cannot substitute for the real thing.
Second, unmasking disturbing memories when awake would defeat the very
purpose of repressing them and could have a profound destabilizing efect on
the brain. But unmasking such memories during dreams may permit a realistic
and emotionally charged simulation to take place while preventing the penalties
that would result if you were to do this when awake.
NO T E S I 2 8 3
There are many opinions on the fnctions of dreams. For sti mulating reviews
on the subject see Hobson, 1988, and Winson, 1986.
14. This isn't true for all peopl e. One patient, George, vividly remembered that he
had denied his paralysis. "I could see that it wasn't moving," he said, "but my
mind didn' t want to accept it. It was the strangest thing. I guess I was in denial . "
Why one person remembers and the other forgets i s not clear, but i t could have
something to do with residual damage to the right hemisphere. Perhaps George
had recovered more flly than Mumtaz or Jean and was therefore able to con
font reality squarely. It is clear from my experiments, though, that at least some
patients who recover from denial will "deny their denials" even though they are
mentally lucid and have no other memory problems .
Our memory experiments also raise another interesting question: What if a per
son were to have an automobile accident that caused peripheral nere damage and
rendered her lef arm paralyzed? Then suppose she sufered a stroke some months
later, the kind that leads to lef body paralysis and denial syndrome. Would she
then suddenly say, "Oh, my God, doctor, my arm that has been paralyzed all along
is suddenly moving again. " Going back to my theory that the patient tends to
cling to a preexisting worldview, would she cling to her updated worldview and
therefore say that the lef arm was paralyzed-or would she go back to her earlier
body image and assert that her arm was in fact moving again?
1 5 . I emphasize that this is a single case study and we need to repeat the experiment
more careflly on additional patients. Indeed, not every patient was as cooper
ative as Nancy. I vividly recall one patient, Susan, who vigorously denied her lef
arm paralysis and who agreed to be pan of our experiments . When I told her
that I was going to inject her lef arm with a local anesthetic, she stifened in
her wheelchair, leaned forard to look me straight in the eye and without batting
an eyelid, said, "But doctor, is that fair? " It was as though Susan was playing
some son of game with me and I had suddenly changed the rules and this was
forbidden. I didn't continue the experiment.
I wonder, though, whether mock injections may pave the way for an entirely
new form of psychotherapy.
1 6. Another fndamental problem arises when the lef hemisphere tries to read
and interpret messages from the right hemisphere. You will recall from Chap
ter 4 that the visual centers of the brain are segregated into two streams,
called the how and what pathways ( parietal and temporal lobes ) . Crudely
speaking, the right hemisphere tends to use an analogue-rather than digital
medium of representation, emphasizing body image, spatial vision and other
fnctions of the how pathway. The lef hemisphere, on the other hand, prefers
a more logical style related to language, recognizing and categorizing objects,
tagging objects with verbal labels and representing them in logical sequences
( done mainly by the what pathway) . This creates a profound translation bar
rier. Every time the lef hemisphere tries to interpret information coming from
the right-such as trying to put into words the inefable qualities of music or
art-at least some forms of confabulation may arse because the lef hemi
sphere starts spinning a yarn when it doesn't get the expected information
from the right ( because the latter is either damaged or disconnected from the
lef) . Can such a failure of translation explain at least some of the more florid
2 8 4 I NO T E S
confabulations that we see in patients with anosognosia? ( See Rmachandran
and Hirstein, 1997. )
l . J. Capgras and J. Reboul - Lachaux, 1923; H. D. Ellis and A.W. Young, 1990;
Hirstein and Ramachandran, 1 997.
2. This disorder i s called prosopagnosia. See Farah, 1 990; Damasio, Damasio and
Van Hoesen, 1982.
Cells in the visual cortex ( area 1 7) respond to simple features like bars of
light, but in the temporal lobes they ofen respond to complex features such as
faces. These cells may be part of a complex network specialized for recognizing
faces. See Gross, 1992; Rolls, 1 995; Tovee, Rolls and Rmachandran, 1996.
The fnctions of the amygdala which fgures prominently in this chapter, have
been discussed in detail by LeDoux, 1996, and Damasio, 1994.
3. The clever idea that Capgras' delusion may be a mirror image of prosopagnosia
was frst proposed by Young and Ellis ( 1 990) , but they postulate a disconnection
between dorsal stream and limbic strctures rather than the IT amygdala discon
nection that we suggest in this chapter. Aso see Hirstein and Rmachandran, 1997.
4. Another question: Why does the mere absence of this emotional arousal lead to
such an extraordinarily far-fetched delusion? Why doesn' t the patient j ust think,
I know that this is my father but for some reason I no longer feel the warmth?
One answer is that some additional lesion, perhaps in the right frontal cortex,
may be required to generate such extreme delusions. Recall the denial patients
in the last chapter whose lef hemispheres sought to presere global consistency
by explaining away discrepancies and whose right hemispheres kept things in
balance by monitoring and responding to inconsistency. To develop fll- blown
Capgras' syndrome, one might need a conjunction of two lesions-one that
afects the brain's ability to attach emotional signifcance to a familiar face and
one that disturbs the global "consistency-checkng" mechanism in the right
hemisphere. Additional brain imaging studies are needed to resolve this.
5. Baron- Cohen, 1995.
1 . At present the device i s efective mainly for stimulating parts of the brain near
the surface but we may eventually be able to stimulate deeper structures.
2. See Papez, 1937, for the original description and Maclean, 1973, for a compre
hensive review fll of fascinating speculatons.
It's no coincidence that the rabies virus "chooses" to lodge itself mainly in the
limbic structures. When dog A bites dog B, the virus travels fom the peripheral
neres near the bite into the spinal cord and then eventually up to the victim's lim
bic system, turning Benji into Damien. Snarling and foaming at the mouth, the
once-placid pooch bites another victim and the virus is thus passed on, infecting
those very brain structures that drive aggressive biting behavior. And as part of
this diabolical strategy, the virus initially leaves other brain structures completely
NO T E S I 2 8 5
unafected so that the dog can remain alive j ust long enough to transmit the
virus. But how the devil does a virus travel all the way from peripheral neres
near the bite to cells deep inside the brain while sparing all other brain structures
along the way? When I was a student I ofen wondered whether it might be
possible to stain the virus with a fuorescent dye in order to "light up" these
brain areas-thereby allowing us to discover pathways specifcally concerned with
biting and aggression, in much the same way one uses PET scans these days . In
any event, it is clear that as far as the rabies virus is concerned, a dog is j ust
another way of making a virus-a temporar vehicle for passing on its genome.
3. Usefl descriptions of temporal lobe epilepsy can be found in Trimble, 1992,
and Bear and Fedio, 1 977. Waxman and Geschwind, 1975 , have championed
the view that there is a constellation of personality traits more frequently found
in temporal lobe epilepsy patients than in age-matched controls. Although this
notion is not without its critics, several studies have confrmed such an associa
tion: Gibbs, 1 95 1 ; Gastaut, 1956; Bear and Fedio, 1977; Nielsen and Kistensen,
198 1 ; Rodin and Schmaltz, 1984: Adamec, 1989; Wieser, 1983.
The presumed link between "psychiatric disturbances" and epilepsy, of
course, goes back to antiquity, and, in the past, there has been an unfortunate
stigma attached to the disorder. But as I have stressed repeatedly in this chapter,
there is no basis for concluding that any of these traits is "undesirable" or that
the patient is worse of because of them. The best way to eliminate the stigma,
of course, is to explore the syndrome in greater depth.
Slater and Beard ( 1963) noted "mystical experiences" in 38 percent of their
series of cases, and Bruens ( 1 971 ) made a similar obseration. Frequent religious
conversions are also seen in some patients ( Dewhurst and Beard, 1970) .
It i s important t o recognize that only a minority of patients display esoteric
traits, like religiosity or hypergraphia, but that does not make the association any
less real . By way of analogy, consider the fact that kidney or eye changes ( com
plications of diabetes) occur only in a minority of diabetics, but no one would
deny that the association exists. A Trimble ( 1 992) has noted, "It is most likely
that personality traits such as religiosity and hypergraphia seen in patients with
epilepsy represent an all- or- none phenomenon and are seen in a minority of
patients. It is not a graded characteristic, for example like obsessionality, and
therefore does not emerge as a prominent factor in questionnaire studies unless
a sufciently large number of patients are evaluated. "
4. To complicate matters, it is entirely possible that some clinically undetectable
damage in the temporal lobes also underlies schizophrenia and manic-depressive
disorders, so the fact that psychiatric patients sometimes experience religious
feelings doesn't negate my argument.
5. Similiar views have been put forard by Crick, 1993; Ridley, 1997; and Wright,
1 994, although they do not invoke specialized structures in the temporal lobe.
This argument smacks of group selection-a taboo phrase in evolutionary psy
chology-but it doesn't have to. Afer all, most religions, even though they pay lip
serice to the "brotherhood" of mankind, tend mainly to emphasize loyalty to
one's own clan or tribe ( hence those who probably share many of the same genes) .
6. Bear and Fedio ( 1977) ofered the ingenious suggestion that there has been
hyperconnectivity in the limbic system that makes the patients see cosmic sig-
2 8 6 I NO T E S
nifcance in everything. Their idea predicts a heightened GSR to everything the
patient looks at, a prediction that held up in some preliminary studies. But other
studies showed either no change or a reduction in GSR to most categories. The
picture is complicated also by the extent to which the patient is on medication
while the GSR is measured.
Our own preliminary studies, on the other hand, suggest that there can be a se
lective enhancement of GSR responses to some categories and not others
thereby altering the patients' emotional landscape permanently ( Rmachandran,
Hirstein, Armel, Tecoma and Iragui, 1997) . But this fnding, too, should be taken
with a generous scoop of salt until it is confrmed on a large number of patients.
7. Moreover, even if the changes in the patient's brain were orginally mediated by
the temporal lobes-the actual repository of the changes-"a religious outlook"
probably involves many diferent brain areas.
8. For lucid and lively expositions of Darin's ideas, see Dawkins, 1976; Maynard
Smith, 1978; Dennett, 1 995.
There i s an acrimonious debate going on at the high table of evolution over
whether every trait ( or almost every trai t) is a direct result of natural selection or
whether there are other laws or principles governing evolution. We will take up
this debate in Chapter 1 0, where I discuss the evolution of humor and laughter.
9. Much of this discussion appears in a book by Loren Eisley ( 1958) .
1 0. This idea i s clearly described i n a delightfl book by Christopher Wills ( 1 993) .
See also Leakey, 1993, and Johanson and Edward, 1996.
1 1 . The savant who could produce the cube- root is described by Hi l l , 1978. The
idea that savants have learned some simple shortcuts or tricks for discovering
primes or for factoring has been around for some time. But it doesn't work.
When a professional mathematician learned the appropriate algorithm, he still
took almost a minute to generate all primes between 1 0, 037 and 1 0, 1 33-
whereas a nonverbal autistic man, naive to this task, took only ten seconds ( Her
melin and O' Connor, 1990) .
There are algorithms for generating primes at a high fequency-with occa
sional rare errors. It would be interesting to see whether prime number savants
make exactly the same rare errors that these algorithms do; that would tell us
whether the savants were tacitly using the same algorithm.
1 2. Aother possible explanation of the savant syndrome is based on the notion that the
absence of certain abilities may actually make it easier to take advantage of what's lef
over and to focus attention on more esoteric skills. For instance, as you encounter
events in the external world, you obviously do not record ever trivial detail in your
mind; that would be maladaptive. Our brains frst gauge the signifcance of events
and engage in an elaborate censoring and editing of the information-before storing
it. But what if this mechanism goes awry? Then you might start recording at least
some events in needless detail like the words in a book that you read ten years ago.
This, to you or me, might seem to be an astounding talent. But in truth, it emerges
from a damaged brain that cannot censor daily experience. Similarly, an autistic child
is locked in a world where others are not welcome, save one or two channels of in
terest to the outside. The child's ability to focus all her attention on a single subject
to the exclusion of all else can lead to apparently exotic abilties-but, again, her
brain is not normal and she remains profoundly retarded.
NO T E S I 2 8 7
A related but more ingenious argument is proposed by Snyder and Thomas
( 1 997) , who suggest that savants are for some reason less concept-driven because
of their retardation and this in turn allows them access to earlier levels of the
processing hierarchy, which is not available to most of us ( hence the obsessively
detailed drawings of Stephen Wiltshire, which contrast sharply with the tadpole
fgures or the conceptual cartoonlike drawings of normal children) .
This idea i s not inconsistent with mine. One could argue that the shif i n em
phasis from concept-driven perception (or conception) to allow access to early
processes may depend on the hypertrophy of the "early" modules in precisely the
manner I have suggested. Snyder's idea could therefore be seen as being halfay
between the traditional attention theory and my theory proposed in this chapter.
