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Pathology, Diagnosis, and the DSM-5 – due in 12 hours

4 pages

Pathology, Diagnosis, and the DSM-5

Prior to beginning work on this assignment, review

Chapter 3

and

Chapter 6

in the course text and view the videos

Depression and Its Treatments (Links to an external site.)

OCD: One Patient’s Story (Links to an external site.)

, Diagnostic and Statistical Manual of Mental Disorders (5th ed.) (Links to an external site.) and The DSM-5 (Links to an external site.) screencast on how to access and use this resource and how to cite and reference the DSM-5. Utilize the

Diagnostic and Statistical Manual of Mental Disorders (5th ed.) (Links to an external site.)

to support your analysis. Note that, in keeping with the focus of this class, the emphasis of your paper should be on the pathological aspects of the disorder you select to analyze.

To successfully complete this writing assignment,

1. Select a psychological disorder for comprehensive analysis from the following list (Choose only one.):

· Major depressive disorder

· Bipolar disorder

· Anxiety

o Focus on only one of the anxiety disorders (e.g., generalized anxiety disorder or social anxiety disorder).

· Post-traumatic stress disorder

· Obsessive-compulsive disorder

· Substance use disorder (substance abuse and addiction)

o Provide both an overview of this topic plus a focus on a single drug of your choice.

§ Your selection of topic should be based on your personal or professional experience or your own academic or personal interest in the topic. Be sure to use current terminology from the Diagnostic and Statistical Manual (DSM-5).

2. Based on the following requirements, create an

outline (Links to an external site.)

for your paper. Use this outline to determine the appropriate APA headings to be applied to your paper. To see APA guidelines for headings, visit

APA Style Elements (Links to an external site.)

in the Ashford Writing Center. Include the following in your paper:

· Introduction of the diagnosis

· Explanation of at least one theory of etiology (causes) of the disorder

· Explanation of the associated factors in development of the disorder (genetic, environmental, familial, lifestyle)

· A summary of the diagnostic and research technologies employed in clinical diagnosis, clinical and behavioral healthcare, and clinical interventions

· Discussion of treatment options of the disorder

· An analysis of the predominance of the disorder in our current society

· Conclusion

3. Next, research your topic and obtain a minimum of two scholarly and/or peer-reviewed sources published within the last five years. These sources should provide evidence-based information regarding the psychological features of the disorder. Be sure to cite these sources accurately in your paper and include them on your references page. Consider the following for this step:

· You may utilize required or recommended course materials in your work, but these will not count toward the reference requirements; however, you may cite and reference the DSM-5 as one of your sources used for the grading credit.

· For support formatting your paper in APA, visit the Ashford Writing Center’s

APA: Citing Within Your Paper (Links to an external site.)

and

Formatting Your References List (Links to an external site.)

4. Write your assignment.

· Suggestion: Complete your paper by the weekend to also take advantage of running a

Paper Review (Links to an external site.)

in the Ashford Writing Center to support your success.

5. Access the

rubric (Links to an external site.)

to confirm all required components have been addressed.

The Pathology, Diagnosis, and the DSM-5 writing assignment

· Must be a minimum of four double-spaced pages in length (not including title and references pages) and formatted according to APA Style as outlined in the Ashford Writing Center’s

APA Style (Links to an external site.)

· Must include a separate title page with the following:

o Title of paper

o Student’s name

o Course name and number

o Instructor’s name

o Date submitted

§ For further assistance with the formatting and the title page, refer to

APA Formatting for Word 2013 (Links to an external site.)

· Must utilize academic voice. See the

Academic Voice (Links to an external site.)

resource for additional guidance.

· Must include an introduction and conclusion paragraph. Your introduction paragraph needs to end with a clear thesis statement that indicates the purpose of your paper.

o For assistance on writing

Introductions & Conclusions (Links to an external site.)

as well as

Writing a Thesis Statement (Links to an external site.)

, refer to the Ashford Writing Center resources.

· Must include APA headings. For formatting support, visit APA Style Elements (Links to an external site.) in the Ashford Writing Center.

· Must use at least two scholarly or peer-reviewed sources published within the last five years in addition to the course text or other course materials. You may also use required and recommended materials from the course but these will not count toward the research component of your grade.

o The

Scholarly, Peer-Reviewed, and Other Credible Sources (Links to an external site.)

table offers additional guidance on appropriate source types. If you have questions about whether a specific source is appropriate for this assignment, please contact your instructor. Your instructor has the final say about the appropriateness of a specific source for a particular assignment.

o To assist you in completing the research required for this assignment, view this

Ashford University Library Quick ‘n’ Dirty (Links to an external site.)

tutorial, which introduces the Ashford University Library and the research process, and provides some library search tips.

· Must document any information used from sources in APA Style as outlined in the Ashford Writing Center’s APA: Citing Within Your Paper (Links to an external site.)

· Must include a separate references page that is formatted according to APA Style as outlined in the Ashford Writing Center. See the

APA: Formatting Your References List (Links to an external site.)

resource in the Ashford Writing Center for specifications.

Required Resources

Text

Getzfeld, A. R. (2018).

Abnormal psychology

(2nd ed.). Retrieved from https://content.ashford.edu

· Chapter 3: Anxiety and Obsessive-Compulsive Disorders

· Chapter 6: Depressive Disorders and Bipolar and Related Disorders

Book

American Psychiatric Association. (2013).

Diagnostic and statistical manual of mental disorders (5th ed.) (Links to an external site.)

. https://doi.org/10.1176/appi.books.9780890425596

· This manual will support your understanding of diagnosis and treatment for mental illness. Note you will only be reviewing one to three pages and it will be based on specific disorders you choose to evaluate this week. It will assist you in your Anxiety and Depression: A Case Study discussion forum and Pathology, Diagnosis, and the DSM-5 assignment this week.

Accessibility Statement (Links to an external site.)

Multimedia

Ashford University. (2018, August 8).

The DSM-5 (Links to an external site.)

[Video file]. Retrieved from https://ashford.mediaspace.kaltura.com/media/The%2BDSM-5/0_wa13z8fy

· This web page provides information about how to access and use the DSM-5 and will assist you in your Anxiety and Depression: A Case Study discussion forum and Pathology, Diagnosis discussion forum and the DSM-5 assignment this week. This video has closed captioning.
Accessibility Statement does not exist.
Privacy Policy (Links to an external site.)

nature video. (2014, December 19).

Depression and its treatments (Links to an external site.)

[Video file]. Retrieved from https://youtu.be/Yy8e4sw70ow

· This video provides information about the neural circuits affected in depression, as well as the molecular and cellular changes becoming better understood for treatment. This video will assist you in your Anxiety and Depression: A Case Study discussion forum and Pathology, Diagnosis, and the DSM-5 assignment this week. This video has closed captioning and a transcript.
Accessibility Statement (Links to an external site.)
Privacy Policy (Links to an external site.)

Sunnybrook Hospital. (2012, October 4).

OCD: One patient’s story (Links to an external site.)

[Video file]. Retrieved from https://youtu.be/x2JAXAmXd2w

· This video features a patient who has been diagnosed with OCD, as well as Dr. Peggy Richter, and discusses the illness as well as potential treatments. This resource will support your Anxiety and Depression: A Case Study discussion forum and Pathology, Diagnosis, and the DSM-5 discussion forum assignment this week. This video has closed captioning and a transcript.
Accessibility Statement (Links to an external site.)
Privacy Policy (Links to an external site.)

Web Page

Society of Clinical Psychology: Division 12. (n.d.).

Case studies search (Links to an external site.)

. Retrieved from https://www.div12.org/case-studies/

· This web page will be utilized to identify a case study to analyze associated with your Anxiety and Depression: A Case Study discussion forum this week.
Accessibility Statement does not exist.
Privacy Policy (Links to an external site.)

Supplemental Material

Rosser-Majors, M. (2019).

Week 2 Study Guide

. Retrieved from https://www.ashford.instructure.com

· This study guide will help you prepare for your Week 2 Terminology Quiz and Week 2 Content Review this week.

Recommended Resources

Book

Ledley, D. R., Pai, A., & Franklin, M. E. (2007).

Treating comorbid presentations: Obsessive-compulsive disorder, anxiety disorders, and depression

. In M. M. Anthony, C. Purdon, & L. J. Summerfeldt (Eds.), Psychological treatment of obsessive-compulsive disorder: Fundamentals and beyond. (pp. 281–293). https://doi.org/10.1037/11543-013

· The full-text version of this chapter is available through the EBSCOhost database in the Ashford University Library. The chapter researches individuals with obsessive compulsive disorder (OCD) and additional psychological disorders, including other anxiety disorders and depression. The study reviews guidelines to differentiate OCD from other anxiety disorders and depression. This resource may helpful in supporting you with your assignments this week.

Article

Finley, E. P., Garcia, H. A., Ramirez, V. A., Haro, E. K., Mignogna, J., DeBeer, B., & Wiltsey-Stirman, S. (2019).

Treatment selection among post-traumatic stress disorder (PTSD) specialty care providers in the Veterans Health Administration: A thematic analysis

. Psychological Trauma: Theory, Research, Practice, and Policy. https://doi.org/10.1037/tra0000477

· The full-text version of this article is available through the EBSCOhost database in the Ashford University Library. This article researches several treatment options specific to veterans experiencing post-traumatic stress disorder (PTSD). Specific psychotherapies are assessed. This article may helpful in supporting you with your assignments this week.

Supplemental Material
Maryland Recovery. (n.d.).

Holistic remedies to help with mental disorders and substance abuse cravings (Links to an external site.)

[Educational brochure]. Retrieved from https://www.marylandrecovery.com/wp-content/uploads/2017/05/marylandRecovery_HolisticRemedies

· The brochure offers insight into holistic methods for addressing addiction and may support you in your assignments this week, as well as future writing assignments in this course.
Accessibility Statement does not exist.
Privacy Policy (Links to an external site.)

12 hours

6 Depressive Disorders and Bipolar and Related Disorders

tommaso79/iStock/Thinkstock

Learning Objectives

After reading this chapter, you should be able to:

• Understand the difference between normal emotions and pathological emotions.

• Explain what depressive disorders are.

• Explain what bipolar and related disorders are.

• Know and discuss what causes depressive, bipolar, and related disorders.

• Explain and discuss how depressive, bipolar, and related disorders are treated.

• Analyze the relationships among depressive, bipolar, and related disorders and suicide.

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146

Depressive Disorders and Bipolar and Related Disorders

It is mid-June in a city known for a temperate climate. You awaken to a blue sky with puffy
clouds; the sun is bright but not too hot, with low humidity. After eating your favorite break-
fast, you go for a walk before heading off to your summer job. All seems right with the world,
yet you are not happy. The sky appears gray to you, the sun covered by clouds. Breakfast
seemed bland, almost tasteless. You didn’t sleep well; in fact, you awakened, again, in the
middle of the night and couldn’t fall back to sleep. You were hoping to be intimate with your
partner last night, but the desire and the drive remain missing.

Does this scenario sound familiar to you? Perhaps it sounds like an everyday experience for
many people. Have you ever had days with some, if not all, of these experiences? Before we
continue, consider the next scenario.

You awaken to the same sunny day, although this time the sun seems exceptionally bright and
energizing. After making yourself a gourmet breakfast and wolfing it down in about three
minutes, you go for a power walk, completing your usual course in record time and engag-
ing everyone you pass in conversation, though the conversations have no connection to each
other. Returning home, you decide, after showering, to clean the entire house as well as clean
the windows and mow the lawn. You then head to work, put in a 13-hour day with a 15-min-
ute lunch break, during which you consume a PowerBar and some Red Bull. At home you pre-
pare a four-course meal from scratch. You should be tired but you’re not, so you call your best
friend and see if she wants to go out to a bar for a few drinks. She calls it a night at 11 p.m., but
you are going strong. You meet an attractive person and go back to his or her apartment for a
while. You return home at about 2 a.m. and go to sleep. . .until 4 a.m., when you awaken, ready
to start the new day, repeating this pattern for at least seven days.

How does the second scenario sound to you? Does this sound like a normal day and night for
some people? Let’s take a closer look at what these scenarios seem to describe.

The first scenario could illustrate some of the classic signs of depression, including sadness,
hopelessness, self-blame, anger, insomnia, and loss of appetite. Depression is one of several
depressive, bipolar, and related disorders, abnormal conditions characterized by persistent
extremes of mood. Depression represents one pole of a person’s mood (see Figure 6.1) and

is typically characterized by extreme sadness, lack
of energy and sex drive, low self-worth, guilt, and
oftentimes thoughts of suicide.

The second scenario might illustrate the other pole,
which is known as mania. Mania is marked by
extreme elation. People who are in the grip of mania
have lots of energy, form grandiose plans (to make
a fortune or cure cancer), display a cavalier attitude
toward money, and usually have a strong sex drive.
At first glance, this may not seem to be much of a
problem; left unchecked, however, mania can cause
just as many difficulties as depression.

Happily, most of us spend the bulk of our time some-
where in the middle of the mood spectrum, neither
very high nor very low. A telephone conversation,
a walk in the park, or a dinner with friends can lift

EgudinKa/iStock/Thinkstock
Typically, the majority of people are
somewhere in the middle of the mood
spectrum and experience a range of
emotions that are neither very high
nor very low.

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147

Depressive Disorders and Bipolar and Related Disorders

our mood. By contrast, a bad day at work, failing an exam, losing a tennis match, indeed any
of life’s disappointments can bring on the “blues.” When our mood rises, we feel happy, ener-
gized, confident, and optimistic. When we get the blues, we feel sad, tired, and pessimistic.
When we are low, we may decide to drown our sorrows in a drink, or maybe just go to bed.

The main difference between the blues, an emotion we all experience, and a depressive disor-
der is one of degree (Oyama & Piotrowski, 2017). The blues pass quickly. In a day or two, we
pick ourselves up and start again. However, when a negative mood persists for a long period
of time, affecting social and occupational functioning, clinicians begin to suspect the presence
of a depressive disorder.

This chapter is concerned with the diagnosis, etiology, treatment, and prevention of depres-
sive, bipolar, and related disorders. It also includes a discussion of suicide, which is some-
times (but not always) caused by one of these disorders.

Figure 6.1: The mood spectrum

Most of the time, we find ourselves in the middle of the spectrum, not too high or too low. Notice that the
two extremes, mania and depression, are closer to one another than they are to the normal mood state.
In fact, some people cycle between depression and mania, and a few manage to be both depressed and
manic at the same time.

Source: Adapted from S. Schwartz, Abnormal Psychology: A Discovery Approach. Mountain View, CA: Mayfield Publishing Company, 2000,
Figure 8.1, p. 319.

Normal mood

Joy

Depression Mania

The
“blues”

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148

Section 6.1 Emotions: Normal and Pathological

Before we continue, let’s examine the case of Bernard Louis, a man whose manic episodes
severely affected his life.

The Case of Bernard Louis: Part

Note Dictated by Psychiatrist, Dr. Kahn, When Admitting Bernard Louis
to the Hospital
UNIVERSITY HOSPITAL

Intake Note

CONFIDENTIAL

Admitting Psychiatrist: Dr. Sally Kahn

Bernard Louis was brought involuntarily to the admitting ward by county police who were
acting on a court order to have him committed for 24 hours of psychiatric observation.

Mr. Louis is a large man, well over 6 feet tall. He weighs more than 200 pounds. When he
appeared at the hospital, his face was very red, and his hair and clothing were disheveled.
Otherwise, he seemed normal. According to his wife, who accompanied him to the hospital,
Mr. Louis had been working alone, 18 hours a day, building a “golf course” in their suburban
backyard. His plan was to turn their half-acre lot into a private country club with a clubhouse.
He hoped to sell memberships at $5,000 a year. The clubhouse would offer catering facilities
as well as a bar and pro shop. He planned to build sand and water traps and to invest in a
fleet of motorized golf carts. When his wife suggested that he might be getting a little carried
away, Mr. Louis lost his temper, shouted in rage, and threatened to leave her for another
woman. He claimed to have four girlfriends whom he regularly “satisfied” ten times a night.
Two days earlier, when his wife had left the house, Mr. Louis had taken all her jewelry to a
pawnshop. He had used the money to invite strangers off the street to an all-night party that
finally had to be stopped by the police. Mr. Louis had not slept at all for three days before his
wife obtained the court order that brought him to the hospital.

Mr. Louis was difficult to interview because he talked nonstop. He complained that he was
being persecuted and that his wife was just jealous of the many women who were after him
because of his sexual prowess. There was nothing wrong with him. In fact, he claimed, “I’ve
never felt better in my life.” When asked if he was happy, Mr. Louis responded, “Am I happy?
Why, if I felt any happier, you could sell tickets. I’m so happy, it should be illegal.”

See appendix for full case study.

6.1 Emotions: Normal and Pathological
Admirers of the original (and often-replicated) Star Trek television series and films will
recall the Starship Enterprise’s Vulcan officer, Mr. Spock. Spock differed from earthlings in
two ways: He had odd, pointy ears, and he was rarely emotional. Unlike Captain Kirk, Spock
was never tempted by the seductive outer-space sirens who regularly tried to lure the space
mariners to destruction. Even when the murderous Romulans seemed certain to destroy the
Enterprise, Spock never panicked. As he coldly evaluated the ship’s predicament, the other

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149

Section 6.1 Emotions: Normal and Pathological

crew members would accuse Spock of being
“inhuman.” To them, the essential charac-
teristic of a human being is the ability to feel
emotions—and most psychologists agree.

Emotions are so much a part of life, we
never stop to ask ourselves why they exist
in the first place. What is the biological func-
tion of negative emotions, such as fear and
sorrow? Why did they evolve? Would we not
be better off being unemotional like Spock?

As is the case with many questions sur-
rounding evolution, the first place to look
for answers is in the works of Charles Dar-
win (1809–1882). In his book The Expres-
sion of Emotions in Man and Animals (1872),
Darwin hypothesized that emotions evolved
because they have survival value. Fear helps
us to survive because, when we are afraid
of something, we flee and avoid possible harm. Sorrow also has survival value. Parent-child
bonds are cemented by the feelings of sadness parents and their children experience when
they are separated. To avoid sadness, parents stay close to their children, thereby increas-
ing their offspring’s chances of survival. Of course, it is possible to have too much of a good
thing. Unrelenting fear or sorrow can be so debilitating that, instead of increasing a person’s
chances of survival, they can actually decrease those chances.

Grieving
The loss of a loved one or a friend usually sets off a grieving process. The first reaction is usu-
ally emotional numbness and disbelief punctuated with acute bouts of distress. Social sup-
port is an important determinant of how quickly, and how well, people cope with the grieving
process (Prest, 2017).

Within a week or so after a loss, disbelief is replaced with a period of pining for the lost per-
son. The survivors dwell on their loss, have trouble sleeping, neglect other aspects of life, and
display anger at their fate (“Why me?”). This stage may last months or years, but most people
eventually acknowledge the permanency of their loss (“I am now a widow”). In the final stage
of grieving, people gradually regain their interest in life, and their sadness abates. The whole
process may take a year or more and may involve significant periods of psychological distress.
Still, the process is perfectly normal (see the accompanying Highlight). In fact, not grieving
over the death of a loved one would be viewed by most psychologists as abnormal. Because
grieving is normal, treatment is not indicated unless people become dangerous to themselves
or are unable to function (Prest, 2017). In such cases, clinicians would probably consider the
individual to be suffering from one of the depressive, bipolar, or related disorders described
in the DSM–5.

