Compare and contrast two or more anxiety disorders to distinguish them from normal worry

6 panic, anxiety, obsessions, and their disorders

learning objectives 6

· 6.1 What are the essential features of anxiety disorders?

· 6.2 Describe the clinical features of specific and social phobias.

· 6.3 Why do anxiety disorders develop?

· 6.4 What are the clinical features of panic disorder?

· 6.5 What factors are implicated in the development of panic disorder?

· 6.6 Describe the clinical aspects of generalized anxiety disorder.

· 6.7 How are anxiety disorders treated?

· 6.8 What are the clinical features of obsessive-compulsive disorder and how is this disorder treated?

· 6.9 Describe three obsessive-compulsive related disorders.

Leni: Worried About Worrying So Much Leni is a 24-year-old graduate student. Although she is doing exceptionally well in her program, for the past year she has worried constantly that she will fail and be thrown out. When her fellow students and professors try to reassure her, Leni worries that they are just pretending to be nice to her because she is such a weak student. Leni also worries about her mother becoming ill and about whether she is really liked by her friends. Although Leni is able to acknowledge that her fears are excessive (she has supportive friends, her mother is in good health, and, based on her grades, Leni is one of the top students in her program), she still struggles to control her worrying. Leni has difficulty sleeping, often feels nervous and on edge, and experiences a great deal of muscle tension. When her friends suggested she take a yoga class to try and relax, Leni even began to worry about that, fearing that she would be the worse student in the class. “I know it makes no sense,” she says, “But that’s how I am. I’ve always been a worrier. I even worry about worrying so much!”

Anxiety involves a general feeling of apprehension about possible future danger, and fear is an alarm reaction that occurs in response to immediate danger. Today the DSM has identified a group of disorders—known as the anxiety disorders—that share obvious symptoms of clinically significant fear or anxiety. Anxiety disorders affect approximately 25 to 29 percent of the U.S. population at some point in their lives and are the most common category of disorders for women and the second most common for men (Kessler et al., 1994 ; Kessler, Berglund, Delmar, et al., 2005 ). In any 12-month period, about 18 percent of the adult population suffers from at least one anxiety disorder (Kessler, Chiu, et al., 2005c ). Anxiety disorders create enormous personal, economic, and health care problems for those affected. Some years ago several studies estimated that the anxiety disorders cost the United States somewhere between $42.3 billion and $47 billion in direct and indirect costs (about 30 percent of the nation’s total mental health bill of $148 billion in 1990; Greenberg et al., 1999 ; Kessler & Greenberg, 2002 ). The figure is no doubt even higher now. Anxiety disorders are also associated with an increased prevalence of a number of medical conditions including asthma, chronic pain, hypertension, arthritis, cardiovascular disease, and irritable bowel syndrome (Roy-Byrne et al., 2008 ) and people with anxiety disorders are very high users of medical services (e.g., Chavira et al., 2009 ).

In this chapter, we describe a number of different anxiety disorders. We also focus on obsessive-compulsive disorder (OCD) . Obsessions are persistent and highly recurrent intrusive thoughts or images that are experienced as disturbing and inappropriate. People affected by such obsessions try to resist or suppress them, or to neutralize them with some other thought or action. Compulsions are repetitive behaviors (such as hand-washing or checking) that the person feels must be performed in response to the obsession. Compulsions are sometimes performed as lengthy rituals. These behaviors have the goal of preventing or reducing distress or preventing some dreaded outcome from occurring.

Historically, anxiety and obsessive-compulsive disorders were considered to be classic neurotic disorders. Although individuals with neurotic disorders show maladaptive and self-defeating behaviors, they are not incoherent, dangerous, or out of touch with reality. To Freud, these neurotic disorders developed when intrapsychic conflict produced significant anxiety. Anxiety was, in Freud’s formulation, a sign of an inner battle or conflict between some primitive desire (from the id) and prohibitions against its expression (from the ego and superego). Sometimes this anxiety was overtly expressed (as in those disorders known today as the anxiety disorders). In certain other neurotic disorders, however, he believed that the anxiety might not be obvious, either to the person involved or to others, if psychological defense mechanisms were able to deflect or mask it. The term neurosis was dropped from the DSM in 1980. In addition, in DSM-III, some disorders that did not involve obvious anxiety symptoms were reclassified as either dissociative or somatoform disorders (some neurotic disorders were absorbed into the mood disorders category as well—see Chapters 7 and 8 ). This change was made to group together smaller sets of disorders that shared more obvious symptoms and features. In DSM-5 this trend has gone a step further. Obsessive-compulsive disorder is no longer classified as an anxiety disorder. Instead, it is now listed in a new DSM-5category called obsessive-compulsive and related disorders (see Thinking Critically about DSM-5).

We begin by discussing the nature of fear and anxiety as emotional and cognitive states and patterns of responding, each of which has an extremely important adaptive value but to which humans at times seem all too vulnerable. We will then move to a discussion of the anxiety disorders. Finally, we consider OCD and other disorders from the new obsessive-compulsive and related disorders category.

The Fear and Anxiety Response Patterns

There has never been complete agreement about how distinct the two emotions of fear and anxiety are from each other. Historically, the most common way of distinguishing between the fear and anxiety response patterns has been whether there is a clear and obvious source of danger that would be regarded as real by most people. When the source of danger is obvious, the experienced emotion has been called fear (e.g., “I’m afraid of snakes”). With anxiety, however, we frequently cannot specify clearly what the danger is (e.g., “I’m anxious about my parents’ health”).

Fear

In recent years, however, many prominent researchers have proposed a more fundamental distinction between the fear and anxiety response patterns (e.g., Barlow, 1988 , 2002 ; Bouton, 2005 ; Grillon, 2008 ; McNaughton, 2008 ). According to these theorists, fear is a basic emotion (shared by many animals) that involves activation of the “fight-or-flight” response of the autonomic nervous system. This is an almost instantaneous reaction to any imminent threat such as a dangerous predator or someone pointing a loaded gun.

Its adaptive value as a primitive alarm response to imminent danger is that it allows us to escape. When the fear response occurs in the absence of any obvious external danger, we say the person has had a spontaneous or uncued panic attack . The symptoms of a panic attack are nearly identical to those experienced during a state of fear except that panic attacks are often accompanied by a subjective sense of impending doom, including fears of dying, going crazy, or losing control. These latter cognitive symptoms do not generally occur during fear states. Thus fear and panic have three components:

· 1. cognitive/subjective components (“I feel afraid/terriffied”; “I’m going to die”)

· 2. physiological components (such as increased heart rate and heavy breathing)

· 3. behavioral components (a strong urge to escape or Thee; Lang, 1968 , 1971 )

DSM-5 THINKING CRITICALLY about DSM-5: Why Is OCD No Longer Considered to Be an Anxiety Disorder?

In DSM-5, obsessive-compulsive disorder was removed from the anxiety disorders category and placed into a new category called “obsessive-compulsive and related disorders.” (As you already know from Chapter 5 , PTSD was also removed and put into a new category called “trauma and stressor-related disorders.”)

One reason for moving OCD into the new category was that anxiety is not generally used as an indicator of OCD severity. Indeed, for people with certain forms of OCD such as symmetry-related obsessions and compulsions, anxiety is not even a prominent symptom. It was also noted that anxiety occurs in a wide range of disorders, so the presence of some anxiety is not a valid reason to regard OCD an anxiety disorder. Indeed Stein et al. ( 2010 ) wrote that “the highly stereotyped, driven, repetitive, and nonfunctional quality of compulsive behaviors differentiate OCD from normal acts and from the types of avoidance that occur in other anxiety disorders” ( p. 497 ).

Yet another reason is that the neurobiological underpinnings of OCD appear to be rather different from those of other anxiety disorders, focusing on frontal-striatal neural circuitry including the orbitofrontal cortex, anterior cingulate cortex, and striatum (especially the caudate nucleus). Studies examining the “OCD-related disorders” such as body dysmorphic disorder (obsessing about perceived or imagined flaws in physical appearance) and trichotillomania (chronic hair pulling) also suggest shared involvement of frontal-striatal neural circuitry. Finally, other anxiety disorders respond to a wider range of medication treatments than does OCD, which seems to respond selectively to selective serotonin reuptake inhibitors.

How compelling do these reasons sound to you? What kinds of research findings might further support the grouping of OCD with related disorders such as hoarding or trichotillomania? On the contrary, what research findings might incline you to think that it was wrong to remove OCD from the anxiety disorders category?

Fear or panic is a basic emotion that is shared by many animals, including humans, and may activate the fight-or-flight response of the sympathetic nervous system. This allows us to respond rapidly when faced with a dangerous situation, such as being threatened by a predator. In humans who are having a panic attack, there is no external threat; panic occurs because of some misfiring of this response system.

These components are only “loosely coupled” (Lang, 1985 ), which means that someone might show, for example, physiological and behavioral indications of fear or panic without much of the subjective component, or vice versa.

Anxiety

In contrast to fear and panic, the anxiety response pattern is a complex blend of unpleasant emotions and cognitions that is both more oriented to the future and much more diffuse than fear (Barlow, 1988 , 2002 ). But like fear, it has not only cognitive/subjective components but also physiological and behavioral components. At the cognitive/subjective level, anxiety involves negative mood, worry about possible future threats or danger, self-preoccupation, and a sense of being unable to predict the future threat or to control it if it occurs. At a physiological level, anxiety often creates a state of tension and chronic overarousal, which may reflect risk assessment and readiness for dealing with danger should it occur (“Something awful may happen, and I had better be ready for it if it does”). Although there is no activation of the fight-or-flight response as there is with fear, anxiety does prepare or prime a person for the fight-or-flight response should the anticipated danger occur. At a behavioral level, anxiety may create a strong tendency to avoid situations where danger might be encountered, but there is not the immediate behavioral urge to flee with anxiety as there is with fear (Barlow, 1988 , 2002 ). Support for the idea that anxiety is descriptively and functionally distinct from fear or panic comes both from complex statistical analyses of subjective reports of panic and anxiety and from a great deal of neurobiological evidence (e.g., Bouton, 2005 ; Bouton et al., 2001 ; Davis, 2006 ; Grillon, 2008 ).

The adaptive value of anxiety may be that it helps us plan and prepare for possible threat. In mild to moderate degrees, anxiety actually enhances learning and performance. For example, a mild amount of anxiety about how you are going to do on your next exam, or in your next tennis match, can actually be helpful. But although anxiety is often adaptive in mild or moderate degrees, it is maladaptive when it becomes chronic and severe, as we see in people diagnosed with anxiety disorders.

Although there are many threatening situations that provoke fear or anxiety unconditionally, many of our sources of fear and anxiety are learned. Years of human and nonhuman animal experimentation have established that the basic fear and anxiety response patterns are highly conditionable (e.g., Fanselow & Ponnusamy, 2008 ; Lipp, 2006 ). That is, previously neutral and novel stimuli (conditioned stimuli) that are repeatedly paired with, and reliably predict, frightening or unpleasant events such as various kinds of physical or psychological trauma (unconditioned stimulus) can acquire the capacity to elicit fear or anxiety themselves (conditioned response). Such conditioning is a completely normal and adaptive process that allows all of us to learn to anticipate upcoming frightening events if they are reliably preceded by a signal. Yet this normal and adaptive process can also lead in some cases to the development of clinically significant fears and anxieties, as we will see.

For example, a girl named Angela sometimes saw and heard her father physically abuse her mother in the evening. After this happened four or five times, Angela started to become anxious as soon as she heard her father’s car arrive in the driveway at the end of the day. In such situations a wide variety of initially neutral stimuli may accidentally come to serve as cues that something threatening and unpleasant is about to happen—and thereby come to elicit fear or anxiety themselves. Our thoughts and images can also serve as conditioned stimuli capable of eliciting the fear or anxiety response pattern. For example, Angela came to feel anxious even when thinking about her father.

in review

· ● Compare and contrast fear or panic with anxiety, making sure to note that both emotions involve three response systems.

· ● Explain the significance of the fact that both fear and anxiety can be classically conditioned.

Overview of the Anxiety Disorders and their Commonalities

Anxiety disorders all have unrealistic, irrational fears or anxieties of disabling intensity as their principal and most obvious manifestation. Among the disorders recognized in DSM-5 are:

· 1. specific phobia

· 2. social anxiety disorder (social phobia)

· 3. panic disorder

· 4. agoraphobia

· 5. generalized anxiety disorder

As seen in the following brief overview, people with these varied disorders differ from one another both in terms of the relative preponderance of fear or panic versus anxiety symptoms that they experience and in the kinds of objects or situations that most concern them. For example, people with specific or social phobias exhibit many anxiety symptoms about the possibility of encountering their phobic situation, but they may also experience a fear or panic response when they actually encounter the situation. People with panic disorder experience both frequent panic attacks and intense anxiety focused on the possibility of having another one. People with agoraphobia go to great lengths to avoid a variety of feared situations, ranging from open streets, bridges, and crowded public places. By contrast, people with generalized anxiety disorder (like Leni in the case study that opened this chapter) mostly experience a general sense of diffuse anxiety and worry about many potentially bad things that may happen; some may also experience an occasional panic attack, but it is not a focus of their anxiety. It is also important to note that many people with one anxiety disorder will experience at least one more anxiety disorder and/or depression either concurrently or at a different point in their lives (e.g., Brown & Barlow, 2002 , 2009 ; Kessler, Berglund, Demler, et al., 2005 ).

Given these commonalities across the anxiety disorders, it should come as no surprise that there are some important similarities in the basic causes of these disorders (as well as many differences). Among biological causal factors, we will see that there are genetic contributions to each of these disorders and that at least part of the genetic vulnerability may be nonspecific, or common across the disorders (e.g., Barlow, 2002 ; Craske & Waters, 2005 ). In adults, the common genetic vulnerability is manifested at a psychological level at least in part by the important personality trait called neuroticism—a proneness or disposition to experience negative mood states that is a common risk factor for both anxiety and mood disorders (e.g., Klein et al., 2009 ). The brain structures most centrally involved in most disorders are generally in the limbic system (often known as the “emotional brain”) and certain parts of the cortex, and the neurotransmitter substances that are most centrally involved are gamma aminobutyric acid (GABA), norepinephrine, and serotonin (see Chapter 3 ).

Among common psychological causal factors, we will see that classical conditioning of fear, panic, or anxiety to a range of stimuli plays an important role in many of these disorders (Forsyth et al., 2006 ; Mineka & Oehlberg, 2008 ; Mineka & Zinbarg, 1996 , 2006 ). In addition, people who have perceptions of a lack of control over either their environments or their own emotions (or both) seem more vulnerable to developing anxiety disorders. The development of such perceptions of uncontrollability depends heavily on the social environment people are raised in, including parenting styles (Chorpita & Barlow, 1998 ; Craske & Waters, 2005 ; Mineka & Zinbarg, 2006 ; Hudson & Rapee, 2009 ). For certain disorders, faulty or distorted patterns of cognition also may play an important role. Finally, the sociocultural environment in which people are raised also has prominent effects on the kinds of objects and experiences people become anxious about or come to fear. Ultimately what we must strive for is a good biopsychosocial understanding of how all these types of causal factors interact with one another in the development of anxiety disorders.

Finally, as we will see, there are many commonalities across the effective treatments for the various anxiety disorders (e.g., Barlow, 2004 ; Campbell-Sills & Barlow, 2007 ). For each disorder, graduated exposure to feared cues, objects, and situations—until fear or anxiety begins to habituate—constitutes the single most powerful therapeutic ingredient. Further, for certain disorders the addition of cognitive restructuring techniques can provide added benefit. What these cognitive restructuring techniques for different disorders have in common is that they help the individual understand his or her distorted patterns of thinking about anxiety-related situations and how these patterns can be changed. Medications can also be useful in treating all disorders except specific phobias, and nearly all tend to fall into two primary medication categories: antianxiety medications (anxiolytics) and antidepressant medications.

