The Neurobiology of Language
The Neurobiology of Language
The Neurobiology of Language
I. I N T R O D U C T I O N
One of the most challenging issues related to human language is under-
standing how it is organized and processed in the brain. Such study is
described under the broad rubric of the neurobiology of language and de-
fines the field ofneurolinguistics. The domain of inquiry has largely focused
on investigations of aphasic patients, exploring the clinical and behavioral
manifestations of their disorder and the accompanying lesion localization.
These "experiments in nature" provide the traditional approach to the study
of language/brain relations, and without question, they have provided, the
major insights to date. Nevertheless, in more recent years, the increased
sophistication of electrophysiological and metabolic techniques has pro-
vided a new and exciting approach to the study of the neurobiology of
language. These latter studies allow investigation of neural activity in nor-
mal subjects in addition to the study of brain-damaged patients. Taken
together, these three approaches: clinical/lesion investigations using imag-
ing techniques such as computerized axial tomography (CAT scan) and
magnetic resonance imaging (MRI); electrophysiological studies using
evoked related potentials (ERP); and metabolic techniques using positron
emission tomography (PET), provide converging data on the nature of the
representation of language, the processes involved in language use, and
ultimately its underlying neural organization.
It is the object of this chapter to review the current state of knowledge of
the neurobiology of language. Particular emphasis will be on studies of
339
340 SheilaE. Blumstein
adult aphasia. Studies involving ERP and PET are also reviewed as they
speak to issues concerning language organization and language processing.
A. Research M e t h o d o l o g i e s
All experimental methodologies have both strengths and weaknesses. Clini-
cal/lesion investigations of adult patients provide a view of language break-
down subsequent to brain damage. As such, they serve as a window into the
fractionation of language in individuals who had normal language and cog-
nitive functions prior to the damage. Charting the relation between patterns
of language breakdown and underlying neuropathology provides the closest
analogy to lesion mapping in animal investigations. Unlike lesion mapping
studies in animals, however, it is impossible to control for the site and size
of the lesion. Grouping patients by lesion site then is quite difficult and
usually involves gross localization schemas making it difficult to determine
the precise relation between language behavior and underlying lesion. In
addition, it is problematic to assume a one-to-one relation between brain
structure and language function. As John Hughlings Jackson stated " . . . to
locate the damage which destroys speech and to localise [sic] speech are two
different things" (quoted in Henry Head, 1963, p. 50). It is possible that a
lesion may affect pathways leading to a particular functional area without
damaging that area. Moreover, the processing components ultimately con-
tributing to language are complex and are usually inferred from investiga-
tions of patients' behavior on different language tasks, such as naming and
comprehension, behaviors that in themselves may require different process-
ing components. Finally, studies with aphasic patients typically rely on
behavioral measures and aphasic patients typically show increased vari-
ability compared to neurologically intact control patients on these mea-
sures. As a result, it is often difficult to titrate out statistically reliable effects.
Nonetheless, studies with aphasic patients have provided the basis for the
major hypotheses generated and tested to date in metabolic studies with
neurologically intact subjects.
The advantages of metabolic studies such as PET are that they provide a
potential means of mapping brain function in neurologically intact subjects
and of investigating specific aspects of language without the complicating
factors of lesions, which potentially affect more than one component of
language. PET is a technique that examines changes in cerebral blood flow
in localized brain areas during cognitive activities. The time frame over
which blood flow is measured is about 40 s. The assumption underlying this
methodology is that the greater the involvement of a particular area of the
brain in a particular cognitive activity, the greater will be the metabolic
activity, hence cerebral blood flow, to that area. Nevertheless, this technique
has its own weaknesses and potential problems. Perhaps the biggest chal-
10 The Neurobiology of Language 341
B. T h e o r e t i c a l F r a m e w o r k
As a preliminary step in the discussion of the neurobiology of language, it
may be useful to consider some broad theoretical issues that have guided
research in this field. Much as linguistic research has been guided by consid-
erations of the structural levels of the linguistic grammar, such as phonol-
ogy, lexicon/semantics, and syntax, so have linguistic investigations of
aphasia (see Frazier, Chapter 1, this volume). The major question has been
whether language deficits in aphasia reflect selective impairments to these
342 Sheila E. Blumstein
tory system in the latter, and for that reason the interface of these two
systems with the lexicon for speech production and speech perception re-
quires a unique set of operations (see Fowler, Chapter 2, and Nygaard and
Pisoni, Chapter 3, this volume). For this reason, it is useful to consider the
neurobiology of speech production and speech perception separately.
