Republic of the Philippines

POLYTECHNIC UNIVERSITY OF THE PHILIPPINES

SANTA ROSA CAMPUS
City of Santa Rosa, Laguna

Artwork courtesy from: Leigh T. Cadavos

INSTRUCTIONAL MATERIALS FOR

ABNORMAL PSYCHOLOGY
(PSYC 30093)

COMPILED BY:

MS. SHEINA T. CADAVOS, RPm

Revised
September 2021
 TABLE OF CONTENTS

Module 1: Abnormal Psychology

Part 1: Abnormal Psychology: Overview and Historical Roots …………………………………………….. 2-10
Part 2: Models and Integrative Approaches to Psychopathology ………………………………………... 11-44
Module 2: Anxiety Disorders ………………………………………………………………………………………. 45-59
Module 3: Trauma- and Stressor-Related Disorder and Obsessive-Compulsive and Related Disorders
Part 1: Trauma- and Stressor-Related Disorder …………………………………………………………… 60-71
Part 2: Obsessive-Compulsive and Related Disorders …………………………………………………… 72-81
Module 4: Mood Disorders ……………………………………………………………………………………….. 82-100
Module 5: Eating and Sleep-Wake Disorders
Part 1: Eating Disorders ………………………………………………………………………………….... 101-103
Part 2: Sleep-Wake Disorders …………………………………………………………………………….. 104-106
Module 6: Disruptive, impulse-Control, and conduct disorders ……………………………………………... 107-111
Module 7: Paraphilic Disorder & Dissociative Disorder
Part 1: Paraphilic Disorder ………………………………………………………………………………… 112-115
Part 2: Dissociative Disorder ……………………………………………………………………………… 116-122
Module 8: Personality Disorders ……………………………………………………………………………….. 123-141
Module 9: Schizophrenia Spectrum and Other Psychotic Disorders ………………………………………. 142-155
Module 10: Substance-Related and Addictive Disorders …………………………………………………… 156-166
Module 11: Neurodevelopmental Disorders ………………………………………………………………….. 167-173
Module 12: Neurocognitive Disorder ………………………………………………………………………….. 174-177
References …………………………………………………………………………………………………………. 178

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 MODULE 1: ABNORMAL PSYCHOLOGY

Module Overview:

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Photo from: pinterest.com

In part 1, we will venture the nature of abnormal behaviour by describing what normal
behaviour is, and how history and today’s society view mental disorders, which includes
what research methodologies were used by mental health professionals in general and
how they are adapted to study abnormal behavior/mental disorders.

In part 2, we will tackle the three core models in abnormal psychology namely;
biological, psychological, and sociocultural models. Every model has its own
exceptional perspective to various spectrum of abnormal behaviour but cannot account
solely by defining one. Thus, a multi-dimensional and not a uni-dimensional model will
be advocated for.

Module Objectives:

• Explain what it means to display abnormal behavior.

• Outline the history of mental illness.
• Describe research methods used to study abnormal behavior and mental
illness.
• Differentiate uni- and multi-dimensional models of abnormality.
• Describe how the biological model explains mental illness.
• Describe how psychological perspectives explain mental illness.
• Describe how the sociocultural model explains mental illness.

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Course Materials

PART 1: ABNORMAL PSYCHOLOGY: OVERVIEW AND HISTORICAL ROOTS

I. What is Abnormal Behaviour?

Is a psychological dysfunction within an individual that is associated with distress or
impairment in functioning and a response that is not typical or culturally expected? On the
surface, these three criteria may seem obvious, but they were not easily arrived at and it is
worth a moment to explore what they mean. You will see, importantly, that no one criterion has
yet been developed that fully defines abnormality. The 4D’s of Abnormal Behavior:

a. Dysfunction - Abnormal behaviour has the capacity to make our well-being difficult to obtain
and can be assessed by looking at an individual’s current performance and comparing it to what
is expected in general or how the person has performed in the past.
b. Distress - When the person experiences a disabling condition “in social, occupational, or
other important activities”. Distress can take the form of psychological or physical pain or both
concurrently. Alone though, distress is not sufficient enough to describe behavior as abnormal.
c. Deviance - Closer examination of the word abnormal shows that it indicates a move away
from what is normal, or the mean (i.e. what would be considered average and in this case in
relation to behavior), and so is behavior that occurs infrequently (sort of an outlier in our data).
d. Dangerousness - Though not part of the DSM conceptualization of what abnormal behavior
is, many clinicians add this to the list, or when behavior represents a threat to the safety of the
person or others.
In conclusion, the most widely accepted definition used in DSM-5 describes behavioral,
psychological, or biological dysfunctions that are unexpected in their cultural context and
associated with present distress and impairment in functioning, or increased risk of suffering,
death, pain, or impairment. This definition can be useful across cultures and subcultures if we
pay careful attention to what is functional or dysfunctional (or out of control) in a given society.
But it is never easy to decide what represents dysfunction, and some scholars have argued
persuasively that the health professions will never be able to satisfactorily define disease or
disorder. The best we may be able to do is to consider how the apparent disease or disorder
matches a “typical” profile of a disorder—for example, major depression or schizophrenia—
when most or all symptoms that experts would agree are part of the disorder are present.

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II. The Clinical Description
Clinical description is represents the unique combination of behaviors, thoughts, and
feelings that make up a specific disorder. In hospitals and clinics, we often say that a patient
“presents” with a specific problem or set of problems or we discuss the presenting problem.
Presents is a traditional shorthand way of indicating why the person came to the clinic.
Clearly, one important function of the clinical description is to specify what makes the
disorder different from normal behavior or from other disorders. Statistical data may also be
relevant. For example, how many people in the population as a whole have the disorder? This
figure is called the prevalence of the disorder. Statistics on how many new cases occur during
a given period, such as a year, represent the incidence of the disorder. Other statistics include
the sex ratio—that is, what percentage of males and females have the disorder—and the typical
age of onset, which often differs from one disorder to another. In addition to having different
symptoms, age of onset, and possibly a different sex ratio and prevalence, most disorders
follow a somewhat individual pattern, or course. Closely related to differences in course of
disorders are differences in onset. Some disorders have an acute onset, meaning that they
begin suddenly; others develop gradually over an extended period, which is sometimes called
an insidious onset. Etiology, or the study of origins, has to do with why a disorder begins
(what causes it) and includes biological, psychological, and social dimensions.

III. Historical Conceptions of Abnormal Behavior

For thousands of years, humans have tried to explain and control problematic behavior.
But our efforts always derive from the theories or models of behavior popular at the time. The
purpose of these models is to explain why someone is “acting like that.” Three major models
that have guided us date back to the beginnings of civilization.

A. THE SUPERNATURAL TRADITION

For much of our recorded history, deviant behavior has been considered a reflection of
the battle between good and evil. When confronted with unexplainable, irrational behavior and
by suffering and upheaval, people have perceived evil.

1. Demons and Witches

During the last quarter of the 14th century, religious and lay authorities supported these
popular superstitions and society as a whole began to believe more strongly in the existence
and power of demons and witches. People increasingly turned to magic and sorcery to solve

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their problems. During these turbulent times, the bizarre behavior of people afflicted with
psychological disorders was seen as the work of the devil and witches. It followed that
individuals possessed by evil spirits were probably responsible for any misfortune experienced
by people in the local community, which inspired drastic action against the possessed.
Treatments included exorcism, in which various religious rituals were performed in an effort to
rid the victim of evil spirits. Other approaches included shaving the pattern of a cross in the hair
of the victim’s head and securing sufferers to a wall near the front of a church so that they might
benefit from hearing Mass.

2. Stress and Melancholy

An equally strong opinion, even during this period, reflected the enlightened view that
insanity was a natural phenomenon, caused by mental or emotional stress, and that it was
curable (Alexander & Selesnick, 1966; Maher & Maher, 1985a). Mental depression and anxiety
were recognized as illnesses (Kemp, 1990; Schoeneman, 1977), although symptoms such as
despair and lethargy were often identified by the church with the sin of acedia, or sloth
(Tuchman, 1978). Common treatments were rest, sleep, and a healthy and happy environment.
Other treatments included baths, ointments, and various potions. In the 14th century, one of the
chief advisers to the king of France, a bishop and philosopher named Nicholas Oresme, also
suggested that the disease of melancholy (depression) was the source of some bizarre
behavior, rather than demons. Oresme pointed out that much of the evidence for the existence
of sorcery and witchcraft, particularly among those considered insane, was obtained from
people who were tortured and who, quite understandably, confessed to anything.

3. Treatments for Possession

Possession, is not always connected with sin but may be seen as involuntary and the
possessed individual as blameless. Furthermore, exorcisms at least have the virtue of being
relatively painless. Interestingly, they sometimes work, as do other forms of faith healing, for
reasons we explore in subsequent chapters. But what if they did not? In the Middle Ages, if
exorcism failed, some authorities thought that steps were necessary to make the body
uninhabitable by evil spirits, and many people were subjected to confinement, beatings, and
other forms of torture (Kemp, 1990). Somewhere along the way, a creative “therapist” decided
that hanging people over a pit full of poisonous snakes might scare the evil spirits right out of
their bodies (to say nothing of terrifying the people themselves). Strangely, this approach
sometimes worked; that is, the most disturbed, oddly behaving individuals would suddenly come

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to their senses and experience relief from their symptoms, if only temporarily. Naturally, this was
reinforcing to the therapist, so snake pits were built in many institutions. Many other treatments
based on the hypothesized therapeutic element of shock were developed, including dunkings in
ice-cold water.

4. Mass Hysteria
In Europe, whole groups of people were simultaneously compelled to run out in the
streets, dance, shout, rave, and jump around in patterns as if they were at a particularly wild
party late at night (still called a rave today, but with music). This behavior was known by several
names, including Saint Vitus’s dance and tarantism. It is most interesting that many people
behaved in this strange way at once. In an attempt to explain the inexplicable, several reasons
were offered in addition to possession. One reasonable guess was reaction to insect bites.
Another possibility was what we now call mass hysteria.

5. The Moon and the Stars

Paracelsus, a Swiss physician who lived from 1493 to 1541, rejected notions of
possession by the devil, suggesting instead that the movements of the moon and stars had
profound effects on people’s psychological functioning. Echoing similar thinking in ancient
Greece, Paracelsus speculated that the gravitational effects of the moon on bodily fluids might
be a possible cause of mental disorders (Rotton & Kelly, 1985). This influential theory inspired
the word lunatic, which is derived from the Latin word luna, meaning “moon.”

B. THE BIOLOGICAL TRADITION

Physical causes of mental disorders have been sought since early in history. Important
to the biological tradition are a man, Hippocrates; a disease, syphilis; and the early
consequences of believing that psychological disorders are biologically caused.

1. Hippocrates and Galen

The Greek physician Hippocrates (460–377 b.c.) is considered to be the father of
modern Western medicine. He and his associates left a body of work called the Hippocratic
Corpus, written between 450 and 350 b.c. (Maher & Maher, 1985a), in which they suggested
that psychological disorders could be treated like any other disease. They did not limit their
search for the causes of psychopathology to the general area of “disease,” because they
believed that psychological disorders might also be caused by brain pathology or head trauma

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and could be influenced by heredity (genetics). Hippocrates considered the brain to be the seat
of wisdom, consciousness, intelligence, and emotion. Therefore, disorders involving these
functions would logically be located in the brain. Hippocrates also recognized the importance of
psychological and interpersonal contributions to psychopathology, such as the sometimes-
negative effects of family stress; on some occasions, he removed patients from their families.
One of the more interesting and influential legacies of the Hippocratic-Galenic approach
is the humoral theory of disorders. Hippocrates assumed that normal brain functioning was
related to four bodily fluids or humors: blood, black bile, yellow bile, and phlegm. Blood came
from the heart, black bile from the spleen, phlegm from the brain, and choler or yellow bile from
the liver.
The four humors were related to the Greeks’ conception of the four basic qualities: heat,
dryness, moisture, and cold. Each humor was associated with one of these qualities. Terms
derived from the four humors are still sometimes applied to personality traits. For example,
sanguine (literal meaning “red, like blood”) describes someone who is ruddy in complexion,
presumably from copious blood flowing through the body, and cheerful and optimistic, although
insomnia and delirium were thought to be caused by excessive blood in the brain. Melancholic
means depressive (depression was thought to be caused by black bile flooding the brain). A
phlegmatic personality (from the humor phlegm) indicates apathy and sluggishness but can also
mean being calm under stress. A choleric person (from yellow bile or choler) is hot tempered
(Maher & Maher, 1985a).
In addition to rest, good nutrition, and exercise, two treatments were developed. In one,
bleeding or bloodletting, a carefully measured amount of blood was removed from the body,
often with leeches. The other was to induce vomiting; indeed, in a well-known treatise on
depression published in 1621, Anatomy of Melancholy, Robert Burton recommended eating
tobacco and a half-boiled cabbage to induce vomiting (Burton, 1621/1977).

C. THE PSYCHOLOGICAL TRADITION

If something was wrong in the environment, such as abusive parents, one’s impulses
and emotions would overcome reason. The best treatment was to re-educate the individual
through rational discussion so that the power of reason would predominate (Maher & Maher,
1985a). This was very much a precursor to modern psychosocial treatment approaches to the
causation of psychopathology, which focus not only on psychological factors but also on social
and cultural ones as well.

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1. Moral Therapy
Its basic tenets included treating institutionalized patients as normally as possible in a
setting that encouraged and reinforced normal social interaction (Bockoven, 1963), thus
providing them with many opportunities for appropriate social and interpersonal contact.
Relationships were carefully nurtured. Individual attention clearly emphasized positive
consequences for appropriate interactions and behavior, and restraint and seclusion were
eliminated.

2. Asylum Reform and the Decline of Moral Therapy

Humane treatment declined because it was widely recognized that moral therapy worked
best when the number of patients in an institution was 200 or fewer, allowing for a great deal of
individual attention. A second reason for the decline of moral therapy has an unlikely source.
The great crusader Dorothea Dix (1802–1887) campaigned endlessly for reform in the treatment
of insanity and began the mental hygiene movement and spent much of her life campaigning for
reform in the treatment of the mentally ill. Unfortunately, an unforeseen consequence of Dix’s
heroic efforts was a substantial increase in the number of mental patients. This influx led to a
rapid transition from moral therapy to custodial care because hospitals were inadequately
staffed. Dix reformed our asylums and single-handedly inspired the construction of numerous
new institutions here and abroad. A final blow to the practice of moral therapy was the decision,
in the middle of the 19th century, that mental illness was caused by brain pathology and,
therefore, was incurable.

3. Psychoanalytic Theory
a. Franz Anton Mesmer (1734–1815) suggested to his patients that their problem was caused
by an undetectable fluid found in all living organisms called “animal magnetism,” which could
become blocked.
b. Jean-Martin Charcot (1825–1893) demonstrated that some techniques of mesmerism were
effective with a number of psychological disorders, and he did much to legitimize the fledgling
practice of hypnosis
c. Sigmund Freud teamed up with Josef Breuer (1842–1925), who had experimented with a
somewhat different hypnotic procedure. While his patients were in the highly suggestible state
of hypnosis, Breuer asked them to describe their problems, conflicts, and fears in as much detail
as they could. Breuer observed two extremely important phenomena during this process. Breuer
and Freud had “discovered” the unconscious mind and its apparent influence on the production

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of psychological disorders. A close second was their discovery that it is therapeutic to recall and
relive emotional trauma that has been made unconscious and to release the accompanying
tension. This release of emotional material became known as catharsis. (Read the case of
Anna O.)

4. The Psychoanalytic Model

a. The Structure of the Mind- The mind, according to Freud, has three major parts or functions:
the id, the ego, and the superego.
b. Defense Mechanism - The ego fights a continual battle to stay on top of the warring id and
superego. Occasionally, their conflicts produce anxiety that threatens to overwhelm the ego.
The anxiety is a signal that alerts the ego to marshal defense mechanisms, unconscious
protective processes that keep primitive emotions associated with conflicts in check so that the
ego can continue its coordinating function.
c. Psychosexual Stages of Development - The stages—oral, anal, phallic, latency, and genital—
represent distinctive patterns of gratifying our basic needs and satisfying our drive for physical
pleasure.

5. The Behavioral Model

a. Ivan Petrovich Pavlov (1849–1936) of St. Petersburg, Russia, initiated the study of classical
conditioning, a type of learning in which a neutral stimulus is paired with a response until it
elicits that response.
b. Edward Titchener (1867–1927) emphasized the study of introspection. Subjects simply
reported on their inner thoughts and feelings after experiencing certain stimuli, but the results of
this “armchair” psychology were inconsistent and discouraging to many experimental
psychologists.
c. John B. Watson (1878–1958) decided that to base psychology on introspection was to head
in the wrong direction; that psychology could be made as scientific as physiology, and that
psychology needs introspection or other nonquantifiable methods no more than chemistry and
physics do.
d. Mary Cover Jones (1896–1987), thought that if fear could be learned or classically
conditioned in this way, perhaps it could also be unlearned or extinguished.
e. Joseph Wolpe (1915–1997) He developed a variety of behavioral procedures for treating his
patients, many of whom suffered from phobias. His best-known technique was termed

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systematic desensitization. Wolpe, working with fellow pioneers Hans Eysenck and Stanley
Rachman in London, called this approach behavior therapy.
f. Burrhus Frederic (B. F.) Skinner (1904–1990) he laid out, in a comprehensive manner, the
principles of operant conditioning, a type of learning in which behavior changes as a function of
what follows the behavior.

3. Prevention research can be viewed in four broad categories: health promotion or positive
development strategies, universal prevention strategies, selective prevention strategies, and
indicated prevention strategies.
4. The clinical picture, causal factors, and treatment process and outcome can all be influenced
by cultural factors.
5. The more the findings of a research program are replicated, the more they gain in credibility.
6. Ethics are important to the research process, and ethical guidelines are spelled out by many
professional organizations in an effort to ensure the well-being of research participants.
7. Ethical concerns are being addressed through informed consent and through the inclusion of
consumers in research design, implementation, and interpretation.

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Course Materials
PART 2: MODELS AND INTEGRATIVE APPROACHES IN PSYCHOPATHOLOGY

Lecture:
In order to effectively treat a mental disorder, we have to understand its cause. This
could be a single factor such as a chemical imbalance in the brain, relationship with a parent,
socioeconomic status (SES), a fearful event encountered during middle childhood, or the way in
which the individual copes with life’s stressors. This single factor explanation is called a uni-
dimensional model. Thus, in reality it is better to subscribe to a multi-dimensional model that
integrates multiple causes of psychopathology and affirms that each cause comes to affect
other causes over time. Uni-dimensional models alone are too simplistic to fully understand the
etiology of mental disorders.
Before introducing the main models subscribed to today, it is important to understand what
a model is. In a general sense, a model is defined as a representation or imitation of an object.
For mental health professionals, models help us to understand mental illness since diseases
such as depression cannot be touched or experienced first-hand. So what are the models we
will examine in this module?
• Biological – Includes genetics, chemical imbalances in the brain, the functioning of the
nervous system, etc.
• Psychological – includes learning, personality, stress, cognition, self-efficacy, and early
life experiences. We will examine several perspectives that make up the psychological
model to include psychodynamic, behavioral, cognitive, and humanistic-existential.
• Socicultural – includes factors such as one’s gender, religious orientation, race, ethnicity,
and culture, for example.

I. THE BIOLOGICAL PERSPECTIVE

A. Brain Structure and Chemistry

1. Communication in the Nervous System
To really understand brain structure and chemistry, it is a good idea to understand how
communication occurs within the nervous system. Simply:
1. Receptor cells in each of the five sensory systems detect energy.
2. This information is passed to the nervous system due to the process of transduction and
through sensory or afferent neurons, which are part of the peripheral nervous system.

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 3. The information is received by brain structures (central nervous system) and perception
occurs.
4. Once the information has been interpreted, commands are sent out, telling the body how
to respond (Step E), also via the peripheral nervous system.

2. The Nervous System

a. Central Nervous System (CNS) - is the control center for the nervous system which receives,
processes, interprets, and stores incoming sensory information. It consists of the brain and
spinal cord.
b. Peripheral Nervous System - consists of everything outside the brain and spinal cord. It
handles the CNS’s input and output and divides into the somatic and autonomic nervous
systems.
c. Somatic Nervous System - allows for voluntary movement by controlling the skeletal muscles
and carries sensory information to the CNS.
d. Autonomic Nervous System - regulates functioning of blood vessels, glands, and internal
organs such as the bladder, stomach, and heart. It consists of sympathetic and parasympathetic
nervous systems.
e. Sympathetic Nervous System - is involved when a person is intensely aroused. It provides
the strength to fight back or to flee (fight-or-flight instinct).
f. Parasympathetic Nervous System - calms the body.

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3. The Neuron
The fundamental unit of the nervous system is the neuron, or nerve cell. It has several
structures in common with all cells in the body. The nucleus is the control center of the body
and the soma is the cell body. It terms of structures that make it different, these focus on the
ability of a neuron to send and receive information. The axon sends signals/information to
neighboring neurons while the dendrites receive information from neighboring neurons and
look like little trees. Notice the s on the end of dendrite and that axon has no such letter. In other
words, there are lots of dendrites but only one axon. Also of importance to the neuron is
the myelin sheath or the white, fatty covering which: 1) provides insulation so that signals from
adjacent neurons do not affect one another and, 2) increases the speed at which signals are
transmitted. The axon terminals are the end of the axon where the electrical impulse becomes
a chemical message and is passed to an adjacent neuron.
Though not neurons, glial cells play an important part in helping the nervous system to
be the efficient machine that it is. Glial cells are support cells in the nervous system that serve
five main functions.
1. They act as glue and hold the neuron in place.
2. They form the myelin sheath.
3. They provide nourishment for the cell.
4. They remove waste products.
5. They protect the neuron from harmful substances.
Finally, nerves are a group of axons bundled together like wires in an electrical cable.

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4. Neural transmission
Transducers or receptor cells in the major organs of our five sensory systems – vision
(the eyes), hearing (the ears), smell (the nose), touch (the skin), and taste (the tongue) –
convert the physical energy that they detect or sense, and send it to the brain via the neural
impulse. How so? We will cover this process in three parts:

Part 1. The Axon and Neural Impulse

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• Step 1 – Neurons waiting to fire are said to be in resting potential and polarized, or
having a negative charge inside the neuron and a positive charge outside.
• Step 2 – If adequately stimulated, the neuron experiences an action potential and
becomes depolarized. When this occurs, ion gated channels open allowing positively
charged Sodium ions to enter. This shifts the polarity to positive on the inside and negative
outside.
• Step 3 – Once the action potential passes from one segment of the axon to the next, the
previous segment begins to repolarize. This occurs because the Na channels close and
Potassium channels open. K has a positive charge and so the neuron becomes negative
again on the inside and positive on the outside.
• Step 4 – After the neuron fires it will not fire again no matter how much stimulation it
receives. This is called the absolute refractory period. Think of it as the neuron
ABSOLUTELY will not fire, no matter what.
• Step 5 – After a short period of time, the neuron can fire again, but needs greater than
normal levels of stimulation to do so. This is called the relative refractory period.
• Step 6 – Please note that the process is cyclical. We start at resting potential in Step 1 and
notice that Step 6 is the same as Step 1.

Part 2. The Action Potential

Let’s look at the electrical portion of the process in another way and add some detail.

• Recall that a neuron is normally at resting potential and polarized. The charge inside is -
70mV at rest.
• If it receives sufficient stimulation meaning that the polarity inside the neuron rises from -70
mV to -55mV defined as the threshold of excitation, the neuron will fire or send an
electrical impulse down the length of the axon (the action potential or depolarization). It

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 should be noted that it either hits -55mV and fires or it does not. This is the all-or-nothing
principle. The threshold must be reached.
• Once the electrical impulse has passed from one segment of the axon to the next, the
neuron begins the process of resetting called repolarization.
• During repolarization the neuron will not fire no matter how much stimulation it receives.
This is called absolute refractory period.
• The neuron next moves into relative refractory period meaning it can fire, but needs greater
than normal levels of stimulation. Notice how the line has dropped below -70mV. Hence, to
reach -55mV and fire, it will need more than the normal gain of +15mV (-70 to -55 mV).
• And then we return to resting potential, as you saw in Figure 2.4
Ions are charged particles found both inside and outside the neuron. It is positively charged
Sodium (Na) ions that cause the neuron to depolarize and fire and positively charged Potassium
(K) ions that exit and return the neuron to a polarized state.

Part 3. The Synapse

The electrical portion of the neural impulse is just the start. The actual code passes from
one neuron to another in a chemical form called a neurotransmitter. The point where this
occurs is called the synapse. The synapse consists of three parts – the axon of the sending
neuron; the space in between called the synaptic space, gap, or cleft; and the dendrite of the
receiving neuron. Once the electrical impulse reaches the end of the axon, called the axon
terminal, it stimulates synaptic vesicles or neurotransmitter sacs to release the
neurotransmitter. Neurotransmitters will only bind to their specific receptor sites, much like a
key will only fit into the lock it was designed for. You might say neurotransmitters are part of a
lock-and-key system. What happens to the neurotransmitters that do not bind to a receptor site?
They might go through reuptake which is the process of the presynaptic neuron taking up
excess neurotransmitters in the synaptic space for future use or enzymatic degradation when
enzymes are used to destroy excess neurotransmitters in the synaptic space.

5. Neurotransmitter
What exactly are some of the neurotransmitters which are so critical for neural transmission,
and are important to our discussion of psychopathology?
• Dopamine – controls voluntary movements and is associated with the reward mechanism
in the brain

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• Serotonin – controls pain, sleep cycle, and digestion; leads to a stable mood and so low
levels leads to depression
• Endorphins – involved in reducing pain and making the person calm and happy
• Norepinephrine – increases the heart rate and blood pressure and regulates mood
• GABA – responsible for blocking the signals of excitatory neurotransmitters responsible for
anxiety and panic.
• Glutamate – associated with learning and memory

The critical thing to understand here is that there is a belief in the realm of mental health
that chemical imbalances are responsible for many mental disorders. Chief among these are
neurotransmitter imbalances. For instance, people with Seasonal Affective Disorder (SAD) have
difficulty regulating serotonin. More on this throughout the book as we discuss each disorder.

6. The Brain
The central nervous system consists of the brain and spinal cord; the former we will discuss
briefly and in terms of key structures which include:
• Medulla – regulates breathing, heart rate, and blood pressure
• Pons – acts as a bridge connecting the cerebellum and medulla and helps to transfer
messages between different parts of the brain and spinal cord.
• Reticular formation – responsible for alertness and attention
• Cerebellum – Involved in our sense of balance and for coordinating the body’s muscles so
that movement is smooth and precise. Involved in the learning of certain kinds of simple
responses and acquired reflexes.
• Thalamus – The major sensory relay center for all senses but smell.
• Hypothalamus – Involved in drives associated with the survival of both the individual and
the species. It regulates temperature by triggering sweating or shivering, and controls the
complex operations of the autonomic nervous system
• Amygdala – Responsible for evaluating sensory information and quickly determining its
emotional importance
• Hippocampus – Our “gateway” to memory. Allows us to form spatial memories so that we
can accurately navigate through our environment and helps us to form new memories
about facts and events
• The cerebrum has four distinct regions in each cerebral hemisphere. First, the frontal
lobe contains the motor cortex which issues orders to the muscles of the body that produce

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 voluntary movement. The frontal lobe is also involved in emotion and in the ability to make
plans, think creatively, and take initiative. The parietal lobe contains the somatosensory
cortex and receives information about pressure, pain, touch, and temperature from sense
receptors in the skin, muscles, joints, internal organs, and taste buds. The occipital lobe
contains the visual cortex and receives and processes visual information. Finally, the
temporal lobe is involved in memory, perception, and emotion. It contains
the auditory cortex which processes sound.

Of course, this is not an exhaustive list of structures found in the brain but gives you a
pretty good idea of function and which structure is responsible for it. What is important to mental
health professionals is that for some disorders, specific areas of the brain are involved. For
instance, Parkinson’s disease is a brain disorder which results in a gradual loss of muscle
control and arises when cells in the substantia nigra, a long nucleus considered to be part of
the basal ganglia, stop making dopamine. As these cells die, the brain fails to receive messages
about when and how to move. In the case of depression, low levels of serotonin are
responsible, at least partially. New evidence suggests “nerve cell connections, nerve cell
growth, and the functioning of nerve circuits have a major impact on depression…and areas that
play a significant role in depression are the amygdala, the thalamus, and the hippocampus.”
Also, individuals with borderline personality disorder have been shown to have structural and
functional changes in brain areas associated with impulse control and emotional regulation
while imaging studies reveal differences in the frontal cortex and subcortical structures for those
suffering from OCD.

B. Genes, Hormonal Imbalances, and Viral Infections

1. Genetic issues and explanations

DNA, or deoxyribonucleic acid, is our heredity material, and is found in the nucleus of
each cell packaged in threadlike structures known as chromosomes for which we have 23 pairs
or 46 total. Twenty-two of the pairs are the same in both sexes, but the 23rd pair is called the
sex chromosome and differs between males and females. Males have X and Y chromosomes
while females have two Xs. According to the Genetics Home Reference website as part of NIH’s
National Library of Medicine, a gene is “the basic physical and functional unit of heredity”. They
act as the instructions to make proteins and it is estimated by the Human Genome Project that

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we have between 20,000 and 25,000 genes. We all have two copies of each gene and one is
inherited from our mother and one from our father.
Recent research has discovered that autism, ADHD, bipolar disorder, major depression,
and schizophrenia all share genetic roots. They, “were more likely to have suspect genetic
variation at the same four chromosomal sites. These included risk versions of two genes that
regulate the flow of calcium into cells.” Likewise, twin and family studies have shown that people
with first-degree relatives suffering from OCD are at higher risks to develop the disorder
themselves. The same is true of borderline personality disorder.
WebMd adds, “Experts believe many mental illnesses are linked to abnormalities in
many genes rather than just one or a few and that how these genes interact with the
environment is unique for every person (even identical twins). That is why a person inherits a
susceptibility to a mental illness and doesn’t necessarily develop the illness. Mental illness itself
occurs from the interaction of multiple genes and other factors — such as stress, abuse, or a
traumatic event — which can influence, or trigger, an illness in a person who has an inherited
susceptibility to it”.

2. Hormonal Imbalances
The body has two coordinating and integrating systems in the body. The nervous system
is one and the endocrine system is the second. The main difference between these two systems
is in terms of the speed with which they act. The nervous system moves quickly with nerve
impulses moving in a few hundredths of a second. The endocrine system moves slowly with
hormones, released by endocrine glands, taking seconds, or even minutes, to reach their target.
Hormones are important to psychologists because they organize the nervous system and body
tissues at certain stages of development and activate behaviors such as alertness or
sleepiness, sexual behavior, concentration, aggressiveness, reaction to stress, a desire for
companionship. The pituitary gland is the “master gland” which regulates other endocrine
glands. It influences blood pressure, thirst, contractions of the uterus during childbirth, milk
production, sexual behavior and interest, body growth, the amount of water in the body’s cells,
and other functions as well. The pineal gland helps regulate the sleep-wake cycle while
the thyroid gland regulates the body’s rate of metabolism and so how energetic people are.
Of importance to mental health professionals are the adrenal glands, located on top of
the kidneys, and which release cortisol to help the body deal with stress. Elevated levels of this
hormone can lead to increased weight gain, interfere with learning and memory, reduce bone

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density, increase cholesterol, etc… But the hormone also can cause an increased risk of
depression. Also, overproduction of the hormone melatonin can lead to SAD.

3. Viral Infections
Infections can cause brain damage and lead to the development of mental illness or an
exacerbation of symptoms. For example, evidence suggests that contracting strep infection can
lead to the development of OCD, Tourette’s syndrome, and tic disorder in children (Mell, Davis,
& Owens, 2005; Giedd et al., 2000; Allen et al., 1995). Influenza epidemics have also been
linked to schizophrenia (Brown et al., 2004; McGrath and Castle, 1995; McGrath et al., 1994;
O’callaghan et al., 1991) though more recent research suggests this evidence is weak at best
(Selten & Termorshuizen, 2017; Ebert & Kotler, 2005).

C. Treatments

1. Psychopharmacology and psychotropic drugs

One option to treat severe mental illness is psychotropic medications. These
medications fall under five major categories.
The antidepressants are used to treat depression, but also anxiety, insomnia, or pain.
The most common types of antidepressants are SSRIs or selective serotonin reuptake inhibitors
and include Citalopram, Paroxetine, and Fluoxetine (Prozac). Possible side effects include
weight gain, sleepiness, nausea and vomiting, panic attacks, or thoughts about suicide or dying.
Anti-anxiety medications help with the symptoms of anxiety and include the benzodiazepines
such as Clonazepam, Alprazolam, and Lorazepam. “Anti-anxiety medications such as
benzodiazepines are effective in relieving anxiety and take effect more quickly than the
antidepressant medications (or buspirone) often prescribed for anxiety. However, people can
build up a tolerance to benzodiazepines if they are taken over a long period of time and may
need higher and higher doses to get the same effect.” Side effects include drowsiness,
dizziness, nausea, difficulty urinating, and irregular heartbeat, to name a few.
Stimulants increase one’s alertness and attention and are frequently used to treat
ADHD. They include Lisdexamfetamine, the combination of dextroamphetamine and
amphetamine, and Methylphenidate. Stimulants are generally effective and produce a calming
effect. Possible side effects includeloss of appetite, headache, motor tics or verbal tics, and
personality changes such as appearing emotionless.

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 Antipsychotics are used to treat psychosis or, “conditions that affect the mind, and in
which there has been some loss of contact with reality, often including delusions (false, fixed
beliefs) or hallucinations (hearing or seeing things that are not really there).” They can be used
to treat eating disorders, severe depression, PTSD, OCD, ADHD, and Generalized Anxiety
Disorder. Common antipsychotics include Chlorpromazine, Perphenazine, Quetiapine, and
Lurasidone. Side effects include nausea, vomiting, blurred vision, weight gain, restlessness,
tremors, and rigidity.
Mood stabilizers are used to treat bipolar disorder and at times depression,
schizoaffective disorder, and disorders of impulse control. A common example is Lithium and
side effects include loss of coordination, hallucinations, seizures, and frequent urination.
The use of these drugs has been generally beneficial to patients. Most report that their
symptoms decline leading them to feel better and improve their functioning. Also, long-term
hospitalizations are less likely to occur as a result though the medications do not benefit the
individual in terms of improved living skills.

2. Electroconvulsive Therapy
According to Mental Health America, “Electroconvulsive therapy (ECT) is a procedure in
which a brief application of electric stimulus is used to produce a generalized seizure.” Patients
are placed on a padded bed and administered a muscle relaxant to avoid injury during the
seizures. Annually, approximately 100,000 are treated using ECT for conditions to include
severe depression, acute mania, suicidality, and some forms of schizophrenia. The procedure is
still the most controversial available to mental health professionals due to “its effectiveness vs.
the side effects, the objectivity of ECT experts, and the recent increase in ECT as a quick and
easy solution, instead of long-term psychotherapy or hospitalization”. Its popularity has declined
since the 1960s and 1970s.

3. Psychosurgery
Another option to treat mental disorders is to perform brain surgeries. In the past, we
have conducted trephining and lobotomies, neither of which are used today. Today’s techniques
are much more sophisticated and have been used to treat schizophrenia, depression, and some
personality and anxiety disorders, though critics cite obvious ethical issues with conducting such
surgeries as well as scientific issues.

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II. PSYCHOLOGICAL PERSPECTIVES
A. Psychodynamic Theory
In 1895, the book, Studies on Hysteria, was published by Josef Breuer (1842-1925) and
Sigmund Freud (1856-1939), and marked the birth of psychoanalysis, though Freud did not use
this actual term until a year later. The book published several case studies, including that of
Anna O., born February 27, 1859 in Vienna to Jewish parents Siegmund and Recha
Pappenheim, strict Orthodox adherents and considered millionaires at the time. Bertha, known
in published case studies as Anna O., was expected to complete the formal education of a girl in
the upper middle class which included foreign language, religion, horseback riding, needlepoint,
and piano. She felt confined and suffocated in this life and took to a fantasy world she called her
“private theater.” Anna also developed hysteria to include symptoms as memory loss, paralysis,
disturbed eye movements, reduced speech, nausea, and mental deterioration. Her symptoms
appeared as she cared for her dying father and her mother called on Breuer to diagnosis her
condition (note that Freud never actually treated her). Hypnosis was used at first and relieved
her symptoms, as it had done for many patients. Breuer made daily visits and allowed her to
share stories from her private theater which she came to call “talking cure” or “chimney
sweeping.” Many of the stories she shared were actually thoughts or events she found troubling
and reliving them helped to relieve or eliminate the symptoms. Breuer’s wife, Mathilde, became
jealous of her husband’s relationship with the young girl, leading Breuer to terminate treatment
in the June of 1882 before Anna had fully recovered. She relapsed and was admitted to
Bellevue Sanatorium on July 1, eventually being released in October of the same year. With
time, Anna O. did recover from her hysteria and went on to become a prominent member of the
Jewish Community, involving herself in social work, volunteering at soup kitchens, and
becoming ‘House Mother’ at an orphanage for Jewish girls in 1895. Bertha (Anna O.) became
involved in the German Feminist movement, and in 1904 founded the League of Jewish
Women. She published many short stories; a play called Women’s Rights, in which she
criticized the economic and sexual exploitation of women, and wrote a book in 1900 called The
Jewish Problem in Galicia, in which she blamed the poverty of the Jews of Eastern Europe on
their lack of education. In 1935 she was diagnosed with a tumor and was summoned by the
Gestapo in 1936 to explain anti-Hitler statements she had allegedly made. She died shortly after
this interrogation on May 28, 1936. Freud considered the talking cure of Anna O. to be the origin
of psychoanalytic therapy and what would come to be called the cathartic method.

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1. The Structure of Personality
Freud’s psychoanalysis was unique in the history of psychology because it did not arise
within universities as most of the majors schools in our history did but from medicine and
psychiatry, it dealt with psychopathology, and examined the unconscious. Freud believed that
consciousness had three levels – 1) consciousness which was the seat of our awareness,
2) preconscious that included all of our sensations, thoughts, memories, and feelings, and 3)
the unconscious which was not available to us. The contents of the unconscious could move
from the unconscious to preconscious, but to do so, it had to pass a Gate Keeper. Content that
was turned away was said to be repressed by Freud.
According to Freud, our personality has three parts – the id, superego, and ego, and
from these our behavior arises. First, the id is the impulsive part that expresses our sexual and
aggressive instincts. It is present at birth, completely unconscious, and operates on the pleasure
principle, resulting in our selfishly seeking immediate gratification of our needs no matter what
the cost. The second part of personality emerges after birth with early formative experiences
and is called the ego. The ego attempts to mediate the desires of the id against the demands of
reality, and eventually the moral limitations or guidelines of the superego. It operates on
the reality principle, or an awareness of the need to adjust behavior to meet the demands of our
environment. The last part of personality to develop is the superego which represents society’s
expectations, moral standards, rules, and represents our conscience. It leads us to adopt our
parent’s values as we come to realize that many of the id’s impulses are unacceptable. Still, we
violate these values at times which lead to feelings of guilt. The superego is partly conscious but
mostly unconscious, and part of it becomes our conscience. The three parts of personality
generally work together well and compromise, leading to a healthy personality, but if the conflict
is not resolved, intrapsychic conflicts can arise and lead to mental disorders.
Personality develops over the course of five distinct stages, in which the libido is focused
on different parts of the body. First, libido is the psychic energy that drives a person to
pleasurable thoughts and behaviors. Our life instincts, or Eros, are manifested through it and
are the creative forces that sustain life. They include hunger, thirst, self-preservation, and sex.
In contrast, Thanatos, or our death instinct, is either directed inward as in the case of suicide
and masochism or outward via hatred and aggression. Both types of instincts are sources of
stimulation in the body and create a state of tension which is unpleasant, thereby motivating us
to reduce them. Consider hunger, and the associated rumbling of our stomach, fatigue, lack of
energy, etc., that motivates us to find and eat food. If we are angry at someone we may engage
in physical or relational aggression to alleviate this stimulation.

