006 - Chapter 6 - Panic, Anxiety, And Their Disorders

Panic, Anxiety, andTheir Disorders

THE FEAR AND ANXIETY RESPONSE PATTERNS

OVERVIEW OF THE ANXIETY DISORDERS ANDTHEIR COMMONALITIES

SPECIFIC PHOBIASBlood- Injection- Injury PhobiaAge of Onset and Gender Differences in

Specific PhobiasPsychosocial Causal FactorsGenetic and Temperamental Causal FactorsTreating Specific Phobias

SOCIAL PHOBIASInteraction of Psychosocial and Biological

Causal FactorsTreating Social Phobias

PANIC DISORDER WITH AND WITHOUTAGORAPHOBIAPanic DisorderAgoraphobiaPrevalence, Gender, and Age of Onset of Panic

Disorder with and without AgoraphobiaComorbidity with Other Disorders

The Timing of a First Panic AttackBiological Causal FactorsBehavioral and Cognitive Causal FactorsTreating Panic Disorder and Agoraphobia

GENERALIZED ANXIETY DISORDERGeneral CharacteristicsPrevalence and Age of OnsetComorbidity with Other DisordersPsychosocial Causal FactorsBiological Causal FactorsTreating Generalized Anxiety Disorder

OBSESSIVE-COMPULSIVE DISORDERPrevalence, Age of Onset, and ComorbidityCharacteristics of OCDPsychosocial Causal FactorsBiological Causal FactorsTreating Obsessive-Compulsive Disorder

SOCIOCULTURAL CAUSAL FACTORS FOR ALLANXIETY DISORDERSCultural Differences in Sources of WorryTaijin Kyofusho

s we noted in Chapter 5, even stable, well-adjusted people may break down ifforced to face extensive combat stress, torture, or devastating natural disaster. Butfor some people, simply performing everyday activities can be stressful. Faced withthe normal demands of life-socializing with friends, waiting in line for a bus, beingon an airplane, touching a doorknob-they become seriously fearful or anxious. Inthe most severe cases, people with anxiety problems may be unable even to leavetheir homes for fear of having a panic attack, or may spend much of their time inmaladaptive behavior such as constant hand washing.

Anxiety-a general feeling of apprehension about possible danger-was, inFreud's formulation, a sign of an inner battle or conflict between some primitivedesire (from the id) and prohibitions against its expression (from the ego and super-ego). Today the DSM has identified a group of disorders that share obvious symp-toms and features of fear and anxiety. These anxiety disorders, as they are known,affect approximately 25 to 29 percent of the U.s. population at some point in theirlives (over 23 million Americans) and are the most common category of disorders forwomen and the second most common for men (Kessler et aI., 1994; Kessler, Berglund,et aI., 2005b). In any 12-month period, about 23 percent of women and 12 percent ofmen suffer from at least one anxiety disorder (Kessler et aI., 1994). Anxiety disorderscreate enormous personal, economic, and health care problems for those affected.For example, in 1990 anxiety disorders cost the United States $42.3 billion in directand indirect costs, with 90 percent of these being direct costs (about 30 percent ofthe nation's total mental health bill of $148 billion in 1990; Greenberg et aI., 1999).

Consider the following case of an anxious electrician:

A 27-year-old married electrician complains of dizziness,sweating palms, heart palpitations, and ringingof the earsof more than 18 months' duration. Hehas also experienceddry mouth and throat, periods of extreme muscle tension,and a constant "edgy" and watchful feeling that has ofteninterfered with his ability to concentrate. These feelingshave been present most of the time during the previous 2years ... Because of these symptoms the patient has seena family practitioner, a neurologist, a neurosurgeon, a chi-ropractor, and an ear-nose-throat specialist. ... Healso hasmany worries. He constantly worries about the health ofhis parents ... Healso worries about whether he is a "goodfather," whether his wife will ever leave him (there is noindication that she is dissatisfied with the marriage), andwhether he is liked by co-workers on the job. Although herecognizes that his worries are often unfounded, he can'tstop worrying. Forthe past 2 years the patient has had fewsocial contacts because of his nervous symptoms ... hesometimes has to leave work when the symptoms becomeintolerable. (Adapted fromSpitzer et aI., 2002.)

Source: Adapted with permission from the DSM-/V- TR Casebook(Copyright 2000.) American Psychiatric Publishing, Inc.)

The physicians this man consulted could not determinethe cause of his physical symptoms, and one of themfinally referred him for treatment at a mental health clinic,where he was diagnosed as having generalized anxiety dis-order-one of seven primary anxiety disorders.

Historically, cases like this and other cases of anxietydisorders were considered to be classic examples ofneurotic behavior. Although neurotic behavior is mal-adaptive and self-defeating, a neurotic person is not out oftouch with reality, incoherent, or dangerous. To Freud,neuroses were psychological disorders that resulted whenintrapsychic conflict produced significant anxiety. Some-times this anxiety was overtly expressed (as in those dis-orders known today as the anxiety disorders). In certainother neurotic disorders, however, he believed that theanxiety might not be obvious, either to the person involvedor to others, if psychological defense mechanisms wereable to deflect or mask it. In 1980 the DSM -III dropped theterm neurosis and reclassified most of these disorders thatdid not involve obvious anxiety symptoms as either disso-ciative or somatoform disorders (see Chapter 8). DSM-IIImade this change in order to group together smaller sets ofdisorders that share more obvious symptoms and features.

We begin by discussing the nature of fear and anxietyas emotional states, both of which have an extremelyimportant adaptive value but to which humans at timesseem all too vulnerable. We will then move to a discussionof the anxiety disorders.

THE FEAR AND ANXIETY__ RESPONSE PATTERNS

It is difficult to define fear and anxiety, and there hasnever been complete agreement about how distinct thetwo emotions are from each other. Historically, the mostcommon way of distinguishing between fear and anxietyhas been whether there is a clear and obvious source ofdanger that would be regarded as real by most people.When the source of danger is obvious, the experiencedemotion has been called fear (e.g., ''I'm afraid of snakes").With anxiety, however, we frequently cannot specifyclearly what the danger is (e.g., ''I'm anxious about myparents' health"). Intuitively, anxiety seems to be experi-enced as an unpleasant inner state in which we are antic-ipating something dreadful happening that is not entirelypredictable from our actual circumstances (e.g., Barlow,2002a).