A. Speech Production
Linguistic theory makes a clear distinction between phonology and phonet-
ics, and the facts of aphasia support such a distinction, particularly in the
investigation of speech production deficits. In some cases, patients may
produce a wrong sound segment, but its phonetic implementation is cor-
rect, that is, for teams the patient says keams. In other cases, patients may
produce the correct sound segments but their phonetic implementation is
distorted, that is, for teams the patient produces an i n i t i a l / t / t h a t is overly
aspirated.
Research investigations have focused on the patterns of speech produc-
tion errors of aphasic patients. A number of different methodologies have
been used to elicit productions from patients including conversational
speech, naming, and repetition. Despite the different methodologies used, a
consistent finding is that nearly all aphasic patients, regardless of the aphasia
syndrome, display impairments implicating a deficit at the phonological
level. Critically, the patterns of impairment are similar, suggesting that
despite the different underlying neuropathology, a common mechanism is
impaired. The similar patterns of performance are particularly striking giv-
en the different clinical characteristics and neuropathology of the patients
investigated. The mechanism impaired in the phonological output impair-
ment of all of these patients relates to the selection and/or organization of
the features comprising the candidate lexical entries. Selection impairments
reflect the inappropriate choice of a feature and hence the appearance of an
inappropriate segment in a particular position. Planning impairments reflect
the inappropriate ordering of the segments or alternatively the inappropriate
influence of phonetic context on the ultimate feature or segment selected.
The patterns of sound substitutions indicate that it is indeed the selection of
an inappropriate feature and not the selection of an inappropriate segment
that underlies these types of errors.
The types of errors produced by aphasic patients can be categorized in
terms of four descriptive categories. Together they suggest that the basis of
the errors reflects a selection as well as a planning deficit (Blumstein, 1973).
These errors include: phoneme substitution errors in which a segment is
substituted for another (e.g., teams ~ keams); simplification errors in which
a phoneme or syllable is deleted (e.g., green ~ geen); addition errors in
which an extra phoneme or syllable is added to a word (e.g., see ~ stee); and
10 The Neurobiology of Language 345
become voiceless (e.g., /d/ --o /t/), and a voiceless stop consonant may
become voiced ( e . g . , / t / ~ / d / ) . Thus, the patterns of errors reflect statisti-
cal tendencies. Because patients are able to produce the correct utterance and
because their errors are systematic (although not predictable), it suggests
that the underlying phonological representations are intact, but that either
the level of activation of the features has been changed or there has been a
failure to select the appropriate phonological representation from the lexi-
con. Even though virtually all aphasic patients regardless of lesion site dis-
play similar patterns of phonological impairment, they vary in the severity
of the impairment. Patients with Broca's aphasia and damage to anterior
brain structures produce many more such errors than do patients with
Wernicke's aphasia (Blumstein, 1973).
While the phonological patterns are similar across patients, phonetic defi-
cits seem to be more selective. A long-held observation is that patients with
anterior aphasia produce phonetic errors. The implied basis for these errors
is one of articulatory implementation; that is, the commands to the articula-
tors to encode the word are incorrect, poorly timed, and so forth. A num-
ber of studies have explored these phonetic patterns of speech by investigat-
ing the acoustic properties or the articulatory parameters underlying the
production of particular phonetic dimensions. The dimensions investigated
include voicing in stop consonants (e.g., /p t k / v s . /b d g/) and fricatives
(e.g., / f s / v s . /v z/), place of articulation in stop consonants (e.g., / b / v s .
/ d / v s . /g/) and fricatives (e.g., / f / v s . /s/), and the nasal and stop manner
of articulation (e.g., /n m/ vs. /d b/). Studies of speech production in
aphasia patients with damage to anterior brain structures (including patients
with Broca's aphasia) have shown that these patients have difficulty produc-
ing phonetic dimensions that require the timing of two independent articu-
lators. These findings have emerged in the analysis of two phonetic dimen-
sions, voicing and nasality. In the case of the feature voicing, the dimension
studied is voice-onset time, that is, the timing relation between the release
of a stop consonant and the onset of vocal cord vibration. The production of
nasal consonants also requires appropriate timing between two articulators,
in this case, the release of the closure in the oral cavity and the velum
opening.