Kimberley French/© Paramount Pictures/
Courtesy Everett Collection

As Star Trek fans know, Mr. Spock differs from
humans because he, as a half Vulcan, does not
express emotions. Sometimes his cold ratio-
nality is an advantage, but at other times his
lack of emotion cuts him off from intuition and
social connection.

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Section 6.1 Emotions: Normal and Pathological

DSM–5 Depressive, Bipolar, and Related Disorders
By definition, a mood disorder is an abnormal condition characterized by persistent
extremes of mood. The DSM–IV–TR categorized depressive and bipolar disorders in a single
chapter titled “Mood Disorders.” The DSM–5 has divided the categories into two separate
chapters: “Depressive Disorders” and “Bipolar and Related Disorders.” According to the DSM–
5, there are two general types of mood disorder: unipolar mood disorder and bipolar mood
disorder. The “poles” referred to by these diagnostic labels are the extremes of the mood
spectrum—depression and mania. Unipolar mood disorders are characterized by depres-
sion, whereas bipolar disorders combine depression with manic periods. Both unipolar and

Highlight: Removal of the Bereavement Exclusion Criterion
From Depressive Disorders

How do you handle the loss of a loved one? Most likely you go into a period of mourning,
handling the situation in a way that is unique to you. This is called bereavement, a normal
part of the grieving process. In the DSM–IV–TR (American Psychiatric Association [APA],
2000), psychologists, psychiatrists, and psychiatric social workers were advised (by the
authors of the DSM–IV–TR) not to diagnose major depression in individuals within the first
two months following the death of a loved one. This was called the “bereavement exclusion.”
The inclusion of this criterion in the DSM–IV–TR meant that grieving a recent loss prevented
a person from being diagnosed with major depression.

The bereavement exclusion was removed from the DSM–5 (APA, 2013) in order to ensure
that unipolar depression (major depressive disorder) was not overlooked and that
appropriate treatment could be implemented quickly before trouble ensued. The rationale
behind this is simple enough: Normal grieving and unipolar depression, while sharing some
common facets like withdrawal from everyday activities and intense overwhelming sadness,
also differ in some very important ways.

For example, during grieving, the painful feelings come in waves of grief when they occur;
positive memories of the deceased individual also occur. However, in major depressive
disorder (MDD), the mood and feelings and ideas are almost always negative and unpleasant.
Second, while you are grieving, self-esteem (positive feelings about yourself) is usually
maintained, whereas in MDD, feelings of worthlessness and self-loathing are common.
Normal grieving can lead to MDD, but clinicians are cautioned not to confuse a normal
process with a mental disorder.

There is another perspective. The DSM–5 characterizes bereavement as a severe psychological
stressor that can incite a major depressive episode even shortly after the loss of a loved one.
Some critics say the risk is that of pathologizing grief, a normal human process. Individuals
may be diagnosed with depression even in the absence of severe depressive symptoms (such
as suicidal ideation) and even though their symptoms may be transient.

A person who meets the diagnostic criteria for MDD will no longer be excluded from that
diagnosis solely because the person recently lost a loved one and is in the process of normal
grieving or bereavement. The death of a loved one may or may not be the main, underlying
cause of the person’s unipolar depression.

What are your views on the bereavement exclusion?

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151

Section 6.2 Depressive (Unipolar) Disorders

bipolar disorders are divided into subtypes. The unipolar subtypes include a relatively mild
condition known as persistent depressive disorder (dysthymia) and a more serious one
called major depressive disorder. Bipolar disorders are divided into bipolar I disorder,
which includes both depression and mania; bipolar II disorder (depression and hypomanic
episodes, or episodes that do not cause as much impairment as manic episodes); and cyclo-
thymic disorder (cycling between hypomanic periods and mildly depressed periods without
ever fulfilling criteria for episodes of mania, hypomania, or major depression; APA, 2013). For
adults to be diagnosed with cyclothymic disorder, the symptoms must be present for at least
two years; for children, they must be present for at least one year (APA, 2013). Hypomanic
episodes, unlike mania, do not require hospitalization (APA, 2013).

6.2 Depressive (Unipolar) Disorders
Depression is as old as recorded history. The Hippocratic Oath contains numerous refer-
ences to depression, or as it was known during Hippocrates’s time (approximately 2,400
years ago in Greece), “melancholia.” Melancholia is derived from the Greek word melanchole,
which means “black bile.” According to Hippocrates,
the human body is filled with four basic substances, or
bodily “humors,” which are in balance when a person
is healthy. Ancient healers believed that depression,
a “black” mood, resulted from an excess of black bile.
Even though modern medicine has proved this to be
incorrect, the idea that depression is caused by a chem-
ical imbalance in the body remains popular today and
will be discussed later in the chapter.

Clearly, depression takes an enormous toll not only on
the individual but also on society—particularly on the
economy. Each year, the costs of major depressive dis-
order for the U.S. workplace average about $43 billion
(Greenberg, Fournier, Sisitsky, Pike, & Kessler, 2014).
The overall costs of treating depression are estimated
to be $210.5 billion per year (Greenberg, Fournier, Sis-
itsky, Pike, & Kessler, 2014).

The signs of depression are common. We all experience
periods of sadness and self-doubt, although these are
not usually severe enough to qualify for a psychological
diagnosis (Oyama & Piotrowski, 2017). Typically, these
feelings begin with a reaction to some stressful life cir-
cumstance (losing one’s job, for example). If these feel-
ings dissipate within six months after the stressor or its
consequences end, the DSM–5 labels them an adjust-
ment disorder with depressed mood—a transient
reaction to a stressful circumstance. A major depres-
sive episode may appear superficially similar to an
adjustment disorder, but it is more extreme.

gameover2012/iStock/Thinkstock
In approximately the 5th century
BCE, Hippocrates inscribed what
is now known as the “Hippocratic
Oath.” The oath includes references
to “melancholia,” or depression,
and this ancient idea posited that
depression resulted from an excess
of black bile in the body. Although
this antiquated conclusion was
proved incorrect by modern medi-
cine, it contributed to the possibil-
ity that depression is caused by a
chemical imbalance.

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Section 6.2 Depressive (Unipolar) Disorders

Major Depressive Episodes
Major depressive episodes are part of the diagnostic criteria for bipolar I disorder. Although
we can expect to see them in bipolar I disorder, they are not required to make a bipolar I
disorder diagnosis (APA, 2013). The hallmark of a major depressive episode is a sad mood.
Depressed people feel down and apathetic. They may go through the motions of daily exis-
tence—get up, go to class, go to the library—but there is no enjoyment in it. Life seems dull
and gray, and formerly pleasurable activities no longer bring any enjoyment. (This inability to
feel pleasure is known as anhedonia.) Starting a new activity seems impossibly difficult. Suf-
ferers describe themselves as constantly tired and just barely dragging themselves through
life. Depressed people may talk and think slowly; some may be unable to get out of bed in
the morning. Although slowness is more typical, some depressed people become agitated.
Instead of lying around in bed, they are unable to sit still. They pace the floor, shaking their
heads and restlessly wringing their hands.

A major depressive episode may affect the way people sleep; they may wake in the night
or early morning and be unable to return to sleep. (However, some depressed people sleep
most hours of the day.) Changes in appetite (usually eating less but sometimes eating more)
and loss of interest in sex are also associated with a major depressive episode. Some writers
believe that the presence of these so-called vegetative symptoms (appetite change, sleep dis-
turbance, loss of sex drive, fatigue) is what distinguishes a major depressive episode from less
severe forms of depression (Jaffe & Holle, 2017).

Although a down mood and vegetative symptoms are the most obvious signs of a major
depressive episode, cognition and memory are often affected as well (Jaffe & Holle, 2017).
Depressed people have difficulty concentrating on cognitive tasks (Jaffe & Holle, 2017). They
tend to see the downside of everything, dwelling on their failures and ignoring their suc-
cesses. Because of their pessimism, they lose motivation. Depressed people judge themselves
to be less liked and less capable than other people rate them (Ledrich & Gana, 2012). In chil-
dren and adolescents, a depressive episode may look different. Children are more likely to be
irritable than sad, for example, and they may show different symptoms at different develop-
mental stages (Jaffe & Holle, 2017).

It is difficult for depressed people to change because depression has a tendency to feed on
itself. The vicious cycle begins with depressed people becoming irritable and short-tempered.
They snap at their partners and their children. Regretting their behavior, they then feel guilty
about mistreating their loved ones. These feelings of guilt, in turn, make them even more
depressed (Roepke & Seligman, 2016). (See Table 6.1 for a summary of the diagnostic criteria
for major depressive disorder.)

Depression and physical symptoms often go together; for instance, headaches, dizzy spells,
and general pain have been associated with depression (Trivedi, 2004). In addition to comor-
bid physical conditions, there is considerable psychological comorbidity. Depressed children
frequently display other problems, especially unruly misbehavior and conduct disorder (Rig-
lin et al., 2016). In adults, depression is often accompanied by substance abuse. In addition,
depression and anxiety are often related and show some clinical similarities in most adults
(Jaffe & Holle, 2017).

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Section 6.2 Depressive (Unipolar) Disorders

Persistent Depressive Disorder (Dysthymia)
Persistent depressive disorder (dysthymia) is a chronic, relatively mild, depressive disor-
der that lasts at least two years but may last for decades (Oyama & Piotrowski, 2017). In
children or adolescents, the diagnosis requires that the symptoms last at least one year. The
person may experience occasional symptom-free days, but symptoms never disappear com-
pletely for more than two months at a time. In addition to a depressed mood (or irritability in
children and adolescents), the DSM–5 diagnostic criteria for persistent depressive disorder
( dysthymia) require the presence of at least two specific depressive symptoms.

Table 6.1: DSM–5 diagnostic criteria for a major depressive disorder

A. Five (or more) of the following symptoms have been present during the same 2-week period and repre-
sent 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) or observation made by others (e.g., appears fearful). (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.

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.
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 impor-

tant 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 unspecified schizo-
phrenia spectrum and other psychotic disorders.

E. There has never been a manic episode or a hypomanic 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.

Source: Reprinted with permission from the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, (Copyright
©2013), p.160-161. American Psychiatric Association. All Rights Reserved.

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Section 6.2 Depressive (Unipolar) Disorders

Prevalence and Course of Depressive Disorders
Clinical depression is the “common cold” of psychological disorders (Lorenzo-Luaces, 2015).
About 300 million people worldwide suffer from depression, and the number of cases seems
to be rising in most countries, putting considerable pressure on health expenditures (World
Health Organization [WHO], 2017). The widespread use of psychoactive substances, mass
international migrations, the breakdown of the traditional family, crime, unemployment, and
poverty all make some contribution to the rising incidence of depressive disorders.

A person’s first major depressive episode is now more likely to occur before age 19 than
after (Gotlib & Hammen, 2009; Kessler, Berglund, Borges, Nock, & Wang, 2005). Most major
depressive episodes begin gradually, usually with a prolonged period of anxiety or mild
depression. Although they can last for years, most episodes improve within nine months to
one year (Hasin, Goodwin, Stinson, & Grant, 2005; Kessler, 2002).

Sex, Ethnic, and Cultural Differences
In general, women are about twice as likely as men to be diagnosed as depressed (Oyama &
Piotrowski, 2017). Why women should be more prone to depression than men has been the
subject of substantial debate. Some researchers say women are more likely to seek assistance
for psychological problems than men, so they turn up more often in the statistics (Rutter et
al., 2016). Depressed men presumably cope
in other ways such as hiding behind anger,
but these theories have not received much
support (Ramirez & Badger, 2014).

If women seek psychological help more
often than men, we would expect to find
more women than men in all of the DSM–5
diagnostic groups. Because we do not, alter-
native explanations have been offered that
specifically target depression. For example,
critics of the DSM–IV–TR and the DSM–5
allege that the diagnostic criteria for mood
disorders are subtly biased to include more
women than men. Still another explanation
for the sex difference is that women blame
themselves for being depressed and rumi-
nate on this more than men, who tend to ignore their feelings (Ramirez & Badger, 2014).
Instead of being diagnosed as depressed, men are diagnosed as substance abusers or as suf-
fering from an antisocial personality disorder (discussed, respectively, in Chapters 4 and 9).

In the Pennsylvania Amish (where all women work), depression is equally common in both
sexes (Parker & Brotchie, 2010). The prevalence of depression varies across ethnic groups.
For example, Native Americans are reputed to have higher rates of depression than the rest
of the population (Roh et al., 2015). In addition, Latinos have higher rates of depression than
African Americans, with Asians having the lowest rate of those ethnic groups sampled in one
rather dated study (Algeria et al., 2008).

natalie_board/iStock/Thinkstock
Commonly, women are more likely than men
to be diagnosed with depression. There are
several explanations for this statistic, yet all
possibilities are still under debate.

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Section 6.3 Bipolar and Related Disorders

Otake (2008) looked at how unipolar depression is viewed in Japan. According to the Japa-
nese Health, Labor and Welfare Ministry, 1 in 15 people in Japan suffer clinical depression
at some point in their lives. Depression is considered one of the leading causes of suicide;
in the industrialized world, Japan has the highest rate (Otake, 2008). Out of 100,000 people,
12.8 females and 35.6 males will kill themselves. This has translated into more than 30,000
suicides annually in recent years. Although these statistics are somewhat dated, they speak to
the fact that untreated unipolar depression is a serious mental health concern in Japan. One
reason the numbers appear as high as they are is that treatment options are limited. Most
people in Japan use antidepressants and other drugs. More important, according to Otake
(2008), few have access to, or seek out, psychotherapy. Japan’s national health insurance
system discourages doctors from spending a lot of time with patients, and there is a short-
age of professionals trained in verbal forms of therapy (Otake, 2008). One thing to ponder is
whether increasing awareness of the seriousness of unipolar depression, or increasing the
number of trained clinicians, would help to reduce the numbers of suicides.

6.3 Bipolar and Related Disorders
Although it is possible to experience manic episodes without any periods of depression, clini-
cians dating back to ancient Greece have noted that this is exceedingly rare. In the vast major-

ity of people, manic episodes are either preceded
or followed by depression (although there may be
intervening periods of relative calm). By the 19th
century, it was taken for granted that depression
and mania go together. This is why Kraepelin coined
the term manic-depressive to describe people with
wide mood swings. The DSM–5 term bipolar con-
veys a similar picture: episodes of elevated mood
(one pole) alternating with periods of depression
(the other pole). (See Part 2 of Bernard Louis’s case
in the appendix.)

Manic, Hypomanic, and
Mixed Episodes
The hallmark of a manic episode is an overly ele-
vated mood. Manic people feel high and excited,
although, like Bernard Louis, they are also easily
irritated. In addition to an expansive mood, manic
episodes are marked by grandiosity. In the grip of
mania, people believe that they have unusual abili-
ties and that they can accomplish anything. Con-
vinced of their great wealth, manic people have
been known to hand out money to strangers they
meet on the street or to make enormous wagers at
racecourses or casinos.

STUDIOGRANDQUEST/iStock/Thinkstock
Bipolar disorders are characterized by
feelings of extreme elation followed by
depression. Individuals suffering from
bipolar disorders usually experience
symptoms starting at around age 18.

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Section 6.3 Bipolar and Related Disorders

In the midst of a manic episode, people find it impossible to focus on a single task. Their
minds race from one idea to another, known as flight of ideas. They begin various grand proj-
ects but do not see them through to completion. Not only are their thoughts rapid and unfo-
cused, but their physical activities are also energized and chaotic. They have little need for
sleep, and their sex drive is heightened. Manic individuals speak quickly and rarely fall silent.
Their speech is so rapid, and they switch topics so often, that they may become incoherent.
See Table 6.2 for a summary of the diagnostic criteria for a manic episode.

Table 6.2: Main DSM–5 diagnostic criteria for a manic episode

A. A distinct period of abnormally and persistent elevated, expansive, or irritable mood, lasting at least one
week (or any duration if hospitalization is necessary).

B. During the period of mood disturbance, three or more of the following symptoms have persisted (four if
the mood is only irritable) and have been present to a significant degree:
1. Inflated self-esteem or grandiosity
2. Decreased need for sleep
3. More talkative than usual or a perceived pressure to keep talking
4. Flight of ideas or subjective experience that thoughts are racing
5. Distractibility (attention is easily drawn to unimportant or irrelevant stimuli)
6. Increase in goal-directed activity (either socially, at work or school, or sexually), or psychomotor

agitation
7. Excessive involvement in pleasurable activities that have a high potential for painful consequences

(buying sprees, sexual indiscretions, foolish business ventures)
C. The mood disturbance is sufficiently severe to cause marked impairment in occupational functioning or

in usual activities or relationships with others or to necessitate hospitalization to prevent harm to self
or others, or there are psychotic features. The symptoms are not the result of substance abuse, a medical
condition, or drug treatment.

D. The episode is not attributable to the physiological effects of a substance, or to another medical condition.

Source: Reprinted with permission from the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, (Copyright
©2013), p. 124. American Psychiatric Association. All Rights Reserved.

Some people display manic symptoms while suffering from a depressed mood. They are said
to have a mixed episode. A milder form of a manic episode is called a hypomanic episode,
which is marked by an elated mood, little need for sleep, and intense periods of activity. Unlike
a manic episode, a hypomanic episode need only last at least four consecutive days, whereas
a manic episode needs to last at least one week. Additionally, an individual with a hypomanic
episode can function and does not require hospitalization. If psychotic features are present
(hallucinations and so on), by definition the episode is manic (APA, 2013). Because they feel
energetic and healthy, hypomanic (and manic) people do not seek professional assistance,
nor do they recognize that anything is wrong with them.

Specific Bipolar Disorders
There are three main bipolar disorders:

• Bipolar I disorder consists of one or more manic or mixed episodes. In most cases,
individuals will also have had one or more major depressive episodes.

• Bipolar II disorder is characterized by recurrent major depressive episodes and at
least one hypomanic episode.

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Section 6.3 Bipolar and Related Disorders

• Cyclothymic disorder involves periods
during which hypomanic symptoms are
present alternating with periods of mild
depression over the course of two years
(or one year in children and adolescents).
These periods may be mixed with periods
of normal moods.

There is a high comorbidity between bipolar dis-
orders and substance abuse, but the reasons for
this remain unclear (Gooding, Wolford, & Good-
ing, 2016). Because substances such as cocaine can
cause manic behavior, and because many people use
alcohol and drugs to control their moods, it is often
impossible to tell whether changes in mood are the
result of substance abuse or are responsible for it.

Prevalence and Course of
Bipolar Disorders
Bipolar disorders are rarer than unipolar disorders.
More recent figures place the prevalence rate at
1.8% in the U.S. population, with a prevalence rate
of 2.7% in children aged 12 or older (APA, 2013).
Between 1% and 2.6% of all adults will develop a
bipolar disorder in their lifetime (Gooding et al.,
2016). Although it is not the case with unipolar dis-
orders, men and women are equally likely to be diag-
nosed with a bipolar disorder (APA, 2013; Gooding
et al., 2016). Many famous people have allegedly
suffered from bipolar disorders (from Herman Mel-
ville, Ernest Hemingway, and Vincent van Gogh to
actors Carrie Fisher and Catherine Zeta-Jones and
singer Demi Lovato).