FEAR In recent years, many prominent researchers haveproposed a more fundamental distinction between fear andanxiety (e.g., Barlow, 1988, 2002a; Gray & McNaughton,1996). According to these theorists, fear or panic is a basicemotion (shared by many animals) that involves activationof the "fight-or-flight" response of the sympathetic ner-vous system. This is an almost instantaneous reaction toany imminent threat such as a dangerous predator orsomeone pointing a loaded gun. Its adaptive value is that itallows us to escape from imminent danger. When thefear/panic response occurs in the absence of any obviousexternal danger, we say the person has had a spontaneousor uncued panic attack. The symptoms of a panic attackare nearly identical to those experienced during a state offear except that panic attacks are often accompanied by asubjective sense of impending doom, including fears ofdying, going crazy, or losing control. These latter cognitivesymptoms do not generally occur during fear states. Thusfear and panic have three components:

1. cognitive/subjective components ("I feelafraid/terrified"; ''I'm going to die");

2. physiological components (such as increased heartrate and heavy breathing);

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

These components are only "loosely coupled" (Lang,1985), which means that someone might show, for exam-ple, physiological and behavioral indications of fear with-out much of the subjective component, or vice versa. As aprimitive alarm response to danger, the fear response mustbe activated with great speed to serve its adaptive purpose:enabling us to escape or avoid danger. Indeed, we oftenseem to go from a normal state to a state of intense fearalmost instantaneously.

Fear or panic is a basic emotion that is shared by many animals,including humans, and may activate the "fight-or-flight" responseof the sympathetic nervous system. This allows us to respondrapidly when faced with a dangeraus situation, such as beingthreatened by a predator. In humans who are having a panicattack, there is no external threat; panic occurs because of somemisfiring of this response system.

ANXIETY In contrast to fear and panic, anxiety is acomplex blend of unpleasant emotions and cognitionsthat is both more oriented to the future and much morediffuse than fear (Barlow, 1988, 2002a). But like fear, ithas not only cognitive/subjective components but alsophysiological and behavioral components. At thecognitive/subjective level, anxiety involves negativemood, worry about possible future threat or danger, self-preoccupation, and a sense of being unable to predict thefuture threat or to control it if it occurs. At a physiologicallevel, anxiety often creates a state of tension and chronicoverarousal, which may reflect readiness for dealing withdanger should it occur ("Something awful may happenand I had better be ready for it if it does"). Although thereis no activation of the fight-or-flight response as in fear,anxiety does prepare or prime a person for the fight-or-flight response should the anticipated danger occur. At abehavioral level, anxiety may create a strong tendency toavoid situations where danger might be encountered, butthere is not the immediate urge to flee with anxiety asthere is with fear (Barlow, 1988, 2002a). Support for theidea that anxiety is descriptively and functionally distinct

from panic comes both from complex statistical analysesof subjective reports of panic and anxiety, and from agreat deal of neurobiological evidence (e.g., Bouton,Mineka, & Barlow, 2001; Gorman et aI., 2000).

The adaptive value of anxiety may be that it helps usplan and prepare for possible threat. In mild to moderatedegrees, anxiety actually enhances learning and perfor-mance. For example, a mild amount of anxiety about howyou are going to do on your next exam, or in your next ten-nis match, can actually be helpful. But although anxiety isoften adaptive in mild or moderate degrees, it is maladap-tive when it becomes chronic and severe, as we see in peo-ple diagnosed with anxiety disorders.

Although there are many threatening situations thatprovoke fear or anxiety unconditionally, many of oursources of fear and anxiety are learned. Years of humanand nonhuman animal experimentation have estab-lished that the basic fear and anxiety response patternsare highly conditionable. That is, previously neutral andnovel stimuli that are repeatedly paired with, and reliablypredict, frightening or unpleasant events such as variouskinds of physical or psychological trauma can acquire thecapacity to elicit fear or anxiety themselves. Such condi-tioning is a completely normal and adaptive process thatallows all of us to learn to anticipate upcoming frighten-ing events if they are reliably preceded by a signal. Yet thisnormal and adaptive process can also lead in some casesto the development of clinically significant fears and anx-ieties, as we will see.

For example, a girl named Angela sometimes sawand heard her father physically abuse her mother in theevening. After this happened four or five times, Angelastarted to became anxious as soon as she heard herfather's car arrive in the driveway at the end of the day. Insuch situations a wide variety of initially neutral stimulimay accidentally come to serve as cues that somethingthreatening and unpleasant is about to happen-andthereby come to elicit fear or anxiety themselves. Ourthoughts and images can also serve as conditioned stim-uli capable of eliciting the fear or anxiety response pat-tern. For example, Angela came to feel anxious even whenthinking about her father.

In ReVIew~ Compare and contrast fear or panic with

anxiety, making sure to note that bothemotions involve three response systems.

~ Explain the significance of the fact that bothfear and anxiety can be classicallyconditioned.

OVERVIEW OF THEANXIETY DISORDERSAND THEIRCOMMONALITIES _

Anxiety disorders all have unrealistic, irrational fears oranxieties of disabling intensity as their principal and mostobvious manifestation. DSM -IV-TR recognizes seven pri-mary types of anxiety disorders:

phobic disorders of the "specific" or of the"social" type;

panic disorder with or without agoraphobia;generalized anxiety disorder;

obsessive-compulsive disorder;

post-traumatic stress disorder (discussed in Chapter 5).

