Abnormal psychology-i

Module2: stress disorders and anxiety disorders 10 hours

Stress and stressors- coping strategies, stress disorders: adjustment disorder-post traumatic stress
disorder; anxiety disorder: specific phobia, social phobias, generalized anxiety disorders, obsessive
compulsive disorder. Causal factors

Stress and stressors

Remember the distinction between stressors and stress, which can be tricky: stressors (like an exam)
cause stress (the physiological and psychological reaction that comes from the exam).

With its deadlines, interpersonal tensions, financial pressures, and everyday hassles, daily life places
many demands on us.

We are all exposed to stress, and this exposure affects our physical and our psychological well-being.

Sometimes even leisure activities can be stressful. For example, a loss in the Superbowl is followed
by an increase in heart attacks and death over the following two weeks in the losing team’s city. And
watching a stressful soccer match more than doubles the risk of having acute cardiovascular
problems.

How are you affected by stress? Does it make you anxious? Does it give you migraines?

The field of health psychology is concerned with the effects of stress and other psychological factors
in the development and maintenance of physical problems. Health psychology is a subspecialty
within behavioral medicine.

A behavioral medicine approach to physical illness is concerned with psychological factors that may
predispose an individual to medical problems. These may include such factors as stressful life events,
certain personality traits, particular coping styles, and lack of social support. Within behavioral
medicine there is also a focus on the effects of stress on the body, including the immune, endocrine,
gastrointestinal, and cardiovascular systems.

But stress affects the mind as well as the body. the role that stress can play in triggering the onset of
mental disorders in vulnerable people is explicitly acknowledged in the diathesis-stress model.
Moreover, exposure to extreme and traumatic stress may overwhelm the coping resources of
otherwise apparently healthy people, leading to mental disorders such as posttraumatic stress
disorder (PTSD).

stress plays important role in the development of physical and mental disorders. Stress causes both
physical (heart disease) and mental problems (PTSD ) because the mind and the body are powerfully
connected and because stress takes its toll on both. Although the problems that are linked to stress
are many, we limit our discussion to the most severe stress-related mental disorders. In the physical
realm, we focus on.

What Is Stress?
Stress: A person’s response to events that are threatening or challenging.

Stress, the response or experience of an individual to demands that he or she perceives as taxing or
exceeding his or her personal resources. It usually occurs when an individual experiences chronic or
episodic events that are undesirable and lead to behavioral, physiological, and cognitive
accommodations
Life would be very simple if all of our needs were automatically satisfied. In reality, however, many
obstacles, both personal and environmental, get in the way. A promising athletic career may be
brought to an end by injury; we may have less money than we need; we may be rejected by the
person we love. The demands of life require that we adjust. When we experience or perceive
challenges to our physical or emotional well-being that exceed our coping resources and abilities, the
psychological condition that results is typically referred to as stress (see Shalev, 2009). To avoid
confusion, we will refer to external demands as stressors, to the effects they create within the
organism as stress, and to efforts to deal with stress as coping strategies. It is also important to note
that stress is fundamentally an interactive and dynamic construct because it reflects the interaction
between the organism and the environment over time (Monroe, 2008).

All situations that require adjustment can be regarded as potentially stressful. Prior to the influential
work of Canadian physician and endocrinologist Hans Selye (1956, 1976), stress was a term used by
engineers. Selye took the word and used it to describe the difficulties and strains experienced by
living organisms as they struggled to cope with and adapt to changing environmental conditions. His
work provided the foundation for current stress research. Selye also noted that stress could occur
not only in negative situations (such as taking an examination) but also in positive situations (such as
a wedding). Both kinds of stress can tax a person’s resources and coping skills, although bad stress
(distress) typically has the potential to do more damage. Stress can also occur in more than one
form—not just as a simple catastrophe but also as a continuous force that exceeds the person’s
capability of managing it.

Stress and the DSM

The relationship between stress and psychopathology is considered so important that the role of
stress is recognized in diagnostic formulations. Nowhere is this more apparent than in the diagnosis
of PTSD. PTSD was classified as an anxiety disorder in DSM-IV. However, DSM-5 introduced a new
diagnostic category called trauma- and stressor related disorders. PTSD is now included there. Other
disorders in this new category are adjustment disorder and acute stress disorder. These disorders
involve patterns of psychological and behavioral disturbances that occur in response to identifiable
stressors. The key differences among them lie not only in the severity of the disturbances but also in
the nature of the stressors and the time frame during which the disorders occur.

Factors Predisposing a Person to Stress

Everyone faces a unique pattern of demands to which he or she must adjust. This is because people
perceive and interpret similar situations differently and also because, objectively, no two people are
faced with exactly the same pattern of stressors. Some individuals are also more likely to develop
long-term problems under stress than others. This may be linked, in part, to coping skills and the
presence of particular resources. Children, for example, are particularly vulnerable to severe
stressors such as war and terrorism. Research also suggests that adolescents with depressed parents
are more sensitive to stressful events; these adolescents are also more likely to have problems with
depression themselves after experiencing stressful life events than those who do not have depressed
parents.

Individual characteristics that have been identified as improving a person’s ability to handle life stress
include higher levels of optimism, greater psychological control or mastery, increased self-esteem,
and better social support (Declercq et al., 2007; Taylor & Stanton, 2007). These stable factors are
linked to reduced levels of distress in the face of life events as well as more favorable health
outcomes. There is also some evidence from twin studies that differences in coping styles may be
linked to underlying genetic differences.

A major development in stress research was the discovery that a particular form of a particular gene
(the 5HTTLPR gene) was linked to how likely it was that people would become depressed in the face
of life stress. Caspi and colleagues (2003) found that people who had two “short” forms of this gene
(the s/s genotype) were more likely to develop depression when they experienced four or more
stressful life events than were people who had two “long” forms of this gene (the l/l geneotype).
Although this specific finding was controversial for a while a recent meta-analysis has provided clear
support for the original finding (Karg et al., 2011). More generally, it is now widely accepted that our
genetic makeup can render us more or less “stress-sensitive.”

The amount of stress we experience early in life may also make us more sensitive to stress later on.
The effects of stress may be cumulative, with each stressful experience serving to make the system
more reactive. Evidence from animal studies shows that being exposed to a single stressful
experience can enhance responsiveness to stressful events that occur later. Rats that were exposed
to stressful tail shocks produced more of the stress hormone cortisol when they were later exposed
to another stressful experience (being placed on a platform). Other biological changes associated
with stress were also more pronounced in these rats. These results suggest that prior stressful
experiences may sensitize us biologically, making us more reactive to later stressful experiences. The
term stress tolerance refers to a person’s ability to withstand stress without becoming seriously
impaired.

Stressful experiences may also create a self-perpetuating cycle by changing how we think about, or
appraise, the things that happen to us. Stressful situations may be related to or intensified by a
person’s cognitions. This may explain why people with a history of depression tend to experience
negative events as more stressful than other people do. For example, if you’re feeling depressed or
anxious already, you may perceive a friend’s canceling a movie date as an indication that she doesn’t
want to spend time with you. Even though the reality may be that a demand in her own life has kept
her from keeping your date, when you feel bad you will be much more inclined to come to a negative
conclusion about what just happened rather than see the situation in a more balanced or more
optimistic way.

Characteristics of Stressors

Why is misplacing our keys so much less stressful than being in an unhappy marriage or being fired
from a job? At some level we all intuitively understand what makes one stressor more serious than
another. The key factors involve (1) the severity of the stressor, (2) its chronicity (i.e., how long it
lasts), (3) its timing, (4) how closely it affects our own lives, (5) how expected it is, and (6) how
controllable it is.

Stressors that involve the more important aspects of a person’s life—such as the death of a loved
one, a divorce, a job loss, a serious illness, or negative social exchanges—tend to be highly stressful
for most people (Aldwin, 2007; Newsom et al., 2008). Furthermore, the longer a stressor operates,
the more severe its effects. A person may be frustrated in a boring and unrewarding job from which
there is seemingly no escape, suffer for years in an unhappy and conflict-filled marriage, or be
severely frustrated by a physical limitation or a long-term health problem. As we have already noted,
stressors also often have cumulative effects (Miller, 2007). A married couple may endure a long
series of difficulties and frustrations, only to divorce after experiencing what might seem to be a
minor precipitating stressor. Encountering a number of stressors at the same time also makes a
difference. If a man loses his job, learns that his wife is seriously ill, and receives news that his son
has been arrested for selling drugs, all at the same time, the resulting stress will be more severe than
if these events occurred separately and over an extended period. Symptoms of stress also intensify
when a person is more closely involved in an immediately traumatic situation. Learning that the
uncle of a close friend was injured in a car accident is not as stressful as being in an accident oneself.

Extensive research has shown that events that are unpredictable and unanticipated (and for which
no previously developed coping strategies are available) are likely to place a person under severe
stress. A devastating house fire and the damage it brings are not occurrences with which anyone has
learned to cope. Likewise, recovery from the stress created by major surgery can be improved when
a patient is given realistic expectations beforehand; knowing what to expect adds predictability to
the situation. In one study, patients who were about to undergo hip replacement surgery watched a
12-minute film the evening before they had the operation. The film described the entire procedure
from the patient’s perspective. Compared to controls who did not see the film, patients who saw the
video were less anxious on the morning of the surgery, were less anxious after the surgery, and
needed less pain medication (Doering et al., 2000).

Finally, with an uncontrollable stressor, there is no way to reduce its impact, such as by escape or
avoidance. In general, both people and animals are more stressed by unpredictable and
uncontrollable stressors than by stressors that are of equal physical magnitude but are either
predictable or controllable or both (e.g., Evans & Stecker, 2004; Maier & Watkins, 1998).

THE EXPERIENCE OF CRISIS

Most of us experience occasional periods of especially acute (sudden and intense) stress. The term
crisis is used to refer to times when a stressful situation threatens to exceed or exceeds the adaptive
capacities of a person or a group. Crises are often especially stressful, because the stressors are so
potent that the coping techniques we typically use do not work. Stress can be distinguished from
crisis in this way: A traumatic situation or crisis overwhelms a person’s ability to cope, whereas stress
does not necessarily overwhelm the person.

Measuring Life Stress

Life changes, even positive ones such as being promoted or getting married, place new demands on
us and may therefore be stressful. The stress from life changes can trigger problems, even in
disorders, such as bipolar disorder, that have strong biological underpinnings (see Johnson & Miller,
1997). The faster life changes occur, the greater the stress that is experienced.

A major focus of research on life changes has concerned the measurement of life stress. Years ago,
Holmes and Rahe (1967) developed the Social Readjustment Rating Scale. This is a selfreport
checklist of fairly common, stressful life experiences (see also Chung et al., 2010; Cooper & Dewe,
2007). Although easy to use, limitations of the checklist method later led to the development of
interview-based approaches such as the Life Events and Difficulties Schedule (LEDS; Brown & Harris,
1978). One advantage of the LEDS is that it includes an extensive manual that provides rules for
rating both acute and chronic forms of stress. The LEDS system also allows raters to consider a
person’s unique circumstances when rating each life event. For example, if a woman who is happily
married and in good financial circumstances learns that she is going to have a baby, she may
experience this news in a way that is quite different from that of an unmarried teenager who is faced
with the prospect of having to tell her parents that she is pregnant. Although interview-based
approaches are more time consuming and costly to administer, they are considered more reliable
and are preferred for research in this area (see Monroe, 2008).
Resilience

After experiencing a potentially traumatic event, some people function well and experience very few
symptoms in the following weeks and months. This kind of healthy psychological and physical
functioning after a potentially traumatic event is called resilience. You might be surprised to learn
that resilience is not rare. In fact, resilience is the most common reaction following loss or trauma
(Bonnano et al., 2011; Quale & Schanke, 2010).

But why are some people more resilient than others? Research suggests that there is no single factor
that predicts resilience. Rather, resilience is linked to a variety of different characteristics and
resources. Factors that increase resilience include being male, being older, and being well educated.
Having more economic resources is also beneficial. Some earlier studies suggested that, after the
9/11 attacks in New York, African Americans and members of some Latino groups fared more poorly
and showed lower levels of resilience compared to whites. However, race and ethnicity are often
confounded with social class. Importantly, when social class is controlled for, statistics show that race
and ethnicity are no longer predictive of reduced resiliency.

It also helps to be a positive person. Research shows that people who can still show genuine positive
emotions when talking about their recent loss also tend to adjust better after bereavement (see
Bonnano et al., 2011). In contrast, having more negative affect, being more inclined to ruminate, and
trying to find meaning in what has happened is associated with people doing less well after a
traumatic event.

The importance of positive and negative emotions is nicely illustrated in a study of 80 people who
were being treated in a specialized rehabilitation hospital (Quale & Schanke, 2010). All had multiple
traumatic injuries or severe spinal cord injuries, usually caused by accidents. The people who showed
most resilience in the months after their injuries were those who, when interviewed shortly after
arriving in the hospital, reported that they generally had an optimistic approach to life. In addition to
optimism, being generally high on positive affect and low on negative affect also predicted having a
more resilient trajectory (as opposed to a distress trajectory) over the period of rehabilitation
treatment.

Finally, it is interesting to note that people who are very selfconfident and who view themselves in an
overly positive light also tend to cope remarkably well in the face of trauma. Although people with
this kind of self-enhancing style are sometimes unpleasant to interact with, such a style may serve
them well in times of crisis. For example, in a recent prospective study, Gupta and Bonanno (2010)
showed that college students with this self-enhancing style coped much better over a four-year
period than people who did not.

CATEGORIZING STRESSORS

There are three general types of stressors: cataclysmic events, personal stressors, and background
stressors.

Cataclysmic events are strong stressors that occur suddenly and typically affect many people
simultaneously. Disasters such as tornadoes and plane crashes as well as terrorist attacks are
examples of cataclysmic events that can affect hundreds or thousands of people simultaneously.
Although it might seem that cataclysmic events would produce potent, lingering stress, in many cases
they do not. In fact, cataclysmic events involving natural disasters may produce less stress in the long
run than events that initially are not as devastating. One reason is that natural disasters have a clear
resolution. Once they are over, people can look to the future knowing that the worst is behind them.
Moreover, others who also experienced the disaster share the stress induced by cataclysmic events.
Such sharing permits people to offer one another social support and a firsthand understanding of the
difficulties others are going through. In contrast, terrorist attacks like the one on the World Trade
Center in 2001 are cataclysmic events that produce considerable stress. Terrorist attacks are
deliberate, and victims (and observers) know that future attacks are likely.

Personal stressors include major life events such as the death of a parent or spouse, the loss of
one’s job, a major personal failure, or even something positive such as getting married. Typically,
personal stressors produce an immediate major reaction that soon tapers off. For example, stress
arising from the death of a loved one tends to be greatest just after the time of death, but people
begin to feel less stress and are better able to cope with the loss after the passage of time.

Background stressors , or more informally, daily hassles, are the third major category of stressors.
Exemplified by standing in a long line at a bank and getting stuck in a traffic jam, daily hassles are the
minor irritations of life that we all face time and time again. Another type of background stressor is a
long-term, chronic problem, such as experiencing dissatisfaction with school or a job, being in an
unhappy relationship, or living in crowded quarters without privacy.

Stress and the Stress Response

To understand why stress can lead to physical and psychological problems, we need to know what
happens to our bodies when we experience stress. Faced with the threat of a perceived stressor, the
body undergoes a cascade of biological changes. Two distinct systems are involved here. The
sympathetic-adrenomedullary (SAM) system (see Gunnar & Quevedo, 2007) is designed to mobilize
resources and prepare for a fight-or-flight response. The stress response begins in the hypothalamus,
which stimulates the sympathetic nervous system (SNS). This, in turn, causes the inner portion of the
adrenal glands (the adrenal medulla) to secrete adrenaline (epinephrine) and noradrenaline
(norepinephrine). As these circulate through the blood, they cause an increase in heart rate (familiar
to all of us). They also get the body to metabolize glucose more rapidly.

The second system involved in the stress response is called the hypothalamus-pituitary-adrenal (HPA)
system (which we introduced in Chapter 3; also see Figure 5.1). In addition to stimulating the SNS,
the hypothalamus releases a hormone called “corticotrophin-releasing hormone” (or CRH). Traveling
in the blood, this hormone stimulates the pituitary gland. The pituitary then secretes
adrenocorticotrophic hormone (ACTH). This induces the adrenal cortex (the outer portion of the
adrenal gland) to produce the stress hormones called glucocorticoids. In humans, the stress
glucocorticoid that is produced is called cortisol.

Cortisol is a good hormone to have around in an emergency. It prepares the body for fight or flight. It
also inhibits the innate immune response. This means that if an injury does occur, the body’s
inflammatory response to it is delayed. In other words, escape has priority over healing, and tissue
repair is secondary to staying alive. This obviously has survival value if you need to run away from a
lion that has just mauled you. It also explains why cortisone injections are sometimes used to reduce
inflammation in damaged joints.

But there is also a downside to cortisol. If the cortisol response is not shut off, cortisol can damage
brain cells, especially in the hippocampus (see Sapolsky, 2000). At a very fundamental level, stress is
bad for your brain. It may even stunt growth (babies who are stressed don’t gain weight in the
normal way and “fail to thrive”). Accordingly, the brain has receptors to detect cortisol. When these
are activated, they send a feedback message that is designed to dampen the activity of the glands
involved in the stress response. But if the stressor remains, the HPA axis stays active and cortisol
release continues. Although short-term cortisol production is highly adaptive, a chronically overactive
HPA axis, with high levels of circulating cortisol, may be problematic.

The Mind–Body Connection

The link between stress and physical illness involves diseases (like colds) that are not directly related
to nervous system activity. This suggests that stress may cause an overall vulnerability to disease by
compromising immune functioning. Psychoneuroimmunology is the study of the interaction
between the nervous system and the immune system. Although it was once thought that the
immune system was essentially “closed” and responsive only to challenges from foreign substances,
we now realize that this is not the case. The nervous system and the immune system communicate in
ways that we are now beginning to understand.

Evidence continues to grow that the brain influences the immune system and that the immune
system influences the brain. In other words, a person’s behavior and psychological states do indeed
affect immune functioning, but the status of the immune system also influences current mental
states and behavioral dispositions by affecting the blood levels of circulating neurochemicals; these,
in turn, modify brain states. For example, we have already seen that glucocorticoids can cause
stress-induced immunosuppression. In the short term, this can be adaptive (escape first, heal later).
However, it makes sense that longer-term stress might create problems for the immune system. To
appreciate why this might be, we need to describe briefly the basics of immune functioning.