We now turn to a more detailed discussion of each disorder, highlighting their common and their distinct features as well as what is known about their causes. We start with phobic disorders—the most common anxiety disorders. A phobia is a persistent and disproportionate fear of some specific object or situation that presents little or no actual danger and yet leads to a great deal of avoidance of these feared situations. As we will see in our discussion of DSM-5, there are three main categories of pho-bias: (1) specific phobia, (2) social phobia, and (3) agoraphobia.

in review

· ● What is the central feature of all anxiety disorders? That is, what do they have in common?

· ● What differentiates the anxiety disorders from one another?

· ● What are some common kinds of biological and psychosocial causes of the different anxiety disorders?

· ● What is the most important ingredient across effective psychosocial treatments for the anxiety disorders?

Specific Phobias

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 (see DSM-5 box for diagnostic criteria). When individuals with specific phobias encounter a phobic stimulus, they often show an immediate fear response that often resembles a panic attack except for the existence of a clear external trigger (APA, 2013 ). Not surprisingly, such individuals also experience anxiety if they anticipate they may encounter a phobic object or situation and so go to great lengths to avoid encounters with their phobic stimulus. Indeed, they often even avoid seemingly innocent representations of it such as photographs or television images. For example, claustrophobic persons may go to great lengths to avoid entering a closet or an elevator, even if this means climbing many flights of stairs or turning down jobs that might require them to take an elevator. Generally, people with specific phobias recognize that their fear is somewhat excessive or unreasonable although occasionally they may not have this insight.

DSM-5 criteria for: Specific Phobia

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

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).

This avoidance is a cardinal characteristic of phobias; it occurs both because the phobic response itself is so unpleasant and because of the phobic person’s irrational appraisal of the likelihood that something terrible will happen. Table 6.1 on page 168 lists the five subtypes of specific phobias recognized in DSM-5, along with some examples.

People with claustrophobia may find elevators so frightening that they go to great lengths to avoid them. If for some reason they have to take an elevator, they will be very frightened and have thoughts about the elevator falling, the doors never opening, or there not being enough air to breathe.

The following case is typical of specific phobia:

A Pilot’s Wife’s Fear Mary, a married mother of three, was 47 at the time she first sought treatment for both claustrophobia and acrophobia. She reported having been intensely afraid of enclosed spaces (claustrophobia) and of heights (acrophobia) since her teens. She remembered having been locked in closets by her older siblings when she was a child; the siblings also confined her under blankets to scare her and added to her fright by showing her pictures of spiders after releasing her from under the blankets. She traced the onset of her claustrophobia to those traumatic incidents, but she had no idea why she was afraid of heights. While her children had been growing up, she had been a housewife and had managed to live a fairly normal life in spite of her two specific phobias. However, her children were now grown, and she wanted to find a job outside her home. This was proving to be very difficult because she could not take elevators and was frightened being on anything other than the first floor of an office building. Moreover, her husband had for some years been working for an airline, which entitled him to free airline tickets. The fact that Mary could not fly (due to her phobias) had become a sore point in her marriage because they both wanted to be able to take advantage of these free tickets to see distant places. Thus, although she had had these phobias for many years, they had become truly disabling only in recent years as her life circumstances had changed and she could no longer easily avoid heights or enclosed spaces.

TABLE 6.1 Subtypes of Specific Phobias in DSM-5

Phobia Type	Examples
Animal	Snakes, spiders, dogs, insects, birds
Natural Environment	Storms, heights, water
Blood-Injection-Injury	Seeing blood or an injury, receiving an injection, seeing a person in a wheelchair
Situational	Public transportation, tunnels, bridges, elevators, flying, driving, enclosed spaces
Other	Choking, vomiting, “space phobia” (fear of falling down if away from walls or other support)

If people who suffer from phobias attempt to approach their phobic situation, they are overcome with fear or anxiety, which may vary from mild feelings of apprehension and distress (usually while still at some distance) to full-fledged activation of the fight-or-flight response. Regardless of how it begins, phobic behavior tends to be reinforced because every time the person with a phobia avoids a feared situation his or her anxiety decreases. In addition, the secondary benefits derived from being disabled, such as increased attention, sympathy, and some control over the behavior of others, may also sometimes reinforce a phobia.

One category of specific phobias that has a number of interesting and unique characteristics is blood-injection-injury phobia . It probably occurs in about 3 to 4 percent of the population (Ayala et al., 2009 ; Öst & Hellström, 1997 ). People afflicted with this phobia typically experience at least as much (if not more) disgust as fear (Schienle et al., 2005 ; Teachman & Saporito, 2009 ). They also show a unique physiological response when confronted with the sight of blood or injury. Rather than showing the simple increase in heart rate and blood pressure seen when most people with phobias encounter their phobic object, these people show an initial acceleration, followed by a dramatic drop in both heart rate and blood pressure. This is very frequently accompanied by nausea, dizziness, or fainting, which do not occur with other specific phobias (Öst & Hellström, 1997 ; Page & Tan, 2009 ).

Interestingly, people with this phobia show this unique physiological response pattern only in the presence of blood and injury stimuli; they exhibit the more typical physiological response pattern characteristic of the fight-or-flight response to their other feared objects (see Dahlloef & Öst, 1998 ; Öst & Hugdahl, 1985 ). From an evolutionary and functional standpoint, this unique physiological response pattern may have evolved for a specific purpose: By fainting, the person being attacked might inhibit further attack, and if an attack did occur, the drop in blood pressure would minimize blood loss (Craske, 1999 ; Marks & Nesse, 1991 ). This type of phobia appears to be highly heritable (Czajkowski et al., 2011).

In blood-injection-injury phobia, the afflicted person experiences disgust and fear at the sight of someone receiving an injection. When confronted with the sight of blood or injury, people with this phobic disorder often experience nausea, dizziness, and fainting.

Prevalence, Age of Onset, and Gender Differences

Specific phobias are quite common. Results of the National Comorbidity Survey-Replication, which used DSM-IV criteria, revealed a lifetime prevalence rate of about 12 percent (Kessler, Chiu, et al., 2005c ). Among people with one specific phobia, over 75 percent have at least one other specific fear that is excessive (Curtis, Magee, et al., 1998 ). The relative gender ratios vary considerably according to the type of specific phobia, but phobias are always considerably more common in women than in men. For example, about 90 to 95 percent of people with animal phobias are women, but the gender ratio is less than 2:1 for blood-injection-injury phobia. The average age of onset for different types of specific phobias also varies widely. Animal phobias usually begin in childhood, as do blood-injection-injury phobias and dental phobias. However, other phobias such as claustrophobia and driving phobia tend to begin in adolescence or early adulthood (Barlow, 2002 ; Öst, 1987 ).

Psychological Causal Factors

A variety of psychological causal factors have been implicated in the origins of specific phobias, ranging from deep-seated psychodynamic conflicts to relatively straightforward traumatic conditioning of fear and a multitude of individual differences in who is at risk for such conditioning.

PSYCHOANALYTIC VIEWPOINT

According to the psychoanalytic view, phobias represent a defense against anxiety that stems from repressed impulses from the id. Because it is too dangerous to “know” the repressed id impulse, the anxiety is displaced onto some external object or situation that has some symbolic relationship to the real object of the anxiety (Freud, 1909 ). However, this prototypical psychodynamic account of how phobias are acquired was long criticized as being far too speculative, and an alternative, simpler account from learning theory was first proposed by Wolpe and Rachman ( 1960 ), which has now been further refined and expanded as discussed below.

PHOBIAS AS LEARNED BEHAVIOR

As an alternative to psychoanalytic accounts, Wolpe and Rachman ( 1960 ) developed an account based on learning theory, which sought to explain the development of phobic behavior through classical conditioning. Numerous other theorists in the 1960s and 1970s also agreed that the principles of classical conditioning appeared to account for the acquisition of irrational fears and phobias. The fear response can readily be conditioned to previously neutral stimuli when these stimuli are paired with traumatic or painful events. We would also expect that, once acquired, phobic fears would generalize to other, similar objects or situations. Recall, for example, that Mary’s claustrophobia had probably been caused by multiple incidents as a child when her siblings locked her in closets and confined her under blankets to scare her. But as an adult, Mary feared elevators and caves as well as other enclosed places. The powerful role of classical conditioning in the development of pho-bias was supported in a survey by Öst and Hugdahl ( 1981 ), who administered questionnaires to 106 adult phobic clients that concerned, among other things, the purported origins of their fears (see Mineka & Sutton, 2006 , for a review). Fifty-eight percent cited traumatic conditioning experiences as the sources of their phobias. Some of these traumatic conditioning events were simply uncued panic attacks, which are now known to effectively condition fear (e.g., Acheson et al., 2007 ; Forsyth & Eifert, 1998 ).

Vicarious Conditioning Direct traumatic conditioning in which a person has a terrifying experience in the presence of a neutral object or situation is not the only way that people can learn irrational, phobic fears. Simply watching a phobic person behaving fearfully with his or her phobic object can be distressing to the observer and can result in fear being transmitted from one person to another through vicarious or observational classical conditioning. In addition, watching a nonfearful person undergoing a frightening experience can also lead to vicarious conditioning. For example, one man, as a boy, had witnessed his grandfather vomit while dying. Shortly after this traumatic event (his grandfather’s distress while dying) the boy had developed a strong and persistent vomiting phobia. Indeed, when this man was in middle age he even contemplated suicide one time when he was nauseated and feared vomiting (Mineka & Zinbarg, 2006 ). Related experimental findings have been observed in laboratory analogue studies of human children. For example, two studies showed that 7- to 9-year-old children who saw pictures of an unfamiliar animal (an Australian marsupial) paired 10 times with fearful facial expressions showed increased fear beliefs and behavioral avoidance of this conditioned stimulus (CS) relative to children who saw the unfamiliar animal paired with happy facial expressions. These effects persisted for at least one week (Askew & Field, 2007 ; see Askew & Field, 2008 , for a review).

Animal research using rhesus monkeys has increased our confidence that vicarious conditioning of intense fears can indeed occur. In these experiments, Mineka and Cook and their colleagues (e.g., Cook & Mineka, 1989 ; Mineka & Cook, 1993 ; Mineka, Davidson, et al., 1984 ) showed that laboratory-reared monkeys who were not initially afraid of snakes rapidly developed a phobic-like fear of snakes simply through observing a wild-reared monkey behaving fearfully with snakes. Significant fear was acquired after only 4 to 8 minutes of exposure to the wild-reared monkey with snakes, and there were no signs that the fear had diminished 3 months later. The monkeys could also learn the fear simply through watching a videotape of the wild-reared model monkey behaving fearfully with snakes. This suggests that the mass media also play a role in the vicarious conditioning of fears and phobias in people (Cook & Mineka, 1990 ; Mineka & Sutton, 2006 ).

Monkeys who watch a model monkey (such as the one illustrated here) behaving fearfully with a live boa constrictor will rapidly acquire an intense fear of snakes themselves. Fears can thus be learned vicariously without any direct traumatic experience.

Individual Differences in Learning Does the direct and vicarious conditioning model really explain the origins of most phobias? Given all the traumas that people undergo, why don’t more people develop phobias (Mineka & Oehlberg, 2008 ; Mineka & Zinbarg, 1996 , 2006 ; Rachman, 1990 )? The answer seems to be, at least in good part, that differences in life experiences among individuals strongly affect whether or not conditioned fears or phobias actually develop. For example, years of positive experiences with friendly dogs before being bitten by one will probably keep a dog bite victim from developing a full-blown dog phobia. Thus, to understand individual differences in the development and maintenance of phobias, we need to understand the role of the different life experiences of people who undergo the same trauma.

Some life experiences may serve as risk factors and make certain people more vulnerable to phobias than others, and other experiences may serve as protective factors for the development of phobias (Mineka & Sutton, 2006 ). For example, children who have had more previous nontraumatic experiences with a dentist are less likely to develop dental anxiety after a bad and painful experience than are children with fewer previous nontraumatic experiences (Kent, 1997 ; Ten Berge et al., 2002 ). This shows the importance of the individual’s prior familiarity with an object or situation in determining whether a phobia develops following a fear-conditioning experience. Moreover, Mineka and Cook ( 1986 ) showed that monkeys who first simply watched nonfearful monkeys behaving nonfearfully with snakes were immunized against acquiring a fear of snakes when they later saw fearful monkeys behaving fearfully with snakes. By analogy, if a child has extensive exposure to a nonfearful parent behaving nonfearfully with the phobic object (e.g., spiders) or situation (e.g., heights) of the other, phobic parent, this may serve as a protective factor and immunize the child against the effects of later seeing the phobic parent behaving fearfully with the phobic object (Mineka & Oehlberg, 2008 ; Mineka & Sutton, 2006 ). Egliston and Rapee ( 2007 ) reported related results in an analogue study of human toddlers who either watched their mothers reacting positively to a snake or spider, or watched the snake or spider alone. Subsequently both groups of toddlers watched an experimenter reacting with fear and disgust toward the stimulus. Those in the group who had first watched their mother behaving positively acquired less fear than those who had first watched the stimulus alone.

A person who has had good experiences with a potentially phobic stimulus, such as the little girl playing here with her dog, is likely to be immunized from later acquiring a fear of dogs even if she has a traumatic encounter with one.

Events that occur during a conditioning experience, as well as before it, are also important in determining the level of fear that is conditioned. For example, experiencing an inescapable and uncontrollable event, such as being attacked by a dog that one cannot escape from after being bitten, is expected to condition fear much more powerfully than experiencing the same intensity of trauma that is escapable or to some extent controllable (e.g., by running away after the attack; Mineka, 1985a ; Mineka & Zinbarg, 1996 , 2006 ). In addition, the experiences that a person has after a conditioning experience may effect the strength and maintenance of the conditioned fear (Rescorla, 1974 ; White & Davey, 1989 ). For example, the inflation effect suggests that a person who acquired, a mild fear of driving following a minor crash might be expected to develop a full-blown phobia if he or she later were physically assaulted, even though no automobile was present during the assault (Dadds et al., 2001 ; Mineka, 1985b ; Mineka & Zinbarg, 1996 , 2006 ). Even verbal information that later alters one’s interpretation of the dangerousness of a previous trauma can inflate the level of fear (e.g., being told, “You’re lucky to be alive because the man who crashed into your car last week had lost his license due to a record of drunk driving leading to fatal car crashes”; Dadds et al., 2001 ). Another way in which fear of a CS can be inflated following conditioning is if the organism later is exposed to uncontrollable stress (Baratta et al., 2007 ). These examples show that the factors involved in the origins and maintenance of fears and phobias are more complex than suggested by the traditional, simplistic conditioning view, although they are nevertheless consistent with contemporary views of conditioning (Mineka & Oehlberg, 2008 ; see also Coelho & Purkis, 2009 ; Laborda & Miller, 2011 ).

It has also been shown that our cognitions, or thoughts, can help maintain our phobias once they have been acquired. For example, people with phobias are constantly on the alert for their phobic objects or situations and for other stimuli relevant to their phobia (McNally & Reese, 2009 ). Nonphobic persons, by contrast, tend to direct their attention away from threatening stimuli (see Mineka, Rafaeli, & Yovel, 2003 ). In addition, phobics also markedly overestimate the probability that feared objects have been, or will be, followed by frightening events. This cognitive bias may help maintain or strengthen phobic fears with the passage of time (Muhlberger et al., 2006 ; Öhman & Mineka, 2001 ; Tomarken, Mineka, & Cook, 1989 ).

Evolutionary Preparedness for Learning Certain Fears and Phobias Consider the observation that people are much more likely to have phobias of snakes, water, heights, and enclosed spaces than of motorcycles and guns, even though the latter objects may be at least as likely to be associated with trauma. This is because our evolutionary history has affected which stimuli we are most likely to come to fear. Primates and humans seem to be evolutionarily prepared to rapidly associate certain objects—such as snakes, spiders, water, and enclosed spaces—with frightening or unpleasant events (e.g., Mineka & Öhman, 2002 ; Öhman, 1996 ; Seligman, 1971 ). This prepared learning occurs because, over the course of evolution, those primates and humans who rapidly acquired fears of certain objects or situations that posed real threats to our early ancestors may have enjoyed a selective advantage. Thus “prepared” fears are not inborn or innate but rather are easily acquired or especially resistant to extinction. Guns and motorcycles, by contrast, were not present in our early evolutionary history and so did not convey any such selective advantage.