Results of analyses of the production of the voicing and nasal phonetic
dimensions have shown that aphasic patients with anterior brain-damage
(including patients with Broca's aphasia) evidence significant deficits
(Blumstein, Cooper, Goodglass, Statlender, & Gottlieb, 1980; Blumstein,
Cooper, Zurif, & Caramazza, 1977; Freeman, Sands, & Harris, 1978; Gan-
dour & Dardarananda, 1984a, Itoh, Sasanuma, Hirose, Yoshioka, & Ushi-
jima, 1980, Itoh et al., 1982; Itoh, Sasanuma, & Ushijima, 1979; Shewan,
Leeper, & Booth, 1984). These same patterns emerge across different lan-
guages. They occur not only in English and Japanese, for which voice-onset
10 The Neurobiology of Language 347
outlined above with particular areas of brain damage, and PET and ERP
data with neurologically intact subjects. In particular, CAT scan correla-
tions with patterns of speech production deficits suggest the involvement of
Broca's area, lower motor cortex regions for larynx, tongue, and face, and
some white matter structures as well in the phonetic implementation of
speech (Baum et al., 1990). PET studies with neurologically intact subjects
determining regions of cerebral blood flow activity during speech produc-
tion also show the importance of these areas as well as the precentral gyrus
and premotor areas surrounding Broca's area (Petersen, Fox, Posner, Mint-
un, & Raichle, 1989). It is interesting that ERP studies with these subjects
suggest that these areas seem to be involved in the production of articula-
tory maneuvers related specifically to the production of speech sounds and
not more generally to vocal tract maneuvers that do not relate to speech
(McAdam & Whitaker, 1971).
B. Speech Perception
Similar to production studies with aphasic patients, most studies exploring
the role of speech perception deficits in auditory comprehension impair-
ments have focused on the ability of aphasic patients to perceive phonemic
or segmental contrasts. Studies on segmental perception have indeed shown
that aphasic patients evidence deficits in processing segmental contrasts.
These studies have explored patients' abilities to discriminate pairs of words
or nonwords (e.g. pear vs. bear, pa vs. ba) or they have asked subjects to
point to the appropriate word or consonant from an array of names or
syllables that are phonologically confusable. Results show that patients with
both anterior and posterior aphasia display some problems in discriminating
phonological contrasts (Blumstein, Baker, & Goodglass, 1977; Jauhiainen &
Nuutila, 1977; Miceli, Calatgirone, Gainotti, & Payer-Rego, 1978; Miceli,
Gainotti, Caltagirone, & Masullo, 1980) or in labeling or identifying conso-
nants presented in a consonant-vowel context (Basso, Casati, & Vignolo,
1977; Blumstein, Cooper et al., 1977; cf. also Boatman, Lesser, & Gordon,
1994). These problems emerge in the perception of both real words and
nonsense syllables. Although there are more errors in the perception of
nonsense syllables than in the perception of real words, the overall patterns
of performance are similar, and essentially mirror the patterns found in the
analysis of phonological errors in speech production. Namely, subjects are
more likely to make speech perception errors when the test stimuli contrast
by a single feature than when they contrast by two or more features (Baker,
Blumstein, & Goodglass, 1981; Blumstein, Baker, & Goodglass, 1977; Mic-
eli et al., 1978; Sasanuma, Tatsumi, & Fujisaki, 1976). Among the various
types of feature contrasts, the perception of place of articulation is partic-
ularly vulnerable (Baker et al., 1981; Blumstein, Baker, & Goodglass, 1977;
350 Sheila E. Blumstein
with the lexicon. Consistent with this view is the finding that although
patients may show speech perception impairments, their performance is
variable; they do not show selective impairments relating to a particular
phonetic feature; and the pattern of errors is bidirectional, for example,
voiced consonants may be perceived as voiceless, and voiceless consonants
may be perceived as voiced. This pattern of results mirrors that found in
speech production studies with aphasic patients.