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2. The Development of Personality
Freud’s psychosexual stages of personality development are listed below. Please note that
a person may become fixated at any stage, meaning they become stuck, thereby affecting later
development and possibly leading to abnormal functioning, or psychopathology.
1. Oral Stage – Beginning at birth and lasting to 24 months, the libido is focused on the
mouth and sexual tension is relieved by sucking and swallowing at first, and then later by
chewing and biting as baby teeth come in. Fixation is linked to a lack of confidence,
argumentativeness, and sarcasm.
2. Anal Stage – Lasting from 2-3 years, the libido is focused on the anus as toilet training
occurs. If parents are too lenient children may become messy or unorganized. If parents
are too strict, children may become obstinate, stingy, or orderly.
3. Phallic Stage – Occurring from about age 3 to 5-6 years, the libido is focused on the
genitals and children develop an attachment to the parent of the opposite sex and are
jealous of the same sex parent. The Oedipus complex develops in boys and results in
the son falling in love with his mother while fearing that his father will find out and
castrate him. Meanwhile, girls fall in love with the father and fear that their mother will
find out, called the Electra complex. A fixation at this stage may result in low self-
esteem, feelings of worthlessness, and shyness.
4. Latency Stage – From 6-12 years of age, children lose interest in sexual behavior and
boys play with boys and girls with girls. Neither sex pays much attention to the opposite
sex.
5. Genital Stage – Beginning at puberty, sexual impulses reawaken and unfulfilled desires
from infancy and childhood can be satisfied during lovemaking.

3. Dealing with Anxiety

The ego has a challenging job to fulfill, balancing both the will of the id and the
superego, and the overwhelming anxiety and panic this creates. Ego-defense
mechanisms are in place to protect us from this pain but are considered maladaptive if they are
misused and become our primary way of dealing with stress. They protect us from anxiety and
operate unconsciously, also distorting reality. Defense mechanisms include the following:
• Repression – when unacceptable ideas, wishes, desires, or memories are blocked from
consciousness such as forgetting a horrific car accident that you caused. Eventually
though, it must be dealt with or else the repressed memory can cause problems later in life.

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• Reaction formation – When an impulse is repressed and then expressed by its opposite
such as we are angry with our boss but cannot lash out at him, and so are super friendly
instead. Another example is having lustful thoughts to a coworker than you cannot express
because you are married, and so you are extremely hateful to this person.
• Displacement – When we satisfy an impulse with a different object because focusing on
the primary object may get us in trouble. A classic example is taking out your frustration
with your boss on your wife and/or kids when you get home. If we lash out at our boss we
could be fired. The substitute target is less dangerous than the primary target.
• Projection – When we attribute threatening desires or unacceptable motives to others. An
example is when we do not have the skills necessary to complete a task but we blame the
other members of our group for being incompetent and unreliable.
• Sublimation – When we find a socially acceptable way to express a desire. If we are
stressed out or upset, we may go to the gym and box or lift weights. A person who desires
to cut things may become a surgeon.
• Denial – Sometimes life is so hard all we can do is deny how bad it is. An example is
denying a diagnosis of lung cancer given by your doctor.
• Identification – this is when we find someone who has found a socially acceptable way to
satisfy their unconscious wishes and desires and we model that behavior.
• Regression – When we move from a mature behavior to one that is infantile in nature. If
your significant other is nagging you, you might regress and point your hands over your
ears and say, “La la la la la la la la…”
• Rationalization – When we offer well thought out reasons for why we did what we did but
in reality these are not the real reason. Students sometimes rationalize not doing well in a
class by stating that they really are not interested in the subject or saying the instructor
writes impossible to pass tests.
• Intellectualization– When we avoid emotion by focusing on intellectual aspects of a
situation such as ignoring the sadness we are feeling after the death of our mother by
focusing on planning the funeral.

4. Psychodynamic Techniques
Freud used three primary assessment techniques as part of psychoanalysis, or
psychoanalytic therapy, to understand the personalities of his patients and to expose repressed
material, which included free association, transference, and dream analysis. First, free
association involves the patient describing whatever comes to mind during the session. The

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patient continues but always reaches a point when he/she cannot or will not proceed any
further. The patient might change the subject, stop talking, or lose his/her train of thought. Freud
said this was resistance and revealed where issues were.
Second, transference is the process through which patients transfer to the therapist
attitudes he/she held during childhood. They may be positive and include friendly, affectionate
feelings, or negative, and include hostile and angry feelings. The goal of therapy is to wean
patients from their childlike dependency on the therapist.
Finally, Freud used dream analysis to understand a person’s inner most wishes. The
content of dreams include the person’s actual retelling of the dreams, called manifest content,
and the hidden or symbolic meaning, called latent content. In terms of the latter, some symbols
are linked to the person specifically while others are common to all people.

B. The Behavioral Model

1. What is learning?
The behavioral model concerns the cognitive process of learning. Simply, learning is
any relatively permanent change in behavior due to experience and practice and has two main
forms – associative learning and observational learning. First, associative learning is the linking
together of information sensed from our environment. Conditioning, or a type of associative
learning, occurs which two events are linked and has two forms – classical conditioning, or
linking together two types of stimuli, and operant conditioning, or linking together a response
with its consequence. Second, observational learning occurs when we learn by observing the
world around us.
We should also note the existence of non-associative learning or when there is no
linking of information or observing the actions of others around you. Types include habituation,
or when we simply stop responding to repetitive and harmless stimuli in our environment such
as a fan running in your laptop as you work on a paper, and sensitization, or when our
reactions are increased due to a strong stimulus, such as an individual who experienced a
mugging and now panics when someone walks up behind him/her on the street.
Behaviorism is the school of thought associated with learning that began in 1913 with
the publication of John B. Watson’s article, “Psychology as the Behaviorist Views It,” in the
journal, Psychological Review (Watson, 1913). It was Watson’s belief that the subject matter of
psychology was to be observable behavior and to that end said that psychology should focus on
the prediction and control of behavior. Behaviorism was dominant from 1913 to 1990 before

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being absorbed into mainstream psychology. It went through three major stages – behaviorism
proper under Watson and lasting from 1913-1930 (discussed as respondent conditioning),
neobehaviorism under Skinner and lasting from 1930-1960 (discussed as operant conditioning),
and sociobehaviorism under Bandura and Rotter and lasting from 1960-1990 (discussed as
social learning theory).

2. Respondent Conditioning
You have likely heard about Pavlov and his dogs but what you may not know is that this
was a discovery made accidentally. Ivan Petrovich Pavlov (1906, 1927, 1928), a Russian
physiologist, was interested in studying digestive processes in dogs in response to being fed
meat powder. What he discovered was the dogs would salivate even before the meat powder
was presented. They would salivate at the sound of a bell, footsteps in the hall, a tuning fork, or
the presence of a lab assistant. Pavlov realized there were some stimuli that automatically
elicited responses (such as salivating to meat powder) and those that had to be paired with
these automatic associations for the animal or person to respond to it (such as salivating to a
bell). Armed with this stunning revelation, Pavlov spent the rest of his career investigating the
learning phenomenon.
The important thing to understand is that not all behaviors occur due to reinforcement
and punishment as operant conditioning says. In the case of respondent conditioning, stimuli
exert complete and automatic control over some behaviors. We see this in the case of reflexes.
When a doctor strikes your knee with that little hammer it extends out automatically. You do not
have to do anything but watch. Babies will root for a food source if the mother’s breast is placed
near their mouth. If a nipple is placed in their mouth, they will also automatically suck, as per the
sucking reflex. Humans have several of these reflexes though not as many as other animals
due to our more complicated nervous system.
Respondent conditioning (also called classical or Pavlovian conditioning) occurs when
we link a previously neutral stimulus with a stimulus that is unlearned or inborn, called an
unconditioned stimulus. In respondent conditioning, learning occurs in three phases:
preconditioning, conditioning, and postconditioning. See Figure 2.6 for an overview of Pavlov’s
classic experiment.
Preconditioning. Notice that preconditioning has both an A and a B panel. Really, all
this stage of learning signifies is that some learning is already present. There is no need to learn
it again as in the case of primary reinforcers and punishers in operant conditioning. In Panel A,
food makes a dog salivate. This does not need to be learned and is the relationship of an

27
unconditioned stimulus (UCS) yielding an unconditioned response (UCR). Unconditioned means
unlearned. In Panel B, we see that a neutral stimulus (NS) yields nothing. Dogs do not enter the
world knowing to respond to the ringing of a bell (which it hears).
Conditioning. Conditioning is when learning occurs. Through a pairing of neutral
stimulus and unconditioned stimulus (bell and food, respectively) the dog will learn that the bell
ringing (NS) signals food coming (UCS) and salivate (UCR). The pairing must occur more than
once so that needless pairings are not learned such as someone farting right before your food
comes out and now you salivate whenever someone farts (…at least for a while. Eventually the
fact that no food comes will extinguish this reaction but still, it will be weird for a bit).

Postconditioning or after learning has occurred, establishes a new and not naturally
occurring relationship of a conditioned stimulus (CS; previously the NS) and conditioned
response (CR; the same response). So the dog now reliably salivates at the sound of the bell
because he expects that food will follow, and it does.
One of the most famous studies in psychology was conducted by Watson and Rayner
(1920). Essentially, they wanted to explore “the possibility of conditioning various types of
emotional response(s).” The researchers ran a 9-month-old child, known as Little Albert,
through a series of trials in which he was exposed to a white rat to which no response was
made outside of curiosity (NS–NR not shown). In Panel A of Figure 2.7, we have the naturally
occurring response to the stimulus of a loud sound. On later trials, the rat was presented (NS)

28
and followed closely by a loud sound (UCS; Panel B). After several conditioning trials, the child
responded with fear to the mere presence of the white rat (Panel C).

As fears can be learned, so too they can be unlearned. Considered the follow-up to
Watson and Rayner (1920), Jones (1924; Figure 2.8) wanted to see if a child who learned to be
afraid of white rabbits (Panel B) could be conditioned to become unafraid of them. Simply, she
placed the child in one end of a room and then brought in the rabbit. The rabbit was far enough
away so as to not cause distress. Then, Jones gave the child some pleasant food (i.e.,
something sweet such as cookies [Panel C]; remember the response to the food is unlearned,
i.e., Panel A). The procedure in Panel C continued with the rabbit being brought in a bit closer
each time until eventually the child did not respond with distress to the rabbit (Panel D).

29
 This process is called counterconditioning, or the reversal of previous learning.
Another respondent conditioning way to unlearn a fear is what is called flooding or exposing
the person to the maximum level of stimulus and as nothing aversive occurs; the link between
CS and UCS producing the CR of fear should break, leaving the person unafraid. That is the
idea at least and if you were afraid of clowns, you would be thrown into a room full of clowns.
Finally, several properties of respondent conditioning should be mentioned:
• Respondent Generalization – When a number of similar CSs or a broad range of CSs
elicit the same CR. An example is the sound of a whistle eliciting salivation the same as the
sound of a bell, both detected via audition.
• Respondent Discrimination – When the CR is elicited by a single CS or a narrow range
of CSs. Teaching the dog to not respond to the whistle but only to the bell, and just that
type of bell. Other bells would not be followed by food, eventually leading to….
• Respondent Extinction – When the CS is no longer paired with the UCS. The sound of a
school bell ringing (new CS that was generalized) is not followed by food (UCS), and so
eventually the dog stops salivating (the CR).
• Spontaneous recovery – When the CS elicits the CR after extinction has occurred.
Eventually, the school bell will ring making the dog salivate. If no food comes, the behavior
will not continue on. If food comes, the salivation response will be re-established.

3. Operant Conditioning
Influential on the development of Skinner’s operant conditioning, Thorndike proposed
the law of effect (Thorndike, 1905) or the idea that if our behavior produces a favorable
consequence, in the future when the same stimulus is present, we will be more likely to make
the response again, expecting the same favorable consequence. Likewise, if our action leads to
dissatisfaction, then we will not repeat the same behavior in the future. He developed the law of
effect thanks to his work with the Puzzle Box. Cats were food deprived the night before the
experimental procedure was to occur. The next morning, they were placed in the puzzle box
and a small amount of food was placed outside the box close enough to be smelled, but the cat
could not reach the food. To get out, a series of switches, buttons, levers, etc. had to be
manipulated and once done, the cat could escape the box and eat some of the food. But just
some. The cat was then promptly placed back in the box to figure out how to get out again, the
food being its reward for doing so. With each subsequent escape and re-insertion into the box,
the cat became faster until he/she knew exactly what had to be done to escape. This is
called trial and error learning or making a response repeatedly if it leads to success.

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Thorndike also said that stimulus and responses were connected by the organism and this lead
to learning. This approach to learning was called connectionism.
Operant conditioning is a type of associate learning which focuses on consequences
that follow a response or behavior that we make (anything we do, say, or think/feel) and whether
it makes a behavior more or less likely to occur. This should sound much like what you just read
about in terms of Thorndike’s work. Skinner talked about contingencies or when one thing
occurs due to another. Think of it as an If-Then statement. If I do X then Y will happen. For
operant conditioning, this means that if I make a behavior, then a specific consequence will
follow. The events (response and consequence) are linked in time.
What form do these consequences take? There are two main ways they can present
themselves.
• Reinforcement – Due to the consequence, a behavior/response is more likely to
occur in the future. It is strengthened.
• Punishment – Due to the consequence, a behavior/response is less likely to occur in
the future. It is weakened.
Reinforcement and punishment can occur as two types – positive and negative. These
words have no affective connotation to them meaning they do not imply good or
bad. Positive means that you are giving something – good or bad. Negative means that
something is being taken away – good or bad. Check out the figure below for how these
contingencies are arranged.

• Positive Punishment (PP) – If something bad or aversive is given or added, then the
behavior is less likely to occur in the future. If you talk back to your mother and she slaps

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 your mouth, this is a PP. Your response of talking back led to the consequence of the
aversive slap being delivered or given to your face.
• Positive Reinforcement (PR) – If something good is given or added, then the behavior is
more likely to occur in the future. If you study hard and earn, or are given, an A on your
exam, you will be more likely to study hard in the future. Similarly, your parents may give
you money for your stellar performance.
• Negative Reinforcement (NR) – This is a tough one for students to comprehend because
the terms don’t seem to go together and are counterintuitive. But it is really simple and you
experience NR all the time. This is when something bad or aversive is taken away or
subtracted due to your actions, making it that you will be more likely to make the same
behavior in the future when the same stimuli presents itself. For instance, what do you do if
you have a headache? You likely answered take Tylenol. If you do this and the headache
goes away, you will take Tylenol in the future when you have a headache. NR can either
result in current escape behavior or future avoidance behavior. What does this
mean? Escape occurs when we are presently experiencing an aversive event and want it to
end. We make a behavior and if the aversive event, like the headache, goes away, we will
repeat the taking of Tylenol in the future. This future action is an avoidance event. We
might start to feel a headache coming on and run to take Tylenol right away. By doing so
we have removed the possibility of the aversive event occurring and this behavior
demonstrates that learning has occurred.
• Negative Punishment (NP) – This is when something good is taken away or subtracted
making a behavior less likely in the future. If you are late to class and your professor
deducts 5 points from your final grade (the points are something good and the loss is
negative), you will hopefully be on time in all subsequent classes.

The type of reinforcer or punisher we use is important. Some are naturally occurring
while some need to be learned. We describe these as primary and secondary reinforcers and
punishers. Primary refers to reinforcers and punishers that have their effect without having to be
learned. Food, water, temperature, and sex, for instance, are primary reinforcers while extreme
cold or hot or a punch on the arm are inherently punishing. A story will illustrate the latter. When
I was about 8 years old I would walk up the street in my neighborhood saying, “I’m Chicken
Little and you can’t hurt me.” Most ignored me but some gave me the attention I was seeking, a
positive reinforcer. So I kept doing it and doing it until one day, another kid was tired of hearing
about my other identity and punched me in the face. The pain was enough that I never walked

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up and down the street echoing my identity crisis for all to hear. This was a positive punisher
and did not have to be learned. That was definitely not one of my finer moments in life.
Secondary or conditioned reinforcers and punishers are not inherently reinforcing or
punishing, but must be learned. An example was the attention I received for saying I was
Chicken Little. Over time I learned that attention was good. Other examples of secondary
reinforcers include praise, a smile, getting money for working or earning good grades, stickers
on a board, points, getting to go out dancing, and getting out of an exam if you are doing well in
a class. Examples of secondary punishers include a ticket for speeding, losing television or
video game privileges, being ridiculed, or a fee for paying your rent or credit card bill late.
Really, the sky is the limit with reinforcers in particular.
In operant conditioning, the rule for determining when and how often we will reinforce a
desired behavior is called the reinforcement schedule. Reinforcement can either
occur continuously meaning every time the desired behavior is made the person or animal will
receive some reinforcer, or intermittently/partially meaning reinforcement does not occur with
every behavior. Our focus will be on partial/intermittent reinforcement.

The figure shows that that are two main components that make up a reinforcement
schedule – when you will reinforce and what is being reinforced. In the case of when, it will be
either fixed or at a set rate, or variable and at a rate that changes. In terms of what is being
reinforced, we will either reinforce responses or time. These two components pair up as follows:
• Fixed Ratio schedule (FR) – With this schedule, we reinforce some set number of
responses. For instance, every twenty problems (fixed) a student gets correct (ratio), the
teacher gives him an extra credit point. A specific behavior is being reinforced – getting

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 problems correct. Note that if we reinforce each occurrence of the behavior, the definition of
continuous reinforcement, we could also describe this as a FR1 schedule. The number
indicates how many responses have to be made and in this case it is one.
• Variable Ratio schedule (VR) – We might decide to reinforce some varying number of
responses such as if the teacher gives him an extra credit point after finishing between 40
and 50 correct problems. This is useful after the student is obviously learning the material
and does not need regular reinforcement. Also, since the schedule changes, the student
will keep responding in the absence of reinforcement.
• Fixed Interval schedule (FI) – With a FI schedule, you will reinforce after some set
amount of time. Let’s say a company wanted to hire someone to sell their product. To
attract someone, they could offer to pay them $10 an hour 40 hours a week and give this
money every two weeks. Crazy idea but it could work. J Saying the person will be
paid every indicates fixed, and two weeks is time or interval. So, FI.
• Variable Interval schedule (VI) – Finally, you could reinforce someone at some changing
amount of time. Maybe they receive payment on Friday one week, then three weeks later
on Monday, then two days later on Wednesday, then eight days later on Thursday. Etc.
This could work, right? Not for a job but maybe we could say we are reinforced on a VI
schedule if we are.
Finally, four properties of operant conditioning – extinction, spontaneous recovery,
stimulus generalization, and stimulus discrimination – are important. These are the same four
discussed under respondent conditioning. First, extinction is when something that we do, say,
think/feel has not been reinforced for some time. As you might expect, the behavior will begin to
weaken and eventually stop when this occurs. Does extinction just occur as soon as the
anticipated reinforcer is not there? The answer is yes and no, depending on whether we are
talking about continuous or partial reinforcement. With which type of reinforcement would you
expect a person to stop responding to immediately if reinforcement is not there?
Do you suppose continuous? Or partial?
The answer is continuous. If a person is used to receiving reinforcement every time the
correct behavior is made and then suddenly no reinforcer is delivered, he or she will cease the
response immediately. Obviously then, with partial, a response continues being made for a
while. Why is this? The person may think the schedule has simply changed. ‘Maybe I am not
paid weekly now. Maybe it changed to biweekly and I missed the email.’ Due to this we say that
intermittent or partial reinforcement shows resistance to extinction, meaning the behavior does
weaken, but gradually.

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 Second, you might have wondered if the person or animal will try to make the response
again in the future even though it stopped being reinforced in the past. The answer is yes and
one of two outcomes is possible. First, the response is made and nothing happens. In this case
extinction continues. Second, the response is made and a reinforcer is delivered. The response
re-emerges. Consider a rat that has been trained to push a lever to receive a food pellet. If we
stop delivering the food pellets, in time, the rat will stop pushing the lever. The rat will push the
lever again sometime in the future and if food is delivered, the behavior spontaneously recovers.
Hence why this phenomenon is called spontaneous recovery.

4. Observational Learning
There are times when we learn by simply watching others. This is called observational
learning and is contrasted with enactive learning, which is learning by doing. There is no
firsthand experience by the learner in observational learning unlike enactive. As you can learn
desirable behaviors such as watching how your father bags groceries at the grocery store (I did
this and still bag the same way today) you can learn undesirable ones too. If your parents resort
to alcohol consumption to deal with the stressors life presents, then you too might do the same.
What is critical is what happens to the model in all of these cases. If my father seems genuinely
happy and pleased with himself after bagging groceries his way, then I will be more likely to
adopt this behavior. If my mother or father consumes alcohol to feel better when things are
tough, and it works, then I might do the same. On the other hand, if we see a sibling constantly
getting in trouble with the law then we may not model this behavior due to the negative
consequences.
Albert Bandura conducted the pivotal research on observational learning and you likely
already know all about it. In Bandura’s experiment, children were first brought into a room to
watch a video of an adult playing nicely or aggressively with a Bobo doll. This was a model.
Next, the children are placed in a room with a lot of toys in it. In the room is a highly prized toy
but they are told they cannot play with it. All other toys are fine and a Bobo doll is in the room.
Children who watched the aggressive model behaved aggressively with the Bobo doll while
those who saw the nice model, played nice. Both groups were frustrated when deprived of the
coveted toy.

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 Bandura said if all behaviors are learned by observing others and we model our
behaviors on theirs, then undesirable behaviors can be altered or relearned in the same
way. Modeling techniques are used to change behavior by having subjects observe a model in
a situation that usually causes them some anxiety. By seeing the model interact nicely with the
fear evoking stimulus, their fear should subside. This form of behavior therapy is widely used in
clinical, business, and classroom situations. In the classroom, we might use modeling to
demonstrate to a student how to do a math problem. In fact, in many college classrooms this is
exactly what the instructor does. In the business setting, a model or trainer demonstrates how to
use a computer program or run a register for a new employee.
But keep in mind that we do not model everything we see. Why? First, we cannot pay attention
to everything going on around us. We are more likely to model behaviors by someone who
commands our attention. Second, we must remember what a model does in order to imitate it. If
a behavior is not memorable, it will not be imitated. We must try to convert what we see into
action. If we are not motivated to perform an observed behavior, we probably will not show what
we have learned.
The greatest strength or appeal of the behavioral model is that its tenets are easily
tested in the laboratory unlike those of the psychodynamic model. Also, a large number of
treatment techniques have been developed and proven to be effective over the years. For
example, desensitization (Wolpe, 1997) teaches clients to respond calmly to fear producing
stimuli. It begins with the individual learning a relaxation technique such as diaphragmatic
breathing. Next, a fear hierarchy, or list of feared objects and situations, is constructed in which

36
the individual moves from least to most feared. Finally, the individual either imagines
(systematic) or experiences in real life (in-vivo) each object or scenario from the hierarchy and
uses the relaxation technique while doing so. This represents individual pairings of feared object
or situation and relaxation and so if there are 10 objects/situations in the list, the client will
experience ten such pairings and eventually be able to face each without fear. Outside of
phobias, desensitization has been shown to be effective in the treatment of Obsessive
Compulsive Disorder symptoms (Hakimian and Souza, 2016) and limitedly with the treatment of
depression when co-morbid with OCD (Masoumeh and Lancy, 2016).

C. The Cognitive Model

1. What is it?
As noted earlier, the idea of people being machines, called mechanism, was a key
feature of behaviorism and other schools of thought in psychology until about the 1960s or
1970s. In fact, behaviorism said psychology was to be the study of observable behavior. Any
reference to cognitive processes was dismissed as this was not overt, but covert according to
Watson and later Skinner. Of course removing cognition from the study of psychology ignored
an important part of what makes us human and separates us from the rest of the animal
kingdom. Fortunately, the work of George Miller, Albert Ellis, Aaron Beck, and Ulrich Neisser
demonstrated the importance of cognitive abilities in understanding thoughts, behaviors, and
emotions, and in the case of psychopathology, show that people can create their own problems
by how they come to interpret events experienced in the world around them. How so?

2. Schemas and Cognitive Errors

First, consider the topic of social cognition or the process of collecting and assessing
information about others. So what do we do with this information? Once collected or sensed
(sensation is the cognitive process of detecting the physical energy given off or emitted by
physical objects), the information is sent to the brain. This occurs through the neural impulse.
Once in the brain, it is processed and interpreted. This is where assessing information about
others comes in and involves the cognitive process of perception, or adding meaning to raw
sensory data. We take the information just detected and use it to assign people to categories,
or groups. For each category, we have a schema, or a set of beliefs and expectations about a
group of people, presumed to apply to all members of the group, and based on experience.
Can our schemas lead us astray, or be false? Consider where students sit in a class. It
is generally understood that the students who sit in the front of the class are the overachievers

37
and want to earn an A in the class. Those who sit in the back of the room are underachievers
and really don’t care. Right? Where do you sit in class, if you are on a physical campus and not
an online student? Is this correct? What about other students in the class that you know? What
if you found out that a friend who sits in the front row is a C student but sits there because he
cannot see the screen or board, even with corrective lenses? What about your friend or
acquaintance in the back? This person is an A student but does not like being right under the
nose of the professor, especially if he/she has a tendency to spit when lecturing. The person in
the back could also be shy and prefer sitting there so that she does not need to chat with others
as much, or is easily distracted and so sits in the back so that all stimuli are in front of her.
Again, your schema about front row and back row students is incorrect and causes you to make
certain assumptions about these individuals. This might even affect how you interact with them.
Would you want notes from the student in the front or back of the class?

3. Attributions and Cognitive Errors

Second, consider the very interesting topic from social psychology of attribution theory,
or the idea that people are motivated to explain their own and other people’s behavior by
attributing causes of that behavior to personal reasons or dispositional factors that are in the
person themselves or linked to some trait they have; or situational factors that are linked to
something outside the person. Like schemas, the attributions we make can lead us astray. How
so? The fundamental attribution error occurs when we automatically assume a dispositional
reason for another person’s actions and ignore situational factors. In other words, we assume
the person who cut us off is an idiot (dispositional) and do not consider that maybe someone in
the car is severely injured and this person is rushing them to the hospital (situational). Then
there is the self-serving bias which is when we attribute our success to our own efforts
(dispositional) and our failures to outside causes (situational). Obviously, our attribution in these
two cases is in error but still, it comes to affect how we see the world and our subjective well-
being.

4. Maladaptive Cognitions
Irrational thought patterns can be the basis of psychopathology. Throughout this book,
we will discuss several treatment strategies that are used to change unwanted, maladaptive
cognitions, whether they are present as an excess such as with paranoia, suicidal ideation, or
feelings of worthlessness; or as a deficit such as with self-confidence and self-efficacy. More
specifically, cognitive distortions/maladaptive cognitions can take the following forms:

38
• Overgeneralizing – You see a larger pattern of negatives based on one event.
• Mind Reading – Assuming others know what you are thinking without any evidence.
• What if? – Asking yourself what if? Something happens without being satisfied by any of
the answers.
• Blaming – You focus on someone else as the source of your negative feelings and do not
take any responsibility for changing yourself.
• Personalizing – Blaming yourself for negative events rather than seeing the role that others
play.
• Inability to disconfirm – Ignoring any evidence that may contradict your maladaptive
cognition.
• Regret orientation – Focusing on what you could have done better in the past rather than
on making an improvement now.
• Dichotomous thinking – Viewing people or events in all-or-nothing terms.

5. Cognitive Therapies
According to the National Alliance on Mental Illness (NAMI), cognitive behavioral
therapy “focuses on exploring relationships among a person’s thoughts, feelings and behaviors.
During CBT a therapist will actively work with a person to uncover unhealthy patterns of thought
and how they may be causing self-destructive behaviors and beliefs.” CBT attempts to
identifying negative or false beliefs and restructure them. They add, “Oftentimes someone being
treated with CBT will have homework in between sessions where they practice replacing
negative thoughts with more realistic thoughts based on prior experiences or record their
negative thoughts in a journal.” For more on CBT, visit: https://www.nami.org/Learn-
More/Treatment/Psychotherapy. Some commonly used strategies include cognitive
restructuring, cognitive coping skills training, and acceptance techniques.
First, you can use cognitive restructuring, also called rational restructuring, in which
maladaptive cognitions are replaced with more adaptive ones. To do this, the client must be
aware of the distressing thoughts, when they occur, and their effect on them. Next, help the
client stop thinking these thoughts and replace them with more rational ones. It’s a simple
strategy, but an important one. Psychology Today published a great article on January 21, 2013
which described 4 ways to change your thinking through cognitive restructuring. Briefly, these
included:

39
 1. Notice when you are having a maladaptive cognition such as making “negative
predictions.” They suggest you figure out what is the worst thing that could happen and
what over outcomes are possible.
2. Track the accuracy of the thought as if you believe focusing on a problem generates a
solution. Write down each time you ruminate and then the result. You can generate a
percentage of times you ruminated to the number of successful problem-solving
strategies you generated.
3. Behaviorally test your thought by figuring out if you really do not have time to go to the
gym. Recording what you do each day and then look at open times of the day. Add them
up and see if you make some minor, or major, adjustments to your schedule if you can
allow yourself an hour to get in valuable exercise.
4. Examine the evidence both for and against your thought. If you do not believe you do
anything right, list evidence of when you did not do something right and then evidence of
when you did. Then write a few balanced statements such as the one the article
suggests, “I’ve made some mistakes that I feel embarrassed about but a lot of the time, I
make good choices.”
A second major strategy is to use what is called cognitive coping skills training. This
strategy teaches social skills, communication, and assertiveness through direct instruction, role
playing, and modeling. For social skills, identify appropriate social behavior such as making eye
contact, saying no to a request, or starting up a conversation with a stranger and whether the
client is inhibited from making this behavior due to anxiety. For communication, determine if the
problem is with speaking, listening, or both and then develop a plan for use in various
interpersonal situations. Finally, assertiveness training aids the client protect their rights and
obtain what they want from others. Those who are not assertive are often overly passive and
never get what they want, or are overly aggressive and only get what they want. Treatment
starts with determining situations in which assertiveness is lacking and coming up with a
hierarchy of assertiveness opportunities. Least difficult situations are handled first, followed by
more difficult situations, all while rehearsing and mastering all the situations present in the
hierarchy. For more on these techniques, visit http://cogbtherapy.com/cognitive-behavioral-
therapy-exercises/.
Finally, acceptance techniques can be used to reduce a client’s worry and anxiety. Life
involves a degree of uncertainty and at times we need to just accept this. Techniques might
include weighing the pros of fighting uncertainty against the cons of doing so. The cons should
outweigh the pros and help you to end the struggle and accept what is unknown. Chances are

40
you are already accepting the unknown in some areas of life and identifying these can help you
to see why it is helpful in these areas, and how you can also think like this in more difficult
areas. Finally, does uncertainty unnecessarily lead to a negative end? We may think so but
review of the evidence for and against this statement will show that it does not and reduce how
threatening it seems.

D. The Humanistic and Existential Perspectives

1. The Humanistic Perspective
The humanistic perspective, or third force psychology (psychoanalysis and behaviorism
being the other two forces), emerged in the 1960s and 1970s as an alternative viewpoint to the
largely deterministic view of personality espoused by psychoanalysis and the view of humans as
machines advocated by behaviorism. Key features of the perspective include a belief in human
perfectibility, personal fulfillment, valuing self-disclosure, placing feelings over intellect, an
emphasis on the present, and hedonism. Its key figures were Abraham Maslow who proposed
the hierarchy of needs and Carl Rogers who we will focus on here.
Rogers said that all people want to have positive regard from significant others in their
life. When the individual is accepted as they are they receive unconditional positive regard and
become a fully functioning person. They are open to experience, live every moment to the
fullest, are creative, accepts responsibility for their decisions, do not derive their sense of self
from others, strive to maximize their potential, and are self-actualized. Their family and friends
may disapprove of some of their actions but overall, respect and love them. They then realize
their worth as a person but also that they are not perfect. Of course most people do not
experience this but instead are made to feel that they can only be loved and respected if they
meet certain standards, called conditions of worth. Hence, they experience conditional positive
regard. Their self-concept is now seen as having worth only when these significant others
approve and so becomes distorted, leading to a disharmonious state and psychopathology.
Individuals in this situation are unsure what they feel, value, or need leading to dysfunction and
the need for therapy. Rogers stated that the humanistic therapist should be warm,
understanding, supportive, respectful, and accepting of his/her clients. This approach came to
be called client-centered therapy.

2. The Existential Perspective

This approach stresses the need for people to continually re-create themselves and be
self-aware, acknowledges that anxiety is a normal part of life, focuses on free will and self-

41
determination, emphasizes that each person has a unique identity known only through
relationships and the search for meaning, and finally, that we develop to our maximum potential.
Abnormal behavior arises when we avoid making choices, do not take responsibility, and fail to
actualize our full potential. Existential therapy is used to treat substance abuse, “excessive
anxiety, apathy, alienation, nihilism, avoidance, shame, addiction, despair, depression, guilt,
anger, rage, resentment, embitterment, purposelessness, psychosis, and violence. They also
focus on life-enhancing experiences like relationships, love, caring, commitment, courage,
creativity, power, will, presence, spirituality, individuation, self-actualization, authenticity,
acceptance, transcendence, and awe”.

3. Evaluating the Humanistic and Existential Perspectives

The biggest criticism of these models is that the concepts are abstract and fuzzy and so
very difficult to research. The exception to this was Rogers who did try to scientifically
investigate his propositions, though most other humanistic-existential psychologists rejected the
use of the scientific method. They also have not developed much in the way of theory and the
perspectives tend to work best with people suffering from adjustment issues and not as well with
severe mental illness. The perspectives do offer hope to people suffering tragedy by asserting
that we control our own destiny and can make our own choices.

E. The Sociocultural Model

1. Socioeconomic Factors
Low socioeconomic status has been linked to higher rates of mental and physical illness
(Ng, Muntaner, Chung, & Eaton, 2014) due to persistent concern over unemployment or under-
employment, low wages, lack of health insurance, no savings, and the inability to put food on
the table, which then leads to feeling hopeless, helpless, and dependent on others. This
situation places considerable stress on an individual and can lead to higher rates of anxiety
disorders and depression. Borderline personality disorder has also been found to be higher in
people in low income brackets (Tomko et al., 2012) and group differences for personality
disorders have been found between African and European Americans (Ryder, Sunohara, and
Kirmayer, 2015).

2. Gender Factors
Gender plays an important, though at times, unclear role in mental illness. It is important to
understand that gender is not the cause of mental illness, though differing demands placed on

42
males and females by society and their culture can influence the development and course of a
disorder. Consider the following:
• Rates of eating disorders are higher among women than, men, though both genders are
affected. In the case of men, muscle dysphoria is of concern and is characterized by
extreme concern over being more muscular.
• OCD has an earlier age of onset in girls than boys, with most people being diagnosed by
age 19.
• Females are at greater risk for developing an anxiety disorder than men.
• ADHD is more common in males than females, though females are more likely to have
inattention issues.
• Boys are more likely to be diagnosed with Autism Spectrum Disorder.
• Depression occurs with greater frequency in women than men.
• Women are more likely to develop PTSD compared to men.
• Rates of SAD (Seasonal Affective Disorder) are four times greater in women than men.
Interestingly younger adults are more likely to develop SAD than older adults.

3. Environmental Factors
Environmental factors also play a role in the development of mental illness. How so?
• In the case of borderline personality disorder, many people report experiencing traumatic
life events such as abandonment, abuse, unstable relationships or hostility, and adversity
during childhood.
• Cigarette smoking, alcohol use, and drug use during pregnancy are risk factors for ADHD.
• Divorce or the death of a spouse can lead to anxiety disorders.
• Trauma, stress, and other extreme stressors are predictive of depression.
• Malnutrition before birth, exposure to viruses, and other psychosocial factors are potential
causes of schizophrenia.
• SAD occurs with greater frequency for those living far north or south from the equator
(Melrose, 2015). Horowitz (2008) found that rates of SAD are just 1% for those living in
Florida while 9% of Alaskans are diagnosed with the disorder.

4. Multicultural Factors
Racial, ethnic, and cultural factors are also relevant to understanding the development
and course of mental illness. Multicultural psychologists assert that both normal behavior and
abnormal behavior need to be understood in relation to the individual’s unique culture and the

43
group’s value system. Racial and ethnic minorities must contend with prejudice, discrimination,
racism, economic hardships, etc. as part of their daily life and this can lead to disordered
behavior (Lo & Cheng, 2014; Jones, Cross, & DeFour, 2007; Satcher, 2001), though some
research suggests that ethnic identity can buffer against these stressors and protect mental
health (Mossakowski, 2003). To address this unique factor, culture-sensitive therapies have
been developed and include increasing the therapist’s awareness of cultural values, hardships,
stressors, and/or prejudices faced by their client; the identification of suppressed anger and
pain; and raising the client’s self-worth (Prochaska & Norcross, 2013). These therapies have
proven efficacy for the treatment of depression (Kalibatseva & Leong, 2014) and schizophrenia
(Naeem et al., 2015).

Watch:
1. What is abnormal psychology? (https://www.youtube.com/watch?v=-mj48nOh-yc)
2. How do we determine abnormal behaviour? (youtube.com/watch?v=cwKJ0juPIrQ or
https://www.youtube.com/watch?v=fgmyK0-GxHA)
3. Overview on the history of mental illness and treatment.
(https://www.youtube.com/watch?v=8eR3i0oT_B0)
4. Current status of mental health in the Philippines.
(https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6646843/)
5. Overview on some models and approaches in abnormal psychology.
(https://www.youtube.com/watch?v=5t6cralIJbE)
6. What is neuroscientific perspective in abnormal behaviour?
(https://www.youtube.com/watch?v=W4N-7AlzK7s)
7. How the foods you eat affect your brain? (https://www.youtube.com/watch?v=xyQY8a-ng6g)

Read:
1. (For Deeper Understanding) Chapter 1, 2, & 4 – An Integrative Approach to
Psychopathology on Abnormal Psychology: An Integrative Approach, Seventh Edition by David
H. Barlow, V. Mark Durand.
2. (For Review) Module 1 & 2: Models of Abnormal Psychology by Washington State University
(https://opentext.wsu.edu/abnormal-psych/chapter/module-2-models-of-abnormal-psychology/)

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 MODULE 2: ANXIETY DISORDERS

Module Overview:

In Module 4, we will discuss matters related to anxiety disorders to include

their clinical presentation, and comorbidity. Our discussion will include
Generalized Anxiety Disorder, Specific Phobias, Agoraphobia, Social Anxiety
Disorder, and Panic Disorder.

Module Learning Outcomes:

• Describe how Generalized Anxiety Disorder presents itself and its

comorbidity, etiology, and treatment options.
• Describe how Specific Phobias presents itself its comorbidity etiology, and
treatment options.
• Describe how Agoraphobia presents itself its comorbidity etiology, and
treatment options.
• Describe how Social Anxiety Disorder presents itself its comorbidity
etiology, and treatment options.
• Describe how Panic Disorder presents itself its comorbidity etiology, and
treatment options.

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Course Materials
Lecture:
The hallmark symptoms of anxiety related disorders are excessive fear or anxiety related
to behavioral disturbances. Fear is considered an adaptive response, as it often prepares your
body for an impending threat. Anxiety, however, is more difficult to identify as it is often the
response to a vague sense of threat. The two can be distinguished from one another as fear is
related to either a real or a perceived threat, while anxiety is the anticipation of a future threat
(APA, 2013).
As you will see throughout the chapter, individuals may experience anxiety in many
different forms. Generalized anxiety disorder, the most common of the anxiety disorders, is
characterized by a global and persistent feeling of anxiety. A specific phobia is observed when
an individual experiences anxiety related to a specific object or subject. Similarly, individuals
may also experience agoraphobia when they experience fear specific to leaving their home and
traveling to public places. Social anxiety disorder occurs when an individual experiences anxiety
related to social or performance situations, where there is the possibility that they will be
evaluated negatively. And finally, there is panic disorder, where an individual experiences
recurrent panic attacks consisting of physical and cognitive symptoms.