About 15% of people initially diagnosed with some
form of depression go on to experience manic
or hypomanic episodes (Angst, Gamma, Rössler,
Ajdacic, & Klein, 2009). Although some people with
bipolar disorder have only a few manic episodes
over the course of their lives, others, known as
rapid cyclers, can have four or more. The first signs
of bipolar disorder usually appear from ages 18 to
25 and appear rather suddenly (APA, 2013; Angst
et al., 2009; Simon & Zieve, 2013). Bipolar disor-
der rarely appears after age 40. Follow-up studies
have found the prognosis for bipolar disorder to be
poor. Even among those who are treated, relapse

Nordic Photos/SuperStock
American author Ernest Hemingway
allegedly suffered from a bipolar
disorder.

Sylvain Grandadam/age fotostock/SuperStock
Painter Vincent van Gogh was also
thought to suffer from bipolar disorder.
Van Gogh voluntarily entered a sanato-
rium in 1889 and completed this self-
portrait during the year he spent there.

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Section 6.4 Etiology of Mood Disorders

is common, and social and occupational functioning becomes progressively worse over the
years (Gitlin & Miklowitz, 2017).

Diagnostic Specifiers
Postpartum depressions are those that occur in the four weeks following childbirth (APA,
2013). Most of these episodes are mild and brief. In severe cases, the depression is probably
not caused solely by the birth of a child but is likely to be the end result of many preexisting
factors, including low self-esteem (Cabrera & Schub, 2017). The specifier with peripartum
onset is used to designate an unspecified depressive disorder with an onset either during
pregnancy or in the four weeks following delivery (APA, 2013).

Premenstrual dysphoric disorder was moved from the DSM–IV–TR’s Appendix B, “Criteria
Sets and Axes Provided for Further Study,” to the main body of the DSM–5. In this disorder, a
majority of symptoms must be present in the week before menstruation, improve a few days
after menstruation begins, and remit in the week following the end of menstruation (APA,
2013). Symptoms include, but are not limited to, mood swings, feeling overwhelmed or out of
control, hypersomnia or insomnia, and difficulty in concentration (APA, 2013).

6.4 Etiology of Mood Disorders
Biologically oriented researchers have concluded that mood disorders must have a physi-
ological etiology. Psychologically oriented researchers have focused on possible social and
psychological causes. The etiology of bipolar disorders remains poorly understood.

Genetic Factors
Although the diagnostic criteria for mood disorders have been revised repeatedly, the
research data accumulated over the decade or more strongly suggest that these disorders run
in families (Gooding et al., 2016). Most studies have found that first-degree relatives (parents,
siblings, and children) of people with mood disorders are more likely to have mood disorders
themselves than are people without affected relatives (Gooding et al., 2016). (See Table 6.3.)
(See Part 3 of Bernard Louis’s case in the appendix.)

Table 6.3: Average risk for mood disorders in first-degree relatives of people
with mood disorders

Percentage of Relatives With

Patient’s Disorder Major Depressive Disorder Bipolar Disorder

Major depression 9.1 0.6

Bipolar disorder 11.4 7.8

No disorder (general population) 8 <1

Source: Katz and McGuffin (1993) and various epidemiological studies, as appearing in S. Schwartz, Abnormal Psychology: A
Discovery Approach. Mountain View, CA: Mayfield Publishing Company, 2000, Table 8.6, p. 334.

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Section 6.4 Etiology of Mood Disorders

Searches for the gene(s) responsible for
mood disorders began with a search for spe-
cific genetic markers, genetic material pres-
ent in relatives with mood disorders. Find-
ing such material requires two important
ingredients: technology capable of identify-
ing parts of chromosomes and a sufficiently
large number of affected family members
who can be studied over several genera-
tions. Nevertheless, given the accumulated
data, it seems reasonable to conclude that
genetics plays a role in rendering people
susceptible to mood disorders (Gooding et
al., 2016).

What Is Inherited?
If genetics plays a role in the development
of mood disorders, then it follows that suf-

ferers must inherit something that renders them especially susceptible to mood disorders.
This “something” turns out to be faulty neurotransmitter regulation.

In Hippocrates’s time, mood disorders were attributed to an imbalance in the chemicals
(humors) of the body. In the 1950s, it was observed that about 15% of patients treated with
reserpine to reduce their high blood pressure were found to develop major depressive epi-
sodes. Because reserpine was thought to reduce the level of a neurotransmitter known as
norepinephrine, researchers hypothesized that depression might be the result of diminished
levels of norepinephrine. Around the same time that these observations were being made,
clinicians using the drug iproniazid to treat tuberculosis noted that their patients not only
improved physically but also seemed to be in a much better mood. By the late 1950s, the drug
was being widely used to treat depression even though no one had any idea how it worked.

Ultimately, scientists discovered that iproniazid, like reserpine, affects neurotransmitter lev-
els. Specifically, iproniazid inhibits the activity of an enzyme known as monoamine oxidase
(MAO), a chemical that plays a crucial role in neurotransmitter regulation. MAO facilitates the
chemical breakdown and reuptake of neurotransmitters such as norepinephrine, dopamine,
and serotonin after they have done their job (see Figure 6.2). Because iproniazid inhibits
the activity of MAO, it slows the reuptake process. The result is a higher concentration of
norepinephrine.

Pharmaceutical companies rushed to market other MAO inhibitors (MAOIs). Unfortunately,
these drugs had a serious drawback; they interact with certain foods to cause potentially
life-threatening conditions such as stroke. This is why MAO inhibitors have been largely aban-
doned in favor of much less lethal antidepressant drugs such as fluoxetine (Prozac) and ser-
traline (Zoloft). (See Thase [2005] for further discussion of low serotonin levels being impli-
cated in unipolar depression.)

Dino Fracchia/agf photo/SuperStock
Researchers believe the causes of mood dis-
orders may relate to biology (physiological
etiology) or psychology (social environment).
Studies within the Amish community proved
there may be a genetic marker within families,
but the study was difficult to replicate.

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Section 6.4 Etiology of Mood Disorders

Figure 6.2: The neurotransmitter cycle

Disruption of any stage of this process can lead to over- or underproduction of a neurotransmitter
or interfere with its reuptake. A variety of drugs have been created to regulate the cycle of specific
neurotransmitters.

Source: From S. Schwartz, Abnormal Psychology: A Discovery Approach. Mountain View, CA: Mayfield Publishing Company, 2000,
Figure 8.3, p. 336.

Neurotransmitter diffuses and
is metabolized and/or transported
back into presynaptic neuron.

Postsynaptic neuron

C22+
Synaptic

cleft

Transporter

Precursor

Presynaptic neuron

Neurotransmitter

Neurotransmitter
molecules

Neurotransmitter
is synthesized in
presynaptic neuron

Neurotransmitter
is packaged into
vesicles.

Neurotransmitter
is released when
vesicles fuse with
cell membrane.

Neurotransmitter
binds to and activates
postsynaptic receptors

1
2
4
5
3

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Section 6.4 Etiology of Mood Disorders

Psychosocial Factors
Although there is clear evidence that genet-
ics plays a role in mood disorders, and we
have several plausible candidates for the
biological diathesis, it is important to keep in
mind that the concordance rate, even among
identical twins, is less than 100% (concor-
dance rate refers to the proportion of identi-
cal twins in a random sample who share a
certain characteristic with their twin; Flint &
Kendler, 2014). Thus, the environment must
also play a role in determining who develops
a mood disorder. In this section, we look at
how psychoanalytic, behavioral, cognitive,
and social psychologists explain how stress
interacts with preexisting vulnerabilities to
produce mood disorders.

Psychoanalytic Views
According to Freud (1917/1959) and his followers, depression is a form of grief produced
in reaction to a loss, especially the loss of an important personal relationship through death,
divorce, or separation. People who become clinically depressed tend to blame themselves for
their loss. This pattern of self-blame is established early in life, usually because of the loss of
parental affection. Rejecting parents, or early separation from one’s parents through death,
divorce, or desertion, can cause a child to become fixated at the oral stage of psychosexual
development. Because children at this early developmental stage depend on their caregivers
to satisfy their physical and psychological needs, fixation produces a passive and emotionally
dependent adult. They blame themselves for their loss of parental affection; these children
grow up feeling unwanted and worthless. They are angry about their loss, but they turn their
anger inward, thereby setting the stage for a lifetime habit of self-blame and a consequent
vulnerability to depression.

Psychoanalysts now believe that mood disorders can be traced back not just to the loss of
parental affection but also to the loss, early in life, of any person who was of special impor-
tance to the child (Keyes et al., 2014). Related to this is the concept that stressful life events
often lead to a mood disorder (Gooding et al., 2016).

Behavioral Views
Behavioral psychologists originally emphasized the loss of important relationships in the eti-
ology of depression. Their basic premise was that the behavior of other people is an important
source of reinforcement for our own behavior. When we lose a friend or loved one, we also
lose the reinforcement they provided. As a consequence, we may go out less, tell fewer jokes,
and lose interest in social activities; in other words, once people become depressed, they
set in motion a vicious cycle. Depressed people are bad company, so they are avoided. This
furthers their isolation and makes them even more depressed. Even worse, if other people

James Woodson/Digital Vision/Thinkstock
Although genetics plays a role in mood dis-
orders, an individual’s environment is also
important when determining the cause of a
mood disorder.

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Section 6.4 Etiology of Mood Disorders

show sympathy for depressed friends and relatives, then the depressive behaviors may be
reinforced and the depression may become chronic. Behavioral psychologists now believe
that any life event that disrupts habitual behaviors can potentially lead to the loss of reinforc-
ers and, therefore, to depression (Gooding et al., 2016).

The main problem with these behavioral formulations is their lack of specificity. We know
that many people experience the loss of a loved one without becoming clinically depressed.
Similarly, very few people respond to praise and success by becoming manic.

Cognitive Views
Cognitive psychologists such as Aaron Beck (1991) view mood disorders as mainly the result of
distorted attributions. They believe that depressed people are biased toward negative attribu-
tions. These negative attributions constitute what Beck calls the negative cognitive triad of
depression: negative feelings about the self, the world, and the future. People with depressive
mood disorders also have characteristic ways of interpreting and responding to life events.

People who feel worthless distort events to justify their low opinion of themselves. These dis-
torted appraisals then make them depressed. Once depression sets in, they tend to make more
negative self-appraisals, assuring further “failures” and making them feel more worthless and
even more depressed. Once this process takes hold, depression becomes self-perpetuating.
Like psychoanalysts and behaviorists, cognitive psychologists make room for individual dif-
ferences in their theory. The main tenet of the cognitive view is indisputable; the research
evidence showing that depressed people are self-critical is overwhelming (Kannan & Levitt,
2013).

Learned Helplessness
In contrast to Beck’s cognitive theory, which was derived from clinical observations, Mar-
tin Seligman’s theory of learned helplessness was derived from animal research (Seligman,
1975). In the typical experiment, dogs were confined in a box with an electrified floor. They
received electric shocks, which they could not avoid because there was no escape route. Later,
the same dogs were tested in an apparatus known as a “shuttle box.” This box consisted of two
compartments separated by a small partition. One side of the box had an electrified floor; the
other did not. Once again electric shocks were delivered through the floor, but this time they
were preceded by a buzzer or a light signal. The animals who were attracted to the electrified
compartment by food or drink could avoid the pain of a shock by jumping over the wall when-
ever they heard or saw the signal (see Figure 6.3). Animals that had never been exposed to the
inescapable shock eventually learned to jump out of the electrified side of the box whenever
the signal was presented. This allowed them to eat or drink in the electrified box without ever
feeling any shock. The animals that had previously been exposed to the unavoidable shock
never learned to make the required escape response. Instead, they just lay down on the grid,
cowered, whined, and accepted their fate. According to Seligman, these animals had learned
that painful outcomes were beyond their control. Instead of learning to avoid shock, they
simply learned to act helpless.

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Section 6.4 Etiology of Mood Disorders

Seligman noted parallels between the animal research and human depression. For example,
many depressed people have experienced tragedy and loss over which they have had no con-
trol. In response, they may give up trying to cope and react to life’s problems with passivity
and helplessness.

Over the years, Seligman and his colleagues have gathered additional evidence for his learned
helplessness theory (Peterson, Maier, & Seligman, 1993) and have revised it. According to
the revised theory, we attribute our failures and losses to either internal or external causes.
External attributions (where the individual attributes failure to environmental events and to
other people) lead to temporary feelings of helplessness and depression but not to self-blame.
Internal attributions (where the individual attributes negative events to a personal failing of
some sort), by contrast, produce more chronic forms of depression in which low self-esteem
and self-blame play an important role. An important prediction of the revised helplessness
theory is that serious depressions require not only a triggering event (such as failing to make
the Olympic team) but also a depressive internal attributional style that assigns such failure
to personal, usually global, failings (Liu, Kleiman, Nestor, & Cheek, 2015).

Figure 6.3: Learned helplessness

In Martin Seligman’s (1975) research into learned helplessness, dogs that had been confined in a box
with an electrified floor and were unable to avoid being shocked were subsequently unable to learn to
jump to safety over the partition in a half-electrified shuttle box at the signal of a buzzer or a light.

Source: S. Schwartz, Abnormal Psychology: A Discovery Approach. Mountain View, CA: Mayfield Publishing Company, 2000, Figure 6.6,
p. 343.

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Section 6.5 Treatment of Mood Disorders

Interpersonal and Social Support
As we have seen, loss and stressful life events, especially the deaths of loved ones, are often
associated with mood disorders. The effects of stress and loss can be minimized by support-
ive friends and family (Gooding et al., 2016). Recovery from depression can be accelerated by
strong social support (Gooding et al., 2016). This is why mood disorders are less likely among
people who have strong social support networks (Liu et al., 2015).

6.5 Treatment of Mood Disorders
As mentioned earlier, Hippocrates believed that depression was caused by the supposed
excess of black bile in the body. Bloodletting, the administration of drugs that caused vomit-
ing and diarrhea, diets, massages, baths, and exercise were all prescribed. Even when doctors
no longer believed in the four humors, regular exercise continued to be prescribed (Jaffe &
Holle, 2017).

Biological Treatments
Biological treatments cover a wide range, including electroconvulsive therapy, light treat-
ment, and many other interventions. However, by far the most common biological treatment
is the administration of mood-altering drugs.

Drug Treatment
As mentioned earlier, MAO inhibitors’ side effects, and the difficulty in maintaining dietary
restrictions to avoid potentially life-threatening reactions, are too serious to make them the
drug of first choice. MAO inhibitors were first replaced by imipramine, which was originally
synthesized to treat schizophrenia. It did not do much to help the symptoms of schizophre-
nia, but it did seem to lift people’s depression. Thus, by accident rather than by design, imip-
ramine became the first in a series of tricyclic antidepressants (TCAs). Tricyclic refers to
the chemical structure of these substances, which
contains three rings of atoms. Although these drugs
work differently from MAO inhibitors, they also
increase neurotransmitter levels. Specifically, they
block the proteins that transport neurotransmitter
residues back to synaptic terminals. This keeps the
neurotransmitters from being reabsorbed, thereby
increasing their levels (Nelson, 2016).

More recent drugs have targeted another neu-
rotransmitter, serotonin. Fluoxetine (Prozac), for
example, is an antidepressant drug that blocks the
reuptake of serotonin (thereby increasing serotonin
levels) while leaving other neurotransmitters unaf-
fected. Fluoxetine and related drugs are known as
selective serotonin reuptake inhibitors (SSRIs).

Elizabeth Cardoso/Hemera/Thinkstock
Modern drug treatments focus on
blocking the reuptake of serotonin, or
SSRIs. These drugs increase serotonin
levels and are effective against depres-
sion with minimal side effects.

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Section 6.5 Treatment of Mood Disorders

The drug has become popular because it not only is effective against depression but also has
relatively mild side effects, such as increased agitation, lowered libido, insomnia, and stom-
ach upset (Nelson, 2016).

These reduced side effects are especially important. It takes a minimum of two weeks before
any of the antidepressant drugs exert their therapeutic effect. During these two weeks,
patients develop the side effects of the drugs but receive no benefits. Some give up the drugs
in disgust. Because fluoxetine has few side effects, people are more likely to stick with it long
enough to obtain the benefits. Reduced side effects also save money because drug side effects
often require treatment (Auday, 2016).

Because most depressions eventually lift whether they are treated or not, the main goal of
drug treatment is to hasten recovery and prevent recurrence (Safer, 2017). The latter goal
may require that patients be given “maintenance” doses of antidepressant medication for
prolonged periods lasting months or even years (Safer, 2017). Antidepressants do not “cure”
depression and recurrences may still occur, even among those treated with maintenance
doses (Auday, 2016).

Drug treatment for bipolar disorder was discovered by John Cade (1912–1980) in the 1940s.
Cade, an Australian psychiatrist, studied people who had mania, trying to find some biochem-
ical cause for their behavior. One of his experiments involved injecting guinea pigs with urine
samples taken from manic patients and noting whether the animals’ behavior changed. Noth-
ing happened. Cade could not find any particular ingredient that caused mania. Instead, he
found that lithium urate (a salt found in everyone’s urine) caused the guinea pigs to become
lethargic. Since lithium carbonate, a naturally occurring salt, had the same effect, he con-
cluded that it was the lithium that was calming down the animals. Cade himself took lithium
first and, noting no ill effects, he tried lithium on one of his patients. The patient, whom Cade
described as “dirty, destructive, mischievous, and interfering” and who had “enjoyed pre-
eminent nuisance value in a back ward for years,” became perfectly well.

Perhaps Cade’s most extraordinary discovery was that lithium not only was effective against
mania but also seemed to prevent the depressive episodes of bipolar disorder. Thus, although
antidepressants helped relieve depression and strong tranquilizers calmed mania, lithium
helped both conditions. Moreover, unlike imipramine or fluoxetine, lithium does not affect
neurotransmitters. Instead, it seems to reduce the excitability of the nervous system.

Although Cade initially reported that bipolar disorder patients will not have a recurrent manic
episode if they take lithium indefinitely, more recent studies estimate the recurrence rate
among treated patients to be around 40% to 50% (Goodwin & Jamison, 2007). One difficulty
in judging lithium’s effectiveness is ensuring that people take their medication as prescribed.
Some people stop taking lithium because they like the feeling of well-being and energy that
accompanies a manic state (Goodwin & Jamison, 2007). Others forego lithium because of its
side effects: diarrhea, stomach upset, weakness, and frequent urination. In high dosages, lith-
ium can even be fatal. Ensuring patient compliance is especially important because discon-
tinuing lithium actually increases the probability of a manic episode. In other words, discon-
tinuing lithium is not recommended as relapse may occur (Sportiche et al., 2016).