In contrast to the segmental features of speech, the prosodic cues (i.e.,
intonation and stress) are consistently less affected in aphasia. Severely im-
paired aphasic patients have been shown to retain some ability to recognize
and distinguish the syntactic forms of commands, yes-no questions, and
information questions when marked only by intonation cues (Green &
Boller, 1974), even when they are unable to do so when syntactic forms are
marked by lexical and syntactic cues. Nonetheless, as with intonation cues,
patients' performance is not completely normal. A number of studies have
revealed impairments in the comprehension of lexical/phrasal stress con-
trasts (e.g., h6tdog vs. hotd6g) (Baum, Kelsch Daniloff, & Daniloff, 1982;
Emmorey, 1987), as well as sentential contrasts (e.g., he fed her d6g biscuits
vs. he fed her dog biscuits) (Baum et al., 1982). Similar findings emerged for
the perception of tone contrasts serving as lexical cues in Thai (Gandour &
Daradarananda, 1983) and Chinese (Naeser &Chan, 1980). No differences
have emerged in any studies between the performance of patients with
anterior and posterior aphasia, an important finding consistent with the
results for the perception of phonemic contrasts.
That speech perception deficits emerge in patients with both anterior and
posterior aphasia suggests that the neural basis for speech perception and the
auditory processing of speech is neurally complex, and includes far greater
neural involvement than simply the primary auditory areas and auditory
association areas in the temporal lobe. While the number of neuro-
physiological and electrophysiological studies focusing particularly on
speech reception are few, these results provide converging evidence consis-
tent with this view. PET studies have shown that the primary auditory
cortex is activated in the processing of simple auditory stimuli (Lauter,
Herscovitch, Formby, & Raichle, 1985), and both the primary auditory
cortex and the superior temporal gyrus are activated in passive word recog-
nition (Petersen, Fox, Posner, Mintun, & Raichle, 1988, 1989). These re-
sults are of no surprise. What is of interest, however, is that other cortical
areas seem to be activated as well. For example, Zatorre, Evans, Meyer, and
Gjedde (1992) showed increased activity in Broca's area near the junction
with premotor cortex as well as the superior parietal area near the supra-
marginal gyrus when subjects were required to make a phonetic decision or
phonetic judgment about auditorily presented CVC stimuli. Further,
Ojemann (1983) has shown impairments in the ability of patients to identify
352 SheilaE. Blumstein
III. T H E L E X I C O N
One of the most c o m m o n clinical attributes in aphasia is a naming deficit.
Such a deficit is operationally defined as an inability or inconsistency in
giving the appropriate name for an object, the depiction of an action, and so
on. This deficit may also manifest itself in word-finding difficulty (i.e.,
groping for the appropriate word), semantic paraphasias (i.e., word substi-
tutions), or empty speech (i.e., the use ofnonspecific words, as thing, be) in
the patient's spontaneous speech output. A number of attributes contribute
to the evocation of a name and can influence a subject's overall performance,
including word frequency (Howes, 1964; Rochford & Williams, 1962) and
its concreteness or picturability (Goodglass, Hyde, & Blumstein, 1969). In
fact, some patients have been identified with selective impairments in nam-
ing particular semantic categories or classes of words (cf. Hart, Berndt, &
Caramazza, 1985). Nonetheless, most aphasic patients do not have such
selective deficits, but rather have a naming deficit cutting across semantic
categories and word classes. The question remains as to what is the basis for
these nonspecific and pervasive naming deficits. Two possibilities have been
proposed. One possibility is that the patients have a lexical access impair-
ment. In this case, the underlying lexical representation and organizational
properties are intact, but the processes required to access this information
are impaired. A second possibility is that the patients have an impairment in
the lexical representation or semantic structure of the words themselves.
Whether the deficit is one of access or representation, such lexical impair-
ments would not only influence naming but could also affect the compre-
hension of language (see Cutler, Chapter 4, and Seidenberg, Chapter 5, this
volume).
There is a fair amount of clinical evidence suggesting that the basis of
naming impairments reflects a retrieval or access problem. A patient who is
unable to name a particular object in one context or at one time may be able
to do so at another. This inconsistency in object naming suggests that the
representation of the lexical item is intact, but the patient may be unable to
354 SheilaE. Blumstein
evoke its name. In support of this interpretation is the fact that the patient
who has failed to name or has misnamed an object may recognize the
appropriate name of the object when it is offered by the examiner. Further,
having failed to name an object, patients can often say what it is used for
(e.g., for cup they may say drink). In addition, they may be able to provide
the generic properties of the word such as the letter it begins with and the
number of syllables it contains (Goodglass, Kaplan, Weintraub, & Acker-
man, 1976). Presumably, the representation of the word must be in the
internal lexicon in order for the patient to be able to recall these properties.