Etiology
1. Biological
1.1. Biological – Genetic influences. While genetics have been known to contribute to the
presentation of anxiety symptoms, the interaction between genetics and stressful environmental
influences appears to actually account for more of anxiety disorders than genetics alone
(Bienvenu, Davydow, & Kendler, 2011). The quest to identify specific genes that
may predispose individuals to develop anxiety disorders has lead researchers to the serotonin
transporter gene (5-HTTLPR). Mutation of the 5-HTTLPR gene has been found to be related to
a reduction in serotonin activity and an increase in anxiety-related personality traits (Munafo,
Brown, & Hairiri, 2008).
1.2. Biological – Neurobiological structures. Researchers have identified several brain
structures and pathways that are likely responsible for anxiety responses. Among those
structures is the amygdala, the area of the brain that is responsible for storing memories related
to emotional events (Gorman, Kent, Sullivan, & Coplan, 2000). When presented with a fearful
situation, the amygdala initiates a reaction in efforts to prepare the body for a response. First,
the amygdala triggers the hypothalamic-pituitary-adrenal (HPA) axis to prepare for immediate

46
action— either to fight or flight. The second pathway is activated by the feared stimulus itself, by
sending a sensory signal to the hippocampus and prefrontal cortex, for determination if threat
is real or imagined. If it is determined that no threat is present, the amygdala sends a calming
response to the HPA axis, thus reducing the level of fear. If there is a threat present, the
amygdala is activated, producing a fear response.
Specific to panic disorder is the implication of the locus coeruleus, the brain structure that
serves as an “on-off” switch for norepinephrine neurotransmitters. It is believed that increased
activation of the locus coeruleus results in panic like symptoms; therefore, individuals with panic
disorder may have a hyperactive locus coeruleus, leaving them more susceptible to experience
more intense and frequent physiological arousal than the general public (Gorman, Kent,
Sullivan, & Coplan, 2000). This theory is supported by studies in which individuals experienced
increased panic symptoms following injection of norepinephrine (Bourin, Malinge, & Guitton,
1995).
Unfortunately, norepinephrine and the locus coeruleus fail to fully explain the
development of panic disorder, as treatment would be much easier if only norepinephrine was
implicated. Therefore, researchers argue that a more complex neuropathway is likely implicated
in the development of panic disorder. More specifically, the corticostriatal-thalamocortical
(CSTC) circuit, also known as the fear-specific circuit, is theorized as a major contributor to
panic symptoms (Gutman, Gorman, & Hirsch, 2004). When an individual is presented with a
frightening object or situation, the amygdala is activated, sending a fear response to the anterior
cingulate cortex and the orbitofrontal cortex. Additional projection from the amygdala to the
hypothalamus activates endocrinologic responses to fear- releasing adrenaline and cortisol to
help prepare the body to fight or flight (Gutman, Gorman, & Hirsch, 2004). This complex
pathway supports the theory that panic disorder is mediated by several neuroanatomical
structures and their associated neurotransmitters.

2. Psychological
2.1. Psychological – Cognitive. The cognitive perspective on the development of anxiety
related disorders centers around dysfunctional thought patters. As seen in
depression, maladaptive assumptions are routinely observed in individuals with anxiety
related disorders, as they often engage in interpreting events as dangerous or overreacting to
potential stressful events, which contributes to a heightened overall anxiety level.
These negative appraisals, in combination with a biological predisposition to anxiety likely
contribute to the development of anxiety symptoms (Gallagher et al., 2013).

47
 Sensitivity to physiological arousal not only contributes to anxiety disorders in general,
but also for panic disorder where individuals experience various physiological sensations and
misinterpret them as catastrophic. One explanation for this theory is that individuals with panic
disorder are actually more susceptible to more frequent and intensive physiological symptoms
than the general public (Nillni, Rohan, & Zvolensky, 2012). Others argue that these individuals
have had more trauma-related experiences in the past, and therefore, are quick to misevaluate
their symptoms as a potential treat. This misevaluation of symptoms as impending disaster
likely maintain symptoms as the cognitive misinterpretations to physiological arousal creates a
negative feedback loop, leading to more physiological changes.
Social anxiety is also largely explained by cognitive theorists. Individuals with social
anxiety disorder tend to hold unattainable or extremely high social beliefs and expectations.
Furthermore, they often engage in preconceived maladaptive assumptions that they will behave
incompetently in social situations, and that their behaviors will lead to terrible consequences.
Because of these beliefs, they anticipate social disasters will occur and therefore, avoid social
encounters (or limit them to close friends/family members) in efforts to prevent the disaster
(Moscovitch et al., 2013). Unfortunately, these cognitive appraisals are not only isolated to
before and during the event. Individuals with social anxiety disorder will also evaluate the social
event after it has taken place, often obsessively reviewing the details. This overestimation of
social performance negatively reinforces future avoidance of social situations.
2.2. Psychological – Behavioral. The behavioral explanation for the development of
anxiety disorders is largely reserved for phobias- both specific and social phobia. More
specifically, behavioral theorists focus on classical conditioning– when two events that occur
close together become strongly associated with one another, despite their lack of causal
relationship. Watson and Rayner’s (1920) infamous Little Albert experiment is an example of
how classical conditioning can be used to induce fear through associations. In this study, Little
Albert developed a fear of white rats by pairing a white rate with a loud sound. This experiment,
although lacking ethical standards, was ground breaking in the development of learned
behaviors. Over time, researchers have been able to replicate these findings (in more ethically
sound ways) to provide further evidence of the role of classical conditioning in the development
of phobias.
2.3. Psychological – Modeling is another behavioral explanation of the development of
specific and social phobias. In modeling, an individual acquires a far though observation and
imitation (Bandura & Rosenthal, 1966). For example, when a young child observes their parent
display irrational fears of an animal, the child may then begin to display similar behaviors.

48
Similarly, observing another individual being ridiculed in a social setting may increase the
chances of the development of social anxiety, as the individual may become fearful that they
would experience a similar situation in the future. It is speculated that the maintenance of these
phobias is due to the avoidance of the feared item or social setting, thus preventing the
individual from learning that the item/social situation is not something that should be feared.
While modeling and classical conditioning largely explain the development of phobias,
there is some speculation that the accumulation of a large number of these learned fears will
develop into GAD. Through stimulus generalization, or the tendency for the conditioned
stimulus to evoke similar responses to other conditions, a fear of one item (such as the dog)
may become generalized to other items (such as all animals). As these fears begin to grow, a
more generalized anxiety will present, as opposed to a specific phobia.

3. Sociocultural
Seeing how prominent the biological and psychological constructs are in explaining the
development of anxiety related disorders, we also need to review the social constructs that
contribute and maintain anxiety disorders. While characteristics such as living in poverty,
experiencing significant daily stressors, and increased exposure to traumatic events are all
identified as major contributors to anxiety disorders, additional sociocultural influences such as
gender and discrimination have also received great attention, particularly because due to the
epidemiological nature of the disorder.
Gender has largely been researched within anxiety disorders due to the consistent
discrepancy in diagnosis rate between men and women. As previously discussed, women are
routinely diagnosed with anxiety disorders more often than men, a trend that is observed
throughout the entire lifespan. One potential explanation for this discrepancy is the influence of
social pressures on women. Women are more susceptible to experience traumatic experiences
throughout their life, which may contribute to anxious appraisals of future events. Furthermore,
women are more likely to use emotion-focused coping, which is less effective in reducing
distress than problem-focused coping (McLean & Anderson, 2009). These factors may
increase levels of stress hormones within women that leave them susceptible to develop
symptoms of anxiety. Therefore, it appears a combination of genetic, environmental, and social
factors may explain why women tend to be diagnosed more often with anxiety related disorders.
Exposure to discrimination and prejudice, particularly relevant to ethnic minority and other
marginalized groups, can also impact an individual’s anxiety level. Discrimination and prejudice
contribute to negative interactions, which is directly related to negative affect and an overall

49
decline in mental health (Gibbons et al., 2014). The repeated exposure to discrimination and
prejudice over time can lead to fear responses in individuals, along with subsequent avoidance
of social situations in efforts to protect themselves emotionally.

I. Generalized Anxiety Disorder (GAD)

Commonly referred to as GAD, is a disorder characterized by an underlying excessive
worry related to a wide range of events or activities. While many individuals experience some
levels of worry throughout the day, individuals with GAD experience worry of a greater intensity
and for longer periods of times than the average person. Additionally, they are often unable to
control their worry through various coping strategies, which directly interferes with their ability to
engage in daily social and occupational tasks. Individuals with GAD will also experience somatic
symptoms during intensive periods of anxiety as listed below.
There is a high comorbidity between generalized anxiety disorder and the other anxiety
related disorders, as well as major depressive disorder, suggesting them all share common
vulnerabilities, both biological and psychological.

Diagnostic Criteria for Generalized Anxiety Disorder

A. Excessive anxiety and worry (apprehensive expectation), occurring more days than not
for at least 6 months about a number of events or activities (such as work or school
performance).

B. The individual finds it difficult to control the worry.

C. The anxiety and worry are associated with at least three (or more) of the following six
symptoms (with at least some symptoms present for more days than not for the past 6
months) [Note: Only one item is required in children]:
1. Restlessness or feeling keyed up or on edge
2. Being easily fatigued.
3. Difficulty concentrating or mind going blank
4. Irritability
5. Muscle tension
6. Sleep disturbance (difficulty falling or staying asleep or restless, unsatisfying sleep)

D. The anxiety, worry or physical symptoms cause clinically significant distress or

impairment in social, occupational, or other important areas of functioning.

E. The disturbance is not due to the direct physiological effects of a substance (e.g., a drug
of abuse, a medication) or a general medical condition (e.g., hyperthyroidism).

F. The disturbance is not better explained by another mental disorder (e.g., anxiety or worry
about having panic attacks in panic disorder).
From American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed.).
Washington, DC.

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Comorbidity
There is a high comorbidity between generalized anxiety disorder and the other anxiety
related disorders, as well as major depressive disorder, suggesting they all share common
vulnerabilities, both biological and psychological.

II. Specific Phobia

Distinguished by an individual’s fear or anxiety specific to an object or a situation. While
the amount of fear or anxiety related to the specific object or situation varies among individuals,
it also varies related to the proximity of the object/situation. When individuals are face-to-face
with their specific phobia, immediate fear is present. It should also be noted that these fears are
more excessive and more persistent than a “normal” fear, often severely impacting one’s daily
functioning (APA, 2013).
Individuals can experience multiple specific phobias at one time. In fact, nearly 75% of
individuals with a specific phobia report fear in more than one object (APA, 2013). When
making a diagnosis of specific phobia, it is important to identify the specific phobic stimulus.
Among the most commonly diagnosed specific phobias are animals, natural environments
(height, storms, water), blood-injection-injury (needles, invasive medical procedures), or
situational (airplanes, elevators, enclosed places; APA, 2013). Given the high percentage of
individuals who experience more than one specific phobia, all specific phobias should be listed
as a diagnosis in efforts to identify an appropriate treatment plan.
Seeing as the onset of specific phobias occurs at a younger age than most other anxiety
disorders, it is generally the primary diagnosis with the occasional generalized anxiety disorder
comorbid diagnosis. It should be noted that children/teens diagnosed with a specific phobia are
at an increased risk for additional psychopathology later in life. More specifically, other anxiety
disorders, depressive disorders, substance related disorders and somatic symptom disorders.

Diagnostic Criteria for Specific Phobia

A. Marked fear or anxiety about a specific object or situation (e.g., flying, heights, animals,
receiving an injection, seeing blood).

B. The phobic object or situation almost always provokes immediate fear or anxiety.
Note: In children, the anxiety may be expressed by crying, tantrums, freezing, or clinging.

C. The phobic object or situation is actively avoided or endured with intense fear or anxiety.

51
 D. The fear or anxiety is out of proportion to the actual danger posed by the specific object or
situation, and to the sociocultural context.

E. The fear, anxiety or avoidance is persistent, typically lasting for 6 months or more.

F. The fear, anxiety, or avoidance causes clinically significant distress or impairment in social,
occupational or other important areas of functioning.

G. The disturbance is not better explained by the symptoms of another mental disorder,
including fear, anxiety and avoidance of: situations associated with panic-like symptoms or
other incapacitating symptoms (as in agoraphobia); objects or situations related to obsessions
(as in obsessive-compulsive disorder); reminders of traumatic events (as in posttraumatic
stress disorder); separation from home or attachment figures (as in separation anxiety
disorder); or social situations (as in social anxiety disorder).

Specify type:
1. Animal
2. Natural environment (e.g., heights, storms, and water)
3. Blood–injection–injury
4. Situational (e.g., planes, elevators, or enclosed places)
5. Other (e.g., phobic avoidance of situations that may lead to choking, vomiting, or contracting
an illness; or in children, avoidance of loud sounds or costumed characters)
From American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed.).
Washington, DC.

Comorbidity
Seeing as the onset of specific phobias occurs at a younger age than most other anxiety
disorders, it is generally the primary diagnosis with the occasional generalized anxiety disorder
comorbid diagnosis. It should be noted that children/teens diagnosed with a specific phobia are
at an increased risk for additional psychopathology later in life. More specifically, other anxiety
disorders, depressive disorders, substance related disorders and somatic symptom disorders.

III. Agoraphobia

Similar to GAD, agoraphobia is defined as an intense fear triggered by a wide range of

situations; however, unlike GAD, agoraphobia’s fears are related to situations in which the
individual is in public situations where escape may be difficult. In order to receive a diagnosis of
agoraphobia, there must be a presence of fear in at least two of the following situations: using
public transportation such as planes, trains, ships, buses; being in large, open spaces such as
parking lots or on bridges; being in enclosed spaces like stores or movie theaters; being in a
large crowd similar to those at a concert; or being outside of the home in general (APA, 2013).

52
 When an individual is in one (or more) of these situations, they experience significant
fear, often reporting panic-like symptoms (see Panic Disorder). It should be noted that fear and
anxiety related symptoms are present every time the individual is presented with these
situations. Should symptoms only occur occasionally, a diagnosis of agoraphobia is not
warranted.
Due to the intense fear and somatic symptoms, individuals will go to great lengths to
avoid these situations, often preferring to remain within their home where they feel safe, thus
causing significant impairment in one’s daily functioning. They may also engage in active
avoidance, where the individual will intentionally avoid agoraphobic situations. These avoidance
behaviors may be behavioral, including having food delivery to avoid going to grocery store or
only taking a job that does not require the use of public transportation, or cognitive, by using
distraction and various other cognitive techniques to successfully get through the agoraphobic
situation.
Similar to the other anxiety disorders, comorbid diagnoses include other anxiety
disorders, depressive disorders, and substance use disorders, all of which typically occur after
the onset of agoraphobia (APA, 2013). Additionally, there is also a high comorbidity between
agoraphobia and PTSD. While agoraphobia can be a symptom of PTSD, an additional
diagnosis of agoraphobia is made when all symptoms of agoraphobia are met in addition to the
PTSD symptoms.

Diagnostic Criteria for Agoraphobia

A. Marked fear or anxiety about two or more of the following five situations: Public
transportation, open spaces, enclosed places, standing in line or being in a crowd, being
outside the home alone.

B. The individual fears or avoids these situations due to thoughts that escape might be
difficult or help might not be available in the event of developing panic-like symptoms or
other incapacitating or embarrassing symptoms (e.g., fear of falling in the elderly, fear of
incontinence).

C. The agoraphobic situations almost always provoke fear or anxiety.

D. The agoraphobic situations are actively avoided, require the presence of a companion, or
are endured with intense fear or anxiety.

E. The fear or anxiety is out of proportion to the actual danger posed by the agoraphobic
situations, and to the sociocultural context.

F. The fear, anxiety or avoidance is persistent, typically lasting for 6 months or more.

53
 G. The fear, anxiety or avoidance causes clinically significant distress or impairment in
social, occupational or other important areas of functioning.

H. If another medical condition is present (e.g., inflammatory bowel disease, Parkinson’s

disease) is present, the fear, anxiety or avoidance is clearly excessive.

I. The fear, anxiety or avoidance is not better explained by the symptoms of another mental
disorder, e.g., the symptoms are not confined to specific phobia, situational type; do not
involve only social situations (as in social anxiety disorder) and are not related exclusively to
obsessions (as in obsessive-compulsive disorder), perceived deficits or flaws in physical
appearance (as in body dysmorphic disorder), reminders of traumatic events (as in
posttraumatic stress disorder), or fear of separation (as in separation anxiety disorder).
From American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed.).
Washington, DC.

Comorbidity
Similar to the other anxiety disorders, comorbid diagnoses include other anxiety
disorders, depressive disorders, and substance use disorders, all of which typically occur after
the onset of agoraphobia (APA, 2013). Additionally, there is also a high comorbidity between
agoraphobia and PTSD. While agoraphobia can be a symptom of PTSD, an additional
diagnosis of agoraphobia is made when all symptoms of agoraphobia are met in addition to the
PTSD symptoms.

IV. Social Anxiety Disorder

For social anxiety disorder, the anxiety is directed toward the fear of social situations,
particularly those in which an individual can be evaluated by others. More specifically, the
individual is worried that they will be judged negatively and viewed as stupid, anxious, crazy,
boring, unlikeable, or boring to name a few. Some individuals report feeling concerned that their
anxiety symptoms will be obvious to others via blushing, stuttering, sweating, trembling, etc.
These fears severely limit an individual’s behavior in social settings. For example, and individual
may avoid holding drinks or plates if they know they will tremble in fear of dropping or spilling
food/water. Additionally, if one is known to sweat a lot in social situations, they may limit
physical contact with others, refusing to shake hands.
Unfortunately, for those with social anxiety disorder, all or nearly all social situations
provoke this intense fear. Some individuals even report significant anticipatory fear days or
weeks before a social event is to occur. This anticipatory fear often leads to avoidance of social
events in some individuals; others will attend social events with a marked fear of possible

54
threats. Because of these fears, there is a significant impact in one’s social and occupational
functioning.
It is important to note that the cognitive interpretation of these social events is often
excessive and out of proportion to the actual risk of being negatively evaluated. There are
instances where one may experience anxiety toward a real threat such as bullying or
ostracizing. In this instance, social anxiety disorder would not be diagnosed as the negative
evaluation and threat are real.
Among the most common comorbid diagnoses with social anxiety disorder are other
anxiety related disorders, major depressive disorder, and substance related disorders.
Generally speaking, social anxiety disorders will precede that of other mental health disorders,
with the exception of separation anxiety disorder and specific phobia, seeing as these two
disorders are more commonly diagnosed in childhood (APA, 2013). The high comorbidity rate
among anxiety related disorders and substance related disorders is likely related to the efforts of
self-medicating. For example, and individual with social anxiety disorder may consume larger
amounts of alcohol in social settings in efforts to alleviate the anxiety of the social situation.

Diagnostic Criteria for Social Anxiety Disorder (Social Phobia)

A. Marked fear or anxiety about one or more social situations in which the person is exposed
to possible scrutiny by others. Examples include social interactions (e.g., having a
conversation; meeting unfamiliar people), being observed (e.g., eating or drinking), or
performing in front of others (e.g., giving a speech). Note: In children, the anxiety must occur
in peer settings and not just in interactions with adults.

B. The individual fears that he or she will act in a way, or show anxiety symptoms, that will be
negatively evaluated (i.e., will be humiliating, embarrassing, lead to rejection, or offend
others).

C. The social situations almost always provoke fear or anxiety. Note: in children, the fear or
anxiety may be expressed by crying, tantrums, freezing, clinging, shrinking, or failing to speak
in social situations.

D. The social situations are avoided or endured with intense fear or anxiety.

E. The fear or anxiety is out of proportion to the actual threat posed by the social situation,
and to the sociocultural context.

F. The fear, anxiety or avoidance is persistent, typically lasting for 6 months or more.

G. The fear, anxiety or avoidance causes clinically significant distress or impairment in social,
occupational or other important areas of functioning.

H. The fear, anxiety or avoidance is not attributable to the effects of a substance (e.g., a drug

55
 of abuse, a medication) or another medical condition.

I. The fear, anxiety or avoidance is not better explained by the symptoms of another mental
disorder, such as panic disorder (e.g., anxiety about having a panic attack) or separation
anxiety disorder (e.g., fear of being away from home or a close relative).

J. If another medical condition (e.g., stuttering, Parkinson’s disease, obesity, disfigurement

from burns or injury) is present, the fear, anxiety or avoidance is clearly unrelated or is
excessive. Specify if: Performance only: If the fear is restricted to speaking or performing in
public.
From American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed.).
Washington, DC.

Comorbidity
Among the most common comorbid diagnoses with social anxiety disorder are other
anxiety related disorders, major depressive disorder, and substance related disorders.
Generally speaking, social anxiety disorders will precede that of other mental health disorders,
with the exception of separation anxiety disorder and specific phobia, seeing as these two
disorders are more commonly diagnosed in childhood (APA, 2013). The high comorbidity rate
among anxiety related disorders and substance related disorders is likely related to the efforts of
self-medicating. For example, and individual with social anxiety disorder may consume larger
amounts of alcohol in social settings in efforts to alleviate the anxiety of the social situation.

V. Panic Disorder

Panic disorder consists of a series of recurrent, unexpected panic attacks coupled with
the fear of future panic attacks. A panic attack is defined as a sudden or abrupt surge or fear or
impending doom along with at least four physical or cognitive symptoms (listed below). The
symptoms generally peak within a few minutes, although it seems much longer for the individual
experiencing the panic attack.
There are two key components to panic disorder—the attacks are unexpected meaning
there is nothing that triggers them, and they are recurrent meaning they occur multiple times.
Because these panic attacks occur frequently and essentially “out of the blue,” they cause
significant worry or anxiety in the individual as they are unsure of when the next attack will
occur. In some individuals, significant behavioral changes such as fear of leaving their home or
attending large events occurs as the individual is fearful an attack will happen in one of these
situations, causing embarrassment. Additionally, individuals report worry that other’s will think
they are “going crazy” or losing control if they were to observe an individual experiencing a
panic attack. Occasionally, an additional diagnosis of agoraphobia is given to an individual with

56
panic disorder if their behaviors meet diagnostic criteria for this disorder as well (see more
below).
The frequency and intensity of these panic attacks vary widely among individuals. Some
people report panic attacks occurring once a week for months on end, others report more
frequent attacks multiple times a day, but then experience weeks or months without any attacks.
Intensity of symptoms also varies among individuals, with some patients reporting experiencing
nearly all 14 symptoms and others only reporting the minimum 4 required for the diagnosis.
Furthermore, individuals report variability within their own panic attack symptoms, with some
panic attacks presenting with more symptoms than others. It should be noted that at this time,
there is no identifying information (i.e. demographic information) to suggest why some
individuals experience panic attacks more frequently or more severe than others.
Panic disorder rarely occurs in isolation, as many individuals also report symptoms of other
anxiety disorders, major depression, and substance abuse. There is mixed evidence as to
whether panic disorder precedes other comorbid psychological disorders—estimates suggest
that 1/3 of individuals with panic disorder will experience depressive symptoms prior to panic
symptoms whereas the remaining 2/3 will experience depressive symptoms concurrently or
after the onset of panic disorder (APA, 2013).
Unlike some of the other anxiety disorders, there is a high comorbid diagnosis with
general medical symptoms. More specifically, individuals with panic disorder are more likely to
report somatic symptoms such as dizziness, cardia arrhythmias, asthma, irritable bowel
syndrome, and hyperthyroidism (APA, 2013). The relationship between panic symptoms and
somatic symptoms is unclear; however, there does not appear to be a direct medical cause
between the two.
Diagnostic Criteria for Panic Disorder

A. Recurrent unexpected panic attacks. A panic attack is an abrupt surge of intense fear or
intense discomfort that reaches a peak within minutes, and during which time four (or more)
of the following symptoms occur:
Note: The abrupt surge can occur from a calm state or an anxious state.

1. Palpitations, pounding heart, or accelerated heart rate.

2. Sweating.
3. Trembling or shaking.
4. Sensations of shortness of breath or smothering.
5. Feelings of choking.
6. Chest pain or discomfort.
7. Nausea or abdominal distress.
8. Feeling dizzy, unsteady, light-headed, or faint.
9. Chills or heat sensations.

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 10. Paresthesias (numbness or tingling sensations).
11. Derealization (feelings of unreality) or depersonalization (being detached from oneself).
12. Fear of losing control or “going crazy.”
13. Fear of dying. Note: Culture-specific symptoms (e.g., tinnitus, neck soreness, headache,
uncontrollable screaming or crying) may be seen. Such symptoms should not count as one of
the four required symptoms.

B. At least one of the attacks has been followed by 1 month (or more) of one or both of the
following:
1. Persistent concern or worry about additional panic attacks or their consequences (e.g.,
losing control, having a heart attack, “going crazy”).
2. A significant maladaptive change in behavior related to the attacks (e.g., behaviors
designed to avoid having panic attacks, such as avoidance of exercise or unfamiliar
situations).

C. The disturbance is not attributable to the physiological effects of a substance (e.g., a drug
of abuse, a medication) or another medical condition (e.g., hyperthyroidism, cardiopulmonary
disorders).

D. The disturbance is not better explained by another mental disorder (e.g., the panic attacks
do not occur only in response to feared social situations, as in social anxiety disorder: in
response to circumscribed phobic objects or situations, as in specific phobia: in response to
obsessions, as in obsessive-compulsive disorder: in response to reminders of traumatic
events, as in posttraumatic stress disorder: or in response to separation from attachment
figures, as in separation anxiety disorder).
From American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed.).
Washington, DC.

Comorbidity
Panic disorder rarely occurs in isolation, as many individuals also report symptoms of
other anxiety disorders, major depression, and substance abuse. There is mixed evidence as to
whether panic disorder precedes other comorbid psychological disorders—estimates suggest
that 1/3 of individuals with panic disorder will experience depressive symptoms prior to panic
symptoms whereas the remaining 2/3 will experience depressive symptoms concurrently or
after the onset of panic disorder (APA, 2013).
Unlike some of the other anxiety disorders, there is a high comorbid diagnosis with
general medical symptoms. More specifically, individuals with panic disorder are more likely to
report somatic symptoms such as dizziness, cardia arrhythmias, asthma, irritable bowel
syndrome, and hyperthyroidism (APA, 2013). The relationship between panic symptoms and
somatic symptoms is unclear; however, there does not appear to be a direct medical cause
between the two.

58
Watch:
1. Anxiety Disorders: What you need to know?
(https://www.youtube.com/watch?v=_MtLaiCThT0)
2. A glimpse on living a life with anxiety.
(https://www.youtube.com/watch?v=mRqR4mOC4gc&t=221s)
Read:
1. (For Deeper Understanding) Chapter 5: Anxiety, Trauma-and Stressor-Related, and
Obsessive - Compulsive and Related Disorders on Abnormal Psychology: An Integrative
Approach, Seventh Edition by David H. Barlow, V. Mark Durand.
2. (For Review) Module 7: Anxiety Disorders by Washington State University
(https://opentext.wsu.edu/abnormal-psych/chapter/module-7-models-of-abnormal-psychology/)

59
 MODULE 3: TRAUMA- AND STRESSOR-RELATED
DISORDERS OBSESSIVE-COMPULSIVE AND
RELATED DISORDERS

Module Overview:

Photo from: thecomicstrips.com

In part 1, we will discuss matters related to trauma- and stressor-related disorders to

include their clinical presentation, epidemiology, comorbidity, etiology, and treatment
options. Our discussion will include PTSD, acute stress disorder, and adjustment
disorder. Before getting started with all this, we will explain what stressors are.

In part 2, we will discuss matters related to obsessive-compulsive and related disorders

to include their clinical presentation, epidemiology, comorbidity, etiology, and treatment
options. Our discussion will include obsessive compulsive disorder (OCD), body
dysmorphic disorder (BDD), and hoarding.

Module Learning Outcomes:

• Explain what stressors are.

• Describe how trauma- and stressor-related disorders present.
• Describe comorbidity in relation to trauma- and stressor-related
disorders.
• Describe the etiology of trauma- and stressor-related disorders.
• Describe how obsessive-compulsive disorders present.
• Describe comorbidity in relation to obsessive-compulsive disorders.
• Describe the etiology of obsessive-compulsive disorders.

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Course Materials:
PART 1: TRAUMA- AND STRESSOR-RELATED DISORDERS

Lecture:
A stress disorder occurs when an individual has difficulty coping with or adjusting to a
recent stressor. Stressors can be any event- witnessed first-hand, experienced personally or
experienced by a close family member- that increases physical or psychological demands on an
individual. These events are significant enough that they pose a threat, whether real or
imagined, to the individual. While many people experience similar stressors throughout their
lives, only a small percentage of individuals experience significant maladjustment to the event
that psychological intervention is warranted.
Among the most commonly studied triggers for trauma related disorders are combat and
physical/sexual assault. Symptoms of combat related trauma date back to World War I, when
soldiers would return home with “shell shock” (Figley, 1978). Unfortunately, it wasn’t until after
the Vietnam War that significant progress was made in both identifying and treating war-related
psychological difficulties (Roy-Byrne et al., 2004). With the more recent wars in Iraq and
Afghanistan, attention was again brought to posttraumatic stress disorder (PTSD) symptoms
due to the large number of service members returning from deployments and reporting
significant trauma symptoms.
Physical assault, more specifically sexual assault, is another commonly studied
traumatic event. Rape, or forced sexual intercourse or other sexual act committed without an
individual’s consent, occurs in one out of every five women and one in every 71 men (Black et
al., 2011). Unfortunately, this statistic is likely an underestimate of the actual number of cases
that occur due to the reluctance of many individuals to report their sexual assault. Of the
reported cases, it is estimated that nearly 81% of female and 35% of male rape victims report
both acute stress disorder and posttraumatic stress disorder symptoms (Black et al., 2011).

Etiology
1. HPA axis
One theory for the development of trauma and stress related disorders is the over
involvement of the hypothalamic-pituitary-adrenal (HPA) axis. The HPA axis is involved in
the fear producing response and some speculate that a dysfunction within this axis is to blame
for the development of trauma symptoms. Within the brain, the amygdala serves as the

61
integrative system that essentially elicits the physiological response to a traumatic/stressful
environmental situation. The amygdala sends this response to the HPA axis in effort to prepare
the body to “fight or flight.” The HPA axis then releases hormones- epinephrine and cortisol–
to help the body to prepare to respond to a dangerous situation (Stahl & Wise, 2008). While
epinephrine is known to cause physiological symptoms such as increased blood pressure,
increased heart rate, increased alertness, and increased muscle tension to name a few, cortisol
is responsible for returning the body back to homeostasis once the dangerous situation is
resolved.
Researchers have studied the amygdala and HPA axis in individuals with PTSD, and
have identified heightened amygdala reactivity in stressful situations, as well as excessive
reactivity to stimuli that is related to one’s specific traumatic event (Sherin & Nemeroff, 2011).
Additionally, studies have indicated that individuals with PTSD also show a diminished fear
extinction, suggesting an overall higher level of stress during non-stressful times. These findings
may explain why individuals with PTSD experience an increased startle response and
exaggerated sensitivity to stimuli associated with their trauma (Schmidt, Kaltwasser, & Wotjak,
2013).

2. Cognitive
Preexisting conditions of depression and/or anxiety may predispose an individual to
develop PTSD or other stress disorders. One theory is that these individuals may ruminate, or
over analyze the traumatic event, thus bringing more attention to the traumatic event which in
return leads to the development of stress related symptoms. Furthermore, negative cognitive
styles or maladjusted thoughts about themselves and the environment may also contribute to
PTSD symptoms. For example, individuals who identify life events as “out of their control” report
more severe stress symptoms than those who feel as though they have some control over their
lives (Catanesi et al., 2013).

3. Social
While this may hold true for many psychological disorders, social and family support
have been identified as protective factors for individuals prone to develop PTSD. More
specifically, rape victims who are loved and cared for by their friends and family members as
opposed to judge for their actions prior to the rape, report fewer trauma symptoms and faster
psychological improvement (Street et al., 2011).

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4. Sociocultural
As was mentioned previously, different ethnicities report different prevalence rates of
PTSD. While this may be due to increased exposure to traumatic events, there is some
evidence to suggest that cultural groups also interpret traumatic events differently, and
therefore, may be more vulnerable to the disorder. Hispanic Americans have routinely been
identified as a cultural group that experiences a higher rate of PTSD. Studies ranging from
combat related PTSD to on-duty police officer stress, as well as stress from a natural disaster,
all identify Hispanic Americans as the cultural group experiencing the most traumatic symptoms
(Kaczkurkin et al., 2016; Perilla et al., 2002; Pole et al., 2001).
Women also report a higher incidence of PTSD symptoms than men. Some possible
explanations for this discrepancy are stigmas related to seeking psychological treatment, as well
as a greater risk of exposure to traumatic events that are related to PTSD (Kubiak,
2006). Studies exploring rates of PTSD symptoms for military and police veterans have failed to
report a significant gender difference in the diagnosis rate of PTSD suggesting that there is not
a difference in the rate of occurrence of PTSD in males and females in these settings (Maguen,
Luxton, Skopp, & Madden, 2012).

I. POSTTRAUMATIC STRESS DISORDER

It is identified by the development of physiological, psychological, and emotional
symptoms following exposure to a traumatic event. Individuals must have been exposed to a
situation where actual or threatened death occurred. Examples of these situations include but
are not limited to: witnessing a traumatic event as it occurred to someone else; learning about a
traumatic event that occurred to a family member or close friend; or being exposed to repeated
events where one experiences an aversive event (e.g. victims of child abuse/neglect, ER
physicians in trauma center, etc.). It should be understood that while the presentation of these
symptoms varies among individuals, to meet criteria for a diagnosis of PTSD, individuals need
to report symptoms among the four different categories of symptoms.
The first category involves recurrent experiences of the traumatic event. This can occur
via flashbacks, distinct memories (which may be voluntary or involuntary), or even distressing
dreams. In order to meet criteria for PTSD, these recurrent experiences must be specific to the
traumatic event or the moments immediately following. Regardless of the method, the recurrent
experiences can last a short time- several seconds- or extend for several days. They are often
initiated by physical sensations similar to those experienced during the traumatic events, or
even environmental triggers such as a specific location. Because of these triggers, individuals

63
with PTSD are known to avoid stimuli (i.e. activities, objects, people, etc.) associated with the
traumatic event.
The second category involves avoidance of stimuli that is related to the traumatic event.
Individuals with PTSD may be observed trying to avoid the distressing thoughts and/or feelings
related to the memories of the traumatic event. One way individuals will avoid these memories
is by avoiding physical stimuli such as locations, individuals, activities, or even specific
situations that trigger the memory of the traumatic event.
The third category experienced by individuals with PTSD is negative alterations in
cognitions or mood. This is often reported as difficulty remembering an important aspect of the
traumatic event. It should be noted that this amnesia is not due to a head injury, loss of
consciousness, or substances, but rather, due to the traumatic nature of the event. The
impaired memory may also leading individuals to have false beliefs about the causes of the
traumatic event, often blaming themselves or others. An overall persistent negative state,
including a generalized negative belief about oneslf or others is also reported by those with
PTSD. Similar to those with depression, individuals with PTSD may report a reduced interest in
participation of previously enjoyable activities, as well as the desire to socially engage with
others.
The fourth and final category is alterations in arousal and reactivity. Because of the
negative mood and increased irritability, individuals with PTSD may be quick tempered and act
out in aggressive manners, both verbally and physically. While these aggressive responses may
be provoked, they are also sometimes unprovoked. It is believed these behaviors occur due to
the heightened sensitivity to potential threats, especially if the threat is similar in nature to their
traumatic event. More specifically, individuals with PTSD have a heightened startle response
and easily jump or respond to unexpected noises just as a telephone rings or a car
backfiring. Given this heightened arousal state, it should not be surprising that individuals with
PTSD also experience significant sleep disturbances, with difficulty falling asleep, as well as
staying asleep due to nightmares.
Although somewhat obvious, these symptoms likely cause significant distress in social,
occupational, and other (i.e. romantic, personal) areas of functioning. Duration of symptoms is
also important, as PTSD cannot be diagnosed unless symptoms have been present for at least
one month. If they have not been present for a month, the individual may meet criteria for
Acute Stress Disorder (see below).

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 Diagnostic Criteria for Posttraumatic Stress Disorder

A. Exposure to actual or threatened death, serious injury, or sexual violence in one (or more)
of the following ways:
1. Directly experiencing the traumatic event(s).
2. Witnessing, in person, the event(s) as they occurred to others.
3. Learning that the event(s) occurred to a close relative or close friend. In cases of actual or
threatened death of a family member or friend, the event(s) must have been violent or
accidental.
4. Experiencing repeated or extreme exposure to aversive details of the traumatic event(s)
(e.g., first responders collecting human remains; police officers repeatedly exposed to details
of child abuse).
Note: Criterion A4 does not apply to exposure through electronic media, television, movies, or
pictures, unless this exposure is work related.

B. Presence of one (or more) of the following intrusion symptoms associated with the
traumatic event(s), beginning after the traumatic event(s) occurred:
1. Recurrent, involuntary and intrusive distressing memories of the traumatic event(s). Note:
In young children, repetitive play may occur in which themes or aspects of the traumatic
event(s) are expressed.
2. Recurrent distressing dreams in which the content and/or affect of the dream are related to
the traumatic event(s). Note: In children, there may be frightening dreams without
recognizable content.
3. Dissociative reactions (e.g., flashbacks) in which the individual feels or acts as if the
traumatic event(s) were recurring. (Such reactions occur on a continuum, with the most
extreme expression being a complete loss of awareness of present surroundings.) Note: In
young children, trauma-specific reenactment may occur in play.
4. Intense or prolonged psychological distress at exposure to internal or external cues that
symbolize or resemble an aspect of the traumatic event(s).
5. Marked physiological reactions to internal or external cues that symbolize or resemble an
aspect of the traumatic event(s).

C. Persistent avoidance of stimuli associated with the traumatic event(s), beginning after the
traumatic event(s) occurred, as evidenced by one or both of the following:
1. Avoidance of or efforts to avoid distressing memories, thoughts, feelings, or conversations
about or closely associated with the traumatic event(s).
2. Avoidance of or efforts to avoid external reminders (people, places, conversations,
activities, objects, situations) that arouse distressing memories, thoughts, or feelings about or
closely associated with the traumatic event(s).
3. Inability to recall an important aspect of the trauma
4. Markedly diminished interest or participation in significant activities
5. Feeling of detachment or estrangement from others
6. Restricted range of affect (e.g., unable to have loving feelings)
7. Sense of a foreshortened future (e.g., does not expect to have a career, marriage, children,

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 or a normal life span)

D. Negative alterations in cognitions and mood associated with the traumatic event(s),
beginning or worsening after the traumatic event(s) occurred, as evidenced by two (or more)
of the following:
1. Inability to remember an important aspect of the traumatic event(s) (typically due to
dissociative amnesia and not to other factors such as head injury, alcohol, or drugs).
2. Persistent and exaggerated negative beliefs or expectations about oneself, others, or the
world (e.g., “I am bad,” “no one can be trusted,” “the world is completely dangerous,” “My
whole nervous system is permanently ruined”).
3. Persistent distorted cognitions about the cause or consequences of the traumatic event(s)
that lead the individual to blame himself/herself or others.
4. Persistent negative emotional state (e.g., fear, horror, anger, guilt, or shame).
5. Markedly diminished interest or participation in significant activities.
6. Feelings of detachment or estrangement from others.
7. Persistent inability to experience positive emotions (e.g., inability to experience happiness,
satisfaction, or loving feelings).

E. Duration of the disturbance (Criteria B, C, D and E) is more than one month.

F. The disturbance causes clinically significant distress or impairment in social, occupational,

or other important areas of functioning.

Specify if:
With delayed expression: If the diagnostic threshold is not exceeded until at least 6 months
after the event (although it is understood that onset and expression of some symptoms may
be immediate).
Specify if:
With Dissociative Symptoms: The individual’s symptoms meet the criteria for posttraumatic
stress disorder, and in addition, in response to the stressor, the individual experiences
persistent or recurrent symptoms of depersonalization or derealization.
From American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed.).
Washington, DC.

Comorbidity
Given the traumatic nature of the disorder, it should not be surprising that there is a high
comorbidity rate between PTSD and other psychological disorders. In fact, individuals with
PTSD are 80% more likely than those without PTSD to report clinically significant levels of
depressive, bipolar, anxiety, or substance abuse related symptoms (APA, 2013). There is also a
strong relationship between PTSD and major neurocognitive disorders, which may be due to the
overlapping symptoms between these disorders.

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II. ACUTE STRESS DISORDER
Acute stress disorder is very similar to PTSD except for the fact that symptoms must be
present from 3 days to 1 month following exposure to one or more traumatic events. If the
symptoms are present after 1 month, the individual would then meet criteria for PTSD.
Additionally, if symptoms present immediately following the traumatic event but resolve by day
3, an individual would not meet criteria for acute stress disorder.
Symptoms of acute stress disorder follow that of PTSD with a few exceptions. PTSD
requires symptoms within each of the four categories discussed above; however, acute stress
disorder requires that the individual experience nine symptoms across five different categories
(intrusion symptoms, negative mood, dissociative symptoms, avoidance symptoms, and arousal
symptoms). For example, an individual may experience several arousal and reactivity symptoms
such as sleep issues, concentration issues, and hypervigilance, but does not experience issues
regarding a negative mood. Regardless of the category of the symptoms, so long as nine
symptoms are present and the symptoms cause significant distress or impairment in social,
occupational, and other functioning, an individual will meet criteria for acute stress disorder.