There is now a large amount of experimental evidence supporting the preparedness theory of phobias. In one important series of experiments using human subjects, Öhman and his colleagues (see Öhman, 1996 ; Öhman, 2009 ; Öhman & Mineka, 2001 , for reviews) found that fear is conditioned more effectively to fear-relevant stimuli (slides of snakes and spiders) than to fear-irrelevant stimuli (slides of flowers and mushrooms). These researchers also found that once the individuals acquired the conditioned responses to fear-relevant stimuli, these responses (including activation of the relevant brain area, the amygdala) could be elicited even when the fear-relevant stimuli (but not the fear-irrelevant stimuli) were presented subliminally (i.e., presentation was so brief that the stimuli were not consciously perceived; e.g., Carlsson et al., 2004 ; Öhman et al., 2007 ). This subliminal activation of responses to phobic stimuli may help to account for certain aspects of the irrationality of phobias. That is, people with phobias may not be able to control their fear because the fear may arise from cognitive structures that are not under conscious control (Öhman & Mineka, 2001 ; Öhman & Soares, 1993 ).

Another series of experiments showed that lab-reared monkeys in a vicarious conditioning paradigm can easily acquire fears of fear-relevant stimuli such as toy snakes and toy crocodiles but not of fear-irrelevant stimuli such as flowers and a toy rabbit (Cook & Mineka, 1989 , 1990 ). Thus, both monkeys and humans seem selectively to associate certain fear-relevant stimuli with threat or danger. Moreover, these lab-reared monkeys had had no prior exposure to any of the stimuli involved (e.g., snakes or flowers) before participating in these experiments. Thus, the monkey results support the evolutionarily based preparedness hypothesis even more strongly than the human experiments. For example, human subjects (unlike the lab-reared monkeys) might show superior conditioning to snakes or spiders because of preexisting negative associations to snakes or spiders rather than because of evolutionary factors (Mineka & Öhman, 2002 ).

Biological Causal Factors

Genetic and temperamental variables affect the speed and strength of conditioning of fear (e.g., Gray, 1987 ; Hettema et al., 2003 ; Oehlberg & Mineka, 2011 ). That is, depending on their genetic makeup or their temperament and personality (all of which are clearly related; see Chapter 3 ), people are more or less likely to acquire fears and phobias. For example, Lonsdorf and colleagues ( 2009 ) found that individuals who are carriers of one of the two variants on the serotonin-transporter gene (the s allele, which has been linked to heightened neuroticism) show superior fear conditioning relative to individuals who do not carry the s allele. However, those with one of two variants of a different gene (the COMT met/met genotype) did not show superior conditioning but did show enhanced resistance to extinction (see also Lonsdorf & Kalisch, 2011). Relatedly, Kagan and his colleagues ( 2001 ) found that behaviorally inhibitedtoddlers (who are excessively timid, shy, easily distressed, etc.) at 21 months of age were at higher risk of developing multiple specific phobias by 7 to 8 years of age than were uninhibited children (32 versus 5 percent). The average number of reported fears in the inhibited group was three to four per child (Biederman et al., 1990 ).

Several behavior genetic studies also suggest a modest genetic contribution to the development of specific phobias. For example, a large female twin study found that monozygotic (identical) twins were more likely to share animal phobias and situational phobias (such as of heights or water) than were dizygotic (nonidentical) twins (Kendler et al., 1999b ). Very similar results were later also found for men (Hettema et al., 2005 ). However, the same studies also found evidence that nonshared environmental factors (i.e., individual specific experiences not shared by twins) also played a very substantial role in the origins of specific phobias, a result that supports the idea that phobias are learned behaviors. Another study found that the heritability of animal phobias was separate from the heritability of complex phobias such as social phobia and agoraphobia (Czajkowski et al., 2011).

Treatments

A form of behavior therapy called exposure therapy —which is the best treatment for specific phobias—involves controlled exposure to the stimuli or situations that elicit phobic fear (Choy et al., 2007 ; Craske & Mystkowski, 2006 ). Clients are gradually placed—symbolically or increasingly under “real-life” conditions—in those situations they find most frightening. In treatment, clients are encouraged to expose themselves (either alone or with the aid of a therapist or friend) to their feared situations for long enough periods of time so that their fear begins to subside. One variant on this procedure, known as participant modeling, is often more effective than exposure alone. Here the therapist calmly models ways of interacting with the phobic stimulus or situation (Bandura, 1977 , 1997 ). These techniques enable clients to learn that these situations are not as frightening as they had thought and that their anxiety, while unpleasant, is not harmful and will gradually dissipate (Craske & Mystkowski, 2006 ; Craske & Rowe, 1997 ). The new learning is probably mediated by changes in brain activation in the amygdala, which is centrally involved in the emotion of fear.

One variation on exposure therapy is called participant modeling. Here the therapist models how to touch and pick up a live tarantula and encourages the spider-phobic client to imitate her behavior. This treatment is graduated, with the client’s first task being simply to touch the tarantula from the outside of the cage, then to touch the tarantula with a stick, then with a gloved hand, then with a bare hand, and finally to let the tarantula crawl over his hand. This is a highly effective treatment, with the most spider-phobic clients being able to reach the top of the hierarchy within 60 to 90 minutes.

For certain phobias such as small-animal phobias, flying phobia, claustrophobia, and blood-injury phobia, exposure therapy is often highly effective when administered in a single long session (of up to 3 hours) (Öst, 1997 ; Öst et al., 2001 ). This can be an advantage because some people are more likely to seek treatment if they have to go only once. This treatment has also been shown to be highly effective in youth with specific phobias (e.g., Ollendick et al., 2009 ).

An example of the use of exposure therapy comes from the treatment of Mary, the housewife whose acrophobia and claustrophobia we described earlier.

Mary’s Treatment Treatment consisted of 13 sessions of graduated exposure exercises in which the therapist accompanied Mary first into mildly fear-provoking situations and then gradually into more and more fear-provoking situations. Mary also engaged in homework, doing these exposure exercises by herself. The prolonged in vivo (“real-life”) exposure sessions lasted as long as necessary for her anxiety to subside. Initial sessions focused on Mary’s claustrophobia and on getting her to be able to ride for a few floors in an elevator, first with the therapist and then alone. Later she took longer elevator rides in taller buildings. Exposure for the acrophobia consisted of walking around the periphery of the inner atrium on the top floor of a tall hotel and, later, spending time at a mountain vista overlook spot. The top of the claustrophobia hierarchy consisted of taking a tour of an underground cave. After 13 sessions, Mary successfully took a flight with her husband to Europe and climbed to the top of many tall tourist attractions there.

Recently, some therapists have begun to use virtual reality environments to simulate certain kinds of phobic situations, such as heights and airplanes, as places to conduct exposure treatment. If such techniques were highly effective and widely available, there would be no need to conduct treatment in real situations (such as real airplanes or tall buildings). About a dozen controlled studies have yielded very promising results. Moreover, although the results are not yet entirely conclusive, it appears that the relative efficacy of virtual reality versus live exposure is comparable (e.g., Choy et al., 2007 ; Parsons & Rizzo, 2008 ; Rothbaum et al., 2006 ).

New treatments using virtual reality environments allow therapists to simulate certain kinds of phobic situations, such as standing at heights or sitting in airplanes, in a contrived setting.

Some researchers have also tried combining cognitive restructuring techniques or medications with exposure-based techniques to see if this can produce additional gains. In general, studies using cognitive techniques alone have not produced results as good as those using exposure-based techniques, and the addition of cognitive techniques has generally not added much (Craske & Mystkowski, 2006 ; Wolitzky-Taylor et al., 2008 ). Similarly, medication treatments are ineffective by themselves, and there is even some evidence that antianxiety medications may interfere with the beneficial effects of exposure therapy (Antony & Barlow, 2002 ; Choy et al., 2007 ). Recently, however, some studies have shown that a drug called d-cycloserine, which is known to facilitate extinction of conditioned fear in animals (e.g., Davis et al., 2005 ; Davis et al., 2006 ), may enhance the effectiveness of small amounts of exposure therapy for fear of heights in a virtual reality environment (Ressler et al., 2004 ; Norberg et al., 2008 ). D-cyloserine by itself, however, has no effect. These results are very promising, but much more work is necessary before it will be known how useful this drug will be in enhancing the effects of exposure therapy for many different kinds of phobias.

in review

· ● What are the five subtypes of specific phobias?

· ● Describe the original classical conditioning explanation for the origins of specific phobias as well as how vicarious conditioning may be involved.

· ● Explain several sources of individual differences in learning that have improved and expanded the basic conditioning hypothesis of phobia acquisition.

· ● Explain how evolutionary factors have influenced which objects and situations we are most likely to learn to fear.

· ● Describe the most effective treatment for specific phobias.

Social Phobias

Social phobia (or social anxiety disorder), as the DSM-5 describes it, is characterized by disabling fears of one or more specific social situations (such as public speaking, urinating in a public bathroom, or eating or writing in public; see the DSM-5 box). In these situations, a person fears that she or he may be exposed to the scrutiny and potential negative evaluation of others or that she or he may act in an embarrassing or humiliating manner. Because of their fears, people with social phobias either avoid these situations or endure them with great distress. Intense fear of public speaking is the single most common type of social phobia. DSM-5 also identifies two subtypes of social phobia, one of which centers on performance situations such as public speaking and one of which is more general and includes nonperformance situations (such as eating in public). Indeed, people with the more general subtype of social phobia often have significant fears of most social situations (rather than simply a few) and often also have a diagnosis of avoid-ant personality disorder (see Chapter 10 ; e.g., Skodol et al., 1995 ; Stein & Stein, 2008 ). Watch the Video Steve: Social Phobia on MyPsychLab

Prevalence, Age of Onset, and Gender Differences

The diagnosis of social phobia is very common and occurs even in famous performers such as Barbra Streisand and Carly Simon. The National Comorbidity Survey-Replication estimated that about 12 percent of the population will qualify for a diagnosis of social phobia at some point in their lives (Kessler, Berglund, Demler, et al., 2005 ; Ruscio et al., 2008 ). This disorder is somewhat more common among women than men (about 60 percent of sufferers are women). Unlike specific phobias, which most often originate in childhood, social phobias typically begin somewhat later, during early or middle adolescence or certainly by early adulthood (Bruce et al., 2005 ; Ruscio et al., 2008 ). Nearly two-thirds of people with social phobia suffer from one or more additional anxiety disorders at some point in their lives, and about 50 percent also suffer from a depressive disorder at the same time (Kessler, Chiu, et al., 2005; Ruscio et al., 2008 ). Approximately one-third abuse alcohol to reduce their anxiety and help them face the situations they fear (for example, drinking before going to a party; Magee et al., 1996 ). Moreover, because of their distress and avoidance of social situations, people with social phobia, on average, have lower employment rates and lower socioeconomic status, and approximately one-third have severe impairment in one or more domains of their life (Harvey et al., 2005 ; Ruscio et al., 2008 ). Finally, the disorder is remarkably persistent, with one study finding that only 37 percent recovered spontaneously over a 12-year period (Bruce et al., 2005 ).

Intense fear of public speaking is the single most common social phobia.

The case of Paul is typical of social phobia (except that not all people with social phobia have full-blown panic attacks, as Paul did, in their socially phobic situations).

A Surgeon’s Social Phobia Paul was a single white male in his mid-30s when he first presented for treatment. He was a surgeon who reported a 13-year history of social phobia. He had very few social outlets because of his persistent concerns that people would notice how nervous he was in social situations, and he had not dated in many years. Convinced that people would perceive him as foolish or crazy, he particularly worried that people would notice how his jaw tensed up when around other people. Paul frequently chewed gum in public situations, believing that this kept his face from looking distorted. Notably, he had no particular problems talking with people in professional situations. For example, he was quite calm talking with patients before and after surgery. During surgery, when his face was covered with a mask, he also had no trouble carrying out surgical tasks or interacting with the other surgeons and nurses in the room. The trouble began when he left the operating room and had to make small talk—and eye contact—with the other doctors and nurses or with the patient’s family. He frequently had panic attacks in these social situations. During the panic attacks he experienced heart palpitations, fears of “going crazy,” and a sense of his mind “shutting down.” Because the panic attacks occurred only in social situations, he was diagnosed as having social phobia rather than panic disorder.

Paul’s social phobia and panic had begun about 13 years earlier when he was under a great deal of stress. His family’s business had failed, his parents had divorced, and his mother had had a heart attack. It was in this context of multiple stressors that a personally traumatic incident probably triggered the onset of his social phobia. One day he had come home from medical school to find his best friend in bed with his fiancée. About a month later he had his first panic attack and started avoiding social situations.

Psychological Causal Factors

Social phobias generally involve learned behaviors that have been shaped by evolutionary factors. Such learning is most likely to occur in people who are genetically or temperamentally at risk.

SOCIAL PHOBIAS AS LEARNED BEHAVIOR

Like specific phobias, social phobias often seem to originate from simple instances of direct or vicarious classical conditioning such as experiencing or witnessing a perceived social defeat or humiliation, or being or witnessing the target of anger or criticism (Harvey et al., 2005 ; Mineka & Zinbarg, 1995 , 2006 ; Tillfors, 2004 ). In two studies, 56 to 58 percent of people with social phobia recalled and identified direct traumatic experiences as having been involved in the origin of their social phobias (Öst & Hugdahl, 1981 ; Townsley et al., 1995 ). Another study reported that 92 percent of an adult sample of people with social phobia reported a history of severe teasing in childhood, compared to only 35 percent in a group of people with obsessive-compulsive disorder (McCabe et al., 2003 ). Moreover, a recent laboratory study of people with social phobia revealed that they showed especially robust conditioning of fear when the unconditioned stimulus was socially relevant (critical facial expressions and verbal insults) as opposed to more nonspecifically negative stimuli (such as unpleasant odors and painful pressure) (Lissek et al., 2008 ).

Öst and Hugdahl ( 1981 ) reported that another 13 percent of their subjects recalled vicarious conditioning experiences of some sort. One study interviewed a group of people with social phobia about their images of themselves in socially phobic situations and asked where those images had originated (Hackmann et al., 2000 ). Ninety-six percent of these people remembered some socially traumatic experience that was linked to their own current image of themselves in socially phobic situations. The themes of these memories included having been “criticized for having an anxiety symptom” (e.g., being red or blushing), and having felt “self-conscious and uncomfortable in public as a consequence of past criticism” such as “having previously been bullied and called a ‘nothing’” (Hackmann et al., 2000 , p. 606).

People with generalized social phobia also may be especially likely to have grown up with parents who were emotionally cold, socially isolated, and avoidant. Not surprisingly, such parents devalued sociability and did not encourage their children to go to social events. All these factors thus provided ample opportunity for vicarious learning of social fears (Harvey et al., 2005 ; Morris, 2001 ; Rapee & Melville, 1997 ). Harvey and colleagues ( 2005 ) also found that many people with social phobia reported that the onset of their social phobia had occurred during a time when they were having problems with their peers such as not fitting in. Nevertheless, as with specific phobias, it is important to recognize that not everyone who experiences direct or vicarious conditioning in social situations, or who grows up with socially avoidant parents, or who has problems with peers, develops social phobia. This is because individual differences in experiences play an important role in who develops social phobia, as is the case with specific phobias.

DSM-5 criteria for: Social Anxiety Disorder (Social Phobia)

· 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 dysmorphic disorder, or autism spectrum disorder.

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

SOCIAL FEARS AND PHOBIAS IN AN EVOLUTIONARY CONTEXT

Social fears and phobias by definition involve fears of members of one’s own species. By contrast, animal fears and phobias usually involve fear of potential predators. Although animal fears probably evolved to trigger activation of the fight-or-flight response to potential predators, Öhman and colleagues proposed that social fears and phobias evolved as a byproduct of dominance hierarchies that are a common social arrangement among animals such as primates (Dimberg & Öhman, 1996 ; Öhman et al., 1985 ). Dominance hierarchies are established through aggressive encounters between members of a social group, and a defeated individual typically displays fear and submissive behavior but only rarely attempts to escape the situation completely. Thus, these investigators argued, it is not surprising that people with social phobia endure being in their feared situations rather than running away and escaping them, as people with animal phobias often do (see also Longin et al., 2010 ; Öhman, 2009 ).