Anticonvulsant medications typically used to treat seizures have also been used to treat bipo-
lar disorder (Gooding et al., 2016). Individuals who have at least four episodes of mania or

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Section 6.5 Treatment of Mood Disorders

depression within a 12-month time period are specified as having a rapid-cycling pattern. This
type of bipolar disorder is quite difficult to treat effectively (for example, Gooding et al., 2016);
nevertheless, anticonvulsants have shown some efficacy for this group (Gooding et al., 2016).

Electroconvulsive Therapy
Electroconvulsive therapy (ECT) was introduced in the 1930s. ECT involves sending elec-
trical impulses through the brain with the goal of inducing a seizure. Like many drug treat-
ments, it also had its origins in an accident. A Viennese doctor named Manfred Sakel noted
that a patient who had accidentally been put in a coma by an overdose of insulin became
less anxious and depressed. Because it was difficult to determine the exact amount of insu-

lin required to produce a seizure without inflicting seri-
ous harm or even killing the patient, clinicians experi-
mented with “safer” methods to induce seizures. One
method was ECT. ECT fell out of use in the 1950s due
to the memory loss that often occurred and the scary
nature of the procedure itself. In addition, antidepres-
sant medications made the use of ECTs less warranted
(Piotrowski & Hartmann, 2017). By the 1970s, however,
it began to make a comeback. Today, ECT is used to treat
depression in patients who do not respond to drugs or
psychological therapy.

Today’s ECT patients are given a general anesthetic so
that they are not conscious during the procedure. They
also receive drugs that inhibit body movements. Elec-
trodes are then placed on the head, usually on the right
side only. Because the left side of the brain normally
contains the speech centers, applying shock only to the
right minimizes any disruption in communicative abil-

ity (Heering & Schub, 2017). Once the electrodes are in place, a current is passed through the
head for about half a second. The patient’s response is a convulsion (seizure) that lasts for
around a minute, followed by a coma that lasts from a few minutes to half an hour.

ECT can rapidly clear a depression without needing to wait the weeks required with drugs
or psychotherapy (Piotrowski, 2016). However, ECT may have side effects. One of these is
memory loss, especially for events just before the seizure. Modern practice is to minimize the
number of treatments so that memory loss is not extensive and new learning is unaffected.
ECT is generally reserved for people who do not respond to other forms of interventions.
After more than 80 years of use, we still have no theory to explain the therapeutic effects of
ECT. The lack of a theory about how ECT works, coupled with reports of serious side effects,
even death, have made ECT controversial.

Light Treatment
For hundreds of years, clinicians have prescribed a trip to a sunny climate as the best cure for
the winter blues. Light treatment provides similar benefits, but without the travel. Unspecified
depressive disorder with seasonal pattern (commonly called seasonal affective disorder
[SAD]) is a unipolar depression that occurs only during a particular time of year—typically in

SSPL/Getty Images
This early electroconvulsive ther-
apy machine was first used in the
1930s and by the 1970s, ECT treat-
ment was administered to patients
who failed to respond to drugs or
therapy.

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Section 6.5 Treatment of Mood Disorders

winter, when the days are shorter. Light treatment for people with this disorder involves expo-
sure to a few hours of bright light every morning (Piotrowski, 2016). The light is designed to
mimic the spectrum of sunlight. In any event, side effects are rare, although exposure to light
may cause eyestrain and headache (Piotrowski, 2016). (See Figure 6.4.)

Figure 6.4: Prevalence of seasonal affective disorder by latitude

Source: Data from Rosen et al. (1990), from S. Schwartz, Abnormal Psychology: A Discovery Approach. Mountain View, CA: Mayfield
Publishing Company, 2000, Figure 8.5, p. 340.

New York

ALMS

CA
NV

AZ
NM

MEXICO

CANADA

KSCO

WI
MN

Sarasota

Atlantic
Ocean

Pacific
Ocean

NC
TN

IN OH
PA

WV VA

MEVT

MA
NH

MD DE
NJ
CT

0
0

250 Miles

27.0°

39.0°

40.5°

42.5°

250 Kilometers

42.5°: Nashua, NH
40.5°: New York, NY
39.0°: Montgomery County, MD
27.0°: Sarasota, FL

Montgomery
County

Nashua

20.7%

17.2%

16.7%

4.0%

Transcranial Magnetic Stimulation
Transcranial magnetic stimulation (TMS) is a painless, noninvasive procedure that uses
magnetic fields to stimulate nerve cells in the brain to improve symptoms of depression, typi-
cally when other treatments haven’t been effective (see also Chapter 1). Even though we are
unsure why TMS works, it may activate regions of the brain that have decreased activity in
people with depression.

Psychological Treatments
Medications, ECT, light, and TMS are aimed at alleviating the symptoms of depression. They
do not teach people who are prone to depression how to cope with the loss of a loved one,
unemployment, or any of the other triggers of depression. Psychological treatment, by con-
trast, is designed to help people learn more effective ways of behaving. Most psychological
treatments have focused on depression rather than bipolar disorder (other than those that
try to devise ways of making sure that people with bipolar disorder take their lithium).

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Section 6.5 Treatment of Mood Disorders

Psychoanalytic and Interpersonal Treatment
Psychoanalytic treatment is designed to help patients achieve insight into the repressed con-
flicts that are presumed to be responsible for their mood disorder. Most often, these conflicts
involve the loss of a loved one, accompanied by guilt and self-blame. Once the therapist has
helped the person to recognize the conflict, the therapist encourages the person to release the
inwardly directed hostility and, through this catharsis, eliminate inner-directed anger.

Interpersonal Psychotherapy (IPT)
Interpersonal psychotherapy (IPT), developed by Gerald Klerman in 1988, aims to help
clients examine the ways in which their present social behavior keeps them from forming
satisfactory interpersonal relationships (Lemmens et al., 2017). Instead of focusing on the
past, IPT is concerned with the present, especially problems in adjusting to grief; fights with
friends, coworkers, and relatives; role transitions (new job, divorce); and social deficits (such
as a difficulty in acquiring new relationships). In addition to gaining insight, clients are taught
assertiveness and communication skills as well as other ways of improving their ability to
form supportive relationships.

Cognitive-Behavioral Treatment
As its name suggests, cognitive-behavioral treatment combines cognitive and behavioral
interventions. The cognitive component involves teaching clients to identify self-critical and
negative thoughts, to note the connection between such thoughts and depression, and to chal-
lenge negative thoughts to see if they are supportable. If they are not, the client is taught to
replace them with more realistic evaluations of present and future circumstances.

Outside of cognitive-behavioral therapy sessions, some clients find that programmed aero-
bic exercise (such as spinning or aqua-aerobics) can help them understand and control their
depression and lead to better relapse prevention (Olson, Brush, Ehmann, & Alderman, 2017).

Drugs Versus Psychological Treatment
One of the first studies to compare psychological with drug treatments found that
cognitive-behavioral therapy was superior to imipramine in the treatment of depression
(Rush, Beck, Kovacs, & Hollon, 1977). Several studies found that cognitive-behavioral treat-
ment and IPT reduce the probability of a relapse (Hollon et al., 1992; Hollon, Shelton, & Davis,
1993; Lewinsohn, Clarke, Hops, & Andrews, 1990). But combining psychological treatments
with antidepressant medication seems to produce a greater prevention effect than use of
either treatment alone (Nelson, 2016). One reason for this is that people in psychotherapy
are more likely to take their drugs regularly (Jin, Sklar, Oh, & Li, 2008).

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Section 6.6 Suicide

Undertreatment
Some people do not seek help because they fail to recognize the signs of depression, others
fear the stigma of “mental illness,” and still others cannot afford treatment costs. Medical pro-
fessionals also contribute to undertreatment. Many medical practitioners are poorly informed
about mood disorders and the benefits of treatment (Vermani, Marcus, & Katzman, 2011).
The worst outcome of an untreated mood disorder is a despair that becomes so extreme that
the person takes his or her own life. However, mood disorders are not the only cause of sui-
cide. (See Part 4 of Bernard Louis’s case in the appendix.)

6.6 Suicide
Suicide, self-inflicted death in which the person deliberately, consciously, and intentionally
acted to kill himself or herself, is a disorder under further study in the DSM–5; the disorder
is called suicidal disorder (APA, 2013). In some times and places, suicide has been socially
acceptable. For example, in 2014 in the United States, Brittany Maynard announced that she
intended to end her life by physician-assisted suicide. In early 2014, Maynard had been diag-
nosed with a brain tumor, which quickly advanced and eventually became terminal. She then
moved from California to Oregon, where physician-assisted suicide is legal, and ultimately
ended her life by that means (Pierre, 2015). In Japan it was, and still is to a certain extent, con-
sidered socially acceptable to commit seppuku, or suicide, to save the family from disgrace.
Even though social views are thought to be more tolerant in the United States, suicide is often
still considered a social disgrace here. Suicidal behavior is surrounded by many myths. Some
of these are highlighted in the accompanying Highlight.

Suicidology (the study of suicide, suicidal behavior, and suicide prevention) has become a
scientific field in its own right. Still, many people who take their own lives do suffer from a
mental disorder (Piotrowski & Hartmann, 2017). Because suicide is frequently associated
with depression, it has been included in this chapter.

Prevalence and Incidence
Suicide is universal and has occurred throughout history. It is among the top 10 causes of
death in the United States and a common cause of death among young people (Centers for
Disease Control and Prevention [CDC], 2015). The reported suicide rate in the United States
is 42,826 per year; the actual number is probably higher (CDC, 2017). About 50% of suicides
involve the use of firearms (CDC, 2017). The remaining are by suffocation and poisoning.
Many suicides go unreported because of the ambiguity surrounding the death or because
families try to cover up the circumstances to avoid social stigma (Piotrowski & Hartmann,

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Section 6.6 Suicide

Highlight: Suicide Myths and Reality

Over the centuries, myths have developed around suicide. Some of the more prevalent myths,
and the corresponding realities, are addressed in the table that follows.

Suicide Myth Suicide Reality

Those who talk about suicide never do it. The vast majority of people who kill them-
selves give some warning.

Suicide is related to social class. People of all social and educational classes kill
themselves. Although more educated people
are less likely to turn to suicide, there are some
notable exceptions. Highly educated people,
such as doctors, have among the highest sui-
cide rates (Kent, 2010). Some occupations that
require advanced education—such as dentists
and physicians—are associated with higher
suicide rates, presumably because they often
are highly stressful professions, and perhaps
because practitioners have easy access to lethal
drugs such as barbiturates and narcotics.

Everyone who dies by suicide is depressed. Many people who kill themselves are not
depressed. Indeed, suicides are most likely to
occur just when it appears that a person has
recovered from depression.

Suicide is influenced by weather (“the suicide
season”).

Suicides can occur at any time of year.

Suicidal people always want to die. Most people who kill themselves are not sure
they want to die. Many gamble with their lives,
hoping that others will save them.

Only insane people contemplate suicide. Suicidal thoughts are common in the general
population. Among the terminally ill, suicide
may be considered a rational act.

Once people try suicide, they remain forever
suspect.

Most people attempt suicide only once, but up
to 40% of those who complete suicide will have
made previous attempts (Cavanagh, Carson,
Sharpe, & Lawrie, 2003).

Those who unsuccessfully attempt suicide
were never serious.

Some people are poorly informed about the
lethality of different acts.

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Section 6.6 Suicide

Age, Sex, and Ethnic Differences
Although suicide is a relatively more common cause of death
among young people than among older ones (because young
people are less likely to die from disease), suicide is not uncom-
mon among older persons (CDC, 2005). For example, in 2000,
when 12.5% of the U.S. population was older than 65, this group
accounted for almost 20% of all suicides (CDC, 2003). It is par-
ticularly prevalent among white males older than age 65 (CDC,
2003). Divorced, widowed, and other single people have higher
suicide rates than married people. In all instances, more men
than women take their own lives (APA, 2003).

The circumstances of people who take their own lives are remark-
ably similar across cultures. Suicides are most common among
people whose families have been affected by death or divorce,
who have unhappy love affairs, who suffer serious illness, or who
experience severe economic setbacks.

Assessing Suicidal Intentions
It is not easy to predict who will kill themselves; many suicides
seem to happen without prior warning (Apter et al., 1993; Maris,
Berman, Maltsberger, & Yuflt, 1992). Nevertheless, suicidologists
have been able to identify a set of risk factors that seem to be cor-
related with suicide (see Table 6.5).

Table 6.4: Suicide attempts versus suicide completers

Characteristic Attempters Completers

Sex Female Male

Age Under 35 Over 60

Means Low lethality (pills) High lethality (firearms)

Diagnosis None or rare Depression; substance abuse

Setting Public, easy to discover Private and isolated

Source: From S. Schwartz, Abnormal Psychology: A Discovery Approach. Mountain View, CA: Mayfield Publishing Company, 2000,
Table 8.7, p. 357.

2017). Although suicide occurs everywhere, cross-cultural comparisons are difficult because
cultures may record suicides differently, based on how suicide is treated in a given culture.
According to recent research, a large disparity exists between suicide attempters and suicide
completers in terms of demographics, means, and the setting (see Table 6.4).

KMazur/WireImage/Getty Images
Rock musician Kurt
Cobain, of the 1990s
band Nirvana, died by
suicide on April 5, 1994.
Cobain suffered from
depression and also had
severe issues coping
with worldwide media
attention.

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Section 6.6 Suicide

Causes of Suicide
The motive for attempting suicide varies from person to person (Piotrowski & Hartmann,
2017). Some suicides are attempts to extract retribution or obtain martyrdom, others are a
way to end a life of intolerable pain, and still others are the result of risk taking or “playing
with death.” Edwin Shneidman, who studied risk factors for suicide, noted that there are cer-
tain commonalities among people who display suicidal behavior (Shneidman, 1992): They
are seeking a solution to a problem, wish to end consciousness, have either psychological or
physical pain (or both), have frustrated psychological needs, feel hopeless, cannot see alter-
natives, and are “escapers” rather than problem solvers. (See Figure 6.5.)

Psychological Disorders and Suicide
A psychological disorder, usually a bipolar disorder or a major depression, appears in the
history of many cases of suicide (Piotrowski & Hartmann, 2017; Shneidman, 1992). Interest-
ingly, people rarely attempt suicide while in the depths of depression. The year following a
major depressive episode is the most dangerous period (Isometsä, Sund, & Pirkola, 2014),
perhaps because the person is still unhappy but now has the energy required to carry out
self-destructive intentions.

Most people with mood disorders do not kill themselves; however, alcohol abuse makes sui-
cide more likely. The presence of a psychological disorder, such as depression, combined with
the poor judgment and reduced inhibition produced by alcohol create a lethal combination
(Piotrowski & Hartmann, 2017).

Table 6.5: Risk factors and suicide

Factor Low Risk High Risk

Sex Female Male

Marital status Married Single/divorced/living alone

Age Middle years Adolescence/old age

Psychiatric status Normal/character disorders/
situational disturbances

Depression/alcoholism/conduct disorder/
schizophrenia

Setting Rural Urban/prisons

Assault victim No history Multiple physical and sexual assaults

Religious activity Regular churchgoer Non-churchgoer

Nationality Italian/Dutch/Spanish Scandinavian/Japanese/German-speaking countries

Source: Adapted from Nock and Kessler (2006), Nock et al. (2008), and Stevenson et al. (1972).

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Section 6.6 Suicide

Psychological Factors
Freud and his followers construe suicide as a form of murderous anger at another person
turned inward against oneself. A child whose mother dies may become angry about this loss,
but the child is unable to vent this anger because its target, the dead mother, is unavailable.
Instead, the child turns this anger inward.

Figure 6.5: Threshold model for suicidal

behavior

Source: Adapted from “Clinical Assessment and Treatment of Youth Suicide,” by S. J. Blumenthal and D. J. Kupfer, 1988, Journal of Youth
and Adolescence, 17, 1–24. Copyright © 1988 by Plenum Publishing Corporation. Reprinted with kind permission of Springer Science +
Business Media.

Suicidal behavior

Risk
factors

Protective
factors

Precipitating
factors

Environmental
factors/suicide

exposure

Cognitive flexibility
Strong social support
Hopefulness
No losses

Lack of precipitating life events
Treatment of psychiatric disorder
Treatment of personality disorder

Availability
of method

Humiliating
precipitating

life event
Threshold

Vulnerability
for suicidal

behavior

Psychiatric
diagnosis

Genetic/family
history

Biological factors
(for example, SHIAA,

perinatal factors)

Personality traits
(for example,
impulsivity)

Predisposing
risk factors

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Section 6.6 Suicide

Despite the confirmation of early loss in the childhood of many people who kill themselves,
the overall evidence for the psychoanalytic view of suicide is far from compelling. Although
hate and revenge are sometimes the motives for suicide, they are not the only reasons people
take their own lives (Tucker, Crowley, Davidson, & Gutierrez, 2015). Shame, guilt, and hope-
lessness are considerably more common motives. Hopelessness is particularly important
(Piotrowski & Hartmann, 2017; Sadock & Sadock, 2007; Shneidman, 2005).

Genetics and Physiology
Suicide, like depression, tends to run in families (Zai et al., 2012). The concordance rate
for suicide among monozygotic twins is 20 times higher than it is among dizygotic twins,
0.7% compared with 14.9% (Brent & Melhem, 2008). Because most suicidal twins are also
depressed (or suffering from some other mental disorder), it may be the mental disorder,
rather than the tendency toward suicide, that is inherited. In any event, there does seem to be
a genetic factor involved, although it is worth noting that, even among monozygotic twins, the
concordance rate for suicide is not 100%.

Treatment and Prevention
Since medical science can now keep some people alive indefinitely, there is considerable
debate about the ethics of doing so. Perhaps people should be able to die with dignity when
they no longer wish to live. Some say yes, others no. For psychologists, their stance is more
clearly defined. Because suicide is an irreversible act, the professional ethics of psychologists
require that they try to prevent people from harming themselves, even if this means breaking
client-therapist confidentiality.

Crisis Intervention
Crisis intervention is aimed at overcoming immediate problems. This is often done through
telephone crisis lines and walk-in prevention centers that were first established in most cities
in the 1960s. The counselors who answer these phones and who work in these centers have
been taught to maintain contact with the person in crisis, develop a relationship, clarify the
source of stress, and recommend an action plan—usually a place the person can go for help.

Psychological Interventions
The first issue to be faced in the treatment of suicide is the potential for another attempt. If the
likelihood seems high (and that is often difficult to judge), then the safest place for the person
is in the hospital, even if this means involuntary commitment and breaking therapist-client
confidentiality. Once the immediate danger subsides, treatment is usually aimed at overcom-
ing any immediate life-stress and at teaching clients how to go about solving problems before
they become hopeless. (See the accompanying Highlight.)

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Section 6.6 Suicide

Postvention
Suicide has a shattering impact on the survivors (Piotrowski & Hartmann, 2017). Family and
friends must cope not only with the death of a loved one but also with the circumstances of the
death. Postvention (Shneidman, Farberow, & Litman, 1970) is aimed at helping relatives and
friends cope with grief. Friends and relatives of a suicide victim often feel guilty and anxious
because they believe that they should have done something to prevent the death. Sometimes
they may become suicidal themselves (Piotrowski & Hartmann, 2017). Group therapy can
sometimes help provide a supportive environment, but postvention involves more than just
group therapy. Postvention also includes rumor control and identifying those people at high
risk of imitation. A number of postvention programs have been developed, mainly for schools.