People with these varied disorders differ from oneanother both in terms of the relative preponderance offear/panic versus anxiety symptoms that they experience,and in the kinds of objects or situations that they are mostconcerned about. For example, people with specific orsocial phobias exhibit many anxiety symptoms about thepossibility of encountering their phobic situation, but theymay also experience a fear/panic response when they actu-ally encounter the situation. People with panic disorderexperience both frequent panic attacks and intense anxietyfocused on the possibility of having another one. By con-trast, people with generalized anxiety disorder mostlyexperience a general sense of diffuse anxiety and worryabout many potentially bad things that may happen; somemay also experience an occasional panic attack, but it is nota focus of their anxiety. Finally, people with obsessive-compulsive disorder experience intense anxiety or distressin response to intrusive thoughts or images and feel com-pelled to engage in compulsive, ritualistic activities thattemporarily help to reduce the anxiety. It is also importantto note that many people with one anxiety disorder willexperience at least one more anxiety disorder and/ordepression either concurrently or at a different point intheir lives (e.g., Brown & Barlow, 2002; Kessler, Berglund,et aI., 2005c; see also Developments in Thinking 7.2).

Given these commonalities across the anxiety disor-ders, it should come as no surprise that there are someimportant similarities in the basic causes of these disor-ders (as well as many differences). Among biologicalcauses, we will see that there are modest genetic contribu-tions to each of these disorders, and that at least part ofthe genetic vulnerability may be nonspecific, or commonacross the disorders (e.g., Barlow, 2002a). The commongenetic vulnerability is manifested at a psychological levelby the personality trait called neuroticism-a proneness toexperience negative mood states. The brain structures

most centrally involved are generally in the limbic system(often known as the emotional brain), and the neurotrans-mitter substances that are most centrally involved areGABA, norepinephrine, and serotonin (see Chapter 3).

Among common psychological causes, we will see thatclassical conditioning of fear/panic and/or anxiety to arange of stimuli plays a prominent role in most of thesedisorders (Mineka & Zinbarg, 1996, 2006). In addition,people who have perceptions of a lack of control over theirenvironments and/or their own emotions seem more vul-nerable to developing anxiety disorders. The developmentof such perceptions of un controllability depends heavilyon the social environment people are raised in (Chorpita &Barlow, 1998; Mineka & Zinbarg, 1996). Finally, the socio-cultural environment that people are raised in also hasprominent effects on the kinds of things people becomeafraid of, or anxious about. Moreover, parenting styles cansignificantly influence the likelihood that children willdevelop phobic fears and other anxiety disorders (e.g.,Craske & Waters, 2005; Rapee, 2002). Ultimately what wemust strive for is a good biopsychosocial understanding ofhow all these different kinds of causes interact with oneanother in the development of these disorders. Now wewill turn to a more detailed discussion of each disorder tohighlight both their common and distinct features, as wellas what is known about their causes.

Finally, there are many commonalities across the effec-tive treatments for these different anxiety disorders, as wewill see (e.g., Barlow, 2002a, 2004). For each disorder, grad-uated exposure to feared cues, objects, and situations-until fear/anxiety begins to habituate-constitutes thesingle most powerful therapeutic ingredient. Further, forcertain disorders the addition of cognitive-restructuringtechniques can provide added benefit, although for otherdisorders the addition of these techniques does not seem tobe especially beneficial. What these cognitive-restructuringtechniques for different disorders have in common is thatthey help the individual understand his or her distortedpatterns of thinking about anxiety-related situations andhow these patterns can be changed. Medications can alsobe useful for all disorders except specific phobias, andnearly all tend to fall into two primary medication cate-gories: benzodiazepines (known as anti-anxiety drugs)and antidepressants. The advantages of behavioral and cog-nitive-behavioral treatments over medications are that theyproduce much lower relapse rates than medications oncethey are discontinued, and they do not have unpleasant sideeffects that medications often have.

We start with the phobic disorders, which are are themost common anxiety disorders. A phobia is a persistentand disproportionate fear of some specific object or situ-ation that presents little or no actual danger and yet leadsto a great deal of avoidance of these feared situations. Aswe will see in DSM-IV-TR, there are three main cate-gories of phobias: (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 incommon?

~ What differentiates the anxiety disordersfrom one another?

~ What are some common kinds of biologicaland psychosocial causes of the differentanxiety disorders?

~ What is the most important commonalityacross effective psychosocial treatments forthe anxiety disorders?

SPECIFIC PHOBIASA person is diagnosed as having a specific phobia if sheor he shows strong and per-sistent fear that is excessiveor unreasonable and is trig-gered by the presence of aspecific object or situation(see DSM table on page 184).When individuals with spe-cific phobias encounter aphobic stimulus, they oftenshow an immediate fearresponse that often resem-bles a panic attack exceptfor the existence of a clearexternal trigger (APA,DSM-IV-TR, 2000). Notsurprisingly, such individu-als go to great lengths toavoid encounters with theirphobic stimulus and some-times even avoid seeminglyinnocent representations ofit such as photographs ortelevision images. For exam-ple, claustrophobic personsmay go to great lengths toavoid entering a closet or anelevator, even if this meansclimbing many flights ofstairs or turning down jobsthat might require them totake an elevator. This avoid-ance is a cardinal character-istic of phobias; it occursboth because the phobic

People with claustrophobia may findelevators so frightening that they goto great lengths to avoid them. Ifforsome reason they have to take anelevator, they will be very frightenedand may have thoughts about theelevator falling, the doors neveropening, or there not being enoughair to breathe.

response itself is so unpleasant and because of the phobicperson's irrational appraisal of the likelihood that somethingterrible will happen. Table 6.1 lists the five subtypes of spe-cific phobias in DSM -IV- TR, along with some examples.

The following case is typical of specific phobia:

Mary, a married mother of three, was 47 at the time shefirst sought treatment for both claustrophobia and acro-phobia. She reported having been intensely afraid ofenclosed spaces and of heights since her teens. Sheremembered having been locked in closets by her oldersiblings when she was a child; the siblings also confinedher under blankets to scare her and added to her fright byshowing her pictures of spiders after releasing her fromunder the blankets. She traced the onset of her claustro-phobia to those traumatic incidents, but she had no ideawhy she was afraid of heights. While her children hadbeen growing up, she had been a housewife and hadmanaged to live a fairly normal life in spite of her two spe·cific phobias. However, her children were now grown, andshe wanted to find a job outside her home. This was prov-ing to be very difficult, however, because she could nottake elevators and was not comfortable being on any-thing other than the first floor of an office building. More-over, her husband had for some years been working foran airline, which entitled him to free airline tickets. Thefact that Mary could not fly (due to her phobias) hadbecome a sore point in her marriage because they bothwanted to be able to take advantage of these free ticketsto see distant places. Thus, although she had had thesephobias for many years, they had become truly disablingonly in recent years as her life circumstances hadchanged and she could no longer easily avoid heights orenclosed spaces.