If social phobias evolved as a byproduct of dominance hierarchies, it is not surprising that humans have an evolution-arily based predisposition to acquire fears of social stimuli that signal dominance and aggression from other humans. These social stimuli include facial expressions of anger or contempt, which on average all humans seem to process more quickly and readily than happy or neutral facial expressions (Öhman et al., 2001 ; Öhman, 2009 ; Schupp et al., 2004 ). In a series of experiments that paralleled ones for specific phobias, Öhman and colleagues demonstrated that subjects develop stronger conditioned responses when slides of angry faces are paired with mild electric shocks than when happy or neutral faces are paired with the same shocks (Dimberg & Öhman, 1996 ). Indeed, even very brief subliminal (not consciously perceived) presentations of the angry face that had been paired with shock were sufficient to activate the conditioned responses (e.g., Parra et al., 1997 ), probably because even these subliminal angry faces activate the amygdala—the central structure involved in fear learning (Öhman et al., 2007 ). Relatedly, recent results have also shown that people who have social phobia show greater activation of the amygdala (and other brain areas involved in emotion processing) in response to negative facial expressions (such as angry faces) than do normal controls (Goldin et al., 2009 ; Phan et al., 2006 ). Such results may help explain the seemingly irrational quality of social phobia, in that the angry faces are processed very quickly and an emotional reaction can be activated without a person’s awareness of any threat. The hyperactivity to negative facial expressions is paralleled by heightened neural responses to criticism (Blair et al., 2008 ; see Shin & Liberzon, 2009 , for a review).

PERCEPTIONS OF UNCONTROLLABILITY AND UNPREDICTABILITY

Being exposed to uncontrollable and unpredictable stressful events (such as parental separation and divorce, family conflict, or sexual abuse) may play an important role in the development of social phobia (Mathew et al., 2001 ; Mineka & Zinbarg, 1995 , 2006 ; Rapee & Spence, 2004 ). In the case of Paul, the precipitating event seemed to be finding his fiancée in bed with his best friend. Perceptions of uncontrollability and unpredictability often lead to submissive and unassertive behavior, which is characteristic of socially anxious or phobic people. This kind of behavior is especially likely if the perceptions of uncontrollability stem from an actual social defeat, which is known in animals to lead to both increased submissive behavior and increased fear (Mineka & Zinbarg, 1995 , 2006 ). Consistent with this, people with social phobia have a diminished sense of personal control over events in their lives (Leung & Heimberg, 1996 ). This diminished expectation of personal control may develop, at least in part, as a function of having been raised in families with somewhat overprotective (and sometimes rejecting) parents (Lieb et al., 2000 ).

COGNITIVE BIASES

Cognitive factors also play a role in the onset and maintenance of social phobia. Beck and Emery (1985) suggested that people with social phobia tend to expect that other people will reject or negatively evaluate them. They argued that this leads to a sense of vulnerability when they are around people who might pose a threat. Clark and Wells ( 1995 ; Wells & Clark, 1997 ) later further proposed that these danger schemas of socially anxious people lead them to expect that they will behave in an awkward and unacceptable fashion, resulting in rejection and loss of status. Such negative expectations lead to their being preoccupied with bodily responses and with stereotyped, negative self-images in social situations; to their overestimating how easily others will detect their anxiety; and to their misunderstanding how well they come across to others (Hirsch et al., 2004 ). Such intense self-preoccupation during social situations, even to the point of attending to their own heart rate, interferes with their ability to interact skillfully (Hirsch et al., 2003 ; Pineles & Mineka, 2005 ). A vicious cycle may evolve: Social phobics’ inward attention and somewhat awkward behavior may lead others to react to them in a less friendly fashion, confirming their expectations (D. M. Clark, 1997 ; Clark & McManus, 2002 ).

Another cognitive bias seen in social phobia is a tendency to interpret ambiguous social information in a negative rather than a benign manner (e.g., when someone smiles at you, does it mean they like you or that they think you’re foolish?). Moreover, it is the negatively biased interpretations that socially anxious people make that are what is remembered (Hertel et al., 2008 ). It has also been suggested that these biased cognitive processes combine to maintain social phobia and possibly even contribute to its development (Hirsch, Clark, & Mathews, 2006 ).

Biological Causal Factors

GENETIC AND TEMPERAMENTAL FACTORS

Infants and young children who are fearful and easily distressed by novel people or situations are sometimes high on the temperamental variable called behavioral inhibition. Such infants show an increased risk of developing social phobia in adolescence.

The most important temperamental variable is behavioral inhibition, which shares characteristics with both neuroticism and introversion (Bienvenu et al., 2007 ). Behaviorally inhibited infants who are easily distressed by unfamiliar stimuli and who are shy and avoidant are more likely to become fearful during childhood and, by adolescence, to show increased risk of developing social phobia (Hayward et al., 1998 ; Kagan, 1997 ). For example, one classic study was conducted on behavioral inhibition as a risk factor in a large group of children, most of whom were already known to be at risk for anxiety because their parents had an emotional disorder. Among these children, those who had been assessed as being high on behavioral inhibition between 2 and 6 years of age were nearly three times more likely to be diagnosed with social phobia (22 percent) even in middle childhood (average age of 10) than were children who were low on behavioral inhibition at 2 to 6 years (8 percent; Hirshfeld-Becker et al., 2007 ; see also Hayward et al., 1998 ). In another study, 60 children were assessed yearly for behavioral inhibition from grades 1 to 9. If they showed chronically high levels of behavioral inhibition throughout this time period, 50 percent had developed social anxiety disorder by grade 9. By contrast, none had developed social anxiety disorder in the group with chronic low behavioral inhibition (Essex et al., 2010 ).

Results from several studies of twins have also shown that there is a modest genetic contribution to social phobia; estimates are that about 30 percent of the variance in liability to social phobia is due to genetic factors (Hettema et al., 2005 ; Smoller et al., 2008 ). Nevertheless, these studies suggest that an even larger proportion of variance in who develops social phobia is due to nonshared environmental factors, which is consistent with a strong role for learning.

Treatments

COGNITIVE AND BEHAVIORAL THERAPIES

There are very effective forms of behavior therapy and cognitive-behavior therapy for social phobia. As for specific phobias, behavioral treatments were developed first and generally involve prolonged and graduated exposure to social situations that evoke fear. More recently, as research has revealed the underlying distorted cognitions that characterize social phobia, cognitive restructuring techniques have been added to the behavioral techniques, generating a form of cognitive-behavioral therapy (Barlow et al., 2007 ). In cognitive restructuring the therapist attempts to help clients with social phobia identify their underlying negative, automatic thoughts (“I’ve got nothing interesting to say” or “No one is interested in me”). After helping clients understand that such automatic thoughts (which usually occur just below the surface of awareness but can be accessed) often involve cognitive distortions, the therapist helps the clients change these inner thoughts and beliefs through logical reanalysis. The process of logical reanalysis might involve asking oneself questions to challenge the automatic thoughts: “Do I know for certain that I won’t have anything to say?” “Does being nervous have to lead to or equal looking stupid?”

In one highly effective version of such treatments, clients may be assigned exercises in which they manipulate their focus of attention (internally versus externally) to demonstrate to themselves the adverse effects of internal self-focus. They may also receive videotaped feedback to help them modify their distorted self-images. Such techniques have now been very successfully applied to the treatment of social phobia (Clark, Ehlers, et al., 2003 , 2006 ; Heimberg, 2002 ; Mörtberg et al., 2007 ). Many studies over the years have shown that exposure therapy and cognitive-behavioral therapy produce comparable results. However, one study suggests that this new, very effective variant on cognitive treatment may be more effective than exposure therapy (Clark et al., 2006 ). Moreover, at least one study has now shown that simply training individuals with social phobia to disengage from negative social cues during a 15-minute lab task that is repeated 8 times over 4 to 6 weeks produced such remarkable reductions in social anxiety symptoms that nearly 3 out of 4 of the participants no longer met criteria for social anxiety disorder (Schmidt et al., 2009 ).

An example of successful combined treatment can be seen in the case of Paul, the surgeon described earlier who had social phobia.

Paul’s Treatment Since the onset of his social phobia 13 years earlier, Paul had taken an antidepressant at one point. The drug had helped stop his panic attacks, but he continued to fear them intensely and still avoided social situations. Thus, there was little effect on his social phobia. He had also been in supportive psychotherapy, which had helped his depression at the time but not his social phobia or his panic. When he went for treatment at an anxiety clinic, he was not on any medication or in any other form of treatment. Treatment consisted of 14 weeks of cognitive-behavioral therapy. By the end of treatment, Paul was not panicking at all and was quite comfortable in most social situations that he had previously avoided. He was seeing old friends whom he had avoided for years because of his anxiety, and he was beginning to date. Indeed, he even asked his female therapist for a date during the last treatment session! Although such a request was clearly inappropriate, it did indicate how much progress he had made.

MEDICATIONS

Unlike specific phobias, social phobias can also sometimes be treated with medications. The most effective and widely used medications are several categories of antidepressants (including the monoamine oxidase inhibitors [MAOIs] and the selective serotonin reuptake inhibitors [SSRIs] discussed extensively in Chapters 7 and 16 ; Ipser et al., 2008 ; Roy-Byrne & Cowley, 2007 ). In some studies, the effects of these antidepressant medications have been comparable to those seen with cognitive-behavioral treatments. However, in several studies, the newer version of cognitive-behavior therapy discussed earlier produced much more substantial improvement than did medication (e.g., Clark, Ehlers, et al., 2003 ). Moreover, the medications must be taken over a long period of time to help ensure that relapse does not occur (Blanco et al., 2002 ; Stein & Stein, 2008 ). A distinct advantage of behavioral and cognitive-behavioral therapies over medications, then, is that they generally produce more long-lasting improvement with very low relapse rates; indeed, clients often continue to improve after treatment is over. Finally, several studies have also suggested that when d-cycloserine (discussed with treatment of specific phobias) is added to exposure therapy, the treatment gains occur more quickly and are more substantial (e.g., Guastella et al., 2008 ).

in review

· ● What are the primary diagnostic criteria for social phobia and its two subtypes?

· ● Identify three of the psychological causal factors for social phobia and two of the biological causal factors.

· ● Describe the major treatment approaches used for social phobias.

Panic Disorder

Diagnostically, panic disorder is defined and characterized by the occurrence of panic attacks that often seem to come “out of the blue.” According to the DSM-5 criteria for panic disorder, the person must have experienced recurrent, unexpected attacks and must have been persistently concerned about having another attack or worried about the consequences of having an attack for at least a month (often referred to as anticipatory anxiety). For such an event to qualify as a full-blown panic attack, there must be abrupt onset of at least 4 of 13 symptoms, most of which are physical, although three are cognitive: (1) depersonalization (a feeling of being detached from one’s body) or derealization (a feeling that the external world is strange or unreal); (2) fear of dying; or (3) fear of “going crazy” or “losing control” (see the DSM-5 box for diagnostic criteria). Panic attacks are fairly brief but intense, with symptoms developing abruptly and usually reaching peak intensity within 10 minutes; the attacks usually subside in 20 to 30 minutes and rarely last more than an hour. Periods of anxiety, by contrast, do not usually have such an abrupt onset and are more long lasting.

Panic attacks are often “unexpected” or “uncued” in the sense that they do not appear to be provoked by identifiable aspects of the immediate situation. Indeed, they sometimes occur in situations in which they might be least expected, such as during relaxation or during sleep (known as nocturnal panic). In other cases, however, panic attacks are said to be situationally predisposed, occurring only sometimes while the person is in a particular situation such as while driving a car or being in a crowd.

Because most symptoms of a panic attack are physical, it is not surprising that as many as 85 percent of people having a panic attack may show up repeatedly at emergency rooms or physicians’ offices for what they are convinced is a medical problem—usually cardiac, respiratory, or neurological (White & Barlow, 2002 ; see also Korczak et al., 2007 ). Of course, medical causes have to be ruled out. However, if a person experiences panic attacks and becomes very concerned about having additional attacks or worries about the possible consequences of the attack (e.g., having a heart attack or going crazy), a diagnosis of panic disorder will eventually be given.

Unfortunately, a correct diagnosis is often not made for years due to the normal results on numerous costly medical tests. Further complications arise because cardiac patients are at a nearly twofold elevated risk for developing panic disorder (Korczak et al., 2007 ). Prompt diagnosis and treatment is also important because panic disorder causes approximately as much impairment in social and occupational functioning as that caused by major depressive disorder (Roy-Byrne et al., 2008 ) and because panic disorder can contribute to the development or worsening of a variety of medical problems (White & Barlow, 2002 ).

DSM-5 criteria for: Panic Disorder

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

Note: The abrupt surge can occur from a calm state or an anxious state.

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

· 2. Sweating.

· 3. Trembling or shaking.

· 4. Sensations of shortness of breath or smothering.

· 5. Feelings of choking.

· 6. Chest pain or discomfort.

· 7. Nausea or abdominal distress.

· 8. Feeling dizzy, unsteady, light-headed, or faint.

· 9. Chills or heat sensations.

· 10. Paresthesias (numbness or tingling sensations).

· 11. Derealization (feelings of unreality) or depersonalization (being detached from oneself).

· 12. Fear of losing control or “going crazy.”

· 13. Fear of dying.

Note: Culture-specific symptoms (e.g., tinnitus, neck soreness, headache, uncontrollable screaming or crying) may be seen. Such symptoms should not count as one of the four required symptoms.

· B. At least one of the attacks has been followed by 1 month (or more) of one or both of the following:

· 1. Persistent concern or worry about additional panic attacks or their consequences (e.g., losing control, having a heart attack, “going crazy”).

· 2. A significant maladaptive change in behavior related to the attacks (e.g., behaviors designed to avoid having panic attacks, such as avoidance of exercise or unfamiliar situations).

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

· D. The disturbance is not better explained by another mental disorder (e.g., the panic attacks do not occur only in response to feared social situations, as in social anxiety disorder; in response to circumscribed phobic objects or situations, as in specific phobia; in response to obsessions, as in obsessive-compulsive disorder; in response to reminders of traumatic events, as in posttraumatic stress disorder; or in response to separation from attachment figures, as in separation anxiety disorder).

The case of Mindy Markowitz is typical:

Art Director’s Panic Attacks Mindy Markowitz is an attractive … 25-year-old art director … who comes to an anxiety clinic … seeking treatment for “panic attacks” that have occurred with increasing frequency over the past year, often two or three times a day. These attacks begin with a sudden, intense wave of “horrible fear” that seems to come out of nowhere, sometimes during the day, sometimes waking her from sleep. She begins to tremble, is nauseated, sweats profusely, feels as though she is choking, and fears that she will lose control and do something crazy, like run screaming into the street….

Mindy has had panic attacks intermittently over the 8 years since her first attack, sometimes not for many months, but sometimes, as now, several times a day. There have been extreme variations in the intensity of the attacks, some being so severe and debilitating that she has had to take a day off from work.

Mindy has always functioned extremely well in school, at work, and in her social life, apart from her panic attacks…. She is a lively, friendly person … who has never limited her activities … She says … she is as likely to have an attack at home in her own bed as on the subway, so there is no point in avoiding the subway…. [Wherever] she has an attack … she says, “I just tough it out.”

Source: Adapted with permission from DSM-IV-TR Casebook: A Learning Companion to the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision (Copyright © 2002). American Psychiatric Association.

Agoraphobia

Historically, agoraphobia was thought to involve a fear of the agora—the Greek word for public places of assembly (Marks, 1987 ). In agoraphobia the most commonly feared and avoided situations include streets and crowded places such as shopping malls, movie theaters, and stores. Standing in line can be particularly difficult (see Table 6.2 on p. 180 for commonly avoided situations). What is the common theme that underlies this seemingly diverse cluster of fears? Sometimes, agoraphobia develops as a complication of having panic attacks in one or more such situations. Concerned that they may have a panic attack or get sick, people with agoraphobia are anxious about being in places or situations from which escape would be physically difficult or psychologically embarrassing, or in which immediate help would be unavailable if something bad happened (see the DSM-5 box for diagnostic criteria). Typically people with agoraphobia are also frightened by their own bodily sensations, so they also avoid activities that will create arousal such as exercising, watching scary movies, drinking caffeine, and even engaging in sexual activity.