Highlight: Celebrities and Suicide

We can safely say that you know about Robin Williams. Perhaps you know of, or saw, Chris
Cornell of Soundgarden. Maybe you know about Chester Bennington of Linkin Park. Robin
Williams of course was a multitalented actor and comedian, while Cornell and Bennington
were successful rock stars, front men for their bands. What is it that led these three men, as
well as a number of other celebrities, to take their own lives? Fast (2017) has an interesting
perspective. Many articles mentioned that Cornell and Bennington were tormented by “inner
demons” and that they dealt with them through their music and singing, almost like a form of
catharsis. Bennington was very candid about being sexually molested by a close friend from
age 7 until 13, and he talked about how he never completely got past this history, leading to
addictions, among other issues. Fast (2017) says that part of the problem is that we and the

media are too quick to characterize depression
as fighting with inner demons, not recognizing
it as an illness similar to diabetes or cancer. In
other words, we are ascribing mythical aspects
to a very real illness that affects tens of millions
of people worldwide and that plays no favorites,
multitalented or not. When people suffering
from depression take their lives, they are doing
so because of a treatable illness, not because
of inner demons. Perhaps if more people
understood this, lives could be saved through
prevention, treatment, and education.HOME BOX OFFICE/SuperStock

Robin Williams took his own life in
2014.

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176

Chapter Summary

Chapter Summary
• Mood disorders (depressive, bipolar, and related disorders) tend to occur most often

among people who have experienced a severe loss early in life.

• Mood disorders run in families.

• Pharmaceuticals, electroconvulsive therapy, and psychological treatments (alone or

in combination) seem to help shorten depressive and manic episodes and prevent
relapses.

Emotions: Normal and Pathological
• Emotions are normal. They help us survive. We flee from danger when afraid. Sad-

ness at parting cements parent-child bonds. Overwhelming fear or sadness can
hinder normal life processes.

• Mood disorders (depressive, bipolar, and related disorders) tend to occur most often
among people who have experienced a severe loss early in life.

• Mood disorders run in families.

Depressive (Unipolar) Disorders
• Depression is marked by a sad mood, loss of interest in formerly pleasurable activi-

ties, sleep disturbances, changes in appetite, loss of interest in sex, irritability, inabil-
ity to concentrate, and a wide variety of aches and pains.

• In adults, depression, physical illness, and substance abuse often go together.
• In children, the most frequently reported comorbid conditions are disorders of

conduct.
• Persistent depressive disorder (dysthymia) is a moderate depression that lasts two

years or more (one year in children and adolescents).
• Depression is common, and the number of cases seems to be rising, especially

among young people.
• Women are more than twice as likely to be depressed as men.

Bipolar and Related Disorders
• Manic episodes are marked by an expansive mood, grandiosity, diminished sleep,

heightened sex drive, and rapid-fire speech.
• Hypomanic episodes are similar to manic episodes but milder.
• When the depressions are mild and mood is highly variable, the diagnosis is cyclo-

thymic disorder.
• Bipolar disorders are less common than unipolar disorders and affect men and

women of different ethnic groups equally.
• The first signs of bipolar disorder usually appear in early adulthood, but the inci-

dence of bipolar disorders seems to be rising among young people.
• Typically, onset is sudden; follow-up studies have found the prognosis to be poor.

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177

Chapter Summary

Etiology of Mood Disorders
• The response of some mood disorders to light therapy, the effectiveness of antide-

pressant drugs, the evidence for heredity, and the relationship between mood and
hormonal imbalances are all compatible with a biological etiology.

• Psychoanalysts focus on the loss of affection and “fixation” in early childhood.
• Behavioral theories emphasize learned helplessness and loss of reinforcement.
• Cognitive theories focus on faulty attributions.

Treatment of Mood Disorders
• Biological treatments for mood disorders cover a wide range and include drug

therapy, ECT, light treatment, and transcranial magnetic stimulation.
• Psychological treatment attempts to teach people more effective ways of coping with

problems.

Suicide
• Suicide is the tragic result of the complex interaction of social, psychological, and

biological forces.
• People who take their own lives are seeking a solution to a problem, wish to end

consciousness, have intolerable psychological or physical pain, have frustrated
psychological needs, feel hopeless, cannot see alternatives, and are “escapers” rather
than problem solvers.

• Suicide is among the world’s top 10 causes of death and a common cause of death
among young people.

• Divorced, widowed, and other single people have higher suicide rates than do mar-
ried people; in all instances, more men than women take their own lives.

• Early life events, genetic predispositions, and psychological disorders all play some
role in suicide, though none of these factors by itself is a good predictor of who will
complete suicide.

• Crisis intervention is aimed at overcoming current problems and reducing the prob-
ability of a suicide attempt; if the probability seems high, then the safest place for
the person is in the hospital.

• Once the immediate danger subsides, cognitive-behavioral treatment can be used to
teach clients how to go about solving problems before they become hopeless.

• Family therapy may also be useful in helping to improve family communication and
joint problem solving.

• Postvention is aimed at helping relatives and friends cope with the grief of a suicide.

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178

Chapter Summary

Key Terms
adjustment disorder with depressed
mood A temporary reaction to a stressful
circumstance.

anhedonia A loss of pleasure in all activi-
ties; the inability to feel pleasure.

bipolar I disorder A mood disorder
in which the individual’s moods fluctu-
ate between mania (abnormal highs) and
depression (lows).

bipolar II disorder A mood disorder
in which the individual’s moods fluctu-
ate between hypomania (a milder form of
mania) and depression.

cyclothymic disorder When the individual
cycles between hypomanic and mildly
depressed moods.

depression An abnormally low mood state
typically characterized by extreme sadness,
lack of energy and sex drive, low self-worth,
guilt, and oftentimes thoughts of suicide.

electroconvulsive therapy (ECT) A treat-
ment for unipolar depression, where elec-
tricity is passed through the brain to induce
a seizure. ECT is used to treat depression
in people who do not respond to drugs or
psychological therapy.

hypomanic episode A milder form of a
manic episode.

interpersonal psychotherapy (IPT) A
mood disorder therapy aimed at helping cli-
ents examine the ways in which their pres-
ent social behavior keeps them from forming
satisfactory interpersonal relationships.

learned helplessness When, based on past
experiences, individuals determine that they
have no control over the reinforcements
and/or the stress in their lives.

lithium carbonate Lithium, a naturally
occurring salt, used to treat bipolar disorder.

major depressive disorder A mood disor-
der in which an individual has one or more
major depressive episodes.

major depressive episode An episode of
unipolar depression.

mania A state of extreme elation and giddi-
ness, accompanied by excessive energy.

manic episode A condition characterized
by extreme elation as well as other mania
features. Left untreated, a manic episode
might last six months.

Critical Thinking Questions

1. Based on what you have read, think about and discuss why it would be difficult
to distinguish between unipolar depression and an adjustment disorder with
depressed mood.

2. What, in your opinion, is the best method for treating unipolar depression?
3. Presume you have a friend who has bipolar I disorder. She tells you that she is on

lithium and has decided not to take it because she wants her “highs” to return and
says that she is all better. Discuss what you would say to her based on what you have
read and discussed in class.

4. Freudians believe that depression is anger turned inward and is also a result of a loss
that occurred during childhood. Give your views on what causes depression.

5. If you had a friend who you thought was suicidal, how would you handle it, based on
what you have read?

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179

Chapter Summary

MAO inhibitors (MAOIs) A type of antide-
pressant medication typically used if other
antidepressants are ineffective; an example
is phenelzine (Nardil).

melancholia Hippocrates’s term for
depression.

mixed episode A condition in which an
individual has manic symptoms while also
having a depressed mood.

mood disorder An abnormal condition
characterized by persistent extremes of
mood.

negative cognitive triad Attributions in
which the individual has negative feelings
about the self, the world, and the future.

persistent depressive disorder (dysthy-
mia) A chronic, relatively mild, depressive
disorder that lasts at least two years but may
last for decades.

postpartum depression A unipolar
depression that occurs in the four weeks fol-
lowing childbirth.

postvention After a suicide, a program that
is aimed at helping relatives and friends
cope with grief.

rapid-cycling pattern The diagnosis given
when an individual has at least four episodes
of mania or depression within a 12-month
time period.

selective serotonin reuptake inhibitor
(SSRI) Medications that increase serotonin
reuptake and thus increase the serotonin
activity in the brain; typically used as antide-
pressant medications; fluoxetine (Prozac) is
an example.

suicide Self-inflicted death in which the
person deliberately, consciously, and inten-
tionally acted to kill himself or herself.

suicidology The study of suicide, suicidal
behavior, and suicide prevention.

transcranial magnetic stimulation
(TMS) A noninvasive procedure that
uses magnetic fields to stimulate nerve
cells in the brain to improve symptoms of
depression. TMS is typically used when
other depression treatments haven’t been
effective.

tricyclic antidepressant (TCA) One of the
earliest types of antidepressant medication
classes; imipramine is an example.

unipolar mood disorder A mood disorder
characterized by depression.

unspecified depressive disorder with
seasonal pattern (seasonal affective
disorder, or SAD) A seasonal mood disor-
der that typically recurs at specific times of
the year. Typically, people feel depressed in
winter, improve in spring, and then become
depressed again as autumn turns to winter.

with peripartum onset A diagnostic
specifier used to designate an unspecified
depressive disorder with onset either during
pregnancy or in the four weeks following
delivery.

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3 Anxiety and Obsessive-Compulsive Disorders

lolloj/iStock/Thinkstock

Learning Objectives

After reading this chapter, you should be able to:

• Differentiate among anxiety, fear, and panic.

• Understand the causes and treatments of specific phobias.

• Discuss the causes and treatment of social anxiety disorder (social phobia).

• Summarize the causes and treatment of generalized anxiety disorder.

• Explain the causes and treatment of panic disorder and agoraphobia.

• Discuss the causes and treatment of obsessive-compulsive disorder and related disorders.

• Understand anxiety related to substance use and medical conditions.

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Section 3.1 Anxiety, Fear, and Panic

3.1 Anxiety, Fear, and Panic
When we encounter any kind of threat or stressor, we experience a number of physiologi-
cal responses: Heart rate, blood pressure, and breathing increase; muscles tense; blood ves-
sels constrict; the liver releases glucose to provide quick energy to muscles; and the spleen
releases red blood cells to help carry oxygen. We feel fear or dread; we may also feel irri-
table or restless. We scan our environment for signs of danger. The intensity of our responses
depends on the perceived magnitude of the stressor or threat.

The Anxiety Spectrum
For people with anxiety disorders, these responses occur continuously or intermittently
when no real threat or stressor is present or when they encounter a stimulus that is similar in
some way to the original threat or stressor. Typically, their reaction is out of proportion to the
degree of danger. Anxiety manifests itself in a spectrum from mild to severe (see Figure 3.1).

Figure 3.1: Anxiety spectrum

Anxiety can manifest itself as something as mild as worry or something as severe as a panic attack.

Source: Adapted from S. Schwartz, Abnormal Psychology: A Discovery Approach. Mountain View, CA: Mayfield Publishing Company, 2000,
Figure 4.4, p. 143.

Mild worry

Mild

Severe

Fears

Phobias

Agoraphobia

Obsessive-compulsive disorder

Panic Attack

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Section 3.1 Anxiety, Fear, and Panic

Anxiety Disorders Related to Medical Conditions
and Substance or Medication Use
A variety of medical conditions can cause symptoms similar to those associated with anxi-
ety disorders. An overactive thyroid gland, heart disease, vitamin deficiencies, respiratory
disease, and brain tumors are among the conditions that share symptoms with the anxiety
disorders. Alcohol, caffeine, and many prescription and illicit drugs can also cause anxiety
symptoms. Before diagnosing an anxiety disorder, we need to be sure that an individual’s
anxiety is not related to a medical condition or to substance use or withdrawal from a sub-
stance. A prudent method is to make sure the individual has had a complete physical before
starting psychotherapy.

Let’s consider the case of Carole Ballodi.

The Case of Carole Ballodi: Part 1

On the night of February 24, three seriously injured infantry soldiers were transported by
helicopter to Medivac Unit 4 CB, which was under the command of Captain Carole Ballodi.
Captain Ballodi and her team of medics and nurses began to stabilize the wounded in
preparation for surgery, when they found themselves under fire. They called for assistance,
but before air strikes could be ordered, their Medivac unit was hit by a rocket. One of the
wounded soldiers was struck in the head by shrapnel and killed instantly while Captain
Ballodi was taking his pulse. A nurse was gravely injured. Although electrical supplies were
cut off, and the shelling continued, Captain Ballodi and her team managed to tend to the
wounded until the shelling stopped. She then assisted in an emergency surgery that required
the amputation of one soldier’s leg. Captain Ballodi’s actions during that night saved the lives
of the injured soldiers. She is worthy of the highest commendation.

Initial Interview Between Carole Ballodi and Psychiatrist Dr. Sally Kahn
UNIVERSITY HOSPITAL

Psychiatry Service

Consultation Transcript

Referring Physician: Dr. Berg

Reason for Referral: Carole Ballodi is an internal medicine specialist at University Hospital.
She was brought to the emergency room complaining of chest pain. A physical examination
proved negative. Because of her agitation, she was referred for a psychiatric consultation.

Posttraumatic stress disorder (PTSD) appeared in the “Anxiety Disorders” chapter of the
DSM–IV–TR. In the DSM–5 it was moved to the “Trauma and Stressor-Related Disorders”
chapter. Because Carole demonstrates signs and symptoms of panic disorder as well as PTSD
we have decided to keep her case in this chapter.

(continued)

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Section 3.1 Anxiety, Fear, and Panic

The Case of Carole Ballodi: Part 1 (continued)

DR. KAHN: Tell me, what do you consider your main problem?

CAROLE: I have these pains in my chest and feel like I can’t catch my breath.

DR. KAHN: When does this occur?

CAROLE: One time was in my car. I was just about to get on the bridge. I was at the toll booth
when I heard a helicopter overhead. I panicked. I couldn’t catch my breath. I broke out in a
sweat, and I could feel my heart pounding. I felt like there was a tight band across my chest. I
got dizzy, hot, and nauseous. And I was very frightened. I thought I was dying.

DR. KAHN: Can you recall what thoughts were going through your head when this happened?

CAROLE: Actually, I can. I thought that the helicopter sounded like the ones that delivered the
wounded to the Medivac unit in Iraq. I think I just panicked.

DR. KAHN: You panicked?

CAROLE: Yes. I was afraid that the helicopter would come down and crash into my car.

DR. KAHN: What would happen to you?

CAROLE: I would be disabled for life and have to use a wheelchair.

DR. KAHN: So, you were thinking about these things and then began to feel the chest pain?

CAROLE: I’m not sure—it all seemed to happen together. I was thinking about the helicopters
and my car, and then I felt the pain in my chest and had trouble breathing.

DR. KAHN: What happened next?

CAROLE: I pulled over to the side and just sat there. Traffic backed up behind me, but there
was nothing I could do. It was like it was happening to someone else. Finally, someone called
an ambulance.

DR. KAHN: What happened in the hospital?

CAROLE: I felt better by the time I got to the hospital. They ran the usual tests but found
nothing. They suggested that I see you.

DR. KAHN: Have you “panicked” at any other time?

CAROLE: Yes. Mostly at night. I wake up at two or three in the morning. I’m covered in sweat
and my heart is racing. I can hardly catch my breath. I think I’m going to die.

DR. KAHN: Is there anything specific that set all this off ?

CAROLE: I had a patient die in my office. It brought back the war. I never used to, but now
I spend hours each night going over things that have happened in the past. I relive what
happened in Iraq. It’s like a videotape that I play over and over again in my mind while I ask
myself whether I could have done things differently.

DR. KAHN: What do you do when you wake up during the night?

CAROLE: I usually check all the windows and door locks and then I go back to sleep.

DR. KAHN: What about your work?

CAROLE: I can’t concentrate on anything. I’ve taken practically all of my sick days.

(continued)

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Section 3.1 Anxiety, Fear, and Panic

Before we continue, we need to define anxiety, fear, and panic. These concepts may seem simi-
lar if not identical, but you will soon see that they are not.

Anxiety
Anxiety is an emotional state marked by an intense feeling of foreboding and somatic signs
such as a racing heart, sweating, and difficulty breathing. The individual is afraid that the
future will bring only bad results. Anxiety is a feature of everyday life. Anxiety is similar to
fear but with a less specific focus. Whereas fear is usually a response to some immediate
threat, anxiety is characterized by apprehension about imagined or real unpredictable dan-
gers that may lie in the future. The limbic system, a complex set of brain structures that
controls our emotions (see Figure 3.2), is involved in mediating anxiety levels. Low levels of
anxiety are adaptive; they help us avoid danger (“I don’t like the look of that dark street”) and
plan for the future (“I better study for the final exam or I will fail”). Anxiety becomes maladap-
tive when it interferes with a person’s relationships and daily functioning. Table 3.1 lists the
DSM–5 anxiety disorders.

The Case of Carole Ballodi: Part 1 (continued)

DR. KAHN: What are you doing about your problems?

CAROLE: Mostly I stay home, hoping that rest will help. I have a few drinks to help me sleep.

DR. KAHN: Has this worked?

CAROLE: Well, the drinks knock me out, but I’m missing lots of work.

DR. KAHN: Do you go out with friends?

CAROLE: No. I’m afraid to leave home. I’m afraid to get in my car. I might have another
incident. I’m not interested in seeing anyone, and sex leaves me cold.

DR. KAHN: Do you ever see anyone you served with in Iraq?

CAROLE: No. I was never really bothered by the war, but I don’t want to talk to anyone. Who
knows what they might think? I don’t know what’s happening to me. I think I’m going mad.

On the basis of their discussion, Dr. Kahn felt certain that Carole Ballodi was suffering
from an anxiety disorder or a trauma or stressor-related disorder, probably related to her
war experiences. Before Dr. Kahn could be more certain, however, she had to consider the
possibility that Carole’s behavior was the result of a general medical condition. A variety
of medical disorders can cause symptoms similar to Carole’s. Because alcohol, caffeine,
and many prescription and illicit drugs can also cause anxiety symptoms, Dr. Kahn had to
be sure that Carole’s behavior was not substance related (or related to withdrawal from
a substance). Thus, Dr. Kahn began by ordering a medical history as well as physical and
laboratory examinations. These found no evidence of a relevant medical condition or
substance-induced anxiety.

See appendix for full case study.

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Section 3.1 Anxiety, Fear, and Panic

Figure 3.2: The limbic system

Except for the pituitary, all the highlighted areas in the forebrain are part of the limbic system
and normally receive signals from neurons that secrete mood-altering neurotransmitters. Some
neurotransmitter pathways are indicated by arrows.

Source: Adapted from S. Schwartz, Abnormal Psychology: A Discovery Approach. Mountain View, CA: Mayfield Publishing Company, 2000,
Figure 4.3, p. 141.