One problem is that although drawings of some savants seem excessively
detailed ( for example, Stephen Wiltshire's, described by Sacks ), there are others
whose drawings seem genuinely beautifl ( for example, the da Vinci-like draw
ings of horses produced by Nadia) . Her sense of perspective, shading and so on
seem hypernormal in a manner predicted by my argument.
What all these ideas have in common is that they imply a shi in emphasis
from one set of modules to the other. Whether this results simply from the lack
of fnction of one set (with more attention paid to others ) or from actual hy
pertrophy of what's lef remains to be seen.
The attention shi f i dea also doesn't appeal to me for two other reasons. First,
saying that you automatically become skilled at something by deploying attention
doesn't really tell us very much unless you kow what attention is, and we don' t.
Second, if this argument is correct, then why don' t adult patients with damaged
large portions of their brains suddenly become ver skilled at other things-by
shifing attention? I have yet to come across a dyscalculic who suddenly became a
musical savant or a neglect patient who became a calculating prodigy. In other
words, the argument doesn't explain why savants are born, not made.
The hypertrophy theory can, of course, be readily tested by using magnetic
resonance imaging ( MR) on diferent types of savants.
1 3 . Patients like Nadia also bring us face-to-face with an even deeper question: What
is art? Wy are some things pretty, while others are not? Is there a universal
grammar underlying all visual aesthetics?
A artist is skilled at grasping the essential features ( what Hindus call rasa)
of an image he is trying to portray and eliminating superfluous detail , and in
doing so he is essentially imitating what the brain itself has evolved for. But the
real question is: Why should this be aesthetically pleasing?
In my view, all art is "caricature" and hyperbole, so if you understand why
caricatures are efective you understand art. If you teach a rat to discriminate a
square from, say, a rectangle and reward it for the latter, then it will soon star
recognizing the rectangle and show a preference for it. But paradoxically, it will
respond even more vigorously to a sknnier "caricature" rectangle ( e. g. , with an
aspect ratio of 3 : 1 instead of 2: 1 ) than to the original prototype! The paradox
is resolved when you realize that what the rat learns is a rule-"rectangularity"
rather than a particular exemplar of that rule. Ad the way the visual form area
in the brain is structured, amplifing the rule (a skinnier rectangl e) is especially
reinforcing ( pleasing) to the rat, providing an incentive for the rat's visual system
to "discover" the rule. In a similar vein, if you subtract a generic average face
2 8 8 I NO T E S
from Nixon's face and then amplif the diferences, you end up with a caricature
that is more Nixon- like than the original . In fact, the visual system is constantly
struggling to "discover the rul e. " My hunch is that ver early in evolution, many
of the extrastriate visual areas that are specialized for extracting correlations and
rules and binding features along diferent dimensions ( form, motion, shading,
color, etc . ) are directly linked to limbic strctures to produce a pleasant sensa
tion, since this would enhance the animal 's surival . Consequently, amplifing a
specifc rule and eliminating irrelevant detail makes the picture look even more
attractive. I would suggest also that these mechanisms and associated limbic
connections are more prominent in the right hemisphere. There are many cases
in the literature of patients with lef- hemisphere stroke whose drawings actually
improved afer the stroke-perhaps because the right hemisphere is then free to
amplif the rul e. A great painting is more evocative than a photograph because
the photograph's details may actually mask the underlying rule-a masking that
is eliminated by the artist's touch ( or by a lef-hemisphere stroke ! ) .
This i s not a complete explanation of art, but it's a good start. We still need
to explain why artists ofen use incongruous j uxtapositions deliberately ( as in
humor) and why a nude seen behind a shower curtain or a diaphanous veil is
more attractive tan a nude photograph. It's as though the rle discovered afer
a struggle is even more reinforcing than one that is instantly obvious, a point
that has also been made by the art historian Ernest Gombrich. Perhaps natural
selection has wired up the visual areas in such a way that the reinforcement is
actually stronger if it obtained afer "work"-in order to ensure that the efort
itself is pleasant rather than unpleasant. Hence the eternal appeal of puzzle
pictures such as te dalmatian dog on page 239 or "abstract" pictures of faces
with strong shadows. A pleasant feeling occurs when the picture fnally clicks
and the splotches are correctly linked together to form a fgure.
Chapter 1o, The Woman Who Di ed Laughi ng
1 . Ruth and Willy (pseudonyms ) are reconstructions of patients originally described
in an article by Ironside ( 1 955 ). The clinical details and autopsy reports, how
ever, have not been altered.
2. Fred, Wilson, MacDonald and Behnke, 1998.
3. The discipline of evolutionary psychology was foreshadowed by the early writings
of Hamil ton ( 1964) , Wilson ( 1 978) and Williams ( 1966) . The modern manifesto
of this discipline is by Barkow, Cosmides and Tooby ( 1992) , who are regarded as
founders of the feld. (Also see Daly and Wilson, 1983, and Symons, 1979. )
The clearest exposition of these ideas can be found i n Pinker's book How the
Mind Works, which contains many stimulating ideas. My disagreement with him
on specifc details of evolutionary theory doesn't detract from the value of his
contributions.
4. This idea is intriguing, but as with all problems in evolutionary psychology it is dif
fcult to test. To emphasize this frther, I' l l mention another equally untestable
idea. Consider Margie Profet's clever suggestion that women get morning sickness
in the frst three months of pregnancy to curtail appetite, thus avoiding the natural
poisons in many foods that might lead to abortion ( Profet, 1 997) . My colleague
NO T E S I 2 8 9
Dr. Anthony Deutsch has proposed an even more ingenious argument. He sug
gests, tongue-i n-cheek, that the odor of vomitus prevents the male from wanting
to have sex with a pregnant woman, thereby reducing the likelihood of inter
course, which in turn is known to increase the risk of abortion. It's instantly obvi
ous this is a silly argument, but why is the argument about toxins any less silly?
5. V. S. Rmachandran, 1997. Here is what they fell for:
Now ask yourself, "Why do gentlemen prefer blondes? " In Western cultures,
it is widely believed that men have a distinct sexual and aesthetic preference for
blondes over brunettes (Alley and Hildebrandt, 1988) . A similar preference for
women of lighter than average skn color is also seen in many non-Western
cultures. ( This has been formally confrmed by "scientifc" sureys; Van der
Berghe and Frost, 1986. ) Indeed, in many countries, there is an almost obsessive
preoccupation with "improving one's complexion"-a mania that the cosmetic
industry has been quick to pander to with innumerable useless skin products.
( Interestingly, there appears to be no such preference for men of lighter ski n,
hence the phrase "tall, dark and handsome. ")
The well - known American psychologist Havelock Ellis suggested ffy years
ago that men prefer rotund features (which indicate fecundity) in women and that
blonde hair emphasizes the roundness by blending in better with the body outline.
Aother view is that infants' skin and hair color tend to be lighter than adults' and
the preference for blonde women may simply reflect the fact that in humans, neo
tenous babylike features in females may be secondary sexual characteristics.
I' d like to propose a third theory, which is not incompatible with these two
but has the added advantage of being consistent wth more general biological
theories of mate selection. But to understand my theory, you have to consider
why sex evolved in the frst place. Wy not reproduce asexually since you could
then pass on all your genes to your ofspring rather than just half of them? The
surprising answer is that sex evolved mainly to avoid parasites ( Hamilton and
Zuk, 1982) ! Parasitic infestation is extremely common in nature and parasites
are always trying to fool the host immune system into thinking that they are
part of the host body. Sex evolved to help the host species shufle its genes so
that it always stays one step ahead of the parasites. ( This is called the Red Queen
strategy, a term inspired by the queen in Alice in Wonderland, who had to keep
running just to stay in one place. ) Similarly, we can ask why secondary sexual
characteristics such as the peacock's tail or the rooster's wattles evolved. The
answer again is parasites. These displays-a shimmering large tail or blood red
wattles-may sere the purpose of "informing" the female that the suitor is
healthy and free of skin parasites.
Might being blonde or light skinned sere a similar purpose? Every medical
student knows that anemia, usually caused by either intestinal or blood parasites;
cyanosis (a sign of heart disease) ; jaundice (a sick liver) and skin infection are
much easier to detect in fair-skinned people than in brunettes. This is true for
both skn and eyes. Infestation with intestinal parasites must have been very
common in early agricultural settlements, and such infestation can cause severe
anemia in the host. There must have been considerable selection pressures for
the early detection of anemia in nubile young women since anemia can interfere
with fertility, pregnancy and the birth of a healthy child. So the blonde is in
efect telling your eyes, "I am pink, healthy and free of parasites. Don't trust
2 9 0 I NO T E S
that brunette. She could be concealing her ill health and parasitic infestation. "
A second, related reason for the preference might be that the absence of protec
ton from ultraviolet radiation by melanin causes the skin of blondes to "age" fas
ter than that of brunettes and the dermal signs of aging-age spots and wrinkles
are usually easier to detect. Since fertility in women declines rapidly with age, per
haps aging men prefer very young women as sexual partners ( Stuart Anstis, per
sonal communication) . So blondes might be preferred not only because the signs
of aging occur earlier but also because the signs are easier to detect in them.
Third, certain external signs of sexual interest like social embarrassment and
blushing, as well as sexual arousal ( the "flush" of orgasm) , might be more dif
fcult to detect in dark-skinned women. Thus the likelihood that one's courtship
gestures will be reciprocated and consummated can be predicted with greater
confdence when courting blondes.
The reason that the preference is not so marked for light-skinned men might
be that anemia and parasites are mainly a risk during pregnancy and men don't
get pregnant. Furthermore, a blonde woman would have greater difculty than
a brunette in lying about an afair she just had since the blush of embarrassment
and guilt would give her away. For a man, detecting such a blush in a woman
would be especially important because he is terrifed of being cuckolded, whereas
a woman need not worry about this-her main goals are to fnd and keep a
good provider. ( This paranoia in the man is not unreasonable; recent sureys
show that as many as 5 to l 0 percent of fathers are not genetic fathers. There
are probably many more milkman genes in the population than anyone realizes. )
One last reason for preferring blondes concerns the pupil s. Pupil dilation-an
other obvious sign of sexual interest-would be more evident when seen against
the blue iris of a blonde than against the dark iris of a brunette. This may also ex
plain why brunettes are ofen considered "sultry" and mysterious ( or why women
use belladonna to dilate pupils and why men tr to seduce women by candlelight;
the drug and dim light dilate the pupils, enhancing the sexual interest display) .
Of course, all these arguments would apply equally well t o any woman of
lighter ski n. Wy does the blond hair make any diference, if indeed it does?
The preference for lighter skin has been established by conducting sureys, but
the question of blond hair has not been studied. ( The existence of bleached
blondes doesn't negate our argument since evolution couldn't have anticipated
the invention of hydrogen peroxide. Indeed, the fact that there is no such thing
as a "fake brunette" but only a "fake blonde" suggests that such a preference
does exist; afer all, most blondes don't dye their hair black. ) I suggest that the
blond hair serves as a "flag" so that even from a great distance it's obvious to
a male that a light-skinned woman is in the neighborhood.
The take-home message: Gentlemen prefer blondes so they can easily detect
the early signs of parasitic infection and aging, both of which reduce fertility and
ofspring viability and can also detect blushing and pupil size, which are indices
of sexual interest and fdelity. ( That fair skin may itself be an indicator of youth
and hormonal status was proposed in 1995 by Don Symons, a distinguished
evolutionary psychologist from UCSB, but he did not put forard specifc ar
guments concerning the easier detection of parasites, anemia, blushing or pupils
in blondes being advocated here. )
A I said earlier, I concocted this whole ridiculous story as a satire on ad hoc
NO T E S I 2 9 1
sociobiological theories of human mate selection-the mainstay of evolutionary
psychology. I give it less than a 10 percent chance of being true, but even so it's
at least as viable as many other theories of human courtship currently in vogue.
If you think my theory is silly, then you should read some of the others .
6. Ramachandran, 1 998.
7. The important link between humor and creativity has also been emphasized by
the English physician, playwright and polymath Jonathan Miller.
8. The notion that a smile is related to a threat grimace goes all the way back to
Darin and ofen resurfaces in the literature. But to my knowledge, no one has
pointed out that it has the same logical form as laughter: an aborted response
to a potential threat when an approaching stranger turns out to be a friend.
9. Any theory that purports to explain humor and laughter has to account for all
of the following features-not j ust one or two: frst, the logical structure of j okes
and events that elicit laughter-that is, the input; second, the evolutionary reason
why the input has to take the particular form that it does, a buildup of a model
followed by a sudden paradigm shif that is of trivial consequence; third, the
loud explosive sound; fourth, the relation of humor to ticking and why tickling
might have evolved (I suggest it has the same logical form as humor but may
represent "play" rehearsal for adult humor) ; ffh, the neurological structures
involved and how the fnctional logic of humor maps onto the "structural logic"
of these parts of the brai n; sixth, whether humor has any other fnctions than the
one it originally evolved for ( for example, we suggest that adult cognitive humor
may provide rehearsal for creativity and may also sere internally to "deflate" po
tentially disturbing thoughts that you can't do anything about) ; seventh, why a
smile is a "half laugh" and ofen precedes laughter ( the reason I suggest is that it
has the same logical form-deflation of potential threat-that humor and laughter
have because it evolved in response to approaching strangers ) .