Diagnostic Criteria for Acute Stress Disorder

A. Exposure to actual or threatened death, serious injury, or sexual violation in one (or more)
of the following ways:
1. Directly experiencing the traumatic event(s).
2. Witnessing, in person, the event(s) as it occurred to others.
3. Learning that the event(s) occurred to a close family member or close friend. Note: In
cases of actual or threatened death of a family member or friend, the event(s) must have
been violent or accidental.
4. Experiencing repeated or extreme exposure to aversive details of the traumatic event(s)
(e.g., first responders collecting human remains, police officers repeatedly exposed to details
of child abuse). Note: This does not apply to exposure through electronic media, television,
movies, or pictures, unless this exposure is work related.

B. Presence of nine (or more) of the following symptoms from any of the five categories of
intrusion, negative mood, dissociation, avoidance, and arousal, beginning or worsening after
the traumatic event(s) occurred:

Intrusion Symptoms
1. Recurrent, involuntary, and intrusive distressing memories of the traumatic event(s). Note:
In children, repetitive play may occur in which themes or aspects of the traumatic event(s) are
expressed.
2. Recurrent distressing dreams in which the content and/or affect of the dream are related to

67
the event(s). Note: In children, there may be frightening dreams without recognizable content.
3. Dissociative reactions (e.g., flashbacks) in which the individual feels or acts as if the
traumatic event(s) were recurring. (Such reactions may occur on a continuum, with the most
extreme expression being a complete loss of awareness of present surroundings.) Note: In
children, trauma-specific re-enactment may occur in play.
4. Intense or prolonged psychological distress or marked physiological reactions in response
to internal or external cues that symbolize or resemble an aspect of the traumatic event(s).

Negative Mood
5. Persistent inability to experience positive emotions (e.g., inability to experience happiness,
satisfaction, or loving feelings).

Dissociative Symptoms
6. An altered sense of the reality of one’s surroundings or oneself (e.g., seeing oneself from
another’s perspective, being in a daze, time slowing).
7. Inability to remember an important aspect of the traumatic event(s) (typically due to
dissociative amnesia and not to other factors such as head injury, alcohol, or drugs).

Avoidance Symptoms
8. Efforts to avoid distressing memories, thoughts, or feelings about or closely associated with
the traumatic event(s).
9. Efforts to avoid external reminders (people, places, conversations, activities, objects,
situations) that arouse distressing memories, thoughts, or feelings about or closely associated
with the traumatic event(s).

Arousal Symptoms
10. Sleep disturbance (e.g., difficulty falling or staying asleep, restless sleep).
11. Irritable behavior and angry outbursts (with little or no provocation), typically expressed as
verbal or physical aggression toward people or objects.
12. Hypervigilance.
13. Problems with concentration.
14. Exaggerated startle response.

C. Duration of the disturbance (symptoms in Criterion B) is 3 days to 1 month after trauma

exposure. Note: Symptoms typically begin immediately after the trauma, but persistence for at
least 3 days and up to a month is needed to meet disorder criteria.

D. The disturbance causes clinically significant distress or impairment in social, occupational,

or other important areas of functioning.

E. The disturbance is not attributable to the physiological effects of a substance (e.g.,

medication or alcohol) or another medical condition (e.g., mild traumatic brain injury) and is
not better explained by brief psychotic disorder.
From American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed.).

68
 Washington, DC.

Comorbidity
Due to the fact that 30 days after the traumatic event, ASD becomes PTSD (or the
symptoms remit), the comorbidity of ASD with other psychological disorders has not been
studied. While ASD and PTSD cannot be comorbid disorders, several studies have explored the
relationship between ASD and PTSD in efforts to identify individuals most at risk for developing
PTSD. Research studies indicate roughly 80% of motor vehicle accident survivors, as well as
assault victims, who met criteria for ASD went on to develop PTSD (Brewin, Andrews, Rose, &
Kirk, 1999; Bryant & Harvey, 1998; Harvey & Bryant, 1998). While some researchers indicated
ASD is a good predictor of PTSD, others argue further research between the two and
confounding variables should be further explored to determine more consistent findings.

III. ADJUSTMENT DISORDER

Adjustment disorder is the least intense of the three stress related disorders discussed in
this chapter. An adjustment disorder occurs following an identifiable stressor that has occurred
within the past 3 months. This stressor can be a single event (loss of job, death of a family
member) or a series of multiple stressors (cancer treatment, divorce/child custody issues).
Unlike PTSD and acute stress disorder, adjustment disorder does not have a set of
specific symptoms an individual must meet for diagnosis, rather, whatever symptoms the
individual is experiencing must be related to the stressor and must be significant enough to
impair social, occupational, or other important areas of functioning. It should be noted that
bereavement can be diagnosed as an adjustment disorder in extreme cases where an
individual’s grief exceeds the intensity or persistence that is expected.
It should be noted that there are modifiers associated with adjustment disorder. Due to
the variety of behavioral and emotional symptoms that can be present with an adjustment
disorder, clinicians are expected to classify a patient’s adjustment disorder as one of the
following: with depressed mood; with anxiety; with mixed anxiety and depressed mood; with
disturbance of conduct; with mixed disturbance of emotions and conduct; or unspecified for
behaviors that do not meet criteria for one of the aforementioned categories. Depending on the
individual’s presenting symptoms, the clinician will determine which category best classifies the
patient’s symptoms. These modifiers are also important in determining treatment options for
patients.

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 Diagnostic Criteria for Adjustment Disorder

A. The development of emotional or behavioral symptoms in response to an identifiable

stressor(s) occurring within 3 months of the onset of the stressor(s).

B. These symptoms or behaviors are clinically significant, as evidenced by one or both of the
following:
1. Marked distress that is out of proportion to the severity or intensity of the stressor, taking
into account the external context and the cultural factors that might influence symptom
severity and presentation.
2. Significant impairment in social, occupational, or other important areas of functioning.

C. The stress-related disturbance does not meet the criteria for another mental disorder and
is not merely an exacerbation of a preexisting mental disorder.

D. The symptoms do not represent normal bereavement.

E. Once the stressor or its consequences have terminated, the symptoms do not persist for
more than an additional 6 months.

Specify whether:
309.0 (F43.21) With depressed mood: Low mood, tearfulness, or feelings of hopelessness
are predominant.
309.24 (F43.22) With anxiety: Nervousness, worry, jitteriness, or separation anxiety is
predominant.
309.28 (F43.23) With mixed anxiety and depressed mood: A combination of depression
and anxiety is predominant.
309.3 (F43.24) With disturbance of conduct: Disturbance of conduct is predominant.
309.4 (F43.25) With mixed disturbance of emotions and conduct: Both emotional
symptoms (e.g., depression, anxiety) and a disturbance of conduct are predominant.
309.9 (F43.20) Unspecified: For maladaptive reactions that are not classifiable as one of the
specific subtypes of adjustment disorder.
From American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed.).
Washington, DC.

Comorbidity
Unlike most of the disorders we have reviewed thus far, adjustment disorders actually
have a high comorbidity rate with various other medical conditions (APA, 2013). Often following
a critical or terminal medical diagnosis, and individual will meet criteria for adjustment disorder
as they process the news about their health and the impact their new medical diagnosis will
have on their life. Other psychological disorders are also diagnosed with adjustment disorder;
however, symptoms of adjustment disorder must be met independently of the other

70
psychological condition (APA, 2013). For example, and individual with adjustment disorder with
depressive features must not meet criteria for a major depressive episode, otherwise, the
diagnosis of major depression should be made over the adjustment disorder.

Watch:
1. What is Posttraumatic Stress Disorder or most commonly known as PTSD?
(https://www.youtube.com/watch?v=hzSx4rMyVjI)
2. What PTSD is really like? (https://www.youtube.com/watch?v=PFW4hYsYF-o)
Read:
1. (For Deeper Understanding) Chapter 5: Anxiety, Trauma-and Stressor-Related, and
Obsessive - Compulsive and Related Disorders on Abnormal Psychology: An Integrative
Approach, Seventh Edition by David H. Barlow, V. Mark Durand.
2. (For Review) Module 5: Trauma- and Stressor-Related Disorders by Washington State
University (https://opentext.wsu.edu/abnormal-psych/chapter/module-5-models-of-abnormal-
psychology/)

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Course Materials
PART 2: OBSESSIVE-COMPULSIVE AND RELATED DISORDERS
Lecture:
Among the persons suffering from anxiety and related disorders, a client who needs
hospitalization is likely to have obsessive-compulsive disorder (OCD). A client referred for
psychosurgery (neurosurgery for a psychological disorder) because every psychological and
pharmacological treatment has failed, and the suffering is unbearable, probably has OCD. OCD
is the devastating culmination of the anxiety disorders. It is not uncommon for someone with
OCD to experience severe generalized anxiety, recurrent panic attacks, debilitating avoidance,
and major depression, all occurring simultaneously with obsessive-compulsive symptoms. With
OCD, establishing even a foothold of control and predictability over the dangerous events in life
seems so utterly hopeless that victims resort to magic and rituals (Barlow & Durand, 2013).

Etiology
1. Biological
There are a few biological explanations for obsessive-compulsive related disorders
including: hereditary transmission, neurotransmitter deficits, and abnormal functioning in brain
structures.
1.1. Hereditary transmission. With regards to heritability studies, twin studies routinely
support the role of genetics in the development of obsessive compulsive behaviors, as
monozygotic twins have a substantially greater concordance rate (80-87%) than dizygotic twins
(47-50%; Carey & Gottesman, 1981; van Grootheest, Cath, Beekman, & Boomsma,
2005). Additionally, first degree relatives of patients diagnosed with OCD are at a 5-fold
increase to develop OCD at some point throughout their lifespan (Nestadt, et al., 2000).
Interestingly, a study conducted by Nestadt and colleagues (2000) exploring the familial role in
the development of obsessive-compulsive disorder found that family members of individuals
with OCD had higher rates of both obsessions and compulsions than control families; however,
obsessions were more specific to the family members than that of the disorder. This suggests
that there is a stronger heritability association for obsessions than compulsions.
This study also found a relationship between age of onset of OCD symptoms and family
heritability. Individuals who experienced an earlier age of onset, particularly before age 17, were
found to have more first-degree relatives diagnosed with OCD. In fact, after the age of 17, there
was no relationship between family diagnoses, suggesting those who develop OCD at an older
age may have a different diagnostic origin (Nestadt, et al., 2000).

72
 Initial studies exploring genetic factors for BDD and hoarding also indicate a likely
hereditary influence; however, environmental factors appear to play a larger role in the
development of these disorders than that of OCD (Ahmed, et al., 2014; Lervolino et al., 2009).
1.2. Neurotransmitters. Neurotransmitters, particularly serotonin have been identified as a
contributing factor to obsessive and compulsive behaviors. This discovery was actually on
accident, when individuals with depression and comorbid OCD were given antidepressant
medications clomipramine and/or fluoxetine- both of which increase levels of serotonin- to
mediate symptoms of depression. Not only did these patients report a significant reduction in
their depressive symptoms, but also significant improvement in their OCD symptoms (Bokor &
Anderson, 2014). Interestingly enough, antidepressant medications that do not effect serotonin
levels are not effective in managing obsessive and compulsive symptoms, thus offering
additional support for deficits of serotonin levels as an explanation of obsessive and compulsive
behaviors (Sinopoli, Burton, Kronenberg, & Arnold, 2017; Bokor & Anderson, 2014). More
recently, there has been some research implicating the involvement of additional
neurotransmitters- glutamate, GABA, and dopamine- in the development and maintenance of
OCD, although future studies are still needed to draw definitive conclusions (Marinova, Chuang,
& Fineberg, 2017).
1.3. Brain structures. Seeing as neurotransmitters have a direct involvement in the
development of obsessive compulsive behaviors, it’s only logical that brain structures that house
these neurotransmitters also likely play a role in symptom development. Neuroimaging studies
implicate the brain structures and circuits in the frontal lobe, more specifically, the orbitofrontal
cortex, which is located just above each eye (Marsh et al., 2014). This brain region is
responsible for mediating strong emotional responses and converts them into behavioral
responses. Once the orbitofrontal cortex receives sensory/emotional information via sensory
inputs, it transmits this information through impulses. These impulses are then passed on to the
caudate nuclei which filters through the many impulses received, passing along only the
strongest impulses to the thalamus. Once the impulses reach the thalamus, the individual
essentially reassesses the emotional response and decides whether or not to act behaviorally
(Beucke et al., 2013). It is believed that individuals with obsessive compulsive behaviors
experience over activity of the orbitofrontal cortex and a lack of filtering in the caudate nuclei,
thus causing too many impulses transferred to the thalamus (Endrass et al., 2011). Further
support for this theory has been shown when individuals with OCD experience brain damage to
the orbitofrontal cortex or caudate nuclei and experience remission of OCD symptoms (Hofer et
al., 2013).

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2. Cognitive
Cognitive theorists believe that OCD behaviors occur due to an individual’s distorted
thinking and negative cognitive biases. More specifically, individuals with OCD are more likely to
overestimate the probability of harm, control, or uncertainty in their life, thus leading them to
over interpret potential negative outcomes of events. Additionally, some research has indicated
that those with OCD also experience disconfirmatory bias, which causes the individual to seek
out evidence that proves they failed to perform the ritual or compensatory behavior incorrectly
(Sue, Sue, Sue, & Sue, 2017). Finally, individuals with OCD often report the inability to trust
themselves and their instincts, and therefore, feel to repeat the compulsive behavior multiple
times to ensure it is done correctly. These cognitive biases are supported throughout research
studies that repeatedly find individuals with OCD experience more intrusive thoughts than those
without OCD (Jacob, Larson, & Storch, 2014).
Now that we have identified that individuals with OCD experience cognitive biases, and
that these biases contribute to the obsessive and compulsive behaviors, we have yet to identify
why these cognitive biases occur so often why does this happen? Everyone has times when
they have repetitive or intrusive thoughts such as: “Did I shut the oven off after cooking dinner?”
or “Did I remember to lock the door before I left home?” Fortunately, most individuals are able to
either check up on their thoughts once, or even forgo checking their thoughts after they
confidently talk themselves through their actions, ensuring that the behavior in question was or
was not completed. Unfortunately, individuals with OCD are unable to neutralize these thoughts
without performing a ritual as a way to put themselves at ease. As you will see in more detail in
the behavioral section below, the behaviors (compulsions) used to neutralize the thoughts
(obsessions) provide a temporary relief to the individual. As the individual is continually exposed
to the obsession and repeatedly engages in the compulsive behaviors to neutralize their
anxiety, the behavior is repeatedly reinforced, thus becoming a compulsion.
This theory is supported by studies where individuals with OCD report using more
neutralizing strategies and report significant reductions in anxiety after employing these
neutralizing techniques (Jacob, Larson, & Storch, 2014; Salkovskis, et al., 2003).

3. Behavioral
The behavioral explanation of obsessive compulsive related disorders focuses on the
explanation of compulsions rather than obsessions. Behaviorists believe that these compulsions
begin with and are maintained by the classical conditioning theory. As you may remember,
classical condition occurs when an unconditioned stimulus is paired with a conditioned stimulus

74
to produce a conditioned response. How does this explain OCD? Well, an individual with OCD
may experience negative thoughts or anxieties related to an unpleasant event (obsession;
unconditioned stimulus). These thoughts/anxieties cause significant distress to the individual,
and therefore, they seek out some kind of behavior (compulsion) to alleviate these threats
(conditioned stimulus). This provides temporary relief to the individual, thus reinforcing the
compulsive behaviors used to alleviate the threat. Over time, the conditioned stimulus
(compulsive behaviors) are reinforced due to the repeated exposure of the obsession and the
temporary relief that comes with engaging in these compulsive behaviors.
Strong support for this theory is the fact that the behavioral treatment option for OCD-
exposure and response prevention, is among the most effective treatments for these disorders.
As you will read below, this treatment essentially breaks the patients classical conditioning
associated with the obsessions and compulsions by preventing the individual from engaging in
the conditioned stimulus until anxiety is reduced.

I. OBSESSIVE COMPULSIVE DISORDER

Obsessive compulsive disorder, more commonly known as OCD, requires the presence
of obsessions, compulsions, or both obsessions and compulsions together (the most
common presentation of the disorder). Obsessions are defined as repetitive and persistent
thoughts, urges, or images. These obsessions are intrusive, time consuming, and unwanted,
often causing significant distress in an individual’s daily functioning. Common obsessions are
contamination (dirt on self or objects), errors of uncertainty regarding daily behaviors (locking
door, turning off appliances), thoughts of physical harm or violence, and orderliness, to name a
few (Cisler, Adams, et. al., 2011; Yadin & Foa, 2009). Often the individual will try to ignore these
thoughts, urges, or images. When they are unable to ignore them, the individual will engage in
compulsatory behaviors to alleviate the anxiety.
Compulsions are defined as repetitive behaviors or mental acts that an individual
performs in response to an obsession. Common examples of compulsions are checking (i.e.
repeatedly checking if the stove is turned off even though the first four times they checked it
was), counting (i.e. flicking the lights off and on for 5 times), hand washing, symmetry, or
repeating specific words. These compulsive behaviors essentially alleviate the anxiety
associated with the obsessive thoughts. For example, an individual may feel as though their
hands are dirty after using utensils at a restaurant. They may obsess over this thought for a
period of time, impacting their ability to interact with others or complete a specific task. This
obsession will ultimately lead to the individual performing a compulsion where they will wash

75
their hands with extremely hot water to rid all the germs, or even wash their hands a specified
number of times if they also have a counting compulsion. At this point, the individual’s anxiety
should be temporarily relieved.
These obsessions and compulsions are more excessive than the typical “cleanliness” as
they consume a large part of the individual’s day. Additionally, they cause significant impairment
in one’s daily functioning. Given the example above, an individual with a fear of contamination
may refuse to eat out at restaurants, or maybe bring their own utensils with them and insist on
using them when they are not eating at home.
Diagnostic Criteria for Obsessive-Compulsive Disorder

A. Presence of obsessions, compulsions or both:

Obsessions are defined by 1 and 2:
1. Recurrent and persistent thoughts, urges, or images that are experienced, at some time
during the disturbance, as intrusive and inappropriate and that in most individuals cause
marked anxiety or distress
2. The individual attempts to ignore or suppress such thoughts, impulses, or images, or to
neutralize them with some other thought or action

Compulsions are defined by 1 and 2:

1. Repetitive behaviors (e.g., handwashing, ordering, checking) or mental acts (e.g., praying,
counting, repeating words silently) that the individual feels driven to perform in response to an
obsession, or according to rules that must be applied rigidly
2. The behaviors or mental acts are aimed at preventing or reducing distress or preventing
some dreaded event or situation; however, these behaviors or mental acts either are not
connected in a realistic way with what they are designed to neutralize or prevent or are clearly
excessive

B. The obsessions or compulsions are time-consuming (e.g., take more than 1 hour per day),
or cause clinically significant distress or impairment in social, occupational or other important
areas of functioning.

C. The disturbance is not due to the direct physiological effects of a substance (e.g., a drug of
abuse, a medication) or another medical condition.

D. The disturbance is not better explained by the symptoms of another mental disorder (e.g.,
excessive worries, as in generalized anxiety disorder, or preoccupation with appearance, as
in body dysmorphic disorder).

Specify if:
With good or fair insight: the individual recognizes that obsessive-compulsive disorder
beliefs are definitely or probably not true or that they may or may not be true.

76
 With poor insight: The individual thinks obsessive-compulsive disorder beliefs are probably
true.
With absent insight/delusional: the person is completely convinced that obsessive-
compulsive disorder beliefs are true.

Specify if:
Tic-related: The individual has a current or past history of a tic disorder.
From American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed.).
Washington, DC.

Comorbidity
There is a high comorbidity rate between OCD and other anxiety disorders. Nearly 76%
of individuals with OCD will be diagnosed with another anxiety disorder, most commonly panic
disorder, social anxiety disorder, generalized anxiety disorder, or a specific phobia (APA, 2013).
Additionally, due to the nature of OCD and its symptoms, nearly 41% of those with OCD will
also be diagnosed with a major depressive episode (APA, 2013).
There is a high comorbidity rate between OCD and tic disorder, particularly in males with
an onset of OCD in childhood. Children presenting with early onset OCD typically have a
different presentation of symptoms than traditional OCD. Research has also indicated a strong
triad of OCD, Tic disorder, and attention-deficit/hyperactivity disorder in children. Due to this
psychological disorder triad, it is believed there is a neurobiological mechanism at fault for
development and maintenance of the disorders.
It should be noted that there are several disorders- schizophrenia, bipolar disorder,
eating disorders, and Tourettes– where there is a higher incidence of OCD than the general
public (APA, 2013). Therefore, clinicians who have a patient diagnosed with one of the
disorders above, should also routinely assess patients for OCD.

II. BODY DYSMORPHIC DISORDER

Body Dysmorphic Disorder (BDD) is another obsessive disorder, however, the focus of
these obsessions are with ones perceived defects or flaws in their physical appearance. A key
feature of these obsessions are that they are not observable to others. An individual who has a
congenital facial defect or a burn victim who is concerned about their scars are not examples of
an individual with BDD. The obsessions related to one’s appearance can run the spectrum from
feeling “unattractive” to “looking hideous.” While any part of the body can be a concern for an
individual with BDD, the most commonly reported areas are skin- such as acne, wrinkles, skin
color, hair-particularly thinning or excessive body hair, or nose- size.

77
 Due to the distressing nature of the obsessions regarding one’s body, individuals with
BDD also engage in compulsive behaviors that take up a considerable amount of time in one’s
day. For example, one may repeatedly compare their body to other people’s bodies in the
general public; repeatedly look at themselves in the mirror; engage in excessive grooming which
includes using make-up to modify their appearance. Some individuals with BDD will go as far as
having numerous plastic surgeries in attempts to obtain their “perfect” appearance. While most
of us are guilty of engaging in some of these behaviors, to meet criteria for BDD, one must
spend a considerable amount of time preoccupied with their appearance (i.e on average 3-8
hours a day), as well as display significant impairment in social, occupational, or other areas of
functioning.
Diagnostic Criteria for Body Dysmorphic Disorder

A. Preoccupation with one or more defects or flaws in physical appearance that are not
observable or appear slight to others.

B. At some point during the course of the disorder, the individual has performed repetitive
behaviors (e.g., mirror checking, excessive grooming, skin picking, reassurance seeking) or
mental acts (e.g., comparing his or her appearance with that of others) in response to the
appearance concerns.

C. The preoccupation causes clinically significant distress or impairment in social,

occupational, or other important areas of functioning.

D. The appearance preoccupation is not better explained by concerns with body fat or weight
in an individual whose symptoms meet diagnostic criteria for an eating disorder.

Specify if:
With good or fair insight: The individual recognizes that the body dysmorphic disorder
beliefs are definitely or probably not true or that they may or may not be true.
With poor insight: The individual thinks that the body dysmorphic disorder beliefs are
probably true.
With absent insight/delusional beliefs: the individual is completely convinced that the body
dysmorphic disorder beliefs are true.
With muscle dysmorphia: The individual is preoccupied with the idea that his or her body
build is too small or insufficiently muscular. This specifier is used even if the individual is
preoccupied with other body areas, which is often the case.
From American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed.).
Washington, DC.

78
Comorbidity
While research on BDD is still in its infancy, initial studies suggest that major depressive
disorder is the most common comorbid psychological disorder (APA, 2013). MDD typically
occurs after the onset of BDD. Additionally, there are some reports of social anxiety, OCD, and
substance-related disorders (likely related to muscle enhancement; APA, 2013).

III. HOARDING DISORDER

In hoarding, the key feature is the persistent over accumulation of possessions. While
we all obtain items throughout our life, individuals with hoarding disorder continue to accumulate
items without discarding possessions, regardless of their value or sentiment. This lack of
discarding occurs over a long period of time, and is not explained by a recent significant
stressor (i.e. lost house in fire so now keeps everything). For example, last week’s newspaper
that had no relevance to me or any historical value- those with hoarding disorder would keep
this newspaper despite the lack of value or sentiment.
The most common items that are hoarded are newspapers, magazines, clothes, bags,
books, mail, and paperwork (APA, 2013). While these items may be stored in attics and
garages, individuals with a hoarding disorder also have these items cluttering their living space,
sometimes to the extent that they are unable to even utilize their furniture because it is covered
in stuff. Cognitive factors contributing to the need to hold onto these non-sentimental items are
fear of losing important information and fear of being wasteful. When asked to “clean out” their
house or get rid of these items, individuals with hoarding disorder experience significant
distress. One’s hoarding behaviors also impacts their daily functioning, and causes impairment
in social and occupational functioning.

Diagnostic Criteria for Hoarding Disorder

A. Persistent difficulty discarding or parting with possessions, regardless of their actual value.

B. This difficulty is due to a perceived need to save the items and to distress associated with
discarding them.

C. The difficulty discarding possessions results in the accumulation of possessions that

congest and clutter active living areas and substantially compromises their intended use. If
living areas are uncluttered, it is only because of the interventions of third parties (e.g., family
members, cleaners, authorities).

79
 D. The hoarding causes clinically significant distress or impairment in social, occupational, or
other important areas of functioning (including maintaining a safe environment for self and
others).

E. The hoarding is not attributable to another medical condition (e.g., brain injury,
cerebrovascular disease, Prader-Willi syndrome).

F. The hoarding is not better explained by the symptoms of another mental disorder (e.g.,
obsessions in obsessive-compulsive disorder, decreased energy in major depressive
disorder, delusions in schizophrenia or another psychotic disorder, cognitive deficits in major
neurocognitive disorder, restricted interests in autism spectrum disorder).

Specify if:
With excessive acquisition: If difficulty discarding possessions is accompanied by excessive
acquisition of items that are not needed or for which there is no available space.

Specify if:
With good or fair insight: The individual recognizes that hoarding-related beliefs and
behaviors (pertaining to difficulty discarding items, clutter, or excessive acquisition) are
problematic.
With poor insight: The individual is mostly convinced that hoarding-related beliefs and
behaviors (pertaining to difficulty discarding items, clutter, or excessive acquisition) are not
problematic despite evidence to the contrary.
With absent insight/delusional beliefs: The individual is completely convinced that
hoarding-related beliefs and behaviors (pertaining to difficulty discarding items, clutter, or
excessive acquisition) are not problematic despite evidence to the contrary
From American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed.).
Washington, DC.

Comorbidity
Hoarding has an extremely high comorbidity rate with other mood and/or anxiety
disorders, with approximately 75% of individuals meeting diagnostic criteria for either major
depressive disorder, social anxiety disorder, or generalized anxiety disorder (APA, 2013).
Additionally, nearly 20% also meet criteria for OCD, which is not surprising seeing the similarity
in their etiology.

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Watch:
1. Debunking myths on Obsessive-Compulsive Disorder
(https://www.youtube.com/watch?v=DhlRgwdDc-E)
2. Living a life with OCD. (https://www.youtube.com/watch?v=TD-xPiwtyHA)
3. How individuals who suffer with Body Dysmorphic Disorder view themselves?
(https://youtu.be/vf4Sigud3Pw)
Read:
1. (For Deeper Understanding) Chapter 5: Anxiety, Trauma-and Stressor-Related, and
Obsessive - Compulsive and Related Disorders on Abnormal Psychology: An Integrative
Approach, Seventh Edition by David H. Barlow, V. Mark Durand.
2. (For Review) Module 9: Obsessive-Compulsive and Related Disorders by Washington State
University (https:// opentext.wsu.edu/abnormal-psych/chapter/module-9-models-of-abnormal-
psychology/)

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 MODULE 4: MOOD DISORDERS
Module Overview:

Photo from: herald.net

In Module 4, we will discuss matters related to mood disorders to include their

clinical presentation, comorbidity, etiology, and treatment options. Our
discussion will include Major Depressive Disorder, Persistent Depressive
Disorder (formerly Dysthymia), Bipolar I disorder, Bipolar II disorder, and
Cyclothymic disorder. Throughout our discussion, we will also cover major
depressive, manic, and hypomanic episodes.

Module Learning Outcomes:

• Describe how depressive disorders present.

• Describe how bipolar disorders present.
• Describe comorbidity in relation to mood disorders.
• Describe the etiology of mood disorders.

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Course Materials

Lecture:
Mood disorders are among the most common psychological disorders, and the risk of
developing them is increasing worldwide, particularly in younger people. Two fundamental
experiences can contribute either singly or in combination to all specific mood disorders: a major
depressive episode and mania. A less severe episode of mania that does not cause impairment
in social or occupational functioning is known as a hypomanic episode. An episode of mania
coupled with anxiety or depression is known as a mixed episode or mixed state. The causes of
mood disorders lie in a complex interaction of biological, psychological, and social factors. From
a biological perspective, researchers are particularly interested in the stress hypothesis and the
role of neurohormones. Psychological theories of depression focus on learned helplessness and
the depressive cognitive schemas, as well as interpersonal disruptions. A variety of treatments,
both biological and psychological, have proved effective for the mood disorders, at least in the
short term. For those individuals who do not respond to antidepressant drugs or psychosocial
treatments, a more dramatic physical treatment, electroconvulsive therapy, is sometimes used.
Two psychological treatments—cognitive therapy and interpersonal psychotherapy— seem
effective in treating depressive disorders (Barlow & Durand, 2013).

I. MAJOR DEPRESSIVE DISORDER

Major depressive disorder represents the classic condition in this group of disorders. It is
characterized by discrete episodes of at least 2 weeks' duration (although most episodes last
considerably longer) involving clear-cut changes in affect, cognition, and neurovegetative
functions and inter-episode remissions. A diagnosis based on a single episode is possible,
although the disorder is a recurrent one in the majority of cases. Careful consideration is given
to the delineation of normal sadness and grief from a major depressive episode. Bereavement
may induce great suffering, but it does not typically induce an episode of major depressive
disorder. When they do occur together, the depressive symptoms and functional impairment
tend to be more severe and the prognosis is worse compared with bereavement that is not
accompanied by major depressive disorder. Bereavement-related depression tends to occur in
persons with other vulnerabilities to depressive disorders, and recovery may be facilitated by
antidepressant treatment.

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 Diagnostic Criteria for Major Depressive Disorder

A. Five (or more) of the following symptoms have been present during the same 2-week
period and represent a change from previous functioning: at least one of the symptoms is
either (1) depressed mood or (2) loss of interest or pleasure.

Note: Do not include symptoms that are clearly attributable to another medical condition.
1. Depressed mood most of the day, nearly every day, as indicated by either subjective report
(e.g., feels sad, empty, hopeless) or observation made by others (e.g., appears tearful).
(Note: In children and adolescents, can be irritable mood.)
2. Markedly diminished interest or pleasure in all, or almost all, activities most of the day,
nearly every day (as indicated by either subjective account or observation).
3. Significant weight loss when not dieting or weight gain (e.g., a change of more than 5% of
body weight in a month), or decrease or increase in appetite nearly every day. (Note: In
children, consider failure to make expected weight gain.)
4. Insomnia or hypersomnia nearly every day.
5. Psychomotor agitation or retardation nearly every day (observable by others, not merely
subjective feelings of restlessness or being slowed down).
6. Fatigue or loss of energy nearly every day.
7. Feelings of worthlessness or excessive or inappropriate guilt (which may be delusional)
nearly every day (not merely self-reproach or guilt about being sick).
8. Diminished ability to think or concentrate, or indecisiveness, nearly every day (either by
subjective account or as observed by others).
9. Recurrent thoughts of death (not just fear of dying), recurrent suicidal ideation without a
specific plan, or a suicide attempt or a specific plan for committing suicide.

B. The symptoms cause clinically significant distress or impairment in social, occupational, or

other important areas of functioning.

C. The episode is not attributable to the physiological effects of a substance or to another

medical condition.

Note: Criteria A-C represent a major depressive episode.

Note: Responses to a significant loss (e.g., bereavement, financial ruin, losses from a natural
disaster, a serious medical illness or disability) may include the feelings of intense sadness,
rumination about the loss, insomnia, poor appetite, and weight loss noted in Criterion A, which
may resemble a depressive episode. Although such symptoms may be understandable or
considered appropriate to the loss, the presence of a major depressive episode in addition to
the normal response to a significant loss should also be carefully considered. This decision
inevitably requires the exercise of clinical judgment based on the individual’s history and the
cultural norms for the expression of distress in the context of loss.

D. The occurrence of the major depressive episode is not better explained by schizoaffective
disorder, schizophrenia, schizophreniform disorder, delusional disorder, or other specified and

84
 unspecified schizophrenia spectrum and other psychotic disorders.

E. There has never been a manic episode or a hypomanie episode. Note: This exclusion does
not apply if all of the manic-like or hypomanic-like episodes are substance-induced or are
attributable to the physiological effects of another medical condition.
From American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed.).
Washington, DC.

II. PERSISTENT DEPRESSIVE DISORDER (DYSTHYMIA)

A more chronic form of depression, persistent depressive disorder (dysthymia), can be
diagnosed when the mood disturbance continues for at least 2 years in adults or 1 year in
children. This diagnosis, new in DSM-5, includes both the DSM-IV diagnostic categories of
chronic major depression and dysthymia.
Diagnostic Criteria for Persistent Depressive Disorder

This disorder represents a consolidation of DSM-lV-defined chronic major depressive disorder

and dysthymic disorder.
A. Depressed mood for most of the day, for more days than not, as indicated by either
subjective account or observation by others, for at least 2 years. Note: In children and
adolescents, mood can be irritable and duration must be at least 1 year.

B. Presence, while depressed, of two (or more) of the following:

1. Poor appetite or overeating.
2. Insomnia or hypersomnia.
3. Low energy or fatigue.
4. Low self-esteem.
5. Poor concentration or difficulty making decisions.
6. Feelings of hopelessness.

C. During the 2-year period (1 year for children or adolescents) of the disturbance, the
individual has never been without the symptoms in Criteria A and B for more than 2 months at
a time.

D. Criteria for a major depressive disorder may be continuously present for 2 years.

E. There has never been a manic episode or a hypomanic episode, and criteria have never
been met for cyclothymic disorder.

F. The disturbance is not better explained by a persistent schizoaffective disorder,

schizophrenia, delusional disorder, or other specified or unspecified schizophrenia spectrum
and other psychotic disorder.

85
 G. The symptoms are not attributable to the physiological effects of a substance (e.g., a drug
of abuse, a medication) or another medical condition (e.g. hypothyroidism).

H. The symptoms cause clinically significant distress or impairment in social, occupational, or

other important areas of functioning.

Note: Because the criteria for a major depressive episode include four symptoms that are
absent from the symptom list for persistent depressive disorder (dysthymia), a very limited
number of individuals will have depressive symptoms that have persisted longer than 2 years
but will not meet criteria for persistent depressive disorder. If full criteria for a major
depressive episode have been met at some point during the current episode of illness, they
should be given a diagnosis of major depressive disorder. Otherwise, a diagnosis of other
specified depressive disorder or unspecified depressive disorder is warranted.

Specify if:
Early onset: If onset is before age 21 years.
Late onset: If onset is at age 21 years or older.
Specify if (for most recent 2 years of persistent depressive disorder):
With pure dysthymic syndrome: Full criteria for a major depressive episode have not been
met in at least the preceding 2 years.
With persistent major depressive episode: Full criteria for a major depressive episode
have been met throughout the preceding 2-year period.
With intermittent major depressive episodes, with current episode: Full criteria for a
major depressive episode are currently met, but there have been periods of at least 8 weeks
in at least the preceding 2 years with symptoms below the threshold for a full major
depressive episode.
With intermittent major depressive episodes, without current episode: Full criteria for a
major depressive episode are not currently met, but there has been one or more major
depressive episodes in at least the preceding 2 years.
From American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed.).
Washington, DC.

III. BIPOLAR I DISORDER

The bipolar I disorder criteria represent the modern understanding of the classic manic-
depressive disorder or affective psychosis described in the nineteenth century, differing from
that classic description only to the extent that neither psychosis nor the lifetime experience of a
major depressive episode is a requirement. However, the vast majority of individuals whose
symptoms meet the criteria for a fully syndromal manic episode also experience major
depressive episodes during the course of their lives (APA, 2013).

86
 Diagnostic Criteria for Bipolar I Disorder

For a diagnosis of bipolar I disorder, it is necessary to meet the following criteria for a manic
episode. The manic episode may have been preceded by and may be followed by hypomanic
or major depressive episodes.

Manic Episode
A. A distinct period of abnormally and persistently elevated, expansive, or irritable mood and
abnormally and persistently increased goal-directed activity or energy, lasting at least 1 week
and present most of the day, nearly every day (or any duration if hospitalization is necessary).

B. During the period of mood disturbance and increased energy or activity, three (or more) of
the following symptoms (four if the mood is only irritable) are present to a significant degree
and represent a noticeable change from usual behavior:
1. Inflated self-esteem or grandiosity.
2. Decreased need for sleep (e.g., feels rested after only 3 hours of sleep).
3. More talkative than usual or pressure to keep talking.
4. Flight of ideas or subjective experience that thoughts are racing.
5. Distractibility (i.e., attention too easily drawn to unimportant or irrelevant external stimuli),
as reported or observed.
6. Increase in goal-directed activity (either socially, at work or school, or sexually) or
psychomotor agitation (i.e., puφoseless non-goal-directed activity).
7. Excessive involvement in activities that have a high potential for painful consequences
(e.g., engaging in unrestrained buying sprees, sexual indiscretions, or foolish business
investments).

C. The mood disturbance is sufficiently severe to cause marked impairment in social or

occupational functioning or to necessitate hospitalization to prevent harm to self or others, or
there are psychotic features.
D. The episode is not attributable to the physiological effects of a substance (e.g., a drug of
abuse, a medication, other treatment) or to another medical condition.
Note: A full manic episode that emerges during antidepressant treatment (e.g., medication,
electroconvulsive therapy) but persists at a fully syndromal level beyond the physiological
effect of that treatment is sufficient evidence for a manic episode and, therefore, a bipolar I
diagnosis.
Note: Criteria A-D constitute a manic episode. At least one lifetime manic episode is required
for the diagnosis of bipolar I disorder.

Hypomanic Episode
A. A distinct period of abnormally and persistently elevated, expansive, or irritable mood and
abnormally and persistently increased activity or energy, lasting at least 4 consecutive days
and present most of the day, nearly every day.

B. During the period of mood disturbance and increased energy and activity, three (or more)

87
of the following symptoms (four if the mood is only irritable) have persisted, represent a
noticeable change from usual behavior, and have been present to a significant degree:
1. Inflated self-esteem or grandiosity.
2. Decreased need for sleep (e.g., feels rested after only 3 hours of sleep).
3. More talkative than usual or pressure to keep talking.
4. Flight of ideas or subjective experience that thoughts are racing.
5. Distractibility (i.e., attention too easily drawn to unimportant or irrelevant external stimuli),
as reported or observed.
6. Increase in goal-directed activity (either socially, at work or school, or sexually) or
psychomotor agitation.
7. Excessive involvement in activities that have a high potential for painful consequences
(e.g., engaging in unrestrained buying sprees, sexual indiscretions, or foolish business
investments).

C. The episode is associated with an unequivocal change in functioning that is

uncharacteristic of the individual when not symptomatic.

D. The disturbance in mood and the change in functioning are observable by others.

E. The episode is not severe enough to cause marked impairment in social or occupational
functioning or to necessitate hospitalization. If there are psychotic features, the episode is, by
definition, manic.

F. The episode is not attributable to the physiological effects of a substance (e.g., a drug of
abuse, a medication, other treatment).
Note: A full hypomanic episode that emerges during antidepressant treatment (e.g.,
medication, electroconvulsive therapy) but persists at a fully syndromal level beyond the
physiological effect of that treatment is sufficient evidence for a hypomanic episode diagnosis.
However, caution is indicated so that one or two symptoms (particularly increased irritability,
edginess, or agitation following antidepressant use) are not taken as sufficient for diagnosis of
a hypomanic episode, nor necessarily indicative of a bipolar diathesis.
Note: Criteria A-F constitute a hypomanic episode. Hypomanic episodes are common in
bipolar I disorder but are not required for the diagnosis of bipolar I disorder.

Major Depressive Episode

A. Five (or more) of the following symptoms have been present during the same 2-week
period and represent a change from previous functioning; at least one of the symptoms is
either (1) depressed mood or (2) loss of interest or pleasure.
Note: Do not include symptoms that are clearly attributable to another medical condition.
1. Depressed mood most of the day, nearly every day, as indicated by either subjective report
(e.g., feels sad, empty, or hopeless) or observation made by others (e.g., appears tearful).
(Note: In children and adolescents, can be irritable mood.)
2. Markedly diminished interest or pleasure in all, or almost all, activities most of the day,
nearly every day (as indicated by either subjective account or observation).