Further insight into naming deficits can be provided by analyzing the
types of misnaming errors a patient may make. When patients cannot name
a particular stimulus, they may often substitute a word in the same semantic
field or produce a word that is a semantic associate to the target (Rinnert &
Whitaker, 1973) (e.g., for chair, they may say sofa; for mother, father). Nev-
ertheless, although consistent with an access deficit, these results could also
reflect a representation impairment. That is, if patients were operating with
a restricted semantic field or a modified conceptual framework for lexical
items, they could well access the appropriate semantic category without
having a full sense of the word and its appropriate name. Semantically
associated verbal paraphasias would then be a natural consequence of such a
deficit.
Consistent with the view that patients' deficit reflects a representation
impairment are results from a study by Zurif, Caramazza, Myerson, and
Galvin (1974) who investigated patients' judgments about semantic related-
ness. In particular, they asked subjects to group the two words of three that
best went together. The words (mother, father, partner, knight, husband,
shark, trout, dog, tiger, turtle, crocodile)varied along several semantic
dimensions (human-nonhuman, gender, functional attribute). Results
showed that neurologically intact control subjects grouped the words along
these semantic dimensions; patients with Broca's aphasia did so, too, with
only one minor exception. In contrast, patients with Wernicke's aphasia
showed no specific pattern--they were as likely to group mother with father
as mother with trout. These results were used as evidence supporting the view
that patients with Wernicke's aphasia have an impairment in the underlying
organization of the lexicon, hence a deficit in lexical representation (cf.
Goodglass & Baker, 1976).
More recently, however, a series of studies have been conducted that
challenge this view. These studies have explored on-line lexical processing
by exploring semantic priming in a lexical decision task. Using an adapta-
tion of a procedure developed by Meyer and Schvaneveldt (1971), the ex-
perimenters asked aphasic patients to make a lexical decision about words
and nonwords presented either visually (Milberg & Blumstein, 1981) or
auditorily (Blumstein, Milberg, & Shrier, 1982). The target word to be
10 The Neurobiology of Language 355
judged (e.g., dog) was preceded by a prime that "was semantically related
(e.g., cat), semantically unrelated (e.g., table), or neutral that is, a nonword
(e.g., glub) with respect to the prime. In both studies, patients with Wer-
nicke's aphasia showed, as do control subjects, semantic facilitation, that is,
they responded faster to a real-word target preceded by a semantically
related prime than to one preceded by a semantically unrelated or nonword
prime. Surprisingly, patients with Broca's aphasia did not show this seman-
tic facilitation as consistently as did patients with Wernicke's aphasia. When
the prime-target pairs included highly associated words, patients with
Broca's aphasia showed evidence of priming (Blumstein et al., 1982). When
the semantic relationships were more subtle, that is, ambiguous words
(Milberg, Blumstein, & Dworetzky, 1987), or when the lexical decision
target word was not temporally paired with the preceding prime (i.e., the
subject was required to make a lexical decision response to each stimulus
presented) (Milberg & Blumstein, 1981), they did not as a group show
evidence of semantic priming. In contrast, when the same patients were
asked to make judgments about the semantic relatedness of the word pairs,
patients with Wernicke's aphasia performed randomly, and patients with
Broca's aphasia performed well.
To account for the dichotomy between the performance of patients with
Broca's and Wernicke's aphasia on these tasks, it was proposed that lexical
deficits in aphasia are better characterized in terms of the processing opera-
tions required for lexical access, rather than on the integrity of the stored
lexical knowledge base. In particular, it has been suggested that there are
two distinct processes involved in lexical access, one called automatic process-
ing that is fast acting, of short duration, not under voluntary control, and
thus largely automatic, and a second called controlled processing that is slower
acting, under a subject's voluntary control, and thus influenced by a sub-
ject's expectancies or attentional demands (Posner & Snyder, 1975; Shif-
frin & Schneider, 1977). Subjects with Wernicke's aphasia show consistent
evidence of semantic facilitation in the lexical decision tasks, but do not
appear to be able to analyze word meaning in a simple semantic judgment
task. Therefore, they seem to be able to automatically access words, and yet
are unable to use the knowledge about semantic features or semantic rela-
tions in making decisions about the meanings of words. For subjects with
Broca's aphasia, results are less clear-cut. The lack of consistent priming
effects suggests that the automatic activation of lexical candidates may be
impaired. However, these patients appear to have little difficulty analyzing
word meaning using controlled processing. In fact, recent debate in the
literature has centered on whether the impairment of subjects with Broca's
aphasia reflects slowed access to lexical representations (Hagoort, 1993), or
alternatively, a diminished activation of word candidates (Milberg, Blums-
tein, Katz, & Gershberg, 1995). Whatever the correct interpretation, it is
356 SheilaE. Blumstein
worth noting that in both cases the explanation turns on the processing
routines used for lexical access.