Laughter may also facilitate a kind of social bonding or "grooming," espe
cially since it frequently occurs in response to a spurious violation of social con
tracts or taboos ( e. g. , when someone is lecturing on the podium with his fly
open) . Telling jokes or laughing at someone may allow an individual to recali
brate frequently the social mores of the group to which he belongs and help
consolidate a shared sense of values. ( Hence the popularity of ethnic jokes. )
The psychologist Wallace Chafe ( 1987) has proposed an ingenious theory of
laughter that is in some ways the converse of mine-although he doesn' t consider
the neurobiology. The main fnction of laughter, he says, is to sere as a "disa
bling" device-the physical act is so exhausting that it literally immobilizes you
momentarily and allows you to relax when you realize that the threat isn't genuine.
I fnd this idea attractive for two reasons. First, when you stimulate the lef supple
mentary motor cortex, not only do you get fts oflaughter but the patient is efec
tively immobilized; he can' t do anything else ( Fried et al . , 1998) . Second, in a
strange disorder called catalepsy, listening to a joke causes the patient to become
paralyzed and collapse to the ground while remaining flly conscious. It seems
plausible that this might be a pathological expression of the "immobilization re
flex" that Chafe is alluding to. However, Chafe' s theory doesn't explain how a
laugh is related to a smile or how it is related to ticking; nor why a laugh should
take the particular form that it does-the rhythmic, loud explosive sounds.
2 9 2 I NO T E S
Wy not just stop dead in your tracks like an opossum? This, of course, is a general
problem in evolutionary psychology; you can come up with several reasonable
sounding scenarios of how something might have evolved, but it is ofen difcult
to retrace the particular route taken by the trait to get where it is now.
Finally, even if l am correct in asserting that laughter evolved as an "it's OK"
or "all is well" signal for communication, we have to explain the rhythmic head
and body movements (in addition to the sounds ) that accompany laughter. Can it
be a coincidence that so many other pleasurable activities such as dancing, sex and
music also involve rhythmic movements? Could it be that they all tap partially into
the same circuits? Jacobs ( 1994) has proposed that both autistic children and nor
mal people may enjoy rhyhmic movements because such movements activate the
serotinergic raphe system, releasing the "reward transmitter" serotoni n. One
wonders whether laughter activates the same mechanism. I knew of at least one
autistic child who frequently engaged in uncontrollable, socially inappropriate
laughter for relief
1 0. In saying this, I have no intention of providing ammunition for creationists.
These "other factors" should be seen as mechanisms that complement rather
than contradict the principle of natural selection. Here are some examples:
a. Contingency-plain old luck-must have played an enormous role in ev
olution. Imagine two diferent species that are slightly diferent genetically-let's
call them hippo A and hippo B-on two diferent islands, island A and island
B. Now if a huge asteroid hits both islands, perhaps hippo B is better adapted
to asteroid impacts, surives and passes on its gene via natural selection. But it's
equally possible that the asteroid may not have hit island B and its hippos. Say
it hit only island A and wiped out all hippo A's. Hippo B' s therefore surived
and passed on their genes not because they had "asteroid- resistance genes" but
simply because they were lucky and the asteroid never hit them.
This idea is so obvious that I fnd it astonishing that people argue about i t. In
my view, it encapsulates the whole debate over the Burgess shale creatures.
Whether Gould is right or wrong about the particular creatures unearthed there,
his general argument about the role of contingency is surely correct. The only sen
sible counterargument would be the many instances of convergent evolution. My
favorite example is the evolution of intelligence and complex types of learning
such as imitation learning-independently in octopuses and higher vertebrates.
How does one explain the independent emergence of such complex traits in both
vertebrates and invertebrates, if contingency rather than natural selection was play
ing the major role? Doesn't it imply that if the tape of evolution were played again,
intelligence would evolve yet again? If it evolved twice, why not three times?
Yet such instances of astonishing convergence are not fatal to the notion of
contingency; afer all , they occur very rarely. Intelligence evolved twice, not
dozens of times. Even the apparent convergent evolution of eyes in vertebrates
and invertebrates-such as squids-is probably not a true case of convergence,
since it has recently been shown that the same genes are involved.
b. When certain neural systems reach a critical level of complexity, they may
suddenly acquire unforeseen propertes, which again are not a direct result of se
lection. There is nothing mystical about these properties; one can show mathe
matically that even completely random interactions can lead to these little eddies
of order from complexity. Stuart Kaufman, a theoretical biologist at the Santa Fe
NO T E S I 2 9 3
Institute, has argued that this might explain the punctuated nature of organic ev
olution-that is, the sudden emergence of new species in novel phylogenetic lines.
c. The evolution of morphological traits may be driven, to a signifcant extent,
by perceptual mechanisms. If you teach a rat to discriminate a square ( l : l aspect
rati o) from a rectangle ( of l : 2 aspect rati o) and reward it for the rectangle alone,
then the rat is found to respond even more vigorously to a skinnier ( l : 4 ratio)
rectangle than to the original prototype rectangle, which it was trained on. This
paradoxical result-called the "peak shif efect" -suggests that the animal is
learning a rule-rectangularity-rather than a response to a single stimulus. I
suggest that this basic propensity-wired into the visual pathways of all ani
mals-can help explain the emergence of new species and of new phylogenetic
trends. Consider the classic problem of how the girafe got its long neck. Assume
frst that an ancestral group of girafes evolved a slightly longer neck as a result
of competition for food, that is, through conventional Darwinian selection. Once
such a trend had been set up, however, it would be important for long-necked
girafes to mate only with other long- necked girafes to ensure viability and
fertility of the ofspring. Once the longer neck became a distinguishing trait for
the new species, then this trait must become "wired" into the visual centers of
the girafe' s brain to help locate potential mates. Once this "girafe = long neck"
rule has been wired into a freely interbreeding group of girafes, given the peak
shif principle, any girafe would tend to prefer mating with the most "girafe
like" individual that it could spot-that is, the most long- necked individual i n
the herd. The net result would be a progressive increase in "long neck" alleles
in the population even in the absence ofa specifc selection pressure fom the en
vironment. The fnal outcome would be a race of girafes with almost comically
exaggerated necks of the kind we see today.
This process will lead to a positive feedback "gain amplifcation" of any preex
isting evolutionary trends; it will exaggerate morphological and behavioral difer
ences between a given species and its immediate ancestor. This amplifcation will
occur as a direct consequence of a psychological law rather than a result of envi
ronmental selection pressures. The theory makes the interesting prediction that
there should be many instances in evolution of progressive caricaturization of spe
cies. Such trends do occur and can be seen clearly in the evolution of elephants,
horses and rhinoceroses. As we trace their evolution, they appear to become more
and more "mammothlike" or "horselike" or "rhinolike" with the passage of time.
This idea is quite similar to Darwin's own explanation for the origin of second
ary sexual characteristics-his so-called theory of sexual selection. The progressive
enlargement of the male peacock tai l , for example, is thought to arise from a fe
male's preference for mates with larger tails. The key diference between our idea
and Darwinian sexual selection is that the latter idea was put forth specifcally to
explain diferences between the sexes, whereas our idea accounts for morphologi
cal diferences between species as well. Mate selection involves choosing partners
that have more salient "sexual markers" ( secondary sexual characterstics) and have
species "markers" ( labels that sere to diferentiate one species fom another) . Con
sequently, our idea might help explain the evolution of exteral morphological traits
in general and the progressive caricaturization of species, and not just the emer
gence of flamboyant sexual display signals and ethological "releasers. "
One wonders whether the explosive enlargement of brain ( and head) size in
2 9 4 I NO T E S
hominid evolution is a consequence of the same principle. Perhaps we fnd in
fantile, neotenous features, such as a disproportionately large head, appealing
because such features are usually diagnostic of a helpless infant, and genes that
promote the care of infants would quickly multiply in a population. But once
this perceptual mechanism is in place, infants' heads would become larger and
larger ( since large-head genes would produce neotenous features and elicit
greater care) and a large brain might simply be a bonus!
To this long list we can add others-Lynn Margulis's idea that symbiotic
organisms can "fse" to evolve into new phylogenetic lines ( for example, mito
chondria have their own DNA and may have started out as intracellular para
sites ) . A detailed description of her ideas is outside the scope of this book, which,
afer all, is about the brain, not evolution.
Chapter 11 "You forgot to Del i ver the Twi n"
1 . This story is a reconstruction based on a case originally described by Silas Weir
Mitchell . See Bivin and Kinger, 1937.
2. Christopher Wills told me the story of an eminent professor of obstetrics who was
fooled by a patient sufciently that he actually presented her as a case of normal
pregnancy to his residents and medical students during Grand Rounds. The stu
dents promptly elicited all the classic symptoms and signs of pregnancy in the un
fortunate lady. They even claimed to hear the fetal heartbeat with their gleaming
new stethoscopes-until one student remembered the "protruding umbilicus"
sign and risked embarrassing her professor by revealing the correct diagnosis.
3. Pseudocyesis is a fossil disease, so rare that one hardly sees it anymore. The
condition was frst described by Hippocrates in 300 B. C. It aficted Mary Tudor,
queen of England, who was falsely pregnant twice, with one episode lasting
thirteen months. Ana 0. , one of Freud's most famous patients, sufered
through a false pregnancy. And the more recent medical literature even describes
two transsexuals who experienced it! For recent work on pseudocyesis, see
Brown and Barglow, 1971 , and Starkman et a! . , 1985.
4. Follicle- stimulating hormone ( FSH) , luteinizing hormone ( LH) and prolactn
are produced by the anterior pituitary; they regulate the menstrual cycle and
ovulation. FSH causes the initial ripening of the ovarian follicle and LH causes
ovulation. The combined action of FSH and LH augments the release of estro
gen by the ovaries and later of both estrogen and progesterone by the corpus
luteum (what remains of the follicle afer release of the egg) . Last, prolactin also
acts on the corpus luteum, causing it to secrete estrogen and progesterone and
preventing it from becoming involuted ( and therefore preventing subsequent
menstruation if the ovum is fertilized) .
5 . For the efects of suggestion on warts, see Spanos, Stenstom and Johnston, 1988.
For a report on unilateral wan remission, see Sinclair- Gieben and Chalmers, 1959.
6. See Ader, 198 1 , and Friedman, Klein and Friedman, 1996.
7. Hypnosis i s a good example. Its a topic that's sometimes taught even in the
most conserative medical establishments, and yet every time the word is men
tioned at scientifc meetings, there is an uncomfortable shufling of feet. Even
NO T E S I 2 9 5
though hypnosis has a venerable tradition going all the way back to one of the
founding fathers of modern neurology, Jean Marin Charcot, it seems to enjoy
a curious dual reputation, being accepted as real on the one hand and yet also
regarded as the orphan child of "fringe medicine. " Charcot claimed that if the
right side of a normal person's body is temporarily paralyzed as the result of a
hypnotic suggestion, then that person also has problems with language, sug
gesting that the trance is actually inhi biting brain mechanisms in the lef hemi
sphere ( recall that language is in the lef) . A similar trance- induced paralysis of
the lef side of the body does not produce language problems. We have tried
replicating this result in our lab, without success.
The key question about hypnosis is whether it is simply an elaborate form of
"role playing" (in which you temporarily suspend disbelief as you do while
watching a horror movie) or whether it is a fndamentally diferent mental state.
Richard Brown, Eric Altschuler, Chris Foster and I have begun to try to
answer this question using a technique called Stroop interference. The words
"red" and "green" are printed either in the correct color ( red ink for the word
"red," green for "green") or with the colors reversed ( the word "green" in red
ink) . If a normal subject is asked j ust to name the color of the ink and ignore
the word, he is slowed down considerably if the word and color don't match.
He's apparently unable voluntarily to ignore the word, and so the word interferes
with color naming ( Stroop interference) . Now the question arises, Wat would
happen if you implanted the hypnotic suggestion in the subject's mind that he's
a native Chinese who can't read the English alphabet but can still name colors?
Would this suddenly eliminate Stroop interference? This test would prove once
and for all that hypnosis is real-not playacting-for there is no way a subject
can voluntarily ignore the word. (As a "control " one could simply ofer him a
large cash reward for voluntarily overcoming the interference. )
8. The placebo response i s a much maligned but poorly understood phenomenon.
Indeed, the phrase has come to acquire a pejorative connotation in clinical medi
cine. Imagine that you are testing a new painklling drug for back pain. Assume
also that no one gets better spontaneously. To determine the efcacy of the drug,
you give the pills to one hundred patients and fnd that, say, ninety patients get
better. In a controlled clinical trial, it is customary for the comparison group of
one hundred patients to receive a dummy pili-a placebo-( of course, the patient
doesn't know this) to see what proportion of them, if any, get better simply as a re
sult of the belief in the drug. If only 50 percent get better ( instead of90 percent) ,
we are j ustifed i n concluding that the drug i s indeed an efective painkiller.