DSM-IV-TR

A. Marked or persistent fear that is excessive orunreasonable, cued by the presence or anticipation of aspecific object or situation.

B. Exposure to phobic stimulus almost invariably provokesan immediate anxiety response or panic attack.

C. Person recognizes that the fear is excessive orunreasonable.

D. Phobic situation avoided or endured with intense anxietyor distress.

E. Symptoms interfere significantly with normal functioning,or there is marked distress about the phobia.

F. Duration of at least 6 months.

Source: Adapted with permission from the Diagnostic andStatistical Manual of Mental Disorders, Fourth Edition,TextRevision(Copyright 2000). American Psychiatric Association.

Although people who suffer from phobias usuallyknow that their fears are somewhat irrational, they saythat they cannot help themselves. If they attempt toapproach the phobic situation, they are overcome withfear or anxiety, which may vary from mild feelings ofapprehension and distress (usually while still at some dis-tance) to full-fledged activation of the fight-or-flightresponse. Regardless of how it begins, phobic behaviortends to be reinforced because every time the person witha phobia avoids a feared situation, his or her anxietydecreases. In addition, the benefits derived from being dis-abled, such as increased attention, sympathy, and somecontrol over the behavior of others, may also sometimesreinforce a phobia.

Phobia TypeAnimalNatural EnvironmentBlood- Injection- InjurySituationalOther

ExamplesSnakes, spiders, dogs, insects, birdsStorms, heights, waterSeeing blood or an injury, receiving an injection, seeing a person in a wheelchairPublic transportation, tunnels, bridges, elevators, flying, driving, enclosed spacesChoking, vomiting, "space phobia" (fear of falling down if away from walls or othersupport)

Source: Reprinted with permission from the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision (Copyright2000). American Psychiatric Association.

This boy suffers from height phobia and can only barely peer overthe end of the diving board after watching his friends all divesuccessfully.

Blood-Injection-Injury PhobiaOne category of specific phobias that probably occurs inabout 3 to 4 percent of the population has a number ofinteresting and unique characteristics (Ost & Hellstrom,1997; Page, 1994). In blood-injection-injury phobia,afflicted people typically experience at least as much (if notmore) disgust as fear (Woody & Teachman, 2000). Theyalso show a unique physiological response when con-fronted with the sight of blood or injury. Rather thanshowing the simple increase in heart rate and blood pres-sure seen when most people with phobias encounter theirphobic object, these people show an initial acceleration,followed by a dramatic drop in both heart rate and bloodpressure. This is very frequently accompanied by nausea,

In blood-injection-injury phabia, the afflicted person experiencesdisgust and fear at the sight af someane receiving an injection.When confronted with the sight of blood or injury, people with thisphobic disorder aften experience nausea, dizziness, and fainting.

dizziness, and/or fainting, which do not occur with otherspecific phobias (Ost & Hellstrom, 1997).

Interestingly, people with this phobia show thisunique physiological response pattern only in the presenceof blood and injury stimuli; they exhibit the more typicalphysiological response pattern characteristic of the fight-or-flight response to other feared objects (see Dahlloef &Ost, 1998; Ost & Hugdahl, 1985). From an evolutionaryand functional standpoint, this unique physiologicalresponse pattern may have evolved for a specific purpose:By fainting, the person being attacked might inhibit fur-ther attack, and if an attack did occur, the drop in bloodpressure would minimize blood loss (Craske, 1999; Marks& Nesse, 1991).

Age of Onset and Gender Differencesin Specific PhobiasSpecific phobias are quite common, especially in women.Results of the National Comorbidity Survey-Replicationrevealed a lifetime prevalence rate of about 12 percent(Kessler, Chiu, et al., 2005c). Among people with one spe-cific phobia, over 75 percent have at least one other specificfear that is excessive (Curtis, Magee, et al., 1998). The rela-tive gender ratios vary considerably according to the typeof specific phobia, but phobias are always considerablymore common in women than in men. For example, about90 to 95 percent of people with animal phobias are women,but the gender ratio is less than 2:1 for blood-injury pho-bia. The average age of onset for different types of specificphobias also varies widely. Animal phobias usually begin inchildhood, as do blood-injury phobias and dental phobias.However, other phobias such as claustrophobia and dri-ving phobia tend to begin in adolescence or early adult-hood (Barlow, 2002a; Ost, 1987).

Psychosocial Causal FactorsA variety of psychosocial causal factors has been implicatedin the origins of specific phobias, ranging from deep-seatedpsychodynamic conflicts to relatively straightforward trau-matic conditioning of fear. According to the psychodynamicview, phobias represent a defense against anxiety that stemsfrom repressed impulses from the id. Because it is too dan-gerous to "know" the repressed id impulse, the anxiety is dis-placed onto some external object or situation that has somesymbolic relationship to the real object of the anxiety. Forexample, in his classic case of Little Hans, Freud (1909) pos-tulated that 5-year-old Hans had developed a phobia forhorses as a result of anxiety stemming from a repressedOedipal conflict in which Hans unconsciously desired hismother and wanted to kill his father so that he could have hismother all to himself. This led him unconsciously to fearthat his father would want to "kill" or castrate him. Theintense internal conflict created by all these unconscious

feelings was not acceptable to Hans's conscious mind, so theanxiety was displaced onto horses, which supposedly boresome symbolic relationship to his father.

This prototypical psychodynamic account of howphobias are acquired has long been criticized as being fartoo speculative, and an alternative, simpler account of theorigins of Hans's phobia for horses derives from learningtheory (e.g., Wolpe & Rachman, 1960). When Hans was4 years old, he had witnessed a horse being badly hurt in anaccident; Hans had become very upset witnessing this inci-dent (an example of traumatic classical conditioning) andlater began to avoid leaving the house so as not toencounter horses in the street.