DSM-5 criteria for: Agoraphobia

· A. Marked fear or anxiety about two (or more) of the following five situations:

· 1. Using public transportation (e.g., automobiles, buses, trains, ships, planes).

· 2. Being in open spaces (e.g., parking lots, marketplaces, bridges).

· 3. Being in enclosed places (e.g., shops, theaters, cinemas).

· 4. Standing in line or being in a crowd.

· 5. Being outside of the home alone.

· B. The individual fears or avoids 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 (e.g., fear of falling in the elderly; fear of incontinence).

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

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

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

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

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

· H. If another medical condition (e.g., inflammatory bowel disease, Parkinson’s disease) is present, the fear, anxiety, or avoidance is clearly excessive.

· I. The fear, anxiety, or avoidance is not better explained by the symptoms of another mental disorder—for example, the symptoms are not confined to specific phobia, situational type; do not involve only social situations (as in social anxiety disorder); and are not related exclusively to obsessions (as in obsessive-compulsive disorder), perceived defects or flaws in physical appearance (as in body dysmorphic disorder), reminders of traumatic events (as in posttraumatic stress disorder), or fear of separation (as in separation anxiety disorder).

Note: Agoraphobia is diagnosed irrespective of the presence of panic disorder. If an individual’s presentation meets criteria for panic disorder and agoraphobia, both diagnoses should be assigned.

As agoraphobia first develops, people tend to avoid situations in which attacks have occurred, but usually the avoidance gradually spreads to other situations where attacks might occur. In moderately severe cases, people with agoraphobia may be anxious even when venturing outside their homes alone. In very severe cases, agoraphobia is an utterly disabling disorder in which a person cannot go beyond the narrow confines of home—or even particular parts of the home.

TABLE 6.2 Situations Frequently Avoided by People with Agoraphobia

Crowds	Standing in line
Theaters	Restaurants
Shopping malls	Sports arenas
Cars and buses	Trains and airplanes
Bridges	Tunnels
Escalators	Elevators
Being home alone	Being far away from home
Aeorbic exercise	Sauna baths
Getting angry	Sexual activity
Watching exciting or scary movies

The case of John D. is typical of someone with both panic disorder and agoraphobia.

John D. John D. was a 45-year-old married Caucasian man with three sons. Although well educated and successful … John had been experiencing difficulties with panic attacks for 15 years … experiencing two to five panic attacks per month. The previous week John had had a panic attack while driving with his family to a computer store. He recollected that before the panic attack he might have been “keyed up” over the kids making a lot of noise in the back seat; the attack began right after he had quickly turned around to tell the kids to “settle down.” Immediately after he turned back to look at the road, John felt dizzy. As soon as he noticed this, John experienced a rapid and intense surge of other sensations including sweating, accelerated heart rate, hot flushes, and trembling. Fearing that he was going to crash the car, John quickly pulled to the side of the road ….

John was having only a few panic attacks per month, but he was experiencing a high level of anxiety every day, focused on the possibility that he might have another panic attack at any time. Indeed, John had developed extensive apprehension or avoidance of driving, air travel, elevators, wide-open spaces, taking long walks alone, movie theaters, and being out of town.

[His] first panic attack had occurred 15 years ago. John had fallen asleep on the living room sofa at around 1:00 A.M. after returning from a night of drinking with some of his friends. Just after awakening at 4:30, John felt stomach pains and a pulsating sensation in the back of his neck. All of a sudden, John noticed that his heart was racing, too…. Although he did not know what he was suffering from, John was certain that he was dying.

John remembered having a second panic attack about a month later. From then on, the panic attacks began to occur more regularly. When the panic attacks became recurrent, John started to avoid situations in which the panic attacks had occurred as well as situations in which he feared a panic attack was likely to occur. On three occasions during the first few years of his panic attacks, John went to the emergency room of his local hospital because he was sure that his symptoms were a sign of a heart attack.

Source: Adapted from Brown & Barlow, 2001 , pp. 19–22.

Agoraphobia is a frequent complication of panic disorder. The case of John D. is typical. However, many patients with agoraphobia do not experience panic. Recognizing this, in DSM-5 agoraphobia is now listed as a distinct disorder. As agoraphobia develops, there is often a gradually spreading fearfulness in which more and more aspects of the environment outside the home become threatening. The most recent estimate of the lifetime prevalence of agoraphobia without panic from the National Comorbidity Survey-Replication is 1.4 percent (e.g., Kessler, Chiu, et al., 2006 ).

Prevalence, Age of Onset, and Gender Differences

Many people suffer from panic disorder and from agoraphobia. The National Comorbidity Survey-Replication study found that approximately 4.7 percent of the adult population has had panic disorder with or without agoraphobia at some time in their lives, with panic disorder without agoraphobia being more common (Kessler, Chiu, et al., 2005c ). Panic disorder with or without agoraphobia often starts in the late teenage years, but the average age of onset is 23 to 34 years. However, it can begin, especially for women, in a person’s 30s or 40s (Hirschfeld, 1996 ; Kessler, Chiu, et al., 2006 ). Once panic disorder develops, it tends to have a chronic and disabling course, although the intensity of symptoms often waxes and wanes over time (Keller et al., 1994 ; White & Barlow, 2002 ). Indeed, one 12-year longitudinal study found that less than 50 percent of patients with panic disorder with agoraphobia had recovered in 12 years, and 58 percent of those who had recovered at some point had had a recurrence (new onset; Bruce et al., 2005 ). Panic disorder is about twice as prevalent in women as in men (Eaton et al., 1994 ; White & Barlow, 2002 ). Agoraphobia also occurs much more frequently in women than in men, and the percentage of women increases as the extent of agoraphobic avoidance increases. Among people with severe agoraphobia, approximately 80 to 90 percent are female (Bekker, 1996 ; White & Barlow, 2002 ). Table 6.3 outlines gender differences in the prevalence of other anxiety disorders for comparison purposes.

The most common explanation of the pronounced gender difference in agoraphobia is a sociocultural one (McLean & Anderson, 2009 ). In our culture (and many others as well), it is more acceptable for women who experience panic to avoid the situations they fear and to need a trusted companion to accompany them when they enter feared situations. Men who experience panic are more prone to “tough it out” because of societal expectations and their more assertive, instrumental approach to life (Bekker, 1996 ). Although there is very little research on this topic, one study consistent with this idea was conducted by Chambless and Mason ( 1986 ), who administered a sex-role scale to both male and female agoraphobics and found that the less “masculine” one scored on the scale, the more extensive the agoraphobic avoidance, for both males and females. Another study found that cultures and societies that delineate rigid gender roles at a sociocultural level tend to have higher levels of agoraphobia. In addition, some evidence indicates that men with panic disorder may be more likely to self-medicate with nicotine or alcohol as a way of coping with and enduring panic attacks rather than developing agoraphobic avoidance (Starcevic et al., 2008 ).

TABLE 6.3 Gender Differences in the Anxiety Disorders: Lifetime Prevalence Estimates

Disorder	Prevalence in Men (%)	Prevalence in Women (%)	Ratio
Specific phobias	6.7	15.7	2.34
Social phobia	11.1	15.5	1.4
Panic disorder	2.0	5.0	2.5
Generalized anxiety disorder	3.6	6.6	1.8

Note: Because these figures are from different studies and may not be strictly comparable, they should be taken as approximations of current estimates of gender differences.

Sources: Eaton et al. ( 1994 ); Karno et al. ( 1988 ); Kessler et al. ( 1994 , 1995 ); Magee et al. ( 1996 ).

Comorbidity With Other Disorders

The National Comorbidity Survey-Replication found that 83 percent of people with panic disorder have at least one comorbid disorder (Kessler, Chiu, et al., 2006 ). Most commonly these include generalized anxiety disorder, social phobia, specific phobia, PTSD, depression, and substance-use disorders (especially smoking and alcohol dependence; Bernstein et al., 2006; Kessler, Chiu, et al., 2006 ; Zvolensky & Bernstein, 2005 ). It is estimated that 50 to 70 percent of people with panic disorder will experience serious depression at some point in their lives (Kessler, Chiu, et al., 2006 ). They may also meet criteria for dependent or avoidant personality disorder (see Chapter 10 ). The issue of whether people with panic disorder show an increased risk of suicidal ideation and suicide attempts has been quite controversial, with a number of studies suggesting that any increased risk is due to indirect factors such as comorbid depression and substance abuse, which are known risk factors themselves (e.g., Vickers & McNally, 2004 ). However, two recent very large epidemiological studies (one in the United States, which had nearly 10,000 adults from the National Comorbidity Survey-Replication study, and one including over 100,000 people from 21 countries) have indeed found that panic disorder is associated with increased risk for suicidal ideation and attempts independent of its relationship with comorbid disorders (Nock et al., 2009 ; Nock et al., 2010 ).

The Timing of a First Panic Attack

Although panic attacks themselves appear to come “out of the blue,” the first one frequently occurs following feelings of distress or some highly stressful life circumstance such as loss of a loved one, loss of an important relationship, loss of a job, or criminal victimization (see Barlow, 2002 ; Klauke et al., 2010 , for reviews). Although not all studies have found this, some have estimated that approximately 80 to 90 percent of clients report that their first panic attack occurred after one or more negative life events.

Nevertheless, not all people who have a panic attack following a stressful event go on to develop full-blown panic disorder. Current estimates from the recent National Comorbidity Survey-Replication are that nearly 23 percent of adults have experienced at least one panic attack in their lifetimes, but most have not gone on to develop full-blown panic disorder (Kessler, Chiu, et al., 2006 ). People who have other anxiety disorders or major depression often experience occasional panic attacks as well (Barlow, 2002 ; Kessler, Chiu, et al., 2006 ). Given that panic attacks are much more frequent than panic disorder, this leads us to an important question: What causes full-blown panic disorder to develop in only a subset of these people? Several different prominent theories about the causes of panic disorder have addressed this question.

Biological Causal Factors

GENETIC FACTORS

According to family and twin studies, panic disorder has a moderate heritable component (e.g., Kendler et al., 1992b , 1992c ; Kendler et al., 2001 ; Norrholm & Ressler, 2009 ). In a large twin study, Kendler and colleagues ( 2001 ) estimated that 33 to 43 percent of the variance in liability to panic disorder was due to genetic factors. As noted earlier, this genetic vulnerability is manifested at a psychological level at least in part by the important personality trait called neuroticism (which is in turn related to the temperamental construct of behavioral inhibition). Recently, several studies have begun to identify which specific genetic polymorphisms are responsible for this moderate heritability (e.g., Strug et al., 2010 ), either alone or in interaction with certain types of stressful life events (e.g., Klauke et al., 2010 ), but this preliminary work needs to be replicated.

People with severe agoraphobia are often fearful of venturing out of their homes into public places, in part because of their fear of having a panic attack in a place in which escape might prove physically difficult or psychologically embarrassing. They may even become housebound unless accompanied by a spouse or trusted companion.

Some studies have suggested that this heritability is at least partly specific for panic disorder (rather than for all anxiety disorders; see Barlow, 2002 , for a review), but one large female twin study suggested that there is overlap in the genetic vulnerability factors for panic disorder and phobias (Kendler, Walters, et al., 1995 ). This would be consistent with some preliminary evidence that people with a history of social or specific phobia are at heightened risk for developing panic disorder (Biederman et al., 2006 ). However, another study suggests overlap in the genetic vulnerability for panic disorder, generalized anxiety disorder, and agoraphobia (Hettema, Prescott, et al., 2005 ). Only further research can resolve these inconsistencies in findings (e.g., Norrholm & Ressler, 2009 ).

PANIC AND THE BRAIN

One relatively early prominent theory about the neurobiology of panic attacks implicated the locus coeruleus in the brain stem (see Figure 6.1 on p. 183 ) and a particular neurotransmitter—norepinephrine—that is centrally involved in brain activity in this area (e.g., Goddard et al., 1996 ). However, today it is recognized that it is increased activity in the amygdala that plays a more central role in panic attacks than does activity in the locus coeruleus. The amygdala is a collection of nuclei in front of the hippocampus in the limbic system of the brain that is critically involved in the emotion of fear. Stimulation of the central nucleus of the amygdala is known to stimulate the locus coeruleus as well as the other autonomic, neuroendocrine, and behavioral responses that occur during panic attacks (e.g., Gorman et al., 2000 ; LeDoux, 2000 ). Other recent research has also implicated the periaqueductal gray area in the midbrain (e.g., Del-Ben & Graeff, 2008 ; Graeff & Del-Ben, 2008 ).

Some research has suggested that the amygdala is the central area involved in what has been called a “fear network,” with connections not only to lower areas in the brain like the locus coeruleus but also to higher brain areas like the prefrontal cortex (e.g., Gorman et al., 2000 ). According to this view, panic attacks occur when the fear network is activated, either by cortical inputs or by inputs from lower brain areas. So according to this influential theory, panic disorder is likely to develop in people who have abnormally sensitive fear networks that get activated too readily to be adaptive. This theory about abnormally sensitive fear networks is also consistent with findings that individuals with panic disorder showed heightened startle responses to loud noise stimuli as well as slower habituation of such responding (Ludewig et al., 2005 ; see also Shin & Liberzon, 2010). Sakai and colleagues ( 2005 ), using functional neuroimaging techniques, also found support for this neuroanatomical hypothesis. Abnormally sensitive fear networks may have a partially heritable basis but may also develop as a result of repeated stressful life experiences, particularly early in life (e.g., Gorman et al., 2000 ; Ladd et al., 2000 ).

But panic attacks are only one component of panic disorder. People with panic disorder also become anxious about the possibility of another attack, and those with agoraphobia also engage in phobic avoidance behavior (e.g., Gorman et al., 1989 , 2000 ). Different brain areas are probably involved in these different aspects of panic disorder. The panic attacks themselves arise from activity in the amygdala, either by cortical inputs (e.g., evaluating a stimulus as highly threatening) or by activity coming from more downstream areas like the locus coeruleus. For people who have one or more panic attacks and who go on to develop significant conditioned anxiety about having another one in particular contexts, the hippocampus (also a part of the limbic system, below the cortex, which is very involved in the learning of emotional responses; see Figure 6.1 ) is thought to generate this conditioned anxiety (e.g., Charney et al., 1998 ; Gray & McNaughton, 1996 , 2000 ) and is probably also involved in the learned avoidance associated with agoraphobia (Gorman et al., 2000 ). Finally, the cognitive symptoms that occur during panic attacks (fears of dying or of losing control) and overreactions to the danger posed by possibly threatening bodily sensations are likely to be mediated by higher cortical centers (see Gorman et al., 2000 ; Etkin, 2010 ).

BIOCHEMICAL ABNORMALITIES

Over 30 years ago, Klein ( 1981 ) and others (Sheehan, 1982 , 1983 ) argued that panic attacks are alarm reactions caused by biochemical dysfunctions. This hypothesis initially appeared to be supported by numerous studies over the past 40 years, showing that people with panic disorder are much more likely to experience panic attacks when they are exposed to various biological challenge procedures than are normal people or people with other psychiatric disorders. For example, some of these laboratory tests involve infusions of sodium lactate (a substance resembling the lactate our bodies produce during exercise; e.g., Gorman et al., 1989 ), inhaling air with altered amounts of carbon dioxide (e.g., Woods et al., 1987 ), or ingesting large amounts of caffeine (e.g., Uhde, 1990 ). In each case, such procedures produce panic attacks in panic disorder clients at a much higher rate than in normal subjects (see Barlow, 2002 , for review). There is a broad range of these so-called panic provocation procedures , and some of them are associated with quite different and even mutually exclusive neurobiological processes. Thus, no single neurobiological mechanism could possibly be implicated (Barlow 2002 ; Roy-Byrne et al., 2006 ). However, as explained later in the section on causal factors, simpler biological and psychological explanations can account for this pattern of results. These alternative explanations stem from the observation that what all these biological challenge procedures have in common is that they put stress on certain neurobiological systems, which in turn produce intense physical symptoms of arousal (such as increased heart rate, respiration, and blood pressure).