But now let us turn to the mysterious 50 percent who got better as a result
of the "placebo. " Wy did they get better? It was shown about a decade ago
that these patients actually release painkilling chemicals, called endorphins, in
their brains ( indeed, in some cases the efect of the placebo can be counteracted
by naloxone, a drug that blocks endorphins ) .
A fascinating but largely unexplored question concerns the specifcity of the
placebo response, and our laboratory has recently become very interested in this
issue. Recall that only 50 percent got better from taking the placebo. Is this
because there is something special about this group? What if the same one hun
dred patients ( treated with a placebo for pai n) went on to develop depression a
few months later and you were to give a "new" placebo-telling them that it
2 9 6 I NO T E S
was a powerl new antidepressant? Would the same ffy patients get better, or
would a new set of patients show improvement, overlapping only parally with
the frst set? In other words, is there such a thing as a "placebo responder"? Is
the response specifc to the malady, the pill, the person or all three? Indeed,
consider what would happen if the same one hundred patients once again de
veloped pain a year later and again you gave them the original placebo "pain
killer. " Would the same ffy get better or would it be a new group of patients?
Dr. Erc Atschuler and I are presently conducting such a study.
Other aspects of placebo specifcity also remain to be investigated. Imagine
that a patient simultaneously develops a migraine and an ulcer-and you give
him a placebo that you tell him is a new "antiulcer drug. " Then would only the
ulcer pain go away ( assuming that he is a "placebo responder") , or would his
brain become so flushed with endorphins that the migraine pain would also
disappear as a bonus? This sounds unlikely, but if antipain neurotransmitters,
such as endorphins, are released difsely in his brain, then he may also get relief
from his other aches and pains even though his belief pertains only to the ulcer.
The question of how sophisticated beliefs are translated and understood by prm
itive brain mechanisms concerned with pain is a fascinating one.
9. For a review of multiple personality disorders, see Birnbaum and Thompson,
1996.
For ocular changes, see Miller, 1989.
Captu 12, Do Marti ans See Red?
l . For clear introductions to the problem of consciousness, see Humphrey, 1992;
Searle, 1992; Dennett, 1991 ; P. Churchland, 1986; P. M. Churchland, 1993; Galin,
1992; Baars 1997; Block, Rmachandran and Hirstein, 1997; Penrose, 1989.
The idea that consciousness-especially introspection-may have evolved
mainly to allow you to simulate other minds ( which inspired the currently popular
noton of a "theory of other minds" modul e) was frst proposed by Nick Hum
phrey at a conference that I had organized in Cambridge over twenty years ago.
2. Aother very diferent type of translation problem also arises between the code or
language of the lef hemisphere and that of the right ( see note 16, Chapter 7) .
3. Some philosophers are utterly bafled by this possibility, but it's no more mys
terious than striking your ulnar nere at the el bow with a hammer to generate
a totally novel electrical "tingling" qualia even though you may have never ex
perienced anything quite like it before (or even the very frst time a boy or girl
experiences an orgasm) .
4. Thus an ancient philosophical riddle going back to David Hume and William
Molyneux can now be answered scientifcally. Researchers at NIH have used
magnets to stimulate the visual cortex of blind people to see whether visual
pathways have degenerated or become reorganized, and we have also begun
some experi ments here at UCSD. But to my knowledge, the specifc question
of whether a person can experience a quale or subjective sensation totally novel
to him or her has never been explored empirically.
5 . The pioneering experiments in this feld were perormed by Singer, 199 3, and
Gray and Singer, 1989.
NO T E S I 2 9 7
6. It is sometimes asserted-on grounds of parsimony-that one does not need
qualia for a complete description of the way the brain works, but I disagree with
this view. Occam's razor-the idea that the simplest of competing theories is
preferable to more complex explanations of unknown phenomena-is a usefl
rule of thumb, but it can sometimes be an actual impediment to scientifc dis
covery. Most science begins with a bold conjecture of what might be true. The
discovery of relativity, for example, was not the product of applying Occam's
razor to our knowledge of the universe at that time. The discovery resulted from
rejecting Occam's razor and asking what if some deeper generalization were true,
which was not required by the available data, but which made unexpected pre
dictions (which later turned out to be parsimonious, afer all ) . It' s ironic that
most scientifc discoveries result not fom brandishing or sharpening Occam's
razor-despite the view to the contrary held by the great majority of scientists
and philosophers-but fom generating seemingly ad hoc and ontologically pro
miscuous conjectures that are not called for by the current data.
7. Please note that I am using the phrase "flling in" in a strictly metaphorical
sense-simply for lack of a better one. I don't want to leave you with the im
pression that there is a pixel- by-pixel rendering of the visual image on some
internal neural screen. But I disagree with Dennett's specifc claim that there is
no "neural machinery" corresponding to the blind spot. There is, in fact, a patch
of cortex corresponding to each eye's blind spot that receives input from the
other eye as well as the region surrounding the blind spot in the same eye. What
we mean by "flling in" is simply this: that one quite literally sees visual stimuli
( such as patterns and colors) as arising fom a region of the visual feld where
there is actually no visual input. This is a purely descriptive, theory- neutral def
inition of flling in, and one does not have to invoke-or debunk-homunculi
watching screens to accept it. We would argue that the visual system flls in not
to beneft a homunculus but to make some aspects of the information explicit
for the next level of processing.
8. Tovee, Rolls and Rmachandran, 1 996. Kthleen Amel, Chris Foster and I have
recently shown that if two completely diferent "views" of this dog are presented
in rapid succession, naive subjects can see only chaoti c, incoherent motion of
the splotches, but once they see the dog, it is seen to jump or turn in the
appropriate manner-emphasizing the role of the "top-down" object knowledge
in motion perception ( see Chapter 5 ) .
9. Sometimes qualia become deranged, leading to a fascinating condition called
synesthesia, in which a person quite literally tastes a shape or sees color in a
sound. For example, one patient, a synesthete, claimed that chicken has a dis
tinctly "pointy" favor and told his physician, Dr. Richard Cyowic, "I wanted
the taste of this chicken to be pointed, but it came out all round . . . well, I
mean it's nearly spherical; I can't sere this if it doesn't have points. " Another
patient claimed to see the letter "U" as being yellow to light brown in color,
whereas the letter "N" was a shiny varnished ebony hue. Some synesthetes see
this union of the senses as a gif to inspire their an, not as brain pathology.
Some cases of synesthesia tend to be a bit dubious. A person claims to see a
sound or taste a color, but it turns out that she is merely being metaphorical
much the same way that you might speak of a sharp taste, a bitter memory or
2 9 8 I NO T E S
a dull sound ( bear in mind, though, that the distinction between the metaphorical
and the literal is extremely blurred in this curious condition) . However, many
other cases are quite genuine. A graduate student, Kthleen Armel, and I recently
examined a patient named John Hamilton who had relatively normal vision up un
til the age of fve, then sufered progressive deterioration in his sight as a result of
retinitis pigmentosa, until fnally at the age of forty he was completely blind. Aer
about two or three years, John began to notice that whenever he touched objects
or simply read Braille, his mind would conjure up vivid visual images, including
flashes of light, pulsating hallucinations or sometimes the actual shape of the ob
ject he was touching. These images were highly intrusive and actually interfered
with his Braille reading and ability to recognize obj ects through touch. Of course,
if you or I close our eyes and touch a ruler, we don't hallucinate one, even though
we may visualize it in our mind's eye. The diference, again, is that your visualiza
tion of the ruler is usually helpfl to your brain since it is tentative and revocable
you have control over it-whereas John's hallucinations are ofen irrelevant and al
ways irrevocable and intrusive. He can't do anything about them, and to him they
are a spurious and distracting nuisance. It seems that the tactile signals evoked in
John's somatosensory areas-his Penfeld map-are being sent all the way back to
his deprived visual areas, which are hungry for input. This is a radical idea, but it
can be tested by using modern imaging techniques.
Interestingly, synesthesia is sometimes seen in temporal lobe epilepsy, sug
gesting that the merging of sense modalities occurs not only in the angular gyrus
( as is ofen asserted) but also in certain limbic structures.
1 0. This question arose in a conversation I had with Mark Hauser.
1 1 . Searle, 1 992.
1 2. Jackendorf, 1987.
1 3 . The patient may also say, "This is i t; I fnally see the truth. I have no doubts
anymore. " It seems ironic that our convictions about the absolute truth or false
hood of a thought should depend not so much on the propositional language
system, which takes great pride in being logical and infallible, but on much more
primitive limbic structures, which add a form of emotional qualia to thoughts,
giving them a "ring of truth. " ( This might explain why the more dogmatic
assertions of priests as well as scientists are so notoriously resistant to correction
through intellectual reasoning! )
14. Damasio, 1 994.
1 5 . I am, of course, simply being metaphorical here. At some stage in science, one
has to abandon or refne metaphors and get to the actual mechanism-the nitty
gritty of it. But in a science that is still in its infancy, metaphors are ofen usefl
pointers. ( For example, seventeenth-centur scientists ofen spoke of light as
being made of waves or particles, and both metaphors were usefl up to a point,
until they became assimilated into the more mature physics of quantum theory.
Even the gene-the independent particle of beabag genetics-continues to be
a usefl word, although its actual meaning has changed radically over the years . )
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I ndex
Page numbers in italics refer to illustrations.