PHOBIAS AS LEARNED BEHAVIOR Building on theseobservations of Wolpe and Rachman (1960), numeroustheorists in the 1960s proposed that the principles of classi-cal conditioning appeared to account for the acquisition ofirrational fears and phobias. The fear response can readilybe conditioned to previously neutral stimuli when thesestimuli are paired with traumatic or painful events. Wewould also expect that, once acquired, phobic fears wouldgeneralize to other, similar objects or situations. Recall, forexample, that Mary's claustrophobia had probably beencaused by multiple incidents as a child when her siblingslocked her in closets and confined her under blankets toscare her. But as an adult Mary feared elevators and caves aswell as other enclosed places. The powerful role of classicalconditioning in the development of phobias was sup-ported in a survey by Ost and Hugdahl (1981), whoadministered questionnaires to 106 adult phobic clientsthat concerned, among other things, the purported originsof their fears (see Mineka & Sutton, in press, for a review).Fifty-eight percent cited traumatic conditioning experi-ences as the sources of their phobias. Some of these trau-matic conditioning events were simply uncued panicattacks, which are now known to effectively condition fear(e.g., Forsyth & Eiffert, 1998). Direct traumatic condition-ing may be especially common in the onset of dental pho-bia (Kent, 1997), claustrophobia (Rachman, 1997), andaccident phobia (Kuch, 1997).

Vicarious Conditioning of Phobic Fears Direct trau-matic conditioning is not the only way people can learnirrational, phobic fears. Simply watching a phobic personbehaving fearfully with his or her phobic object can be dis-tressing to the observer and can result in fear being trans-mitted from one person to another through vicarious orobservational classical conditioning. For example, oneman, as a boy, had witnessed his grandfather vomit whiledying. Shortly after this traumatic event, the boy haddeveloped a strong and persistent vomiting phobia. Indeed,when this man was in middle age he even contemplatedsuicide one time when he was nauseated and feared vomit-ing (Mineka & Zinbarg, 2006).

Monkeys who watch a model monkey (such as the one illustratedhere) behaving fearfully with a live boa constrictor will rapidlyacquire an intense fear of snakes themselves. Fears can thus belearned vicariously, without any direct traumatic experience.

Animal research using rhesus monkeys has increasedour confidence that vicarious conditioning of intensefears can indeed occur. In these experiments, Mineka andCook and their colleagues (e.g., Mineka, Davidson,Cook, & Keir, 1984; Mineka & Cook, 1993; Cook &Mineka, 1991) showed that laboratory-reared monkeyswho were not initially afraid of snakes rapidly developeda phobic-like fear of snakes simply through observing awild-reared monkey behaving fearfully with snakes. Sig-nificant fear was acquired after only 4 to 8 minutes ofexposure to the wild-reared monkey with snakes, andthere were no signs that the fear had diminished 3months later. The monkeys could also learn the fear sim-ply through watching a videotape of the wild-rearedmodel monkey behaving fearfully with snakes. This sug-gests that the mass media also playa role in the vicariousconditioning of fears and phobias in people (Cook &Mineka, 1990; Mineka & Sutton, in press).

Sources of Individual Differences in the Learning ofPhobias Does the direct and vicarious conditioningmodel really explain the origins of most phobias? Givenall the traumas that people undergo, why don't morepeople develop phobias (Mineka & Sutton, in press;Mineka & Zinbarg, 1996, 2006, Rachman, 1990)? Theanswer seems to be that differences in life experiencesamong individuals strongly affect whether or not condi-tioned fears or phobias actually develop. For example,years of positive experiences with friendly dogs beforebeing bitten by one will probably keep the bite victim

from developing a dog phobia. Thus, to understand indi-vidual differences in the development and maintenanceof phobias, we need to understand the role of the differ-ent life experiences of people who undergo the sametrauma. Some of these life experiences may make certainpeople more vulnerable to phobias than others, andother experiences may serve as protective factors for thedevelopment of phobias (Mineka & Sutton, in press).

Children who have had more previous nontraumaticexperiences with a dentist are less likely to develop dentalanxiety after a bad and painful experience than are chil-dren with fewer previous non traumatic experiences(de Jongh et al., 1995; Kent, 1997). This shows the impor-tance of the individual's prior familiarity with an objector situation in determining whether a phobia developsfollowing a fear-conditioning experience. Moreover,Mineka and Cook (1986) showed that monkeys who firstsimply watched non fearful monkeys behaving nonfear-fully with snakes were immunized against acquiring a

A person who has had good experiences with a potentially phobicstimulus, such as the young woman romping here with her dog, islikely to be immunized from later acquiring a fear of dogs even ifshe has a traumatic encounter with one.

fear of snakes when they later saw fearful monkeys behav-ing fearfully with snakes. By analogy, if a child has exten-sive exposure to a nonfearful parent behavingnonfearfully with the phobic object (e.g., spiders) or situ-ation (e.g., heights) of the other parent, this may immu-nize the child against the effects of later seeing the phobicparent behaving fearfully with the phobic object (Mineka& Sutton, in press).

Events that occur during a conditioning experience,as well as before it, are also important in determining thelevel of fear that is conditioned. For example, experienc-ing an inescapable and uncontrollable event, such as beingattacked by a dog that one cannot escape from after beingbitten, is expected to condition fear much more power-fully than experiencing the same intensity of trauma thatis escapable or to some extent controllable (e.g., by run-ning away after the attack; Mineka, 1985a; Mineka & Zin-barg, 1996, 2006). In addition, the experiences that aperson has after a conditioning experience may affect thestrength and maintenance of the conditioned fear(Rescorla, 1974; White & Davey, 1989). For example, theinflation effect suggests that a person who acquired, forexample, a mild fear of driving following a minor crashmight be expected to develop a full-blown phobia if he orshe later were physically assaulted, even though no auto-mobile was present during the assault (Dadds, Davey, &Field, 2001; Mineka, 1985a; Mineka & Zinbarg, 1996,2006). Even verbal information that later alters one'sinterpretation of the dangerousness of a previous traumacan inflate the level of fear (e.g., being told, "You're luckyto be alive because the man who crashed into your car lastweek had lost his license due to a record of drunk drivingleading to fatal car crashes"; Dadds et al., 2001). Theseexamples show that the factors involved in the origins andmaintenance of fears and phobias are more complex thansuggested by the traditional, simplistic conditioning view,although they are nevertheless consistent with contempo-rary views of conditioning.