THE COURSE OF STRESS

General adaptation syndrome (GAS) A theory developed by Selye that suggests that a person’s
response to a stressor consists of three stages: alarm and mobilization, resistance, and exhaustion.

alarm and mobilization —occurs when people become aware of the presence of a stressor. On a
biological level, the sympathetic nervous system becomes energized, which helps a person cope
initially with the stressor.

if the stressor persists, people move into the second response stage: resistance. During this stage,
the body is actively fi ghting the stressor on a biological level. During resistance, people use a variety
of means to cope with the stressor— sometimes successfully but at a cost of some degree of physical
or psychological well-being. For example, a student who faces the stress of failing several courses
might spend long hours studying seeking to cope with the stress.

If resistance is inadequate, people enter the last stage of the GAS: exhaustion. During the
exhaustion stage, a person’s ability to fi ght the stressor declines to the point where negative
consequences of stress appear: physical illness and psychological symptoms in the form of an
inability to concentrate, heightened irritability, or, in severe cases, disorientation and a loss of touch
with reality. In a sense, people wear out, and their physiological resources to fi ght the stressor are
used up.

Cost of Stress

Three major types of consequences result from stress: direct physiological eff ects, harmful
behaviors, and indirect health-related behaviors.

Direct physiological effects • Elevated blood pressure • Decrease in immune system functioning •
Increased hormonal activity • Psychophysiological conditions
Harmful behaviors • Increased smoking, alcohol use • Decreased nutrition • Decreased sleep •
Increased drug use

Indirect health-related behaviors • Decreased compliance with medical advice • Increase in delays
in seeking medical advice • Decrease in likelihood of seeking medical advice

Coping strategies
Coping: The efforts to control, reduce, or learn to tolerate the threats that lead to stress.

coping is defined as the dynamic efforts, which involve “the thoughts and behaviors used to manage
the internal and external demands of situations that are appraised as stressful”

Stress is a normal part of life—and not necessarily a completely bad part. For example, without
stress, we might not be sufficiently motivated to complete the activities we need to accomplish.
However, it is also clear that too much stress can take a toll on physical and psychological health.

We habitually use certain coping responses to deal with stress. Most of the time, we’re not aware of
these responses—just as we may be unaware of the minor stressors of life until they build up to
harmful levels.

Coping behaviors and strategies have been traditionally dichotomized into categories, such as
problem- versus emotion-focused, functional versus dysfunctional, approach versus avoidance,
engagement versus disengagement, and primary versus secondary control coping

We also have other, more direct and potentially more positive ways of coping with stress, which fall
into two main categories.

Emotion-focused coping. In emotion-focused coping, people try to manage their emotions in the
face of stress by seeking to change the way they feel about or perceive a problem. Examples of
emotion-focused coping include strategies such as accepting sympathy from others and looking at
the bright side of a situation. (distancing, self-controlling, accepting responsibility, escape/avoidance,
confrontive coping, and positive reappraisal)

Problem-focused coping. Problem-focused coping attempts to modify the stressful problem or

source of stress. Problem-focused strategies lead to changes in behavior or to the development of a
plan of action to deal with stress. Starting a study group to improve poor classroom performance is
an example of problem focused coping. In addition, one might take a time-out from stress by creating
positive events. For example, taking a day off from caring for a relative with a serious, chronic illness
to go a health club or spa can bring significant relief from stress. (planful problem-solving)

seeking social support can be conceptualized as both problem and emotion-focused.

Functional coping includes active and internal coping and refers to attempts to deal with problems
by seeking support, taking concrete action, or reflecting on possible solutions. Dysfunctional coping
includes withdrawal and refers to denial or repression, controlling feelings, and having a fatalistic
attitude.

Primary control coping involves changing the existing environment to fit the individual’s needs and
secondary control coping includes changing one’s feelings and thoughts to adjust to the objective
environment and it is the type of control that people use when they are unable to exert traditional
primary control. Four types of secondary control have been identified: individuals may use secondary
control to restore a sense of primary control by aligning with powerful others who might have
primary control (vicarious), by aligning with luck to arrange a positive outcome (illusory), by
predicting what will happen to them in future situations (predictive), or by interpreting some
outcome in a way that restores their feeling of primary control. When comparing primary control
coping to secondary control coping, studies indicate that individuals from Asian cultures engage in
more secondary control coping than those from Western cultures.

Some forms of coping are less successful. One of the least effective forms of coping is avoidant
coping. In avoidant coping, a person may use wishful thinking to reduce stress or use more direct
escape routes, such as drug use, alcohol use, and overeating. An example of wishful thinking to avoid
a test would be to say to oneself, “Maybe it will snow so hard tomorrow that the test will be
canceled.”

One of the major findings from coping research is that action-oriented coping is strongly related to
positive psychological outcomes, while avoidance and emotion focused strategies tend to be
associated with poorer mental health.

Another way of dealing with stress occurs unconsciously through the use of defense mechanisms.
Defense mechanisms are unconscious strategies that people use to reduce anxiety by concealing the
source from themselves and others. Defense mechanisms permit people to avoid stress by acting as
if the stress were not even there. Eg: A defense mechanism used to cope with stress is emotional
insulation in which a person stops experiencing any emotions at all and thereby remains unaffected
and unmoved by both positive and negative experiences. The problem with defense mechanisms, of
course, is that they merely hide the problem and do not deal with reality.

While coping behaviors such as developing and maintaining a sense of competence and self-esteem
(i.e., use of skills, talents, and cognitive abilities to feel good about oneself) have been labeled
positive coping strategies assumed to result in positive consequences, coping behaviors such as
relieving tension through diversions (i.e., activities that provide ways of escape, denial, and
sublimation), and avoiding confrontation and withdrawing (e.g., avoiding people, situations, or
stimuli that are difficult, uncomfortable, or unpleasant) have been labeled negative strategies of
coping which can be expected to result in negative consequences

Stress disorders
Comes under the category of Trauma- and Stressor-Related Disorders in DSM 5 (7th category)

Reactive Attachment Disorder

Disinhibited Social Engagement
Disorder Posttraumatic Stress Disorder
Acute Stress Disorder
Adjustment Disorders
Other Specified Trauma- and Stressor-Related Disorder
Unspecified Trauma- and Stressor-Related Disorder

Adjustment disorder-
It was the 15th category of disorders in DSM IV, now it is a part of the category of Trauma- and
Stressor-Related Disorders in DSM 5

No number in ICD

An adjustment disorder is a psychological response to a common stressor (e.g., divorce, death of a

loved one, loss of a job) that results in clinically significant behavioral or emotional symptoms. The
stressor can be a single event, such as going away to college, or involve multiple stressors, such as a
business failure and marital problems. People undergoing severe stress that exceeds their coping
resources may warrant the diagnosis of adjustment disorder. For the diagnosis to be given, symptoms
must begin within 3 months of the onset of the stressor. In addition, the person must experience
more distress than would be expected given the circumstances or be unable to function as usual.

In adjustment disorder, the person’s symptoms lessen or disappear when the stressor ends or when
the person learns to adapt to the stressor. In cases where the symptoms continue beyond 6 months,
the diagnosis is usually changed to some other mental disorder. Adjustment disorder is probably the
least stigmatizing and mildest diagnosis a therapist can assign to a client.

Adjustment disorders affect how you feel and think about yourself and the world and may also affect
your actions or behavior. Some examples include:

Symptoms
Feeling sad, hopeless or not enjoying things you used to enjoy
Frequent crying
Worrying or feeling anxious, nervous, jittery or stressed out
Trouble sleeping
Lack of appetite
Difficulty concentrating
Feeling overwhelmed
Difficulty functioning in daily activities
Withdrawing from social supports
Avoiding important things such as going to work or paying bills
Suicidal thoughts or behavior
Diagnostic Criteria
A. The development of emotional or behavioral symptoms in response to an identifiable stressor(s)
occurring within 3 months of the onset of the stressor(s).
B. These symptoms or behaviors are clinically significant, as evidenced by one or both of the
following:
1. Marked distress that is out of proportion to the severity or intensity of the stressor,
taking into account the external context and the cultural factors that might influence
symptom severity and presentation.
2. Significant impairment in social, occupational, or other important areas of functioning.
C. The stress-related disturbance does not meet the criteria for another mental disorder and is not
merely an exacerbation of a preexisting mental disorder.
D. The symptoms do not represent normal bereavement. E. Once the stressor or its consequences
have terminated, the symptoms do not persist for more than an additional 6 months.

Diagnostic Features
The presence of emotional or behavioral symptoms in response to an identifiable stressor is the
essential feature of adjustment disorders (Criterion A). The stressor may be a single event (e.g., a
termination of a romantic relationship), or there may be multiple stressors (e.g., marked business
difficulties and marital problems). Stressors may be recurrent (e.g., associated with seasonal business
crises, unfulfilling sexual relationships) or continuous (e.g., a persistent painful illness with increasing
disability, living in a crime-ridden neighborhood). Stressors may affect a single individual, an entire
family, or a larger group or community (e.g., a natural disaster). Some stressors may accompany
specific developmental events (e.g., going to school, leaving a parental home, reentering a parental
home, getting married, becoming a parent, failing to attain occupational goals, retirement).

Adjustment disorders may be diagnosed following the death of a loved one when the intensity,
quality, or persistence of grief reactions exceeds what normally might be expected, when cultural,
religious, or age-appropriate norms are taken into account. A more specific set of
bereavement-related symptoms has been designated persistent complex bereavement disorder.

Adjustment disorders are associated with an increased risk of suicide attempts and completed
suicide.

Prevalence
Adjustment disorders are common, although prevalence may vary widely as a function of the
population studied and the assessment methods used. The percentage of individuals in outpatient
mental health treatment with a principal diagnosis of an adjustment disorder ranges from
approximately 5% to 20%. In a hospital psychiatric consultation setting, it is often the most common
diagnosis, frequently reaching 50%.

Development and Course

By definition, the disturbance in adjustment disorders begins within 3 months of onset of a stressor
and lasts no longer than 6 months after the stressor or its consequences have ceased. If the stressor
is an acute event (e.g., being fired from a job), the onset of the disturbance is usually immediate (i.e.,
within a few days) and the duration is relatively brief (i.e., no more than a few months). If the
stressor or its consequences persist, the adjustment disorder may also continue to be present and
become the persistent form.

Risk and Prognostic Factors/ Causes

Environmental. Individuals from disadvantaged life circumstances experience a high rate of stressors
and may be at increased risk for adjustment disorders.

Adjustment disorder is caused by one or more life stressors. In adults, these stressors are most
commonly related to marital discord, finances, or work. In adolescents, common stressors include
school problems, family or parents' marital problems, or issues around sexuality. Other types of
stressors include the death of a loved one, life changes, unexpected catastrophes, and medical
conditions (such as cancer) and their subsequent treatments.

Factors that influence how well a person reacts to stress may include economic conditions, as well as
the availability of social supports and occupational and recreational opportunities. Factors leading an
individual to be more susceptible to stressors include social skills, intelligence, genetics, and mastery
of existing coping strategies.

Treatment
The primary goal of treatment for adjustment disorder is to relieve symptoms and to help an
individual achieve a level of functioning comparable to what they demonstrated prior to the stressful
event.

Recommended treatments include individual psychotherapy, family therapy, behavior therapy, and
self-help groups. Realistic short-term goals should be established at the start of therapy, as the
course of adjustment disorder tends to be short-term in nature.

Goals of therapy will often center around recognizing and taking advantage of the social supports
available to an individual in the form of family, friends, and community. The individual's coping and
problem-solving skills will be explored and developed. Relaxation techniques might be explored to
deal with feelings of stress. Treatment will include eliciting the patient's concern and helping the
individual understand his or her role in the stressors, reviewing and reinforcing any positive steps the
patient may have already taken to deal with the stressors, teaching additional ways to cope with or
avoid future stressors, helping the individual put stressors in perspective to their life overall, helping
the person better understand his or her reaction to the stressors, and helping the patient come to
perceive stressors as an opportunity for positive change or improvement.

Family therapy, as well as effective communication and coping skills, may be recommended when the
patient is a child or adolescent. When medication is used, it is typically in addition to psychotherapy.
Treatment of adjustment disorder typically excludes the use of prescription medications, but in some
cases, medication may be helpful in easing the depression or the anxiety associated with the
disorder.

Most people recover from adjustment disorder without any remaining symptoms if they have no
previous history of mental illness and have access to stable social support. Individuals suffering from
adjustment disorder should work to develop and maintain a healthy diet and sleep pattern, as well as
a strong social support system.

Psychotherapy

Psychotherapy remains the treatment of choice for adjustment disorders. Group therapy can be
particularly useful for patients who have had similar stresses—for example, a group of retired
persons or patients having renal dialysis. Individual psychotherapy oers the opportunity to explore
the meaning of the stressor to the patient so that earlier traumas can be worked through. After
successful therapy, patients sometimes emerge from an adjustment disorder stronger than in the
premorbid period, although no pathology was evident during that period. Because a stressor can be
clearly delineated in adjustment disorders, it is often believed that psychotherapy is not indicated
and that the disorder will remit spontaneously. This viewpoint, however, ignores the fact that many
persons exposed to the same stressor experience dierent symptoms, and in adjustment disorders,
the response is pathological. Psychotherapy can help persons adapt to stressors that are not
reversible or time limited and can serve as a preventive intervention if the stressor does remit.
Psychiatrists treating adjustment disorders must be particularly aware of problems of secondary gain.
The illness role may be rewarding to some normally healthy persons who have had little experience
with illness’s capacity to free them from responsibility. Thus, patients can nd therapists’ attention,
empathy, and understanding, which are necessary for success, rewarding in their own right, and
therapists may thereby reinforce patients’ symptoms. Such considerations must be weighed before
intensive psychotherapy is begun; when a secondary gain has already been established, therapy is
dicult. Patients with an adjustment disorder that includes a conduct disturbance may have diculties
with the law, authorities, or school. Psychiatrists should not attempt to rescue such patients from the
consequences of their actions. Too often, such kindness only reinforces socially unacceptable means
of tension reduction and hinders the acquisition of insight and subsequent emotional growth. In
these cases, family therapy can help.

Crisis Intervention

Crisis intervention and case management are short-term treatments aimed at helping persons with
adjustment disorders resolve their situations quickly by supportive techniques, suggestion,
reassurance, environmental modification, and even hospitalization, if necessary. The frequency and
length of visits for crisis support vary according to patients’ needs; daily sessions may be necessary,
sometimes two or three times each day. Flexibility is essential in this approach.

Pharmacotherapy

No studies have assessed the ecacy of pharmacological interventions in individuals with adjustment
disorder, but it may be reasonable to use medication to treat specic symptoms for a brief time. The
judicious use of medications can help patients with adjustment disorders, but they should be
prescribed for brief periods. Depending on the type of adjustment disorder, a patient may respond to
an antianxiety agent or to an antidepressant. Patients with severe anxiety bordering on panic can
benet from anxiolytics such as diazepam (Valium), and those in withdrawn or inhibited states may be
helped by a short course of psychostimulant medication. Antipsychotic drugs may be used if there
are signs of decompensation or impending psychosis. Selective serotonin reuptake inhibitors have
been found useful in treating symptoms of traumatic grief. Recently, there has been an increase in
antidepressant use to augment psychotherapy in patients with adjustment disorders.
Pharmacological intervention in this population is most often used, however, to augment
psychosocial strategies rather than serving as the primary modality.

Post traumatic stress disorder

309.81_ICD-9 (F43.10_ ICD-10)

Post-traumatic stress disorder (PTSD) is a mental health condition that's triggered by a terrifying
event — either experiencing it or witnessing it. Symptoms may include flashbacks, nightmares and
severe anxiety, as well as uncontrollable thoughts about the event.

The diagnosis of PTSD first entered the DSM in 1980 (see the DSM table for current clinical criteria).
At this time, psychiatry began to realize that many veterans were emotionally scarred and unable to
return to normal civilian life after their military service in Vietnam. The proposal to include PTSD in
the diagnostic system was initially opposed, not least because including a disorder that had a clear
and explicit cause (trauma) was inconsistent with the atheoretical nature of the DSM. Nonetheless, a
consensus emerged that any extreme, terrifying, and stressful event that was life-threatening and
outside the ordinary bounds of everyday experience could lead to psychological symptoms similar to
those experienced by the Vietnam veterans. In other words, at the time of its entry into the DSM
(which is after all a manual of mental disorders), PTSD was viewed as a normal response to an
abnormal stressor.

Traumatic stressors include combat, rape, being confined in a concentration camp, and experiencing
a natural disaster such as a tsunami, earthquake, or tornado.

Stress symptoms are very common in the immediate aftermath of a traumatic event. However, for
most people, these symptoms decrease with time. Rothbaum and Foa (1993) reported that 95
percent of women who had been raped met the symptom criteria for PTSD within 2 weeks of the
assault. One month after the rape, this figure had declined to 63.3 percent of women, and after 3
months, 45.9 percent of the women were diagnosed with the PTSD. Natural recovery with time is
therefore a common pattern.

Symptoms
Post-traumatic stress disorder symptoms may start within one month of a traumatic event, but
sometimes symptoms may not appear until years after the event. These symptoms cause significant
problems in social or work situations and in relationships. They can also interfere with your ability to
go about your normal daily tasks.
PTSD symptoms are generally grouped into four types: intrusive memories, avoidance, negative
changes in thinking and mood, and changes in physical and emotional reactions. Symptoms can vary
over time or vary from person to person.

Intrusive memories

Symptoms of intrusive memories may include:

● Recurrent, unwanted distressing memories of the traumatic event

● Reliving the traumatic event as if it were happening again (flashbacks)

● Upsetting dreams or nightmares about the traumatic event

● Severe emotional distress or physical reactions to something that reminds you of the
traumatic event

Avoidance

Symptoms of avoidance may include:

● Trying to avoid thinking or talking about the traumatic event

● Avoiding places, activities or people that remind you of the traumatic event

Negative changes in thinking and mood

Symptoms of negative changes in thinking and mood may include:

● Negative thoughts about yourself, other people or the world

● Hopelessness about the future

● Memory problems, including not remembering important aspects of the traumatic event

● Difficulty maintaining close relationships

● Feeling detached from family and friends

● Lack of interest in activities you once enjoyed

● Difficulty experiencing positive emotions

● Feeling emotionally numb

Changes in physical and emotional reactions

Symptoms of changes in physical and emotional reactions (also called arousal symptoms) may
include:

● Being easily startled or frightened

● Always being on guard for danger

● Self-destructive behavior, such as drinking too much or driving too fast

● Trouble sleeping

● Trouble concentrating
 ● Irritability, angry outbursts or aggressive behavior

● Overwhelming guilt or shame

For children 6 years old and younger, signs and symptoms may also include:

● Re-enacting the traumatic event or aspects of the traumatic event through play

● Frightening dreams that may or may not include aspects of the traumatic event

Diagnostic Criteria for adult

Note: The following criteria apply to adults, adolescents, and children older than 6 years.