Prefrontal cortex

Amygdala

Hypothalamus

Septum

Cingulate gyrus

Major Brain Structure

Fornix
Basal ganglia

Thalamus

Thalamus
Hypothalamus

Spinal cord

Brain stem
Hindbrain

Midbrain

Hippocampus
Amygdala

Forebrain

Cerebral cortex

Pituitary

Raphe nuclei
Hippocampus

Locus Coeruleus

Cerebellum
Medulla oblongata
Pons

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Section 3.1 Anxiety, Fear, and Panic

Fear
Fear is an emotion that occurs in response to some real immediate threat or danger. Fear serves
a positive purpose: It helps mobilize the body’s defenses quickly in situations requiring fight
or flight (defending oneself or running away) from a dangerous situation or an enemy. Lin-
eage studies have found a tendency for fear to run in families (Van Houtem et al., 2013). Twin
studies, for example, help us to determine whether behavior and mental illness, among other
things, are caused by the environment or by biology. Because identical twins have the same
genes and DNA, differences can be attributed to their environments. Identical twins raised apart
are equally likely to develop fears and to be afraid of similar things (Kendler et al., 2008).

Panic and Panic Attacks
Panic is an extreme anxiety reaction that can result when a real threat suddenly emerges.
Some definitions might add that the threat can be perceived instead of an actual threat. The
experience of panic attacks, however, is different. Panic attacks are periodic, short bouts of
panic that occur suddenly, reach a peak, and pass. Sufferers often fear they will die, go crazy,
or lose control. Attacks happen in the absence of a real threat. We will discuss panic, panic
attacks, and panic disorder in depth later in this chapter.

Panic attack was not a diagnosis in the DSM–IV–TR and is not in the DSM–5. However, the
specifiers for different types of panic attacks have been changed from cued, situationally pre-
disposed, and uncued to unexpected and expected panic attacks. Panic attack is a specifier
that can now apply to all DSM–5 diagnoses (American Psychiatric Association [APA], 2013).

Comorbidity and the Anxiety Disorders
Recall the term comorbidity from Chapter 1. Comorbidity (when a disorder has a high level of
co-occurrence with other disorders) is common with the anxiety disorders. Anxiety disorders
are frequently accompanied by depression (Kessler, Sampson, et al., 2015). This association is
so common that Brown and Barlow (2002) theorized that anxiety and depression may share
a common feature: They both involve emotional distress, but they vary in how the distress
is expressed. People with other psychological disorders (for example, schizophrenia) com-
monly report anxiety symptoms as well.

Table 3.1: The DSM–5 anxiety disorders

• Separation anxiety disorder • Agoraphobia

• Selective mutism • Generalized anxiety disorder

• Specific phobia • Substance/medication-induced anxiety disorder

• Social anxiety disorder (social phobia) • Anxiety disorder due to another medical condition

• Panic disorder • Other specified anxiety disorder

Note: The DSM–5 includes an additional diagnostic category for “Unspecified anxiety disorder.” Vague references to
“unspecified” disorders appear throughout the DSM–5. Because they have no specific symptoms, etiology, or treatment,
these disorders are not discussed in this book.

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Section 3.2 Specific Phobias

3.2 Specific Phobias
At one time or another, everyone is afraid of something: snakes, storms, airplanes, or dentists.
Fear is an important evolutionary adaptation (LeDoux & Pine, 2016). But fear can also be
debilitating. It can torment us, destroy our sleep, and rob our lives of pleasure. In extreme
cases, it can cause disease or even death. Rational fears are not phobias. If you hurry home
after hearing a storm warning on your car radio, you do not have a phobia—no matter how
frightened you may feel. However, if your fear of storms is so intense that you board up all

your windows and at the slightest threat of a rain
shower you run home and barricade all of the doors
and windows, and head to the basement, then you
probably have a phobia. Fears become phobias
when they disrupt daily life enough to justify clini-
cal intervention (APA, 2013).

A specific phobia consists of a persistent, exces-
sive, and irrational fear of an object or situation cou-
pled with a strong desire to avoid the feared object
or situation. People with phobias display extreme
fear reactions when exposed to the feared stimuli.
They recognize that their reaction is excessive and
unreasonable, yet their fear disrupts their everyday
lives (APA, 2013).

Etiology of Phobias
It has been estimated that anywhere from 7.7% to 12.5% of the world’s population will
meet the criteria for a specific phobia disorder at some time in their lives (Wardenaar et
al., 2017). The overall average lifetime prevalence is estimated to be approximately 7.4%
(Wardenaar et al., 2017). Once a phobia is established, it tends to last a lifetime unless
it is specifically treated. The Encyclopedia of
Phobias, Fears, and Anxieties (Doctor, Kahn, &
Adamec, 2008) has more than 2,000 entries.
Phobias are determined by the complex inter-
action of cultural and social norms (fears
vary across cultures), learning experiences
(your best friend screams when she sees a
spider and you become afraid of spiders),
and cognitive components (your thoughts
and beliefs). Table 3.2 lists some of the more
common phobias.

Cultural and Social Determinants
To a large extent, our culture and society determine the objects and situations we fear (Sato,
Yuki, & Norasakkunkit, 2014; Yeh, Nguyen, & Lizarraga, 2014). The Aborigines of Central Aus-
tralia, for example, have an intense fear of violating sacred tribal sites (Strehlow, 1985). Those

william87/iStock/Thinkstock
For some people, going to the dentist
can be a frightening experience, lead-
ing to heightened anxiety about going
for necessary checkups.

Table 3.2: Common fears and phobias

• Death • Storms

• Flying • Enclosed places

• Snakes • Illness/injury

• Dentists • Traveling alone

• Heights

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Section 3.2 Specific Phobias

who violate taboo areas are subject to “bone-pointing,” in which a tribal elder takes the leg
bone of a kangaroo, dips it into an anthill, covers the end with human hairs, and points it at
the transgressor while chanting a curse. Aborigines fear bone-pointing so much that some of
those subjected to the curse have reportedly died from fright (Basedow, 1925). When culture-
bound fears become extreme enough to interfere with normal daily functioning, they cross
over into becoming phobias.

Learning Experiences
According to behavioral psychologists, a phobia is acquired initially through classical con-
ditioning: A neutral stimulus that is repeatedly paired with a fear-inducing stimulus will, in
time, elicit the fear response even in the absence of the primary fear-inducing stimulus. A bell
doesn’t evoke a fear response, but if it is paired with a feared stimulus—a painful shock—it
will eventually evoke a fear response even in the absence of the painful shock. Over time, a
person comes to avoid situations related to the one that originally caused a fear response.
Once the phobia is generalized (occuring in situations similar but not identical to the original
situation), the avoidance response continues because avoiding feared objects reduces anxi-
ety, which in turn reinforces future avoidance.

Behaviorists note that phobias may be acquired indirectly by observing fear in others (Bunaciu,
Fleschin, & Aboul-Enein, 2014). Mineka (1985) found that rhesus monkeys raised in captivity
were not afraid of snakes until they observed the fearful reactions of monkeys raised in the
wild. Although observational learning may account for many fears acquired in the absence of
aversive experiences, exposure alone may not be sufficient for phobias to develop. Mineka’s
monkeys did not develop fears of flowers or a toy rabbit, even when exposed to apparently
fearful models (Mineka 1985; see also Cook & Mineka, 1991). Perhaps observational learn-
ing produces phobias only for dangerous objects and situations that evolution has geneti-
cally “prepared” us to fear (McNally, 2016). For example, humans are genetically prepared to
acquire a fear of heights (we can fall from a high place and be injured or killed) and spiders
(some spider bites can be lethal). Through evolution, we have developed phobias to make our
survival more likely. Of course, even this “preparedness” hypothesis has difficulty determin-
ing whether our fears are due to evolution or to the environment (McNally, 2016).

Cognitive Determinants
Cognitive therapists believe that some people habitually make fearful attributions to objects
or situations, overestimate the probability of risk, and underestimate their personal ability
to cope (Beck & Haigh, 2014). Bandura (1986) suggested that, for some people, perceived
inability to cope is responsible for anxiety and avoidance behaviors. In other words, the real
cause of fear is not the feared stimulus but rather the feelings of inadequacy in dealing with
the challenge it presents. Fearful thoughts may become self-fulfilling prophecies: For exam-
ple, fearing failure on an examination may cause people to fail.

Treatment for Specific Phobias
Therapeutic and drug treatments for specific phobias are described in the treatment sections
related to social anxiety disorder, since the treatment approaches are similar.

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Section 3.3 Social Anxiety Disorder (Social Phobia)

3.3 Social Anxiety Disorder (Social Phobia)
The fear of examinations and speaking in front of other people (“stage fright”) are both forms
of performance anxiety. For example, employment tests, driver’s license tests, and medi-
cal examinations can produce feelings of apprehension and dread in many people, and can
significantly impact one’s life (Cooper, Hildebrandt, & Gerlach, 2014; Morrison & Heimberg,
2013; Sloboda, 1990). Although low to moderate levels of anxiety may facilitate performance,
high levels of anxiety lower performance (Sodhi, Luthra, & Mehta, 2016). In some instances,
extreme anxiety may render people unable to perform at all. It can produce eating and sleep-
ing disorders, and it can make sufferers physically ill (Culbert, Racine, & Klump, 2015; Shana-
han, Copeland, Angold, Bondy, & Costello, 2014; Vogelzangs, Beekman, De Jonge, & Penninx,
2013). Performance anxiety occurs in both Western and Eastern cultures (Ruscio et al., 2007),
but cultural sensitivity is necessary when interpreting performance anxiety. Among Native
American cultures, for instance, it is considered improper, impolite, and even disloyal to stand
out from one’s peers (Dasen, Berry, & Sartorius, 1988; Kagitçibasi & Berry, 1989). Because

people with performance anxiety can usually inter-
act successfully with others (provided they do not
have to perform), few seek professional help. For
some people, however, the fear of being evaluated
by others extends to most aspects of social inter-
action. These people may curtail their social lives,
even sacrifice their careers, to avoid threatening
social situations. Such persons are likely to be suf-
fering from social anxiety disorder (also known as
social phobia; APA, 2013).

Social phobia, which usually begins in adolescence,
represents an extreme form of performance anxiety
in which the fear of social evaluation may severely
restrict a person’s life (Iverach & Rapee, 2014). Like
most anxiety disorders, social phobia affects more
females than males (Pesce et al., 2016). Social pho-
bias may sometimes be traced to a specific trigger-

ing event, such as an inability to find a date for the senior prom or being bullied during early
adolescence (McEvoy & Saulsman, 2014). It is more often due to innately fearing angry, criti-
cal, or rejecting people or their faces (McEvoy & Saulsman, 2014; Prater, Hosanagar, Klumpp,
Angstadt, & Phan, 2013).

Therapeutic Treatment for Specific and Social Phobias
Many different treatments have been developed to deal with specific phobias and social pho-
bia (Arroll, Wallace, Mount, Humm, & Kingsford, 2017; Mayo-Wilson et al., 2014). Although
each has its specific aspects, they all seek to motivate people to change, ensure that they pre-
pare, and expose them to the feared stimulus. No matter what treatment is used, an important
factor in helping someone to overcome any problem is to establish a trusting therapeutic
relationship.

Evan Agostini/Invision/AP Photos
Barbra Streisand, the famous singer,
actress, director, and producer
is a well-known individual with
social phobia.

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Section 3.3 Social Anxiety Disorder (Social Phobia)

Psychoanalytic Treatment of Specific and Social Phobias
Psychoanalysts view phobias as surface manifestations of unconscious conflicts that are dis-
placed onto an object or situation with some symbolic connection to the conflict. Psycho-
analytic treatment consists of uncovering the repressed memories assumed to underlie fear
and avoidance. Dream interpretation, free association, and other psychoanalytic techniques
are used to lift repression and make unconscious conflicts conscious. Psychoanalysts may
expose patients to the object they fear (Karon & Widener, 2013). In such cases, exposure is
not expected to extinguish the fear but to help retrieve repressed conflicts and desires. Psy-
choanalytic treatments are rarely used today in the treatment of specific phobias and social
anxiety disorder.

Behavioral Treatment of Specific and Social Phobias
Behavioral treatments focus on exposure. Perhaps the best-known exposure technique is sys-
tematic desensitization, developed by Joseph Wolpe (1997). The technique has three parts.
The first is relaxation training; the second is the construction of an anxiety hierarchy in which
fear-related images are arranged according to the degree of anxiety they elicit. The third part
involves the gradual presentation of the hierarchy images while the person attempts to main-
tain a relaxed state. The rationale is that one cannot
be both fearful and relaxed at the same time. Thus, a
fearful person who can learn to relax while imagin-
ing anxiety-provoking scenes will eventually cease
being afraid.

Another behavioral technique, flooding, requires
fearful individuals to become “flooded” with emo-
tion through exposure to the feared stimulus.
Because their fear is not “reinforced” (nothing bad
actually happens), repeated exposure should even-
tually cause them to no longer feel afraid. Implo-
sive therapy is a type of flooding in which exposure
is done through imagery rather than in real life
(Schare & Wyatt, 2013).

Cognitive-Behavioral Treatment of Specific and Social Phobias
The goal of cognitive-behavioral treatment is to help clients learn to reappraise feared situa-
tions so that they can replace maladaptive cognitions (thoughts and attributions) about dan-
gerous objects or situations and fear of failure with positive cognitions (McAleavey, Caston-
guay, & Goldfried, 2014).

One cognitive-behavioral technique that has been applied to social phobia is stress inocula-
tion (Jackson, Compton, Thorton, & Dimmock, 2017). Stress inoculation begins with an edu-
cational phase in which people are taught about the role that negative self-statements play
in performance anxiety. Next, clients are taught more accurate self-statements that they can
then practice in stressful evaluative situations. In the final stage, clients are taught coping
skills designed to help them deal with, rather than avoid, evaluative situations.

lemhartley/iStock/Thinkstock
Part of the flooding technique involves
exposing the fearful individual to the
feared stimulus.

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Section 3.3 Social Anxiety Disorder (Social Phobia)

Drug Treatment for Specific and Social Phobias
Many people with performance anxiety, specific phobia, social phobia, or any other anxiety
disorder might be offered anxiolytic drugs (lysis is Greek for “dissolve”; anxiolytics dissolve
anxiety). The most popular anxiolytic medications today are the benzodiazepines. All ben-
zodiazepines are descendants of chlordiazepoxide (Librium), whose anxiolytic effects were
discovered accidentally by researchers observing how various chemical compounds affect
animal behavior (Calcaterra & Barrow, 2014; Dell’osso & Lader, 2013). Diazepam (Valium)
remains one of the most widely prescribed medications. Xanax (alprazolam), a high-potency
benzodiazepine, is a reasonable alternative medication (Calcaterra & Barrow, 2014; Griffin,
Kaye, Bueno, & Kaye, 2013). Table 3.3 contains the chemical (generic) names and the U.S.
trade (brand) names of some of the most commonly prescribed benzodiazepines.

Table 3.3: Common benzodiazepines

Common U.S. Trade Name Generic Name

Xanax alprazolam

Librium chlordiazepoxide

Tranxene clorazepate

Valium diazepam

Dalmane flurazepam

Serax oxazepam

Note: Medication trade names always begin with a capital letter. Generic names
always begin with a lowercase letter.

Even though benzodiazepines can temporarily relieve anxiety (Starcevic, 2014), they are not
without risk. Benzodiazepines are known to cause drowsiness (so they may adversely affect
school or work performance), and they may harm cognitive functioning (Chen et al., 2016;
Starcevic, 2014). Starcevic et al. (2014) note that findings about benzodiazepines causing
cognitive changes are conflicting, which may be the result of confounding variables. Benzodi-
azepines may cause sleep issues, but again the evidence is conflicting. Chen et al. (2016) found
that subjects who used long-acting benzodiazepines (that is, those with a longer half-life) had
higher quality nighttime sleep than did those who used short-acting ones or who had longer
daytime naps. They concluded that the subjects’ improvements were modest at best, and the
evidence remains inconclusive. Benzodiazepines are also associated with injury due to fall-
ing (hip fractures), especially in senior citizens (Ham et al., 2017; Starcevic, 2014). Starcevic
et al. (2014) note that antidepressants and antipsychotics also increase fall risks in senior
citizens, which indicates other factors may be involved in the increased risk. Finally, even
standard doses of benzodiazepines may cause tolerance, in which people require larger and
larger doses to achieve the same therapeutic effect (Calcaterra & Barrow, 2014). For example,
a 2013 SAMHSA study found that, on a typical day, 31 out of 174 emergency department vis-
its for drug misuse or abuse by children aged 12 to 17 (about 18%) were for benzodiazepine
abuse. If a medication not only calms you down but also relaxes your muscles, it has potential
to become physiologically addicting. Benzodiazepine abuse is a real problem, and clinicians
need to be especially aware of it.

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Section 3.4 Generalized Anxiety Disorder (GAD)

3.4 Generalized Anxiety Disorder (GAD)
People with generalized anxiety disorder (GAD) feel apprehensive about vague or future
events that may or may not occur. As soon as one cause for worry is eliminated, they become
anxious about another or they worry about several things simultaneously. Their anxiety
arises without any provocation; it is “free-floating.” Along with their many worries, people
with GAD are often restless and irritable. They describe themselves as being “on edge,” and
their muscles are habitually tense.

Etiology of GAD
Although probably the most common anxiety disorder after phobias, GAD is not frequently
diagnosed in the psychology clinic. One researcher (Allgulander, 2012; Mackenzie, Reynolds,
Chou, Pagura, & Sareen, 2011) estimated that only about 28.3% of individuals who have GAD
sought treatment over a 12-month timeframe. For older individuals who did not have a con-
current diagnosis, the percentage fell to 18%. Allgulander (2012) found that in Great Britain
only 8% of those diagnosed with GAD sought treatment. Many individuals never get to the
clinic because they “treat” themselves with alcohol or other means. The individuals who do
get to the clinic frequently receive some other diagnosis because GAD is often co-morbid with
other disorders (Allgulander, 2012; Moreno-Peral et al., 2014). (See Part 2 of Carole Ballodi’s
case in the appendix.)

Psychoanalytic Views of GAD
Psychoanalysts attribute GAD to a subconscious conflict between the ego and the id. The ego
attempts to prevent the id’s sexual impulses from breaking through to the surface because it
fears the punishment that might ensue. But the ego’s repressive strategy is only partly suc-
cessful. Sexual impulses remain unconscious but not the associated fear of punishment. The
result is that the person is always fearful and apprehensive but does not know why. Like most
psychoanalytic hypotheses, this explanation for GAD relies on clinical observations rather
than controlled research for its support.

Behavioral Views of GAD
Behaviorists view GAD as a form of classically conditioned (learned) fear that differs from a
specific phobia or social phobia only by its greater generality (Lissek et al., 2014). People with
GAD are always afraid because they are always encountering feared stimuli.

Cognitive-Behavioral Views of GAD
Cognitive psychologists propose that people with GAD fear loss of control and helplessness.
Experimental support for this theory comes from several classical experiments conducted
in the 1940s by Mowrer and Viek (1948). These researchers administered electric shocks to
rats while the animals ate (see Figure 3.3). Rats that were unable to control the shock came
to fear and avoid the area in which they were shocked, even though this was also the place
in which they were fed. Rats that were taught how to terminate the shock—given a means of
control—did not avoid the feeding area (Mineka, 1992).