Similar results emerged in studying the time course of lexical access in
sentences. Swinney, Zurif, and Nicol (1989) explored the extent to which
aphasic patients use sentence context in accessing the meanings of ambigu-
ous words. In a cross-modal lexical decision task in which the sentence is
presented auditorily and the lexical target is presented visually, neuro-
logically intact subjects show access to all meanings of an ambiguous word
at its initial presentation even with a preceding biasing context toward one
interpretation. Only further downstream is the meaning appropriate to the
context uniquely retained. For example, in the sentence, the man saw several
spiders, roaches, and other bugs (1) in the corner (2) of the room, subjects show
semantic facilitation to all meanings of the word bugs (i.e., ant and spy) at
time (1), but at time (2) show semantic facilitation only to ant (Onifer &
Swinney, 1981). Swinney and his colleagues (1989) explored semantic facili-
tation in aphasic patients investigating whether they showed semantic facili-
tation to both meanings of an ambiguous word at time (1) [they did not
investigate semantic facilitation downstream at time (2)]. They showed that
similar to neurologically intact subjects, Wernicke's aphasia patients showed
priming for both meanings of the ambiguous words at time (1), irrespective
of the biasing context. In contrast, patients with Broca's aphasia showed
semantic facilitation only to the most frequent meaning of the ambiguous
word regardless of the biasing context. Thus, while patients with Broca's
aphasia clearly show an impairment in accessing word meanings from the
lexicon, similar to control subjects and Wernicke's aphasia patients, such
access is not affected by the sentence context in which the word appears.
Evidence consistent with the observation that the emergence of word
meaning is influenced by contextual factors and is not all-or-none comes
from ERP studies, beginning with the seminal work of Kutas and Hillyard
(1980). In a series of studies, they showed that while there are no ERP
"signatures" tied to either a specific word such as dog or a semantic category
such as fruit, there is a marker, the N400, which is sensitive to semantic
anomaly and semantic expectations (e.g., I take my coffee with cream and dog).
The N400 is a time-locked component that occurs between 350 and 800 ms
after stimulus presentation. The N400 emerges whether the anomaly occurs
in sentence-final or sentence-medial position, and whether the anomaly is in
a sentence or in a more natural prose context (Kutas & Hillyard, 1980,
1983).
O f critical importance, the N400 "marker" relates specifically to seman-
tics; it does not emerge for syntactic anomalies (i. e., tense or number errors)
nor for physical changes to the stimulus (i.e., unexpected differences such as
change of letter size) (Kutas & Hillyard, 1983). Moreover, lexical processing
is dependent on the activation level of candidate lexical items. In particular,
ERP studies have shown that the amplitude of the N400 varies as a function
10 The Neurobiology of Language 357
of the likelihood that a word will appear in a context. The N400 signifi-
cantly decreases if an anomalous word is semantically related to an appro-
priate completion; for example, in the 2ame was called off because it started to
umbrella, umbrella is semantically related to the word rain, the natural com-
pletion of the sentence, and thus shows a significantly smaller N400 than for
coffee, which bears no semantic relationships between coffee and the natural
completion of the sentence. These results suggest that lexical access is
graded, changing as a function of the level of activation of a word candidate
(Kutas & Hillyard, 1984) and the extent to which the word candidate acti-
vates a semantic network (Kutas, Lindamood, & Hillyard, 1984). These
priming effects also emerge for single words; the N400 is larger to weakly
primed versus strongly primed lexical associates and is larger to unrelated
than to related words (Kutas & Hillyard, 1988).
PET studies also provide important converging evidence concerning the
processing components involved in lexical access (Petersen, et al., 1988,
1989; Posner, Petersen, Fox, & Raichle, 1988). These studies have shown
the involvement of anterior brain structures in the semantic processing
of single words in non-brain-damaged subjects, a result consistent with
the impairments shown in lexical priming for Broca's aphasia subjects de-
scribed above. They also showed the role of different brain areas in the
perception of visually and auditorily presented words, even though each
share access to a common output (articulatory) and meaning (semantic)
system. Thus, the PET studies show that the performance of cognitive tasks
requires the integration of a large number of component computations and
in this sense such tasks seem not to be performed in a single area of the
brain.