FIGURE 6.1 A Biological Theory of Panic, Anxiety, and Agoraphobia. According to one theory, panic attacks may arise from abnormal activity in the amygdala, a collection of nuclei in front of the hippocampus in the limbic system. The anticipatory anxiety that people develop about having another panic attack is thought to arise from activity in the hippocampus of the limbic system, which is known to be involved in the learning of emotional responses. Agoraphobic avoidance, also a learned response, may also involve activity of the hippocampus and higher cortical centers (Gorman et al., 2000 ).

At present, two primary neurotransmitter systems are most implicated in panic attacks—the noradrenergic and the serotonergic systems (Gorman et al., 2000 ; Graeff & Del-Ben, 2008 ; Neumeister et al., 2004 ). Noradrenergic activity in certain brain areas can stimulate cardiovascular symptoms associated with panic (Gorman et al., 2000 ). Increased serotonergic activity also decreases noradrenergic activity. This fits with results showing that the medications most widely used to treat panic disorder today (the selective serotonin reuptake inhibitors—SSRIs) seem to increase serotonergic activity in the brain but also to decrease noradrenergic activity. By decreasing noradrenergic activity, these medications decrease many of the cardiovascular symptoms associated with panic that are ordinarily stimulated by noradrenergic activity (Gorman et al., 2000 ).

The inhibitory neurotransmitter GABA has also been implicated in the anticipatory anxiety that many people with panic disorder have about experiencing another attack. GABA is known to inhibit anxiety and has been shown to be abnormally low in certain parts of the cortex in people with panic disorder (Goddard, Mason, et al., 2001 , 2004 ).

Psychological Causal Factors

COMPREHENSIVE LEARNING THEORY OF PANIC DISORDER

Certain investigators have proposed a comprehensive learning theory of panic disorder that accounts for most of the known findings about panic disorder (Bouton, Mineka, & Barlow, 2001 ; see also Barlow, 2002 ; Bouton, 2005 ; Mineka & Zinbarg, 2006 ). Along with advances in the study of classical conditioning, this theory builds on the earlier theory that initial internal bodily sensations of anxiety or arousal (such as heart palpitations) effectively become interoceptive conditioned stimuli associated with higher levels of anxiety or arousal (Goldstein & Chambless, 1978 ). According to this theory, initial panic attacks become associated with initially neutral internal (interoceptive) and external (exteroceptive) cues through an interoceptive conditioning (or exteroceptive conditioning ) process (e.g., Acheson et al., 2007 ; Forsyth & Eifert, 1998 ). One primary effect of this conditioning is that anxiety becomes conditioned to these CSs, and the more intense the panic attack, the more robust the conditioning that will occur (Forsyth et al., 2000 ). Other types of instrumental and avoidance learning are also involved but will not be explained here.

This conditioning of anxiety to the internal or external cues associated with panic thus sets the stage for the development of two of the three components of panic disorder: anticipatory anxiety and sometimes agoraphobic fears. Specifically, when people experience their initial panic attacks (which are terrifying emotional events replete with strong internal bodily sensations), interoceptive and exeroceptive conditioning can occur to multiple different kinds of cues, ranging from heart palpitations and dizziness to shopping malls. Because anxiety becomes conditioned to these CSs, anxious apprehension about having another attack, particularly in certain contexts, may develop, as may agoraphobic avoidance of contexts in which panic attacks might occur in a subset of individuals. Moreover, a recent study demonstrated that once an individual has developed panic disorder they show greater generalization of conditioned responding to other similar cues than do controls without panic disorder (Lissek et al., 2010 ). In individuals who have panic disorder, a recent study showed that extinction of conditioned anxiety responses occurs more slowly than in normal controls (Michael, Blechert, et al., 2007 ). Because extinction involves inhibitory learning, which seems to be impaired in panic disorder, it is not surprising that individuals with panic disorder also show impaired discriminative conditioning because of their deficits in learning that a CS is a safety cue (Lissek et al., 2009 ).

However, another important effect is that panic attacks themselves (the third component of panic disorder) are also likely to be conditioned to certain internal cues. This leads to the occurrence of panic attacks that seemingly come out of the blue when people unconsciously experience certain internal bodily sensations (CSs). For example, one young man with panic disorder who was particularly frightened of signs that his heart was racing experienced a surprising and unexpected panic attack after hearing that his favorite presidential candidate had won. The panic attack thus occurred when he was happy and excited (which is what made it so surprising for him). However, from the standpoint of this theory, the attack was actually not surprising. Because the man was excited, his heart was racing, which probably served as an internal CS that triggered the panic (Mineka & Zinbarg, 2006 ). This theory also underscores why not everyone who experiences an occasional panic attack goes on to develop panic disorder. Instead, people with certain genetic, temperamental or personality, or cognitive-behavioral vulnerabilities will show stronger conditioning of both anxiety and panic (Barlow, 2002 ; Bouton et al., 2001 ; Mineka & Zinbarg, 2006 ). For example, the personality variable that clearly serves as a risk variable is neuroticism.

COGNITIVE THEORY OF PANIC

FIGURE 6.2 The Panic Circle. Any kind of perceived threat may lead to apprehension or worry, which is accompanied by various bodily sensations. According to the cognitive model of panic, if a person then catastrophizes about the meaning of his or her bodily sensations, this will raise the level of perceived threat, thus creating more apprehension and worry as well as more physical symptoms, which fuel further catastrophic thoughts. This vicious circle can culminate in a panic attack. The initial physical sensations need not arise from the perceived threat (as shown at the top of the circle) but may come from other sources (exercise, anger, psychoactive drugs, etc., as shown at the bottom of the circle). (Adapted from D. M. Clark, 1986 , 1997 .)

An earlier cognitive theory of panic disorder proposed that individuals with panic disorder are hypersensitive to their bodily sensations and are very prone to giving them the direst possible interpretation (Beck & Emery, 1985; D. M. Clark, 1986 , 1997 ). Clark referred to this as a tendency to catastrophize about the meaning of their bodily sensations. For example, a person who develops panic disorder might notice that his heart is racing and conclude that he is having a heart attack, or notice that he is dizzy, which may lead to fainting or to the thought that he may have a brain tumor. These very frightening thoughts may cause many more physical symptoms of anxiety, which further fuel the catastrophic thoughts, leading to a vicious circle culminating in a panic attack (see Figure 6.2 ). The person is not necessarily aware of making these catastrophic interpretations; rather, the thoughts are often just barely out of the realm of awareness (Rapee, 1996 ). These automatic thoughts, as Beck calls them, are in a sense the triggers of panic. Although it is not yet clear how the tendency to catastrophize develops, the cognitive model proposes that only people with this tendency to catastrophize go on to develop panic disorder (e.g., D. M. Clark, 1997 ).

Several lines of evidence are consistent with the cognitive theory of panic disorder. For example, people with panic disorder are much more likely to interpret their bodily sensations in a catastrophic manner (e.g., see D. M. Clark, 1997 ; Teachman et al., 2007 ), and the greater the tendency to do so, the greater the severity of panic (Casey et al., 2005 ). The model also predicts that changing their cognitions about their bodily symptoms should reduce or prevent panic. Evidence that cognitive therapy for panic works is consistent with this prediction (D. M. Clark et al., 1994 , 1999 ). In addition, a brief explanation of what to expect in a panic provocation study can apparently prevent or reduce panic symptoms (D. M. Clark, 1997 ). People with panic disorder either were given a brief, but detailed, explanation of what physical symptoms to expect from an infusion of sodium lactate and why they should not worry about these symptoms, or were given a minimal explanation. The people with the cognitive rationale about what to expect were significantly less likely to say that they had had the subjective experience of a panic attack in response to the lactate (30 percent) than were control individuals (90 percent) (see Schmidt et al., 2006 , for related results).

LEARNING AND COGNITIVE EXPLANATIONS OF RESULTS FROM PANIC PROVOCATION STUDIES

Earlier, we noted that there are simpler psychological explanations that provide a common mechanism for understanding how so many varied panic provocation agents can all provoke panic at high rates in people with panic disorder. Because these agents produce arousal, they mimic the physiological cues that normally precede a panic attack or may be taken as a sign of some other impending catastrophe (Barlow, 2002 ; Bouton et al., 2001 ; Margraf et al., 1986a , 1986b ). People with panic disorder already start at a higher level of arousal than others and are very familiar with these early warning cues. Thus, according to the cognitive theory, people with panic attacks frequently misinterpret these symptoms as the beginning of a panic attack or a heart attack, which in turn induces the vicious circle of panic described in the previous section; this would not happen in controls who do not have the same tendency to catastrophize. Alternatively, according to the learning theory of panic disorder, it would be only those with panic disorder for whom these cues might serve as interoceptive CSs that can trigger anxiety and panic because of their prior associations with panic.

The key difference between these two theories in explaining the results of panic provocation studies lies in the great importance that the cognitive model places on the meaning that people attach to their bodily sensations; they will experience panic only if they make catastrophic interpretations of certain bodily sensations. Such catastrophic cognitions are not necessary with the interoceptive conditioning model because anxiety and panic attacks can be triggered by unconscious interoceptive (or exteroceptive) cues (Bouton et al., 2001 ). Thus the learning theory model is better able to explain the occurrence of the panic attacks that often occur without any preceding negative (catastrophic) automatic thoughts, as well as the occurrence of nocturnal panic attacks that occur during sleep; the occurrence of both of these kinds of attacks is difficult for the cognitive model to explain (see the Developments in Research box below).

developments in RESEARCH: Nocturnal Panic Attacks

Although the majority of panic attacks experienced by people with panic disorder occur during waking hours, approximately 50 to 60 percent of people report that they have experienced a panic attack during sleep at least once (Barlow, 2002 ; O’Mahony & Ward, 2003 ). Nocturnal panic refers to waking from sleep in a state of panic. It seems to occur with some regularity in about 20 to 40 percent of people with panic disorder and is frequently associated with insomnia and frequent awakenings during sleep (Craske et al., 2002 ; Overbeek et al., 2005 ; Papadimitriou & Linkowski, 2005 ). Although one might think that such panic attacks occur in response to nightmares, considerable research shows that this is not the case. Sleep has five stages that occur in a fairly invariant sequence multiple times throughout the night: one stage called REM sleep (rapid eye movement sleep) when vivid dreaming occurs, and four stages of non-REM sleep (Stages 1–4) when vivid dreams do not occur. If nocturnal panic attacks occurred in response to dreams, we would expect them to occur during REM sleep (when nightmares usually occur), but in fact they occur during Stage 2 and early Stage 3 sleep, usually a few hours after falling asleep.

It is important to note that nocturnal panic attacks are different from “sleep terrors” or “night terrors,” which usually occur during Stage 4 sleep. Night terrors are usually experienced by children, who often scream and then fear that someone or something is chasing them around the room; however, they do not wake up (Barlow, 2002 ). Nocturnal panic attacks also differ from isolated sleep paralysis, which can sometimes occur during the transition from sleep to waking. It involves awareness of one’s surroundings accompanied by a stark sense of terror (resembling that during a panic attack) and an inability to move, which seems to occur because the individuals are waking from REM (dream) sleep, when there is suppression of muscle activity below the neck (e.g., Hinton et al, 2005 ).

ANXIETY SENSITIVITY AND PERCEIVED CONTROL

Other cognitive and learning explanations of panic and agoraphobia have looked at a number of different factors that can generally be explained within either the learning or cognitive perspective. For example, several researchers have shown that people who have high levels of anxiety sensitivity are more prone to developing panic attacks and perhaps panic disorder (McNally, 2002 ; Pagura et al., 2009 ). Anxiety sensitivity is a trait-like belief that certain bodily symptoms may have harmful consequences. Such a person would endorse statements such as, “When I notice that my heart is beating rapidly, I worry that I might have a heart attack.” In one important study, Schmidt and colleagues ( 1997 ) followed over 1,400 young adults undergoing basic military training for 5 weeks. They found that high levels of anxiety sensitivity predicted the development of spontaneous panic attacks during this highly stressful period. Several other studies examining the same issues obtained very similar results, thus boosting confidence in the reliability of anxiety sensitivity as a predictor of panic attacks (e.g., Hayward et al., 2000 ; Li & Zinbarg, 2007 ). However, Schmidt and colleagues ( 2006 ) have reported results showing that high anxiety sensitivity also serves to predict the onset of other anxiety disorders as well as panic attacks, thus raising some questions about the specificity of its role for panic versus other anxiety disorders (see also Starcevic & Berle, 2006 ).

In addition, several important studies have shown that simply having a sense of perceived control—for instance, over the amount of carbon-dioxide-altered air that is inhaled (a panic provocation procedure known frequently to bring on anxiety and panic)—reduces anxiety and even blocks panic (e.g., Sanderson et al., 1989 ; Zvolensky et al., 1998 , 1999 ). In addition, if a person with panic disorder is accompanied by a “safe” person when undergoing a panic provocation procedure, that person is likely to show reduced distress, lowered physiological arousal, and reduced likelihood of panic relative to someone who came alone (without a “safe” person; Carter et al., 1995 ). Moreover, a recent study has shown that anxiety sensitivity has a greater effect on panic symptoms in people with low perceived control (Bentley et al., 2012). Finally, individuals with panic disorder may also be protected against the development of agoraphobic avoidance if they have relatively high levels of perceived control over their emotions and threatening situations (Suarez et al., 2009; White et al., 2006 ).

Many people experiencing a panic attack mistake their symptoms (for example, chest pain and shortness of breath) for another medical problem—most often a heart attack.

SAFETY BEHAVIORS AND THE PERSISTENCE OF PANIC

Why do people who have developed panic disorder continue to have panic attacks in spite of the fact that their direst predictions rarely, if ever, come true? Some people with panic disorder may, for example, have three or four panic attacks a week for 20 years; each time they may believe they are having a heart attack, and yet they never do. After experiencing hundreds or thousands of panic attacks without having a heart attack, one would think, from the cognitive perspective, that this catastrophic thought would have been proved wrong so many times that it would finally go away. However, evidence suggests that such disconfirmation does not occur because people with panic disorder frequently engage in safety behaviors (such as breathing slowly or carrying a bottle with anxiolytic medication) before or during an attack. They then mistakenly tend to attribute the lack of catastrophe to their having engaged in this safety behavior rather than to the idea that panic attacks actually do not lead to heart attacks. Similarly, people who think they may faint will tend to lean against solid objects (D. A. Clark, 1997 ; Salkovskis et al., 1996 ). Research suggests that it is important during treatment to identify these safety behaviors so that the person can learn to give them up and finally see that the feared catastrophe still does not occur. Indeed, a good number of studies have found that asking people to drop their safety behaviors during cognitive-behavioral treatment can increase the effectiveness of the treatment (e.g., Rachman et al., 2008 ).

COGNITIVE BIASES AND THE MAINTENANCE OF PANIC

Finally, many studies have shown that people with panic disorder are biased in the way they process threatening information. Such people not only interpret ambiguous bodily sensations as threatening (D. A. Clark, 1997 ; Teachman et al., 2006 ), but they also interpret other ambiguous situations as more threatening than do controls. People with panic disorder also seem to have their attention automatically drawn to threatening information in their environment such as words that represent things they fear, such as palpitations, numbness, or faint (see Lim & Kim, 2005 ; Mathews & MacLeod, 2005 ; Mineka et al., 2003 , for reviews). One study using fMRI techniques demonstrated that people with panic disorder showed greater activation to threat words than did normals in brain areas involved in memory processing of threatening material (Maddock et al., 2003 ). Whether these information-processing biases are present before the disorder begins and help to cause it is as yet unclear, but these biases are certainly likely to help maintain the disorder once it has begun. For example, having one’s attention automatically drawn to threatening cues in the environment is likely to provoke more attacks.