acquired immunodefciency syndrome
(AIDS) , 2 1 5
acupuncture, 5 1
Adamec, R. E. , 285n
Adler, Rlph, 220
Aglioti , Salvatore A. , 37, 82-83, 268n
akinetic mutism, 252, 253, 298n
alcoholism, 1 5 , 1 34, 149
Alkon, Dan, 265 n
Alley, T. R. , 289n
Allman, John, 272n
Altschuler, Eric, 277n, 278n, 295 n,
296n
amnesia, 1 60
Capgras' syndrome compared with,
1 69-1 70
H. M. case and, xiii, 1 5 , 148, 149,
265 n
amputation stump, shortening of, vii ,
32-33
amygdala, 1 6, 1 62, 1 63, 1 66, 167-168,
1 77, 1 78, 1 82, 185, 1 86, 228
consciousness and, 244-245 , 247,
252
Anderson, Willy, 199-200, 201 , 202,
208, 288n
angular gyrus, 19, 195-196
Anna 0. , 294n
anomalies, 222-224
anorexia nerosa, 149, 1 5 5-1 56
anosognosia, vii , 2, 127-1 57, 249,
278n-283n
asymmetr of, 1 32
experiments wit, 1 37-141
Freudian view of, 1 3 1-1 32, 133
hemispheric specialization and, 1 34-
1 36, 279n-280n
"i ce water in the ear" stimulation
and, 144-148
neurological view of, 1 3 1 , 1 32, 1 39-
142
temporary remission of, 144-146,
148
of Wernicke's aphasics, 280n
Anstis, Stuart, 290n
anterior thalmic nuclei, 1 78
Anthropologist on Mars, An ( Sacks) ,
73
antibiotics, 2 14
Anton's syndrome, 280n
anxiety, 1 3, 207
apes, 195, 197
appendix, phantom, 24-25
argus pheasant, tail feathers of, 68, 70
Aristotle, 24, 266n
Amel, Kthleen, 286n, 297n, 298n
arms, 14, 26
denial of paralysis in, 2, 127-1 32,
1 39-142, 149-1 55
of monkeys, 27-28
paralysis of, 43-44, 47
phantom, vii , l , 2 1-24, 28-30, 30,
34, 40-2, 45-50, 270n
prosthetic, 41 , 270n
swinging of, 41-42
see also fngers; hands
art, 1 89, 192, 193, 1 94, 196, 197,
287n-288n
arthritic pai n, 5 1
Ahur case, 2, 3-4, 1 58-1 73
auditory recognition in, 1 60, 1 68
duplication in, 1 72
galvanic skin response in, 1 64-165
visual categories problem i n, 1 70-
1 71
asthma, 21 9-220
Asonishing Hypothesis, Te ( Crick) , xii
attention, 1 1 6-1 1 7, 120
attention shif idea, 286n, 287n
auditory cortex, 14, 1 68
auditory nere, 37
auditory nucleus, 37-38
Austen, Jane, 1 52
autistic children, 195, 286n, 292n
autonomic nerous system, 1 63-1 64,
1 63, 1 77, 21 9, 247
Avery, Oswald, 263n
axon terminals, 8
3 1 4
Baars, B. , 296n
Babinski , Joseph Franoois, vii , 128
bacteria, as cause of ulcers, xv, xvi
Balint's syndrome, 80
Barglow, P. , 294n
Barkow, J . H. , 288n
Barlow, Horace, 264n
basal ganglia, 10, 1 3, 14, 16
Bayatch ( T program) , l l
Bear, D. M. , 248, 285 n
Beard, A.W. , 285n
bee waggle dance, 243-244
behaviorism, 229, 264n
belief system, 140, 142, 1 5 5-1 56,
279n
experiment on, 1 5 1-1 52
l ef hemisphere and, 1 34-1 36, 1 41 ,
147, 282n
Benson, F. , 269n
Bhagavad Gita, 12 7
bicycle wheel experiment, 94-95, 97
Bill ( denial patient) , 142-143, 28 1 n
binding problem, 80-8 1
binocular vision, 89-90
biological variability, 2 1 5
Birnbaum, M. H. , 296n
Bisiach, Edoardo, 144, 276n-277n
black box approach, 263n-264n
Blakemore, Colin, xii
blindness, 63-65, 71
in Charles Bonnet syndrome, 87-88,
1 04-1 1 2, 274n-275 n
color, 72-73, 230
motion, 72, 8 1 , 272n
of Thurber, 85-87
blindsight, xvi , 2, 75-76, 1 1 8, 272n
blind spots, 70, 71, 89-96, 235-237,
236, 272n-274n
artifcial, 273n-274n
in bicycle wheel experiment, 94-95,
97
i n corner-of-a- square experiment, 94,
96
decapitation and, 91 , 94
demonstration of, 89, 90
flling in, ix, 89-96, 90, 1 04, 236-
237, 23 242-243, 273 297n
swastika pattern and, 94, 95
vertical black line run through, 91 ,
92
Block, N. , 296n
Bloom, Floyd, 3 1
boasting, 255, 279n
I N D E X I 3 1 5
body image, xi, 3, 253, 282n, 283n
anorexia and, 1 49, 1 5 5-1 56
cars and, 60-61 , 1 36-1 37
coining of phrase, 44
malleability of, 58-62, 247
mirror in altering of, 49
nature vs. nurture and, 22, 27-3 1 ,
41-42, 56-58, 267n
parietal lobe and, 44, 45, 46, 49-50,
142, 1 56, 246, 247
reorganization of, vii-viii, 22
self and, 61 -62, 247, 250
body parts, denial of ownership of, see
somatoparaphrenia
Bogen, J. E. , 279n, 280n, 298n
Bonnet, Charles, 1 04
see also Charles Bonnet syndrome
Borsook, David, 35, 268n
brain, human:
black box approach to, 263n-264n
as computer, 56, 277n
discrepancy in sensory inputs and,
1 41 , 142
hippocampus, 1 5 , 1 6, 1 7, 148, 1 63,
1 78, 265 n
j udgments of, 67-68
modularist vs . holistic view of, 1 0-l l
motor system of, 445, 53-54
phantom limbs and, vii-viii, 22, 25-
40, 45-46, 54-58
redundancy within, 34
size of, 1 91 , 196-197, 265 n, 293n-
294n
split, xiii, 10, 280n
structure of, 7-10, 8, 9, 16
symbolic description in, 66-67
unifed theory of, 4, 5
see also cerebral cortex; frontal lobes;
lef hemisphere; right hemisphere;
temporal lobes; specic topics
Brain, Lord Russell, 44
Brain, Mind and Behavior ( Bloom and
Laserson) , 1 6, 1 78
brain, monkey, 27-28, 30, 77-78, 267n
brain damage, 1 2-19, 3 1 , 196
vision and, 64-65, 72, 73, 75
see also stroke
brain mapping, brain maps, 39-40,
266n-267n
Penfeld homunculus and, 25-27, 26,
29, 3 1 , 32, 37, 39, 44, 50, 267n,
268n, 298n
vision and, 70, 71
3 1 6 I I N D E X
brain remapping, 27-31 , 32, 33-40,
45, 56, 268n-269n
abnormal, 50-5 1
in monkeys, 27-28, 29, 33
savants and, 196
vision and, 274n
brain stem, 14, 1 7, 37, 1 1 6, 1 78, 234
superior colliculus in, 73, 74
brain tumor, denial of, 142-143
breast cancer, 2 14
breasts, phantom, 24, 37
Breiter, Hans, 268n
Brewster, Si r David, 273n
Broca, Pierre Paul, 1 77
Brown, E. , 294n
Brown, Richard, 295 n
Brown-Sequard, Charles, 279n
Bruens, ]. H. , 285n
Bucy, Paul, 78
Buerger's disease, 5 1
Burgess shale creatures, 292n
Caccace, A. T. , 37
California, University of, Medical
Center of, 1 27-1 29
Canadian Journal ofPschiat, 23
cancer, 7, 214-21 5 , 21 8
Capgras' syndrome, ix, xvi , 2, 3-4, l 58-
l73, 248, 284n
amnesia compared with, 1 69-1 70
auditory recognition and, 160, 1 68
Cotard's syndrome as exaggerated
form of, 1 67
Freudian view of, 1 61-1 62
galvanic skin response and, 1 64-1 65
gaze direction and, 1 68-1 69
memory and, 1 69-1 72
self and, 1 71-173
caricature, 287n-288n
Carroll, Lewis, 1 24, 1 58, 277n
cars:
body image and, 60-61 , 1 36-1 37
in reariew mirrors, 120
cartoons, 2, 72, 1 08-1 09, I l l
of Thurber, 86, 86, 87
cataracts, 87, 1 04-1 05
catastrophic reaction, 1 29, 149
cats, seeing vs. imagining of, 88, 1 09-
1 1 0
Cecilia ( denial patient), 1 30
cell body, 8
central ( rolandi c) sulcus, 9
cerebellum, 9, 9, 16, 45, 1 78
cerebral cortex, 9, 1 0, 1 3, 16, 1 1 6,
l 78, 264n
lying and, 278n
Penfeld homunculus and, 25-27,
26
cerix, cancer of, 21 8
Chafe, Wallace, 29l n
Chalmers, D. , 294n
Charcot, Jean Marin, 295 n
Charles Bonnet syndrome, 87-88, 1 04-
1 1 2, 274n-275 n
Charles II, king of England, 91 , l 03
Chemical Histor ofa Candle ( Faraday) ,
i x, xi
chess playing, 250
child abuse, 225
children, 279n
autisti c, 1 95, 286n, 292n
in Charles Bonnet hallucinations, 1 05-
1 06
phantom limbs in, 57, 269n, 270n
Chopra, Deepak, 221 , 249
Chudamani, Viveka, 39
Churchland, Patricia, 1 75, 275 n, 296n
Churchland, P. M. , 296n
cingulate cortex, 163, 1 78
cingulate gyrus, 201 , 208, 228, 249,
252
Civil War, U. S. , vii , 23
Clark, Atley, 200
Clark, Stephanie, 268n
Cobb, S. , 269n
cognitive neuropsychiatr, 3
cognitive science, 272n
coherence and continuity, 1 33, 1 34-
1 35, l47, 280 282n
cold, 33-34, 50
color blindness, 72-73, 230
color vision, 1 1 , 64, 72-73, 79-80, 8 1 ,
1 02, 1 1 0, 1 1 1 , 1 8 5 , 230, 264n,
272n, 275 n
computer model of brain, 56, 277n
conceptual flling in, 1 03-1 04, 1 1 0
conceptual self, 253-254
confabulation, 1 54, 1 5 5 , 254, 283n
connectionism, l 0
consciousness, 76, 77, 1 03, 1 37, 1 56,
227-257, 296n-298n
as epiphenomenon, 235
selective fnction of, 1 1 6-1 1 7, 2 7 6 n
see alo qualia; self
continental drif, 223
contingency, evolution and, 209, 292n
contradictory evidence, visual system
and, 91 , 93, 93
convergent evolution, 292n
Cooper, Larry, 1 39-140
Copernican revolution, xiv, 1 56
cordotomy, 33
corneal damage, l 05
corner-of-a-square experiment, 94, 96,
1 02-103
corpus callosum, 9, 10, 12, 1 6, 163,
1 78, 280n
stroke i n, 1 2-1 3
Cosmides, L. , 288n
cosmology, xiv, 1 56, 1 57
Cotard's syndrome, 167, 248
courtship ritual, of birds, 68, 70
couvade syndrome ( sympathetic
pregnancy) , 21 8
creativity, 7, 197-198
humor and, 206, 291 n
of Thurber, 85-87, 86, 1 12
Crick, Francis, xii, 1 75, 1 86, 199, 229,
234, 263 271 285n
Critchley, M. , 276n, 278n
Cro-Magnon, 190, 191
Cronholm, B. , 267n
Cutting, ]. , 278n
cyclophosphamide, 220
Cytowic, Richard, 297 n
Daly, M. , 288n
Damasio, A. , 278n, 284n
Damasio, Hanna, 274n, 284n
Darwi n, Charles, ix, xi , x, 68, 70,
1 33, 1 89-191 , 2 1 1 , 224, 227,
240, 286n, 29ln
Darinian revolution, 1 56
Darinism (Wallace), 1 89
Davies, Paul, xii, 256-257
Davy, Humphry, i x, xi
Dawkins, Richard, xii, 197, 286n
D. B. ( Drew) , 75-77, 81
death:
Cotard's syndrome and, 1 67
laughter and, 199-200, 207
decapitation:
blind spot and, 91, 94
Capgras' syndrome and, 1 66
scotoma and, 1 03
defense mechanism( s ), viii-ix, 1 30-1 33,
1 36, l 52-l 56, 280n-28 l n
humor as, 1 54, 207
in normal people, 1 31-1 35
I N D E X I 3 1 7
rationale behind, 1 34-1 35
rationalizations as, 1 52, 1 54, 1 55,
1 56
reaction formation as, 1 39, 1 53-1 54,
1 5 5
repression as, 1 35, 143-144, 146,
148, 149, 1 53, 1 55, 1 61 , 282n
selection of, 1 5 5
Dehaene, S. , 265 n
de Kuif, Paul , xii
dendrites, 8
denial , 50, 127-1 53, 1 55-1 57, 253-
254, 278n-283n
depth of, 143, 28 l n-282n
global, 142
location of brain lesions and, 142-
143
memor and, 148-150, 283n
mock injections and, 1 5 1-1 52, 283n
neglect syndrome and, 1 33, 1 39-
1 41 , 144
normal vs. exaggerated, 1 3 1-1 32