Recently it has been shown that our cognitions, orthoughts, can help maintain our phobias once they havebeen acquired. For example, people with phobias are con-stantly on the alert for their phobic objects or situationsand for other stimuli relevant to their phobia. Nonphobicpersons tend to direct their attention away from threaten-ing stimuli (see Mineka, Rafaeli, &Yovel, 2003). In addi-tion, phobics also markedly overestimate the probabilitythat feared objects have been, or will be, followed byfrightening events. This cognitive bias may help maintainor strengthen phobic fears with the passage of time(Ohman & Mineka, 2001; Tomarken, Mineka, & Cook,1989).

Evolutionary Preparedness for the Development ofFears and Phobias Consider the observation that peo-ple 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 beassociated with trauma. This is because our evolutionaryhistory has affected which stimuli we are most likely tocome to fear. Primates and humans seem to be evolution-arily prepared to rapidly associate certain objects-such assnakes, spiders, water, and enclosed spaces-with frighten-ing or unpleasant events (e.g., Mineka & Ohman, 2002;Ohman, 1996; Seligman, 1971). This preparedness occursbecause, over the course of evolution, those primates andhumans who rapidly acquired fears of certain objects orsituations that posed real threats to our early ancestorsmay have enjoyed a selective advantage. Thus "prepared"fears are not inborn or innate but, rather, are easilyacquired or especially resistant to extinction. Guns andmotorcycles, by contrast, were not present in our early evo-lutionary history and so did not convey any such selectiveadvantage.

There is now a large amount of experimental evidencesupporting the preparedness theory of phobias. In oneimportant series of experiments using human subjects,Ohman and his colleagues (see Ohman, 1996; Ohman &Mineka, 2001, for reviews) found that fear is conditionedmore effectively to fear-relevant stimuli (slides of snakesand spiders) than to fear-irrelevant stimuli (slides of flow-ers and mushrooms). These researchers also found thatonce the individuals acquired the conditioned responses tofear-relevant stimuli, these responses (including activationof the relevant brain area, the amygdala) could be elicitedeven when the fear-relevant stimuli (but not the fear-irrel-evant stimuli) were presented subliminally (that is, presen-tation was so brief that the stimuli were not consciouslyperceived; e.g., Carlsson et al., 2004). This subliminal acti-vation of responses to phobic stimuli may help to accountfor certain aspects of the irrationality of phobias. That is,people with phobias may not be able to control their fearbecause the fear may arise from cognitive structures thatare not under conscious control (Ohman & Mineka, 2001;Ohman & Soares, 1993).

Another series of experiments showed that lab-rearedmonkeys in a vicarious conditioning paradigm can easilyacquire fears of fear-relevant stimuli such as toy snakes andtoy crocodiles, but not of fear-irrelevant stimuli such asflowers and a toy rabbit (Cook & Mineka, 1989, 1990).Thus both monkeys and humans seem selectively to asso-ciate certain fear-relevant stimuli with threat or danger.Moreover, these lab-reared monkeys had had no priorexposure to any of the stimuli (e.g., snakes or flowers)before participating in these experiments. Thus the mon-key results support the evolutionarily based preparednesshypothesis even more strongly than the human experi-ments. For example, human subjects (unlike the lab-rearedmonkeys) might show superior conditioning to snakes orspiders because of preexisting negative associations tosnakes or spiders, rather than because of evolutionary fac-tors (Mineka & Ohman, 2002).

Genetic and TemperamentalCausal FactorsGenetic and temperamental variables affect the speed andstrength of conditioning of fear (e.g., Gray, 1987; Zinbarg& Mohlman, 1998). That is, depending on their tempera-ment or personality, people are more or less likely toacquire phobias. Indeed, Kagan and his colleagues (2001)have found that behaviorally inhibited toddlers (who areexcessively timid, shy, easily distressed, ete.) at 21 monthsof age were at higher risk of developing multiple specificphobias at 7 to 8 years of age than were uninhibited chil-dren (32 versus 5 percent). The average number ofreported fears in the inhibited group was three to four perchild (Biederman et al., 1990).

Several studies also suggest a modest genetic contri-bution to the development of specific phobias. For exam-ple, a large female twin study found that monozygotic(identical) twins were more likely to share animal pho-bias, blood-injury phobias, and situational phobias (suchas of heights or water) than were dizygotic (nonidentical)twins (Kendler, Karkowski, & Prescott, 1999b; Kendleret al., 1992b). However, the same study also found evi-dence that nonshared environmental factors (i.e., individ-ual specific experiences not shared by twins) also played avery substantial role in the origins of specific phobias, aresult that supports the idea that phobias are learnedbehaviors.

Treating Specific PhobiasExposure therapy-the best treatment for specific pho-bias-involves controlled exposure to the stimuli or situa-tions that elicit phobic fear (Antony & Barlow, 2002;Craske & Mystkowski, in press). Clients are graduallyplaced-symbolically or increasingly under "real-life"conditions-in those situations they find most frighten-ing. In treatment, clients are encouraged to expose them-selves (either alone, or with the aid of a therapist orfriend) to their feared situations for long enough periodsof time that their fear begins to subside. One variant onthis procedure, known as participant modeling, is oftenmore effective than exposure alone. Here the therapistcalmly models ways of interacting with the phobic stimu-lus or situation (Bandura, 1977a, 1997b). These tech-niques enable clients to learn that these situations are notas frightening as they had thought and that their anxiety,while unpleasant, is not harmful and will gradually dissi-pate (Craske & Mystkowski, in press; Craske & Rowe,1997). For certain phobias such as small-animal phobias,flying phobia, claustrophobia, and blood-injury phobia,exposure therapy is often highly effective when adminis-tered in a single long session (up to 3 hours; Ost, 1997;Ost, AIm, Brandberg, & Breitholtz, 2001). This can be anadvantage, because some people are more likely to seektreatment if they have to go only once.