In summary, research into both biological and psychosocial factors involved in panic disorder has provided important insights into this disorder since it was first identified as a distinct disorder in 1980. It seems unlikely that research from either tradition alone will ever provide a complete account of this disorder, and we eagerly await more attempts at synthesizing these findings into a biopsychosocial theory.

Treatments

MEDICATIONS

Many people with panic disorder (with or without agoraphobia) are prescribed anxiolytics (antianxiety medications) from the benzodiazepine category such as alprazolam (Xanax) or clonazepam (Klonopin). These people frequently show some symptom relief from these medications, and many can function more effectively. One major advantage of these drugs is that they act very quickly (30–60 minutes) and so can be useful in acute situations of intense panic or anxiety. However, these anxiolytic medications can also have quite undesirable side effects such as drowsiness and sedation, which can lead to impaired cognitive and motor performance. Also, with prolonged use, most people using moderate to high doses develop physiological dependence on the drug, which results in withdrawal symptoms when the drug is discontinued (e.g., nervousness, sleep disturbance, dizziness, and further panic attacks). Withdrawal from these drugs can be very slow and difficult, and it precipitates relapse in a high percentage of cases (Pollack & Simon, 2009 ; Roy-Byrne & Cowley, 2007 ). These are the reasons why benzodiazepines are no longer considered as a first-choice treatment (Katon, 2006 ).

The other category of medication that is useful in the treatment of panic disorder and agoraphobia is the antidepressants (including primarily the tricyclics, the SSRIs, and most recently the serotonin-norepinephrine reuptake inhibitors—SNRIs). These medications have both advantages and disadvantages compared with anxiolytics. One major advantage is that they do not create physiological dependence in the way benzodiazepines can, and they also can alleviate any comorbid depressive symptoms or disorders (Pollack & Simon, 2009 ; Roy-Byrne & Cowley, 2007 ). However, it takes about 4 weeks before they have any beneficial effects, so they are not useful in an acute situation where a person is having a panic attack. Troublesome side effects (such as dry mouth, constipation, and blurred vision with the tricyclics, and interference with sexual arousal with the SSRIs) mean that large numbers of people refuse to take the medications or discontinue their use. Moreover, relapse rates when the drugs are discontinued are quite high (although not as high as with the benzodiazepines; Roy-Byrne & Cowley, 2007 ).

Today the SSRIs are more widely prescribed than the tricyclics because the SSRIs are generally better tolerated by most patients. Moreover, both are generally preferred by physicians to benzodiazepines because of the risks associated with the latter (Roy-Byrne & Cowley, 2007 ).

BEHAVIORAL AND COGNITIVE-BEHAVIORAL TREATMENTS

The original behavioral treatment for agoraphobia from the early 1970s involved prolonged exposure to feared situations, often with the help of a therapist or family member. Similar to what is done with specific and social phobias, the idea was to make people gradually face the situations they feared and learn that there was nothing to fear. Such exposure-based treatments were quite effective and helped about 60 to 75 percent of people with agoraphobia show clinically significant improvement (Barlow et al., 2007 ). These effects were generally well maintained at 2- to 4-year follow-up. But this left approximately 25 to 40 percent not improved to a clinically significant degree (Barlow et al., 2002 ).

One limitation of these original treatments was that they did not specifically target panic attacks. In the mid-1980s, two new techniques were developed as clinical researchers increasingly recognized the importance of panic attacks to most people with agoraphobia. One technique involves the variant on exposure known as interoceptive exposure, meaning deliberate exposure to feared internal sensations. The idea was that fear of these internal sensations should be treated in the same way that fear of external agoraphobic situations is treated—namely, through prolonged exposure to those internal sensations so that the fear may extinguish. For example, people are asked to engage in various exercises that bring on various internal sensations (e.g., spinning in a chair, hyperventilating, running in place) and to stick with those sensations until they subside, thereby allowing habituation of their fears of these sensations.

research CLOSE-UP: Clinically Significant

Not all statistically significant changes are of sufficient magnitude to be clinically significant. Clinical significance reflects how large the effects of a particular treatment or intervention are with respect to how much meaningful change they provide in a person’s level of functioning or well-being.

The second set of techniques that were developed is cognitive restructuring techniques, in recognition that catastrophic automatic thoughts may help maintain panic attacks. One kind of integrative cognitive-behavioral treatment for panic disorder—panic control treatment—targets both agoraphobic avoidance and panic attacks. There are several aspects to PCT. First, clients are educated about the nature of anxiety and panic and how the capacity to experience both is adaptive. A second part of the treatment involves teaching people with panic disorder to control their breathing. Third, clients are taught about the logical errors that pople who have panic disorders are prone to making and learn to subject their own automatic thoughts to a logical reanalysis. Finally, they are exposed to feared situations and feared bodily sensations to build up a tolerance to the discomfort. Generally, this integrative treatment produces better results than the original exposure-based techniques that focused exclusively on exposure to external situations (D. M. Clark, 1997 ; Arch & Craske, 2009 ). In many of the studies conducted using one of the variants on these treatments, 70 to 90 percentof people with panic disorder were panic free at the end of 8 to 14 weeks of treatment, and gains were well maintained at 1- to 2-year follow-up (Arch & Craske, 2008 ; McCabe & Gifford, 2009 ). Overall, the magnitude of improvement is often greater with these cognitive and behavioral treatments than with medications (Arch & Craske, 2009 ; Barlow et al., 2002 ). Moreover, these treatments have been extended and shown to be very useful in treating people who also have nocturnal panic (Arch & Craske, 2008 ).

What about the combination of antianxiety medication and cognitive-behavioral therapy? In the short term, such combined treatment sometimes produces a slightly superior result compared to either type of treatment alone (Barlow et al., 2007 ; Mitte, 2005 ). In addition, one study showed that those individuals who had received combined treatment showed fewer medication side effects and fewer dropouts than those who had used medication alone (Marcus, Gorman, et al., 2007 ). However, in the long term, after medication has been tapered (especially benzodiazepine medications), clients who have been on medication with or without cognitive or behavioral treatment seem to show a greater likelihood of relapse (Arch & Craske, 2008 ; Barlow et al., 2002 ; Marks et al., 1993 ). Perhaps this is because they have attributed their gains to the medication rather than to their personal efforts (Başoĝlu et al., 1994 ; Mitte, 2005 ). The one medication that has shown promise for enhancing responsiveness to CBT of panic disorder is D-cyloserine—the same medication discussed earlier that can enhance the speed of treating specific and social phobias (Otto et al., 2009).

in review

· ● You are experiencing a panic attack. What are your symptoms?

· ● Describe the major diagnostic features of both panic disorder and agoraphobia. Why do the two disorders often occur together?

· ● What biological causal factors have been implicated in panic disorder?

· ● Compare and contrast the learning or conditioning theory and cognitive models of panic disorder.

· ● Describe the major treatment approaches for panic disorder and their relative advantages and disadvantages.

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. DSM-5 criteria specify that the worry must occur on more days than not for at least 6 months and that it must be experienced as difficult to control (see DSM-5 criteria box). The worry must be about a number of different events or activities, and its content cannot be exclusively related to the worry associated with another concurrent disorder, such as the possibility of having a panic attack. The subjective experience of excessive worry must also be accompanied by at least three of six other symptoms, as listed in the table, such as muscle tension or being easily fatigued. There was much discussion among the task force working on revisions for DSM-5 as to whether this is the optimal set of criteria for GAD (e.g., the 6-month duration requirement and the excessive worry requirement; e.g., Andrews et al., 2010 ; Lee et al., 2009; Ruscio et al., 2005 ) and whether this is the optimal name for the disorder (versus generalized worry disorder or pathological worry disorder) (Andrews et al., 2010 ). However, in the end a conservative approach was taken and no changes were made from DSM-IV to DSM-5.

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 general picture of people suffering from generalized anxiety disorder is that they live in a relatively constant future-oriented mood state of anxious apprehension, chronic tension, worry, and diffuse uneasiness that they cannot control. They also show marked vigilance for possible signs of threat in the environment and frequently engage in subtle avoidance activities such as procrastination, checking, or calling a loved one frequently to see if he or she is safe (Barlow, 2002 ; Barlow et al., 1996 ). Such anxious apprehension also occurs in other anxiety disorders (for example, the person with agoraphobia shows anticipatory anxiety about future panic attacks and about dying, and the person with social phobia is anxious about possible negative social evaluation). But this apprehension is the essence of GAD, leading Barlow and others to refer to GAD as the “basic” anxiety disorder (Roemer et al., 2002 ; Wells & Butler, 1997 ). Watch the Video Philip: Generalized Anxiety Disorder on MyPsychLab.

DSM-5 criteria for: Generalized Anxiety Disorder

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

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

· C. The anxiety and worry are associated with 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).

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 (Roemer et al., 1997 ). Not only do they have difficulty making decisions, but after they have managed to make a decision they worry endlessly, even after going to bed, over possible errors and unforeseen circumstances that may prove the decision wrong and lead to disaster. They have no appreciation of the logic by which most of us conclude that it is pointless to torment ourselves about possible outcomes over which we have no control. As two researchers in this area put it, “The result is that they fail to escape the illusory world created in their thoughts and images and rarely experience the present moment that possesses the potential to bring them joy” (Behar & Borkovec, 2006 , p. 184). It is not surprising then that a recent study of the personal and economic burden of GAD found that those with GAD experienced a similar amount of role impairment and lessened quality of life to those with major depression (Hofmann et al., 2010).

The case below is fairly typical of generalized anxiety disorder.

A Graduate Student with GAD John was a 26-year-old, single graduate student in the social sciences at a prestigious university. He reported that he had had problems with anxiety nearly all his life, but they had become worse since he had left home and gone to an Ivy League college. During the past year his anxiety had seriously interfered with his functioning, and he worried about several different spheres of his life such as his own and his parents’ health. During one incident a few months earlier, he had thought that his heart was beating more slowly than usual, and he had experienced some tingling sensations; this led him to worry that he might die. In another incident he had heard his name spoken over a loudspeaker in an airport and had worried that someone at home must be dying. He was also very worried about his future because his anxiety had kept him from completing his master’s thesis on time. John also worried excessively about getting a bad grade even though he had never had one either in college or in graduate school. In classes he worried excessively about what the professor and other students thought of him. Although he had a number of friends, he had never had a girlfriend because of his shyness about dating. He had no problem talking or socializing with women as long as it was not defined as a dating situation. He worried that he should date a woman only if he was quite sure, from the outset, that it could be a serious relationship. He also worried excessively that if a woman did not want to date him, it meant that he was boring.

In addition to his worries, which he perceived as uncontrollable, John reported muscle tension and becoming easily fatigued. He also reported great difficulty concentrating and a considerable amount of restlessness and pacing. At times he had difficulty falling asleep if he was particularly anxious, but at other times he slept excessively, in part to escape from his worries. He frequently experienced dizziness and palpitations, and in the past he had had full-blown panic attacks.

John’s mother was also quite anxious and had been treated for panic disorder. John was obviously extremely bright and had managed to do very well in school in spite of his lifelong problems with anxiety. But as the pressures of finishing graduate school and starting his career loomed before him, and as he got older and had still never dated, the anxiety became so severe that he sought treatment.

Prevalence, Age of Onset, and Gender Differences

Generalized anxiety disorder is a relatively common condition; current estimates from the National Comorbidity Survey-Replication are that approximately 3 percent of the population suffers from it in any 1-year period and 5.7 percent at some point in their lives (Kessler et al., 1994 ; Kessler, Berglund, Demler, et al., 2005; Kessler, Chiu, et al., 2005c). It also tends to be chronic. One 12-year follow-up study of people diagnosed with GAD found that 42 percent had not remitted 13 years later and of those who had remitted, nearly half had had a recurrence (Bruce et al., 2005 ; see also Hofmann et al., 2010). However, after age 50 the disorder seems to disappear for many people (Rubio & Lopez-Ibor, 2007 ). If it disappears it tends to be replaced by a somatic symptom disorder and characterized by physical symptoms and health concerns.

GAD is approximately twice as common in women as in men (a somewhat less dramatic difference than is seen with many specific phobias or severe agoraphobia; see Table 6.3 for summaries of gender differences in the different anxiety disorders). Although GAD is quite common, most people with this disorder manage to function (albeit with some role impairment) in spite of their high levels of worry and low perceived well-being (Hofmann et al., 2010; Stein et al., 2004 ). They are less likely to go to clinics for psychological treatment than are people with panic disorder or major depressive disorder, which are frequently more debilitating conditions. However, people with GAD do frequently show up in physicians’ offices with medical complaints (such as muscle tension or gastrointestinal and/or cardiac symptoms) and are known to be overusers of health care resources (similar to people with panic disorder; Greenberg et al., 1999 ; Hofmann et al., 2010; Katon et al., 2002 ).

Age of onset is often difficult to determine because 60 to 80 percent of people with GAD remember having been anxious nearly all their lives, and many others report a slow and insidious onset (Roemer et al., 2002 ; Wells & Butler, 1997 ). However, research has also documented that GAD often develops in older adults, for whom it is the most common anxiety disorder (e.g., Mackenzie et al., 2011 ; Stein, 2004 ).

Comorbidity With Other Disorders

Generalized anxiety disorder often co-occurs with other disorders, especially other anxiety and mood disorders such as panic disorder, social phobia, specific phobia, PTSD, and major depressive disorder (Brown, Campbell, et al., 2001 ; Kessler, Chiu, et al., 2005c ; Tyrer & Baldwin, 2006 ). In addition, many people with GAD (like John) experience occasional panic attacks without qualifying for a diagnosis of panic disorder (Barlow, 1988 , 2002 ). Nor is it surprising that excessive use of tranquilizing drugs, sleeping pills, and alcohol often complicates the clinical picture in generalized anxiety disorder (Tyrer & Baldwin, 2006 ). Watch the Video Christy: Generalized Anxiety Disorder with Insomnia on MyPsychLab.

Psychological Causal Factors

THE PSYCHOANALYTIC VIEWPOINT

According to this viewpoint, generalized or free-floating anxiety results from an unconscious conflict between ego and id impulses that is not adequately dealt with because the person’s defense mechanisms have either broken down or have never developed. Freud believed that it was primarily sexual and aggressive impulses that had been either blocked from expression or punished upon expression that led to free-floating anxiety. Defense mechanisms may become overwhelmed when a person experiences frequent and extreme levels of anxiety, as might happen if id impulses are frequently blocked from expression (e.g., under periods of prolonged sexual deprivation). According to this view, the primary difference between specific pho-bias and free-floating anxiety is that in phobias, the defense mechanisms of repression and displacement of an external object or situation actually work, whereas in free-floating anxiety these defense mechanisms do not work, leaving the person anxious nearly all the time. Unfortunately this viewpoint is not testable and has therefore been largely abandoned among clinical researchers.

PERCEPTIONS OF UNCONTROLLABILITY AND UNPREDICTABILITY

Uncontrollable and unpredictable aversive events are much more stressful than controllable and predictable aversive events, so it is perhaps not surprising that the former create more fear and anxiety, as we discussed with specific and social pho-bias (Barlow, 2002 ; Craske & Waters, 2005 ; Mineka, 1985b ; Mineka & Oehlberg, 2008 ; Mineka & Zinbarg, 1996 , 2006 ). Conversely, experience with controlling aspects of one’s life may immunize one against developing general anxiety (Chorpita, 2001 ; Mineka & Kelly, 1989 ).

This has led researchers to hypothesize that people with GAD may have a history of experiencing many important events in their lives as unpredictable or uncontrollable. For example, having a boss or spouse who has unpredictable bad moods or outbursts of temper for seemingly trivial reasons might keep a person in a chronic state of anxiety. Although the unpredictable and uncontrollable events involved in GAD are generally not as severe and traumatic as those involved in the origins of PTSD, there is some evidence that people with GAD may be more likely to have had a history of trauma in childhood than individuals with several other anxiety disorders (Borkovec et al., 2004 ; see also Kendler, Hettema, et al., 2003 ). Moreover, people with GAD clearly have far less tolerance for uncertainty than nonanxious controls and than people with panic disorder (Dugas et al., 2004 , 2005 ; Koerner & Dugas, 2008 ). This low tolerance for uncertainty in people with GAD suggests that they are especially disturbed by not being able to predict the future (as none of us can; Roemer et al., 2002 ). Some findings also show the greater the intolerance of uncertainty, the more severe the GAD (Dugas et al., 2007 ). Intolerance for uncertainty also seems to be elevated in individuals with obsessive compulsive disorder (e.g., Behar et al., 2008 ).