Dennett, Dan, xii, 80, 254, 272n,
286n, 296n, 297n
depression, 3, 1 3, 182, 21 7, 280n-
28 l n
depth, 1 1 0, I l l
Descent ofMan, Te ( Darin) , 70,
2 1 1
Deutsch, Anthony, 289n
Deutsch, G. , 280n
Devil's Advocate, 1 35-1 36
Dewhurst, K. , 285n
DeYoe, Ted, 272n
diabetes, 285n
diabetic retinopathy, 87, 1 05
dichotomania, 279n
Dickens, Charles, viii
digestive system, 264n
disease, sensory identifcation of, 6-7
Disraeli , Benjamin, 2 1 1
DNA ( deoxyribonucleic acid) , 8 1 , 234,
246, 263 264 272 294n
Dr. Jekyl and Mr. Hyde (Stevenson) ,
224
Dodds, Mrs . , 127-129, 1 32, 1 36, 1 38-
1 39, 1 54
Dolan, Ry, 141-142, 280n
dorsal rhizotomy, 27-28, 33
dreams, 3, 147, 195
RM sleep and, 147-148, 282n
dyscalculias, 1 7-19, 265 n, 277n
dyslexia, temporary, 1 01
3 1 8 I I N D E X
ears, 37-38
hallucinations and, 1 05, 1 06
nystagmus and, 1 44146
Eddington, Sir Thomas, 222-223
Edelman, Gerald M. , 1 09, 278n
Edward, B. , 286n
eggs and cavities images, 68, 69, 70,
271 n
ego, defense of, 1 30, 1 35
Einstein, Albert, 4, l i S, 1 74, 1 95, 235
Ekman, P. , 278n
Electra complex, 1 61
electricity, magnetism and, 45
Ellen ( neglect syndrome patient) , l l 3-
l l 7, 120-125
Ellis, Havelock, 289n
Ellis, H. D. , 284n
embodied self, 247, 250
emotion, 1 1 6, l l 7, 282n
appropriate, l i S , 1 66
Capgras' syndrome and, 1 62-1 67,
1 70, l 72, 284n
eye contact and, 1 68
limbic system and, 1 3, 16, 1 7, l l6,
1 62-1 64, 163, 1 67, 171, 1 77, 1 82-
1 83, 1 85, 247, 248-249
right hemisphere and, 1 33-1 34,
280n
self and, 247-249
temporal lobe epilepsy and, 1 80,
1 82, 1 87
empathy, 61 , 21 8, 250
epilepsy, I S
grand mal seizure of, 1 79
temporal lobe, see temporal lobe
epilepsy
epistemology, experimental , 3, 1 5 1-1 52
erections:
of gay bashers, 1 5 3
health and, 197
phantom, 25, 37
Esmerelda ( denial patient) , 1 30
estrogen, 294n
evolution, 1 56, 1 57, 224
contingency and, 209, 292n
convergent, 292n
Lamarckian, 190
natural selection in, 175, 183, 1 84,
1 89-19 1 , 196, 201 , 209-2 1 1 ,
235, 286n, 288n, 292n-293n
perception and, 68, 70, 76, 1 03,
271 n
of self- deception, 278n-279n
evolutionary psychology ( sociobiolog) ,
l 83-l 84, 20l-202, 288n-291 n
executive self, 249-250
experimental method, Galilean, 24,
266n
eye movement, 38, 1 44, 145, 271 n
rapid ( RM) , 147-148, 282n
eyes, 6, 73, 74, 1 68
retina of, 70, 71, 74, 8 1 , 89, l i S,
274n, 275 n
face, 33
brain mapping and, 26-31 , 26, 30,
3 34, 40, 267n-268n
phantom, 25
face cells, 77-78
face recognition, 1 0, 64, 77-78, 1 69
Capgras' syndrome and, 1 62-167,
l72, 284n
Fregoli syndrome and, 1 71
prosopagnosia and, 1 62, 284n
false alarm theory, 206, 207
Faraday, Michael, ix, xi, 45, 263n
Farah, Martha, 266n, 278n, 284n
feces, disgust for, 202
Fedio, Paul, 248, 285n
feet:
brain mapping and, 26, 26, 27, 35,
36, 266n-267n
phantom, 35-36, 57, 270n
sexuality and, 3, 35-37
Feinberg, T. , 278n
Fermat, Pierre de, 1 88
Feynman, Richard, 120
flling-in phenomenon, 88-96, 90,
273n-274n
blind spots and, ix, 89-96, 90, 1 04,
236-237, 236, 242-243, 273n,
297n
in Charles Bonnet syndrome, I I 0
defned, 88, 273n
perceptual vs. conceptual, 1 03-1 04,
1 1 0
scotomas and, 89, 98-1 04, 272n-
273n
fnger agnosia, 19
fngers:
brain mapping and, 26, 26, 50
disease identifcation and, 6-7
phantom, vii , I , 2 1-22, 28-30, 30,
41 , 43, 47, 49-55, l l l , 270n
Finkelstein, Rita, 28
fsts, phantom, 52-55, I l l
Fletcher, Diane, 63-65, 69, 79-83
flower drawing, 1 21-122, 122
follicle-stimulating hormone ( FSH) ,
21 7, 294n
foot fetishes, 26, 36-37
Foster, Chris, 295 n, 297n
foveal vision, 80
Fregoli syndrome, 1 71
Freud, Anna, 1 30, 1 53
Freud, Sigmund, viii-ix, 3, 36, 41 , 1 35,
147, 1 52-1 57, 205, 224
Capgras' syndrome as viewed by, 1 61-
1 62
defense mechanisms and, 1 30-1 33,
1 39, 1 52-1 56
Fried, I . , 291 n
Frith, Chris, 141-142, 280n
frontal lobes, 9, 9, 1 7, 1 1 6, 1 66, 1 75,
1 77, 228, 234, 247, 264n-265 n,
282n, 284n
consciousness and, 244, 248
movement and, 44
ventromedial, 142-143
frontal lobe syndrome, 1 82
Frost, P. , 289n
fnctionalists, 264n
fnctional magnetic resonance imaging
( tR) , 1 41 , 263n, 266n, 270n
fnhouse, images in, 1 09, 274n
Fuster, J. M. , 269n
Gage, Phineas, 248
Gainotti, G. , 280n
Galileo, xi , xiv, 24, 266n
Galin, D. , 278n, 279n, 296n
Gall, Franz, 264n-265 n
Gallen, Chris, 3 1
galvanic skin response ( GSR), 61 ,
1 66, 248, 250, 270n, 279n,
282n
Capgras' syndrome and, 1 64-
1 65
of Cotard's syndrome patients, 167
temporal lobe epilepsy and, 1 85-
. 1 87, 286n
Gamow, George, i x, xii
Gandhi , Mohandas K. , 1 74
Gardner, H. , 28 l n
Gastaut, H. , 285 n
gate control ( volume control ) , 5 1
gay bashers, 1 5 3
gaze direction, 1 68-1 69
gaze tinnitus, 37-38
I N D E X I 3 1 9
Gazzaniga, M. , 280n
genetic engineering, 197
genitals:
brain mapping and, 25, 26, 27, 35-
36, 266n
see also erections; penis
genius, 1 85, 192-198
George ( denial patient) , 283n
Geschwind, Norman, 265 n, 285 n
gestalt, l 09
Gestalt psychologists, 82
gesticulation, 41 , 42, 44, 140
Gibbs, F.A. , 285n
girafes, long neck of, 293n
glaucoma, 87
God, 3, 39, 1 75-1 76, 1 79-1 82, 1 84-
1 88, l 91 , 235, 273n
Goldberg, E. , 269n
Goldberg, G. , 269n
Goldman- Rakic, P. S. , 269n
Goldstein, Kur, 1 2-1 3, 1 29
Gombrich, Ernest, 288n
Goodale, Mel, 77
Gould, Stephen Jay, i x, xii, 209, 265 n,
292n
Grace ( denial patient) , 142
Gray, C. M. , 296n
Graziano, M. S. A. , 280n
"Greenough, Ruth," 200, 201 , 207,
208, 288n
Gregory, Richard, ix, xii, 65, 120, 190,
27l n, 273n
Grifths, Fred, 263n
Gross, C. G. , 77, 280n, 284n
Haldane, J. B. S. , xxi , 39, 1 1 3
Halligan, Peter, 1 05, 1 1 7-1 1 8, 250,
276n
hallucinations, 33, 1 05-1 1 2, 275 n
auditory, 1 05, 1 06
Charles Bonnet, 87-88, 1 05-1 1 2,
274n-275 n
imagining and, 1 1 0-1 1 2
temporal lobe epilepsy and, 1 7 6-1 77
of Thurber, 85-87, 86
Hamilton, John, 298n
Hamilton, W. D. , 288n, 289n
Hamlet ( Shakespeare) , 1 39
hands, 209
brain mapping and, 26, 26, 27-3 1 ,
30, 32
dummy, 59-60
Parkinson's disease and, 269n-270n
3 2 0 I I N D E X
hands ( continued )
telescoped phantom, 42-3
see also fngers
Hard Times ( Dickens ) , viii
Hardy, G. H. , 1 94
Hari, Riita, 247, 282n
Head, Henry, 44
Hebbian link, 54
Heilman, J. , 276n
Helicobacter pylori, xv
Helmholtz, Hermann von, 68
hemianopia, 75
hemineglect, see neglect syndrome
hemispheric specialization, xiii , 142
anosognosia and, 1 34-1 36, 279n-
280n
see also lef hemisphere; right
hemisphere
heredity, see DNA; nature vs . nurtre
Hermelin, B. , 286n
Hildebrandt, K.A. , 289n
Hill, A. L. , 286n
hippocampus, 1 5 , 1 6, 1 7, 148, 163,
1 78, 265 n
Hippocrates, 294n
Hirstein, W. , 247, 270n, 284n, 286n,
296n
H. M. ( amnesia patient) , xiii, 1 5 , 148,
l49, 265 n
Hobson, J. A. , 283n
Hochberg, J. E. , 271 n
holism, 10-l l , 80
Holmes, Sherlock, l, 3, 12, 1 58, 21 2
homosexuality, latent, 1 5 3
Hooker, Joseph, 1 89
hormones, 1 77, 196, 197
false pregnancy and, 21 6, 21 7, 21 8,
294n
"how" pathway, 74, 77, 78, 79, 8 1 ,
82, 82, 8 3 , 1 1 0, I l l , 1 1 5,
283n
consciousness and, 240-241 , 244,
247
mirror agnosia and, 277n
How the Mind Works ( Pinker), 288n
Hubel, David, 271 n, 272n
Hume, David, 1 71 , 296n
humor, 1 54, 1 88
evolution of, 203-209, 286n, 29l n
false alarm theory of, 206, 207
see also j okes; laughter
Humphrey, Nick, 275 n, 296n
Huxley, Thomas Henry, ix, xi, 1 52
hyperconnectivity, 248
hypertrophy theory, 287n
hypnosis, 21 5 , 21 8-219, 294n-295 n
hypothalamus, 1 0, 16, 1 5 5 , 1 56, 1 63,
1 64, 1 77-1 78, 182, 201 , 228
false pregnancy and, 21 6, 21 7
hypoxia, 1 5
"ice water i n the ear" stimulation, 144-
1 48
ideomotor apraxia, 269n
imaging techniques, 35, 83, 284n
fnctional magnetic resonance
( fR) , 1 41 , 263n, 266n, 270n
magnetic resonance (MR), 32, 287n
magnetoencephalography ( MEG) ,
3 1 , 32, 263n, 270n
positron emission tomography ( PET) ,
1 41 , 142, 263 285n
imagining, imagination, xv-xvi, 87-88
hallucination and, 1 1 0-1 1 2
seeing vs. , 88, 1 09-1 1 0
immune system, 2 14, 2 19-221 , 225
imposters, Capgras' syndrome and, ix,
1 58-1 66
India, 1 83, 193-195, 2 14, 265n
leprosy i n, 57-58
information sequencing, 277n
Ingrid ( Swiss patient) , 72, 8 1
injections, mock, 1 5 1-152, 283n
insular cortex, 1 56, 208, 228
intelligence, 190-193, 292n
general, 192, 193, 195
kineti c, 190
phrenology and, 264n-265 n
potential , 190-1 91
intralaminar thalmic nuclei, 252,
253
Iragui, Vincent, 1 85-1 86, 286n
Irene ( phantom limb patient) , 43, 44,
46
Ironside, R. , 288n
itching, 28, 38
j acksonian seizures, 1 79
Jacobs, B. , 292n
James, William, 267n, 276n
Jean ( denial patient) , 1 50, 1 53-1 54
Joan ( scotoma patient) , 274n
Joe ( amnesia patient) , 1 69-1 70
Johanson, D. , 286n
Johnson, Mark, 28
Johnston, M. A. , 294n
j okes, 3, 1 8-19, 147, 1 54, 203-204,
206, 207, 291 n
Josh ( scotoma patient) , 97-103, 274n
Kaas, John, 272n
Kllio, K. E. , 270n
Kandel, Eric, 265 n
Knt, Immanuel, l l 5, 203
Karen ( phantom li mb patient) , 55
Kufman, Stuart, 292n-293n
kndling hypothesis, 1 82-1 83, 1 85-186
kinetic intelligence, 190
Kinsbourne, M. , 279n, 280n
Klefner, D.A. , 271 n
Kiver, Heinrich, 78
Kliver-Bucy syndrome, 78-79, 248
Knight, Mary, 21 2-21 7
Koch, Christof, 234
Korsakov, Sergei, 265 n
Kristensen, 0. , 285n
Kuhn, Thomas, 1 36, 204, 222
Kumar, Mirabelle, 40-44, 57
Lacker, J. R. , 270n
La Croix, R. , 270n
Lamarckian evolution, 190
Lancet, 105
language, 10, 1 1 , 14, 19, 1 1 7, 1 91 ,
245, 295n

body, 41 , 42, 44
hemispheric specialization and, 1 33,
283n
information sequencing and, 277n
translation barrier and, 231 -232