Taken together, the results of studies with aphasic patients and with
neurologically intact subjects using both ERP and PET suggest that the
neural basis of lexical processing is indeed complex. Both anterior and
posterior brain structures seem to be involved in lexical access, although to
date it is not clear what the contributions of these various structures are to
lexical access and lexical processing. What does seem to be the case is that
there are neurophysiological markers related to access of meaning. More-
over, lexical impairments seem to reflect deficits in lexical access and not
lexical representation. A point of interest is that the processing components
contributing to lexical access may be affected differently as a function of the
type of aphasia and presumably as a function of the different neural struc-
tures involved.
IV. SYNTAX
Nearly all aphasic patients display syntactic impairments in their speech
output. Nevertheless, the hallmark of syntactic production deficits is char-
acterized by patients with Broca's aphasia, who clinically are often de-
358 Sheila E. Blumstein
logically. Additional support for this view comes from the language pat-
terns of congenitally deaf signers who sustain brain damage to these same
neural structures. These patients also display agrammatic deficits, in this
case relating to the syntactic properties of sign (Corina, Vaid, & Bellugi,
1992). In American Sign Language (ASL), syntax is marked by certain
hand-shape and movement configurations. The only common attribute be-
tween hand-shape and movement configurations in ASL and word order,
infixing, and agglutination in aural/oral language is the syntactic function
these attributes play in language.
Further analysis of productive agrammatism also reveals that it is charac-
terized by the substitution of syntactic particles or endings for each other
rather than the "loss" of these endings. For example, in English the singular
form for a word is characterized phonologically by a zero marker [i.e., boy
+ 0 (singular)], whereas the plural is determined by the addition of the
plural f o r m / s / t o the word stem [i.e., boy +/s/(plural)]; thus, for English
it is impossible to ascertain whether the production of the singular boy for
the plural boys reflects the loss of the plural form or alternatively the substitu-
tion of the singular (zero) morphological ending for the plural. However, in
other languages such as Russian, German, Japanese, Hebrew, and Arabic,
the stem itself does not appear alone and all words must be marked with a
morphological ending. Thus, it is possible to determine whether the agram-
matic patient's production reflects the loss or substitution of a morphologi-
cal marker. Results show that in these languages, agrammatic patients al-
ways use a syntactic marker, albeit from time to time, the wrong marker
(Menn & Obler, 1990); thus, the syntactic markers are not lost but rather are
substituted for each other. These results lend credence to the view that the
basis of the agrammatic deficit is primarily a syntactic one and not an
economizing effort by the patient to reduce the amount of language output.
Additional evidence supports the view that agrammatism is primarily a
syntactic deficit. In addition to the deficit with morphology described
above, agrammatic patients also display a reduction in the variety of syntac-
tic structures that they use, as well as a failure to concatenate phrases that
constitute a sentence. Thus, patients have great difficulty in juxtaposing the
noun phrase (NP) and verb phrase (VP) of a sentence, while they may still
be able to maintain the internal cohesion of the NP itself by using adjectives
and the VP itself by concatenating the verb with a following object. More-
over, the occurrence of more complex sentences and phrases containing
embeddings and compound nouns and verbs is rare. The failure to produce
these syntactic structures, however, does not seem to reflect a loss of the
"knowledge" of these structures. Goodglass, Gleason, Bernholtz, and Hyde
(1972) have shown that patients may use alternative strategies to convey a
meaning that they seem to be unable to express using a given syntactic
structure. For example, given a structured story completion test designed to
3(~ SheilaE. Blumstein
ably because reference to one of the two circles requires the use of an
indefinite article. In contrast, agrammatic aphasia patients show no differ-
ences in reaction time to the two commands "press a round one" and "press
the round one," suggesting that they do not appropriately process the
meaning difference between the two articles (Goodenough, Zurif, &
Weintraub, 1977). In other research (Caramazza & Zurif, 1976), patients
with Broca's aphasia showed comprehension deficits in understanding
subject-object relations in embedded sentences in a picture-pointing task. It
is interesting that these deficits emerged only when the test sentences were
10 The Neurobiology of Language 361
stripped of other potential semantic cues that could be used by the subjects.