In addition, perhaps some of these people’s intolerance for uncertainty, as well as their tension and hypervigilance (the sense of always looking for signs of threat), stems from their lacking safety signals in their environment. If a person mostly experiences predictable stressors (e.g., on Mondays the boss is always in a bad mood and is likely to be highly critical), he or she cannot only predict when something bad is likely to happen (e.g., Mondays at work) but can also feel safe when that signal is missing (a safety signal; e.g., Tuesdays through Fridays at work). But if another person has experienced many unpredictable or unsignaled stressors (e.g., the boss is in a bad mood and highly critical on random days of the week), she or he will not have developed safety signals for when it is appropriate to relax and feel safe, and this uncertainty may lead to chronic anxiety (Mineka, 1985a ; Mineka & Zinbarg, 1996 ; Seligman & Binik, 1977 ). Thus a relative lack of safety signals may help explain why people with GAD feel constantly tense and vigilant for possible threats (Rapee, 2001 ).

A SENSE OF MASTERY: THE POSSIBILITY OF IMMUNIZING AGAINST ANXIETY

A person’s history of control over important aspects of his or her environment is another important experiential variable strongly affecting reactions to anxiety-provoking situations. Although we cannot study this experimentally in humans, we can learn a lot from laboratory analogue studies in animals. For example, one longitudinal experiment with infant rhesus monkeys found that infant monkeys reared with a sense of mastery and control over their environments for 7 to 10 months later adapted more readily to frightening events and novel anxiety-provoking situations than did monkeys reared in environments that were identical except for the experiences with control (Mineka, Gunnar, & Champoux, 1986 ; see also Chorpita & Barlow, 1998 ; Craske & Waters, 2005 ; Mineka & Zinbarg, 1996 , 2006 ). In human children, experiences with control and mastery often also occur in the context of the parent–child relationship and so parents’ responsiveness to their children’s needs directly influences their children’s developing sense of mastery (e.g., Chorpita, 2001 ; Craske & Waters, 2005 ; Mineka & Zinbarg, 1996 , 2006 ). Unfortunately, parents of anxious children often have an intrusive, overcontrolling parenting style, which may serve only to promote their children’s anxious behaviors by making them think of the world as an unsafe place in which they require protection and have little control themselves (Craske & Waters, 2005 ).

THE CENTRAL ROLE OF WORRY AND ITS POSITIVE FUNCTIONS

The worry process is now considered the central feature of GAD and has been the focus of much research in the past 20 years. Here we will first consider the nature and functions of worry. Next, we will consider why worry comes to be such a self-sustaining process in some people and why it may be perceived to be uncontrollable.

Borkovec and colleagues (Borkovec, 1994 ; Borkovec et al., 2004 ; Behar & Borkovec, 2006 ) investigated both what people with GAD think the benefits of worrying are and what actual functions worry serves. Several of the benefits that people with GAD most commonly think derive from worrying are:

· • Superstitious avoidance of catastrophe (“Worrying makes it less likely that the feared event will occur”).

· • Avoidance of deeper emotional topics (“Worrying about most of the things I worry about is a way to distract myself from worrying about even more emotional things, things that I don’t want to think about”).

· • Coping and preparation (“Worrying about a predicted negative event helps me to prepare for its occurrence”; Borkovec, 1994 , pp. 16–17; Borkovec et al., 2004 ).

There is some evidence that for a subset of people with GAD, these positive beliefs about worry play a key role in maintaining high levels of anxiety and worry, especially in early phases of the development of GAD (Dugas et al., 2007 ). In addition, exciting new discoveries about the functions that worry actually serves help reveal why the worry process is so self-sustaining. When people with GAD worry, their emotional and physiological responses to aversive imagery are actually suppressed. This suppression of aversive emotional physiological responding may serve to reinforce the process of worry (that is, to increase its probability; Borkovec et al., 2004 ; McLaughlin et al., 2007 ). Because worry suppresses physiological responding, it also insulates the person from fully experiencing or processing the topic that she or he is worrying about, and it is known that such full processing is necessary if extinction of that anxiety is to occur. Thus the threatening meaning of the topic being worried about is maintained (Borkovec et al., 2004 ; Sibrava & Borkovec, 2006 ).

THE NEGATIVE CONSEQUENCES OF WORRY

In spite of these positive functions that worry serves, some of its effects are clearly negative (Mineka, 2004 ; Mineka et al., 2002 ; Newman & Liera, 2011). For example, worry itself is certainly not an enjoyable activity and can actually lead to a greater sense of danger and anxiety (and lower positive mood) because of all the possible catastrophic outcomes that the worrier envisions (McLaughlin et al., 2007 ). In addition, people who worry about something tend subsequently to have more negative intrusive thoughts than people who do not worry. For example, Wells and Papageorgiou ( 1995 ) had people watch a gruesome film. Following the film, some were told to relax and settle down, some were told to imagine the events in the film, and some were told to worry in verbal form about the film. Over the next several days, people in the worry condition showed the most intrusive images from the film. In addition, another study showed that after engaging in worry individuals with GAD experience more intense negative emotions when reacting to a sad film (McLaughlin et al., 2007 ; see also Newman & Liera, 2011).

Finally, there is now considerable evidence that attempts to control thoughts and worry may paradoxically lead to increased experience of intrusive thoughts and enhanced perception of being unable to control them (Abramowitz et al., 2001 ; Wells, 1999 ; Wells & Butler, 1997 ). Somewhat paradoxically, these intrusive thoughts can serve as further trigger topics for more worry, and a sense of uncontrollability over worry may develop in people caught in this cycle that occurs in GAD. As we have noted, perceptions of uncontrollability are also known to be associated with increased anxiety, so a vicious circle of anxiety, worry, and intrusive thoughts may develop (Mineka, 2004 ; Mineka et al., 2002 ; Mineka & Zinbarg, 2006 ).

COGNITIVE BIASES FOR THREATENING INFORMATION

Not only do people with GAD have frequent frightening thoughts, they also process threatening information in a biased way, perhaps because they have prominent danger schemas. Many studies have shown that generally anxious people tend to preferentially allocate their attention toward threatening cues when both threat and nonthreat cues are present in the environment. Nonanxious people do not show a bias except under limited circumstances, in which they actually may show the opposite bias (see Bar-Haim et al., 2007 ; MacLeod & Mathews, 2012; Mathews & MacLeod, 2005 ). Further, this attentional vigilance for threat cues can occur at a very early stage of information processing, even before the information has entered the person’s conscious awareness. If a person is already anxious, having her or his attention automatically focused on threat cues in the environment would seem only to maintain the anxiety or even make it worse. Moreover, recent evidence also strongly supports the idea that such attentional biases play a causal role in anxiety as well (e.g., MacLeod et al., 2004 ; MacLeod & Mathews, 2012; Mathews & MacLeod, 2002 ). For example, several studies have shown that training nonanxious individuals to show an attentional bias toward threat leads to their showing a greater increase in anxiety in stressful situations (e.g., MacLeod et al., 2002 ). Conversely, several other studies have shown that training anxious individuals to attend away from threat leads to a decrease in their anxiety symptom levels (e.g., MacLeod & Mathews, 2012).

Generally anxious people are also more likely than nonanxious people to think that bad things are likely to happen in the future (A. K. MacLeod, 1999 ), and they have a much stronger tendency to interpret ambiguous information in a threatening way. For example, when clinically anxious subjects read a series of ambiguous sentences (e.g., “The doctor examined little Emma’s growth” or “They discussed the priest’s convictions”), they are more likely than nonanxious controls to remember the threatening interpretation of each sentence (Eysenck et al., 1991 ; see also MacLeod et al., 2004 ; Mathews & MacLeod, 2005 ; Ouimet et al., 2009 ). This tendency to interpret ambiguous information negatively has actually been shown to increase anxiety in several situations, including watching a stressful video (Wilson et al., 2006 ).

In summary, several psychosocial variables seem to promote the onset of generalized anxiety as well as its maintenance. Experience with unpredictable and/or uncontrollable life events may create a vulnerability to anxiety and promote current anxiety. People also believe that worry serves a number of important functions, and it may actually be reinforced because it dampens physiological arousal. But worry also has some negative consequences, including the fact that worry begets further worry and creates a sense of perceived uncontrollability over the worry process, which further enhances anxiety. Finally, anxiety is associated with an automatic attentional and interpretive bias toward threatening information.

Biological Causal Factors

GENETIC FACTORS

Although evidence for genetic factors in GAD is mixed, there does seem to be a modest heritability, although perhaps smaller than that for most other anxiety disorders except phobias (Hettema, Prescott, & Kendler, et al., 2001; Kendler et al., 1992a ). Part of the problem for research in this area has been the evolving nature of our understanding of GAD and what its diagnostic criteria should be. Several large twin studies reveal exactly how heritability estimates vary as a function of one’s definition of GAD (Hettema, Neale, & Kendler, et al., 2001; Kendler et al., 1992a ). The largest and most recent of these twin studies using the DSM-IV-TR diagnostic criteria estimate that 15 to 20 percent of the variance in liability to GAD is due to genetic factors.

The evidence is increasingly strong that GAD and major depressive disorder have a common underlying genetic predisposition (Kendler, 1996 ; Kendler et al., 1992d ; Kendler et al., 2007 ). What determines whether individuals with a genetic risk for GAD and/or major depression develop one or the other disorder seems to depend entirely on the specific environmental experiences they have (nonshared environment). At least part of this common genetic predisposition for GAD and major depression is best conceptualized as the basic personality trait commonly known as neuroticism (e.g., Clark, Watson, & Mineka, 1994 ; Hettema et al., 2004 ; Kendler et al., 2007 ).

NEUROTRANSMITTER AND NEUROHORMONAL ABNORMALITIES

A Functional Deficiency in GABA In the 1950s, the benzodiazepine category of medications was found to reduce anxiety. This discovery was followed in the 1970s by the finding that these drugs probably exert their effects by stimulating the action of GABA, a neurotransmitter now strongly implicated in generalized anxiety (Davis, 2002 ; LeDoux, 2002 ; Nutt et al., 2006 ). It appears that highly anxious people have a kind of functional deficiency in GABA, which ordinarily plays an important role in the way our brain inhibits anxiety in stressful situations. The benzodiazepine drugs appear to reduce anxiety by increasing GABA activity in certain parts of the brain implicated in anxiety, such as the limbic system, and by suppressing the stress hormone cortisol. Whether the functional deficiency in GABA in anxious people causes their anxiety or occurs as a consequence of it is not yet known, but it does appear that this functional deficiency promotes the maintenance of anxiety.

More recently, researchers have discovered that another neurotransmitter—serotonin—is also involved in modulating generalized anxiety (Goodman, 2004 ; Nutt et al., 2006 ). At present, it seems that GABA, serotonin, and perhaps norepinephrine all play a role in anxiety, but the ways in which they interact remain largely unknown (LeDoux, 2002 ).

The Corticotropin-Releasing Hormone System and Anxiety An anxiety-producing hormone called corticotropin-releasing hormone (CRH) has also been strongly implicated as playing an important role in generalized anxiety (and depression; Leonardo & Hen, 2006 ; Maier & Watkins, 2005 ). When activated by stress or perceived threat, CRH stimulates the release of ACTH (adrenocorticotropic hormone) from the pituitary gland, which in turn causes release of the stress hormone cortisol from the adrenal gland (Leonardo & Hen, 2006 ); cortisol helps the body deal with stress. The CRH hormone may play an important role in generalized anxiety through its effects on the bed nucleus of the stria terminalis (an extension of the amygdala; see Figure 6.1 ), which is now believed to be an important brain area mediating generalized anxiety (e.g., Davis, 2006 ; Lang et al., 2000 ).

NEUROBIOLOGICAL DIFFERENCES BETWEEN ANXIETY AND PANIC

As we noted at the beginning of this chapter, contemporary theorists are drawing several fundamental distinctions between fear, panic, and anxiety, including their neurobiological bases. Fear and panic involve activation of the fight-or-flight response, and the brain areas and neurotransmitters that seem most strongly implicated in these emotional responses are the amygdala (and locus coeruleus) and the neurotransmitters norepinephrine and serotonin. Generalized anxiety (or anxious apprehension) is a more diffuse emotional state involving arousal and a preparation for possible impending threat; and the brain area, neurotransmitters, and hormones that seem most strongly implicated are the limbic system (especially the bed nucleus of the stria terminalis, an extension of the amygdala), GABA, and CRH (Davis, 2006 ; Lang et al., 2000 ). Although serotonin may play a role in both anxiety and panic, it probably does so in somewhat different ways. Recently, people with GAD have been found to have a smaller left hippocampal region similar to what is seen with major depression (Hettema et al. 2012); this may represent a common risk factor for the two disorders.

Treatments

MEDICATIONS

Many clients with generalized anxiety disorder consult family physicians, seeking relief from their “nerves” or anxieties or their various functional (psychogenic) physical problems. Most often in such cases, medications from the benzodiazepine (anxiolytic) category such as Xanax or Klonopin are used—and misused—for tension relief, reduction of other somatic symptoms, and relaxation. Their effects on worry and other psychological symptoms are not as great. Moreover, they can create physiological and psychological dependence and withdrawal and are therefore difficult to taper. A newer medication called buspirone (from a different medication category) is also effective, and it neither is sedating nor leads to physiological dependence. It also has greater effects on psychic anxiety than do the benzodiazepines. However, it may take 2 to 4 weeks to show results (Roy-Byrne & Cowley, 2002 , 2007 ). Several categories of antidepressant medications like those used in the treatment of panic disorder are also useful in the treatment of GAD, and they also seem to have a greater effect on the psychological symptoms of GAD than do the benzodiazepines (Goodman, 2004 ; Roy-Byrne & Cowley, 2002 , 2007 ). However, they also take several weeks before their effects are apparent.

COGNITIVE-BEHAVIORAL TREATMENT

Cognitive-behavioral therapy (CBT) for generalized anxiety disorder has become increasingly effective as clinical researchers have refined the techniques used. It usually involves a combination of behavioral techniques, such as training in applied muscle relaxation, and cognitive restructuring techniques aimed at reducing distorted cognitions and information-processing biases associated with GAD as well as reducing catastrophizing about minor events (Barlow, Allen, & Basden, 2007 ; Borkovec, 2006 ; Borkovec et al., 2002 ). GAD initially appeared to be among the most difficult of the anxiety disorders to treat, and to some extent this is still true. However, advances have been made, and a quantitative review of many controlled studies showed that CBT approaches resulted in large changes on most symptoms measured (Mitte, 2005 ). The magnitude of the changes seen with cognitive-behavioral treatment was at least as large as those seen with benzodiazepines, and it led to fewer dropouts (i.e., it was better tolerated). Finally, CBT has also been found to be useful in helping people who have used benzodiazepines for over a year to successfully taper their medications (Gosselin et al., 2006 ).

CBT for John’s GAD The case of John, the graduate student with GAD discussed earlier, serves as an example of the success of cognitive-behavioral therapy with this condition. Before receiving cognitive-behavioral therapy, John had seen someone at a student counseling center for several months, but he hadn’t found the “talk therapy” very useful. He had heard that cognitive-behavioral therapy might be useful and had sought such treatment. He was in treatment for about 6 months, during which time he found training in deep muscle relaxation helpful in reducing his overall level of tension. Cognitive restructuring helped reduce his worry levels about all spheres of his life. He still had problems with procrastinating when he had deadlines, but this too was improving. He also began socializing more frequently and had tentatively begun dating when treatment ended for financial reasons. He could now see that if a woman didn’t want to go out with him again, this did not mean that he was boring but simply that they might not be a good match.

in review

Compare and contrast two or more anxiety disorders to distinguish them from normal worry

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