88
 3. Significant weight loss when not dieting or weight gain (e.g., a change of more than 5% of
body weight in a month), or decrease or increase in appetite nearly every day. (Note: In
children, consider failure to make expected weight gain.)
4. Insomnia or hypersomnia nearly every day.
5. Psychomotor agitation or retardation nearly every day (observable by others; not merely
subjective feelings of restlessness or being slowed down).
6. Fatigue or loss of energy nearly every day.
7. Feelings of worthlessness or excessive or inappropriate guilt (which may be delusional)
nearly every day (not merely self-reproach or guilt about being sick).
8. Diminished ability to think or concentrate, or indecisiveness, nearly every day (either by
subjective account or as observed by others).
9. Recurrent thoughts of death (not just fear of dying), recurrent suicidal ideation without a
specific plan, or a suicide attempt or a specific plan for committing suicide.

B. The symptoms cause clinically significant distress or impairment in social, occupational, or

other important areas of functioning.

C. The episode is not attributable to the physiological effects of a substance or another

medical condition.
Note: Criteria A-C constitute a major depressive episode. Major depressive episodes are
common in bipolar I disorder but are not required for the diagnosis of bipolar I disorder.
Note: Responses to a significant loss (e.g., bereavement, financial ruin, losses from a natural
disaster, a serious medical illness or disability) may include the feelings of intense sadness,
rumination about the loss, insomnia, poor appetite, and weight loss noted in Criterion A, which
may resemble a depressive episode. Although such symptoms may be understandable or
considered appropriate to the loss, the presence of a major depressive episode in addition to
the normal response to a significant loss should also be carefully considered. This decision
inevitably requires the exercise of clinical judgment based on the individual’s history and the
cultural norms for the expression of distress in the context of loss.

Bipolar I Disorder
A. Criteria have been met for at least one manic episode (Criteria A-D under “Manic Episode”
above).
B. The occurrence of the manic and major depressive episode(s) is not better explained by
schizoaffective disorder, schizophrenia, schizophreniform disorder, delusional disorder, or
other specified or unspecified schizophrenia spectrum and other psychotic disorder.
From American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed.).
Washington, DC.

IV. BIPOLAR II DISORDER

Bipolar II disorder, requiring the lifetime experience of at least one episode of major
depression and at least one hypomanic episode, is no longer thought to be a "milder" condition
than bipolar I disorder, largely because of the amount of time individuals with this condition

89
spend in depression and because the instability of mood experienced by individuals with bipolar
II disorder is typically accompanied by serious impairment in work and social functioning (APA,
2013).
Diagnostic Criteria for Bipolar I Disorder

For a diagnosis of bipolar II disorder, it is necessary to meet the following criteria for a current
or past hypomanic episode and the following criteria for a current or past major depressive
episode:

Hypomanic Episode
A. A distinct period of abnormally and persistently elevated, expansive, or irritable mood and
abnormally and persistently increased activity or energy, lasting at least 4 consecutive days
and present most of the day, nearly every day.
B. During the period of mood disturbance and increased energy and activity, three (or more)
of the following symptoms have persisted (four if the mood is only irritable), represent a
noticeable change from usual behavior, and have been present to a significant degree:
1. Inflated self-esteem or grandiosity.
2. Decreased need for sleep (e.g., feels rested after only 3 hours of sleep).
3. More talkative than usual or pressure to keep talking.
4. Flight of ideas or subjective experience that thoughts are racing.
5. Distractibility (i.e., attention too easily drawn to unimportant or irrelevant external stimuli),
as reported or observed.
6. Increase in goal-directed activity (either socially, at work or school, or sexually) or
psychomotor agitation.
7. Excessive involvement in activities that have a high potential for painful consequences
(e.g., engaging in unrestrained buying sprees, sexual indiscretions, or foolish business
investments).

C. The episode is associated with an unequivocal change in functioning that is

uncharacteristic of the individual when not symptomatic.

D. The disturbance in mood and the change in functioning are observable by others.

E. The episode is not severe enough to cause marked impairment in social or occupational
functioning or to necessitate hospitalization. If there are psychotic features, the episode is, by
definition, manic.

F. The episode is not attributable to the physiological effects of a substance (e.g., a drug of
abuse, a medication or other treatment).
Note: A full hypomanic episode that emerges during antidepressant treatment (e.g.,
medication, electroconvulsive therapy) but persists at a fully syndromal level beyond the
physiological effect of that treatment is sufficient evidence for a hypomanic episode diagnosis.
However, caution is indicated so that one or two symptoms (particularly increased irritability,

90
edginess, or agitation following antidepressant use) are not taken as sufficient for diagnosis of
a hypomanic episode, nor necessarily indicative of a bipolar diathesis.

Major Depressive Episode

A. Five (or more) of the following symptoms have been present during the same 2-week
period and represent a change from previous functioning; at least one of the symptoms is
either (1 ) depressed mood or (2) loss of interest or pleasure.
Note: Do not include symptoms that are clearly attributable to a medical condition.
1. Depressed mood most of the day, nearly every day, as indicated by either subjective report
(e.g., feels sad, empty, or hopeless) or observation made by others (e.g., appears tearful).
(Note: In children and adolescents, can be irritable mood.)
2. Markedly diminished interest or pleasure in all, or almost all, activities most of the day,
nearly every day (as indicated by either subjective account or observation).
3. Significant weight loss when not dieting or weight gain (e.g., a change of more than 5% of
body weight in a month), or decrease or increase in appetite nearly every day. (Note: In
children, consider failure to make expected weight gain.)
4. Insomnia or hypersomnia nearly every day.
5. Psychomotor agitation or retardation nearly every day (observable by others; not merely
subjective feelings of restlessness or being slowed down).
6. Fatigue or loss of energy nearly every day.
7. Feelings of worthlessness or excessive or inappropriate guilt (which may be delusional)
nearly every day (not merely self-reproach or guilt about being sick).
8. Diminished ability to think or concentrate, or indecisiveness, nearly every day (either by
subjective account or as observed by others).
9. Recurrent thoughts of death (not just fear of dying), recurrent suicidal ideation without a
specific plan, a suicide attempt, or a specific plan for committing suicide.

B. The symptoms cause clinically significant distress or impairment in social, occupational, or

other important areas of functioning.

C. The episode is not attributable to the physiological effects of a substance or another

medical condition.
Note: Criteria A-C above constitute a major depressive episode.
Note: Responses to a significant loss (e.g., bereavement, financial ruin, losses from a natural
disaster, a serious medical illness or disability) may include the feelings of intense sadness,
rumination about the loss, insomnia, poor appetite, and weight loss noted in Criterion A, which
may resemble a depressive episode. Although such symptoms may be understandable or
considered appropriate to the loss, the presence of a major depressive episode in addition to
the normal response to a significant loss should be carefully considered. This decision
inevitably requires the exercise of clinical judgment based on the individual’s history and the
cultural norms for the expression of distress in the context of loss.

Bipolar II Disorder
A. Criteria have been met for at least one hypomanic episode (Criteria A-F under “Hypomanic

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 Episode” above) and at least one major depressive episode (Criteria A-C under “Major
Depressive Episode” above).

B. There has never been a manic episode.

C. The occurrence of the hypomanic episode(s) and major depressive episode(s) is not better
explained by schizoaffective disorder, schizophrenia, schizophreniform disorder, delusional
disorder, or other specified or unspecified schizophrenia spectrum and other psychotic
disorder.

D. The symptoms of depression or the unpredictability caused by frequent alternation

between periods of depression and hypomania causes clinically significant distress or
impairment in social, occupational, or other important areas of functioning.
From American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed.).
Washington, DC.

V. CYCLOTHYMIC DISORDER
The diagnosis of cyclothymic disorder is given to adults who experience at least 2 years
(for children, a full year) of both hypomanic and depressive periods without ever fulfilling the
criteria for an episode of mania, hypomania, or major depression.
Diagnostic Criteria for Cyclothymic Disorder

A. For at least 2 years (at least 1 year in children and adolescents) there have been
numerous periods with hypomanic symptoms that do not meet criteria for a hypomanic
episode and numerous periods with depressive symptoms that do not meet criteria for a
major depressive episode.

B. During the above 2-year period (1 year in children and adolescents), the hypomanic and
depressive periods have been present for at least half the time and the individual has not
been without the symptoms for more than 2 months at a time.

C. Criteria for a major depressive, manic, or hypomanic episode have never been met.

D. The symptoms in Criterion A are not better explained by schizoaffective disorder,

schizophrenia, schizophreniform disorder, delusional disorder, or other specified or
unspecified schizophrenia spectrum and other psychotic disorder.

E. The symptoms are not attributable to the physiological effects of a substance (e.g., a drug
of abuse, a medication) or another medical condition (e.g., hyperthyroidism).

F. The symptoms cause clinically significant distress or impairment in social, occupational, or

other important areas of functioning
From American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed.).

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 Washington, DC.

Etiology
1. Biological
Research throughout the years continues to provide evidence that depressive disorders have
some biological cause. While it does not explain every depressive case, it is safe to say that
some individuals may at least have a predisposition to develop a depressive disorder. Among
the biological factors are genetic factors, biochemical factors and brain structure.
1.1. Genetics. Like with any disorder, researchers often explore the prevalence rate of
depressive disorders among family members, in efforts to determine if there is some genetic
component, whether it be a direct link or a predisposition. If there is a genetic predisposition to
developing depressive disorders, one would expect a higher rate of depression within families
than that of the general population. Researchers support this with regards to depressive
disorders as there is nearly a 30 percent increase in relatives diagnosed with depression,
compared to 10 percent of the general population (Levinson & Nichols, 2014). Similarly, there is
also an elevated prevalence among first-degree relatives for both bipolar I and bipolar II
disorders as well.
Another way to study the genetic component of a disorder is via twin studies. One would
expect identical twins to have a higher rate of the disorder as opposed to fraternal twins, as
identical twins share the same genetic make-up whereas fraternal twins only share that of
siblings, roughly 50%. A large scaled study found that there was nearly a 46% chance that if
one identical twin was diagnosed with depression, that the other was as well. In contrast, the
fraternal twin rate was only 20%. Despite the fraternal twin rate still being higher than that of a
firs-degree relative, this study provided enough evidence that there is a strong genetic link in the
development of depression (McGuffin et al., 1996).
Finally, scientists have more recently been studying depression at a molecular level,
exploring possibilities of gene abnormalities as a cause to developing a depressive disorder.
While much of the research is speculation due to sampling issues and low power, there is some
evidence that depression may be tied to the 5-HTT gene on chromosome 17, as this is
responsible for the activity of serotonin (Jansen et al., 2016).
Bipolar disorders share a similar genetic predisposition to developing the disorder. Twin studies
within bipolar disorder yield concordance rates for identical twins at as high as 72%, and 5-15%
for fraternal twins, siblings, and other close relatives. Both of these percentages are significantly

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higher than that of the general population, suggesting a strong genetic component of bipolar
disorder (Edvardsen et al., 2008).
1.2. Biochemical. As you will read in the treatment section, there is strong evidence of a
biochemical deficit in depression and bipolar disorders. More specifically, low activity levels of
norepinephrine and serotonin, have long been documented as contributing factors to developing
depressive disorders. This was actually discovered accidently in the 1950’s when MAOI’s were
given to tuberculosis patients, and miraculously, their depressive moods were also improved.
Soon thereafter, medical providers found that medications used to treat high blood pressure by
causing a reduction in norepinephrine, also caused depression in their patients (Ayd, 1956).
While these initial findings were premature in the identification of how neurotransmitters effected
development of depressive features, they did provide insight as to what neurotransmitters were
involved in this system. Researchers are still trying to determine exact pathways; however, it
does appear that both norepinephrine and serotonin are involved in the development of
symptoms, whether it be between the interaction between them, or their interaction on other
neurotransmitters (Ding et al., 2014).
Due to the close nature of depression and bipolar disorder, researchers initially believed that
both norepinephrine and serotonin were both implicated in the development of bipolar disorder;
however, the idea was that there was a drastic increase in serotonin during mania episodes.
Unfortunately, research actually supports the opposite. It is believed that mania episodes may in
fact be explained by low levels of serotonin and high levels of norepinephrine (Soreff &
McInnes, 2014). Additional research with this area is needed to conclusively determine exactly
what is responsible for the manic episodes within bipolar disorder.
1.3. Endocrine system. As you may know, the endocrine system is a collection of glands
responsible for regulating hormones, metabolism, growth and development, sleep, and mood
among other things. Some research has implicated hormones, particularly cortisol, a hormone
released as a stress response, in the development of depression (Owens et al, 2014).
Additionally, melatonin, a hormone released when it is dark outside to assist with the transition
to sleep, may also be related to depressive symptoms, particularly during the winter months
(seasonal affective disorder).
1.4. Brain anatomy. Seeing as neurotransmitters are involved in depressive disorders, it
should not be a surprise that the brain anatomy is also involved. While exact anatomy and
pathways are yet to be determined, research studies implicate the prefrontal cortex, the
hippocampus, and the amygdala. More specifically, drastic changes in blood flow throughout the
prefrontal cortex has been linked with depressive symptoms. Similarly, a smaller hippocampus,

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and consequently, fewer number of neurons, have also been linked to depressive symptoms.
Finally, heightened activity and blood flow in the amygdala, the brain area responsible for our
fight or flight emotions, is also consistently found in individuals with depressive symptoms.
There are a number of structural abnormalities in individuals with bipolar disorder; however,
what or why these structures are abnormal is yet to be determined. Researchers continue to
focus on areas of basal ganglia and cerebellum, which appear to be much smaller in individuals
with bipolar disorder as opposed to the general public. Additionally, there appears to be a
decrease in brain activity in regions associated with regulating emotions, as well as increase in
brain activity among structures related to emotional responsiveness (Houenou et al., 2011).
Additional research is still needed to determine exactly how each of these brain structures may
be implicated in the development of bipolar disorder.

2. Cognitive
The cognitive model, arguably the most conclusive model with regards to depressive
disorders, focuses on the negative thoughts and perceptions of an individual. One theory often
equated with the cognitive model of depression is learned helplessness. Coined by Martin
Seligman (1975), learned helplessness was developed based on his laboratory experiment
involving dogs. In this study, Seligman restrained dogs in an apparatus and routinely shocked
the dogs regardless of their behavior. The following day, the dogs were placed in a similar
apparatus; however, this time the dogs were not restrained and there was a small barrier placed
between the “shock” floor and the “safe” floor. What Seligman observed was that despite the
opportunity to escape the shock, the dogs flurried for a bit, and then ultimately laid down and
whimpered while being shocked.
Based on this study, Seligman concluded that the animals essentially learned that they
were unable to avoid the shock the day prior, and therefore, learned that they were helpless in
avoiding the shocks. When they were placed in a similar environment but had the opportunity to
escape the shock, their learned helplessness carried over and they continued to believe they
were unable to escape the shock.
This study has been linked to humans through the research in attributional
style (Nolen-Hoeksema, Girgus & Seligman, 1992). There are two types of attributional style-
positive and negative. A negative attributional style focuses on the internal,
stable and global influence of daily lives, whereas a positive attributional style focuses on
the external, unstable, and specific influence of the environment. Research has found that
individuals with a negative attributional style are more likely to experience depression. This is

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likely due to their negative interpretation of daily events. For example, if something bad were to
happen to them, they conclude that it is their fault (internal), bad things always happen to them
(stable), and bad things happen all day to them. Unfortunately, this maladaptive thinking style
often takes over an individual’s daily view, thus making them more vulnerable to depression.
In addition to attributional style, Aaron Beck also attributed negative thinking as a precursor to
depressive disorders (Beck, 2002, 1991, 1967). Often viewed as the grandfather of Cognitive-
Behavioral Therapy, Beck went on to coin the terms maladaptive attitudes, cognitive triad, errors
in thinking, and automatic thoughts- all of which combine to explain the cognitive model of
depressive disorders.
Maladaptive attitudes, or negative attitudes about one self, others, and the world
around them, are often present in those with depressive symptoms. These attitudes are
inaccurate, and often global. For example, “If I fail my exam, the world will know I’m stupid.” Will
the entire world really know you failed your exam? Not likely. Because you fail the exam, are
you stupid? No. Individual’s with depressive symptoms often develop these maladaptive
attitudes regarding everything in their life, indirectly isolating themselves from others.
The cognitive triad also plays into the maladaptive attitudes in that the individual interprets
these negative thoughts about their experiences, themselves, and their futures.
Cognitive distortions, also known as errors in thinking, are a key component in Beck’s
cognitive theory. Beck identified 15 errors in thinking that are most common in individuals with
depression (see end of chapter). Among the most common are catastrophizing, jumping to
conclusions, and overgeneralization. I always like to use my dad as an example for
overgeneralization- whenever we go to the grocery store, he always comments about
how whatever line he chooses, at every store, it is always the slowest/takes the longest. Does
this happen every time he is at the store? I’m doubtful, but his error in thinking perceives this to
be true.
Finally, automatic thoughts, or the constant stream of negative thoughts, also leads to
symptoms of depression as individuals begin to feel as though they are inadequate or helpless
in a given situation. While some cognitions are manipulated and interpreted in a negative view,
Beck stated that there are another set of negative thoughts that occur automatically, such as
these. Research studies have continue supported Beck’s maladaptive thoughts, attitudes, and
errors in thinking as fundamental issues in those with depressive disorders (Possel & Black,
2014; Lai et al., 2014). Furthermore, as you will see in the treatment section, cognitive
strategies are among the most effective forms of treatment for depressive disorders.

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3. Behavioral
The behavioral model explains depression as a result of change in the number of
rewards and punishments one receives throughout their life. This change can come from work,
intimate relationships, family, or even the environment in general. Among the most influential in
the field of depression is Peter Lewinsohn. He stated depression occurred in most people due to
the reduced positive rewards in their life. Because they were not being positively rewarded, their
constructive behaviors occurred more infrequently until they stop engaging in the behavior
completely (Lewinsohn et al., 1990; 1984). An example of this is a student who continues to
receive bad grades on their exam despite studying for hours. Over time, the individual will
reduce the amount of time they are studying, thus continuing to earn poor grades.

4. Sociocultural
In the sociocultural theory, the role of family and one’s social environment play a strong
role in the development of depressive disorders. There are two sociocultural views- the family-
social perspective and the multi-cultural perspective.
4.1. Family-social perspective. Similar to that of the behavioral theory, the family-social
perspective of depression suggests that depression is related to the unavailability of social
support. This is often supported from research studies that show separated and divorced
individuals are three times more likely to experience depressive symptoms than those that are
married or even widowed (Schultz, 2007). While there are many factors that lead a couple to
separate or even end their marriage, some relationships end due to a spouse’s mental health
issues, particularly depressive symptoms. Depressive symptoms have been positively related to
increased interpersonal conflicts, reduced communication, and intimacy issues, all of which are
often reported in causal factors leading to a divorce (Najman et al., 2014).
The family-social perspective can also be viewed in the opposite way, with stress and
marital discord leading to increased rates of depression in one or both spouses (Nezlek et al.,
2000). While some research indicates that having children provides a positive influence in one’s
life, it can also lead to stress both within the individual, as well as between partners due to
division of work and discipline differences. Research studies have shown that women who had
three or more young children who also lacked a close confidante and outside employment, were
more likely that other mothers to become depressed (Brown, 2002).
4.2. Multi-cultural perspective. While depression is experienced across the entire world,
one’s cultural background may influence what symptoms of depression are presented. Common
depressive symptoms such as feeling sad, lack of energy, anhedonia, difficulty concentrating

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and thoughts of suicide are hallmark in most societies, other symptoms may be more specific to
one’s nationality. More specifically, individuals from non-Western countries (China and other
Asian countries) often focus on the physical symptoms of depression- tiredness, weakness,
sleep issues, and less of an emphasis on the cognitive symptoms. Individuals from Latino and
Mediterranean cultures often experience problems with “nerves” and headaches as primary
symptoms of depression (American Psychiatric Association, 2013).
Within the United States, many researchers have explored potential differences across
ethnic or racial groups in both rates of depression, as well as presenting symptoms of those
diagnosed with depression. These studies continually fail to identify any significant differences
between ethnical and racial groups; however, one major study has identified a difference in the
rate of recurrence of depression in Hispanic and African Americans (Gonzalez et al., 2010).
While the exact reason for this is unclear, the researchers propose lack of treatment
opportunities as a possible explanation. According to Gonzalez and colleagues (2010),
approximately 54 percent of depressed white American seek out treatment, compared to the 34
percent and 40 percent Hispanic and African Americans, respectively. The fact that there is
such a large discrepancy in the use of treatment between non-white Americans and minority
Americans suggests that these individuals are not receiving the effective treatment necessary to
resolve the disorder, thus leaving them more vulnerable for repeated depressive episodes.
4.3. Gender differences. As previously discussed, there is a significant difference between
gender and rates of depression, with women twice as likely to experience an episode of
depression than man (Schuch et al., 2014). There are a few speculations of why there is such
an imbalance in the rate of depression across genders.
The first theory- artifact theory- suggests that the difference between genders is due to
clinician or diagnostic systems being more sensitive to diagnosing women with depression than
men. While women are often thought to be more “emotional,” easily expressing their feelings
and more willing to discuss their symptoms with clinicians and physicians, men often withhold
their symptoms or will present with more traditionally “masculine” symptoms of anger or
aggression. While this theory is often a possible explanation for the gender differences in the
rate of depression, research has failed to support this theory suggesting that men and women
are equally likely to seek out treatment and discuss their depressive symptoms (McSweeney,
2004; Rieker & Bird, 2005).
The second theory- hormone theory– suggests that variations in hormone levels trigger
depression in women more than men (Graziottin & Serafini, 2009). While there is biological
evidence supporting the changes in hormone levels during various phases of the menstrual

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cycle and their impact on women’s ability to integrate and process emotional information,
research fails to support this theory as the reason for higher rates of depression in women
(Whiffen & Demidenko, 2006).
The third theory- life stress theory- suggests that women are more likely to experience
chronic stressors than men, thus accounting for their higher rate of depression (Astbury, 2010).
Women are at an increased risk for facing poverty, lower employment opportunities,
discrimination, and poorer quality of housing than men, all of which are strong predictors of
depressive symptoms (Garcia-Toro et al., 2013).
The fourth theory- gender roles theory- suggests that social and or psychological factors
related to traditional gender roles also influence the rate of depression in women. For example,
men are often encouraged to develop personal autonomy, seek out activities that interest them,
and display achievement oriented goals, women are encouraged to empathize and care for
others, often fostering an interdependent functioning, which may cause women to value the
opinion of others more highly than their male counterparts do.
The final theory- rumination theory– suggests that women are more likely than men to ruminate,
or intently focus, on their depressive symptoms, thus making them more vulnerable to
developing depression at a clinical level (Nolen-Hoeksema, 2012). Several studies have
supported this theory and shown that rumination of negative thoughts is positively related to an
increase depression symptom (Hankin, 2009).
While there are many theories trying to explain the gender discrepancy in depressive
episodes, no one single theory has produced enough evidence to fully explain why women
experience depression more than men. Due to the lack of evidence, gender differences in
depression remains one of the most researched topic within depression, while simultaneously
being the least understood phenomena in the clinical psychology world.

Comorbidity
1. Depressive Disorders
It does not come as a surprise, studies exploring depression symptoms among the
general population show a substantial pattern of comorbidity between depression and other
mental disorders, particularly substance use disorders (Kessler, Berglund, et al., 2003). In fact,
nearly three-fourths of participants with lifetime MDD in a large scale research study also met
criteria for at least one other DSM disorder (Kessler, Berglund, et al., 2003). Among those that
are the most common are anxiety disorders, ADHD, and substance abuse.

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Given the extent of comorbidity among individuals with MDD, researchers have tried to identify
which disorder precipitated the other. Majority of the studies have identified most depression
cases occur secondly to another mental health disorder meaning that the onset of depression is
a direct result to the onset of another disorder (Gotlib & Hammen, 2009).

2. Bipolar Disorders
Bipolar disorder also has a high comorbidity rate with other mental disorders, particularly
anxiety disorders and any disruptive/impulse-control disorders such as ADHD and Conduct
Disorder. Substance abuse disorders are also commonly seen in individuals with Bipolar
Disorder. In fact, over half of those with Bipolar Disorder also meet diagnostic criteria for
Substance Abuse Disorder, particularly alcohol abuse. The combination of Bipolar Disorder and
Substance Abuse Disorder places individuals at a greater risk of suicide attempt (APA, 2013).
While these comorbidities are high across both Bipolar I and Bipolar II, Bipolar II appears to
have more comorbidities, with 60% of individuals meeting criteria for three or more co-occurring
mental disorders (APA, 2013).

Watch:
1. What is Bipolar Disorder (depression and mania)?
(https://www.youtube.com/watch?v=KSvk8LLBo2g)
2. What is depression? (https://www.youtube.com/watch?v=z-IR48Mb3W0)
Read:
1. (For Deeper Understanding) Chapter 7 – Mood Disorders and Suicide on Abnormal
Psychology: An Integrative Approach, Seventh Edition by David H. Barlow, V. Mark Durand.
2. (For Review) Module 4: Mood Disorders by Washington State University
(https://opentext.wsu.edu/abnormal-psych/chapter/module-4-models-of-abnormal-psychology/)

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 MODULE 5: EATING DISORDERS AND SLEEP-
WAKE DISORDERS

Module Overview:

Photo from: brightside.me

In Module 5, we will discuss matters related to eating and sleep-wake

disorders. Our discussion will include anorexia nervosa and bulimia nervosa,
and the insomnia disorder and hypersomnolence disorder.

Module Learning Outcomes:

• Describe how Anorexia Nervosa presents itself.

• Describe how Bulimia Nervosa presents itself.
• Describe how Insomnia Disorder presents itself.
• Describe how Hypersomnolence Disorder presents itself.

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Course Materials:

PART 1: EATING DISORDERS

There are three prevalent eating disorders. In bulimia nervosa, dieting results in out-of-
control binge-eating episodes that are often followed by purging the food through vomiting or
other means. In binge-eating disorder, a pattern of binge eating is not followed by purging.
Anorexia nervosa, in which food intake is cut dramatically, results in substantial weight loss and
sometimes dangerously low body weight. In addition to sociocultural pressures, causal factors
include possible biological and genetic vulnerabilities (the disorders tend to run in families),
psychological factors (low self-esteem), social anxiety (fears of rejection), and distorted body
image (relatively normal weight individuals view themselves as fat and ugly). (Barlow & Durand,
2013).

Etiology

1. Biological

There is some evidence of a genetic predisposition to eating disorders, with relatives of those
diagnosed with an eating disorder are up to six times more likely than other individuals to be
diagnosed with an eating disorder (APA, 2013). Twin concordance studies also support the
gene theory. If an identical twin is diagnosed with anorexia, there is a 70 percent chance the
other twin will develop an anorexia in their lifetime (APA, 2013).

2. Cognitive

Some argue that eating disorders are in fact a variant of Obsessive Compulsive Disorder
(OCD). The obsession with body shape and weight- the hallmark of an eating disorder- is likely
a driving factor in anorexia nervosa. Distorted thought patterns and an over-evaluation of body
size likely contribute to this obsession and one’s desire for thinness. Research has identified
high levels of Impulsivity, particularly in those with binge eating episodes, suggesting a
temporary lack of control is responsible for these episodes. Post binge-eating episode, many
individuals report feelings of disgust or even thoughts of failure.

3. Sociocultural

Eating disorders are overwhelmingly found in Western countries where there is a heavy
emphasis on thinness- a core feature of eating disorders. It is also found in countries where
food is in abundance as in places of deprivation, round figures are more desirable (Polivy &
Herman, 2002).

I. ANOREXIA NERVOSA

Diagnostic Criteria for Anorexia Nervosa

A. Restriction of energy intake relative to requirements, leading to a significantly low body
weight in the context of age, sex, developmental trajectory, and physical health. Significantly
low weight is defined as a weight that is less than minimally normal or, for children and
adolescents, less than that minimally expected.

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B. Intense fear of gaining weight or of becoming fat, or persistent behavior that interferes with
weight gain, even though at a significantly low weight.

C. Disturbance in the way in which one’s body weight or shape is experienced, undue
influence of body weight or shape on self-evaluation, or persistent lack of recognition of the
seriousness of the current low body weight.

Specify type:
Restricting type: During the past 3 months, the individual has not engaged in recurrent
episodes of binge eating or purging behavior (i.e., self-induced vomiting or the misuse of
laxatives, diuretics, or enemas). This subtype describes presentations in which weight loss is
accomplished primarily through dieting, fasting, and/or excessive exercise.
Binge-eating/purging type: During the past 3 months, the individual has engaged in
recurrent episodes of binge eating or purging behavior (i.e., self-induced vomiting or the
misuse of laxatives, diuretics, or enemas).
From American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed.).
Washington, DC.

II. BULIMIA NERVOSA

Diagnostic Criteria for Bulimia Nervosa

A. Recurrent episodes of binge eating. An episode of binge eating is characterized by both of
the following:
1. Eating, in a discrete period of time (e.g., within any 2-hour period), an amount of food that
is definitely larger than most people would eat during a similar period of time and under
similar circumstances
2. A sense of lack of control over eating during the episode (e.g., a feeling that one cannot
stop eating or control what or how much one is eating)

B. Recurrent inappropriate compensatory behavior in order to prevent weight gain, such as

self-induced vomiting; misuse of laxatives, diuretics, or other medications; fasting; or
excessive exercise.

C. The binge eating and inappropriate compensatory behaviors both occur, on average, at
least once a week for 3 months.

D. Self-evaluation is unduly influenced by body shape and weight.

E. The disturbance does not occur exclusively during episodes of anorexia nervosa.
From American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed.).
Washington, DC.

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PART 2: SLEEP-WAKE DISORDERS

Sleep–wake disorders are highly prevalent in the general population and are of two
types: dyssomnias (disturbances of sleep) and parasomnias (abnormal events such as
nightmares and sleepwalking that occur during sleep). Of the dyssomnias, the most common
disorder, insomnia disorder, involves the inability to initiate sleep, problems maintaining sleep,
or failure to feel refreshed after a full night’s sleep. Other dyssomnias include hypersomnolence
(excessive sleep), narcolepsy (sudden and irresistible sleep attacks), circadian rhythm sleep
disorders (sleepiness or insomnia caused by the body’s inability to synchronize its sleep
patterns with day and night), and breathing-related sleep disorders (disruptions that have a
physical origin, such as sleep apnea, that leads to excessive sleepiness or insomnia) (Barlow &
Durand, 2013).

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I. INSOMNIA DISORDER

Diagnostic Criteria for Insomnia Disorder

A. A predominant complaint of dissatisfaction with sleep quantity or quality associated with
one or more of the following symptoms:
1. Difficulty initiating sleep. (In children, this may manifest as difficulty initiating sleep without
caregiver intervention.)
2. Difficulty maintaining sleep, characterized by frequent awakenings or problems returning to
sleep after awakenings. (In children, this may manifest as difficulty returning to sleep without
caregiver intervention.)
3. Early-morning awakening with inability to return to sleep.

B. The sleep disturbance causes clinically significant distress in social, occupational,

educational, academic, behavioral, or other important areas of functioning.

C. The sleep difficulty occurs at least 3 nights per week.

D. The sleep difficulty is present for at least 3 months.

E. The sleep difficulty occurs despite adequate opportunity for sleep.

F. The insomnia is not better explained by and does not occur exclusively during the course
of another sleep–wake disorder (e.g., narcolepsy, breathing-related sleep disorder, a
circadian rhythm sleep–wake disorder, a parasomnia).

G. The insomnia is not attributable to the physiological effects of a substance (e.g., a drug
abuse, a medication).

H. Coexisting mental disorders and medical conditions do not adequately explain the
predominant complaint of insomnia.

Specify if:
Episodic: Symptoms last at least 1 month but less than 3 months Persistent: Symptoms last
3 months or longer
Recurrent: Two (or more) episodes within the space of 1 year
From American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed.).
Washington, DC.

II. HYPERSOMNOLENCE DISORDER

Diagnostic Criteria for Hypersomnolence Disorder

A. Self-reported excessive sleepiness (hypersomnolence) despite a main sleep period lasting
at least 7 hours, with at least one of the following symptoms:
1. Recurrent periods of sleep or lapses into sleep within the same day.
2. A prolonged main sleep episode of more than 9 hours per day that is non-restorative (i.e.,
unrefreshing).
3. Difficulty being fully awake after abrupt awakening.

B. The hypersomnolence occurs at least three times per week, for at least 3 months.

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 C. The hypersomnolence is accompanied by significant distress or impairment in cognitive,
social, occupational, or other important areas of functioning.

D. The hypersomnolence is not better explained by and does not occur exclusively during the
course of another sleep disorder (e.g., narcolepsy, breathing-related sleep disorder, a
circadian rhythm sleep–wake disorder, a parasomnia).

E. The hypersomnolence is not attributable to the physiological effects of a substance (e.g., a

drug abuse, a medication).

F. Coexisting mental and medical disorders do not adequately explain the predominance
complaint of hypersomnolence.

Specify if:
Acute: Duration of less than 1 month
Subacute: Duration of 1–3 months
Persistent: Duration of more than 3 months

Specify current severity:

Specify severity based on degree of difficulty maintaining daytime alertness as manifested by
the occurrence of multiple attacks of irresistible sleepiness within any given day occurring, for
example, while sedentary, driving, visiting with friends, or working.
Mild: Difficulty maintaining daytime alertness 1–2 days/week
Moderate: Difficulty maintaining daytime alertness 3–4 days/week
Severe: Difficulty maintaining daytime alertness 5–7 days/week.
From American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed.).
Washington, DC.

Watch:

1. What is Anorexia Nervosa? (https://youtu.be/KEa_qsm6Kl)

2. Cause of Pica Eating Disorder. (https://youtu.be/oNXFps-aJRk)

3. Discussion on Binge-Eating. (https://youtu.be/BnL869PrmWI)

4. The story of person who suffers from Sleep Apnea (https://youtu.be/Wz-uL1GpT5Q)

5. What is Insomnia? (https://youtu.be/Oo4ncPV02wI)

Read:

1. (For Deeper Understanding) Chapter 8: Eating and Sleep-Wake Disorders on Abnormal

Psychology: An Integrative Approach, Seventh Edition by David H. Barlow, V. Mark Durand.

2. (For Review) Module 10: Eating Disorders by Washington State University

(https://opentext.wsu.edu/abnormal-psych/chapter/module-10-models-of-abnormal-psychology/)

106
 MODULE 6: DISRUPTIVE, IMPULSE-CONTROL,
AND CONDUCT DISORDERS
Module Overview:

Photo from: The Comic Strips

In Module 6, we will discuss Disruptive, impulse-control, and conduct

disorders. Our discussion will include Oppositional Defiant Disorder,
Intermittent Explosive Disorder, and Conduct Disorder.

Module Learning Outcomes:

• Describe how Oppositional Defiant Disorder present.

• Describe how Intermittent Explosive Disorder present.
• Describe how Conduct Disorder present.

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Course Materials

Lecture:
Disruptive, impulse-control, and conduct disorders include conditions involving problems
in the self-control of emotions and behaviors. While other disorders in DSM-5 may also involve
problems in emotional and/or behavioral regulation, the disorders in this chapter are unique in
that these problems are manifested in behaviors that violate the rights of others (e.g.,
aggression, destruction of property) and/or that bring the individual into significant conflict with
societal norms or authority figures.

Although all the disorders in the chapter involve problems in both emotional and
behavioral regulation, the source of variation among the disorders is the relative emphasis on
problems in the two types of self-control. For example, the criteria for conduct disorder focus
largely on poorly controlled behaviors that violate the rights of others or that violate major
societal norms. Many of the behavioral symptoms (e.g., aggression) can be a result of poorly
controlled emotions such as anger. At the other extreme, the criteria for intermittent explosive
disorder focus largely on such poorly controlled emotion, outbursts of anger that are
disproportionate to the interpersonal or other provocation or to other psychosocial stressors.
Intermediate in impact to these two disorders is oppositional defiant disorder, in which the
criteria are more evenly distributed between emotions (anger and irritation) and behaviors
(argumentativeness and defiance).

I. OPPOSITIONAL DEFIANT DISORDER

Diagnostic Criteria for Oppositional Defiant Disorder

A. A pattern of angry/irritable mood, argumentative/defiant behavior, or vindictiveness lasting
at least 6 months as evidenced by at least four symptoms from any of the following categories
and exhibited during interaction with at least one individual who is not a sibling.

Angry/Irritable Mood
1. Often loses temper.
2. Is often touchy or easily annoyed.
3. Is often angry and resentful.

Argumentative/Defiant Behavior
4. Often argues with authority figures or, for children and adolescents, with adults.
5. Often actively defies or refuses to comply with requests from authority figures or with rules.
6. Often deliberately annoys others.
7. Often blames others for his or her mistakes or misbehavior.

Vindictiveness
8. Has been spiteful or vindictive at least twice within the past 6 months.

Note: The persistence and frequency of these behaviors should be used to distinguish a
behavior that is within normal limits from a behavior that is symptomatic. For children younger
than 5 years, the behavior should occur on most days for a period of at least 6 months unless
otherwise noted (Criterion A8). For individuals 5 years or older, the behavior should occur at

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least once per week for at least 6 months, unless otherwise noted (Criterion AS). While these
frequency criteria provide guidance on a minimal level of frequency to define symptoms, other
factors should also be considered, such as whether the frequency and intensity of the
behaviors are outside a range that is normative for the individual’s developmental level,
gender, and culture.

B. The disturbance in behavior is associated with distress in the individual or others in his or
her immediate social context (e.g., family, peer group, work colleagues), or it impacts
negatively on social, educational, occupational, or other important areas of functioning.

C. The behaviors do not occur exclusively during the course of a psychotic, substance use,
depressive, or bipolar disorder. Also, the criteria are not met for disruptive mood dysregulation
disorder.

Specify current severity:

Mild: Symptoms are confined to only one setting (e.g., at home, at school, at work, with
peers)
Moderate: Some symptoms are present in at least two settings.
Severe: Some symptoms are present in three or more settings
From American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed.).
Washington, DC.

II. INTERMITTENT EXPLOSIVE DISORDER

Diagnostic Criteria for Intermittent Explosive Disorder

A. Recurrent behavioral outbursts representing a failure to control aggressive impulses as
manifested by either of the following:
1. Verbal aggression (e.g., temper tantrums, tirades, verbal arguments or fights) or physical
aggression toward property, animals, or other individuals, occurring twice weekly, on average,
for a period of 3 months. The physical aggression does not result in damage or destruction of
property and does not result in physical injury to animals or other individuals.
2. Three behavioral outbursts involving damage or destruction of property and/or physical
assault involving physical injury against animals or other individuals occurring within a 12-
month period.

B. The magnitude of aggressiveness expressed during the recurrent outbursts is grossly out
of proportion to the provocation or to any precipitating psychosocial stressors.

C. The recurrent aggressive outbursts are not premeditated (i.e., they are impulsive and/ or
anger-based) and are not committed to achieve some tangible objective (e.g., money, power,
intimidation).

D. The recurrent aggressive outbursts cause either marked distress in the individual or
impairment in occupational or interpersonal functioning or are associated with financial or
legal consequences.

E. Chronological age is at least 6 years (or equivalent developmental level).

F. The recurrent aggressive outbursts are not better explained by another mental disorder
(e.g., major depressive disorder, bipolar disorder, disruptive mood dysregulation disorder, a

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psychotic disorder, antisocial personality disorder, borderline personality disorder) and are not
attributable to another medical condition (e.g., head trauma, Alzheimer’s disease) or to the
physiological effects of a substance (e.g., a drug of abuse, a medication). For children ages 6-
18 years, aggressive behavior that occurs as part of an adjustment disorder should not be
considered for this diagnosis.

Note: This diagnosis can be made in addition to the diagnosis of attention-deficit/hyperactivity

disorder, conduct disorder, oppositional defiant disorder, or autism spectrum disorder when
recurrent impulsive aggressive outbursts are in excess of those usually seen in these
disorders and warrant independent clinical attention
From American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed.).
Washington, DC.

III. CONDUCT DISORDER

Diagnostic Criteria for Conduct Disorder

A. A repetitive and persistent pattern of behavior in which the basic rights of others or major
age-appropriate societal norms or rules are violated, as manifested by the presence of at
least three of the following 15 criteria in the past 12 months from any of the categories below,
with at least one criterion present in the past 6 months:

Aggression to People and Animals

1. Often bullies, threatens, or intimidates others.
2. Often initiates physical fights.
3. Has used a weapon that can cause serious physical harm to others (e.g., a bat, brick,
broken bottle, knife, gun).
4. Has been physically cruel to people.
5. Has been physically cruel to animals.
6. Has stolen while confronting a victim (e.g., mugging, purse snatching, extortion, armed
robbery).
7. Has forced someone into sexual activity.

Destruction of Property
8. Has deliberately engaged in fire setting with the intention of causing serious damage.
9. Has deliberately destroyed others’ property (other than by fire setting).