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Section 3.4 Generalized Anxiety Disorder (GAD)

Because most people have sexual and aggressive thoughts at one time or another and because
everyone feels frightened or helpless sometimes, psychoanalysts, behaviorists, and cognitive
psychologists agree that GAD develops only when there is a preexisting diathesis (vulnerabil-
ity). Although there is evidence that the diathesis for GAD may be inherited (Newman, Llera,
Erickson, Przeworski, & Castonguay, 2013; Sharma, Powers, Bradley, & Ressler, 2016; Stein &
Sareen, 2015), there is also evidence that it is acquired (Newman et al., 2013). We know that
the social environment contributes to the disorder because GAD is more common in danger-
ous environments, such as in war-torn areas and inner-city ghettos (Sheidow, Henry, Tolan, &
Strachan, 2014). (See the accompanying Highlight.)

Figure 3.3: An experiment illustrating the consequence of controllability

The “executive” rat can control the electric shock to its tail by turning a wheel. The “subordinate” rat
has no control over the shock. The control rat receives no shock at all. Neither the control rat nor the
executive rat avoids the feeding place. The subordinate, by contrast, becomes vigilant and anxious.

Source: J. Maser and M. E. P. Seligman (Eds.), Psychopathology: Experimental Models. San Francisco: W.H. Freeman, 1977. Reprinted by
permission.

“Executive” rat

To shock control To shock source No connection
to shock source

“Subordinate” rat Control rat

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Section 3.4 Generalized Anxiety Disorder (GAD)

Therapeutic Treatment for GAD
Therapeutic treatment for GAD is determined largely by the theoretical orientation of the
practitioner. Psychoanalysts use free association, dream interpretation, and other techniques
to help people confront their repressed impulses and conflicts, whereas practical, traditional
behavioral clinicians use desensitization and other forms of exposure therapies. Relaxation
training may help people reduce their level of anxiety in general, especially if it is used in
conjunction with cognitive therapy (Heimberg & Magee, 2014; Lang, 2004). Cognitive inter-
ventions are usually aimed at the chronic worry that is characteristic of people with GAD
(Hanrahan, Field, Jones, & Davey, 2013). In a safe therapeutic environment, clients can face
the anxiety-producing images, thoughts, and ideas directly. They learn to use coping tech-
niques to control their worrying. Behavioral and cognitive treatments are reported to be
about equally effective in the treatment of GAD, and both are better than no treatment at all
(Newman & Fisher, 2013).

Drug Treatment for GAD
Anxiolytics can be prescribed for GAD; however, the selective serotonin reuptake inhibitors
(SSRIs) fluoxetine (Prozac) and paroxetine (Paxil) are preferred because of their lack of phys-
iological addiction potential (Bandelow et al., 2013; Newman et al., 2013). Of course, even
when medication relieves anxiety temporarily, it does nothing to overcome helplessness or to
teach new coping skills.

Highlight: How Does Hollywood Portray Anxiety Disorders?

Have you ever seen the movie Vertigo? It stars Jimmy Stewart as a police detective who has
a crippling case of acrophobia—an extreme fear of heights. How about Marathon Man, in
which Sir Laurence Olivier stars as a sadistic Nazi dentist who tortures Dustin Hoffman in
an effort to get him to reveal information related to a stash of stolen diamonds? He drills
into Hoffman’s teeth without using Novocain, among other horrors. How about any of the
Peanuts specials? In virtually all of them, Charlie Brown is afraid that something disastrous
will occur to him in the future, so much so that he either avoids situations (asking the little
red-haired girl out) or sets himself up for failure (though, to his credit, he keeps trying). How
accurate are these portrayals of acrophobia, an event that could trigger a dental phobia, and
a child’s experience with what might appear to be GAD? As with anything else, Hollywood
tends to exaggerate and misinterpret anxiety disorders, as well as mental illness in general.
Although Vertigo is a classic film, how likely is it that a police detective could hold down his
job if he suffered from acrophobia? How realistic is it to think that people develop dental
phobias because of sadistic dentists just waiting to work on their patients without using
anesthetic? And how accurate is the portrayal of Charlie Brown’s near-constant experience
of anxiety? He never succeeds in anything; indeed, he cannot even buy a good Christmas tree.
His creator, Charles Schulz, got one aspect of GAD right: Even though Charlie Brown rarely if
ever succeeds, and is convinced he will always fail, he never stops trying. Is this because of
his determination to succeed, his optimism that he will eventually succeed, or his inability to
learn from past experiences?

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Section 3.5 Panic Disorder and Agoraphobia

3.5 Panic Disorder and Agoraphobia
You suddenly feel very scared. Your heart beats so hard you think it will burst through your
chest. You can barely catch your breath. Your mouth is totally dry; you are dizzy and shaking.
You feel like you are going to faint, maybe even die. This is panic. Panic is not, by itself, abnor-
mal. It is the intense fear produced by an especially frightening situation: You lose control of
your car on an icy road; you hear footsteps following you down a dark street. It is perfectly
normal to feel panic in such situations.

Panic attacks are common occurrences; they may occur as part of everyday life. They are
also associated with many psychological disorders (Meuret, Kroll, & Ritz, 2017). When panic
attacks become recurrent and when people become so anxious about them that they change
their lives to avoid them, then panic attacks can become a full-blown panic disorder. In the
United States and in several European countries, panic disorder affects between 2% and 3%
of adults (APA, 2013; Inoue, Kaiya, Hara, & Okazaki, 2016), and women are twice as likely
as men to receive the diagnosis (APA, 2013). Panic disorder and related anxiety conditions
appear to be universal, occurring in all cultures (de Jonge et al., 2016). (See Part 3 of Carole
Ballodi’s case in the appendix.)

Panic disorder usually begins in early adulthood, and most people report clear memories
of their first panic attack. This initial attack, which may come on without warning, is often
followed by further attacks. In such cases, the person comes to associate panic attacks with

the situations in which they occur. Fearing further
attacks, the person avoids these situations. Over time,
panic attacks occur in other situations, which must
then also be avoided. As the number of situations that
must be avoided increases, the person’s movements
become increasingly restricted. In this way, panic dis-
order may give rise to agoraphobia. About one third
to one half of people diagnosed with panic disorder
develop agoraphobia (Wittmann et al., 2014).

The term agoraphobia comes from the Greek for “fear
of the marketplace.” The lifetime prevalence for ago-
raphobia has been estimated at between 1% and 7%
(Taylor & Asmundson, 2016). At least 20% of those
who have agoraphobia are currently in treatment,
based on one survey (National Institute of Mental
Health, 2011). This makes it by far one of the most
common phobias seen in the psychology clinic (Marks,
1987). Agoraphobia begins in late adolescence or
early adulthood and is twice as likely to appear in
women (APA, 2013). People with agoraphobia worry
about having panic-like symptoms or panic attacks in
places or situations from which escape might be dif-
ficult (or embarrassing) or in which help might be
unavailable. (See Figure 3.4.) They avoid feared situ-
ations in the hope that doing so will help them avoid
panic attacks. Some people with agoraphobia cannot

Garo/Phanie/SuperStock
People who have agoraphobia often
avoid going out in public, as they are
afraid of having panic attacks in pub-
lic places or in situations in which
escape would be difficult.

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Section 3.5 Panic Disorder and Agoraphobia

avoid fearful situations, and they enter feared situations full of dread. Agoraphobic people,
men particularly, may resort to alcohol or drugs just to get by. In extreme cases, they may
escape by suicide (Henriksson et al., 1996), although this is rare (Friedman, Jones, Chernen, &
Barlow, 1992). In the DSM–IV–TR, agoraphobia was diagnosed with panic disorder as a speci-
fier: panic disorder with or without agoraphobia. In the DSM–5, agoraphobia is its own diag-
nosis and is diagnosed whether panic disorder is present or not. If both panic disorder and
agoraphobia are present, then both diagnoses are assigned.

Figure 3.4: Causes of panic disorder and agoraphobia

Agoraphobia is determined by cultural, social, and pragmatic factors, and moderated by the presence or
absence of safety signals.

Source: “Panic Disorder and Agoraphobia,” by K. S. White and D. H. Barlow, in Anxiety and Its Disorders: The Nature and Treatment of
Anxiety and Panic, 2nd ed., by D. H. Barlow. New York: Guilford Press. Copyright © 2002 by Guilford Press. Reprinted by permission.

Generalized
psychological vulnerability

Due to life events

Stress

Focused on somatic sensations

Anxious apprehension

Unexplained physical sensations
are dangerous

Specific psychological vulnerability

False alarm

Panic disorder Agoraphobia

Learned alarm

Determined by cultural, social,
and pragmatic factors, and
moderated by presence or
absence of safety signals

Development of agoraphobia

Associated with somatic sensations
(interoceptive cues)

(e.g., pounding heart)

Generalized
biological vulnerability

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Section 3.5 Panic Disorder and Agoraphobia

Etiology of Panic Disorder
About 1% to 7% of people will develop panic disorder at some time (APA, 2013; Kimmel,
Roy-Byrne, & Cowley, 2015; Taylor & Asmundson, 2016); onset usually occurs between late
adolescence and the mid-30s and is more common in women. There is indirect evidence that
some people are predisposed to develop panic disorder. It seems, for example, that panic
disorder runs in families and that there is a greater concordance for such disorders among
identical than fraternal twins (Shimada-Sugimoto, Otowa, & Hettema, 2015). There may even
be a genetic component for panic and/or panic disorders (APA, 2013; Shimada-Sugimoto et
al., 2015). Because of the genetic evidence, considerable research has been devoted to under-
standing the physiological causes of panic disorder (Maron, Hettema, & Shlik, 2010). The bulk
of this research focuses on the way certain physiological processes may interact with cogni-
tions to produce panic disorder.

People prone to panic attacks may have a general tendency to appraise benign physiological
sensations as threatening (Meuret et al., 2017). They may focus on their body’s sensations
too often and may misinterpret them as harmful. Panic-prone individuals are highly sensitive
to their internal physiology. Whenever they detect any change, no matter how slight, they
become fearful.

Therapeutic Treatment for Panic Disorder
Psychological treatment approaches vary according to theoretical orientation. They are aimed
at one or more of the variables that contribute to the vicious “fear of fear” cycle: the preoc-
cupation with internal bodily states, excessive physiological responsiveness to threat, faulty
cognitive appraisals, or the quickly spiraling loss of control. The goal of treatment for panic
disorder is to break the vicious cycle that maintains it. Taylor and Asmundson (2016) have
suggested an integrated treatment program for panic disorder that treats the cognitive, physi-
ological, and behavioral aspects of panic disorder rather than focusing on only one element.

Drug Treatment for Panic Disorder
Medications are often prescribed in an attempt to prevent emergency reactions, or alarm
reactions (see Chapter 2), that trigger panic attacks (see Figure 3.5). Early observations sug-
gested that tricyclic antidepressant medications blocked panic attacks but had little effect on
general anxiety, which responded to benzodiazepines (Klein, 1964). This observation was
taken as support for the idea that the fear felt in a panic attack is physiologically different
from the anxiety felt in GAD. However, we now know that SSRIs such as fluoxetine (Prozac)
or paroxetine (Paxil) (Kimmel et al., 2015), or powerful benzodiazepines like alprazolam
(Xanax), are helpful to people who have panic attacks with agoraphobia (Van Apeldoorn, Van
Hout, Timmerman, Mersch, & den Boer, 2013). Thus, fear and anxiety may not be as different
as once thought. A combination of medications and psychological treatment can be effective
in treating panic disorder with agoraphobia (Van Apeldoorn et al., 2013).

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Section 3.5 Panic Disorder and Agoraphobia

Figure 3.5: Nervous system pathway

The alarm reaction starts a chain of physical responses through both hormonal and nerve pathways
(ACTH = adrenocorticotropic hormone).

Source: Adapted from S. Schwartz, Abnormal Psychology: A Discovery Approach. Mountain View, CA: Mayfield Publishing Company, 2000,
Figure 4.1, p. 140.

Stressor Hypothalamus

Autonomic nervous system

Nervous System Pathway

Pituitary gland

Endocrine Pathway
(via bloodstream)

Releases
hormone
(ACTH)

Release hormones

Increase heart rate

Increase blood pressure

Increase blood sugar (glucose)

Decrease antibody production

Increase fatty acids in blood

Increase perspiration

Adrenal glands

Release hormones
Increase heart rate
Increase blood pressure

Increase body temperature

Increase oxygen consumption

Adrenal glands

Muscles tense

Heart rate increases

Blood pressure increases

Breathing is deeper and faster

Digestion of food stops

Perspiration increases

Secretion of saliva decreases

Releases more red blood cells

Increases blood clotting ability

Produces more white blood cells

Spleen

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Section 3.6 Obsessive-Compulsive Disorder (OCD)

3.6 Obsessive-Compulsive Disorder (OCD)
Obsessions are unwelcome, intrusive, and recurring thoughts or images that appear irratio-
nal and uncontrollable to the individual experiencing them. Compulsions are repetitive ritu-
alistic behaviors (counting, cleaning, checking) that a person feels driven to perform to ward
off some calamity. Compulsive people feel obligated to dress, clean house, or fold clothes in
just the “right” way. Their rituals often involve repetitions: counting certain numbers, touch-
ing some religious icon, or going back several times to check that the doors are locked and
the lights have been switched off. Often, compulsions are linked to obsessive thoughts. Thus,
a person obsessed with infection and contamination may develop compulsive cleanliness
rituals. All of us have obsessive thoughts at times as
well as minor compulsions (Grant, 2014), but peo-
ple with obsessive-compulsive disorder (OCD)
have them often.

Before the DSM–5, obsessive-compulsive disorder
was classified as an anxiety disorder. In the DSM–5,
the disorder was moved to the “Obsessive-Compul-
sive and Related Disorders” chapter, since the dis-
orders here are related to each other diagnostically
(APA, 2013). Despite the new classification, OCD
still has many symptoms in common with anxiety
disorders. In particular, if those with OCD are pre-
vented from performing compulsive rituals, the
typical result is intense anxiety.

Etiology of OCD
Obsessive-compulsive disorder affects anywhere from 1.2% of the U.S. population (APA, 2013)
to as much as 2% to 3% of the population (Grant, 2014). Women are slightly more likely than
men to be affected by OCD (APA, 2013). Even though it does occur in childhood, OCD generally
makes its first appearance in late adolescence or early adulthood, often in conjunction with
some significant life event, such as pregnancy or the start of a new job. The specific nature of
obsessions and compulsions varies across cultures. In some cultures, obsessions and compul-
sions have religious themes. In most modern countries, obsessions center around dirt or con-
tamination (Olatunji, Ebesutani, Haidt, & Sawchuk, 2014), and compulsions center around
checking and cleaning (Coleman et al., 2011; Radomsky, Ashbaugh, Gelfand, & Dugas, 2008).

The diagnosis of OCD is often complicated because clients show considerable comorbidity
(Gillan, Fineberg, & Robbins, 2017). Sometimes it is difficult to determine whether an indi-
vidual has depression, a phobia, OCD, GAD, or all four disorders (Hunt & Andrews, 1995). The
diagnosis is often based on the presumed etiology. People with OCD get no pleasure from
their compulsive behaviors, and they typically know that their obsessions and compulsions
are odd and irrational. Like the anxiety disorders, OCD appears to run in families (Pauls,
Abramovitch, Rauch, & Geller, 2014). Some family studies have found OCD to be related to
anxiety disorders and depression (Bienvenu, Busti, Magill, Ferraguti, & Capogna, 2012). See
the accompanying Highlight.

Adam Gault/Photodisc/Thinkstock
An obsession with infection and con-
tamination may result in compulsive
cleanliness rituals.

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Section 3.6 Obsessive-Compulsive Disorder (OCD)

Psychoanalytic Views of OCD
According to psychoanalytic theory, experiences that produce obsessive-compulsive behav-
ior take place early in life, when children learn to suppress their id impulses because of the
demands of society. In toilet training, for example, children must learn to replace their instinc-
tual impulses to defecate anywhere with socially approved toileting behaviors. The resolution
of this conflict between a child’s biological impulses and society’s demands has important
implications for later behavior. Children who are trained harshly may become obsessively
orderly and conformist and remain this way throughout their lives. As is the case with other
psychoanalytic explanations, there is little experimental evidence for the relationship between
toilet training (or other early conflicts) and the later development of OCD.

Behavioral and Cognitive-Behavioral Views of OCD
Once compulsive behaviors are established, it is not difficult to see how they may be reinforced
by their anxiety-reducing consequences. Hand washing reduces worry about germs and ill-
ness; compulsive checking reduces concern about potential burglary or fire. But how do com-
pulsive rituals get started in the first place? One possibility is that compulsions are learned
“superstitiously” (Skinner, 1948). Pure coincidences (rubbing a lucky rabbit’s foot before win-
ning a sporting event) may lead people into ritualistic behavior patterns (rubbing a rabbit’s
foot before every contest). This explanation seems inadequate, however, because it fails to
explain why all of us are not obsessive-compulsive, given the occurrence of such coincidences
in everyone’s lives. Another problem with the superstitious-learning explanation is that it fails
to explain obsessions. Obsessive thoughts do not reduce anxiety—usually they increase it.

In contrast to behavioral theorists, cognitive behaviorists emphasize the importance of obses-
sive thoughts. From the cognitive-behavioral viewpoint, we all have distressing thoughts at

Highlight: What Is the Difference Between Being an Avid Fan
and Having an Unhealthy Obsession?

As you have just read, obsessions are unwelcome, intrusive, and recurring thoughts or
images that appear irrational and uncontrollable to the individual experiencing them. One
might say, “Oh, of course I can easily distinguish between the two.” Let’s discuss this. You
have all had an “earworm,” a song or a tune that is running constantly through your head,
like elevator music. The award-winning song “Don’t Worry, Be Happy” is an example of such
a song. Heard often on radio, through music streaming services, and on commercials, it
became so ubiquitous that it was impossible to avoid, much less get out of one’s head. This
can be unwelcome (especially if you dislike Bobby McFerrin), intrusive, recurring, and, yes,
uncontrollable. Note, however, that the term song or tune is not a part of the definition of an
obsession. So, can we classify having a song stuck in your head as an obsession? What if you
are a Star Wars devotee? Suppose you see each new movie the day it opens, fully dressed
as your favorite Jedi knight. Is this an obsession, or simply fandom? These behaviors would
classify as diagnosable obsessions if they caused you marked anxiety or distress (APA, 2013).
Like many other concepts we will discuss, the line between what is deemed abnormal and
what is deemed fandom, really liking something, or an earworm is fine and at times blurred.

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Section 3.6 Obsessive-Compulsive Disorder (OCD)

one time or another, but people with a tendency toward anxiety are unable to dismiss them
from their minds (Couge & Lee, 2014). They dwell on the unwanted thoughts, which makes
them feel even more anxious. Compulsive rituals arise to distract people from obsessive
thoughts and reduce the anxiety that accompanies them (Grant, 2014).