A. Exposure to actual or threatened death, serious injury, or sexual violence in one (or more) of the
following ways:

1. Directly experiencing the traumatic event(s).

2. Witnessing, in person, the event(s) as it occurred to others.

3. Learning that the traumatic event(s) occurred to a close family member or close friend. In
cases of actual or threatened death of a family member or friend, the event(s) must have
been violent or accidental.

4. Experiencing repeated or extreme exposure to aversive details of the traumatic event(s)

(e.g., first responders collecting human remains: police officers repeatedly exposed to details
of child abuse).

Note: Criterion A4 does not apply to exposure through electronic media, television, movies, or
pictures, unless this exposure is work related.

B. Presence of one (or more) of the following intrusion symptoms associated with the traumatic
event(s), beginning after the traumatic event(s) occurred:

1. Recurrent, involuntary, and intrusive distressing memories of the traumatic event(s). Note:
In children older than 6 years, repetitive play may occur in which themes or aspects of the
traumatic event(s) are expressed.

2. Recurrent distressing dreams in which the content and/or affect of the dream are related
to the traumatic event(s). Note: In children, there may be frightening dreams without
recognizable content.

3. Dissociative reactions (e.g., flashbacks) in which the individual feels or acts as if the
traumatic event(s) were recurring. (Such reactions may occur on a continuum, with the most
extreme expression being a complete loss of awareness of present surroundings.) Note: In
children, trauma-specific reenactment may occur in play.

4. Intense or prolonged psychological distress at exposure to internal or external cues that

symbolize or resemble an aspect of the traumatic event(s).

5. Marked physiological reactions to internal or external cues that symbolize or resemble an

aspect of the traumatic event(s).

C. Persistent avoidance of stimuli associated with the traumatic event(s), beginning after the
traumatic event(s) occurred, as evidenced by one or both of the following:
 1. Avoidance of or efforts to avoid distressing memories, thoughts, or feelings about or
closely associated with the traumatic event(s).

2. Avoidance of or efforts to avoid external reminders (people, places, conversations,

activities, objects, situations) that arouse distressing memories, thoughts, or feelings about
or closely associated with the traumatic event(s).

D. Negative alterations in cognitions and mood associated with the traumatic event(s), beginning or
worsening after the traumatic event(s) occurred, as evidenced by two (or more) of the following:

1. Inability to remember an important aspect of the traumatic event(s) (typically due to

dissociative amnesia and not to other factors such as head injury, alcohol, or drugs).

2. Persistent and exaggerated negative beliefs or expectations about oneself, others, or the
world (e.g., “I am bad,” “No one can be trusted,” ‘The world is completely dangerous,” “My
whole nervous system is permanently ruined”).

3. Persistent, distorted cognitions about the cause or consequences of the traumatic event(s)
that lead the individual to blame himself/herself or others.

4. Persistent negative emotional state (e.g., fear, horror, anger, guilt, or shame).

5. Markedly diminished interest or participation in significant activities.

6. Feelings of detachment or estrangement from others.

7. Persistent inability to experience positive emotions (e.g., inability to experience happiness,

satisfaction, or loving feelings).

E. Marked alterations in arousal and reactivity associated with the traumatic event(s), beginning or
worsening after the traumatic event(s) occurred, as evidenced by two (or more) of the following:

1. Irritable behavior and angry outbursts (with little or no provocation) typically expressed as
verbal or physical aggression toward people or objects.

2. Reckless or self-destructive behavior.

3. Hypervigilance.

4. Exaggerated startle response.

5. Problems with concentration.

6. Sleep disturbance (e.g., difficulty falling or staying asleep or restless sleep).

F. Duration of the disturbance (Criteria B, C, D, and E) is more than 1 month.

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

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

Specify whether:
With dissociative symptoms: The individual’s symptoms meet the criteria for posttraumatic stress
disorder, and in addition, in response to the stressor, the individual experiences persistent or
recurrent symptoms of either of the following:

1. Depersonalization: Persistent or recurrent experiences of feeling detached from, and as if

one were an outside observer of, one’s mental processes or body (e.g., feeling as though one
were in a dream; feeling a sense of unreality of self or body or of time moving slowly).

2. Derealization: Persistent or recurrent experiences of unreality of surroundings (e.g., the

world around the individual is experienced as unreal, dreamlike, distant, or distorted).

Note: To use this subtype, the dissociative symptoms must not be attributable to the physiological
effects of a substance (e.g., blackouts, behavior during alcohol intoxication) or another medical
condition (e.g., complex partial seizures).

Specify if:

With delayed expression: If the full diagnostic criteria are not met until at least 6 months after the
event (although the onset and expression of some symptoms may be immediate).

Diagnostic Features
The essential feature of posttraumatic stress disorder (PTSD) is the development of characteristic
symptoms following exposure to one or more traumatic events. Emotional reactions to the traumatic
event (e.g., fear, helplessness, horror) are no longer a part of Criterion A. The clinical presentation of
PTSD varies. In some individuals, fear-based re- experiencing, emotional, and behavioral symptoms
may predominate. In others, anhe- donic or dysphoric mood states and negative cognitions may be
most distressing. In some other individuals, arousal and reactive-externalizing symptoms are
prominent, while in others, dissociative symptoms predominate. Finally, some individuals exhibit
combinations of these symptom patterns.

The directly experienced traumatic events in Criterion A include, but are not limited to, exposure to
war as a combatant or civilian, threatened or actual physical assault (e.g., physical attack, robbery,
mugging, childhood physical abuse), threatened or actual sexual violence (e.g., forced sexual
penetration, alcohol/drug-facilitated sexual penetration, abusive sexual contact, noncontact sexual
abuse, sexual trafficking), being kidnapped, being taken hostage, terrorist attack, torture,
incarceration as a prisoner of war, natural or human-made disasters, and severe motor vehicle
accidents. For children, sexually violent events may include developmentally inappropriate sexual
experiences without physical violence or injury. A life-threatening illness or debilitating medical
condition is not necessarily considered a traumatic event. Medical incidents that qualify as traumatic
events involve sudden, catastrophic events (e.g., waking during surgery, anaphylactic shock).
Witnessed events include, but are not limited to, observing threatened or serious injury, unnatural
death, physical or sexual abuse of another person due to violent assault, domestic violence, accident,
war or disaster, or a medical catastrophe in one's child (e.g., a life- threatening hemorrhage). Indirect
exposure through learning about an event is limited to experiences affecting close relatives or friends
and experiences that are violent or accidental (e.g., death due to natural causes does not qualify).
Such events include violent personal assault, suicide, serious accident, and serious injury. The
disorder may be especially severe or long-lasting when the stressor is interpersonal and intentional
(e.g., torture, sexual violence).

The traumatic event can be reexperienced in various ways. Commonly, the individual has recurrent,
involuntary, and intrusive recollections of the event (Criterion Bl). Intrusive recollections in PTSD are
distinguished from depressive rumination in that they apply only to involuntary and intrusive
distressing memories. The emphasis is on recurrent memories of the event that usually include
sensory, emotional, or physiological behavioral components. A common reexperiencing symptom is
distressing dreams that replay the event itself or that are representative or thematically related to
the major threats involved in the traumatic event (Criterion B2). The individual may experience
dissociative states that last from a few seconds to several hours or even days, during which
components of the event are relived and the individual behaves as if the event were occurring at that
moment (Criterion B3). Such events occur on a continuum from brief visual or other sensory
intrusions about part of the traumatic event without loss of reality orientation, to complete loss of
awareness of present surroundings. These episodes, often referred to as "flashbacks," are typically
brief but can be associated with prolonged distress and heightened arousal. For young children,
reenactment of events related to trauma may appear in play or in dissociative states. Intense
psychological distress (Criterion B4) or physiological reactivity (Criterion B5) often occurs when the
individual is exposed to triggering events that resemble or symbolize an aspect of the traumatic
event (e.g., windy days after a hurricane; seeing someone who resembles one's perpetrator). The
triggering cue could be a physical sensation (e.g., dizziness for survivors of head trauma; rapid
heartbeat for a previously traumatized child), particularly for individuals with highly somatic
presentations.

Stimuli associated with the trauma are persistently (e.g., always or almost always) avoided. The
individual commonly makes deliberate efforts to avoid thoughts, memories, feelings, or talking about
the traumatic event (e.g., utilizing distraction techniques to avoid internal reminders) (Criterion Cl)
and to avoid activities, objects, situations, or people who arouse recollections of it (Criterion C2).

Negative alterations in cognitions or mood associated with the event begin or worsen after exposure
to the event. These negative alterations can take various forms, including an inability to remember
an important aspect of the traumatic event; such amnesia is typically due to dissociative amnesia and
is not due to head injury, alcohol, or drugs (Criterion Dl). Another form is persistent (i.e., always or
almost always) and exaggerated negative expectations regarding important aspects of life applied to
oneself, others, or the future (e.g., "I have always had bad judgment"; "People in authority can't be
trusted") that may manifest as a negative change in perceived identity since the trauma (e.g., "I can't
trust anyone ever again"; Criterion D2). Individuals with PTSD may have persistent erroneous
cognitions about the causes of the traumatic event that lead them to blame themselves or others
(e.g., "It's all my fault that my uncle abused me") (Criterion D3). A persistent negative mood state
(e.g., fear, horror, anger, guilt, shame) either began or worsened after exposure to the event
(Criterion D4). The individual may experience markedly diminished interest or participation in
previously enjoyed activities (Criterion D5), feeling detached or estranged from other people
(Criterion D6), or a persistent inability to feel positive emotions (especially happiness, joy,
satisfaction, or emotions associated with intimacy, tenderness, and sexuality) (Criterion D7).

Individuals with PTSD may be quick tempered and may even engage in aggressive verbal and/or
physical behavior with little or no provocation (e.g., yelling at people, getting into fights, destroying
objects) (Criterion El). They may also engage in reckless or selfdestructive behavior such as
dangerous driving, excessive alcohol or drug use, or self- injurious or suicidal behavior (Criterion E2).
PTSD is often characterized by a heightened sensitivity to potential threats, including those that are
related to the traumatic experience (e.g., following a motor vehicle accident, being especially
sensitive to the threat potentially caused by cars or trucks) and those not related to the traumatic
event (e.g., being fearful of suffering a heart attack) (Criterion E3). Individuals with PTSD may be very
reactive to unexpected stimuli, displaying a heightened startle response, or jumpiness, to loud noises
or unexpected movements (e.g., jumping markedly in response to a telephone ringing) (Criterion E4).
Concentration difficulties, including difficulty remembering daily events (e.g., forgetting one's
telephone number) or attending to focused tasks (e.g., following a conversation for a sustained
period of time), are commonly reported (Criterion E5). Problems with sleep onset and maintenance
are common and may be associated with nightmares and safety concerns or with generalized
elevated arousal that interferes with adequate sleep (Criterion E6). Some individuals also experience
persistent dissociative symptoms of detachment from their bodies (depersonalization) or the world
around them (derealization); this is reflected in the ''with dissociative symptoms" specifier.

Prevalence
In the United States, projected lifetime risk for PTSD using DSM-IV criteria at age 75 years is 8.7%.
Twelve-month prevalence among U.S. adults is about 3.5%. Lower estimates are seen in Europe and
most Asian, African, and Latin American countries, clustering around 0.5%-L0%. Although different
groups have different levels of exposure to traumatic events, the conditional probability of
developing PTSD following a similar level of exposure may also vary across cultural groups. Rates of
PTSD are higher among veterans and others whose vocation increases the risk of traumatic exposure
(e.g., police, firefighters, emergency medical personnel). Highest rates (ranging from one-third to
more than one- half of those exposed) are found among survivors of rape, military combat and
captivity, and ethnically or politically motivated internment and genocide. The prevalence of PTSD
may vary across development; children and adolescents, including preschool children, generally have
displayed lower prevalence following exposure to serious traumatic events; however, this may be
because previous criteria were insufficiently developmentally informed. The prevalence of
full-threshold PTSD also appears to be lower among older adults compared with the general
population; there is evidence that subthreshold presentations are more common than full PTSD in
later life and that these symptoms are associated with substantial clinical impairment. Compared
with U.S. non-Latino whites, higher rates of PTSD have been reported among U.S. Latinos, African
Americans, and American Indians, and lower rates have been reported among Asian Americans, after
adjustment for traumatic exposure and demographic variables.

Development and Course

PTSD can occur at any age, beginning after the first year of life. Symptoms usually begin within the
first 3 months after the trauma, although there may be a delay of months, or even years, before
criteria for the diagnosis are met. There is abundant evidence for what DSM-IV called "delayed
onset" but is now called "delayed expression," with the recognition that some symptoms typically
appear immediately and that the delay is in meeting full criteria.

Frequently, an individual's reaction to a trauma initially meets criteria for acute stress disorder in the
immediate aftermath of the trauma. The symptoms of PTSD and the relative predominance of
different symptoms may vary over time. Duration of the symptoms also varies, with complete
recovery within 3 months occurring in approximately one-half of adults, while some individuals
remain symptomatic for longer than 12 months and sometimes for more than 50 years. Symptom
recurrence and intensification may occur in response to reminders of the original trauma, ongoing
life stressors, or newly experienced traumatic events. For older individuals, declining health,
worsening cognitive functioning, and social isolation may exacerbate PTSD symptoms.

The clinical expression of reexperiencing can vary across development. Young children may report
new onset of frightening dreams without content specific to the traumatic event. Before age 6 years
(see criteria for preschool subtype), young children are more likely to express reexperiencing
symptoms through play that refers directly or symbolically to the trauma. They may not manifest
fearful reactions at the time of the exposure or during reexperiencing. Parents may report a wide
range of emotional or behavioral changes in young children. Children may focus on imagined
interventions in their play or storytelling. In addition to avoidance, children may become preoccupied
with reminders. Because of young children's limitations in expressing thoughts or labeling emotions,
negative alterations in mood or cognition tend to involve primarily mood changes. Children may
experience cooccurring traumas (e.g., physical abuse, witnessing domestic violence) and in chronic
circumstances may not be able to identify onset of symptomatology. Avoidant behavior may be
associated with restricted play or exploratory behavior in young children; reduced participation in
new activities in school-age children; or reluctance to pursue developmental opportunities in
adolescents (e.g., dating, driving). Older children and adolescents may judge themselves as cowardly.
Adolescents may harbor beliefs of being changed in ways that make them socially undesirable and
estrange them from peers (e.g., '"Now I'll never fit in") and lose aspirations for the future. Irritable or
aggressive behavior in children and adolescents can interfere with peer relationships and school
behavior. Reckless behavior may lead to accidental injury to self or others, thrill-seeking, or high-risk
behaviors. Individuals who continue to experience PTSD into older adulthood may express fewer
symptoms of hyperarousal, avoidance, and negative cognitions and mood compared with younger
adults with PTSD, although adults exposed to traumatic events during later life may display more
avoidance, hyperarousal, sleep problems, and crying spells than do younger adults exposed to the
same traumatic events. In older individuals, the disorder is associated with negative health
perceptions, primary care utilization, and suicidal ideation.

Causes / Risk and Prognostic Factors

Experience of major stress.

In keeping with the diathesis-stress model, research over the past two decades has made it clear that
certain preexisting vulnerabilities also play an important role. Traumatic stressors include combat,
rape, being confined in a concentration camp, and experiencing a natural disaster such as a tsunami,
earthquake, or tornado.

You can develop post-traumatic stress disorder when you go through, see or learn about an event
involving actual or threatened death, serious injury or sexual violation.

Doctors aren't sure why some people get PTSD. As with most mental health problems, PTSD is
probably caused by a complex mix of:

● Stressful experiences, including the amount and severity of trauma you've gone through in
your life

● Inherited mental health risks, such as a family history of anxiety and depression

● Inherited features of your personality — often called your temperament

● The way your brain regulates the chemicals and hormones your body releases in response to
stress

Risk (and protective) factors are generally divided into pre-traumatic, peritraumatic, and
posttraumatic factors.

Pre-traumatic factors
Temperamental. These include childhood emotional problems by age 6 years (e.g., prior traumatic
exposure, externalizing or anxiety problems) and prior mental disorders (e.g., panic disorder,
depressive disorder, PTSD, or obsessive-compulsive disorder [OCD]).

Environmental. These include lower socioeconomic status; lower education; exposure to prior
trauma (especially during childhood); childhood adversity (e.g., economic deprivation, family
dysRinction, parental separation or death); cultural characteristics (e.g., fatalistic or self-blaming
coping strategies); lower intelligence; minority racial/ethnic status; and a family psychiatric history.
Social support prior to event exposure is protective.

Genetic and physiological. These include female gender and younger age at the time of trauma
exposure (for adults). Certain genotypes may either be protective or increase risk of PTSD after
exposure to traumatic events.

Peritraumatic factors

Environmental. These include severity (dose) of the trauma (the greater the magnitude of trauma,
the greater the likelihood of PTSD), perceived life threat, personal injury, interpersonal violence
(particularly trauma perpetrated by a caregiver or involving a witnessed threat to a caregiver in
children), and, for military personnel, being a perpetrator, witnessing atrocities, or killing the enemy.
Finally, dissociation that occurs during the trauma and persists afterward is a risk factor.

Posttraumatic factors

Temperamental. These include negative appraisals, inappropriate coping strategies, and

development of acute stress disorder.

Environmental. These include subsequent exposure to repeated upsetting reminders, subsequent

adverse life events, and financial or other trauma-related losses. Social support (including family
stability, for children) is a protective factor that moderates outcome after trauma.

Culture-Related Diagnostic issues

The risk of onset and severity of PTSD may differ across cultural groups as a result of variation in the
type of traumatic exposure (e.g., genocide), the impact on disorder severity of the meaning
attributed to the traumatic event (e.g., inability to perform funerary rites after a mass killing), the
ongoing sociocultural context (e.g., residing among unpunished perpetrators in post conflict
settings), and other cultural factors (e.g., acculturative stress in immigrants). The relative risk for
PTSD of particular exposures (e.g., religious persecution) may vary across cultural groups. The clinical
expression of the symptoms or symptom clusters of PTSD may vary culturally, particularly with
respect to avoidance and numbing symptoms, distressing dreams, and somatic symptoms (e.g.,
dizziness, shortness of breath, heat sensations).