Deceitfulness or Theft
10. Has broken into someone else’s house, building, or car.
11. Often lies to obtain goods or favors or to avoid obligations (i.e., “cons” others).
12. Has stolen items of nontrivial value without confronting a victim (e.g., shoplifting, but
without breaking and entering: forgery).

Serious Violations of Rules

13. Often stays out at night despite parental prohibitions, beginning before age 13 years.
14. Has run away from home overnight at least twice while living in the parental or parental
surrogate home, or once without returning for a lengthy period.
15. Is often truant from school, beginning before age 13 years.
B. The disturbance in behavior causes clinically significant impairment in social, academic, or
occupational functioning.
C. If the individual is age 18 years or older, criteria are not met for antisocial personality

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disorder.

Specify whether:
312.81 (F91.1) Childhood-onset type: Individuals show at least one symptom characteristic
of conduct disorder prior to age 10 years.
312.82 (F91.2) Adolescent-onset type: Individuals show no symptom characteristic of
conduct disorder prior to age 10 years.
312.89 (F91.9) Unspecified onset: Criteria for a diagnosis of conduct disorder are met, but
there is not enough information available to determine whether the onset of the first symptom
was before or after age 10 years.

Specify if:
With limited prosocial emotions: To qualify for this specifier, an individual must have
displayed at least two of the following characteristics persistently over at least 12 months and
in multiple relationships and settings. These characteristics reflect the individual’s typical
pattern of interpersonal and emotional functioning over this period and not just occasional
occurrences in some situations. Thus, to assess the criteria for the specifier, multiple
information sources are necessary. In addition to the individual’s self-report, it is necessary to
consider reports by others who have known the individual for extended periods of time (e.g.,
parents, teachers, co-workers, extended family members, peers).
Lack of remorse or guilt: Does not feel bad or guilty when he or she does something
wrong (exclude remorse when expressed only when caught and/or facing
punishment). The individual shows a general lack of concern about the negative
consequences of his or her actions. For example, the individual is not remorseful
after hurting someone or does not care about the consequences of breaking rules.
Callous—lack of empathy: Disregards and is unconcerned about the feelings of
others. The individual is described as cold and uncaring. The person appears more
concerned about the effects of his or her actions on himself or herself, rather than
their effects on others, even when they result in substantial harm to others.
Unconcerned about performance: Does not show concern about poor/problematic
performance at school, at work, or in other important activities. The individual does not
put forth the effort necessary to perform well, even when expectations are clear, and
typically blames others for his or her poor performance.
Shallow or deficient affect: Does not express feelings or show emotions to others,
except in ways that seem shallow, insincere, or superficial (e.g., actions contradict the
emotion displayed; can turn emotions “on” or “off’ quickly) or when emotional
expressions are used for gain (e.g., emotions displayed to manipulate or intimidate
others).

Specify current severity:

Mild: Few if any conduct problems in excess of those required to make the diagnosis are
present, and conduct problems cause relatively minor harm to others (e.g., lying, truancy,
staying out after dark without permission, other rule breaking).
Moderate: The number of conduct problems and the effect on others are intermediate
between those specified in “mild” and those in “severe” (e.g., stealing without confronting a
victim, vandalism).
Severe: Many conduct problems in excess of those required to make the diagnosis are
present, or conduct problems cause considerable harm to others (e.g., forced sex, physical
cruelty, use of a weapon, stealing while confronting a victim, breaking and entering).
From American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed.).
Washington, DC.

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 MODULE 17: PARAPHILIC DISORDERS, AND
DISSOCIATIVE DISORDERS

Module Overview:

In Module 14, we will discuss matters related to Paraphilic Disorders and

Dissociative Disorders. In paraphilic disorders, we will focus the discussion on
fetishistic, voyeuristic, exhibitionistic, frotteuristic, sexual sadism &
masochism, and pedophilic disorder. While in dissociative disorders, our
discussion will include dissociative identity disorder, dissociative amnesia,
and depersonalization/derealization.

Module Learning Outcomes:

• Describe the distinct diagnostic features of paraphilic disorders.

• Describe how dissociative disorders present.

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Course Materials:

PART 1: PRAPHILIC DISORDERS

Paraphilia is sexual attraction to inappropriate people, such as children, or to

inappropriate objects, such as articles of clothing. Paraphilia becomes a paraphilic disorder
when the sexual attraction causes significant distress or impairment to the individual or causes
harm or the risk of harm to others. The paraphilic disorders include fetishistic disorder, in which
sexual arousal occurs almost exclusively in the context of inappropriate objects or individuals;
exhibitionistic disorder, in which sexual gratification is attained by exposing one’s genitals to
unsuspecting strangers; voyeuristic disorder, in which sexual arousal is derived from observing
unsuspecting individuals undressing or naked; transvestic disorder, in which individuals are
sexually aroused by wearing clothing of the opposite sex; sexual sadism disorder, in which
sexual arousal is associated with inflicting pain or humiliation; sexual masochism disorder, in
which sexual arousal is associated with experiencing pain or humiliation; and pedophilic
disorder, in which there is a strong sexual attraction toward children. Incest is a type of
pedophilia in which the victim is related, often a son or daughter (Barlow & Durand, 2013).

Etiology

The development of paraphilic disorders is associated with deficiencies in consensual adult

sexual arousal, deficiencies in consensual adult social skills, deviant sexual fantasies that may
develop before or during puberty and attempts by the individual to suppress thoughts
associated with these arousal patterns.

I. PARAPHILIC DISORDERS

Diagnostic Criteria for Voyeuristic and Exhibitionistic Disorder

Fetishistic Disorder
A. Over a period of at least 6 months, recurrent and intense sexual arousal from the use of
nonliving objects or a highly specific focus on nongenital body part(s), as manifested by
fantasies, urges, or behaviors.
B. The fantasies, sexual urges, or behaviors cause clinically significant distress or impairment
in social, occupational, or other important areas of functioning.
C. The fetish objects are not limited to articles of clothing used in cross-dressing (as in
transvestic disorder) or devices specifically designed for

Voyeuristic Disorder
A. Over a period of at least 6 months, recurrent and intense sexual arousal from observing an
unsuspecting person who is naked, in the process of disrobing, or engaging in sexual activity,
as manifested by fantasies, urges, or behaviors.
B. The person has acted on these sexual urges with a nonconsenting person, or the sexual
urges or fantasies cause clinically significant distress or impairment in social, occupational, or
other important areas of functioning.
C. The individual experiencing the arousal and/or acting on the urges is at least 18 years of
age.

Exhibitionistic Disorder
A. Over a period of at least 6 months, recurrent and intense sexual arousal from the exposure

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of one’s genitals to an unsuspecting person, as manifested by fantasies, urges, or behaviors.
B. The person has acted on these sexual urges with a nonconsenting person, or the sexual
urges or fantasies cause clinically significant distress or impairment in social, occupational, or
other important areas of functioning.

Frotteuristic Disorder
A. Over a period of at least 6 months, recurrent and intense sexual arousal from touching or
rubbing against a nonconsenting person, as manifested by fantasies, urges, or behaviors.
B. The person has acted on these sexual urges with a nonconsenting person, or the sexual
urges or fantasies cause clinically significant distress or impairment in social, occupational, or
other important areas of functioning.

Sexual Sadism Disorder

A. Over a period of at least 6 months, recurrent and intense sexual arousal from the
psychological or physical suffering of another person, as manifested by fantasies, urges, or
behaviors.
B. The person has acted on these sexual urges with a nonconsenting person, or the sexual
urges or fantasies cause clinically significant distress or impairment in social, occupational, or
other important areas of functioning.

Sexual Masochism Disorder

A. Over a period of at least 6 months, recurrent and intense sexual arousal from the act of
being humiliated, beaten, bound, or otherwise made to suffer, as manifested by fantasies,
urges, or behaviors.
B. The fantasies, sexual urges, or behaviors cause clinically significant distress or impairment
in social, occupational, or other important areas of functioning

Pedophilic Disorder
A. Over a period of at least 6 months, recurrent, intense sexually arousing fantasies, sexual
urges, or behaviors involving sexual activity with a prepubescent child or children (generally
age 13 years or younger).
B. The person has acted on these sexual urges, or the sexual urges or fantasies cause
marked distress or interpersonal difficulty.
C. The individual is at least age 16 years and at least 5 years older than the child or children
in Criterion A.

Note: Do not include an individual in late adolescence involved in an ongoing sexual

relationship with a 12- or 13-year-old.
Specify type:
Exclusive type (attracted only to children)
Nonexclusive type

Specify if:
Sexually attracted to males
Sexually attracted to females
Sexually attracted to both

Specify if:
Limited to incest
From American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed.).
Washington, DC.

114
Watch:

1. What is Gender Dysphoria? (https://youtu.be/W669-8aQzTk)

2. What are Paraphilic Disorders? (https://youtu.be/0TtryBLokZc)

Read:

1. (For Deeper Understanding) Chapter 10: Sexual Dysfunctions, Paraphilic Disorders, and
Gender Dysphoria on Abnormal Psychology: An Integrative Approach, Seventh Edition by
David H. Barlow, V. Mark Durand.

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PART 2: DISSOCIATIVE DISORDERS

Dissociative disorders are a group of disorders categorized by symptoms of disruption

in consciousness, memory, identify, emotion, perception, motor control, or behavior (APA,
2013). These symptoms are likely to appear following a significant stressor or years of ongoing
stress (i.e. abuse; Maldonadao & Spiegel, 2014). Occasionally, one may experience temporary
dissociative symptoms due to lack of sleep or ingestion of a substance, however, these would
not qualify as a dissociative disorder due to the lack of impairment in functioning. Furthermore,
individuals who suffer from acute stress disorder and PTSD often experience dissociative
symptoms, such as amnesia, flashbacks, depersonalization and/or derealization; however,
because of the identifiable stressor (and lack of additional symptoms listed below), they meet
diagnostic criteria for a stress disorder as opposed to a dissociative disorder.
There are 3 main types of dissociative disorders: Dissociative Identity Disorder, Dissociative
Amnesia, and Depersonalization/Derealization Disorder.

Comorbidity
Given that dissociative disorders are often precipitated by a traumatic experience, it
should not be surprising that there is a high comorbidity between dissociative disorders and
PTSD. Similarly, depressive disorders are also often found in combination with dissociative
disorders, likely due to the impact the disorders have on social and emotional functioning. In
individuals with dissociative amnesia, a wide range of emotions related to their inability to recall
memories during the episode often present once the amnesia episode is in remission (APA,
2013). These emotions often contribute to the development of a depressive episode.
Due to the rarity of these disorders with respect to other mental health disorders, it is
often difficult to truly determine comorbid diagnoses. There has been some evidence of
comorbid somatic symptom disorder and conversion disorder, particularly for those who
experience dissociative amnesia. Furthermore, dependent, avoidant, and borderline personality
disorders have all been suspected as co-occurring disorders among the dissociative disorder
family.

Etiology
1. Biological
While studies on the involvement of genetic underpinnings need additional research,
there is some suggestion that heritability rates for dissociation rage from 50-60% (Pieper, Out,

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Bakermans-Kranenburg, Van Ijzendoorn, 2011). However, it is suggested that the combination
of genetic and environmental factors may play a larger role in the development of dissociative
disorders than genetics alone (Pieper, Out, Bakermans-Kranenburg, Van Ijzendoorn, 2011).

2. Cognitive
One proposed cognitive theory of dissociative disorders, particularly dissociative
amnesia, is a memory retrieval deficit. More specifically, Kopelman (2000) theorizes that the
combination of psychological stress and various other biopsychosocial predispositions affects
the frontal lobe’s executive system’s ability to retrieve autobiographical memories (Picard et al.,
2013). Neuroimaging studies have supported this theory by showing deficits to several
prefrontal regions, which is one area responsible for memory retrieval (Picard et al.,
2013). Despite these findings, there is still some debate over which specific brain regions
within the executive system that are responsible for the retrieval difficulties, as research studies
have reported mixed findings.
Specific to DID, neuroimaging studies have shown differences in hippocampus activation
between subpersonalities (Tsai, Condie, Wu & Chang, 1999). As you may recall, the
hippocampus is responsible for storing information from short-term to long-term memory. It is
hypothesized that this brain region is responsible for the generation of dissociative states and
amnesia (Staniloiu & Markowitsch, 2010).

3. Sociocultural
The sociocultural model of dissociative disorders has largely been influenced by
Lilienfeld and colleagues (1999) who argue that the influence of mass media and its publications
of dissociative disorders, provide a model for individuals to not only learn about dissociative
disorders, but also engage in similar dissociative behaviors. This theory has been supported by
the significant increase in DID cases after the publication of Sybil, a documentation of a
woman’s 16 subpersonalities (Goff & Simms, 1993).
These mass media productions are also not just suggestive to patients. It has been
suggested that mass media also influences the way clinicians gather information regarding
dissociative symptoms of patients. For example, therapists may unconsciously use questions or
techniques in session that evoke dissociative types of problems in their patients following
exposure to a media source discussing dissociative disorders.

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4. Psychodynamic
The psychodynamic theory of dissociative disorders assumes that the dissociative
disorders are caused by and individual’s repressed thoughts and feelings related to an
unpleasant or traumatic event (Richardson, 1998). In blocking these thoughts and feelings, the
individual is subconsciously protecting himself from painful memories.
While dissociative amnesia may be explained by a single repression, psychodynamic
theorists believe that DID results from repeated exposure to traumatic experiences, such as
childhood abuse, neglect, or abandonment (Dalenberg et al., 2012). According to the
psychodynamic perspective, children who experience repeated traumatic events such as
physical abuse or parental neglect lack the support and resources to cope with these
experiences. In efforts to escape from their current situations, children develop different
personalities to essentially flee the dangerous situation they are in. While there is limited
scientific evidence to support this theory, the nature of severe childhood psychological trauma is
consistent with this theory, as individuals with DID have the highest rate of childhood
psychological trauma compared to all other psychiatric disorders (Sar, 2011).

I. DISSOCIATIVE IDENTITY DISORDER (DID)

The key diagnostic criteria for DID is the presence of two or more distinct personality
states or expressions. The identities are distinct in that they often have their own tone of voice,
engage in different physical gestures (including different gait), and have their own behaviors-
ranging anywhere from cooperative and sweet to defiant and aggressive. Additionally, the
identities can be of varying ages and gender, have different memories, and/or sensory-motor
functioning.
The second main diagnostic criteria for DID is that there must be a gap in recall of
events, information, and/or trauma due to the switching of personalities. These gaps are more
excessive than typical forgetting one may experience due to lack of attention. It is important that
these personalities are not a secondary effect of a substance or medical condition (I.e. gap of
information due to seizure).
While personalities can present at any time, there is generally a dominant
or primary personality that is present majority of the time. From there, an individual may have
several subpersonalities. Although it is hard to identify how many subpersonalities an
individual may have at one time, it is believed that there are on average 15 subpersonalities for
women and 8 for men (APA, 2000).

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 The presentation of switching between personalities varies among individuals and can
be as simple as the individual appearing to fall asleep to very dramatic, involving excessive
bodily movements. While often sudden and unexpected, switching is generally precipitated by a
significant stressor, as the subpersonality best equipped to handle the current stressor will
present. The relationship between subpersonalities varies between individuals- with some
individuals reporting knowledge of other subpersonalities while others have a one-way amnesic
relationship with subpersonalities, meaning they are not aware of other personalities (Barlow &
Chu, 2014). These individuals will experience episodes of “amnesia” when the primary
personality is not present.

Diagnostic Criteria for Dissociative Identity Disorder

A. Disruption of identity characterized by two or more distinct personality states, which may
be described in some cultures as an experience of possession. The disruption of marked
discontinuity in sense of self and sense of agency, accompanied by related alterations in
affect, behavior, consciousness, memory, perception, cognition, and/or sensory-motor
functioning. These signs and symptoms may be observed by others or reported by the
individual.

B. Recurrent gaps in the recall of everyday events, important personal information, and/or
traumatic events that are inconsistent with ordinary forgetting.

C. The symptoms cause clinically significant distress or impairment in social, occupational, or

other important areas of functioning.

D. The disturbance is not a normal part of a broadly accepted cultural or religious practice.
Note: In children, the symptoms are not attributable to imaginary playmates or other fantasy
play.

E. The symptoms are not attributable to the physiological effects of a substance (e.g.,
blackouts or chaotic behavior during alcohol intoxication) or another medical condition (e.g.,
complex partial seizures).
From American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed.).
Washington, DC.

II. DISSOCIATIVE AMNESIA DISORDER

Dissociative amnesia disorder is identified by the inability to recall important
autobiographical information. This type of amnesia is different from what one would consider a
permanent amnesia in that the information was successfully stored in memory, however, the
individual cannot retrieve it. Additionally, individuals experiencing permanent amnesia often
have a neurobiological cause, whereas dissociative amnesia does not (APA, 2013).

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 There are a few types of amnesia within dissociative amnesia. Localized amnesia, the
most common type of dissociative amnesia, is the inability to recall events during a specific
period of time. The length of time within a localized amnesia episode can vary—it can be as
short as the time immediately surrounding a traumatic event, to months or years, should the
traumatic event occur that long (as commonly seen in abuse and combat situations). Selective
amnesia is in a sense, a component of localized amnesia in that the individual can recall some,
but not all, of the details during a specific time period. For example, a soldier may experience
dissociative amnesia during the time they were deployed, yet still have some memories of
positive experiences such as celebrating Thanksgiving dinner or Christmas dinner with their
unit.
Conversely, some individuals experience generalized amnesia where they have a
complete loss of memory of their entire life history, including their own identity. Individuals who
experience this amnesia experience deficits in both semantic and procedural knowledge. This
means that individuals have no common knowledge of (i.e. cannot identify letters, colors,
numbers) nor do they have the ability to engage in learned skills (i.e. typing shoes, driving car).
While generalized amnesia is extremely rare, it is also extremely frightening. The onset is acute,
and the individual is often found wandering in a state of disorientation. Many times, these
individuals are brought into emergency rooms by law enforcement following a dangerous
situation such as an individual walking aimlessly on a busy road.
Dissociative fugue is considered to be the most extreme type of dissociative amnesia
where not only does an individual forget personal information, but they also flee to a different
location (APA, 2013). The degree of the fugue varies among individuals- with some
experiencing symptoms for a short time (only hours) to others lasting years, affording individuals
to take on new identities, careers, and even relationships. Similar to their sudden onset,
dissociative fugues also end abruptly. Post dissociative fugue, the individual generally regains
most of their memory and rarely is there a relapse. Emotional adjustment after the fugue is
dependent on the time the individual spent in the fugue- with those having been in a fugue state
longer experiencing more emotional distress than those who experienced a shorter fugue
(Kopelman, 2002).

Diagnostic Criteria for Dissociative Amnesia Disorder

A. An inability to recall important autobiographical information, usually of a traumatic or

stressful nature, that is inconsistent with ordinary forgetting.
Note: Dissociative amnesia most often consists of localized or selective amnesia for a specific
event or events; or generalized amnesia for identity and life history.

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 B. The symptoms cause clinically significant distress or impairment in social, occupational, or
other important areas of functioning.

C. The disturbance is not attributable to the physiological effects of a substance (e.g., alcohol
or other drug of abuse, a medication) or a neurological or other medical condition (e.g., partial
complex seizures, transient global amnesia, sequelae of a closed head injury/traumatic brain
injury, or other neurological condition).

D. The disturbance is not better explained by dissociative identity disorder, posttraumatic

stress disorder, acute stress disorder, somatic symptom disorder, or major or mild
neurocognitive disorder.

Specify if:
With dissociative fugue:
Apparently purposeful travel or bewildered wandering that is associated with amnesia for
identity or for other important autobiographical information.
From American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed.).
Washington, DC.

III. DEPERSONALIZATION/DEREALIZATION DISORDER

Depersonalization/Derealization disorder is categorized by recurrent episodes of
depersonalization and/or derealization. Depersonalization can be defined as a feeling of
unreality or detachment from oneself. Individuals describe this feeling as an outer
body experience where you are an observer of your thoughts, feelings, and physical being.
Furthermore, some patients report feeling as though they lack speech or motor control, thus
feeling at times like a robot. Distortions of one’s physical body has also been reported, with
various body parts appearing enlarged or shrunken. Emotionally, one may feel detached from
their own feelings, lacking the ability to feel emotions despite knowing they have them.
Symptoms of derealization include feelings of unreality or detachment from the world—
whether it be individuals, objects, or their surroundings. For example, an individual may feel as
though they are unfamiliar with their surroundings, even though they are in a place they have
been to many times before. Feeling emotionally disconnected from close friends or family
members whom they have strong feelings for is another common symptom experienced during
derealization episodes. Sensory changes have also been reported such as feeling as though
your environment is distorted, blurry, or even artificial. Distortions of time, distance, and
size/shape of objects may also occur.
These episodes can last anywhere from a few hours, to days, weeks, or even months
(APA, 2013). The onset is generally sudden, and similar to the other dissociative disorders, is
often triggered by a intense stress or trauma. As one can imagine,

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depersonalization/derealization disorder can cause significant emotional distress, as well as
impairment in one’s daily functioning (APA, 2013).

Diagnostic Criteria for Depersonalization/Derealization Disorder

A. The presence of persistent or recurrent experiences of depersonalization, derealization, or

both:
Depersonalization: Experiences of unreality, detachment, or being an outside observer with
respect to one’s thoughts, feelings, sensations, body or actions (e.g., perceptual alterations,
distorted sense of time, unreal or absent self, emotional and/or physical numbing).
Derealization: Experiences of unreality or detachment with respect to surroundings (e.g.,
individuals or objects are experienced as unreal, dreamlike, foggy, lifeless, or visually
distorted).

B. During the depersonalization or derealization experience, reality testing remains intact.

C. The symptoms cause clinically significant distress or impairment in social, occupational, or

other important areas of functioning.

D. The disturbance is not attributable to the physiological effects of a substance (e.g., a drug
of abuse, medication) or another medical condition (e.g., seizures).
E. The disturbance is not better explained by another mental disorder, such as schizophrenia
or panic disorder.
From American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed.).
Washington, DC.

Watch:
1. What are Dissociative Disorders? (https://youtu.be/XF2zeOdE5GY)
2. Meet the mother with 20 personalities. (https://youtu.be/n2atzoaA2NI)
Read:
1. (For Deeper Understanding) Chapter 6: Somatic Symptom and Related Disorders and
Dissociative Disorders on Abnormal Psychology: An Integrative Approach, Seventh Edition by
David H. Barlow, V. Mark Durand.
2. (For Review) Module 6: Dissociative Disorders by Washington State University
(https://opentext.wsu.edu/abnormal-psych/chapter/module-6-models-of-abnormal-psychology/)

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 MODULE 8: PERSONALITY DISORDERS

Module Overview:

In Module 8, we will discuss matters related to personality disorders to include

their clinical presentation, epidemiology, comorbidity, etiology, and treatment
options. Our discussion will include Cluster A disorders of paranoid, schizoid,
and schizotypal; Cluster B disorders of antisocial, borderline, histrionic, and
narcissistic; and Cluster C personality disorders of avoidant, dependent, and
obsessive-compulsive.

Module Learning Outcomes:

• Describe how personality disorders present.

• Describe comorbidity in relation to personality disorders.
• Describe the etiology of personality disorders.

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Course Materials

Lecture:

A personality disorder is a persistent pattern of emotions, cognitions, and behavior that

results in enduring emotional distress for the person affected and/or for others and may cause
difficulties with work and relationships (American Psychiatric Association, 2013). DSM-5 notes
that having a personality disorder may distress the affected person. Individuals with personality
disorders may not feel any subjective distress, however; indeed, it may in fact be others who
acutely feel distress because of the actions of the person with the disorder. This is particularly
common with antisocial personality disorder, because the individual may show a blatant
disregard for the rights of others yet exhibit no remorse (Hare, Neumann, & Widiger, 2012).
In certain cases, someone other than the person with the personality disorder must
decide whether the disorder is causing significant functional impairment, because the affected
person often cannot make such a judgment. DSM-5 lists 10 specific personality disorders.
Although the prospects for treatment success for people who have personality disorders may be
more optimistic than previously thought (Nelson, Beutler, & Castonguay, 2012), unfortunately,
as you will see later, many people who have personality disorders in addition to other
psychological problems (for example, major depression) tend to do poorly in treatment. One
factor important to the success (or lack of success) of treatment is how the therapist feels about
the client. The emotions of therapists brought out by clients (called “countertransference” by
Sigmund Freud) tend to be negative for those diagnosed with personality disorders, especially
those (as you will see next) in Cluster A (the odd or eccentric cluster) and Cluster B (the
dramatic, emotional, or erratic cluster) (Liebman & Burnette, 2013). Therapists especially need
to guard against letting their personal feelings interfere with treatment when working with people
who have personality disorders (Barlow & Durand, 2013).

Comorbidity
Among the most commonly comorbid diagnoses with personality disorders are mood
disorders, anxiety disorders, and substance abuse disorders (Lenzenweger, Lane, Loranger, &
Kessler, 2007). A large meta-analysis exploring the data on the comorbidity of major depressive
disorder and personality disorders indicated a high diagnosis of major depressive disorder,
bipolar disorder, and dysthymia (Friborg, Martinsen, Martinussen, Kaiser, Overgard, &
Rosenvinge, 2014). Further exploration of major depressive disorder suggested a lowest rate of
diagnosis in cluster A disorders, higher rate in cluster B disorders, and highest rate in cluster C

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disorders. While the relationship between bipolar disorder and personality disorders has not
been consistently clear, the most recent findings report a high comorbidity rate between cluster
B personality disorders, with the exception of OCPD (which is in Cluster C), which had the
highest comorbidity rate than any other personality disorder. Overall analysis of dysthymia
suggested that it is the most commonly diagnosed major depressive disorder among all
personality disorders.
A more detailed analysis exploring the prevalence rates of the four main anxiety
disorders (generalized anxiety disorder (GAD), specific phobia, social phobia, and panic
disorder) among individuals with various personality disorders found a clear relationships
specific to personality disorders and anxiety disorders (Skodol, Geier, Grant, & Hasin, 2014).
More specifically, individuals diagnosed with borderline and schizotypal personality disorders
were found to have an additional diagnosis of each of the four main anxiety disorders.
Individuals with narcissistic personality disorders were more likely to be diagnosed with GAD
and panic disorder. Schizoid and avoidant personality disorders reported significant rates of
GAD; avoidant personality disorder had a higher diagnosis rate of social phobia.
Substance abuse disorders occur less frequently across the ten personality disorders but are
frequently found in individuals diagnosed with antisocial, borderline, and schizotypal personality
disorders (Grant et al., 2015).

Etiology
1. Biological
Research across the personality disorders suggests some underlying biological or
genetic component; however, identification of specific mechanisms have not been identified in
most disorders, with the exception of those below. Because of this lack of specific evidence,
researchers argue that it is difficult to determine what role genetics plays into the development
of these disorders compared to that of environmental influences. Therefore, while there is likely
a biological predisposition to personality disorders, exact causes cannot be determined at this
time.
Research on the development of schizotypal personality disorder has identified similar
biological causes to that of schizophrenia—high activity of dopamine and enlarged brain
ventricles (Lener et al., 2015). Similar differences in neuroanatomy may explain the high
similarity of behaviors in both schizophrenia and schizotypal personality disorder.
Surprisingly, antisocial personality disorder and borderline personality disorder also have
similar neurological changes. More specifically, individuals with both disorders reportedly show

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deficits in serotonin activity (Thompson, Ramos, & Willett, 2014). These low levels of serotonin
activity in combination with deficient functioning of the frontal lobes, particularly the prefrontal
cortex which is used in planning, self-control, and decision making, as well as an overly reactive
amygdala, may explain the impulsive and aggressive nature of both antisocial and borderline
personality disorder (Stone, 2014).

2. Psychological
Psychodynamic, cognitive, and behavioral theories are among the most common
psychological models used to explain the development of personality disorders. Although much
is still speculation, the following are general etiological views with regards to each specific
theory.
2.1. Psychodynamic. The psychodynamic theory places a large emphasis on negative
early childhood experiences and how these experiences impact an individual’s inability to
establish healthy relationships in adulthood. More specifically, individuals with personality
disorders report higher levels of childhood stress such as living in impoverished environments,
exposed to family/domestic violence, and experiencing repeated abuse/maltreatment (Kumari et
al., 2014). Additionally, high levels of childhood neglect and parental rejection are also
observed in personality disorder patients, with early parental loss and rejection leading to fears
of abandonment throughout an individual’s life (Caligor & Clarkin, 2010; Newnham & Janca,
2014; Roepke & Varter, 2014).
Because of these negative early maltreatment experiences, psychodynamic theorists
believe an individual’s sense of self, and consequently, their beliefs of others, is negatively
impacted, thus leading to the development of a personality disorder. For example, an individual
who was neglected as a young child and deprived of love, may report a lack of trust in others as
an adult, a characteristic of antisocial personality disorder (Meloy & Yakeley, 2010). Difficulty
trusting others or beliefs that they are unable to be loved may also impact one’s ability or desire
to establish social relationships as seen in many personality disorders, particularly schizoid
personality disorder. Because of these early childhood deficits, individuals may also
overcompensate in their relationships in efforts to convince themselves that they are worthy of
love and affection (Celani, 2014). Conversely, individuals may respond to their early childhood
experiences by becoming emotionally distant, using relationships as a sense of power and
destructiveness.
2.2. Cognitive. While psychodynamic theory places an emphasis on early childhood
experiences, cognitive theorists focus on the maladaptive thought patterns and cognitive

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distortions displayed by those with personality disorders. Overall deficiencies in thinking place
individuals with personality disorders in a position to develop inaccurate perceptions of others
(Beck, 2015). These dysfunctional beliefs likely originate from the interaction between a
biological predisposition and undesirable environmental experiences. Maladaptive thought
patterns and strategies are strengthened during aversive life events as a protective mechanism
and ultimately come together to form patterns of behaviors displayed in personality disorders
(Beck, 2015).
Cognitive distortions such as dichotomous thinking, also known as all or nothing
thinking, are observed in several personality disorders. More specifically, dichotomous thinking
explains rigidity and perfectionism in OCPD, and the lack of independence observed in
dependent and borderline personality disorders (Weishaar & Beck, 2006). Discounting the
positive also explains the underlying mechanisms for avoidant personality disorder (Weishaar
& Beck, 2006). For example, individuals who have been routinely criticized or rejected during
childhood may have difficulty accepting positive feedback from others, expecting to only receive
rejection and harsh criticism. In fact, they may employ these misattributions to positive feedback
to support their ongoing theory that they are constantly rejected and criticized by others.
2.3. Behavioral. Behavioral theorists identify three major theories in their explanation of the
development of personality disorders: modeling, reinforcement, and lack of social skills. With
regards to modeling, personality disorders are explained by an individual learning maladaptive
social relationship patterns and behaviors due to directly observing family members engaging in
similar behaviors(Gaynor & Baird, 2007). While we cannot discredit the biological component of
the familial influence, research does support an additive modeling or imitating component to the
development of personality disorders (especially antisocial personality disorder; APA, 2013).
Similarly, reinforcement, or rewarding of maladaptive behaviors is another behavioral theory
used to explain the development of personality disorders. Parents may unintentionally reward
aggressive behaviors by giving in to a child’s desires in efforts to cease the situation or prevent
escalation of behaviors. When this is done repeatedly over time, children (and later as adults)
continue with these maladaptive behaviors as they are effective in gaining their needs/wants.
On the other side, there is some speculation that excessive reinforcement or praise
during childhood may contribute to the grandiose sense of self observed in individuals with
narcissistic personality disorder (Millon, 2011).
Finally, failure to develop normal social skills may explain the development of some personality
disorders, such as avoidant personality disorder (Kantor, 2010). While there is some discussion
as to whether lack of social skills leads to avoidance of social settings OR if social skills deficits

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develop as a result of avoiding social situations, most researchers agree that the avoidance of
social situations contributes to the development of personality disorders, whereas, underlying
deficits in social skills may contribute more to social anxiety disorder (APA, 2013).

3. Social
3.1. Family dysfunction. High levels of psychological or social dysfunction within families
has also been identified as a contributing factor to the development of personality disorders.
High levels of poverty, unemployment, family separation, and witnessing domestic violence are
routinely observed in individuals diagnosed with personality disorders (Paris, 1996). While
formalized research has yet to further explore the relationship between SES and personality
disorders, correlational studies suggest a relationship between poverty, unemployment and poor
academic achievement with increased levels of personality disorder diagnoses (Alwin, 2006).
3.2. Childhood maltreatment. Childhood maltreatment is among the most influential
arguments for the development of personality disorders in adulthood. Individuals with
personality disorders often struggle with a sense of self and the ability to relate to others—
something that is generally developed during the first four to six years of a child’s life and it is
affected by the emotional environment of which that child was raised. This sense of self is the
mechanism in which individuals view themselves within their social context, while also informing
attitudes and expectations of others. A child who experiences significant maltreatment, whether
it be though neglect or physical, emotional, or sexual abuse, is at-risk for under or lack of
development of one’s sense of self. Due to the lack of affection, discipline, or autonomy during
childhood, these individuals are unable to engage in appropriate relationships as adults as seen
across the spectrum of personality disorders.
Another way childhood maltreatment contributes to personality disorders is through the
emotional bonds or attachments developed with primary caregivers. The relationship between
attachment and emotional development was thoroughly researched by John Bowlby as he
explored the need of affection in Harlow monkeys (Bowlby, 1998). Based off Bowlby’s research,
four attachment styles have been identified: secure, anxious,
ambivalent, and disorganized. While securely attached children generally do not develop
personality disorders, those with anxious, ambivalent, and disorganized attachment are at an
increased risk to develop various disorders. More specifically, those with an anxious attachment
are at-risk for developing internalizing disorders, ambivalent are at-risk for developing
externalizing disorders, and disorganized are at-risk for dissociative symptoms and personality
related disorders (Alwin, 2006).

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CLUSTER A PERSONALITY DISORDERS (ODD OR ECCENTRIC DISORDERS)
I. PARANOID PERSONALITY DISORDER
Paranoid personality disorder is characterized by a marked distrust or suspicion of
others. Individuals interpret and believe that other’s motives and interactions are intended to
harm them, and therefore, they are skeptical about establishing close relationships outside of
family members—although at times even family members actions are also believed to be
malevolent (APA, 2013). Individuals with paranoid personality disorder often feel as though they
have been deeply and irreversibly hurt by others even though there lacks evidence to support
that others intended to or actually did hurt them. Because of these persistent suspicions, they
will doubt relationships that show true loyalty or trustworthiness.
Individuals with paranoid personality disorder are also hesitant to share any personal
information or confide in others as they fear the information will be used against them (APA,
2013). Additionally, benign remarks or events are often interpreted as demeaning or
threatening. For example, if an individual with paranoid personality disorder was accidently
bumped into at the store, they would interpret this action as intentional, with the purpose of
causing them injury. Because of this, individuals with paranoid personality disorder are quick to
hold grudges and unwilling to forgive insults or injuries- whether intentional or not (APA, 2013).
They are known to quickly, and angrily counterattack either verbally or physically in situations
where they feel they were insulted.
Diagnostic Criteria for Paranoid Personality Disorder

A. A pervasive distrust and suspiciousness of others such that their motives are interpreted as
malevolent, beginning by early adulthood and present in a variety of contexts, as indicated by
four (or more) of the following:
1. Suspects, without sufficient basis, that others are exploiting, harming, or deceiving him or
her.
2. Is preoccupied with unjustified doubts about the loyalty or trustworthiness of friends or
associates.
3. Is reluctant to confide in others because of unwarranted fear that the information will be
used maliciously against him or her.
4. Reads hidden demeaning or threatening meanings into benign remarks or events.
5. Persistently bears grudges, i.e., is unforgiving of insults, injuries, or slights.
6. Perceives attacks on his or her character or reputation that are not apparent to others and
is quick to react angrily or to counterattack.
7. Has recurrent suspicions, without justification, regarding fidelity of spouse or sexual
partner.

B. Does not occur exclusively during the course of schizophrenia, a bipolar disorder or

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 depressive disorder with psychotic features, or another psychotic disorder and is not
attributable to the physiological effects of another medical condition.

Note: If criteria are met prior to the onset of schizophrenia, add “premorbid,” i.e., “paranoid
personality disorder (premorbid).”
From American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed.).
Washington, DC.

II. SCHIZOID PERSONALITY DISORDER

Individuals with schizoid personality disorder display a persistent pattern of avoidance
from social relationships along with a limited range of emotion among social relationships (APA,
2013). Similar to those with paranoid personality disorder, individuals with schizoid personality
disorder do not have many close relationships; however, unlike paranoid personality disorder,
this lack of relationship is not due to suspicious feelings, but rather, the lack of desire to engage
with others and the preference to engage in solitary behaviors. Individuals with schizoid
personality disorder are often viewed as “loners” and prefer activities where they do not have to
engage with others (APA, 2013). Established relationships rarely extends outside that of family
as those diagnosed with schizoid personality disorder make no effort to start or maintain
friendships. This lack of establishing social relationships also extends to sexual behaviors, as
those with schizoid personality disorder report a lack of interest in engaging in sexual
experiences with others.
With regard to limited range of emotion, individuals with schizoid personality disorder are
often indifferent to criticisms or praises of others and appear to not be affected by what others
think of them (APA, 2013). Individuals will rarely show any feelings or expression of emotions
and are often described as having a “bland” exterior (APA, 2013). In fact, individuals with
schizoid personality disorder rarely reciprocate facial expressions or gestures typically displayed
in normal conversations such as smiles or nods. Because of this lack of emotions, there is
limited need for attention or acceptance.

Diagnostic Criteria for Schizoid Personality Disorder

A. A pervasive pattern of detachment from social relationships and a restricted range of

expression of emotions in interpersonal settings, beginning by early adulthood and present in
a variety of contexts, as indicated by four (or more) of the following:
1. Neither desires nor enjoys close relationships, including being part of a family.
2. Almost always chooses solitary activities.
3. Has little, if any, interest in having sexual experiences with another person.
4. Takes pleasure in few, if any, activities.

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 5. Lacks close friends or confidants other than first-degree relatives.
6. Appears indifferent to the praise or criticism of others.
7. Shows emotional coldness, detachment, or flattened affectivity.

B. Does not occur exclusively during the course of schizophrenia, a bipolar disorder or
depressive disorder with psychotic features, another psychotic disorder, or autism spectrum
disorder and is not attributable to the physiological effects of another medical condition.

Note: If criteria are met prior to the onset of schizophrenia, add “premorbid,” e.g., “schizoid
personality disorder (premorbid).”
From American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed.).
Washington, DC.

III. SCHIZOTYPAL PERSONALITY DISORDER

Schizotypal personality disorder is characterized by a range of impairment in social and
interpersonal relationships due to discomfort in relationships, along with odd cognitive and/or
perceptual distortions and eccentric behaviors (APA, 2013). Similar to those with schizoid
personality disorder, individuals also seek isolation and have few, if any established
relationships outside of family members.
One of the most prominent features of schizotypal personality disorder is ideas of
reference, or the belief that unrelated events pertain to them in a particular and unusual way.
Ideas of reference also lead to superstitious behaviors or preoccupation with paranormal
activities that are not generally accepted in their culture (APA, 2013). The perception of special
or magical powers such as the ability to mind read or control other’s thoughts has also been
documented in individuals with schizotypal personality disorder. Similar to schizophrenia,
unusual perceptual experiences such as auditory hallucinations, as well as unusual speech
patterns of derailment or incoherence are also present.
Similar to the other personality disorder within cluster A, there is also a component of
paranoia or suspiciousness of other’s motives. Additionally, individuals with schizotypal
personality disorder also display inappropriate or restricted affect, thus impacting their ability to
appropriately interact with others in a social context. Significant social anxiety is often also
present in social situations, particularly in those involving unfamiliar people. The combination of
limited affect and social anxiety contributes to their inability to establish and maintain personal
relationships; most individuals with schizotypal personality disorder prefer to keep to themselves
in efforts to reduce this anxiety.

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 Diagnostic Criteria for Schizotypal Personality Disorder

A. A pervasive pattern of social and interpersonal deficits marked by acute discomfort with,
and reduced capacity for, close relationships, as well as by cognitive or perceptual distortions
and eccentricities of behavior, beginning by early adulthood and present in a variety of
contexts, as indicated by five (or more) of the following:
1. Ideas of reference (excluding delusions of reference).
2. Odd beliefs or magical thinking that influences behavior and is inconsistent with subcultural
norms (e.g., superstitiousness, belief in clairvoyance, telepathy, or “sixth sense”; in children
and adolescents, bizarre fantasies or preoccupations).
3. Unusual perceptual experiences, including bodily illusions.
4. Odd thinking and speech (e.g., vague, circumstantial, metaphorical, overelaborate, or
stereotyped).
5. Suspiciousness or paranoid ideation.
6. Inappropriate or constricted affect.
7. Behavior or appearance that is odd, eccentric, or peculiar.
8. Lack of close friends or confidants other than first-degree relatives.
9. Excessive social anxiety that does not diminish with familiarity and tends to be associated
with paranoid fears rather than negative judgments about self.
B. Does not occur exclusively during the course of schizophrenia, a bipolar disorder or
depressive disorder with psychotic features, another psychotic disorder, or autism spectrum
disorder.