Biological Views of OCD
Encephalitis, brain tumors, and closed-head injuries can produce obsessive-compulsive behav-
ior (Karadag et al., 2011; Veale & Roberts, 2014). This suggests that the disorder is at least
partly physiological. The precise nature of the biological cause may lie in the metabolism of the
neurotransmitter serotonin, as well as dopamine and glutamate (Bokor & Anderson, 2014b).
Antidepressant drugs that block serotonin reuptake, such as fluoxetine (Prozac), reduce the
intensity and severity of obsessive-compulsive disorder (Bokor & Anderson, 2014b). In the
reuptake process, a neurotransmitter is quickly brought back to the same neuron from which
it was released a short time earlier. (See Figure 3.6.) Serotonin is involved with inhibition and
restraint, and with regulating appetite and sexual and aggressive behaviors. This suggests that
OCD may result from a defect in serotonin metabolism (Stein & Fineberg, 2007).

Figure 3.6: Serotonin receptors and reuptake transporters

Serotonin secreted by a synaptic cell binds to receptors on a postsynaptic cell and directs the postsynaptic
cell to fire or stop firing. Serotonin levels in synapses are reduced by autoreceptors, which direct the
cells to inhibit serotonin production, and reuptake transporters, which absorb the neurotransmitter.
Antidepressants, such as Prozac and Paxil, increase synaptic serotonin by inhibiting its reuptake.
Antidepressants can be similarly used to inhibit the reuptake of the neurotransmitter norepinephrine.

Source: Adapted from S. Schwartz, Abnormal Psychology: A Discovery Approach. Mountain View, CA: Mayfield Publishing Company, 2000,
Figure 4.9, p. 169.

Presynaptic
cell

Serotonin

Reuptake
transporter

Synaptic
cleft

Serotonin
receptors

Regulatory
signal

Postsynaptic cell

“Stop production”
signal

Serotonin in action

Autoreceptor

get83787_03_c03_061-090.indd 82 2/16/18 4:38 PM

Section 3.6 Obsessive-Compulsive Disorder (OCD)

Therapeutic Treatment for Obsessive-Compulsive Disorder
As with other disorders, treatment modalities depend on the orientation of the treating clini-
cian. Although a psychoanalytic approach is still used by some, the biological and cognitive-
behavioral treatment approaches appear to be most helpful for individuals who have OCD.

Psychoanalytic Treatment for OCD
Freud considered OCD to be among the most difficult disorders to treat. This was ironic, he
thought, because people with obsessive-compulsive disorder knew they were “sick,” hated
their symptoms, and were highly motivated to change. Freud’s initial impressions have
proven accurate over time; OCD remains one of the most difficult anxiety disorders to treat.
Psychoanalytic treatment attempts to make conscious the repressed conflicts presumed to be
responsible for obsessive-compulsive behavior. Psychoanalysts do not attempt to inhibit the
intrusive thoughts and ritualistic behaviors directly because they believe that these symp-
toms are keeping even more debilitating anxiety in check.

Behavioral and Cognitive-Behavioral Treatment of OCD
The behavioral approach to OCD treatment usually consists of exposure and response pre-
vention (Veale & Roberts, 2014). Clients who fear germs may be asked to enter a hospital,
touch the walls, and shake hands with patients while refraining from their normal ritualistic
hand-washing response. Inhibiting hand washing causes these individuals to experience the
anxiety that hand washing helps them to avoid. Because nothing untoward actually happens,
their anxiety is not reinforced. Repeated exposure should extinguish the anxiety associated
with the obsession.

In a related manner, behavioral psychologists have treated obsessions using thought stop-
ping, which requires clients to say “stop” to themselves each time they begin to dwell on
an obsessive thought, and then attempt to distract themselves and think of something else
that competes with the obsessive thoughts. Perhaps the major problem faced by behavior
therapists treating OCD is getting clients to complete the treatment. Some people find behav-
ioral treatment too threatening and drop out (Öst, Havnen, Hansen, & Kyale, 2015; Veale &
Roberts, 2014). Cognitive restructuring may help some clients persist with therapy because
it provides them with a set of motivating self-statements that they can use to help deal with
anxiety-producing situations, including the anxiety associated with the therapy itself (Pon-
niah, Magiati, & Hollon, 2013).

Drug Treatment for OCD
People with OCD gain little relief from benzodiazepines or other anxiolytics. However, antide-
pressant medications—SSRIs like fluoxetine (Prozac) and the tricyclic antidepressant clomip-
ramine (Anafranil)—have proven to be quite effective (Veale & Roberts, 2014). These medi-
cations suppress symptoms; they do not teach people new behaviors. Clients treated solely
with medication may require medication indefinitely (Fineberg, Reghunandanan, Brown, &
Pampaloni, 2013). They also run the risk of serious side effects and relapse when the drug is
terminated (Veale & Roberts, 2014).

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Section 3.6 Obsessive-Compulsive Disorder (OCD)

Disorders Related to Obsessive-Compulsive Disorder
Located within the “Obsessive-Compulsive and Related Disorders” chapter in the DSM–5 is a
new disorder, hoarding disorder, which involves a persistent difficulty discarding or parting
with possessions due to a perceived need to save them. Individuals with this disorder experi-
ence significant distress associated with discarding these items if indeed they must. In the
DSM–IV–TR, hoarding was included as a possible symptom of obsessive-compulsive personal-
ity disorder. It was also noted that extreme hoarding (which was not clearly defined) might
occur in obsessive-compulsive disorder (APA, 2000). The DSM–5 notes that data available
at the time of publication (2013) did not indicate that hoarding was a variant of obsessive-
compulsive disorder or another mental disorder. The DSM–5 team determined that this disor-
der warranted its own category.

In some instances, the individual’s entire home is filled with unnecessary and/or unused
items like loads of clothes that are never worn or useless items like broken furniture, dishes,
and toys. The hoarding may be so severe that parts of the individual’s home become inacces-
sible. Furniture may be covered with hoarded items, resulting in a fire hazard or worse. The
individual may be unable to leave his or her home due to the quantity of hoarded items. In
addition, the costs involved with purchasing so many things can be considerable.

Since hoarding disorder is a newly diagnosed condition, some clinicians attempt to treat it in
a fashion similar to the treatment for obsessive-compulsive disorder, since the two disorders
appear to have some aspects in common. This includes using behavioral as well as cognitive-
behavioral techniques, and SSRIs such as fluoxetine (Prozac). Sometimes using professional
“declutterers” can be successful. Interestingly, it is not so much the hoarding that causes dis-
tress as it is the requirement of discarding so many useless objects. Hoarding disorder is asso-
ciated with significant impairment; it may have unique neurobiological correlates and may
respond to clinical intervention (Mathews et al., 2016; Morein-Zamir et al., 2014; Williams &
Viscusi, 2016). The accompanying Highlight describes a well-known case of hoarding.

Highlight: The Strange Case of the Collyer Brothers

Perhaps one of the most famous hoarding cases is that of the Collyer brothers, who were
found dead in their Harlem, New York brownstone in 1947. Homer and Langley Collyer were
born in 1881 and 1885, respectively, to Dr. Herman Livingston Collyer, a gynecologist at
Bellevue Hospital, and Susie Gage Frost, a former opera singer. According to some accounts,
Dr. Collyer was rather eccentric. For example, he would often paddle a canoe from Manhattan
to the City Hospital on Blackwell’s Island (now called Roosevelt Island) where he sometimes
worked. In 1919, Dr. Collyer left the family without explanation. He died in 1923, and his
wife died in 1929. Upon their parents’ deaths, the brothers inherited all their property and
possessions and became shut-ins, never leaving the house, sealing themselves up in their
house, away from the world.

(continued)

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Section 3.6 Obsessive-Compulsive Disorder (OCD)

Highlight: The Strange Case of the Collyer Brothers
(continued)

There were rumors that the brothers were bathing themselves in riches when in fact their
eccentricities moved closer to mental illness. They had their phone disconnected in 1917,
stating that they had been billed for long-distance calls they didn’t make. When their gas
was turned off in 1928, they lived without heat or hot water, using kerosene for cooking and
lighting. When vandals used rocks to smash their windows, the brothers boarded up the
windows rather than fixing them or asking someone to fix them. In fact, asking someone
in was impossible, as the brothers had collected so much garbage and other items that it
became virtually impossible to move in their apartment. As interest in the rather unusual
brothers increased, the younger brother, Langley, became more anxious and paranoid. He
began to arrange his collection of junk into a series of mazes, tunnels, and booby traps lest
anyone try to enter.

On March 21, 1947, the New York City Police Department received an anonymous call that
there was a dead body in the Collyer house. Once they finally breached the front door, they
found it blocked by stacks of boxes. The basement entrance was similarly blocked. After
forcing open a first-floor window, they found the house filled with piles of junk and trash,
and overrun with rats. Around noon of
that day, officers forced open a window
on the second floor, where they found
Homer Collyer dead. He had not eaten or
drunk any water for days. There was no
sign of Langley. After 10 days of searching
the house, and subsequently removing
two organs, multiple guns, bowling balls,
pickled human organs in jars, and eight
live cats (all found in just two rooms on
the first floor), they finally found Langley,
crushed to death by one of his booby
traps (York, 2012).

Of course, this is an extreme case of
hoarding disorder that ended tragically,
but perhaps we can look at this in
another way. According to the blog post
from which the details of this story were
drawn, these men just wanted to be left
alone. Is this a sign of a mental illness, or
were they just extremely eccentric individuals? Did their father’s leaving without explanation
and their parents’ death cause negative reactions? Suppose they just liked to collect various
things. After all, don’t all of us save important papers and articles at times because we know
we will read them eventually, or use them for a term paper or for research (your author,
like many others, does this)? Is this hoarding? Did the brothers die happily? Perhaps most
important, we must ask again: When does an example of extreme behavior such as this cross
the line into a diagnosable illness?

New York Daily News/Getty Images
When the police were finally able to enter
the Collyer brothers’ brownstone, they
found garbage piled to the ceiling.

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Chapter Summary

Anxiety, Fear, and Panic
• Anxiety is a negative emotional state marked by foreboding and somatic signs of ten-

sion, such as a racing heart, sweating, and difficulty breathing.
• Fear is a negative emotion that occurs in response to some immediate threat or

danger.
• Panic is the intense fear produced by an especially frightening situation.
• Anxiety disorders not only seem to occur with one another, but they are also fre-

quently accompanied by depression.

Specific Phobias
• A phobia consists of a persistent and irrational fear coupled with a desire to avoid

the feared object or situation.
• Specific phobias are determined by the interaction of cultural and social norms,

learning experiences, and cognitive components.

Social Anxiety Disorder (Social Phobia)
• Performance anxiety occurs in both Western and Eastern cultures.
• Performance anxiety is rarely the result of a traumatic experience. It is more often

related to shyness and lack of confidence.
• Social anxiety disorder (social phobia) begins in adolescence and represents an

extreme form of performance anxiety in which fear of social evaluation can produce
panic attacks and can severely restrict a person’s life.

• Social phobias usually develop slowly in people who either inherit a tendency
toward shyness or become shy early in life.

• No matter what treatment method is used, an important factor in helping someone
to overcome any problem is to establish a trusting relationship.

• People with phobias habitually avoid the feared object or situation. Successful treat-
ment almost always requires overcoming this avoidance and getting the client to
confront his or her fear.

• Anxiolytic drugs (antianxiety medications) may also be used to treat phobias.

Generalized Anxiety Disorder (GAD)
• People with GAD are not fearful of specific objects or situations; they are apprehen-

sive about everything.
• Many cases of GAD never get to the clinic because people “treat” themselves with

alcohol.
• Psychoanalysts, behaviorists, and cognitive psychologists agree that GAD develops

only when there is a preexisting vulnerability.
• Psychoanalysts attribute GAD to a conflict between the ego and the id.
• Some behaviorists view GAD as a form of classically conditioned (learned) fear that

differs from a simple phobia only in its greater generalization.
• Anxiolytics are frequently prescribed for GAD.

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Chapter Summary

Panic Disorder and Agoraphobia
• A panic attack consists of an abrupt and intense feeling of fear accompanied by

somatic symptoms, usually in the absence of any objective danger.
• When panic attacks become recurrent and when people become so anxious about

them that they change their lives to avoid them, panic attacks can become a full-
blown panic disorder.

• People prone to panic attacks may have a general tendency to appraise benign physi-
ological sensations as threatening.

• Panic disorder usually begins in early adulthood; it is rare in children.
• There is strong evidence that panic disorder is hereditary.
• People with agoraphobia worry about and avoid having panic-like symptoms in

places or situations from which escape might be difficult (or embarrassing) or in
which help might be unavailable.

• Agoraphobia begins in early adulthood and is particularly common in older women.
• Psychoanalysts assume that agoraphobia manifests in children who are fearful by

nature. These children experience an unconscious conflict, wherein they wish to be
independent, but they also fear being on their own.

• Cognitive restructuring and relaxation training are two therapy modalities used to
treat panic disorder and/or agoraphobia.

• Long-acting benzodiazepines are helpful in treating people who have panic disorder
and/or agoraphobia.

Obsessive-Compulsive Disorder (OCD)
• Obsessions are unwelcome, intrusive, and recurring thoughts or images that are

recognized as irrational and are uncontrollable to the individual experiencing them.
• Compulsions are repetitive ritualistic behaviors (counting, cleaning, checking) that a

person feels driven to perform to ward off some calamity.
• OCD generally makes its first appearance in late adolescence or early adulthood,

often in conjunction with some significant life event.
• According to psychoanalytic theory, the special experiences that produce obsessive-

compulsive behavior take place early in life, when children learn to suppress their
id impulses because of the demands of society. Psychoanalysts do not attempt to
inhibit the intrusive thoughts and ritualistic behaviors directly because they believe
that these symptoms are keeping even more debilitating anxiety in check.

• Behaviorists note that compulsive behaviors are reinforced by their anxiety-
reducing consequences and often treat OCD with exposure and response prevention
therapy.

• According to cognitive behaviorists, people with a vulnerability for anxiety are
unable to dismiss distressing thoughts from their minds. Compulsive rituals arise
to distract them from obsessive thoughts and reduce the anxiety that accompanies
them.

• Encephalitis, brain tumors, and closed-head injuries can all produce obsessive-
compulsive behavior. People with obsessive-compulsive disorder gain little relief from
antianxiety drugs, although some seem to respond to antidepressant medications.

• Hoarding disorder is related to obsessive-compulsive disorder; in this disorder, the
individual has persistent difficulty discarding or parting with possessions due to a
perceived need to save the items. Significant distress is associated with discarding
such items.

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Chapter Summary

• Some clinicians attempt to treat hoarding disorder in a fashion similar to treatment
for OCD, since the two disorders appear to have some aspects in common.

• Behavioral as well as cognitive-behavioral treatment techniques, and SSRIs such as
Prozac, may be useful.

Critical Thinking Questions

1. Everyone has a superstition or two (or perhaps even more!). Discuss the difference
between superstitious behavior (yours, or perhaps a friend’s) and a phobia. How do
the two differ?

2. Discuss some of the more common venues in which social anxiety disorder could
present itself. How would you best handle this if a client came to see you with this
concern?

3. Some people say that GAD should have been removed from the DSM–5 because it is
too common a disorder and is difficult to accurately define. Discuss and give your
views on this.

4. Like many people, you most likely enjoy collecting certain things: souvenirs from a
trip, baseball cards, comics, your child’s drawings and accomplishments. You may
have significantly large collections. When does this become hoarding, and then
hoarding disorder? Should hoarding disorder in fact be a diagnostic category?

5. No doubt you have gone back inside your house or apartment to check the stove to
make sure it’s off, to check the lights, and so on. What is the difference between this
kind of behavior and OCD?

6. Some observers believe that certain phobias, such as a fear of snakes and acrophobia
(fear of heights) are innate. Discuss your views on this belief.

Key Terms
agoraphobia The fear of being in a place or
in a situation where escape might be dif-
ficult, impossible, or embarrassing if a panic
attack or panic symptoms occur.

anxiety A negative emotional state marked
by a feeling of foreboding and bodily signs of
tension such as a racing heart, sweating, and
difficulty breathing.

anxiety disorder Any of a number of
disorders characterized by feelings of fear,
dread, or panic plus physiological symptoms
such as racing heart, sweating, and difficulty
breathing.

benzodiazepines A class of antianxiety
medications.

classical conditioning A learning proce-
dure in which a neutral stimulus is paired
repeatedly with a fear-inducing stimulus. In
time, the neutral stimulus will elicit the fear
response even in the absence of the primary
fear-inducing stimulus.

compulsions Repetitive ritualistic behav-
iors (counting, cleaning, checking) that a
person feels driven to perform to ward off
some imagined or unknown calamity.

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Chapter Summary

emergency reaction Another name for an
alarm reaction; how we react in response to
a dangerous situation.

flooding A therapeutic technique that
requires fearful individuals to become
“flooded” with emotion through exposure to
their most feared stimulus in order to realize
that the feared outcome does not occur.

generalized anxiety disorder (GAD) An
anxiety disorder characterized by “free-
floating” anxiety not specific to real objects
or situations but to real or imagined uncon-
trollable future events or situations.

hoarding disorder A disorder related to
OCD, in which the individual has persistent
difficulty discarding or parting with posses-
sions due to a perceived need to save the
items; significant distress is associated with
discarding the items if indeed they must.

implosive therapy A type of flooding in
which exposure is done through imagery
rather than in vivo (real life).

limbic system A complex set of brain struc-
tures that controls our emotions.

obsessions Unwelcome, uncontrollable,
intrusive, and recurring thoughts or images
that are recognized as irrational to the indi-
vidual experiencing them.

obsessive-compulsive disorder (OCD) A
disorder in which individuals suffer from
obsessions and compulsions that may take
up the majority of their time and interfere
with daily functioning.

panic attack An abrupt and intense feeling
of fear accompanied by bodily symptoms,
usually in the absence of any objective
danger.

panic disorder An anxiety disorder char-
acterized by recurrent, unexpected panic
attacks.

performance anxiety The fear of speaking
or performing in front of other people.

response prevention A form of therapy for
OCD in which the individual encounters or is
exposed to the feared stimuli while refrain-
ing from the usual compulsive behavior.

social anxiety disorder (social pho-
bia) An anxiety disorder in which individu-
als have an excessive concern about being in
social situations where they may be evalu-
ated by others.

specific phobia An anxiety disorder in
which a person experiences extreme anxi-
ety or panic when confronted with a spe-
cific object or situation that triggers the
response.

stress inoculation A cognitive-behavioral
treatment modality in which people are
taught about the role that negative self-
statements play in performance anxiety;
more accurate self-statements that they can
then practice in stressful evaluative situ-
ations; and coping skills designed to help
them deal with, rather than avoid, evaluative
situations.

systematic desensitization A behavioral
treatment modality that attempts to reduce
an individual’s anxiety through relaxation
techniques paired with progressive expo-
sure to a hierarchical presentation of feared
stimuli.

thought stopping A cognitive-behavioral
treatment intervention that instructs clients
to say “stop” to themselves each time they
begin to dwell on an obsessive thought.

get83787_03_c03_061-090.indd 89 2/16/18 4:39 PM

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