Cultural syndromes and idioms of distress influence the expression of PTSD and the range of
comorbid disorders in different cultures by providing behavioral and cognitive templates that link
traumatic exposures to specific symptoms. Comprehensive evaluation of local expressions of PTSD
should include assessment of cultural concepts of distress.

Gender-Related Diagnostic issues

PTSD is more prevalent among females than among males across the lifespan. Females in the general
population experience PTSD for a longer duration than do males. At least some of the increased risk
for PTSD in females appears to be attributable to a greater likelihood of exposure to traumatic
events, such as rape, and other forms of interpersonal violence. Within populations exposed
specifically to such stressors, gender differences in risk for PTSD are attenuated or nonsignificant.

Suicide Risk
Traumatic events such as childhood abuse increase a person's suicide risk. PTSD is associated with
suicidal ideation and suicide attempts, and presence of the disorder may indicate which individuals
with ideation eventually make a suicide plan or actually attempt suicide.

Functional Consequences of PTSD

PTSD is associated with high levels of social, occupational, and physical disability, as well as
considerable economic costs and high levels of medical utilization. Impaired functioning is exhibited
across social, interpersonal, developmental, educational, physical health, and occupational domains.
In community and veteran samples, PTSD is associated with poor social and family relationships,
absenteeism from work, lower income, and lower educational and occupational success.

Treatment
When a clinician is faced with a patient who has experienced a signicant trauma, the major
approaches are support, encouragement to discuss the event, and education about a variety of
coping mechanisms (e.g., relaxation). In encouraging persons to talk about the event it is imperative
that the clinician allow the person to proceed at his or her own pace. Some patients will not be
willing to talk until well after the event has passed, and those wishes should be respected. To press a
person who is reluctant to talk about a trauma into doing so is likely to increase rather than decrease
the risk of developing PTSD. The use of sedatives and hypnotics can also be helpful in some cases.
When a patient has experienced a traumatic event in the past and has now developed PTSD, the
emphasis should be on education about the disorder and its treatment, both pharmacological and
psychotherapeutic. The clinician should also work to destigmatize the notion of mental illness and
PTSD. Additional support for the patient and the family can be obtained through local and national
support groups for patients with PTSD.

Pharmacotherapy

Selective serotonin reuptake inhibitors (SSRIs), such as sertraline (Zoloft) and paroxetine (Paxil), are
considered rst-line treatments for PTSD, owing to their efficacy, tolerability, and safety ratings. SSRIs
reduce symptoms from all PTSD symptom clusters and are effective in improving symptoms unique
to PTSD, not just symptoms similar to those of depression or other anxiety disorders. Buspirone
(BuSpar) is serotonergic and may also be of use.

The efficacy of imipramine (Tofranil) and amitriptyline (Elavil), two tricyclic drugs, in the treatment of
PTSD is supported by a number of well-controlled clinical trials. Although some trials of the two
drugs have had negative findings, most of these trials had serious design aws, including too short a
duration. Dosages of imipramine and amitriptyline should be the same as those used to treat
depressive disorders, and an adequate trial should last at least 8 weeks. Patients who respond well
should probably continue the pharmacotherapy for at least 1 year before an attempt is made to
withdraw the drug. Some studies indicate that pharmacotherapy is more effective in treating the
depression, anxiety, and hyperarousal than in treating the avoidance, denial, and emotional
numbing.

Other drugs that may be useful in the treatment of PTSD include the monoamine oxidase inhibitors
(MAOIs) (e.g., phenelzine [Nardil]), trazodone (Desyrel), and the anticonvulsants (e.g.,
carbamazepine [Tegretol], valproate [Depakene]). Some studies have also revealed improvement in
PTSD in patients treated with reversible monoamine oxidase inhibitors (RIMAs). Use of clonidine
(Catapres) and propranolol (Inderal), which are antiadrenergic agents, is suggested by the theories
about noradrenergic hyperactivity in the disorder. There are almost no positive data concerning the
use of antipsychotic drugs in the disorder, so the use of drugs such as haloperidol (Haldol) should be
reserved for the short-term control of severe aggression and agitation. Research is ongoing about the
use of opioid receptor agonists during traumatic events as a preventative against developing PTSD.

Psychotherapy

Psychodynamic psychotherapy may be useful in the treatment of many patients with PTSD. In some
cases, reconstruction of the traumatic events with associated abreaction and catharsis may be
therapeutic, but psychotherapy must be individualized because reexperiencing the trauma
overwhelms some patients.

Psychotherapeutic interventions for PTSD include behavior therapy, cognitive therapy, and hypnosis.
Many clinicians advocate time limited psychotherapy for the victims of trauma. Such therapy usually
takes a cognitive approach and also provides support and security. The short-term nature of
psychotherapy minimizes the risk of dependence and chronicity, but issues of suspicion, paranoia,
and trust often adversely affect compliance. Therapists should overcome patients’ denial of the
traumatic event, encourage them to relax, and remove them from the source of the stress. Patients
should be encouraged to sleep, using medication if necessary. Support from persons in their
environment (e.g., friends and relatives) should be provided. Patients should be encouraged to
review and abreact emotional feelings associated with the traumatic event and to plan for future
recovery. Abreaction—experiencing the emotions associated with the event—may be helpful for
some patients. The amobarbital (Amytal) interview has been used to facilitate this process.

Psychotherapy after a traumatic event should follow a model of crisis intervention with support,
education, and the development of coping mechanisms and acceptance of the event. When PTSD
has developed, two major psychotherapeutic approaches can be taken. The first is exposure therapy,
in which the patient re-experiences the traumatic event through imaging techniques or in vivo
exposure. The exposures can be intense, as in implosive therapy, or graded, as in systematic
desensitization. The second approach is to teach the patient methods of stress management,
including relaxation techniques and cognitive approaches, to coping with stress. Some preliminary
data indicate that, although stress management techniques are effective more rapidly than exposure
techniques, the results of exposure techniques last longer.

Another psychotherapeutic technique that is relatively novel and somewhat controversial is eye
movement desensitization and reprocessing (EMDR), in which the patient focuses on the lateral
movement of the clinician’s finger while maintaining a mental image of the trauma experience. The
general belief is that symptoms can be relieved as patients work through the traumatic event while in
a state of deep relaxation. Proponents of this treatment state it is as effective, and possibly more
effective, than other treatments for PTSD and that it is preferred by both clinicians and patients who
have tried it.

In addition to individual therapy techniques, group therapy and family therapy have been reported to
be effective in cases of PTSD. The advantages of group therapy include sharing of traumatic
experiences and support from other group members. Group therapy has been particularly successful
with Vietnam veterans and survivors of catastrophic disasters such as earthquakes. Family therapy
often helps sustain a marriage through periods of exacerbated symptoms. Hospitalization may be
necessary when symptoms are particularly severe or when a risk of suicide or other violence exists.
Anxiety disorder:
Anxiety disorders include disorders that share features of excessive fear and anxiety and related
behavioral disturbances.

Fear is the emotional response to real or perceived imminent threat, whereas anxiety is anticipation
of future threat (Anxiety involves a general feeling of apprehension about possible future danger, and
fear is an alarm reaction that occurs in response to immediate danger). Obviously, these two states
overlap, but they also differ, with fear more often associated with surges of autonomic arousal
necessary for fight or flight, thoughts of immediate danger, and escape behaviors, and anxiety more
often associated with muscle tension and vigilance in preparation for future danger and cautious or
avoidant behaviors. Sometimes the level of fear or anxiety is reduced by pervasive avoidance
behaviors. Panic attacks feature prominently within the anxiety disorders as a particular type of fear
response. Panic attacks are not limited to anxiety disorders but rather can be seen in other mental
disorders as well.

Anxiety is a state that has many effects: It influences cognition and tends to produce distortions of
perception. It is differentiated from fear, which is an appropriate response to a known threat; anxiety
is a response to a threat that is unknown, vague, or conflictual.

NORMAL ANXIETY

Everyone experiences anxiety. It is characterized most commonly as a disuse, unpleasant, vague

sense of apprehension, often accompanied by autonomic symptoms such as headache, perspiration,
palpitations, tightness in the chest, mild stomach discomfort, and restlessness, indicated by an
inability to sit or stand still for long. The particular constellation of symptoms present during anxiety
tends to vary among persons

Fear versus Anxiety

Anxiety is an alerting signal; it warns of impending danger and enables a person to take measures to
deal with a threat. Fear is a similar alerting signal, but it should be differentiated from anxiety. Fear is
a response to a known, external, definite, or nonconflictual threat; anxiety is a response to a threat
that is unknown, internal, vague, or conflictual. This distinction between fear and anxiety arose
accidentally. When Freud’s early translator mistranslated angst, the German word for “fear,” as
anxiety, Freud himself generally ignored the distinction that associates anxiety with a repressed,
unconscious object and fear with a known, external object. The distinction may be difficult to make
because fear can also be caused by an unconscious, repressed, internal object displaced to another
object in the external world. For example, a boy may fear barking dogs because he actually fears his
father and unconsciously associates his father with barking dogs. Nevertheless, according to
post-freudian psychoanalytic formulations, the separation of fear and anxiety is psychologically
justifiable. The emotion caused by a rapidly approaching car as a person crosses the street differs
from the vague discomfort a person may experience when meeting new persons in a strange setting.
The main psychological difference between the two emotional responses is the suddenness of fear
and the insidiousness of anxiety.

Is Anxiety Adaptive?

Anxiety and fear both are alerting signals and act as a warning of an internal and external threat.
Anxiety can be conceptualized as a normal and adaptive response that has lifesaving qualities and
warns of threats of bodily damage, pain, helplessness, possible punishment, or the frustration of
social or bodily needs; of separation from loved ones; of a menace to one’s success or status; and
ultimately of threats to unity or wholeness. It prompts a person to take the necessary steps to
prevent the threat or to lessen its consequences. This preparation is accompanied by increased
somatic and autonomic activity controlled by the interaction of the sympathetic and parasympathetic
nervous systems. Examples of a person warding o threats in daily life include getting down to the
hard work of preparing for an examination, dodging a ball thrown at the head, sneaking into the
dormitory after curfew to prevent punishment, and running to catch the last commuter train. Thus,
anxiety prevents damage by alerting the person to carry out certain acts that forestall the danger.

Symptoms of Anxiety

The experience of anxiety has two components: the awareness of the physiological sensations (e.g.,
palpitations and sweating) and the awareness of being nervous or frightened. A feeling of shame
may increase anxiety—“Others will recognize that I am frightened.” Many persons are astonished to
find out that others are not aware of their anxiety or, if they are, do not appreciate its intensity. In
addition to motor and visceral effects, anxiety affects thinking, perception, and learning. It tends to
produce confusion and distortions of perception, not only of time and space but also of persons and
the meanings of events. These distortions can interfere with learning by lowering concentration,
reducing recall, and impairing the ability to relate one item to another—that is, to make associations.
An important aspect of emotions is their effect on the selectivity of attention. Anxious persons likely
select certain things in their environment and overlook others in their effort to prove that they are
justified in considering the situation frightening. If they falsely justify their fear, they augment their
anxieties by the selective response and set up a vicious circle of anxiety, distorted perception, and
increased anxiety. If, alternatively, they falsely reassure themselves by selective thinking, appropriate
anxiety may be reduced, and they may fail to take necessary precautions.

Comes under the category of Anxiety Disorders in DSM 5 (category 5), It was the 7th category
of disorders in DSM IV, now it is category 5 in DSM 5, its divisions are given below
Separation Anxiety Disorder
Selective Mutism
Specific Phobia Social Anxiety Disorder (Social Phobia)
Panic Disorder
Panic Attack (Specifier)
Agoraphobia
Generalized Anxiety Disorder
Substance/Medication-Induced Anxiety Disorder
Anxiety Disorder Due to Another Medical Condition
Other Specified Anxiety Disorder
Unspecified Anxiety Disorder

Anxiety disorders can be viewed as a family of related but distinct mental disorders, which include
the above said disorders.

A fascinating aspect of anxiety disorders is the exquisite interplay of genetic and experiential factors.
Little doubt exists that abnormal genes predispose to pathological anxiety states; however, evidence
clearly indicates that traumatic life events and stress are also etiologically important. Thus, the study
of anxiety disorders presents a unique opportunity to understand the relation between nature and
nurture in the etiology of mental disorders.
The anxiety disorders differ from one another in the types of objects or situations that induce fear,
anxiety, or avoidance behavior, and the associated cognitive ideation. Thus, while the anxiety
disorders tend to be highly comorbid with each other, they can be differentiated by close
examination of the types of situations that are feared or avoided and the content of the associated
thoughts or beliefs.

Anxiety disorders differ from developmentally normative fear or anxiety by being excessive or
persisting beyond developmentally appropriate periods. They differ from transient fear or anxiety,
often stress-induced, by being persistent (e.g., typically lasting 6 months or more), although the
criterion for duration is intended as a general guide with allowance for some degree of flexibility and
is sometimes of shorter duration in children (as in separation anxiety disorder and selective mutism).
Since individuals with anxiety disorders typically overestimate the danger in situations they fear or
avoid, the primary determination of whether the fear or anxiety is excessive or out of proportion is
made by the clinician, taking cultural contextual factors into account. Many of the anxiety disorders
develop in childhood and tend to persist if not treated. Most occur more frequently in females than
in males (approximately 2:1 ratio). Each anxiety disorder is diagnosed only when the symptoms are
not attributable to the physiological effects of a substance/medication or to another medical
condition or are not better explained by another mental disorder.

Selective mutism is characterized by a consistent failure to speak in social situations in which there is
an expectation to speak (e.g., school) even though the individual speaks in other situations. The
failure to speak has significant consequences on achievement in academic or occupational settings or
otherwise interferes with normal social communication.

Individuals with specific phobia are fearful or anxious about or avoidant of circumscribed objects or
situations. A specific cognitive ideation is not featured in this disorder, as it is in other anxiety
disorders. The fear, anxiety, or avoidance is almost always immediately induced by the phobic
situation, to a degree that is persistent and out of proportion to the actual risk posed. There are
various types of specific phobias: animal; natural environment; blood-injection-injury; situational;
and other situations.

In social anxiety disorder (social phobia), the individual is fearful or anxious about or avoidant of
social interactions and situations that involve the possibility of being scrutinized. These include social
interactions such as meeting unfamiliar people, situations in which the individual may be observed
eating or drinking, and situations in which the individual performs in front of others. The cognitive
ideation is of being negatively evaluated by others, by being embarrassed, humiliated, or rejected, or
offending others.

In panic disorder, the individual experiences recurrent unexpected panic attacks and is persistently
concerned or worried about having more panic attacks or changes his or her behavior in maladaptive
ways because of the panic attacks (e.g., avoidance of exercise or of unfamiliar locations). Panic
attacks are abrupt surges of intense fear or intense discomfort that reach a peak within minutes,
accompanied by physical and/or cognitive symptoms. Limited-symptom panic attacks include fewer
than four symptoms. Panic attacks may be expected, such as in response to a typically feared object
or situation, or unexpected, meaning that the panic attack occurs for no apparent reason. Panic
attacks function as a marker and prognostic factor for severity of diagnosis, course, and comorbidity
across an array of disorders, including, but not limited to, the anxiety disorders (e.g., substance use,
depressive and psychotic disorders). Panic attack may therefore be used as a descriptive specifier for
any anxiety disorder as well as other mental disorders.
Individuals with agoraphobia are fearful and anxious about two or more of the following situations:
using public transportation; being in open spaces; being in enclosed places; standing in line or being
in a crowd; or being outside of the home alone in other situations. The individual fears these
situations because of thoughts that escape might be difficult or help might not be available in the
event of developing panic-like symptoms or other incapacitating or embarrassing symptoms. These
situations almost always induce fear or anxiety and are often avoided and require the presence of a
companion.

The key features of generalized anxiety disorder are persistent and excessive anxiety and worry about
various domains, including work and school performance, that the individual finds difficult to control.
In addition, the individual experiences physical symptoms, including restlessness or feeling keyed up
or on edge; being easily fatigued; difficulty concentrating or mind going blank; irritability; muscle
tension; and sleep disturbance.

Substance/medication-induced anxiety disorder involves anxiety due to substance intoxication or

withdrawal or to a medication treatment. In anxiety disorder due to another medical condition,
anxiety symptoms are the physiological consequence of another medical condition.

Epidemiology

The anxiety disorders make up one of the most common groups of psychiatric disorders. The
National Comorbidity Study reported that one of four persons met the diagnostic criteria for at least
one anxiety disorder and that there is a 12-month prevalence rate of 17.7 percent. Women (30.5
percent lifetime prevalence) are more likely to have an anxiety disorder than are men (19.2 percent
lifetime prevalence). The prevalence of anxiety disorders decreases with higher socioeconomic
status.

Etiology

A. Biological

1. Anxiety involves an excessive autonomic reaction with increased sympathetic tone.

2. The release of catecholamines is increased with increased production of norepinephrine

metabolites (e.g., 3-methoxy-4-hydroxyphenylglycol).

3. Decreased rapid eye movement (REM), latency, and stage IV sleep (similar to depression) may
develop.
4. Decreased levels of γ-aminobutyric acid (GABA) cause central nervous system (CNS) hyperactivity
(GABA inhibits CNS irritability and is widespread throughout the brain).

5. Alterations in serotonergic system and increased dopaminergic activity are associated with anxiety.

6. Activity in the temporal cerebral cortex is increased.

7. The locus coeruleus, a brain center of noradrenergic neurons, is hyperactive in anxiety states,
especially panic attacks.

8. Recent studies also suggest a role for neuropeptides (substance P, CRF, and cholecystokinin).

9. Hyperactivity and dysregulation in the amygdala may be associated with social anxiety.

B. Psychoanalytic.

According to Freud, unconscious impulses (e.g., sex or aggression) threaten to burst into
consciousness and produce anxiety. Anxiety is related developmentally to childhood fears of
disintegration that derive from the fear of an actual or imagined loss of a love object or the fear of
bodily harm (e.g., castration). Freud used the term signal anxiety to describe anxiety not consciously
experienced but that triggers defense mechanisms used by the person to deal with a potentially
threatening situation. See Table 15–12 for an overview of the psychodynamics of anxiety disorders.

C. Learning theory

1. Anxiety is produced by continued or severe frustration or stress. The anxiety then becomes a
conditioned response to other situations that are less severely frustrating or stressful.

2. It may be learned through identification and imitation of anxiety patterns in parents (social
learning theory).

3. Anxiety is associated with a naturally frightening stimulus (e.g., accident). Subsequent

displacement or transference to another stimulus through conditioning produces a phobia to a new
and different object or situation.