Note: If criteria are met prior to the onset of schizophrenia, add “premorbid,” e.g., “schizoid
personality disorder (premorbid).
From American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed.).
Washington, DC.

CLUSTER B PERSONALITY DISORDERS (DRAMATIC, EMOTIONAL, OR ERRATIC

DISORDERS)
I. ANTISOCIAL PERSONALITY DISORDER
The essential feature of antisocial personality disorder is the persistent pattern of
disregard for, and violation of, the rights of others. The pattern of this behavior begins in late
childhood or early adolescence and continues throughout adulthood. While the presence of this
behavior begins prior to age 15, the individual cannot be diagnosed with antisocial personality
disorder until the age of 18. Prior to age 18, the individual would be diagnosed with Conduct
Disorder. Although not discussed in this course as it is a disorder of childhood, conduct disorder
involves repetitive and persistent pattern of behaviors that violate the rights of others or major
age-appropriate norms (APA, 2013). Common behaviors of individuals with conduct disorder

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that go on to develop antisocial personality disorder are aggression toward people or animals,
destruction of property, deceitfulness or theft, or serious violation of rules (APA, 2013).
While commonly referred to as “psychopaths” or “sociopaths,” individuals with antisocial
personality disorder fail to conform to social norms. This also includes legal rules as individuals
with antisocial personality disorder are often repeatedly arrested for violation of property
destruction, harassing/assaulting others, or stealing (APA, 2013). Deceitfulness is another
hallmark symptom of antisocial personality disorder as individuals often lie repeatedly, generally
as a means to gain profit or pleasure. There is also a pattern of impulsivity- decisions are made
in the moment without forethought of personal consequences or consideration for others (Lang
et al., 2015). This impulsivity also contributes to their inability to withhold jobs as they are more
likely to impulsively quit their jobs (Hengartner et al., 2014). Employment instability, along with
impulsivity, also impacts their ability to manage finances; it is not uncommon to see individuals
with antisocial personality disorder to large debts that they are unable to pay (Derefinko &
Widiger, 2016).
While also likely related to impulsivity, individuals with antisocial personality disorders
tend to be extremely irritable and aggressive, repeatedly getting into fights. The marked
disregard for their own safety, as well as the safety of others, is also observed in reckless
behavior such as speeding, driving under the influence, and engaging in sexual and substance
abuse behavior that may put themselves at risk (APA, 2013).
Of course, the most known and devastating symptom of antisocial personality disorder is
the lack of remorse for the consequences of their actions, regardless of how severe they may
be (APA, 2013). Individuals often rationalize their actions at the fault of the victim, minimize the
harmfulness of the consequences of their behaviors, or display indifference (APA, 2013).
Overall, individuals with antisocial personality disorder have limited personal relationships due
to their selfish desire and lack of moral conscious.

Diagnostic Criteria for Antisocial Personality Disorder

A. A pervasive pattern of disregard for and violation of the rights of others, occurring since
age 15 years, as indicated by three (or more) of the following:
1. Failure to conform to social norms with respect to lawful behaviors, as indicated by
repeatedly performing acts that are grounds for arrest.
2. Deceitfulness, as indicated by repeated lying, use of aliases, or conning others for personal
profit or pleasure.
3. Impulsivity or failure to plan ahead.
4. Irritability and aggressiveness, as indicated by repeated physical fights or assaults.

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 5. Reckless disregard for safety of self or others.
6. Consistent irresponsibility, as indicated by repeated failure to sustain consistent work
behavior or honor financial obligations.
7. Lack of remorse, as indicated by being indifferent to or rationalizing having hurt, mistreated,
or stolen from another. B. The individual is at least age 18 years.

C. There is evidence of conduct disorder with onset before age 15 years.

D. The occurrence of antisocial behavior is not exclusively during the course of schizophrenia
or bipolar disorder.
From American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed.).
Washington, DC.

II. BORDERLINE PERSONALITY DISORDER

Individuals with borderline personality disorder display a pervasive pattern of instability in
interpersonal relationships, self-image, affect, and instability (APA, 2013). The combinations of
these symptoms cause significant impairment in establishing and maintaining personal
relationships. They will often go to great lengths to avoid real or imagined abandonment. Fears
related to abandonment often lead to inappropriate anger as they often interpret the
abandonment as a reflection of their own behaviors. It is not uncommon to experience intense
fluctuations in mood, often observed as volatile interactions with family and friends (Herpertz &
Bertsch, 2014). Those with borderline personality disorder may be friendly one day and hostile
the next.
In efforts to prevent abandonment, individuals with borderline personality disorder will
often engage in impulsive behaviors such as self-harm and suicidal behaviors. In fact,
individuals with borderline personality disorder engage in more suicidal attempts and completion
of suicide is higher among these individuals than the general public (Linehan et al., 2015). Other
impulsive behaviors such as non-suicidal self-injury (cutting) and sexual promiscuity are often
seen within this population, typically occurring during high stress periods (Sansone & Sansone,
2012).
Another key characteristic of borderline personality disorder is the unstable and/or
intense relationships. For example, individuals may idealize or experience intense feelings for
another person immediately after meeting them. Occasionally, hallucinations and delusions are
present, particularly of a paranoid nature; however, these symptoms are often transient, and
recognized as unacceptable by the individual (Sieswerda & Arntz, 2007).

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 Diagnostic Criteria for Borderline Personality Disorder

A pervasive pattern of instability of interpersonal relationships, self-image, and affects, and

marked impulsivity, beginning by early adulthood and present in a variety of contexts, as
indicated by five (or more) of the following:
1. Frantic efforts to avoid real or imagined abandonment. (Note: Do not include suicidal or
self-mutilating behavior covered in Criterion 5.)
2. A pattern of unstable and intense interpersonal relationships characterized by alternating
between extremes of idealization and devaluation.
3. Identity disturbance: markedly and persistently unstable self-image or sense of self.
4. Impulsivity in at least two areas that are potentially self-damaging (e.g., spending, sex,
substance abuse, reckless driving, binge eating). (Note: Do not include suicidal or self-
mutilating behavior covered in criterion 5.)
5. Recurrent suicidal behavior, gestures, or threats, or self-mutilating behavior.
6. Affective instability due to a marked reactivity of mood (e.g., intense episodic dysphoria,
irritability, or anxiety usually lasting a few hours and only rarely more than a few days).
7. Chronic feelings of emptiness.
8. Inappropriate, intense anger or difficulty controlling anger (e.g., frequent displays of temper,
constant anger, recurrent physical fights).
9. Transient, stress-related paranoid ideation or severe dissociative symptoms.
From American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed.).
Washington, DC.

III. HISTRIONIC PERSONALITY DISORDER

Histrionic personality disorder is the first personality disorder that addresses the
pervasive and excessive need for emotion and attention from others. These individuals are
often uncomfortable in social settings unless they are the center of attention. In efforts to gain
the attention, the individual is often very lively and dramatic, using physical gestures and
mannerisms along with grandiose language. These behaviors are initially very charming to their
audience; however, they begin to wear due to the constant need for attention to be on them. If
the theatrical nature does not gain the attention they desire, they may go to great lengths to gain
the attention such as make-up a story or create a dramatic scene (APA, 2013).
To ensure they gain the attention they desire, individuals with histrionic personality
disorder often dress and engage in sexually seductive or provocative ways. These sexually
charged behaviors are not only directed at those in which they have a sexual or romantic
interest, but to the general public as well (APA, 2013). They often spend significant amount of
time on their physical appearance to gain the attention they desire.

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Individuals with histrionic personality disorder are easily suggestable. Their opinions and
feelings are influenced by not only their friends, but also by current fads (APA, 2013). They also
have a tendency to over exaggerate relationships, considering casual acquaintanceships as
more intimate in nature than they really are.

Diagnostic Criteria for Histrionic Personality Disorder

A pervasive pattern of excessive emotionality and attention seeking, beginning by early

adulthood and present in a variety of contexts, as indicated by five (or more) of the following:
1. Is uncomfortable in situations in which he or she is not the center of attention.
2. Interaction with others is often characterized by inappropriate sexually seductive or
provocative behavior.
3. Displays rapidly shifting and shallow expression of emotions.
4. Consistently uses physical appearance to draw attention to self.
5. Has a style of speech that is excessively impressionistic and lacking in detail.
6. Shows self-dramatization, theatricality, and exaggerated expression of emotion.
7. Is suggestible (i.e., easily influenced by others or circumstances).
8. Considers relationships to be more intimate than they actually are.
From American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed.).
Washington, DC.

IV. NARCISSISTIC PERSONALITY DISORDER

Similar to histrionic personality disorder, narcissistic personality disorder also centers
around the individual; however, with narcissistic personality disorder, individuals display a
pattern of grandiosity along with a lack of empathy for others (APA, 2013). The grandiose
sense of self leads to an overvaluation of their abilities and accomplishments. They often come
across as boastful and pretentious, repeatedly proclaiming their superior achievements. These
proclamations may also be fantasized as a means to enhance their success or power.
Oftentimes they identify themselves as “special” and will only interact with others of high status.
Given the grandiose sense of self, it is not surprising that individuals with narcissistic personality
disorder need excessive admiration from others. While it appears that their self-esteem is
extremely inflated, it is actually very fragile and dependent on how others perceive them (APA,
2013). Because of this, they may constantly seek out compliments and expect favorable
treatment from others. When this sense of entitlement is not upheld, they can become irritated
or angry that their needs are not met.
A lack of empathy is also displayed in individuals with narcissistic personality disorder as
they often have difficulty (or choose not to) recognizing the desires or needs of others. This lack
of empathy also leads to exploitation of interpersonal relationships, as they are unable to

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empathize other’s feelings (Marcoux et al., 2014). They often become envious of others who
achieve greater success or possessions than them. Conversely, they believe everyone should
be envious of their achievements, regardless of how small hey may actually be.

Diagnostic Criteria for Narcissistic Personality Disorder

A pervasive pattern of grandiosity (in fantasy or behavior), need for admiration, and lack of
empathy, beginning by early adulthood and present in a variety of contexts, as indicated by
five (or more) of the following:
1. Has a grandiose sense of self-importance (e.g., exaggerates achievements and talents,
expects to be recognized as superior without commensurate achievements).
2. Is preoccupied with fantasies of unlimited success, power, brilliance, beauty, or ideal love.
3. Believes that he or she is “special” and unique and can only be understood by, or should
associate with, other special or high-status people (or institutions).
4. Requests excessive admiration.
5. Has a sense of entitlement (i.e., unreasonable expectations of especially favorable
treatment or automatic compliance with his or her expectations).
6. Is interpersonally exploitative (i.e., takes advantage of others to achieve his or her own
ends).
7. Lacks empathy: is unwilling to recognize or identify with the feelings and needs of others.
8. Is often envious of others or believes that others are envious of him or her.
9. Shows arrogant, haughty behaviors or attitudes.
From American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed.).
Washington, DC.

CLUSTER C PERSONALITY DISORDERS (ANXIOUS OR FEARFUL DISORDERS)

I. AVOIDANT PERSONALITY DISORDERS
Individuals with avoidant personality disorder display a pervasive pattern of social
anxiety due to feelings of inadequacy and increased sensitivity to negative evaluations (APA,
2013). The fear of being rejected drives their reluctance to engage in social situations, in efforts
to prevent others from evaluating them negatively. This fear extends so far that it prevents
individuals from maintaining employment due to their intense fear of a negative evaluation or
rejection.
Socially, they have very few if any friends, despite their desire to establish social
relationships. They actively avoid social situations in which they can establish new friendships
out of the fear of being disliked or ridiculed. Similarly, they are cautious of new activities or
relationships as they often exaggerate the potential negative consequences and
embarrassment that may occur; this is likely a result of their ongoing preoccupation of being
criticized or rejected by others.

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 Despite their view as socially inept, unappealing, or inferior, individuals with avoidant
personality disorder do not typically suffer from social skills deficits, but rather from
misattributions of their own behaviors (APA, 2013).

Diagnostic Criteria for Avoidant Personality Disorder

A pervasive pattern of social inhibition, feelings of inadequacy, and hypersensitivity to negative

evaluation, beginning by early adulthood and present in a variety of contexts, as indicated by
four (or more) of the following:
1. Avoids occupational activities that involve significant interpersonal contact because of fears
of criticism, disapproval, or rejection.
2. Is unwilling to get involved with people unless certain of being liked.
3. Shows restraint within intimate relationships because of the fear of being shamed or
ridiculed.
4. Is preoccupied with being criticized or rejected in social situations.
5. Is inhibited in new interpersonal situations because of feelings of inadequacy.
6. Views self as socially inept, personally unappealing, or inferior to others.
7. Is unusually reluctant to take personal risks or to engage in any new activities because they
may prove embarrassing.
From American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed.).
Washington, DC.

II. DEPENDENT PERSONALITY DISORDER

Dependent personality disorder is characterized by pervasive and excessive need to be
taken care of by others (APA, 2013). This intense need leads to submissive and clinging
behaviors as they fear they will be abandoned or separated from their parent, spouse, or other
person whom they are in a dependent relationship with. They are so dependent on this other
individual that they cannot make even the smallest decisions without first consulting with them
and gaining their approval or reassurance. They often allow others to assume complete
responsibility of their life, making decisions in nearly all aspects of their lives. Rarely will they
challenge these decisions as their fear of losing this relationship greatly outweighs their desire
to express their own opinion. Should the relationship end, the individual experiences significant
feelings of helplessness and quickly seeks out another relationship to replace the old one (APA,
2013).
When they are on their own, individuals with dependent personality disorder express
difficulty initiating and engaging in tasks on their own. They lack self-confidence and feel
helpless when they are left to care for themselves or engage in tasks on their own. In efforts to
not have to engage in tasks alone, individuals will go to great lengths to seek out support of

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others, often volunteering for unpleasant tasks if it means they will get the reassurance they
need (APA, 2013).

Diagnostic Criteria for Dependent Personality Disorder

A pervasive and excessive need to be taken care of that leads to submissive and clinging
behavior and fears of separation, beginning by early adulthood and present in a variety of
contexts, as indicated by five (or more) of the following:
1. Has difficulty making everyday decisions without an excessive amount of advice and
reassurance from others.
2. Needs others to assume responsibility for most major areas of his or her life.
3. Has difficulty expressing disagreement with others because of fear of loss of support or
approval. (Note: Do not include realistic fears of retribution.)
4. Has difficulty initiating projects or doing things on his or her own (because of a lack of self-
confidence in judgment or abilities rather than a lack of motivation or energy).
5. Goes to excessive lengths to obtain nurturance and support from others, to the point of
volunteering to do things that are unpleasant.
6. Feels uncomfortable or helpless when alone because of exaggerated fears of being unable
to care of himself or herself.
7. Urgently seeks another relationship as a source of care and support when a close
relationship ends.
8. Is unrealistically preoccupied with fears of being left to take care of himself or herself.
From American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed.).
Washington, DC.

II. OBSESSIVE-COMPULSIVE PERSONALITY DISORDER

OCPD is defined by an individual’s preoccupation with orderliness, perfectionism, and
ability to control situations that they lose flexibility, openness, and efficiency in everyday life
(APA, 2013). One’s preoccupation with details, rules, lists, orders, organizations or schedules
overshadows the larger picture of the task or activity. In fact, the need to complete the task or
activity is significantly impacted by the individuals self-imposed high standards and need to
complete the task perfectly, that the task often does not get completed. The desire to complete
the task perfectly often causes the individual to spend excessive amount of time on the task,
occasionally repeating it until it is to their standard. Due to repetition and attention to fine detail,
the individual often does not have time to engage in leisure activities or engage in social
relationships. Despite the excessive amount of time spent on activities or tasks, individuals with
OCPD will not seek help from others, as they are convinced that the others are incompetent and
will not complete the task up to their standard.

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 Personally, individuals with OCD are rigid and stubborn, particularly with their morals,
ethics, and values. Not only do they hold these standards for themselves, but they also expect
others to have similar high standards, thus causing significant disruption to their social
interactions. The rigid and stubborn behaviors are also seen in their financial status, as they are
known to live significantly below their means, in order to prepare financially for a potential
catastrophe (APA, 2013). Similarly, they may have difficulty discarding worn-out or worthless
items, despite their lack of sentimental value.
While some argue that OCPD and OCD are one in the same, others argue that there is a
distinct difference in that the personality disorder lacks definitive obsessions and compulsions
(APA, 2013). Although many individuals are diagnosed with both OCD and OCPD, research
indicates that individuals with OCPD are more likely to be diagnosed with major depression,
generalized anxiety disorder, or substance abuse disorder than OCD (APA, 2013).

Diagnostic Criteria for Obsessive-Compulsive Personality Disorder

A pervasive pattern of preoccupation with orderliness, perfectionism, and mental and

interpersonal control, at the expense of flexibility, openness, and efficiency, beginning by early
adulthood and present in a variety of contexts, as indicated by four (or more) of the following:
1. Is preoccupied with details, rules, lists, order, organization, or schedules to the extent that
the major point of the activity is lost.
2. Shows perfectionism that interferes with task completion (e.g., is unable to complete a
project because his or her own overly strict standards are not met).
3. Is excessively devoted to work and productivity to the exclusion of leisure activities and
friendships (not accounted for by obvious economic necessity).
4. Is overconscientious, scrupulous, and inflexible about matters of morality, ethics, or values
(not accounted for by cultural or religious identification).
5. Is unable to discard worn-out or worthless objects even when they have no sentimental
value.
6. Is reluctant to delegate tasks or to work with others unless they submit to exactly his or her
way of doing things.
7. Adopts a miserly spending style toward both self and others; money is viewed as something
to be hoarded for future catastrophes.
8. Shows rigidity and stubbornness.
From American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed.).
Washington, DC.

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Watch:
1. What are Cluster A Personality Disorders? (https://youtu.be/o0slJlpmF-c)
2. What are Cluster B Personality Disorders? (https://youtu.be/kdWnP8FReAI)
3. What are Cluster C Personality Disorders? (https://youtu.be/MAEjhV1xAFk)
Read:
1. (For Deeper Understanding) Chapter 12: Personality Disorders on Abnormal Psychology:
An Integrative Approach, Seventh Edition by David H. Barlow, V. Mark Durand.
2. (For Review) Module 13: Personality Disorders by Washington State University
(https://opentext. wsu.edu/abnormal-psych/chapter/module-13-models-of-abnormal-
psychology/)

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 MODULE 9: SCHIZOPHRENIA SPECTRUM AND
OTHER PSYCHOTIC DISORDERS

Module Overview:

In Module 9, we will discuss matters related to schizophrenia spectrum

disorders to include their clinical presentation, epidemiology, comorbidity,
etiology, and treatment options. Our discussion will include schizophrenia,
schizophreniform disorder, schizoaffective disorder, delusional disorder and
brief psychotic disorder.

Module Learning Outcomes:

• Describe how schizophrenia spectrum disorders present.

• Describe comorbidity in relation to schizophrenia spectrum disorders.
• Describe the etiology of schizophrenia spectrum disorders.

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Course Materials

Lecture:

The schizophrenia spectrum disorders, which for the purpose of this course consists of
Schizophrenia, Schizophreniform disorder, Schizoaffective disorder, and Delusional disorder,
are defined by one of the following main symptoms: delusions, hallucinations, disorganized
thinking (speech), disorganized or abnormal motor behavior, and negative symptoms.
Individuals diagnosed with a schizophrenia spectrum disorder experience psychosis, which is
defined as a loss of contact with reality. Be psychosis episodes make it difficult for individuals
to perceive and respond to environmental stimuli, which causes a significant disturbance in
everyday functioning. While there are a vast number of symptoms displayed in schizophrenia
spectrum disorders, presentation of symptoms varies greatly among individuals, as there are
rarely two cases similar in presentation, triggers, course, or responsiveness to treatment (APA,
2013).
1. Delusions. Delusions are defined as “fixed beliefs that are not amenable to change in
light of conflicting evidence” (APA, 2013, pp. 87). This means that despite evidence
contradicting one’s thoughts, they are unable to distinguish them from reality, likely due to a lack
of insight. There are a variety of delusions that can present in many different ways:
• Delusions of grandeur– belief they have exceptional abilities, wealth, or fame; belief they
are God or other religious saviors
• Delusions of control– belief that their thoughts/feelings/actions are controlled by others
• Delusions of thought broadcasting– belief that one’s thoughts are transparent and
everyone knows what they are thinking
• Delusions of persecution– belief they are going to be harmed, harassed, plotted or
discriminated against by either an individual or an institution
• Delusions of reference– belief that specific gestures, comments, or even larger
environmental cues are directed directly to them
• Delusions of thought withdrawal– belief that one’s thoughts have been removed by
another source
Among the most common delusions are delusions of persecution (Arango & Carpenter,
2010). It is believed that the presentation of the delusion is largely related to the social,
emotional, educational, and cultural background of the individual (Arango & Carpenter, 2010).
For example, an individual with schizophrenia who comes from a highly religious family is more
likely to experience religious delusions (delusions of grandeur) than another type of delusion.

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 2. Hallucinations. Hallucinations can occur in any of the five senses such as hearing
(auditory hallucinations), seeing (visual hallucinations), smelling (olfactory hallucinations),
touching (tactile hallucinations), or tasting (gustatory hallucinations). Additionally, they can occur
in a single modality, or present across a combination of modalities (i.e. having auditory and
visual hallucinations). For the most part, individuals recognize that their hallucinations are not
real and attempt to engage in normal behavior while simultaneously combating ongoing
hallucinations.
According to various research studies, nearly half of all patients with schizophrenia
report auditory hallucinations, 15% report visual hallucinations, and 5% report tactile
hallucinations (DeLeon, Cuesta, & Peralta, 1993). Among the most common types of auditory
hallucinations are voices talking to the patient or various voices talking to one another.
Generally, these hallucinations are not attributable to any one person that the individual knows.
They are usually clear, objective, and definite (Arango & Carpenter, 2010). Additionally, the
auditory hallucinations can be pleasurable, providing comport to the patient; however, in other
individuals, the auditory hallucinations can be unsettling as they produce commands or
malicious intent.
3. Disorganized thinking. Among the most common cognitive impairments displayed in
patients with schizophrenia are disorganized thought, communication, and speech. More
specifically, thoughts and speech patterns may appear to be circumstantial or tangential. For
example, patients may give unnecessary details in response to a question before they finally
produce the desired response. While the question is eventually answered in circumstantiality, in
tangentially, the patient never reaches the point. Another common cognitive symptom is
speech retardation where the individual may take a long period of time before answering a
question. Derailment, or the illogical connection in a chain of thoughts, is another common type
of disorganized thinking. Although not always, derailment is often seen in illogicality, or the
tendency to provide bizarre explanations for things.
These type of distorted thought patterns are often related to concrete thinking. That is, the
individual is focused on one aspect of a concept or thing, and neglects all other aspects. This
type of thinking makes treatment difficult as individuals lack insight into their illness and
symptoms (APA, 2013).
4. Disorganized/Abnormal motor behavior. Psychomotor symptoms can also be
observed in individuals with schizophrenia. These behaviors may manifest as awkward
movements or even ritualistic/repetitive behaviors. They are often unpredictable and
overwhelming, severely impacting their ability to perform daily activities (APA, 2013).

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 5. Catatonic behavior. Catatonic behavior, or the decrease or even lack of reactivity to the
environment, is among the most commonly seen disorganized motor behavior in schizophrenia.
There runs a range of catatonic behaviors from negativism (resistance to
instruction); mutism or stupor (complete lack of verbal and motor
responses); rigidity (maintaining a rigid or upright posture while resisting efforts to be moved);
or posturing (holding odd, awkward postures for long periods of time; APA, 2013). There is one
type of catatonic behavior, catatonic excitement, where the individual experiences a
hyperactivity of motor behavior, in a seemingly excited/delirious way.
6. Negative symptoms. Up until this point, all the schizophrenia symptoms can be
categorized as positive symptoms, or symptoms that are an over-exaggeration of normal brain
processes; these symptoms are also new to the individual. The final symptom included in the
diagnostic criteria of schizophrenia is negative symptoms, which are defined as the inability or
decreased ability to initiate actions, speech, expressed emotion, or to feel pleasure (Barch,
2013). Negative symptoms are often present before positive symptoms and remain once
positive symptoms remit. Because of their prevalence through the course of the disorder, they
are also more indicative of prognosis, with more negative symptoms suggestive of a poorer
prognosis. The poorer prognosis may be explained by the lack of effectiveness antipsychotic
medications have in addressing negative symptoms (Kirkpatrick, Fenton, Carpenter, & Marder,
2006).

There are six main types of negative symptoms seen in patients with schizophrenia. Such
symptoms include:
• Affective flattening – Reduction in emotional expression; reduced display of emotional
expression
• Alogia – Poverty of speech or speech content
• Anhedonia – Inability to experience pleasure
• Apathy – General lack of interest
• Asociality – Lack of interest in social relationships
• Avolition – Lack of motivation of goal-directed behavior

Comorbidity
There is a high comorbidity rate between schizophrenia related disorders and substance abuse
disorders. Furthermore, there is some evidence to suggest that the use of various substances
(specifically marijuana) may place an individual at an increased risk to develop schizophrenia, if

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the genetic predisposition is also present (see diathesis-stress model below; Corcoran et al.,
2003). Additionally, there appears to be an increase in anxiety related disorders—specifically
obsessive-compulsive disorder and panic disorder—among individuals with schizophrenia than
compared to the general public.
It should also be noted that individuals diagnosed with a schizophrenia related disorder
are also at an increased risk for associated medical conditions such as: weight gain, diabetes,
metabolic syndrome, and cardiovascular and pulmonary disease (APA, 2013). This
predisposition to various medical conditions is likely related to medications and poor lifestyle
choices, and also place individuals at risk for a reduced life expectancy.

Etiology
1. Biological
1.1. Genetic/Family studies. Twin and family studies consistently support the biological
theory. More specifically, if one identical twin develops schizophrenia, there is a 48 percent
chance that the other will also develop the disorder within their lifetime (Coon & Mitter, 2007).
This percentage drops to 17 percent in fraternal twins. Similarly, family studies have also found
similarities in brain abnormalities among individuals with schizophrenia and their relatives; the
more similarities, the higher the likelihood that the family member also developed schizophrenia
(Scognamiglio & Houenou, 2014).
1.2. Neurobiological. There is consistent and reliable evidence of a neurobiological
component in the transmission of schizophrenia. More specifically, neuroimaging studies have
found a significant reduction in overall and specific brain regions volumes, as well as tissue
density of individuals with schizophrenia compared to healthy controls (Brugger, & Howes,
2017). Additionally, there has been evidence of ventricle enlargement as well as volume
reductions in the medial temporal lobe. As you may recall, structures such as the amygdala
(involved in emotion regulation), the hippocampus (involved in memory), as well as the
neocortical surface of the temporal lobes (processing of auditory information) are all structures
within the medial temporal lobe (Kurtz, 2015). Additional studies also indicate a reduction in the
orbitofrontal regions of the brain, a part of the frontal lobe that is responsible for response
inhibition (Kurtz, 2015).
1.3. Stress cascade. The stress-vulnerability model suggests that individuals have a
genetic or biological predisposition to develop the disorder, however, symptoms will not present
unless there is a stressful precipitating factor that ilicits the onset of the disorder. Researchers

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have identified the HPA axis and its consequential neurological effects as the likely responsible
neurobiological component responsible for this stress cascade.
The HPA axis is one of the main neurobiological structures that mediates stress. It
involves the regulation of three chemical messengers (cotropin-releasing hormone (CRH),
adrenocorticotropic hormone (ACTH), and glucocorticoids) as they respond to a stressful
situation (Corcoran et al., 2003). Glucocorticoids, more commonly referred to as cortisol, is the
final neurotransmitter released which is responsible for the physiological change that
accompanies stress to prepare the body to “fight” or “flight.”
It is hypothesized that in combination with abnormal brain structures, persistent
increased levels of glucocorticoids in brain structures may be the key to the onset of psychosis
in prodromal patients (Corcoran et al., 2003). More specifically, the stress exposure (and
increased glucocorticoids) affects the neurotransmitter system and exacerbates psychotic
symptoms due to changes in dopamine activity (Walker & Diforio, 1997). While research
continues to explore the relationship between stress and onset of disorder, evidence for the
implication of stress and symptom relapse is strong. More specifically, schizophrenia patients
experience more stressful life events leading up to a relapse of symptoms. Similarly, it is
hypothesized that the worsening or exacerbation of symptoms is also a source of stress as they
interfere with daily functioning (Walker & Diforio, 1997). This stress alone may be enough to
initiate the onset of a relapse.
2. Psychological
2.1. Cognitive. The cognitive model utilizes some of the aspects of the diathesis-stress
model in that it proposes that premorbid neurocognitive impairment places individuals at risk for
aversive work/academic/interpersonal experiences. These experiences in return lead to
dysfunctional beliefs and cognitive appraisals, ultimately leading to maladaptive behaviors such
as delusions/hallucinations (Beck & Rector, 2005).
Beck proposed the following diathesis-stress model of development of schizophrenia:

Adapted from Beck & Rector, 2005, pg. 580

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 Based on this theory, an underlying neurocognitive impairment (as discussed above)
makes an individual more vulnerable to experience aversive life events such as homelessness,
conflict within the family, etc. Individuals with schizophrenia are more likely to evaluate these
aversive life events with a dysfunctional attitude and maladaptive cognitive distortions. The
combination of the aversive events and negative interpretations of them, produces a stress
response in the individual, thus igniting hyperactivation of the HPA axis. According to Beck and
Rector (2005), it is the culmination of these events leads to the development of schizophrenia.

3. Sociocultural
3.1. Expressed emotion. Research in support of a supportive family environment suggests
that families high in expressed emotion, meaning families that have high hostile, critical, or
overinvolved family members, are predictors of relapse (Bebbington & Kuipers, 2011). In fact,
individuals who return to families post hospitalization with high criticism and emotional
involvement are twice as likely to relapse compared to those who return to families with low
expressed emotion (Corcoran et al., 2003). Several meta-analyses have concluded that family
atmosphere are causally related to relapse in patients with schizophrenia, and that these
outcomes can be improved when the family environment is improved (Bebbington & Kuipers,
2011). Therefore, one major treatment goal in families of patients with schizophrenia is to
reduce expressed emotion within family interactions.
3.2. Family dysfunction. Even for families with low levels of expressed emotion, there is
often an increase in family stress due to the secondary effects of schizophrenia. Having a family
member who was diagnosed with schizophrenia increases the likelihood of a disruptive family
environment due to managing the patients symptoms and ensuring their safety while they are
home (Friedrich et al., 2015). Because of the severity of symptoms, families with a loved one
diagnosed with schizophrenia often report more conflict in the home as well as more difficulty
communicating with one another (Kurtz, 2015).

I. SCHIZOPHRENIA
As stated above, the hallmark symptoms of schizophrenia include the presentation of at
least two of the following for at least one month: delusions, hallucinations, disorganized speech,
disorganized/abnormal behavior, or negative symptoms. These symptoms create significant
impairment in an individual’s ability to engage in normal daily functioning such as work, school,
relationships with others, or self-care. It should be noted that presentation of schizophrenia
varies greatly among individuals, as it is a heterogeneous clinical syndrome (APA, 2013).

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 While the presence of symptoms have to persist for a minimum of 6 months to meet
criteria for a schizophrenia diagnosis, it is not uncommon to have prodromal symptoms that
precede the active phase of the disorder and residual symptoms that follow it. These prodromal
and residual symptoms are “subthreshold” forms of psychotic symptoms that do not cause
significant impairment in functioning, with the exception of negative symptoms (Lieberman et al.,
2001). Due to the severity of psychotic symptoms, mood disorder symptoms are also common
among individuals with schizophrenia; however, these mood symptoms are distinct from a mood
disorder diagnosis in that psychotic features will exist beyond the remission of depressive
symptoms.
Diagnostic Criteria for Schizophrenia Disorder

A. Two (or more) of the following, each present for a significant portion of time during a 1-
month period (or less if successfully treated). At least one of these must be (1), (2), or (3):
1. Delusions.
2. Hallucinations.
3. Disorganized speech (e.g., frequent derailment or incoherence).
4. Grossly disorganized or catatonic behavior.
5. Negative symptoms (i.e., diminished emotional expression or avolition).

B. For a significant portion of the time since the onset of the disturbance, level of functioning in
one or more major areas, such as work, interpersonal relations, or self-care, is markedly below
the level achieved prior to the onset (or when the onset is in childhood or adolescence, there
is failure to achieve expected level of interpersonal, academic, or occupational functioning).

C. Continuous signs of the disturbance persist for at least 6 months. This 6-month period must
include at least 1 month of symptoms (or less if successfully treated) that meet Criterion A
(i.e., active-phase symptoms) and may include periods of prodromal or residual symptoms.
During these prodromal or residual periods, the signs of the disturbance may be manifested by
only negative symptoms or by two or more symptoms listed in Criterion A present in an
attenuated form (e.g., odd beliefs, unusual perceptual experiences).

D. Schizoaffective disorder and depressive or bipolar disorder with psychotic features have
been ruled out because either 1) no major depressive or manic episodes have occurred
concurrently with the active-phase symptoms; or 2) if mood episodes have occurred during
active-phase symptoms, they have been present for a minority of the total duration of the
active and residual periods of the illness.

E. The disturbance is not attributable to the physiological effects of a substance (e.g., a drug
of abuse, a medication) or another medical condition.

F. If there is a history of autistic spectrum disorder or a communication disorder of childhood

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 onset, the additional diagnosis of schizophrenia is made only if prominent delusions or
hallucinations, in addition to the other required symptoms of schizophrenia, are also present
for at least 1 month (or less if successfully treated).

Specify if:
With catatonia
From American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed.).
Washington, DC.

II. SCHIZOPHRENIFORM DISORDER

Schizophreniform disorder is similar to schizophrenia with the exception of the length of
presentation of symptoms. Schizophreniform disorder is considered an “intermediate” disorder
between schizophrenia and brief psychotic disorder as the symptoms are present for at least
one month but not longer than 6 months. As you may recall, schizophrenia symptoms must be
present for at least 6 months; A brief psychotic disorder is diagnosed when symptoms are
present for less than 1 month. Approximately two-thirds of individuals who are initially diagnosed
with schizophreniform disorder will have symptoms that last longer than 6 months, at which time
their diagnosis is changed to schizophrenia (APA, 2013).
Another key distinguishing feature of schizophreniform disorder is the lack of criteria
related to impaired functioning. While many individuals with schizophreniform disorder do
display impaired functioning, it is not essential for diagnosis. Finally, any major mood
episodes—either depressive or manic— that are present concurrently with the psychotic
features must only be present for a small period of time, otherwise a diagnosis of schizoaffective
disorder may be more appropriate.
Diagnostic Criteria for Schizophreniform Disorder

A. Two (or more) of the following, each present for a significant portion of time during a 1-
month period (or less if successfully treated). At least one of these must be (1), (2), or (3):
1. Delusions.
2. Hallucinations.
3. Disorganized speech (e.g., frequent derailment or incoherence).
4. Grossly disorganized or catatonic behavior.
5. Negative symptoms (i.e., diminished emotional expression or avolition).

B. An episode of the disorder lasts at least 1 month but less than 6 months. When the
diagnosis must be made without waiting for recovery, it should be qualified as “provisional.”

C. Schizoaffective disorder and depressive or bipolar disorder with psychotic features have
been ruled out because either 1) no major depressive or manic episodes have occurred
concurrently with the active-phase symptoms; or 2) if mood episodes have occurred during

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 activephase symptoms, they have been present for a minority of the total duration of the active
and residual periods of the illness.

D. The disturbance is not attributable to the physiological effects of a substance (e.g., a drug
of abuse, a medication) or another medical condition.

Specify if:
With good prognostic features: This specifier requires the presence of at least two of the
following features: onset of prominent psychotic symptoms within 4 weeks of the first
noticeable change in usual behavior or functioning; confusion or perplexity; good premorbid
social and occupational functioning; and absence of blunted or flat affect.
Without good prognostic features: This specifier is applied if two or more of the above
features have not been present.

Specify if:
With catatonia
From American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed.).
Washington, DC.

III. SCHIZOAFFECTIVE DISORDER

Schizoaffective disorder is characterized by the psychotic symptoms included in criteria
A of schizophrenia and a concurrent uninterrupted period of a major mood episode—either a
depressive or manic episode. It should be noted that because loss of interest in pleasurable
activities is a common symptom of schizophrenia, to meet criteria for a depressive episode
within schizoaffective disorder, the individual must present with a pervasive depressed mood.
While schizophrenia and schizophreniform disorder do not have a significant mood component,
schizoaffective disorder requires the presence of a depressive or manic episode for majority, if
not the total duration of the disorder. While psychotic symptoms are sometimes present in
depressive episodes, they often remit once the depressive episode is resolved. For individuals
with schizoaffective disorder, psychotic symptoms should continue for at least 2 weeks in the
absence of a major mood disorder (APA, 2013). This is the key distinguishing feature between
schizoaffective disorder and major depressive disorder with psychotic features.

Diagnostic Criteria for Schizoaffective Disorder

A. An uninterrupted period of illness during which there is a major mood episode (major
depressive or manic) concurrent with Criterion A of schizophrenia.
Note: The major depressive episode must include Criterion A1: Depressed mood.

B. Delusions or hallucinations for 2 or more weeks in the absence of a major mood episode

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 (depressive or manic) during the lifetime duration of the illness.

C. Symptoms that meet criteria for a major mood episode are present for the majority of the
total durance of the active and residual portions of the illness.

D. The disturbance is not attributable to the effects of a substance (e.g., a drug of abuse, a
medication) or another medical condition.

Specify whether:
Bipolar type: This subtype applies if a manic episode is part of the presentation. Major
depressive episodes may also occur.
Depressive type: This subtype applies only if only major depressive episodes are part of the
presentation.

Specify if:
With catatonia
From American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed.).
Washington, DC.

IV. DELUSIONAL DISORDER

As suggestive of its title, delusional disorder requires the presence of at least one
delusion that lasts for at least one month in duration. It is important to note that should an
individual experience a delusion, but, has also experienced either hallucinations, disorganized
speech, disorganized or catatonic behavior, or negative symptoms (additional criteria of
schizophrenia), they should not be diagnosed with delusional disorder as their symptoms are
more aligned with a schizophrenia diagnosis. Unlike most other schizophrenia related disorders,
daily functioning is not overly impacted due to the delusions. Additionally, if symptoms of
depressive or manic episodes present during delusions, they are typically brief in duration
compared to the duration of the delusions.
The DSM-V (APA, 2013) has identified five main subtypes of delusional disorder in
efforts to better categorize the symptoms of the individuals disorder. When making a diagnosis
of delusional disorder, one of the following modifiers (in addition to mixed presentation) is
included. Erotomanic delusion occurs when an individual reports a delusion of another
person being in love with them. Generally speaking, the individual whom the convictions are
about are of higher status such as a celebrity. Grandiose delusion involves the conviction of
having a great talent or insight. Occasionally, patients will report they have made an important
discovery that benefits the general public. Grandiose delusions may also take on a religious
affiliation, as people believe they are prophets or even God, himself. Jealous delusion revolves
around the conviction that one’s spouse or partner is/has been unfaithful. While many

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individuals may have this suspicion at some point in their relationship, a jealous delusion is
much more extensive and generally based on incorrect inferences that lack
evidence. Persecutory delusion involves the individual believing that they are being conspired
against, spied on, followed, poisoned or drugged, maliciously maligned, harassed, or obstructed
in pursuit of their long-term goals (APA, 2013). Of all subtypes of delusional disorder, those
experiencing persecutory delusions are the most at risk of becoming aggressive or hostile, likely
due to the persecutory nature of their distorted beliefs. Finally, somatic delusion involves
delusions regarding bodily functions or sensations. While these delusions can vary significantly,
the most common beliefs are that the individual emits a foul odor despite attempts to rectify their
smell; there is an infestation of insects on the skin; or that they have an internal parasite (APA,
2013).

Diagnostic Criteria for Delusional Disorder

A. The presence of one (or more) delusions with a duration of 1 month or longer.

B. Criterion A for schizophrenia has never been met.

Note: Hallucinations, if present, are not prominent and are related to the delusional theme
(e.g., the sensation of being infested with insects associated with delusions of infestation).