lateral ( sylvian) fssure, 9
lateral geniculate nucleus ( LGN) , 71,
73, 74
laughter, ix, 3, l l , 199-209
evolution of, 201 , 203-209, 286n,
291 n
nerous, 1 52, 1 54, 207
pathological, 199-201 , 207
uncontrollable, 2, 199-201
Leakey, R. , 286n
learned paralysis, viii, 46, 47-8, 269n
learning, 19, 68, 292n
lef hemisphere, xiii, 9-1 0, 1 2-1 3, 32,
288n
angular gyrus of, 195-196
belief system and, 1 34-1 36, 1 41 ,
147, 282n
as general , 135, 147, 280n
injury in, 13, 14, 1 32, 280n
I N D E X I 3 2 1
interpreter in, 280n
language and, 1 33, 283n, 295n
self-deception and, 279n
structure of, 9, 9
translation barrier and, 283n
visual pathways i n, 74
legs, 26, 1 3 1
phantom, vii , 22, 24, 35-36, 52
Leonardo da Vinci , 1 24, 1 94
leprosy, 57-58
Lettvin, Jerome, 273n
Levi, Leah, 280n
Levine, D. N. , 278n
Levinson, Lilian, 102
limbic system, 61 , 1 56, 288n
Cotard's syndrome and, 1 67
emotion and, 1 3, 16, 1 7, 1 1 6, 162-
1 64, 16 1 67, 1 71 , 1 77, 1 82-
1 83, 1 85, 247, 248-249
fnctions of, 1 77-1 79, 1 78
laughter and, 201 , 207, 208
lying and, 278n
rabies in, 1 77, 284n
racism and, 1 71
line- bisection test, 1 21 , 276n
lines, vertical vs. horizontal , 94, 95,
273n
Lipperhey, Hans, xiv
Lippincot's Journal, 23
lips, 33
brain mapping and, 25, 26, 26, 29
Littlewood, J. E. , 194
Livingstone, Margaret, 272n
Logotethis, Nikos, 272n
looking glass syndrome, see mirror
agnosia
love, 61 , 250
Lullin, Charles, 1 04-105
lung cancer, 7
luteinizing hormone ( LH) , 294n
lying ( self- deception) , 1 35, 254-255,
278n-279n
Lynch, Gary, 265 n
McCarty, Maclyn, 263n
MacDonald, Larry, 1 06-109, 1 1 0,
274n
McGlynn, S. M. , 278n
McGrath, John, 42-43, 45
Mach, Ernst, l l 5
Macken, Mrs . , 144-149, 1 5 5
Maclean, P. , 284n
Macleod, Colin, 263n
3 2 2 I I N D E X
macular degeneration, 87, 1 05
Madonna, 36
Magicicada septendecim, 263n
magnetic resonance ( MR) image, 32,
287n
magnetism, electricity and, 4-5
magnetoencephalography ( MEG) , 3 1 ,
32, 263n, 270n
Mai , N. , 272n
mammillary bodies, 1 63, 1 78, 201
manic depressive illness, 1 82, 285n
Man Wo Mistook His Wi for a Hat,
Te (Sacks ) , 1 62
Margulis, Lynn, 294n
Mariotte, Edme, 89
Marr, David, 27l n, 275 n
Marshall , Bill, xv, 1 7-19, 265n
Marshall, John, 105, 1 1 7-1 1 8
Martin, Purdon, 200
Martinez, Philip, 47-50, 269n
Mary ( phantom limb patient), 55, 270n
Massachusetts General Hospital
( MGH) , 35, 268n
mastectomy, 24, 37
math ability, 10, 1 7-19, 1 88, 190-197,
265n-266n, 277n, 286n
Maunsell, John, 272n
Maxwell, James Clerk, 5
Maynard Smith, J . , 286n
Mazziotta, J. C. , 263n
Medawar, Peter, i x, xii , xv-xvi, 8 1 , 206,
234
medicine, xiv-xv, 6-7
medulla oblongata, 9, 9, 1 6
Melzack, Ron, 267n, 269n
memory, 10, 1 5-17, 19, 44, 48, 238,
282n
Capgras' syndrome and, 1 69-1 72
in Charles Bonnet hallucinations,
1 1 0, 274n
denial and, 148-150, 283n
for faces, 1 69
Hebbian link and, 54
hippocampus and, 1 5 , 1 6, 1 7, 148,
l 69, 250, 265 n
pain, 5 1-52, I l l
perception and, 1 1 2, 238-241
temporal lobe epilepsy and, 1 8 1-182
memory trace, formation of, 148, 149,
250
Mendeleyev, Dmitri , 222
menstrual cramps, phantom, 25
Merzenich, Mike, 266n, 267n
Mesulam, Marcel, 1 1 7
metamorphosis, delay of, 5-6, 263n
metaphors, 197-198
Microbe Hunters, Te ( de Kruif, xii
midbrain, 1 6
middle temporal ( MT) area, 72, 73,
272n
migraines, transient scotomas and, 89,
97
Miller, Jonathan, 29l n
Miller, Lawrence, xxi
Miller, S. O. , 296n
Milner, Brenda, 265 n
Milner, David, 63-65, 79
Milton, John, 1 76
mind- body interactions, 1 77, 2 12-226,
294n-296n
asthma and, 21 9-220
in false pregnancy, 21 2-2 18, 294n
hypnosis in, 21 5 , 21 8-219, 294n-
295 n
in immune conditioning, 21 9-22 1
multiple personality disorder and,
224225, 296n
placebo efect and, 22 1 , 295 n-296n
resistance to idea of, 221-224
mirror agnosia ( looking glass
syndrome) , viii , 123-126
mirrors, 270n
denial patients and, 140-141
neglect syndrome and, 1 1 9-1 25
phantom limbs and, viii, 49, 52-
54, 269n, 270n
real obj ects vs. refection in, 120,
276n
Mischkin, Mortimer, 74
Mismeasure of Man, Te ( Gould) , 265 n
Mitchell, Silas Weir, vii, 23, 214, 267n,
294n
mnemonic self, 250-251
modularity, 1 0-l l , 1 7, 1 9, 55-56, 80,
264n-265 n, 277n
Molyneux, William, 232-233, 296n
monkeys, 280n
brain of, 27-28, 30, 77-78, 267n
monogamy, 1 83
Monroe, Dr . , 21 2-21 3, 21 6
morning sickness, 202, 288 n-289n
motion blindness, 72, 8 1 , 272n
motion perception, 72, 102, 1 1 0, I l l ,
272 274 275 297n
motor cortex, 9, 14, 16, 44, 53-54,
1 74, 1 79
movement:
arm, 41-42
of phantom limbs, 40-8
see also eye movement
Mozart, Wolfgang Amadeus, 188, 195
multiple personality disorder ( MPD) , 6,
146-147, 224-225, 25 1 , 282n
Murray, John, xi
music, 1 88-193, 195
mystical experience, ix, 1 82, 1 84-1 85,
285n
Nadia ( autistic savant) , 193, 1 94, 195,
197, 287n
Nadia ( Selfe) , 1 94
Nancy ( Charles Bonnet patient), 1 08-
1 1 1
Nancy ( denial patient) , 1 5 1-152,
283n
National Institutes of Health, xi , 74,
94, 296n
natural selection, 175, 1 83, 1 84, 1 89-
1 91 , 196, 209-2 1 1 , 235, 286n,
288n, 292n-293n
Nature, 200-201 , 269n
nature vs. nurture, 20, 1 83-1 84
body image and, 22, 27-3 1 , 41-42,
56-58, 267n
Neanderthals, 1 91
Necker, L. A. , 67
Necker cube, 67, 67
neglect syndrome, xvi, 1 1 3-126, 1 55,
266n, 276n-278n
clinical importance of, 1 19
denial and, 1 33, 1 39-141 , 144
mirror agnosia and, 123-126
mirrors and, 1 19-125
recovery from, 1 19, 277n
subconscious awareness in, 1 1 7-1 1 8
testing for, 121-122, 122
Nelson, Lord Horatio, 22-23, 273n
neocortex, 8
neuromas, 23, 3 1-32, 50, 56
neurons ( nere cells) , 8, 8
Newsome, William, 272n
Newton, Sir Isaac, 4, 228-229
New Yorker, 86
Nielsen, H. , 285n
Nietzsche, Friedrich, 199
nose, 209
phantom, 25, 270n
nose illusion, 59, 270n
nystagmus, 144-146, 148
I N D E X I 3 2 3
objective science, 229
object recognition, 1 5-16, 64, 1 01 ,
1 1 0, 1 1 5, 1 1 6, 275 n, 283n
auditory, 1 60, 1 68
see also face recognition
objects, external , projection of
sensations to, 59, 61
Occam's razor, 297n
occipital lobe, 9, 9, 16
ocular change, multiple personality
disorder and, 224, 296n
oculomotor nere nucleus, 38
Oedipus complex, 1 61
Omar Khayyam, 1 , 1 88, 265 n
On the Oriin of Species ( Darwi n), 2 1 1
optic chiasm, 71
optic disk, 89
optic nere, 70, 71 , 73, 74, 89, 275 n
optic radiation, 71
optic tract, 71
orgasm, 36, 1 1 1 , 1 75, 1 79, 296n
orienting behavior, 73, 76, 79, 280n
positive feedback loop in, 1 1 6-1 1 7,
276n
Ornstein, Robert, 279n
Ovid, 21
pain, 49-56
memory of, 5 1-52, 1 1 1
pain, phantom, vii , viii, 1 , 22, 28, 32-
33, 38, 40, 47, 49-55, 1 1 1
abnormal remapping and, 50-5 1
alleviation of, 24, 32-33, 49, 50, 52-
55
causes of, 50-5 1
cup experiment and, 43
pain asymbolia, 207-208
palinopsia, 274n-275 n
Papez, James, 1 77, 284n
paradigm shifs, 1 36, 204, 205, 222-
223, 280n, 291 n
Paradise Lost ( Milton) , 1 76
paralysis, 14
denial of, vii , 2, 127-1 57, 278n-
283n
of denial patient's right arm, 140-
141
learned, viii, 46, 47-48, 269n
i n monkeys, 27-28
in phantom limbs, vii , viii, 43-7
stroke and, 48, 1 19, 127-128
see also anosognosia; somata-
paraphrenia
3 2 4 I I N D E X
Pare, Abroise, 22
parent( s) :
child's sexual attraction to, 161
as imposters, i x, 1 58-1 66
as robot, 1 66
parietal lobe, 9, 9, 46, 49, 73, 1 1 6-
1 1 7
Balint's syndrome and, 80
body image and, 44, 45, 46, 49-50,
142, 1 56, 246, 247
denial and, 1 39, 142
lef, damage to, 1 1 6, 1 1 7
motor system and, 44, 45, 49-50
right, detection of damage to, 1 25
right, stroke i n, 1 14, 1 1 7, 1 42, 277n
spatial representation and, l l 5, 1 20-
1 21 , 1 25
see also "how" pathway
Parkinson's disease, 7, 269n-270n
parthenogenesis, 1 04
passionate self, 247-249
Paul ( temporal lobe personality), 1 80-
1 82
Peggy Sue ( MPD patient), 224-225
penduncular hallucinosis, 252-253
Penfeld, Wilder, 25-27, 26
Penfeld homunculus ( sensory
homunculus) , 25-27, 26, 29, 3 1 ,
32, 37, 39, 44, 50, 267n, 268n,
298n
penis, 25, 37, 270n
see also erections
perception, 63-1 12, 27l n-275 n, 293n
ambiguity i n, 68
comparisons vs. absolute value in,
1 67
eggs and cavities image and, 68, 69
fnhouse imagery view of, l 09
j udgment and, 67
memory and, 1 1 2, 238-241
stability in, 241-242, 27l n
as "unconscious inference, " 68
unity of, 80-8 1
see also vision, visual system
perceptual flling in, 1 00-1 04, l l O
perimetry, 1 02
periodic table, 222
Perrett, David, 77
Persinger, Michael, 1 75, 1 84
pets, Capgras' syndrome and, 1 61-1 62
phantom limbs, vii-viii, xi, l , 3, 2 1-58,
I l l , 266n-270n
"amputation" of, viii, 49-50
being born with, 40-2, 269n
defned, vii, 22
explanations of, 23, 28, 3 1-32
in historical perspective, vii , 22-23
movement of, 40-8
paralysis in, vii , viii, 43- 7
"virtual reality" device and, 46-9,
52-55, 1 41-142
vision and, 43, 46-9, 54-55
Phelps, M. E. , 263n
phrenology, 264n-265 n
physics, 4-5
Pie!, Jonathan, 95-96
Pinker, Steven, xii, 288n
pituitary gland, 1 77, 21 6, 294n
placebo efect, 53, 1 5 1-1 52, 214, 221 ,
295n-296n
Plum, F. , 298n
poetr, 7, 1 88
polyandr, 1 83
polygamy, 1 83, 1 84
pons, 9, 9, 1 6
Pons, Tim, 25, 27-30, 267n, 268n
positron emission tomography ( PET) ,
141, l42, 263 285n
Posner, M. , 263n
potential intelligence, 190-1 91
preadaptation, 209
preformationism, 1 04
pregnancy:
false (pseudocyesis) , 21 2-21 8, 294n
sympathetic ( couvade syndrome) ,
21 8
Pribram, K. , 269n
primary axon, 8
primary visual cortex, 70, 71, 72, 73,
75, 76, 77, 8 1 , 1 09, 1 1 0, 1 1 5,
275 n
Proceedings ofthe Royal Societ of
London, 269n
Profet, Margie, 288n