4. Anxiety disorders involve faulty, distorted, or counterproductive patterns of cognitive thinking.

D. Genetic studies

1. Half of patients with panic disorder have one affected relative.

2. About 5% of persons with high levels of anxiety have a polymorphic variant of the gene associated
with serotonin transporter metabolism.

Specific phobia,
300.29 (___.__) Specific Phobia

A phobia is an irrational fear of an object (e.g., horses, heights, needles). The person experiences
massive anxiety when exposed to the feared object and tries to avoid it at all costs. Up to
25%ofthepopulation have specific phobias. More common in females.

A person is diagnosed as having a specific phobia if she or he shows strong and persistent fear that is
triggered by the presence of a specific object or situation.

The term phobia refers to an excessive fear of a specific object, circumstance, or situation. A specific
phobia is a strong, persisting fear of an object or situation. The diagnosis of specific phobia requires
the development of intense anxiety, even to the point of panic, when exposed to the feared object.
Persons with specific phobias may anticipate harm, such as being bitten by a dog, or may panic at the
thought of losing control; for instance, if they fear being in an elevator, they may also worry about
fainting after the door closes.

The development of specific phobia may result from the pairing of a specific object or situation with
the emotions of fear and panic. Various mechanisms for the pairing have been postulated. In general,
a nonspecific tendency to experience fear or anxiety forms the backdrop; when a specific event (e.g.,
driving) is paired with an emotional experience (e.g., an accident), the person is susceptible to a
permanent emotional association between driving or cars and fear or anxiety. The emotional
experience itself can be in response to an external incident, as a trac accident, or to an internal
incident, most commonly a panic attack. Although a person may never again experience a panic
attack and may not meet the diagnostic criteria for panic disorder, he or she may have a generalized
fear of driving, not an expressed fear of having a panic attack while driving. Other mechanisms of
association between the phobic object and the phobic emotions include modeling, in which a person
observes the reaction in another (e.g., a parent), and information transfer, in which a person is
taught or warned about the dangers of specific objects (e.g., venomous snakes).

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

Note: In children, the fear or anxiety may be expressed by crying, tantrums, freezing, or clinging.

B. The phobic object or situation almost always provokes immediate fear or anxiety.

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

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

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

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

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

Diagnostic Features / Symptoms

A key feature of this disorder is that the fear or anxiety is circumscribed to the presence of a
particular situation or object (Criterion A), which may be termed the phobic stimulus. The categories
of feared situations or objects are provided as specifiers. Many individuals fear objects or situations
from more than one category, or phobic stimulus. For the diagnosis of specific phobia, the response
must differ from normal, transient fears that commonly occur in the population. To meet the criteria
for a diagnosis, the fear or anxiety must be intense or severe (i.e., "marked") (Criterion A). The
amount of fear experienced may vary with proximity to the feared object or situation and may occur
in anticipation of or in the actual presence of the object or situation. Also, the fear or anxiety may
take the form of a full or limited symptom panic attack (i.e., expected panic attack). Another
characteristic of specific phobias is that fear or anxiety is evoked nearly every time the individual
comes into contact with the phobic stimulus (Criterion B). Thus, an individual who becomes anxious
only occasionally upon being confronted with the situation or object (e.g., becomes anxious when
flying only on one out of every five airplane flights) would not be diagnosed with specific phobia.
However, the degree of fear or anxiety expressed may vary (from anticipatory anxiety to a full panic
attack) across different occasions of encountering the phobic object or situation because of various
contextual factors such as the presence of others, duration of exposure, and other threatening
elements such as turbulence on a flight for individuals who fear flying. Fear and anxiety are often
expressed differently between children and adults. Also, the fear or anxiety occurs as soon as the
phobic object or situation is encountered (i.e., immediately rather than being delayed).

The individual actively avoids the situation, or if he or she either is unable or decides not to avoid it,
the situation or object evokes intense fear or anxiety (Criterion C). Active avoidance means the
individual intentionally behaves in ways that are designed to prevent or minimize contact with
phobic objects or situations (e.g., takes tunnels instead of bridges on daily commute to work for fear
of heights; avoids entering a dark room for fear of spiders; avoids accepting a job in a locale where a
phobic stimulus is more common). Avoidance behaviors are often obvious (e.g., an individual who
fears blood refusing to go to the doctor) but are sometimes less obvious (e.g., an individual who fears
snakes refusing to look at pictures that resemble the form or shape of snakes). Many individuals with
specific phobias have suffered over many years and have changed their living circumstances in ways
designed to avoid the phobic object or situation as much as possible (e.g., an individual diagnosed
with specific phobia, animal, who moves to reside in an area devoid of the particular feared animal).
Therefore, they no longer experience fear or anxiety in their daily life. In such instances, avoidance
behaviors or ongoing refusal to engage in activities that would involve exposure to the phobic object
or situation (e.g., repeated refusal to accept offers for work-related travel because of fear of flying)
may be helpful in confirming the diagnosis in the absence of overt anxiety or panic.

The fear or anxiety is out of proportion to the actual danger that the object or situation poses, or
more intense than is deemed necessary (Criterion D). Although individuals with specific phobia often
recognize their reactions as disproportionate, they tend to overestimate the danger in their feared
situations, and thus the judgment of being out of proportion is made by the clinician. The individual's
sociocultural context should also be taken into account. For example, fears of the dark may be
reasonable in a context of ongoing violence, and fear of insects may be more disproportionate in
settings where insects are consumed in the diet. The fear, anxiety, or avoidance is persistent, typically
lasting for 6 months or more (Criterion E), which helps distinguish the disorder from transient fears
that are common in the population, particularly among children. However, the duration criterion
should be used as a general guide, with allowance for some degree of flexibility. The specific phobia
must cause clinically significant distress or impairment in social, occupational, or other important
areas of functioning in order for the disorder to be diagnosed (Criterion F).

Prevalence
In the United States, the 12-month community prevalence estimate for specific phobia is
approximately 7%-9%. Prevalence rates in European countries are largely similar to those in the
United States (e.g., about 6%), but rates are generally lower in Asian, African, and Latin American
countries (2%-4%). Prevalence rates are approximately 5% in children and are approximately 16% in
13- to 17-year-olds. Prevalence rates are lower in older individuals (about 3%-5%), possibly reflecting
diminishing severity to subclinical levels. Females are more frequently affected than males, at a rate
of approximately 2:1, although rates vary across different phobic stimuli. That is, animal, natural
environment, and situational specific phobias are predominantly experienced by females, whereas
blood-injection-injury phobia is experienced nearly equally by both genders.

Causes/ ETIOLOGY and Risk and Prognostic Factors

Temperamental. Temperamental risk factors for specific phobia, such as negative affectivity
(neuroticism) or behavioral inhibition, are risk factors for other anxiety disorders as well.

Environmental. Environmental risk factors for specific phobias, such as parental overprotectiveness,
parental loss and separation, and physical and sexual abuse, tend to predict other anxiety disorders
as well. As noted earlier, negative or traumatic encounters with the feared object or situation
sometimes (but not always) precede the development of specific phobia.

Genetic and physiological. There may be a genetic susceptibility to a certain category of specific
phobia (e.g., an individual with a first-degree relative with a specific phobia of animals is significantly
more likely to have the same specific phobia than any other category of phobia). Individuals with
blood-injection-injury phobia show a unique propensity to vasovagal syncope (fainting) in the
presence of the phobic stimulus.

Functional Consequences of Specific Phobia

Individuals with specific phobia show similar patterns of impairment in psychosocial functioning and
decreased quality of life as individuals with other anxiety disorders and alcohol and substance use
disorders, including impairments in occupational and interpersonal functioning. In older adults,
impairment may be seen in caregiving duties and volunteer activities. Also, fear of falling in older
adults can lead to reduced mobility and reduced physical and social functioning, and may lead to
receiving formal or informal home support. The distress and impairment caused by specific phobias
tend to increase with the number of feared objects and situations. Thus, an individual who fears four
objects or situations is likely to have more impairment in his or her occupational and social roles and
a lower quality of life than an individual who fears only one object or situation. Individuals with
blood-injection-injury specific phobia are often reluctant to obtain medical care even when a medical
concern is present. Additionally, fear of vomiting and choking may substantially reduce dietary
intake.

Treatment
Behavior Therapy.

The most studied and most effective treatment for phobias is probably behavior therapy. The key
aspects of successful treatment are (1) the patient’s commitment to treatment; (2) clearly identified
problems and objectives; and (3) available alternative strategies for coping with the feelings. A
variety of behavioral treatment techniques have been used, the most common being systematic
desensitization, a method pioneered by Joseph Wolpe. In this method, the patient is exposed serially
to a predetermined list of anxiety-provoking stimuli graded in a hierarchy from the least to the most
frightening. Through the use of antianxiety drugs, hypnosis, and instruction in muscle relaxation,
patients are taught how to induce in themselves both mental and physical repose. After they have
mastered the techniques, patients are taught to use them to induce relaxation in the face of each
anxiety-provoking stimulus. As they become desensitized to each stimulus in the scale, the patients
move up to the next stimulus until, ultimately, what previously produced the most anxiety no longer
elicits the painful affect.

Other behavioral techniques that have been used more recently involve intensive exposure to the
phobic stimulus through either imagery or desensitization in vivo. In imaginal ooding, patients are
exposed to the phobic stimulus for as long as they can tolerate the fear until they reach a point at
which they can no longer feel it. Flooding (also known as implosion) in vivo requires patients to
experience similar anxiety through exposure to the actual phobic stimulus.

Insight-Oriented Psychotherapy.

Early in the development of psychoanalysis and the dynamically oriented psychotherapies, theorists
believed that these methods were the treatments of choice for phobic neurosis, which was then
thought to stem from oedipal genital conflicts. Soon, however, therapists recognized that, despite
progress in uncovering and analyzing unconscious conflicts, patients frequently failed to lose their
phobic symptoms. Moreover, by continuing to avoid phobic situations, patients excluded a significant
degree of anxiety and its related associations from the analytic process. Both Freud and his pupil
Sandor Ferenczi recognized that if progress in analyzing these symptoms was to be made, therapists
had to go beyond their analytic roles and actively urge patients with phobia to seek the phobic
situation and experience the anxiety and resultant insight. Since then, psychiatrists have generally
agreed that a measure of activity on the therapist’s part is often required to treat phobic anxiety
successfully. The decision to apply the techniques of psychodynamic insight-oriented therapy should
be based not on the presence of phobic symptoms alone but on positive indications from the
patient’s ego structure and life patterns for the use of this method of treatment. Insight-oriented
therapy enables patients to understand the origin of the phobia, the phenomenon of secondary gain,
and the role of resistance and enables them to seek healthy ways of dealing with anxiety provoking
stimuli.

Virtual Therapy.

A number of computer-generated simulations of phobic disorders have been developed. Patients are
exposed to or interact with the phobic object or situation on the computer screen. Countless
numbers of such programs are available, and others are in continual development. Variable success
rates have been reported, but virtual therapy for phobic disorder is on the cutting edge of using
computers to treat mental illness.

Other Therapeutic Modalities.

Hypnosis, supportive therapy, and family therapy may be useful in the treatment of phobic disorders.
Hypnosis is used to enhance the therapist’s suggestion that the phobic object is not dangerous, and
self-hypnosis can be taught to the patient as a method of relaxation when confronted with the
phobic object. Supportive psychotherapy and family therapy are often useful in helping the patient
actively confront the phobic object during treatment. Not only can family therapy enlist the aid of
the family in treating the patient, but it may also help the family understand the nature of the
patient’s problem.

Specific Phobia

A common treatment for specific phobia is exposure therapy. In this method, therapists desensitize
patients by using a series of gradual, self-paced exposures to the phobic stimuli, and they teach
patients various techniques to deal with anxiety, including relaxation, breathing control, and
cognitive approaches. The cognitive-behavioral approaches include reinforcing the realization that
the phobic situation is, in fact, safe. The key aspects of successful behavior therapy are the patient’s
commitment to treatment, clearly identified problems and objectives, and alternative strategies for
coping with the patient’s feelings. In the special situation of blood-injection-injury phobia, some
therapists recommend that patients tense their bodies and remain seated during the exposure to
help avoid the possibility of fainting from a vasovagal reaction to the phobic stimulation.
β-adrenergic receptor antagonists may be useful in the treatment of specific phobia, especially when
the phobia is associated with panic attacks. Pharmacotherapy (e.g., benzodiazepines),
psychotherapy, or combined therapy directed to the attacks may also be of benefit.

Social phobias
300.23 (F40.10) Social Anxiety Disorder (Social Phobia)

Social phobia is an irrational fear of public situations (e.g., speaking in public, eating in public, using
public bathrooms [shy bladder]). May be associated with panic attacks. It usually occurs during early
teens but can develop during childhood. Affects up to 13% of persons. Equally common in men and
women.

Social anxiety disorder (also referred to as social phobia) involves the fear of social situations,
including situations that involve scrutiny or contact with strangers. The term social anxiety reflects
the distinct differentiation of social anxiety disorder from specific phobia, which is the intense and
persistent fear of an object or situation. Persons with social anxiety disorder are fearful of
embarrassing themselves in social situations (i.e., social gatherings, oral presentations, meeting new
people). They may have specific fears about performing specific activities such as eating or speaking
in front of others, or they may experience a vague, nonspecific fear of “embarrassing oneself.” In
either case, the fear in social anxiety disorder is of the embarrassment that may occur in the
situation, not of the situation itself.

EPIDEMIOLOGY

Various studies have reported a lifetime prevalence ranging from 3 to 13 percent for social anxiety
disorder. In epidemiological studies, females are affected more often than males, but in clinical
samples, the reverse is often true. The reasons for these varying observations are unknown. The
peak age of onset for social anxiety disorder is in the teens, although onset is common as young as 5
years of age and as old as 35 years.

Diagnostic Criteria
A. Marked fear or anxiety about one or more social situations in which the individual is exposed to
possible scrutiny by others. Examples include social interactions (e.g., having a conversation, meeting
unfamiliar people), being observed (e.g., eating or drinking), and performing in front of others (e.g.,
giving a speech).

Note: In children, the anxiety must occur in peer settings and not just during interactions
with adults.

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

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

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

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

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

F. The fear, anxiety, or avoidance is persistent, typically lasting for 6 months or more.
G. The fear, anxiety, or avoidance causes clinically significant distress or impairment in social,
occupational, or other important areas of functioning.

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

I. The fear, anxiety, or avoidance is not better explained by the symptoms of another mental disorder,
such as panic disorder, body dysmoφhic disorder, or autism spectrum disorder.

J. If another medical condition (e.g., Parkinson’s disease, obesity, disfigurement from bums or injury)
is present, the fear, anxiety, or avoidance is clearly unrelated or is excessive.

Diagnostic Features / Symptoms

The essential feature of social anxiety disorder is a marked, or intense, fear or anxiety of social
situations in which the individual may be scrutinized by others. In children the fear or anxiety must
occur in peer settings and not just during interactions with adults (Criterion A). When exposed to
such social situations, the individual fears that he or she will be negatively evaluated. The individual
is concerned that he or she will be judged as anxious, weak, crazy, stupid, boring, intimidating, dirty,
or unlikable. The individual fears that he or she will act or appear in a certain way or show anxiety
symptoms, such as blushing, trembling, sweating, stumbling over one's words, or staring, that will be
negatively evaluated by others (Criterion B). Some individuals fear offending others or being rejected
as a result. Fear of offending others—for example, by a gaze or by showing anxiety symptoms—may
be the predominant fear in individuals from cultures with strong collectivistic orientations. An
individual with fear of trembling of the hands may avoid drinking, eating, writing, or pointing in
public; an individual with fear of sweating may avoid shaking hands or eating spicy foods; and an
individual with fear of blushing may avoid public performance, bright lights, or discussion about
intimate topics. Some individuals fear and avoid urinating in public restrooms when other individuals
are present (i.e., paruresis, or "shy bladder syndrome").

The social situations almost always provoke fear or anxiety (Criterion C). Thus, an individual who
becomes anxious only occasionally in the social situation(s) would not be diagnosed with social
anxiety disorder. However, the degree and type of fear and anxiety may vary (e.g., anticipatory
anxiety, a panic attack) across different occasions. The anticipatory anxiety may occur sometimes far
in advance of upcoming situations (e.g., worrying every day for weeks before attending a social
event, repeating a speech for days in advance). In children, the fear or anxiety may be expressed by
crying, tantrums, freezing, clinging, or shrinking in social situations. The individual will often avoid
the feared social situations. Alternatively, the situations are endured with intense fear or anxiety
(Criterion D). Avoidance can be extensive (e.g., not going to parties, refusing school) or subtle (e.g.,
overpreparing the text of a speech, diverting attention to others, limiting eye contact).

The fear or anxiety is judged to be out of proportion to the actual risk of being negatively evaluated
or to the consequences of such negative evaluation (Criterion E). Sometimes, the anxiety may not be
judged to be excessive, because it is related to an actual danger (e.g., being bullied or tormented by
others). However, individuals with social anxiety disorder often overestimate the negative
consequences of social situations, and thus the judgment of being out of proportion is made by the
clinician. The individual's sociocultural context needs to be taken into account when this judgment is
being made. For example, in certain cultures, behavior that might otherwise appear socially anxious
may be considered appropriate in social situations (e.g., might be seen as a sign of respect).

The duration of the disturbance is typically at least 6 months (Criterion F). This duration threshold
helps distinguish the disorder from transient social fears that are common, particularly among
children and in the community. However, the duration criterion should be used as a general guide,
with allowance for some degree of flexibility. The fear, anxiety, and avoidance must interfere
significantly with the individual's normal routine, occupational or academic functioning, or social
activities or relationships, or must cause clinically significant distress or impairment in social,
occupational, or other important areas of functioning (Criterion G). For example, an individual who is
afraid to speak in public would not receive a diagnosis of social anxiety disorder if this activity is not
routinely encountered on the job or in classroom work, and if the individual is not significantly
distressed about it. However, if the individual avoids, or is passed over for, the job or education he or
she really wants because of social anxiety symptoms. Criterion G is met.