One variation on exposure therapy is called participant modeling. Here the therapist models how to touch and pick up a live tarantula andencourages the spider-phobic client to imitate her behavior. This treatment is graduated, with the client's first task being simply to touch thetarantula 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 letthe tarantula crawl over his hand. This is a highly effective treatment, with the most spider-phobic clients being able to reach the top of thehierarchy within 60--90 minutes.

An example of the use of exposure therapy comesfrom the treatment of Mary, the housewife whose acro-phobia and claustrophobia we described earlier.

Treatment consisted of 13 sessions of graduated expo-sure exercises in which the therapist accompanied Maryfirst into mildly fear-provoking situations and then gradu-ally into more and more fear-provoking situations. Maryalso engaged in homework, doing these exposure exer-cises by herself. The prolonged in vivo ("real-life") expo-sure sessions lasted as long as necessary for her anxietyto subside. Initial sessions focused on Mary's claustro-phobia and on getting her to be able to ride for a fewfloors in an elevator, first with the therapist and thenalone. Later she took longer elevator rides in taller build-ings. Exposure for the acrophobia consisted of walkingaround the periphery of the inner atrium on the top floorof a tall hotel and, later, spending time at a mountain

vista overlook spot. The top of the claustrophobia hierar-chy consisted of taking a tour of an underground cave.After 13 sessions, Mary successfully took a flight with herhusband to Europe and climbed to the top of many talltourist attractions there.

Recently, some therapists have begun to use virtualreality environments to simulate certain kinds of phobicsituations, such as heights and airplanes, as places to con-duct exposure treatment. If such techniques were highlyeffective and widely available, there would be no need toconduct treatment in real situations (such as real air-planes). A few controlled studies have yielded promisingresults, but it is too soon to draw any strong conclusionsabout the relative efficacy of virtual reality versus liveexposure (Craske & Mystkowski, in press; Rothbaum,Hodges, et al., 2002).

Some researchers have also tried combining cognitivetechniques or medications with exposure-based techniquesto see if this can produce additional gains. In general,studies using cognitive techniques alone have not producedresults as good as those using exposure-based techniques,

and the addition of cognitive techniqueshas generally not added much (Antony &Barlow, 2002; Craske & Mystkowski, inpress). Similarly, medication treatments areineffective by themselves, and there is evensome evidence that anti-anxiety medica-tions may interfere with the beneficialeffects of exposure therapy (Antony & Bar-low, 2002). Very recently, however, prelimi-nary evidence has shown that a drug knownas d-cycloserine, which is known to facili-tate extinction of conditioned fear in ani-mals (e.g., Walker, Ressler, Lu, & Davis,2002), may also enhance the effectiveness ofsmall amounts of exposure therapy for fearof heights in a virtual reality environment(Ressler, Rothbaum, et al., 2004). Theseresults are very promising, but much morework is necessary before it will be knownhow useful this drug will be in enhancing the effects ofexposure therapy for many different kinds of phobias.

New treatments using virtual reality environments allow therapists to simulate certainkinds of phobic situations, such as standing at heights or sitting in airplanes, in acontrived setting. Unfortunately, the equipment is currently quite costly, which makesaccess to this treatment somewhat limited.

In ReVIew~ What are the five subtypes of specific

phobias listed in the DSM-IV-TR?~ Describe the original classical-conditioning

explanation for the origins of specificphobias, and identify the primary criticismsof th is hypothesis.

~ Explain how recent behavioral andevolutionary explanations have improvedand expanded the basic conditioninghypothesis of phobia acquisition.

~ Describe the most effective treatment forspecific phobias.

SOCIAL PHOBIASSocial phobia (or social anxiety disorder), as the DSM-IV-TR describes it, is characterized by disabling fears of one ormore specific social situations (such as public speaking, uri-nating in a public bathroom, or eating or writing in public;see the DSM-IV-TR Table). In these situations, a personfears that she or he may be exposed to the scrutiny andpotential negative evaluation of others and/or that she or hemay act in an embarrassing or humiliating manner. Becauseof their fears, people with social phobias either avoid thesesituations or endure them with great distress. Intense fear ofpublic speaking is the single most common type of socialphobia. DSM -IV-TR also identifies one subtype of social

phobia known as generalized social phobia. People with gen-eralized social phobia have significant fears of most socialsituations (rather than simply a few) and often also have adiagnosis of avoidant personality disorder (see Chapter 11;e.g., Hofmann & Barlow, 2002; Skodol et al., 1995).

The diagnosis of social phobia is very common andoccurs even in famous performers such as Barbra Streisandand Carly Simon. The National Comorbidity Survey-Replication estimated that about 12 percent of the popula-tion will qualify for a diagnosis of social phobia at somepoint in their lives (Kessler, Berglund, et al., 2005b; see alsoTillfors, 2004); this disorder is somewhat more commonamong women than men (about 60 percent are women).

A. Marked or persistent fear of one or more social orperformance situations in which the person is exposed tounfamiliar people or possible scrutiny of others.

B. Exposure to feared social situation almost invariablyprovokes anxiety or panic.

C. Person recogn izes that the fear is excessive orunreasonable.

D. Feared social or performance situation avoided or enduredwith great distress or anxiety.

E. Symptoms interfere significantly with person's normalroutine, or occupational or social functioning.

Source: Adapted with permission from the Diagnostic andStatistical Manual of Mental Disorders, Fourth Edition, Text Revision(Copyright 2000). American Psychiatric Association.

Unlike specific phobias, which most often ongmate inchildhood, social phobias typically begin somewhat later,during adolescence or early adulthood (Tillfors, 2004;Wells & Clark, 1997). More than half of people with socialphobia suffer from one or more additional anxiety disor-ders at some point in their lives, and about 50 percent alsosuffer from a depressive disorder at the same time (Kessler,Chiu, et ai., 2005c). Approximately one-third abuse alco-hol to reduce their anxiety and help them face the situa-tions they fear (for example, drinking before going to aparty; Magee et ai., 1996).

The case of Paul is typical of social phobia (except thatnot all people with social phobia have full-blown panicattacks, as Paul did, in their social phobic situations).