progesterone, 294n
projection, 1 54-1 55
prolactin, 21 6, 21 7, 21 8, 294n
prosopagnosia, 1 62, 284n
pseudocyesis ( false pregnancy), 21 2-
2 1 8, 294n
psychological defenses, see defense
mechanism( s )
qualia ( subj ective sensation) , 229-245,
25 l-252, 296n-297n
defned, 229, 230
features of, 238-242, 239
riddle of, 229-231
Queen Square Neurological Hospital
for Neurological Diseases, 141-
142
rabies, 1 77, 284n-285n
racism, 1 71
Rfael, Robert, 278n
Richle, M. , 263n
Rmachandran, Mani, 83
Rmachandran, V. S. , 69, 227, 239,
267n-27l n, 273n, 274n, 275n,
28 1 284 286 296n
Rmanujan, Srinivasa, 188, 193-195
Rmon y Cajal, Santiago, 234
rationalizations, 1 52, 1 54, 1 5 5 , 1 56
reaction formation, 1 39, 1 5 3-1 54, 1 5 5
recticular activating system, 1 1 6
reductionism, 234, 264n
redundancy, 34
religious experience, ix, 1, 3, 6, 1 75-
188, 285n
RM ( rapid eye movement) sleep, 147-
148, 282n
repression, 1 35, 143-144, 146, 148,
149, 1 53, 1 55, 1 61 , 282n
reverse engineering, 209-2 1 0
Rckard, Tim, 266n
Rdley, M. , 285 n
rifle targets, 83
right hemisphere, xiii, 9-10, 9, 12-1 3,
32, 288n
angular gyrs of, 196
anosognosia and, 1 32, 141 , 147,
282n
as Devil's Advocate, 1 35-1 36
discrepancies monitored in, 142,
280n
injury in, 7, 1 3, 14, 1 14, 1 1 7, 127-
128, 1 32, 1 34, 142, 144, 280n,
28 1 n, 282n; see also neglect
syndrome
language and, 1 33
self-deception and, 279n
translation barrier and, 283n
vision and, 1 33-1 34
Rivermead Rehabilitation Center, 1 3 1
Robinson, R. G. , 280n
robot, parent as, 1 66
Rock, 1 . , 271 n
Rodin, E. , 285n
Rogers- Rmachandran, D. , 269n, 270n
I N D E X I 3 2 5
Rolls, E. T. , 77, 239, 284n
Rubiyat ofOmar Khayam, 1e, 1, 188
Sacks, Oliver, xii, 73, 1 1 8, 143, 162,
192, 272n, 287n
Sagan, Carl, ix, xii
Sam ( Ellen's son) , 1 1 3-1 1 5 , 120
Sanders, Mike, 75
San Diego Rehabilitation Center, 1 50
savant syndrome ( idiot savant
syndrome) , 192-197, 1 94, 286n-
287n
explanation of, 195-196, 286n-287n
Schacter, D. L. , 278n
schizophrenia, 1 76, 1 82, 253, 285n
Schmaltz, S. , 285n
Schopenhauer, Ahur, 203
Schrodinger, Erwin, xi i , 1 76
sCience:
exception vs. rule in, 5-6
progress in, 221-222
Scientic American, 95-96, 272n
scientifc revolutions, common
denominator of, 1 56-1 57
scotoma, 71, 96-104, 274n, 275 n
corner-of-a-square experiment and,
1 02-1 03
decapitation and, 1 03
migraines and, 89, 97
perimetry and, 1 02
Searle, John, 245, 296n
"Secret Life of Walter Mitty, The"
( Thurber), 85
Sejnowski , Terry, 265 n, 275 n
self, xviii, 3, 12, 8 1 , 83-84, 227-257,
296n-298n
anosognosia and, 1 37
body image and, 61-62, 247, 250
Capgras' syndrome and, 1 71-173
conceptual, 253-254
executive, 249-250
as illusion, 84, 227-228, 247, 272n
mnemonic, 250-25 1
passionate, 247-249
social , 254
unifed, 25 1-252
vigilant, 252-253
see alo consciousness
self-deception, 1 30, 1 34-1 35, 254-
255, 278n-279n
Selfe, Lorna, 1 94
Sen, Sathyajit, 40
sensory cortex, viii , 9, 1 6
3 2 6 I I N D E X
sensory homunculus, see Penfeld
homunculus
septum, 175, 178, 228
Sergent, Justine, 98, 273n, 274n
Sex ( Madonna) , 36
sexuality, sexual behavior, 1 0, 1 53,
197, 201
children's attraction to parents and,
161
ears and, 37
feet and, 3, 35-37
indiscriminate, 78, 79
temporal lobe epilepsy and, 1 8 1 ,
1 86, 187
see also erections; orgasm; penis
sexual selection, 293n
Shah, Muntaz, 149-150
Shakespeare, William, 85, l l l , 148,
1 52, l98, 241 , 256, 282n
Shallice, T. , 269n
shapes, vision and, l l 0, I l l
shoelace experiment, 1 38-1 39
Simmel, Mary An, 269n
Sinclair- Gieben, A. H. C. , 294n
Singer, W. , 296n
size- contrast illusion, 82-83, 82
skin, sensations arising from, 33-34
Slater, E. , 285n
sleep, REM ( rapid eye movement) , l47-
148, 282n
smell, 6-7, 1 0, 1 77
smiling, 1 3-14, 291 n
grimace compared with, 207, 21 0-
2 1 1 , 29l n
lying and, 278n
Snyder, A. , 287n
social self, 254
sociobiology, see evolutionary
psychology
somatoparaphrenia, vii , 2, 1 3 1 , 143,
249, 278n
Sorenson, Tom, 20-22, 28-3 1 , 33-35,
38, 40, 50, 268n
Spanos, N. P. , 294n
spatial representation, 1 1 5, 1 20-121 ,
1 25
speculation, xv-xvi
Sperry, R.W. , 280n
spinal cord, 9, 9, 1 6, 33, 48
dorsal rhizotomy and, 27, 33
motor system and, 44, 45
split brains, xiii, 10, 280n
spontaneous activity, 275 n
spontaneous remissions, 21 421 5
sports, spatial orientation in, 8 3
Springer, S . , 280n
sprouting, 34, 35
Squire, Larry, 265 n
Starkman, M. , 294n
Star Wars ( movie) , 83
Stenstrom, R. S. , 294n
stereoscopic vision, 94, 273n
Steve ( neglect syndrome patient) , 1 1 8-
1 19, 120
Stevenson, Robert Luis, 224
Stoddard, Rck, 60
"Stream of Thought, The" ( James) ,
276n
stroke, 2, 1 2-1 3, 14
blindness and, 73, 75
neglect syndrome and, l l 3, 1 14,
1 19, 277n
number sense and, 1 7-19
paralysis and, 48, 1 19, 127-128
in right hemisphere, l l4, 1 1 7, 127-
128, 1 34, 142, 144, 277n
Stroop interference, 295 n
subjective sensation, see qualia
suicidal tendencies, 1 2-1 3, 22
sun, xiv, 68, 69n, 271 n
superior colliculus, 73, 74
supplementary motor area, 44, 201 , 249
Susan ( denial patient), 283n
Susan ( epilepsy patient) , 201
Sutherland, Stuart, 228
swastika pattern, blind spot and, 94, 95
sweatng, 1 64
see also galvanic skin response
symbolic description, 66-67
Symons, Don, 288n, 290n
synapses, 8, 8
synesthesia, 297n-298n
table-tapping illusion, 60, 61
tadpoles, regeneration i n, 5-6
Taub, E. , 267n
Tecoma, Evelyn, 1 85-1 86, 286n
telescope, xiv
temporal lobe epilepsy, xvi, 1 , 7, 248-
249, 285n
galvanic skin response and, 1 85-1 87,
285 n-286n
religious experience and, 1 7 5-1 77,
1 79-188, 285 n-286n
temporal lobe personality, 1 80-1 88,
285n
temporal lobes, ix, 9, 9, 74, 77, 78-79,
1 01 , 228, 265 n
consciousness and, 244-246
object recognition and, 1 1 5, 1 1 6,
1 62, 1 65, 284n
religious experience and, 17 5-1 77,
1 79-1 88, 286n
see also amygdala; hypothalamus;
insular cortex; septum
textures, 64, 79-80, 1 01 , 1 02, 1 03,
275 n
thalamus, 9, 1 0, 1 3, 16, 33, 74, 1 09,
163, 1 75, 252
"theory of other minds" module, 296n
Thiruvengadam, K.V. , 6-7
Thomas, Dylan, 1 88
Thomas, Lewis, ix, xii, 1 27, 21 8
Thomas, M. , 287n
Thompson, K. , 296n
threat:
emotional arousal in response to, 1 63-
1 64
perception of, 1 1 6-1 1 7
threat grimace, smile compared with,
207, 21 0-2 1 1 , 29l n
Trough the Looking Glass ( Carroll ) ,
1 24, 1 58
Thurber, James, 85-87, 86, 1 04, 1 1 2,
272n
tickling, ix, 208, 291 n
"tinkering" strategy, 5
toes, sucking of, 3, 37
tokens vs. types, 1 70
Tom (savant) , 192-193, 195
Tooby, J. , 288n
touch, 33-34, 38, 39, 1 77
phantom pain and, 50-5 1 , 54-55
Tovee, M. J. , 239, 284n
Townsend, Robert, 52-54
transcranial magnetic stimulator, 1 74-
175, 284n
translation barrier, 231 -232, 283n,
296n
transsexuals, 270n, 294n
tray experiment, 1 37-1 38
trichromacy, 264n
Trimble, M. R. , 285n
Trvers, Robert, 254-255, 278n-279n
Tudor, Mary, 294n
ulcers, cause of, xv, xvi
ultra-Darinists, 209-21 0
unconscious, viii-ix, 1 56, 235
I N D E X I 3 2 7
unconscious inference, 68, 270n
Ungerleider, Leslie, 74
unifed self, 251 -252
universe, geocentric vs. heliocentric
view of, xiv, 1 56
Upanishads, 1 5 7
Van der Berghe, L. , 289n
Van Essen, David, 272n
Van Hoesen, G. W. , 284n
Venus' s-flytrap, 239-240
vertical black line experiment, 91 , 92
vestibular cortex, 147
vestibular nere, 147
V4 (visual area) , 72-73, 8 1 , 272n
vigilant self, 252-253
"virtual reality" device, viii , 46-49, 52-
55
denial patients and, 1 40-141
Dolan-Frith experiment with, 141-
142, 280n
vision, visual system, 63-1 1 2, 1 77, 232-
233, 27l n-275n
assumptions of, 68, 69, 271 n
binocular, 89-90
bottom-up view of, 1 09, 1 1 0, 1 1 1
color, 1 1 , 64, 72-73, 79-80, 8 1 ,
1 02, 1 1 0, 1 1 1 , 1 8 5 , 230, 264n,
272n, 275 n
contradictory evidence and, 91 , 93,
93
double, 274n
foveal, 80
imagination and, 1 12
multiple specialized areas of, 72-73,
77, 80, 8 1 , 1 02, 272n
neglect syndrome and, 1 1 5
organization of, 73, 74
Parkinson's disease and, 270n
phantom limbs and, 43, 46-9, 54-
55
right hemisphere and, 1 33-1 34
size-contrast illusion and, 82-83, 82
statistical regularities and, 1 03-1 04
stereoscopic, 94, 273n
subjective experience and, 55
top-down view of, 1 09, 1 1 0, 1 1 1 ,
275n, 297n
see also blindness; blind spots; "how"
pathway; "what" pathway
Vision ofthe Brain, A ( Zeki ) , 71
visual categories, Capgras' syndrome
and, 1 70-1 71
3 2 8 I I N D E X
visual cortex, 70, 71, 74, 233, 284n,
296n
migraines and, 89
primary, 70, 71, 72, 73, 75, 76, 77,
8 1 , 1 09, l l O, l l 5, 275n
visualizaton therapy, I l l
volume control ( gate control ) , 5 1
von Cramon, D. , 272n
Wall, Patrick, 267n
Wallace, Alfred Russel, 1 89-192, 198
Ward, Betty, 140-141
warmth, 33-34, 50
Warrington, Elizabeth, 265 n
warts, hypnosis and, 21 8-219, 294n
Watson, James, 63, 263n
Waxman, S. G. , 285n
Wegener, Alfred, 223
Wei!, Andrew, 22 1
Weisel, Torsten, 27l n
Weiskrantz, Larry, 75-76, 265 n, 272n
Wernicke's aphasia, 277n, 280n
Wernicke's area, 245
Wat Is Lie ? ( Schrodinger), xii
"what" pathway, 74, 77-82, l l O, I l l ,
l l 5, 240, 247, 277 283n
Weeler, John Archibald, xi
"where" pathway, see "how" pathway
"Wy Do Gentlemen Prefer Blondes? "
( Rmachandran) , 202, 289n-29l n
Wieser, H. G. , 285n
Williams, G. , 288n
Wills, Christopher, 274n, 286n, 294n
Wilson, E. O. , 288n
Wilson, M. , 288n
Wiltshire, Stephen, 287n
Winson, J. , 283n
Wright, R. , 285n
writer's cramp ( focal dystonia) , 269n
Yang, Tony, 31
Yap, G. S. , 280n
yawning, 14
Young, A.W. , 284n
Zeki , Semir, 9, 71, 221 , 272n
Zihl, J. , 272n
Zuk, M. , 289n