Prevalence
The 12-month prevalence estimate of social anxiety disorder for the United States is approximately
7%. Lower 12-month prevalence estimates are seen in much of the world using the same diagnostic
instrument, clustering around 0.5%-2.0%; median prevalence in Europe is 2.3%. The 12-month
prevalence rates in children and adolescents are comparable to those in adults. Prevalence rates
decrease with age. The 12-month prevalence for older adults ranges from 2% to 5%. In general,
higher rates of social anxiety disorder are found in females than in males in the general population
(with odds ratios ranging from 1.5 to 2.2), and the gender difference in prevalence is more
pronounced in adolescents and young adults. Gender rates are equivalent or slightly higher for males
in clinical samples, and it is assumed that gender roles and social expectations play a significant role
in explaining the heightened help-seeking behavior in male patients. Prevalence in the United States
is higher in American Indians and lower in persons of Asian, Latino, African American, and
Afro-Caribbean descent compared with non-Hispanic whites.

Development and Course

Median age at onset of social anxiety disorder in the United States is 13 years, and 75% of individuals
have an age at onset between 8 and 15 years. The disorder sometimes emerges out of a childhood
history of social inhibition or shyness in U.S. and European studies. Onset can also occur in early
childhood. Onset of social anxiety disorder may follow a stressful or humiliating experience (e.g.,
being bullied, vomiting during a public speech), or it may be insidious, developing slowly.

Causes/ ETIOLOGY and Risk and Prognostic Factors

Several studies have reported that some children possibly have a trait characterized by a consistent
pattern of behavioral inhibition. This trait may be particularly common in the children of parents who
are aected with panic disorder, and it may develop into severe shyness as the children grow older. At
least some persons with social anxiety disorder may have exhibited behavioral inhibition during
childhood. Perhaps associated with this trait, which is thought to be biologically based, are the
psychologically based data indicating that the parents of persons with social anxiety disorder, as a
group, were less caring, more rejecting, and more overprotective of their children than were other
parents. Some social anxiety disorder research has referred to the spectrum from dominance to
submission observed in the animal kingdom. For example, whereas dominant humans may tend to
walk with their chins in the air and to make eye contact, submissive humans may tend to walk with
their chins down and to avoid eye contact.

Temperamental. Underlying traits that predispose individuals to social anxiety disorder include
behavioral inhibition and fear of negative evaluation.

Environmental. There is no causative role of increased rates of childhood maltreatment or other

early-onset psychosocial adversity in the development of social anxiety disorder. However, childhood
maltreatment and adversity are risk factors for social anxiety disorder.
Genetic and physiological. Traits predisposing individuals to social anxiety disorder, such as
behavioral inhibition, are strongly genetically influenced. The genetic influence is subject to
gene-environment interaction; that is, children with high behavioral inhibition are more susceptible
to environmental influences, such as socially anxious modeling by parents. Also, social anxiety
disorder is heritable (but performance-only anxiety less so). First-degree relatives have a two to six
times greater chance of having social anxiety disorder, and liability to the disorder involves the
interplay of disorder-specific (e.g., fear of negative evaluation) and nonspecific (e.g., neuroticism)
genetic factors.

Neurochemical Factors

The success of pharmacotherapies in treating social anxiety disorder has generated two specic
neurochemical hypotheses about two types of social anxiety disorder. Specically, the use of
β-adrenergic receptor antagonists—for example, propranolol (Inderal)—for performance phobias
(e.g., public speaking) has led to the development of an adrenergic theory for these phobias. Patients
with performance phobias may release more norepinephrine or epinephrine, both centrally and
peripherally, than do nonphobic persons, or such patients may be sensitive to a normal level of
adrenergic stimulation. The observation that MAOIs may be more eective than tricyclic drugs in the
treatment of generalized social anxiety disorder, in combination with preclinical data, has led some
investigators to hypothesize that dopaminergic activity is related to the pathogenesis of the disorder.
One study has shown signicantly lower homovanillic acid concentrations. Another study using SPECT
demonstrated decreased striatal dopamine reuptake site density. Thus, some evidence suggests
dopaminergic dysfunction in social anxiety disorder.

Genetic Factors

First-degree relatives of persons with social anxiety disorder are about three times more likely to be
aected with social anxiety disorder than are rst-degree relatives of those without mental disorders.
And some preliminary data indicate that monozygotic twins are more often concordant than are
dizygotic twins, although in social anxiety disorder, it is particularly important to study twins reared
apart to help control for environmental factors.

Prognosis:

Social anxiety disorder tends to have its onset in late childhood or early adolescence. Existing
prospective epidemiological ndings indicate that social anxiety disorder is typically chronic, although
patients whose symptoms do remit tend to stay well. Both retrospective epidemiological studies and
prospective clinical studies suggest that the disorder can profoundly disrupt the life of an individual
over many years. This can include disruption in school or academic achievement and interference
with job performance and social development.

Functional Consequences of Social anxiety disorder/ Social Phobia

Social anxiety disorder is associated with elevated rates of school dropout and with decreased
well-being, employment, workplace productivity, socioeconomic status, and quality of life. Social
anxiety disorder is also associated with being single, unmarried, or divorced and with not having
children, particularly among men. In older adults, there may be impairment in caregiving duties and
volunteer activities. Social anxiety disorder also impedes leisure activities. Despite the extent of
distress and social impairment associated with social anxiety disorder, only about half of individuals
with the disorder in Western societies ever seek treatment, and they tend to do so only after 15-20
years of experiencing symptoms. Not being employed is a strong predictor for ihe persistence of
social aimety disorder.
Treatment
Both psychotherapy and pharmacotherapy are useful in treating social anxiety disorder. Some studies
indicate that the use of both pharmacotherapy and psychotherapy produces better results than
either therapy alone, although the finding may not be applicable to all situations and patients.

Effective drugs for the treatment of social anxiety disorder include (1) SSRIs, (2) the benzodiazepines,
(3) venlafaxine (Effexor), and (4) buspirone (BuSpar). Most clinicians consider SSRIs the rst-line
treatment choice for patients with more generalized forms of social anxiety disorder. The
benzodiazepines alprazolam (Xanax) and clonazepam (Klonopin) are also efficacious in social anxiety
disorder. Buspirone has shown additive effects when used to augment treatment with SSRIs.

In severe cases, successful treatment of social anxiety disorder with both irreversible MAOIs such as
phenelzine (Nardil) and reversible inhibitors of monoamine oxidase such as moclobemide (Aurorix)
and brofaromine (Consonar), which are not available in the United States, has been reported.
Therapeutic dosages of phenelzine range from 45 to 90 mg a day, with response rates ranging from
50 to 70 percent; approximately 5 to 6 weeks is needed to assess the efficacy.

The treatment of social anxiety disorder associated with performance situations frequently involves
the use of β-adrenergic receptor antagonists shortly before exposure to a phobic stimulus. The two
compounds most widely used are atenolol (Tenormin) 50 to 100 mg taken about 1 hour before the
performance, or propranolol, 20 to 40 mg. Another option to help with performance anxiety is a
relatively short- or intermediate-acting benzodiazepine, such as lorazepam or alprazolam. Cognitive,
behavioral, and exposure techniques are also useful in performance situations.

Psychotherapy for social anxiety disorder usually involves a combination of behavioral and cognitive
methods, including cognitive retraining, desensitization, rehearsal during sessions, and a range of
homework assignments.

Generalized anxiety disorders

300.02 (F41.1) Generalized Anxiety Disorder

Most of us worry and get anxious occasionally, and anxiety is an adaptive emotion that helps us plan
and prepare for possible threat. But for some people, anxiety and worry about many different
aspects of life (including minor events) becomes chronic, excessive, and unreasonable. In these
cases, generalized anxiety disorder (GAD) (formerly known as free-floating anxiety) may be
diagnosed.

Involves excessive worry about everyday life circumstances, events, or conflicts. The symptoms may
fluctuate and overlap with other medical and psychiatric disorders (depressive and other anxiety
disorders). The anxiety is difficult to control, is subjectively distressing, and produces impairments in
important areas of a person’s life. Occurs in children and adults with a lifetime prevalence of 45%.
Ratio of women to men is 2:1

Anxiety can be conceptualized as a normal and adaptive response to threat that prepares the
organism for flight or fight. Persons who seem to be anxious about almost everything, however, are
likely to be classified as having generalized anxiety disorder. Generalized anxiety disorder is defined
as excessive anxiety and worry about several events or activities for most days during at least a
6-month period. The worry is difficult to control and is associated with somatic symptoms, such as
muscle tension, irritability, difficulty sleeping, and restlessness. The anxiety is not focused on features
of another disorder, is not caused by substance use or a general medical condition, and does not
occur only during a mood or psychiatric disorder. The anxiety is difficult to control, is subjectively
distressing, and produces impairment in important areas of a person’s life.

Generalized anxiety disorder is characterized by a pattern of frequent, persistent worry and anxiety
that is out of proportion to the impact of the event or circumstance that is the focus of the worry.
The distinction between generalized anxiety disorder and normal anxiety is emphasized by the use of
the word “excessive” in the criteria and by the specification that the symptoms cause significant
impairment or distress.

Muscle tension, restlessness, and difficulty concentrating are all symptoms that people with
generalized anxiety disorder may have. Such individuals also worry excessively and are hypervigilant
for possible signs of threat in their environment.

The nearly constant worries of people with generalized anxiety disorder leave them continually upset
and discouraged. In one study, the most common spheres of worry were found to be family, work,
finances, and personal illness

EPIDEMIOLOGY

Generalized anxiety disorder is a common condition; reasonable estimates for its 1-year prevalence
range from 3 to 8 percent. The ratio of women to men with the disorder is about 2 to 1, but the ratio
of women to men who are receiving inpatient treatment for the disorder is about 1 to 1. A lifetime
prevalence is close to 5 percent with the Epidemiological Catchment Area (ECA) study suggesting a
lifetime prevalence as high as 8 percent. In anxiety disorder clinics, about 25 percent of patients have
generalized anxiety disorder. The disorder usually has its onset in late adolescence or early
adulthood, although cases are commonly seen in older adults. Also, some evidence suggests that the
prevalence of generalized anxiety disorder is particularly high in primary care settings.

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

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

C. The anxiety and worry are associated with three (or more) of the following six symptoms (with at
least some symptoms having been present for more days than not for the past 6 months);

Note: Only one item is required in children.

1. Restlessness or feeling keyed up or on edge.

2. Being easily fatigued.

3. Difficulty concentrating or mind going blank.

4. Irritability.

5. Muscle tension.

6. Sleep disturbance (difficulty falling or staying asleep, or restless, unsatisfying sleep).

D. The anxiety, worry, or physical symptoms cause clinically significant distress or impairment in
social, occupational, or other important areas of functioning.
E. The disturbance is not attributable to the physiological effects of a substance (e.g., a drug of
abuse, a medication) or another medical condition (e.g., hyperthyroidism).

F. The disturbance is not better explained by another mental disorder (e.g., anxiety or worry about
having panic attacks in panic disorder, negative evaluation in social anxiety disorder [social phobia],
contamination or other obsessions in obsessive-compulsive disorder, separation from attachment
figures in separation anxiety disorder, reminders of traumatic events in posttraumatic stress disorder,
gaining weight in anorexia nervosa, physical complaints in somatic symptom disorder, perceived
appearance flaws in body dysmorphic disorder, having a serious illness in illness anxiety disorder, or
the content of delusional beliefs in schizophrenia or delusional disorder).

Diagnostic Features / Symptoms

The essential feature of generalized anxiety disorder is excessive anxiety and worry (apprehensive
expectation) about a number of events or activities. The intensity, duration, or frequency of the
anxiety and worry is out of proportion to the actual likelihood or impact of the anticipated event. The
individual finds it difficult to control the worry and to keep worrisome thoughts from interfering with
attention to tasks at hand. Adults with generalized anxiety disorder often worry about everyday,
routine life circumstances, such as possible job responsibilities, health and finances, the health of
family members, misfortune to their children, or minor matters (e.g., doing household chores or
being late for appointments). Children with generalized anxiety disorder tend to worry excessively
about their competence or the quality of their performance. During the course of the disorder, the
focus of worry may shift from one concern to another.

Several features distinguish generalized anxiety disorder from nonpathological anxiety. First, the
worries associated with generalized anxiety disorder are excessive and typically interfere significantly
with psychosocial functioning, whereas the worries of everyday life are not excessive and are
perceived as more manageable and may be put off when more pressing matters arise. Second, the
worries associated with generalized anxiety disorder are more pervasive, pronounced (marked), and
distressing; have longer duration; and frequently occur without precipitants. The greater the range of
life circumstances about which a person worries (e.g., finances, children's safety, job performance),
the more likely his or her symptoms are to meet criteria for generalized anxiety disorder. Third,
everyday worries are much less likely to be accompanied by physical symptoms (e.g., restlessness or
feeling keyed up or on edge). Individuals with generalized anxiety disorder report subjective distress
due to constant worry and related impairment in social, occupational, or other important areas of
functioning.

Prevalence
The 12-month prevalence of generalized anxiety disorder is 0.9% among adolescents and 2.9%
among adults in the general community of the United States. The 12-month prevalence for the
disorder in other countries ranges from 0.4% to 3.6%. The lifetime morbid risk is 9.0%. Females are
twice as likely as males to experience generalized anxiety disorder. The prevalence of the diagnosis
peaks in middle age, and declines across the later years of life.

Individuals of European descent tend to experience generalized anxiety disorder more frequently
than do individuals of non-European descent (i.e., Asian, African, Native American and Pacific
Islander). Furthermore, individuals from developed countries are more likely than individuals from
nondeveloped countries to report that they have experienced symptoms that meet criteria for
generalized anxiety disorder in their lifetime.
Development and Course
Many individuals with generalized anxiety disorder report that they have felt anxious and nervous all
of their lives. The median age at onset for generalized anxiety disorder is 30 years; however, age at
onset is spread over a very broad range. The median age at onset is later than that for the other
anxiety disorders. The symptoms of excessive worry and anxiety may occur early in life but are then
manifested as an anxious temperament. Onset of the disorder rarely occurs prior to adolescence.
The symptoms of generalized anxiety disorder tend to be chronic and wax and wane across the
lifespan, fluctuating between syndromal and subsyndromal forms of the disorder. Rates of full
remission are very low.

The clinical expression of generalized anxiety disorder is relatively consistent across the lifespan. The
primary difference across age groups is in the content of the individual's worry. Children and
adolescents tend to worry more about school and sporting performance, whereas older adults report
greater concern about the well-being of family or their own physical heath. Thus, the content of an
individual's worry tends to be age appropriate. Younger adults experience greater severity of
symptoms than do older adults.

The earlier in life individuals have symptoms that meet criteria for generalized anxiety disorder, the
more comorbidity they tend to have and the more impaired they are likely to be. The advent of
chronic physical disease can be a potent issue for excessive worry in the elderly. In the frail elderly,
worries about safety—and especially about falling—may limit activities. In those with early cognitive
impairment, what appears to be excessive worry about, for example, the whereabouts of things is
probably better regarded as realistic given the cognitive impairment.

In children and adolescents with generalized anxiety disorder, the anxieties and worries often
concern the quality of their performance or competence at school or in sporting events, even when
their performance is not being evaluated by others. There may be excessive concerns about
punctuality. They may also worry about catastrophic events, such as earthquakes or nuclear war.
Children with the disorder may be overly conforming, perfectionist, and unsure of themselves and
tend to redo tasks because of excessive dissatisfaction with less-than-perfect performance. They are
typically overzealous in seeking reassurance and approval and require excessive reassurance about
their performance and other things they are worried about.

Generalized anxiety disorder may be over diagnosed in children. When this diagnosis is being
considered in children, a thorough evaluation for the presence of other childhood anxiety disorders
and other mental disorders should be done to determine whether the worries may be better
explained by one of these disorders. Separation anxiety disorder, social anxiety disorder (social
phobia), and obsessive-compulsive disorder are often accompanied by worries that may mimic those
described in generalized anxiety disorder. For example, a child with social anxiety disorder may be
concerned about school performance because of fear of humiliation. Worries about illness may also
be better explained by separation anxiety disorder or obsessive-compulsive disorder.

COURSE AND PROGNOSIS

The age of onset is difficult to specify; most patients with the disorder report that they have been
anxious for as long as they can remember. Patients usually come to a clinician’s attention in their 20s,
although the first contact with a clinician can occur at virtually any age. Only one-third of patients
who have generalized anxiety disorder seek psychiatric treatment. Many go to general practitioners,
internists, cardiologists, pulmonary specialists, or gastroenterologists, seeking treatment for the
somatic component of the disorder. Because of the high incidence of comorbid mental disorders in
patients with generalized anxiety disorder, the clinical course and prognosis of the disorder are
difficult to predict. Nonetheless, some data indicate that life events are associated with the onset of
generalized anxiety disorder: The occurrence of several negative life events greatly increases the
likelihood that the disorder will develop. By definition, generalized anxiety disorder is a chronic
condition that may well be lifelong.

Causes/ ETIOLOGY and Risk and Prognostic Factors

The cause of generalized anxiety disorder is not known. As currently defined, generalized anxiety
disorder probably affects a heterogeneous group of persons. Perhaps because a certain degree of
anxiety is normal and adaptive, differentiating normal anxiety from pathological anxiety and
differentiating biological causative factors from psychosocial factors are difficult. Biological and
psychological factors probably work together.

Biological Factors

The therapeutic efficacies of benzodiazepines and the azaspirones (e.g., buspirone [BuSpar]) have
focused biological research efforts on the γ-aminobutyric acid and serotonin neurotransmitter
systems. Whereas benzodiazepines (which are benzodiazepine receptor agonists) are known to
reduce anxiety, flumazenil (Romazicon) (a benzodiazepine receptor antagonist) and the β-carbolines
(benzodiazepine receptor reverse agonists) are known to induce anxiety. Although no convincing
data indicate that the benzodiazepine receptors are abnormal in patients with generalized anxiety
disorder, some researchers have focused on the occipital lobe, which has the highest concentrations
of benzodiazepine receptors in the brain. Other brain areas hypothesized to be involved in
generalized anxiety disorder are the basal ganglia, the limbic system, and the frontal cortex. Because
buspirone is an agonist at the serotonin 5-HT1A receptor, there is the hypothesis that the regulation
of the serotonergic system in generalized anxiety disorder is abnormal. Other neurotransmitter
systems that have been the subject of research in generalized anxiety disorder include the
norepinephrine, glutamate, and cholecystokinin systems. Some evidence indicates that patients with
generalized anxiety disorder may have subsensitivity of their α2-adrenergic receptors, as indicated by
a blunted release of growth hormone after clonidine (Catapres) infusion.