C. Apart from the impact of the delusion(s) or its ramifications, functioning is not markedly
impaired, and behavior is not obviously bizarre or odd.

D. If manic or major depressive episodes have occurred, these have been brief relative to the
duration of the delusional periods.

E. The disturbance is not attributable to the physiological effects of a substance or another

medical condition and is not better explained by another mental disorder, such as body
dysmorphic disorder or obsessive-compulsive disorder.

Specify whether:
Erotomanic type: This subtype applies when the central theme of the delusion is that another
person is in love with the individual.
Grandiose type: This subtype applies when the central theme of the delusion is the
conviction of having some great (but unrecognized) talent or insight or having made some
important discovery.
Jealous type: This subtype applies when the central theme of the individual’s delusion is that
his or her spouse or lover is unfaithful.
Persecutory type: This subtype applies when the central theme of the delusion involves the
individual’s belief that he or she is being conspired against, cheated, spied on, followed,

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 poisoned or drugged, maliciously maligned, harassed, or obstructed in the pursuit of long-term
goals. Somatic type: This subtype applies when the central theme of the delusion involves
bodily functions or sensations.
Mixed type: This subtype applies when no delusional theme predominated.
Unspecified type: This subtype applies when the dominant delusional belief cannot be clearly
determined or is not described in the specific types (e.g., referential delusions without a
prominent persecutory or grandiose component).
From American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed.).
Washington, DC.

V. BRIEF PSYCHOTIC DISORDER

It is characterized by the presence of one or more positive symptoms such as delusions,
hallucinations, or disorganized speech or behavior lasting 1 month or less.
Diagnostic Criteria for Brief Psychotic Disorder

A. Presence of one (or more) of the following symptoms. At least one of these must be (1), (2),
or (3): 1. Delusions.
2. Hallucinations.
3. Disorganized speech (e.g., frequent derailment or incoherence).
4. Grossly disorganized or catatonic behavior.
Note: Do not include a symptom if it is a culturally sanctioned response

B. Duration of an episode of the disturbance is at least 1 day but less than 1 month, with
eventual full return to premorbid level of functioning.

C. The disturbance is not better explained by major depressive or bipolar disorder with
psychotic features, or another psychotic disorder such as schizophrenia or catatonia, and is
not attributable to the physiological effects of a substance (e.g., a drug of abuse, a medication)
or another medical condition.

Specify if:
With marked stressor(s) (brief reactive psychosis): If symptoms occur in response to
events that, singly or together, would be markedly stressful to almost anyone in similar
circumstances in the individual’s culture.
Without marked stressor(s): If symptoms do not occur in response to events that, singly or
together, would be markedly stressful to almost anyone in similar circumstances in the
individual’s culture.
With postpartum onset: If onset is during pregnancy or within 4 weeks postpartum.

Specify if:
With catatonia
From American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed.).
Washington, DC.

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Watch:
1. What is Schizophrenia? (https://youtu.be/K2sc_ck5BZU)
2. Schizophrenia sample simulation (Trigger Warning). (https://youtu.be/Pr8lyNGAqlw)
3. Living a life with Schizophrenia (https://youtu.be/C7Jl9_59tfY)
Read:
1. (For Deeper Understanding) Chapter 13: Schizophrenia Spectrum and Other Psychotic
Disorders on Abnormal Psychology: An Integrative Approach, Seventh Edition by David H.
Barlow, V. Mark Durand.
2. (For Review) Module 12: Schizophrenia Spectrum and Other Psychotic Disorders
by Washington State University (https://opentext.wsu.edu/abnormal-psych/chapter/module-12-
models-of-abnormal-psychology/)

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 MODULE 10: SUBSTANCE-RELATED AND
ADDICTIVE DISORDERS

Module Overview:

In Module 10, we will discuss matters related to substance-related, and

addictive disorders to include their clinical presentation, comorbidity, etiology,
and treatment options.

Module Learning Outcomes:

• Describe how substance-related and addictive disorders present.

• Describe comorbidity in relation to substance-related and addictive
disorders.
• Describe the etiology of substance-related and addictive disorders.
• Describe treatment options for substance-related and addictive disorders.

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Course Materials
Lecture:
In DSM-5, substance-related and addictive disorders include problems with the use of
depressants (alcohol, barbiturates, and benzodiazepines), stimulants (amphetamines, cocaine,
nicotine, and caffeine), opiates (heroin, codeine, and morphine), and hallucinogens (cannabis
and LSD) as well as gambling. Specific diagnoses are further categorized as substance
intoxication and substance withdrawal (Barlow & Durand, 2013).
Substance-related disorders are among the most prevalent psychological disorders with
roughly 100 million people in the United States reporting the use of an illegal substance
sometime throughout their life (SAMHSA, 2014). While this disorder was previously classified as
“drug abuse,” the evolvement of the disorder has sparked abuse of other substances such as
alcohol, tobacco, and caffeine, thus better classifying the disorder as abuse of substances.
What are substances? Substances are any ingested materials that cause temporary cognitive,
behavioral, and/or physiological symptoms within the individual. These changes that are
observed directly after or within a few hours of ingestion of the substance are classified
as substance intoxication (APA, 2013). Substance intoxication symptoms vary greatly, and are
dependent on the type of substance ingested. Specific substances and their effects will be
discussed later in the chapter.
Repeated use of these substances, or frequent substance intoxication can develop into
a long-term problem known as substance abuse. Abuse occurs when an individual consumes
the substance for an extended period of time, or has to ingest large amounts of the substance to
get the same effect a substance provided previously. The need to continually increase the
amount of ingested substance is also known as tolerance. As tolerance builds, additional
physical and psychological symptoms present, often causing significant disturbances in an
individual’s personal and/or professional life. Individuals with substance abuse are often
spending a significant amount of time engaging in activities that revolve around their substance
use, thus spending less time in recreational activities that once consumed their time.
Sometimes, there is a desire to reduce or abstain from substance use, however, cravings
and withdrawal symptoms often prohibit this from occurring on one’s own attempts. Common
withdrawal symptoms include but are not limited to: cramps, anxiety attacks, sweating, nausea,
tremors, and hallucinations. Depending on the substance and the tolerance level, most
withdrawal symptoms last anywhere from a few days to a week. For those with extensive
substance abuse- or multiple substances being abused- withdrawal should be closely monitored

157
in a hospital setting to avoid serious possible consequences such as seizures, stroke, or even
death.
According to the DSM-5 (APA, 2013), an individual is diagnosed with Substance
Intoxication, Use, and/or Withdrawal specific to the substance(s) the individual is ingesting.
While there are some subtle differences in symptoms, particularly psychological, physical, and
behavioral symptoms, the general diagnostic criteria for Substance Intoxication, Use,
and Withdrawal remains the same across substances. Therefore, the general diagnostic criteria
for Substance Intoxication, Use, and Withdrawal is reviewed below, with more specific details of
psychological, physical, and/or behavioral symptoms in the Types of Substances Abused
section.
For a diagnosis of Substance Intoxication, the individual must have recently ingested a
substance (APA, 2013). Immediately following the ingestion of this substance, significant
behavioral and/or psychological change is observed. In addition, physical and physiological
symptoms present as a direct result of the substance ingested. As stated above, these
behavioral, physical and physiological symptoms are dependent on the type of substance that is
ingested and therefore, discussed in more detail within each substance category (i.e.
depressants, stimulants, hallucinogens/cannabis/combination).
In order to meet criteria for Substance Use Disorder, an individual must experience
significant impairment or distress over the course of 12-months due to their use of a substance
(APA, 2013). Distress or impairment can be described as any of the following: inability to
complete or lack of participation in work, school or home obligations/activities; increased time
spent on activities obtaining, using, or recovering from substance use; impairment in social or
interpersonal relationships; use of substance in a potentially hazardous situation; psychological
problems due to recurrent substance abuse; craving for substance; an increase in the amount of
substance used over time (i.e. tolerance); difficulty reducing the amount of substance used
despite desire to reduce/stop using the substance; and/or withdrawal symptoms (APA, 2013).
While the number of these symptoms may vary among individuals, only two symptoms are
required to be present for a diagnosis of a Substance Use Disorder.
Finally, Substance Withdrawal is diagnosed when there is cessation or reduction of a
substance that has been used for a long period of time. Individuals undergoing substance
withdrawal will experience physiological and/or psychological symptoms within a few hours after
cessation/reduction (APA, 2013). These symptoms cause significant distress or impairment in
daily functioning. Similar to Substance Intoxication, physiological and/or psychological

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symptoms during substance withdrawal are often specific to the substance abused and are
discussed in more detail within each substance category later in the module.
We now turn to the individual substances themselves, their effects on our brains and
bodies, and how they are used in our society. We have grouped the substances into six general
categories.
1. Depressants: These substances result in behavioral sedation and can induce relaxation.
They include alcohol (ethyl alcohol) and the sedative and hypnotic drugs in the families of
barbiturates (for example, Seconal) and benzodiazepines (for example, Valium, Xanax).
2. Stimulants: These substances cause us to be more active and alert and can elevate mood.
Included in this group are amphetamines, cocaine, nicotine, and caffeine.
3. Opiates: The major effect of these substances is to produce analgesia temporarily (reduce
pain) and euphoria. Heroin, opium, codeine, and morphine are included in this group.
4. Hallucinogens: These substances alter sensory perception and can produce delusions,
paranoia, and hallucinations. Cannabis and LSD are included in this category.
5. Other Drugs of Abuse: Other substances that are abused but do not fit neatly into one of the
categories here include inhalants (for example, airplane glue), anabolic steroids, and other over-
the-counter and prescription medications (for example, nitrous oxide). These substances
produce a variety of psychoactive effects that are characteristic of the substances described in
the previous categories.
6. Gambling Disorder: As with the ingestion of the substances just described, individuals who
display gambling disorder are unable to resist the urge to gamble which, in turn, results in
negative personal consequences (e.g., divorce, loss of employment).

SUBSTANCE-RELATED AND ADDICTIVE DISORDERS

Overall, the diagnosis of a substance use disorder is based on a pathological pattern of
behaviors related to use of the substance (American Psychological Association, 2013). To
assist with organization:

I. Diagnostic Criteria of Substance Use Disorder (General)

- Criteria can be considered to fit within overall groupings of impaired control, social impairment,
risky use, and pharmacological criteria. Impaired control over substance use is the first criteria
grouping (Criteria 1-4).
- The individual may take the substance in larger amounts or over a longer period than was
originally intended (Criterion 1).

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- The individual may express a persistent desire to cut down or regulate substance use and may
report multiple unsuccessful efforts to decrease or discontinue use (Criterion 2).
- The individual may spend a great deal of time obtaining the substance, using the substance, or
recovering from its effects (Criterion 3).
- In some instances of more severe substance use disorders, virtually all of the individual's daily
activities revolve around the substance.
- Craving (Criterion 4) is manifested by an intense desire or urge for the drug that may occur at
any time but is more likely when in an environment where the drug previously was obtained or
used. Craving has also been shown to involve classical conditioning and is associated with
activation of specific reward structures in the brain. Craving is queried by asking if there has
ever been a time when they had such strong urges to take the drug that they could not think of
anything else.
- Current craving is often used as a treatment outcome measure because it may be a signal of
impending relapse.
- Social impairment is the second grouping of criteria (Criteria 5-7).
- Recurrent substance use may result in a failure to fulfill major role obligations at work, school,
or home (Criterion 5).
- The individual may continue substance use despite having persistent or recurrent social or
interpersonal problems caused or exacerbated by the effects of the substance (Criterion 6).
- Important social, occupational, or recreational activities may be given up or reduced because
of substance use (Criterion 7).
- The individual may withdraw from family activities and hobbies in order to use the substance.
Risky use of the substance is the third grouping of criteria (Criteria 8-9).
- This may take the form of recurrent substance use in situations in which it is physically
hazardous (Criterion 8).
- The individual may continue substance use despite knowledge of having a persistent or
recurrent physical or psychological problem that is likely to have been caused or exacerbated by
the substance (Criterion 9).
- The key issue in evaluating this criterion is not the existence of the problem, but rather the
individual's failure to abstain from using the substance despite the difficulty it is causing.
Pharmacological criteria are the final grouping (Criteria 10 and 11).
- Tolerance (Criterion 10) is signaled by requiring a markedly increased dose of the substance
to achieve the desired effect or a markedly reduced effect when the usual dose is consumed.
The degree to which tolerance develops varies greatly across different individuals as well as

160
across substances and may involve a variety of central nervous system effects. For example,
tolerance to respiratory depression and tolerance to sedating and motor coordination may
develop at different rates, depending on the substance. Tolerance may be difficult to determine
by history alone, and laboratory tests may be helpful (e.g., high blood levels of the substance
coupled with little evidence of intoxication suggest that tolerance is likely). Tolerance must also
be distinguished from individual variability in the initial sensitivity to the effects of particular
substances. For example, some first-time alcohol drinkers show very little evidence of
intoxication with three or four drinks, whereas others of similar weight and drinking histories
have slurred speech and incoordination.
- Withdrawal (Criterion 11) is a syndrome that occurs when blood or tissue concentrations of a
substance decline in an individual who had maintained prolonged heavy use of the substance.
After developing withdrawal symptoms, the individual is likely to consume the substance to
relieve the symptoms. Withdrawal symptoms vary greatly across the classes of substances, and
separate criteria sets for withdrawal are provided for the drug classes. Marked and generally
easily measured physiological signs of withdrawal are common with alcohol, opioids, and
sedatives, hypnotics, and anxiolytics. Withdrawal signs and symptoms with stimulants
(amphetamines and cocaine), as well as tobacco and cannabis, are often present but may be
less apparent. Significant withdrawal has not been documented in humans after repeated use of
phencyclidine, other hallucinogens, and inhalants; therefore, this criterion is not included for
these substances. Neither tolerance nor withdrawal is necessary for a diagnosis of a substance
use disorder. However, for most classes of substances, a past history of withdrawal is
associated with a more severe clinical course (i.e., an earlier onset of a substance use disorder,
higher levels of substance intake, and a greater number of substance-related problems).
Symptoms of tolerance and withdrawal occurring during appropriate medical treatment with
prescribed medications (e.g., opioid analgesics, sedatives, stimulants) are specifically not
counted when diagnosing a substance use disorder. The appearance of normal, expected
pharmacological tolerance and withdrawal during the course of medical treatment has been
known to lead to an erroneous diagnosis of "addiction" even when these were the only
symptoms present. Individuals whose only symptoms are those that occur as a result of medical
treatment (i.e., tolerance and withdrawal as part of medical care when the medications are
taken as prescribed) should not receive a diagnosis solely on the basis of these symptoms.
However, prescription medications can be used inappropriately, and a substance use disorder
can be correctly diagnosed when there are other symptoms of compulsive, drug-seeking
behavior.

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Severity and Specifiers
Substance use disorders occur in a broad range of severity, from mild to severe, with
severity based on the number of symptom criteria endorsed. As a general estimate of severity, a
mild substance use disorder is suggested by the presence of two to three symptoms, moderate
by four to five symptoms, and severe by six or more symptoms. Changing severity across time
is also reflected by reductions or increases in the frequency and/or dose of substance use, as
assessed by the individual's own report, report of knowledgeable others, clinician's
observations, and biological testing. The following course specifiers and descriptive features
specifiers are also available for substance use disorders: "in early remission," "in sustained
remission," "on maintenance therapy," and "in a controlled environment." Definitions of each are
provided within respective criteria sets (APA, 2013).

II. Substance/Medication-Induced Mental Disorders

The substance/medication-induced mental disorders are potentially severe, usually
temporary, but sometimes persisting central nervous system (CNS) syndromes that develop in
the context of the effects of substances of abuse, medications, or several toxins. They are
distinguished from the substance use disorders, in which a cluster of cognitive, behavioral, and
physiological symptoms contribute to the continued use of a substance despite significant
substance-related problems. The substance/medication-induced mental disorders may be
induced by the 10 classes of substances that produce substance use disorders, or by a great
variety of other medications used in medical treatment. Each substance-induced mental
disorder is described in the relevant chapter (e.g., "Depressive Disorders," "Neurocognitive
Disorders"), and therefore, only a brief description is offered here. All substance/medication-
induced disorders share common characteristics. It is important to recognize these common
features to aid in the detection of these disorders. These features are described as follows:
A. The disorder represents a clinically significant symptomatic presentation of a relevant mental
disorder.
B. There is evidence from the history, physical examination, or laboratory findings of both of the
following:
1. The disorder developed during or within 1 month of a substance intoxication or v^ithdrawal or
taking a medication; and
2. The involved substance/medication is capable of producing the mental disorder.

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C. The disorder is not better explained by an independent mental disorder (i.e., one that is not
substance- or medication-induced). Such evidence of an independent mental disorder could
include the following:
1. The disorder preceded the onset of severe intoxication or withdrawal or exposure to the
medication; or
2. The full mental disorder persisted for a substantial period of time (e.g., at least 1 month) after
the cessation of acute withdrawal or severe intoxication or taking the medication. This criterion
does not apply to substance-induced neurocognitive disorders or hallucinogen persisting
perception disorder, which persist beyond the cessation of acute intoxication or withdrawal.
D. The disorder does not occur exclusively during the course of a delirium.
E. The disorder causes clinically significant distress or impairment in social, occupational, or
other important areas of functioning.

Etiology
Most psychotropic drugs seem to produce positive effects by acting directly or indirectly on the
dopaminergic mesolimbic system (the pleasure pathway). In addition, psychosocial factors such
as expectations, stress, and cultural practices interact with the biological factors to influence
drug use.

Comorbidity
It should not come as a surprise that substance abuse in general has a high comorbidity
rate within itself (meaning abuse of multiple different substances), as well as with other mental
health disorders. Researchers believe that substance abuse disorders are often secondary to
another mental health disorder, as the substance abuse develops as a means to “self-medicate”
the underlying psychological disorder. In fact, several large surveys identified alcohol and drug
dependence to be twice as more likely in individuals with anxiety, affective, and psychotic
disorders than the general public (Hartz et al., 2014). While it is difficult to identify exact
estimates of the relationship between substance abuse and serious mental health disorders, the
general consensus among researchers is that there is a strong relationship between substance
abuse and mood, anxiety, posttraumatic stress, and personality disorders (Grant et al., 2016).

163
III. GAMBLING DISORDER (Addictive Disorder)
Problem gamblers display the same types of cravings and dependence as persons who
have substance-related disorders. Similar brain systems appear to be involved with those
addicted to gambling as seen in persons with substance-related disorders (Barlow & Durand,
2013).
The DSM-5 criteria for gambling disorder set forth the associated behaviors that
characterize people who have this addictive disorder. These include the same pattern of urges
we observe in the other substance-related disorders. Note too the parallels with substance
dependence, with the need to gamble increasing amounts of money over time and the
“withdrawal symptoms” such as restlessness and irritability when attempting to stop. These
parallels to substance-related disorders led to the recategorization of gambling disorder as an
“Addictive Disorder” in DSM-5 (Denis, Fatséas, & Auriacombe, 2012).

Diagnostic Criteria for Gambling Disorder

A. Persistent and recurrent problematic gambling behavior leading to clinically significant

impairment of distress, as indicated by the individual exhibiting four (or more) of the following
in a 12-month period:
1. Needs to gamble with increasing amounts of money in order to achieve the desired
excitement.
2. Is restless or irritable when attempting to cut down or stop gambling.
3. Has made repeated unsuccessful efforts to control, cut back, or stop gambling.
4. Is often preoccupied with gambling (e.g., having persistent thoughts of reliving past

164
 gambling experiences, handicapping or planning the next venture, or thinking of ways to get
money with which to gamble).
5. Often gambles when feeling distressed (e.g., helpless, guilty, anxious, depressed).
6. After losing money gambling, often returns another day to get even (“chasing” one’s
losses).
7. Lies to conceal the extent of involvement with gambling.
8. Has jeopardized or lost a significant relationship, job, or educational or career opportunity
because of gambling.
9. Relies on others to provide money to relieve desperate financial situations caused by
gambling.

B. The gambling behavior is not better explained by a manic episode.

Specify current severity:

Mild: 4-5 criteria met
Moderate: 6-7 criteria met
Severe: 8-9 criteria met
From American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed.).
Washington, DC.

Etiology
There is a growing body of research on the nature and treatment of gambling disorder.
For example, work is under way to explore the biological origins of the urge to gamble among
pathological gamblers. In one study, brain-imaging technology (echoplanar functional magnetic
resonance imaging) was used to observe brain function while gamblers observed videotapes of
other people gambling (Potenza et al., 2003). A decreased level of activity was observed in
those regions of the brain that are involved in impulse regulation when compared with controls,
suggesting an interaction between the environmental cues to gamble and the brain’s response
(which may be to decrease the ability to resist these cues). Abnormalities in the dopamine
system (which may account for the pleasurable consequences of gambling) and the serotonin
system (involved in impulsive behavior) have been found in some studies of pathological
gamblers (Moeller, 2009).

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Watch:
1. What are Opioid Dependence and Opioid Use Disorder? (https://youtu.be/VldsyyyBbRw)
Read:
1. (For Deeper Understanding) Chapter 11: Substance-Related, Addictive, and Impulse-
Control on Abnormal Psychology: An Integrative Approach, Seventh Edition by David H. Barlow,
V. Mark Durand.
2. (For Review) Module 11: Substance-Related and Addictive Disorders by Washington State
University (https://opentext.wsu.edu/abnormal-psych/chapter/module-10-models-of-abnormal-
psychology/)

166
 MODULE 11: NEURODEVELOPMENTAL
DISORDERS

Module Overview:

In Module 11, we will discuss matters related to neurodevelopmental disorders

to include their clinical presentation, epidemiology, comorbidity, etiology, and
treatment/prevention options. Our discussion will include Attention-
Deficit/Hyperactivity Disorder, Specific Learning Disorder, Autism Spectrum
Disorder, and Intellectual Disability (Intellectual Development Disorder).

Module Learning Outcomes:

• Describe how Attention Deficit/Hyperactivity Disorder present.

• Describe how Specific Learning Disorder present.
• Describe how Autism Spectrum Disorder present.
• Describe how Intellectual Disability or Intellectual Development Disorder
present.

167
Course Materials:
Almost all disorders described in this module are developmental disorders in the sense
that they change over time. Most disorders originate in childhood, although the full presentation
of the problem may not manifest itself until much later. Disorders that show themselves early in
life often persist as the person grows older, so the term childhood disorder may be misleading.
Because the developmental disorders in this group are all presumed to be neurologically based,
DSM-5 categorizes them as neurodevelopmental disorders (American Psychiatric Association,
2013).

Childhood is considered particularly important, because the brain changes significantly

for several years after birth; this is also when critical developments occur in social, emotional,
cognitive, and other important competency areas. These changes mostly follow a pattern: The
child develops one skill before acquiring the next, and subsequent skills often build upon one
another. Although this pattern of change is only one aspect of development, it is an important
concept at this point because it implies that any disruption in the development of early skills will,
by the very nature of this sequential process, disrupt the development of later skills (Barlow,
Durand, & Hoffmann, 2013).

We will examine several disorders usually diagnosed first in infancy, childhood, or

adolescence, including attention-deficit/hyperactivity disorder, which involves characteristics of
inattention or hyperactivity and impulsivity, and specific learning disorder, which is characterized
by one or more difficulties in areas such as reading and writing. We then focus on autism
spectrum disorder, a more severe disability, in which the child shows significant impairment in
social communication and has restricted patterns of behaviour, interest, and activities. Finally,
we examine intellectual disability, which involves considerable deficits in cognitive abilities,
communication and motor disabilities, which are also considered neurodevelopmental disorders
(Barlow & Durand, 2013).

I. ATTENTION DEFICIT/HYPERACTIVITY DISORDER

Diagnostic Criteria for Attention Deficit/Hyperactivity Disorder

A. A persistent pattern of inattention and/or hyperactivity-impulsivity that interferes with
functioning or development, as characterized by (1) and/or (2):

1. Inattention: Six (or more) of the following symptoms have persisted for at least 6 months
to a degree that is inconsistent with developmental level and that negatively impacts directly
on social and academic/occupational activities:
Note: The symptoms are not solely a manifestation of oppositional behavior, defiance,
hostility, or failure to understand tasks or instructions. For older adolescents and adults (aged
17 and older), at least five symptoms are required.
a. Often fails to give close attention to details or makes careless mistakes in schoolwork, at
work, or during other activities (e.g., overlooks or misses details, work is inaccurate).
b. Often has difficulty sustaining attention in tasks or play activities (e.g., has difficulty
remaining focused during lectures, conversations, or lengthy reading).

168
c. Often does not seem to listen when spoken to directly (e.g., mind seems elsewhere, even
in the absence of any obvious distraction).
d. Often does not follow through on instructions and fails to finish schoolwork, chores, or
duties in the workplace (e.g., starts tasks but quickly loses focus and is easily sidetracked).
e. Often has difficulty organizing tasks and activities (e.g., difficulty managing sequential
tasks; difficulty keeping materials and belongings in order; messy, disorganized work; has
poor time management; fails to meet deadlines).
f. Often avoids, dislikes, or is reluctant to engage in tasks that require sustained mental effort
(e.g., schoolwork or homework; for older adolescents and adults, preparing reports,
completing forms, reviewing lengthy papers).
g. Often loses things necessary for tasks or activities (e.g., school materials, pencils, books,
tools, wallets, keys, paperwork, eyeglasses, or mobile telephones).
h. Is often easily distracted by extraneous stimuli (for older adolescents and adults, may
include unrelated thoughts).
i. Is often forgetful in daily activities (e.g., chores, running errands; for older adolescents and
adults, returning calls, paying bills, keeping appointments).

2. Hyperactivity and impulsivity: Six (or more) of the following symptoms have persisted for
at least 6 months to a degree that is inconsistent with developmental level and that negatively
impacts directly on social and academic/occupational activities:
Note: The symptoms are not solely a manifestation of oppositional behavior, defiance,
hostility, or failure to understand tasks or instructions. For older adolescents and adults (age
17 and older), at least five symptoms are required.
a. Often fidgets with or taps hands or feet or squirms in seat.
b. Often leaves seat in situations when remaining seated is expected (e.g., leaves his or her
place in the classroom, in the office or other workplace, or in other situations that require
remaining in place).
c. Often runs about or climbs in situations where it is inappropriate. (Note: In adolescents or
adults, may be limited to feeling restless.)
d. Often unable to play or engage in leisure activities quietly.
e. Is often “on the go,” acting as if “driven by a motor” (e.g., is unable to be or uncomfortable
being still for an extended time, as in restaurants, meetings; may be experienced by others as
being restless or difficult to keep up with).
f. Often talks excessively.
g. Often blurts out an answer before a question has been completed (e.g., completes people’s
sentences; cannot wait for turn in conversation).
h. Often has difficulty waiting his or her turn (e.g., while waiting in line).
i. Often interrupts or intrudes on others (e.g., butts into conversations, games, or activities;
may start using other people’s things without asking or receiving permission; for adolescents
or adults, may intrude into or take over what others are doing).

B. Several inattentive or hyperactive-impulsive symptoms were present prior to age 12 years.

C. Several inattentive or hyperactive-impulsive symptoms are present in two or more settings

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(e.g., at home, school, or work; with friends or relatives; in other activities).

D. There is clear evidence that the symptoms interfere with, or reduce the quality of, social,
academic, or occupational functioning.

E. The symptoms do not occur exclusively during the course of schizophrenia or another
psychotic disorder and are not better explained by another mental disorder (e.g., mood
disorder, anxiety disorder, dissociative disorder, personality disorder, substance intoxication
or withdrawal).

Specify whether:
Combined presentation: If both Criterion A1 (inattention) and Criterion A2 (hyperactivity-
impulsivity) are met for the past 6 months.
Predominantly inattentive presentation: If Criterion A1 (inattention) is met but Criterion A2
(hyperactivity-impulsivity) is not met for the past 6 months.
Predominantly hyperactive/impulsive presentation: If Criterion A2 (hyperactivity-
impulsivity) is met and Criterion A1 (inattention) is not met for the past 6 months.
From American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed.).
Washington, DC.

II. SPECIFIC LEARNING DISORDER

Diagnostic Criteria for Specific Learning Disorder

A. Difficulty learning and using academic skills, as indicated by the presence of at least one of
the following symptoms that have persisted for at least 6 months, despite the provision of
interventions that target those difficulties:
1. Inaccurate or slow and effortful word reading (e.g., reads single words aloud incorrectly or
slowly and hesitantly, frequently guesses words, has difficulty sounding out words).
2. Difficulty understanding the meaning of what is read (e.g., may read text accurately but not
understand the sequence, relationships, inferences, or deeper meanings of what is read).
3. Difficulties with spelling (e.g., may add, omit, or substitute vowels or consonants).
4. Difficulties with written expression (e.g., makes multiple grammatical or punctuation errors
within sentences; employs poor paragraph organization, written expression of ideas lacks
clarity).
5. Difficulties mastering number sense, number facts, or calculation (e.g., has poor
understanding of numbers, their magnitude, and relationships; counts on fingers to add
single-digit numbers instead of recalling the math fact as peers do; gets lost in the midst of
arithmetic computation and may switch procedures. 6. Difficulties with mathematical
reasoning (e.g., has severe difficulty applying mathematical concepts, facts, or procedures to
solve quantitative problems).

B. The affected academic skills are substantially and quantifiably below those expected for
the individual’s chronological age and cause significant interference with academic or
occupational performance, or with activities of daily living, as confirmed by individually

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administered standardized achievement measures and comprehensive clinical assessment.
For individuals aged 17 years and older, a documented history of impairing learning
difficulties may be substituted for the standardized assessment.

C. The learning difficulties begin during school-age years but may not become fully manifest
until the demands for those affected academic skills exceed the individual’s limited capacities
(e.g., as in timed tests, reading or writing lengthy, complex reports for a tight deadline,
excessively heavy academic loads).

D. The learning difficulties are not better accounted for by intellectual disabilities, uncorrected
visual or auditory acuity, other mental or neurological disorders, psychosocial adversity, lack
of proficiency in the language of academic instruction, or inadequate educational instruction.

Note: The four diagnostic criteria are to be met based on clinical synthesis of the individual’s
history (developmental, medical, family, educational), school reports, and psychoeducational
assessment.

Specify if:
With impairment in reading: Word reading accuracy Reading rate or fluency Reading
comprehension
With impairment in expression: Spelling accuracy Grammar and punctuation accuracy
Clarity or organization of written expression
With impairment in mathematics: Number sense Memorization of arithmetic facts Accurate
or fluent calculation Accurate math reasoning
From American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed.).
Washington, DC.

III. AUTISM SPECTRUM DISORDER

Diagnostic Criteria for Autism Spectrum Disorder

A. Persistent deficits in social communication and social interaction across multiple contexts,
as manifested by the following, currently or by history (examples are illustrative, not
exhaustive; see text):
1. Deficits in social-emotional reciprocity; ranging, for example, from abnormal social
approach and failure of normal back-and-forth conversation; to reduced sharing of interests,
emotions, and affect; to failure to initiate or respond to social interactions.
2. Deficits in nonverbal communicative behaviors used for social interaction, ranging, for
example, from poorly integrated verbal and nonverbal communication; to abnormalities in eye
contact and body language or deficits in understanding and use of gestures; to a total lack of
facial expressions and nonverbal communication.
3. Deficits in developing, maintaining, and understanding relationships, ranging, for example,
from difficulties adjusting behavior to suit various social contexts; to difficulties in sharing
imaginative play and in making friends; to absence of interest in peers.

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B. Restricted, repetitive patterns of behavior, interests, or activities, as manifested by at least
two of the following, currently or by history (examples are illustrative, not exhaustive; see
text):
1. Stereotyped or repetitive motor movements, use of objects, or speech; (e.g., simple motor
stereotypies, lining up toys or flipping objects, echolalia, idiosyncratic phrases).
2. Insistence on sameness, inflexible adherence to routines, or ritualized patterns of verbal or
nonverbal behavior (e.g., extreme distress at small changes, difficulties with transitions, rigid
thinking patterns, greeting rituals, need to take same route or eat same food every day).
3. Highly restricted, fixated interests that are abnormal in intensity or focus (e.g., strong
attachment to or preoccupation with unusual objects, excessively circumscribed or
perseverative interests).
4. Hyper- or hyporeactivity to sensory input or unusual interest in sensory aspects of the
environment (e.g., apparent indifference to pain/temperature, adverse response to specific
sounds or textures, excessive smelling or touching of objects, visual fascination with lights or
movement).

C. Symptoms must be present in the early developmental period (but may not become fully
manifest until social demands exceed limited capacities or may be masked by learned
strategies in later life).

D. Symptoms cause clinically significant impairment in social, occupational, or other important

areas of current functioning.

E. The disturbances are not better explained by intellectual disability (intellectual

developmental disorder) or global developmental delay. Intellectual disability and autism
spectrum disorder frequently co-occur; to make comorbid diagnoses of autism spectrum
disorder and intellectual disability, social communication should be below that expected for
general developmental level
From American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed.).
Washington, DC.

IV. INTELLECTUAL DISABILITY OR INTELLECTUAL DEVELOPMENT DISORDER

Diagnostic Criteria for Intellectual Disability or Intellectual Development Disorder

Intellectual disability (intellectual developmental disorder) is a disorder with onset during the
developmental period that includes both intellectual and adaptive functioning deficits in
conceptual, social, and practical domains. The following three criteria must be met:

A. Deficits in intellectual functions, such as reasoning, problem solving, planning, abstract

thinking, judgment, academic learning, and learning from experience, confirmed by both
clinical assessment and individualized, standardized intelligence testing.

B. Deficits in adaptive functioning that result in failure to meet developmental and

sociocultural standards for personal independence and social responsibility. Without ongoing

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 support, the adaptive deficits limit functioning in one or more activities of daily life, such as
communication, social participation, and independent living, across multiple environments
such as home, school, work, and community.

C. Onset of intellectual and adaptive deficits during the developmental period.

From American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed.).
Washington, DC.

Watch:

1. What is Attention Deficit/Hyperactive Disorder or ADHD?

(https://youtu.be/vQRh_VMA7Vc)

2. What is Autism Spectrum Disorder or ASD? (https://youtu.be/x2hWVgZ8J4A)

3. What are Specific Learning Disorders? (https://youtu.be/RKCNqHEzLwQ)

4. What is Intellectual Disability? (https://youtu.be/9g-6g89sWbk)

Read:

1. (For Deeper Understanding) Chapter 14: Neurodevelopmental Disorders on Abnormal

Psychology: An Integrative Approach, Seventh Edition by David H. Barlow, V. Mark Durand.

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 MODULE 12: NEUROCOGNITIVE DISORDERS

Module Overview:

In Module 12, we will discuss matters related to neurocognitive disorders and

our our discussion will include Delirium, Major Neurocognitive Disorder, and
Mild Neurocognitive Disorder.

Module Learning Outcomes

• Describe how Delirium presents itself.

• Describe how Major Neurocognitive Disorder presents itself.
• Describe how Mild Neurocognitive Disorder presents itself.

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Course Materials:
Unlike many of the disorders we have discussed thus far, neurocognitive disorders often
result from disease processes or medical conditions. Therefore, it is important that individuals
presenting with these symptoms complete a medical assessment to better determine the
etiology behind the disorder.

Most neurocognitive disorders develop much later in life, whereas intellectual disability
and specific learning disorder are believed to be present from birth. In this module, we review
two classes of cognitive disorders: delirium, an often-temporary condition displayed as
confusion and disorientation; and mild or major neurocognitive disorder, a progressive condition
marked by gradual deterioration of a range of cognitive abilities. The label “neurocognitive
disorders” in DSM-5 reflects a shift in the way these disorders are viewed (American Psychiatric
Association, 2013). In early editions of the DSM, they were labeled “organic mental disorders,”
along with mood, anxiety, personality, hallucinosis (an abnormal mental state involving
hallucinations), and delusional disorders. The word organic indicated that brain damage or
dysfunction was believed to be involved. The “organic mental disorders” category, however,
covered so many disorders that the distinction was meaningless. Consequently, the traditional
organic disorders—delirium, dementia, and amnestic disorders—were kept together, and the
others—organic mood, anxiety, personality, hallucinosis, and delusional disorders—were
categorized with disorders that shared their symptoms (such as anxiety and mood disorders)
(Barlow & Durand, 2013).

I. DELIRIUM

Diagnostic Criteria for Delirium

A. A disturbance in attention (i.e., reduced ability to direct, focus, sustain, and shift attention)
and awareness (reduced orientation to the environment).

B. The disturbance develops over a short period of time (usually hours to a few days),
represents a change from baseline attention and awareness, and tends to fluctuate in severity
during the course of a day.

C. An additional disturbance in cognition (e.g., memory deficit, disorientation, language,

visuospatial ability, or perception).

D. The disturbances in Criteria A and C are not better explained by another preexisting,
established, or evolving neurocognitive disorder and do not occur in the context of a severely
reduced level of arousal, such as coma.

E. There is evidence from the history, physical examination, or laboratory findings that the
disturbance is a direct physiological consequence of another medical condition, substance
intoxication or withdrawal (i.e., due to a drug of abuse or to a medication), or exposure to a
toxin, or is due to multiple etiologies.
From American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed.).
Washington, DC.

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II. NEUROCOGNITIVE DISORDERS

Diagnostic Criteria for Neurocognitive Disorders

Major Neurocognitive Disorder
A. Evidence of significant cognitive decline from a previous level of performance in one or
more cognitive domains (complex attention, executive function, learning and memory,
language, perceptual-motor, or social cognition) based on:
1. Concern of the individual, a knowledgeable informant, or the clinician that there has been a
significant decline in cognitive function; and
2. A substantial impairment in cognitive performance, preferably documented by standardized
neuropsychological testing or, in its absence, another quantified clinical assessment.

B. The cognitive deficits interfere with independence in everyday activities (i.e., at a minimum,
requiring assistance with complex instrumental activities of daily living such as paying bills or
managing medications).

C. The cognitive deficits do not occur exclusively in the context of a delirium.

D. The cognitive deficits are not better explained by another mental disorder (e.g., major
depressive disorder, schizophrenia).

Specify whether due to:

Alzheimer’s disease
Frontotemporal lobar degeneration
Lewy body disease Vascular disease
Traumatic brain injury
Substance/medication use
HIV infection Prion disease
Parkinson’s disease
Huntington’s disease
Another medical condition
Multiple etiologies
Unspecified

Mild Neurocognitive Disorder

A. Evidence of modest cognitive decline from a previous level of performance in one or more
cognitive domains (complex attention, executive function, learning and memory, language,
perceptual motor, or social cognition) based on:
1. Concern of the individual, a knowledgeable informant, or the clinician that there has been a
mild decline in cognitive function; and
2. A modest impairment in cognitive performance, preferably documented by standardized
neuropsychological testing or, in its absence, another quantified clinical assessment.

B. The cognitive deficits do not interfere with capacity for independence in everyday activities

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 (i.e., complex instrumental activities of daily living such as paying bills or managing
medications are preserved, but greater effort, compensatory strategies, or accommodation
may be required).

C. The cognitive deficits do not occur exclusively in the context of a delirium.

D. The cognitive deficits are not better explained by another mental disorder (e.g., major
depressive disorder, schizophrenia).

Specify whether due to:

Alzheimer’s disease
Frontotemporal lobar degeneration
Lewy body disease Vascular disease
Traumatic brain injury
Substance/medication use
HIV infection Prion disease
Parkinson’s disease
Huntington’s disease
Another medical condition
Multiple etiologies
Unspecified

From American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed.).
Washington, DC.

Watch:

1. What is Delirium? (https://youtu.be/qmMYsVaZ0zo)

2. What is Lewy Body Dementia? (https://youtu.be/QmLStXU12F0)

3. What is Alzheimer’s disease? (https://youtu.be/v5gdH_Hydes)

Read:

1. (For Deeper Understanding) Chapter 15: Neurocognitive Disorders on Abnormal

Psychology: An Integrative Approach, Seventh Edition by David H. Barlow, V. Mark Durand.

2. (For Review) Module 14: Neurocognitive Disorders by Washington State University

(https://opentext.wsu.edu/abnormal-psych/chapter/module-14-models-of-abnormal-psychology/)

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 REFERENCES

American Psychiatric Association. (2013). Diagnostic and statistical manual of mental

disorders (5th ed.). Washington, D.C.: Author

Barlow D. & Durand M. (2013). Abnormal Psychology An Integrative Approach.

Stamford, USA: Cengage Learning.

Bridley A. & Daffin L. Abnormal Psychology 1st Edition. Retrieved from

https://opentext.wsu.edu/abnormal-psych/front-matter/title-page/

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