That is, their deficit emerged in the context of semantically reversible sen-
tences such as the clown chases the midget, and not when the meaning of the
sentence was constrained by semantic and real-world probabilities such as
the man patted the dog.
The fact that most agrammatic aphasia patients display a syntactic com-
prehension deficit as well as a syntactic production deficit (but cf. Miceli,
Mazzucchi, Menn, & Goodglass, 1983) suggests that a single impairment,
namely, a central syntactic impairment, underlies their language difficulty.
The deficit is considered "central" because it affects syntax independent of
its language modality~speaking, comprehending, reading, and writing.
As to the specific nature of this syntactic deficit, recent research has sug-
gested that the impairment is more likely a deficit in syntactic processing
than it is a deficit in syntactic representation. Several lines of research con-
tribute to this view (although cf. Caplan et al., 1985, and Caplan & Futter,
1986, Grodzinsky, 1984, 1986, for alternative points of view). Patients who
are agrammatic in both production and comprehension, nonetheless are
able to make grammaticality judgments (Linebarger, Schwartz, & Saffran,
1983). Thus, these patients are able to judge the grammaticality of sentences
that violate different types of syntactic structures, for example, *he shut the
window that the door was open (gapless relatives), *the girls laughed the clown
(subcategorization), and *my father knew they would give the job to (empty
elements). This relatively spared ability to make syntactic judgments in the
face of grammatical comprehension and production deficits for the same
type of syntactic structures suggests that syntactic representations are intact.
The comprehension and production impairments probably reflect the fact
that these patients have a processing deficit affecting the "mapping" of
syntactic structures onto their appropriate semantic representations.
Consistent with this view are the results of several on-line syntactic
processing experiments. These studies have shown that agrammatic aphasia
patients do not show a sensitivity to morphological constraints that non-
brain-damaged control subjects show. In particular, unlike control subjects,
they fail to show faster reaction times in a lexical decision task to verbs
when preceded by a grammatically appropriate modal (e.g., is-going) than
when preceded by a grammatically inappropriate modal (e.g., could-going)
(Blumstein, Milberg, Dworetzky, Rosen, & Gershberg, 1991). Nonethe-
less, these same patients show an ability to make correct syntactic judg-
ments of these same verb phrases in an off-line grammaticality judgment
task. Similarly, Friederici and Kilborn (1989) showed a delay in accessing
syntactic information specified by morphological endings in subjects with
Broca's aphasia compared to syntactic information provided by individual
lexical items.
That the syntactic processing impairment extends beyond the processing
362 SheilaE. Blumstein
V. SUMMARY
Investigation of the neurobiology of language provides support for the view
that the organization of the language system is indeed complex. All aphasic
patients display phonological, lexical, and syntactic deficits regardless of
aphasia type and lesion localization, suggesting that the neural instantiation
of these linguistic components requires complex neural structures that are
represented throughout the left hemisphere. Consideration of the neuro-
biology of the sound structure of language and, especially, the studies of
aphasic patients suggest that the organization and ultimate implementation
of the phonological sound structure is broadly represented in the left domi-
nant hemisphere and deficits relate to selection and planning in speech pro-
duction and access in speech perception. In contrast, as shown by studies of
patients with aphasia and results of PET and ERP investigations, the pho-
netic implementation of speech seems to be subserved by specific neural
substrates, and phonetic deficits reflect impairments in particular articula-
tory movements rather than in underlying linguistic features. With respect
to the neurobiology of the lexicon and syntax, ERP and PET studies pro-
vide support for electrophysiological markers for lexical meaning and syn-
tactic structures, and, in conjunction with data from aphasic patients, sug-
gest that with the possible exception of productive agrammatism, the neural
basis of the lexicon and syntax is broadly represented. Studies of both
lexical and syntactic impairments show that these deficits emerge in both
production and comprehension, and they reflect impairments to the pro-
cessing mechanisms accessing lexical and/or syntactic structures rather than
deficits to the representations or structures themselves.
Although this chapter has used a modular approach to language as a
theoretical framework by studying separately phonology, the lexicon, and
syntax, the results of this research suggest that there is little evidence to
support the view that the organization of the language system itself is
modular. In particular, language impairments in aphasia reflect processing
disorders that cut across the linguistic components of the grammar includ-
ing phonology, the lexicon, and syntax. Language impairments in aphasia
10 The Neurobiology of Language 365
Acknowledgment
This research was supported in part by NIH Grant DC00314 to Brown University.
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