Brain imaging studies of patients with generalized anxiety disorder have revealed signicant ndings.
One PET study reported a lower metabolic rate in basal ganglia and white matter in patients with
generalized anxiety disorder than in normal control subjects. A few genetic studies have also been
conducted in the eld. One study found that a genetic relation might exist between generalized
anxiety disorder and major depressive disorder in women. Another study showed a distinct, but
dicult-to-quantitate, genetic component in generalized anxiety disorder. About 25 percent of
rst-degree relatives of patients with generalized anxiety disorder are also aected. Male relatives are
likely to have an alcohol use disorder. Some twin studies report a concordance rate of 50 percent in
monozygotic twins and 15 percent in dizygotic twins. Table 9.6-1 lists relative genetic risks in selected
anxiety disorders.

A variety of electroencephalogram (EEG) abnormalities has been noted in alpha rhythm and evoked
potentials. Sleep EEG studies have reported increased sleep discontinuity, decreased delta sleep,
decreased stage 1 sleep, and reduced rapid eye movement sleep. These changes in sleep
architecture differ from the changes seen in depressive disorders.

Psychosocial Factors
The two major schools of thought about psychosocial factors leading to the development of
generalized anxiety disorder are the cognitivebehavioral school and the psychoanalytic school.
According to the cognitive-behavioral school, patients with generalized anxiety disorder respond to
incorrectly and inaccurately perceived dangers. The inaccuracy is generated by selective attention to
negative details in the environment, by distortions in information processing, and by an overly
negative view of the person’s own ability to cope. The psychoanalytic school hypothesizes that
anxiety is a symptom of unresolved, unconscious conflicts. Sigmund Freud rst presented this
psychological theory in 1909 with his description of Little Hans; before then, Freud had
conceptualized anxiety as having a physiological basis.

Temperamental. Behavioral inhibition, negative affectivity (neuroticism), and harm avoidance have
been associated with generalized anxiety disorder.

Environmental. Although childhood adversities and parental overprotection have been associated
with generalized anxiety disorder, no environmental factors have been identified as specific to
generalized anxiety disorder or necessary or sufficient for making the diagnosis.

Genetic and physiological. One-third of the risk of experiencing generalized anxiety disorder is
genetic, and these genetic factors overlap with the risk of neuroticism and are shared with other
anxiety and mood disorders, particularly major depressive disorder.

Functional Consequences of Generalized Anxiety Disorder

Excessive worrying impairs the individual's capacity to do things quickly and efficiently, whether at
home or at work. The worrying takes time and energy; the associated symptoms of muscle tension
and feeling keyed up or on edge, tiredness, difficulty concentrating, and disturbed sleep contribute
to the impairment. Importantly the excessive worrying may impair the ability of individuals with
generalized anxiety disorder to encourage confidence in their children.

Generalized anxiety disorder is associated with significant disability and distress that is independent
of comorbid disorders, and most non-institutionalized adults with the disorder are moderately to
seriously disabled. Generalized anxiety disorder accounts for 110 million disability days per annum in
the U.S. population.

Treatment
The most effective treatment of generalized anxiety disorder is probably one that combines
psychotherapeutic, pharmacotherapeutic, and supportive approaches. The treatment may take a
significant amount of time for the involved clinician, whether the clinician is a psychiatrist, a family
practitioner, or another specialist.

Psychotherapy

The major psychotherapeutic approaches to generalized anxiety disorder are cognitive-behavioral,

supportive, and insight oriented. Data are still limited on the relative merits of those approaches,
although the most sophisticated studies have examined cognitive-behavioral techniques, which seem
to have both short-term and long-term efficacy. Cognitive approaches address patients’ hypothesized
cognitive distortions directly, and behavioral approaches address somatic symptoms directly. The
major techniques used in behavioral approaches are relaxation and biofeedback. Some preliminary
data indicate that the combination of cognitive and behavioral approaches is more effective than
either technique used alone. Supportive therapy offers patients reassurance and comfort, although
its long-term efficacy is doubtful. Insight-oriented psychotherapy focuses on uncovering unconscious
conflicts and identifying ego strengths. The efficacy of insight-oriented psychotherapy for generalized
anxiety disorder is found in many anecdotal case reports, but large controlled studies are lacking.

Most patients experience a marked lessening of anxiety when given the opportunity to discuss their
difficulties with a concerned and sympathetic physician. If clinicians discover external situations that
are anxiety provoking, they may be able—alone or with the help of the patients or their families—to
change the environment and thus reduce the stressful pressures. A reduction in symptoms often
allows patients to function effectively in their daily work and relationships and thus gain new rewards
and gratification that are themselves therapeutic.

In the psychoanalytic perspective, anxiety sometimes signals unconscious turmoil that deserves
investigation. The anxiety can be normal, adaptive, maladaptive, too intense, or too mild, depending
on the circumstances. Anxiety appears in numerous situations over the course of the life cycle; in
many cases, symptom relief is not the most appropriate course of action.

For patients who are psychologically minded and motivated to understand the sources of their
anxiety, psychotherapy may be the treatment of choice. Psychodynamic therapy proceeds with the
assumption that anxiety can increase with effective treatment. The goal of the dynamic approach
may be to increase the patient’s anxiety tolerance (a capacity to experience anxiety without having
to discharge it), rather than to eliminate anxiety. Empirical research indicates that many patients who
have successful psychotherapeutic treatment may continue to experience anxiety after termination
of the psychotherapy, but their increased ego mastery allows them to use the anxiety symptoms as a
signal to reflect on internal struggles and to expand their insight and understanding. A
psychodynamic approach to patients with generalized anxiety disorder involves a search for the
patient’s underlying fears.

Pharmacotherapy

The decision to prescribe an anxiolytic to patients with generalized anxiety disorder should rarely be
made on the first visit. Because of the long-term nature of the disorder, a treatment plan must be
carefully thought out. The three major drugs to be considered for the treatment of generalized
anxiety disorder are benzodiazepines, the SSRIs, buspirone (BuSpar), and venlafaxine (Effexor). Other
drugs that may be useful are the tricyclic drugs (e.g., imipramine [Tofranil]), antihistamines, and the
β-adrenergic antagonists (e.g., propranolol [Inderal])

Although drug treatment of generalized anxiety disorder is sometimes seen as a 6- to 12-month

treatment, some evidence indicates that treatment should be long term, perhaps lifelong. About 25
percent of patients relapse in the rst month after the discontinuation of therapy, and 60 to 80
percent relapse over the course of the next year. Although some patients become dependent on the
benzodiazepines, tolerance rarely develops to the therapeutic effects of the benzodiazepines,
buspirone, venlafaxine, or the SSRIs.

Treatment_ Anxiety disorder

The treatment of anxiety disorders involves both a psychopharmacological approach as well as
psychotherapy (CBT, psychodynamic, time limited, group and family therapies).

Pharmacological

1. Benzodiazepines. These drugs are generally effective in reducing anxiety. In panic disorder, they
reduce both the number and intensity of attacks. They are also useful in social and specific phobia.
2. Selective serotonin reuptake inhibitors (SSRIs).

3. Tricyclics. Drugs in this class reduce the intensity of anxiety in all the anxiety disorders, especially in
obsessive–compulsive states. however, they are not first-line agents because of a major adverse side
effect.

4. Monoamine oxidase inhibitors (MAOIs). MAOIs are effective for the treatment of panic and other
anxiety disorders; however, they are not first-line agents because of a major adverse side effect,
which is the occurrence of a hypertensive crisis secondary to ingestion of foods containing tyramine.

Psychological

1. Supportive psychotherapy.

This approach involves the use of psychodynamic concepts and a therapeutic alliance to promote
adaptive coping. Adaptive defenses are encouraged and strengthened, and maladaptive ones are
discouraged. The therapist assists in reality testing and may offer advice regarding behavior.

[Link]-oriented psychotherapy.

The goal is to increase the patient’s development of insight into psychological conflicts that, if
unresolved, can manifest as symptomatic behavior (e.g., anxiety, phobias,
obsessionsandcompulsions,andposttraumaticstressreactions).Thismodality is particularly indicated if
(1) anxiety symptoms are clearly secondary to an underlying unconscious conflict, (2) anxiety
continues after behavioral or pharmacological treatments are instituted, (3) new anxiety symptoms
develop after the original symptoms have resolved (symptom substitution), or (4) the anxieties are
more generalized and less specific.

[Link] therapy

The basic assumption is that change can occur without the development of psychological insight into
underlying causes. Techniques include positive and negative reinforcement, systematic
desensitization, flooding, implosion, graded exposure, response prevention, stop thought, relaxation
techniques, panic control therapy, self-monitoring, and hypnosis.

a. Behavior therapy is indicated for clearly delineated, circumscribed, maladaptive behaviors (e.g.,
panic attacks, phobias, compulsions, obsessions). Compulsive behavior generally is more responsive
than obsessional thinking.

b. Most current strategies for the treatment of anxiety disorders include a combination of
pharmacological and behavioral interventions.

c. Although drugs can reduce anxiety early, treatment with drugs alone leads to equally early relapse.
The response of patients who are also treated with cognitive and behavioral therapies appears to be
significantly and consistently better than the response of those who receive drugs alone.

4. Cognitive therapy.

Thisisbasedonthepremisethatmaladaptivebehaviorissecondarytodistortionsinhowpeopleperceivethe
mselvesandin how others perceive them. Treatment is short-term and interactive, with assigned
homework and tasks to be performed between sessions that focus on correcting distorted
assumptions and cognitions. The emphasis is on confronting and examining situations that elicit
interpersonal anxiety and associated mild depression.
5. Group therapy.

Groups range from those that provide only support and an increase in social skills to those that focus
on relief of specific symptoms to those that are primarily insight oriented. Groups may be
heterogeneous or homogeneous in terms of diagnosis. Homogeneous groups are commonly used in
the treatment of such diagnoses as posttraumatic stress disorder, in which therapy is aimed at
education about dealing with stress.

Obsessive compulsive disorder

Comes under the category of Obsessive-Compulsive and Related Disorders in DSM 5 (6th category)

Obsessive-Compulsive Disorder
Body Dysmorphic Disorder
Hoarding Disorder
Trichotillomania (Hair-Pulling Disorder)
Excoriation (Skin-Picking) Disorder
Substance/Medication-Induced Obsessive-Compulsive and Related Disorder
Obsessive-Compulsive and Related Disorder Due to Another Medical Condition
Other Specified Obsessive-Compulsive and Related Disorder
Unspecified Obsessive-Compulsive and Related Disorder
300.3 (F42) Obsessive-Compulsive Disorder _ICD

Obsessive-Compulsive and related disorders include obsessive-compulsive disorder (OCD), body

dysmorphic disorder, hoarding disorder, trichotillomania (hair- pulling disorder), excoriation
(skin-picking) disorder, substance/medication-induced obsessive-compulsive and related disorder,
obsessive-compulsive and related disorder due to another medical condition, and other specified
obsessive-compulsive and related disorder and unspecified obsessive-compulsive and related
disorder (e.g., body-focused repetitive behavior disorder, obsessional jealousy).

OCD is characterized by the presence of obsessions and/or compulsions. Obsessions are recurrent
and persistent thoughts, urges, or images that are experienced as intrusive and unwanted, whereas
compulsions are repetitive behaviors or mental acts that an individual feels driven to perform in
response to an obsession or according to rules that must be applied rigidly. Some other
obsessive-compulsive and related disorders are also characterized by preoccupations and by
repetitive behaviors or mental acts in response to the preoccupations. Other obsessive-compulsive
and related disorders are characterized primarily by recurrent body-focused repetitive behaviors
(e.g., hair pulling, skin picking) and repeated attempts to decrease or stop the behaviors.

The inclusion of a chapter on obsessive-compulsive and related disorders in DSM-5 reflects the
increasing evidence of these disorders' relatedness to one another in terms of a range of diagnostic
validators as well as the clinical utility of grouping these disorders in the same chapter. Clinicians are
encouraged to screen for these conditions in individuals who present with one of them and be aware
of overlaps between these conditions. At the same time, there are important differences in
diagnostic validators and treatment approaches across these disorders. Moreover, there are close
relationships between the anxiety disorders and some of the obsessive-compulsive and related
disorders (e.g., OCD), which is reflected in the sequence of DSM-5 chapters, with
obsessive-compulsive and related disorders following anxiety disorders.

The obsessive-compulsive and related disorders differ from developmentally normative

preoccupations and rituals by being excessive or persisting beyond developmentally appropriate
periods. The distinction between the presence of subclinical symptoms and a clinical disorder
requires assessment of a number of factors, including the individual's level of distress and
impairment in functioning.

The chapter begins with OCD. It then covers body dysmorphic disorder and hoarding disorder, which
are characterized by cognitive symptoms such as perceived defects or flaws in physical appearance or
the perceived need to save possessions, respectively. The chapter then covers trichotillomania
(hair-pulling disorder) and excoriation (skin-picking) disorder, which are characterized by recurrent
body-focused repetitive behaviors. Finally, it covers substance/medication-induced
obsessive-compulsive and related disorder, obsessive-compulsive and related disorder due to
another medical condition, and other specified obsessive-compulsive and related disorder and
unspecified obsessive-compulsive and related disorder.

Obsessive-Compulsive Disorder
300.3 (F42)

Obsessive–compulsive disorder involves recurrent intrusive ideas, images, ruminations, impulses,

thoughts (obsessions), or repetitive patterns of behavior or actions (compulsions). Both obsessions
and compulsions are ego-alien and produce anxiety if resisted. Lifetime prevalence is 2% to 3%. Men
and women are equally affected. Mean age of onset is 22 years.

Obsessive-compulsive disorder (OCD) is represented by a diverse group of symptoms that include

intrusive thoughts, rituals, preoccupations, and compulsions. These recurrent obsessions or
compulsions cause severe distress to the person. The obsessions or compulsions are time consuming
and interfere significantly with the person’s normal routine, occupational functioning, usual social
activities, or relationships. A patient with OCD may have an obsession, a compulsion, or both.

An obsession is a recurrent and intrusive thought, feeling, idea, or sensation. In contrast to an

obsession, which is a mental event, a compulsion is a behavior. Specifically, a compulsion is a
conscious, standardized, recurrent behavior, such as counting, checking, or avoiding. A patient with
OCD realizes the irrationality of the obsession and experiences both the obsession and the
compulsion as ego-dystonic (i.e., unwanted behavior).

Although the compulsive act may be carried out in an attempt to reduce the anxiety associated with
the obsession, it does not always succeed in doing so. The completion of the compulsive act may not
affect the anxiety, and it may even increase the anxiety. Anxiety is also increased when a person
resists carrying out a compulsion.

EPIDEMIOLOGY

The rates of OCD are fairly consistent, with a lifetime prevalence in the general population estimated
at 2 to 3 percent. Some researchers have estimated that the disorder is found in as many as 10
percent of outpatients in psychiatric clinics. These figures make OCD the fourth most common
psychiatric diagnosis after phobias, substance-related disorders, and major depressive disorder.
Epidemiological studies in Europe, Asia, and Africa have confirmed these rates across cultural
boundaries.

Among adults, men and women are equally likely to be affected, but among adolescents, boys are
more commonly affected than girls. The mean age of onset is about 20 years, although men have a
slightly earlier age of onset (mean about 19 years) than women (mean about 22 years). Overall, the
symptoms of about two thirds of affected persons have an onset before age 25, and the symptoms of
fewer than 15 percent have an onset after age 35. The onset of the disorder can occur in adolescence
or childhood, in some cases as early as 2 years of age. Single persons are more frequently affected
with OCD than are married persons, although this finding probably reflects the difficulty that persons
with the disorder have maintaining a relationship. OCD occurs less often among blacks than among
whites, although access to health care rather than differences in prevalence may explain the
variation.

Diagnostic Criteria
A. Presence of obsessions, compulsions, or both:

Obsessions are defined by (1) and (2):

1. Recurrent and persistent thoughts, urges, or images that are experienced, at some time during the
disturbance, as intrusive and unwanted, and that in most individuals cause marked anxiety or
distress. 2. The individual attempts to ignore or suppress such thoughts, urges, or images, or to
neutralize them with some other thought or action (i.e., by performing a compulsion).

Compulsions are defined by (1) and (2):

1. Repetitive behaviors (e.g., hand washing, ordering, checking) or mental acts (e.g., praying,
counting, repeating words silently) that the individual feels driven to perform in response to an
obsession or according to rules that must be applied rigidly.

2. The behaviors or mental acts are aimed at preventing or reducing anxiety or distress, or preventing
some dreaded event or situation; however, these behaviors or mental acts are not connected in a
realistic way with what they are designed to neutralize or prevent, or are clearly excessive. Note:
Young children may not be able to articulate the aims of these behaviors or mental acts.

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

C. The obsessive-compulsive symptoms are not attributable to the physiological effects of a

substance (e.g., a drug of abuse, a medication) or another medical condition.

D. The disturbance is not better explained by the symptoms of another mental disorder (e.g.,
excessive worries, as in generalized anxiety disorder; preoccupation with appearance, as in body
dysmorphic disorder; difficulty discarding or parting with possessions, as in hoarding disorder; hair
pulling, as in trichotillomania [hair-pulling disorder]; skin picking, as in excoriation [skin-picking]
disorder; stereotypies, as in stereotypic movement disorder; ritualized eating behavior, as in eating
disorders; preoccupation with substances or gambling, as in substance-related and addictive
disorders; preoccupation with having an illness, as in illness anxiety disorder; sexual urges or
fantasies, as in paraphilic disorders; impulses, as in disruptive, impulse-control, and conduct
disorders; guilty ruminations, as in major depressive disorder; thought insertion or delusional
preoccupations, as in schizophrenia spectrum and other psychotic disorders; or repetitive patterns of
behavior, as in autism spectrum disorder).

Specify if: With good or fair insight: The individual recognizes that obsessive-compulsive disorder
beliefs are definitely or probably not true or that they may or may not be true. With poor insight: The
individual thinks obsessive-compulsive disorder beliefs are probably true. With absent
insight/deiusionai beiiefs: The individual is completely convinced that obsessive-compulsive disorder
beliefs are true.

Specify if: Tic-reiated: The individual has a current or past history of a tic disorder.
Diagnostic Features / Symptoms
The characteristic symptoms of OCD are the presence of obsessions and compulsions (Criterion A).
Obsessions are repetitive and persistent thoughts (e.g., of contamination), images (e.g., of violent or
horrific scenes), or urges (e.g., to stab someone). Importantly, obsessions are not pleasurable or
experienced as voluntary: they are intrusive and unwanted and cause marked distress or anxiety in
most individuals. The individual attempts to ignore or suppress these obsessions (e.g., avoiding
triggers or using thought suppression) or to neutralize them with another thought or action (e.g.,
performing a compulsion). Compulsions (or rituals) are repetitive behaviors (e.g., washing, checking)
or mental acts (e.g., counting, repeating words silently) that the individual feels driven to perform in
response to an obsession or according to rules that must be applied rigidly. Most individuals with
OCD have both obsessions and compulsions. Compulsions are typically performed in response to an
obsession (e.g., thoughts of contamination leading to washing rituals or that something is incorrect
leading to repeating rituals until it feels "just right")· The aim is to reduce the distress triggered by
obsessions or to prevent a feared event (e.g., becoming ill). However, these compulsions either are
not connected in a realistic way to the feared event (e.g., arranging items symmetrically to prevent
harm to a loved one) or are clearly excessive (e.g., showering for hours each day). Compulsions are
not done for pleasure, although some individuals experience relief from anxiety or distress.

Criterion B emphasizes that obsessions and compulsions must be time-consuming (e.g., more than 1
hour per day) or cause clinically significant distress or impairment to warrant a diagnosis of OCD. This
criterion helps to distinguish the disorder from the occasional intrusive thoughts or repetitive
behaviors that are common in the general population (e.g., double-checking that a door is locked).
The frequency and severity of obsessions and compulsions vary across individuals with OCD (e.g.,
some have mild to moderate symptoms, spending 1-3 hours per day obsessing or doing compulsions,
whereas others have nearly constant intrusive thoughts or compulsions that can be incapacitating).

Prevalence
The 12-month prevalence of OCD in the United States is 1.2%, with a similar prevalence
internationally (1.1%-1.8%). Females are affected at a slightly higher rate than males in adulthood,
although males are more commonly affected in childhood.

Development and Course

In the United States, the mean age at onset of OCD is 19.5 years, and 25% of cases start by age 14
years. Onset after age 35 years is unusual but does occur. Males have an earlier age at onset than
females: nearly 25% of males have onset before age 10 years. The onset of symptoms is typically
gradual; however, acute onset has also been reported.

If OCD is untreated, the course is usually chronic, often with waxing and waning symptoms. Some
individuals have an episodic course, and a minority have a deteriorating course. Without treatment,
remission rates in adults are low (e.g., 20% for those reevaluated 40 years later). Onset in childhood
or adolescence can lead to a lifetime of OCD. However, 40% of individuals with onset of OCD in
childhood or adolescence may experience remission by early adulthood. The course of OCD is often
complicated by the co-occurrence of other disorders (see section "Comorbidity" for this disorder).

Compulsions are more easily diagnosed in children than obsessions are because compulsions are
observable. However, most children have both obsessions and compulsions (as do most adults). The
pattern of symptoms in adults can be stable over time, but it is more variable in children. Some
differences in the content of obsessions and compulsions have been reported when children and
adolescent samples have been compared with adult samples. These differences likely reflect content
appropriate to different developmental stages (e.g., higher rates of sexual and religious obsessions in
adolescents than in children; higher rates of harm obsessions [e.g., fears of catastrophic events, such
as death or illness to self or loved ones] in children and adolescents than in adults).

Causes/ ETIOLOGY and Risk and Prognostic Factors

Biological Factors

Neurotransmitters

SEROTONERGIC SYSTEM. The many clinical drug trials that have been conducted support the
hypothesis that dysregulation of serotonin is involved in the symptom formation of obsessions and
compulsions in the disorder. Data show that serotonergic drugs are more effective in treating OCD
than drugs that affect other neurotransmitter systems, but whether serotonin is involved in the
cause of OCD is not clear. Clinical studies have assayed cerebrospinal fluid (CSF) concentrations of
serotonin metabolites (e.g., 5-hydroxyindoleacetic acid [5-HIAA]) and affinities and numbers of
platelet-binding sites of tritiated imipramine (Tofranil), which binds to serotonin reuptake sites, and
have reported variable findings of these measures in patients with OCD. In one study, the CSF
concentration of 5-HIAA decreased after treatment with clomipramine (Anafranil), focusing attention
on the serotonergic system.

NORADRENERGIC SYSTEM. Currently, less evidence exists for dysfunction in the noradrenergic system
in OCD. Anecdotal reports show some improvement in OCD symptoms with use of oral clonidine
(Catapres), a drug that lowers the amount of norepinephrine released from the presynaptic nerve
terminals.

NEUROIMMUNOLOGY. Some interest exists in a positive link between streptococcal infection and
OCD. Group Aβ-hemolytic streptococcal infection can cause rheumatic fever, and approximately 10
to 30 percent of the patients develop Sydenham’s chorea and show obsessive compulsive symptoms.

Brain-Imaging Studies.

Neuroimaging in patients with OCD has produced converging data implicating altered function in the
neurocircuitry between orbitofrontal cortex, caudate, and thalamus. Various functional brain-imaging
studies—for example, positron emission tomography (PET)—have shown increased activity (e.g.,
metabolism and blood flow) in the frontal lobes, the basal ganglia (especially the caudate), and the
cingulum of patients with OCD. The involvement of these areas in the pathology of OCD appears
more associated with corticostriatal pathways than with the amygdala pathways, which are the
current focus of much anxiety disorder research. Pharmacological and behavioral treatments
reportedly reverse these abnormalities (Fig. 10.1-1). Data from functional brain-imaging studies are
consistent with data from structural brain-imaging studies. Both computed tomographic (CT) and
magnetic resonance imaging (MRI) studies have found bilaterally smaller caudates in patients with
OCD. Both functional and structural brain-imaging study results are also compatible with the
observation that neurological procedures involving the cingulum are sometimes effective in the
treatment of OCD. One recent MRI study reported increased T1 relaxation times in the frontal cortex,
a finding consistent with the location of abnormalities discovered in PET studies.

Genetics.

Available genetic data on OCD support the hypothesis that the disorder has a significant genetic
component. Relatives of probands with OCD consistently have a threefold to fivefold higher
probability of having OCD or obsessive-compulsive features than families of control probands The
data, however, do not yet distinguish the heritable factors from the influence of cultural and
behavioral effects on the transmission of the disorder. Studies of concordance for the disorder in
twins have consistently found a significantly higher concordance rate for monozygotic twins than for
dizygotic twins. Some studies also demonstrate increased rates of a variety of conditions among
relatives of OCD probands, including generalized anxiety disorder, tic disorders, body dysmorphic
disorder, hypochondriasis, eating disorders, and habits such as nail-biting.

Other Biological Data.

Electrophysiological studies, sleep electroencephalogram (EEG) studies, and neuroendocrine studies

have contributed data that indicate some commonalities between depressive disorders and OCD. A
higher than usual incidence of nonspecific EEG abnormalities occurs in patients with OCD. Sleep EEG
studies have found abnormalities similar to those in depressive disorders, such as decreased rapid
eye movement latency. Neuroendocrine studies have also produced some analogies to depressive
disorders, such as nonsuppression on the dexamethasone-suppression test in about one-third of
patients and decreased growth hormone secretion with clonidine infusions.

As mentioned, studies have suggested a possible link between a subset of OCD cases and certain
types of motor tic syndromes (i.e., Tourette’s disorder and chronic motor tics). A higher rate of OCD,
Tourette’s disorder, and chronic motor tics are found in relatives of patients with Tourette’s disorder
than in relatives of controls, whether or not they had OCD. Most family studies of probands with
OCD have found increased rates of Tourette’s disorder and chronic motor tics only among the
relatives of probands with OCD who also have some form of tic disorder. Evidence also suggests
co-transmission of Tourette’s disorder, OCD, and chronic motor tics within families.

Behavioral Factors

According to learning theorists, obsessions are conditioned stimuli. A relatively neutral stimulus
becomes associated with fear or anxiety through a process of respondent conditioning by being
paired with events that are noxious or anxiety producing. Thus, previously neutral objects and
thoughts become conditioned stimuli capable of provoking anxiety or discomfort.

Compulsions are established in a different way. When a person discovers that a certain action
reduces anxiety attached to an obsessional thought, he or she develops active avoidance strategies in
the form of compulsions or ritualistic behaviors to control the anxiety. Gradually, because of their
ecacy in reducing a painful secondary drive (anxiety), the avoidance strategies become xed as
learned patterns of compulsive behaviors. Learning theory provides useful concepts for explaining
certain aspects of obsessive-compulsive phenomena—for example, the anxiety-provoking capacity of
ideas not necessarily frightening in themselves and the establishment of compulsive patterns of
behavior.

Psychosocial Factors

Personality Factors. OCD differs from obsessive-compulsive personality disorder, which is associated
with an obsessive concern for details, perfectionism, and other similar personality traits. Most
persons with OCD do not have premorbid compulsive symptoms, and such personality traits are
neither necessary nor sufficient for the development of OCD. Only about 15 to 35 percent of patients
with OCD have had premorbid obsessional traits.

Psychodynamic Factors. Psychodynamic insight may be of great help in understanding problems with
treatment compliance, interpersonal difficulties, and personality problems accompanying the Axis I
disorder. Many patients with OCD may refuse to cooperate with effective treatments such as
selective serotonin reuptake inhibitors (SSRIs) and behavior therapy. Even though the symptoms of
OCD may be biologically driven, psychodynamic meanings may be attached to them. Patients may
become invested in maintaining the symptomatology because of secondary gains. For example, a
male patient, whose mother stays home to take care of him, may unconsciously wish to hang on to
his OCD symptoms because they keep the attention of his mother.

Another contribution of psychodynamic understanding involves the interpersonal dimensions.

Studies have shown that relatives will accommodate the patient through active participation in
rituals or significant modifications of their daily routines. This form of family accommodation is
correlated with stress in the family, rejecting attitudes toward the patient, and poor family
functioning. Often, the family members are involved in an effort to reduce the patient’s anxiety or to
control the patient’s expressions of anger. This pattern of relatedness may become internalized and
be re-created when the patient enters a treatment setting. By looking at recurring patterns of
interpersonal relationships from a psychodynamic perspective, patients may learn how their illness
affects others.

Finally, one other contribution of psychodynamic thinking is recognition of the precipitants that
initiate or exacerbate symptoms. Often, interpersonal difficulties increase the patient’s anxiety and,
thus, increase the patient’s symptomatology as well. Research suggests that OCD may be
precipitated by a number of environmental stressors, especially those involving pregnancy, childbirth,
or parental care of children. An understanding of the stressors may assist the clinician in an overall
treatment plan that reduces the stressful events themselves or their meaning to the patient.

SIGMUND FREUD. In classic psychoanalytic theory, OCD was termed obsessive-compulsive neurosis
and was considered a regression from the oedipal phase to the anal psychosexual phase of
development. When patients with OCD feel threatened by anxiety about retaliation for unconscious
impulses or by the loss of a significant object’s love, they retreat from the oedipal position and
regress to an intensely ambivalent emotional stage associated with the anal phase. The ambivalence
is connected to the unraveling of the smooth fusion between sexual and aggressive drives
characteristic of the oedipal phase. The coexistence of hatred and love toward the same person
leaves patients paralyzed with doubt and indecision.

Temperamental. Greater internalizing symptoms, higher negative emotionality, and behavioral

inhibition in childhood are possible temperamental risk factors.

Environmental. Physical and sexual abuse in childhood and other stressful or traumatic events have
been associated with an increased risk for developing OCD. Some children may develop the sudden
onset of obsessive-compulsive symptoms, which has been associated with different environmental
factors, including various infectious agents and a post-infectious autoimmune syndrome.

Genetic and physiological. The rate of OCD among first-degree relatives of adults with OCD is
approximately two times that among first-degree relatives of those without the disorder; however,
among first-degree relatives of individuals with onset of OCD in childhood or adolescence, the rate is
increased 10-fold. Familial transmission is due in part to genetic factors (e.g., a concordance rate of
0.57 for monozygotic vs. 0.22 for dizygotic twins). Dysfunction in the orbitofrontal cortex, anterior
cingulate cortex, and striatum have been most strongly implicated.

Treatment
With mounting evidence that OCD is largely determined by biological factors, classic psychoanalytic
theory has fallen out of favor. Moreover, because OCD symptoms appear to be largely refractory to
psychodynamic psychotherapy and psychoanalysis, pharmacological and behavioral treatments have
become common. But psychodynamic factors may be of considerable benefit in understanding what
precipitates exacerbations of the disorder and in treating various forms of resistance to treatment,
such as noncompliance with medication.

Many patients with OCD tenaciously resist treatment efforts. They may refuse to take medication
and may resist carrying out therapeutic homework assignments and other activities prescribed by
behavior therapists. The obsessive-compulsive symptoms themselves, no matter how biologically
based, may have important psychological meanings that make patients reluctant to give them up.
Psychodynamic exploration of a patient’s resistance to treatment may improve compliance.

Well-controlled studies have found that pharmacotherapy, behavior therapy, or a combination of

both is effective in significantly reducing the symptoms of patients with OCD. The decision about
which therapy to use is based on the clinician’s judgment and experience and the patient’s
acceptance of the various modalities.

Pharmacotherapy

The efficacy of pharmacotherapy in OCD has been proved in many clinical trials and is enhanced by
the observation that the studies find a placebo response rate of only about 5 percent.

The drugs, some of which are used to treat depressive disorders or other mental disorders, can be
given in their usual dosage ranges. Initial effects are generally seen after 4 to 6 weeks of treatment,
although 8 to 16 weeks are usually needed to obtain maximal therapeutic benefit. Treatment with
antidepressant drugs is still controversial, and a significant proportion of patients with OCD who
respond to treatment with antidepressant drugs seem to relapse if the drug therapy is discontinued.

The standard approach is to start treatment with an SSRI or clomipramine and then move to other
pharmacological strategies if the serotonin-specific drugs are not effective. The serotonergic drugs
have increased the percentage of patients with OCD who are likely to respond to treatment to the
range of 50 to 70 percent.

Selective Serotonin Reuptake Inhibitors. Each of the SSRIs available in the United States—fluoxetine
(Prozac), fluvoxamine (Luvox), paroxetine (Paxil), sertraline (Zoloft), citalopram (Celexa)—has been
approved by the US Food and Drug Administration (FDA) for the treatment of OCD. Higher dosages
have often been necessary for a beneficial effect, such as 80 mg a day of fluoxetine. Although the
SSRIs can cause sleep disturbance, nausea and diarrhea, headache, anxiety, and restlessness, these
adverse effects are often transient and are generally less troubling than the adverse effects
associated with tricyclic drugs, such as clomipramine. The best clinical outcomes occur when SSRIs
are used in combination with behavioral therapy.

Clomipramine. Of all the tricyclic and tetracyclic drugs, clomipramine is the most selective for
serotonin reuptake versus norepinephrine reuptake and is exceeded in this respect only by the SSRIs.
The potency of serotonin reuptake of clomipramine is exceeded only by sertraline and paroxetine.
Clomipramine was the first drug to be FDA approved for the treatment of OCD. Its dosing must be
titrated upward over 2 to 3 weeks to avoid gastrointestinal adverse effects and orthostatic
hypotension, and as with other tricyclic drugs, it causes significant sedation and anticholinergic
effects, including dry mouth and constipation. As with SSRIs, the best outcomes result from a
combination of drug and behavioral therapy.

Other Drugs. If treatment with clomipramine or an SSRI is unsuccessful, many therapists augment
the first drug by the addition of valproate (Depakene), lithium (Eskalith), or carbamazepine (Tegretol).
Other drugs that can be tried in the treatment of OCD are venlafaxine (Effexor), pindolol (Visken),
and the monoamine oxidase inhibitors (MAOIs), especially phenelzine (Nardil). Other
pharmacological agents for the treatment of unresponsive patients include buspirone (BuSpar),
5-hydroxytryptamine (5-HT), L-tryptophan, and clonazepam (Klonopin). Adding an atypical
antipsychotic such as risperidone (Risperdal) has helped in some cases.

Behavior Therapy

Although few head-to-head comparisons have been made, behavior therapy is as effective as
pharmacotherapies in OCD, and some data indicate that the beneficial effects are longer lasting with
behavior therapy. Many clinicians, therefore, consider behavior therapy the treatment of choice for
OCD. Behavior therapy can be conducted in both outpatient and inpatient settings. The principal
behavioral approaches in OCD are exposure and response prevention. Desensitization, thought
stopping, flooding, implosion therapy, and aversive conditioning have also been used in patients with
OCD. In behavior therapy, patients must be truly committed to improvement.

Psychotherapy

In the absence of adequate studies of insight-oriented psychotherapy for OCD, any valid
generalizations about its effectiveness are hard to make, although there are anecdotal reports of
successes. Individual analysts have seen striking and lasting changes for the better in patients with
obsessive-compulsive personality disorder, especially when they are able to come to terms with the
aggressive impulses underlying their character traits. Likewise, analysts and dynamically oriented
psychiatrists have observed marked symptomatic improvement in patients with OCD in the course of
analysis or prolonged insight psychotherapy.

Supportive psychotherapy undoubtedly has its place, especially for those patients with OCD who,
despite symptoms of varying degrees of severity, are able to work and make social adjustments. With
continuous and regular contact with an interested, sympathetic, and encouraging professional
person, patients may be able to function by virtue of this help, without which their symptoms would
incapacitate them. Occasionally, when obsessional rituals and anxiety reach an intolerable intensity,
it is necessary to hospitalize patients until the shelter of an institution and the removal from external
environmental stresses diminish symptoms to a tolerable level.

A patient’s family members are often driven to the verge of despair by the patient’s behavior. Any
psychotherapeutic endeavors must include attention to the family members through provision of
emotional support, reassurance, explanation, and advice on how to manage and respond to the
patient.

Other Therapies

Family therapy is often useful in supporting the family, helping reduce marital discord resulting from
the disorder, and building a treatment alliance with the family members for the good of the patient.
Group therapy is useful as a support system for some patients. For extreme cases that are treatment
resistant and chronically debilitating, electroconvulsive therapy (ECT) and psychosurgery are
considerations. ECT should be tried before surgery. A psychosurgical procedure for OCD is
cingulotomy, which may be successful in treating otherwise severe and treatment-unresponsive
patients. Other surgical procedures (e.g., sub caudate tractotomy, also known as capsulotomy) have
also been used for this purpose.

Deep Brain Stimulation (DBS)

Nonablative surgical techniques involving indwelling electrodes in various basal ganglia nuclei are
under investigation to treat both OCD and Tourette’s disorder. DBS is performed using MRI-guided
stereotactic techniques in which electrodes are implanted in the brain. Complications of DBS include
infection, bleeding, or the development of seizures, which are almost always controlled by treatment
with phenytoin (Dilantin). Some patients who do not respond to psychosurgery alone and who do
not respond to pharmacotherapy or behavior therapy before the operation do respond to
pharmacotherapy or behavior therapy after psychosurgery.