Paul was a single white male in his mid-thirties when hefirst presented for treatment. He was a surgeon whoreported a 13-year history of social phobia. He had veryfew social outlets because of his persistent concerns thatpeople would notice how nervous he was in social situa-tions, and he had not dated in many years. Convinced thatpeople would perceive him as foolish or crazy, he particu-larly worried that people would notice how his jaw tensedup when around other people. Paul frequently chewedgum in public situations, believing that this kept his facefrom looking distorted. Notably, he had no particular prob-lems talking with people in professional situations. Forexample, he was quite calm talking with patients beforeand after surgery. During surgery, when his face was cov-ered with a mask, he also had no trouble carrying out sur-gical tasks or interacting with the other surgeons andnurses in the room. The trouble began when he left theoperating room and had to make small talk-and eye con-tact-with the other doctors and nurses or with thepatient's family. He frequently had panic attacks in thesesocial situations. During the panic attacks he experiencedheart palpitations, fears of "going crazy," and a sense ofhis mind "shutting down." Because the panic attacksoccurred only in social situations, he was diagnosed ashaving social phobia rather than panic disorder.

Paul's social phobia and panic had begun about 13years earlier when he was under a great deal of stress.His family's business had failed, his parents haddivorced, and his mother had had a heart attack. It was inthis context of multiple stressors that a personally trau-matic incident probably triggered the onset of his socialphobia. One day he had come home from medical schoolto find his best friend in bed with his fiancee. About amonth later he had his first panic attack and startedavoiding social situations.

Interaction of Psychosocial andBiological Causal FactorsSocial phobias generally involve learned behaviors thathave been shaped by evolutionary factors. Such learning ismost likely to occur in people who are genetically or tem-peramentally at risk.

SOCIAL PHOBIAS AS LEARNED BEHAVIOR Like spe-cific phobias, social phobias often seem to originate fromsimple instances of direct or vicarious classical conditioningsuch as experiencing or witnessing aperceived social defeat or humilia-tion, or being or witnessing the tar-get of anger or criticism (Mineka &Zinbarg, 1995,2006; Tillfors, 2004).In two studies, 56 to 58 percent ofpeople with social phobia recalledand identified direct traumaticexperiences as having been involvedin the origin of their social phobias(Ost & Hugdahl, 1981; Townsleyet ai., 1995). Another study reportedthat 92 percent of an adult sample ofpeople with social phobia reported ahistory of severe teasing in child-hood, compared to only 35 percentin a group of people with obsessive-compulsive disorder (McCabe,Antony, et ai., 2003). Ost and Hug-dahl (1981) also reported thatanother 13 percent of their subjects recalled vicarious con-ditioning experiences of some sort. Another recent studyinterviewed a group of people with social phobia abouttheir images of themselves in social phobic situations andasked where those images originated (Hackmann, Clark, &McManus, 2000). Ninety-six percent of these peopleremembered some socially traumatic experience that waslinked to their own current image of themselves in sociallyphobic situations. The themes of these memories includedhaving been "criticized for having an anxiety symptom"(e.g., being red or blushing), and having felt "self-consciousand uncomfortable in public as a consequence of past crit-icism" such as "having previously been bullied and called a'nothing'" (Hackmann et ai., 2000, p. 606).

People with generalized social phobia also may beespecially likely to have grown up with parents who weresocially isolated and avoidant and who devalued sociabil-ity, thus providing ample opportunity for vicariouslearning of social fears (Morris, 2001; Rapee & Melville,1997). More generally, parents with anxiety disorders aremore likely than nonanxious parents to tell their childrenabout the potential dangers of a novel situation such as aplayground, and thereby strengthen anxious children'savoidant tendencies (Morris, 2001). However, as with spe-cific phobias, it is important to recognize that not everyone

Intense fear of publicspeaking is the single mostcornman social phobia.

who experiences direct or vicarious conditioning in socialsituations, or who grows up with socially avoidant parents,develops social phobia. This is because individual differ-ences in experiences play an important role in who devel-ops social phobia, as is the case with specific phobias.

SOCIAL FEARS AND PHOBIAS IN AN EVOLUTIONARYCONTEXT Social fears and phobias by definition involvefears of members of one's own species. By contrast, animalfears and phobias usually involve fear of potential preda-tors. Although animal fears probably evolved to trigger acti-vation of the fight-or-flight response to potential predators,Ohman and colleagues proposed that social fears and pho-bias evolved as a by-product of dominance hierarchies thatare a common social arrangement among animals such asprimates (Dimberg & Ohman, 1996; Ohman et al., 1985).Dominance hierarchies are established through aggressiveencounters between members of a social group, and adefeated individual typically displays fear and submissivebehavior but only rarely attempts to escape the situationcompletely. Thus, these investigators argued, it is not sur-prising that people with social phobia endure being in theirfeared situations rather than running away and escapingthem, as people with animal phobias often do.

If social phobias evolved as a by-product of domi-nance hierarchies, it is not surprising that humans have anevolutionarily based predisposition to acquire fears of socialstimuli that signal dominance and aggression from otherhumans. These social stimuli include facial expressions ofanger or contempt, which on average all humans seem toprocess more quickly and readily than happy or neutralfacial expressions (Ohman et al., 2001; Schupp, Ohman,Junghofer, et al., 2004). In a series of experiments that par-alleled ones for specific phobias, Ohman, Dimberg, andtheir colleagues demonstrated that subjects developstronger conditioned responses when slides of angry facesare paired with mild electric shocks than when happy orneutral faces are paired with the same shocks (Dimberg &Ohman, 1996). Indeed, even very brief subliminal (notconsciously perceived) presentations of the angry facewere sufficient to activate the conditioned responses (e.g.,Parra, Esteves, Flykt, & Ohman, 1997). Such results mayhelp explain the seemingly irrational quality of social pho-bia, in that the angry faces are processed very quickly andan emotional reaction can be activated without a person'sawareness of any threat.

GENETIC AND TEMPERAMENTAL FACTORS As withspecific phobias, not everyone who undergoes or witnessestraumatic social humiliation or defeat goes on to developfull-blown social phobia. Results from one large study offemale twins and another study of male twins suggestedthat there is a modest genetic contribution to social pho-bia; estimates were that the proportion of variance due togenetic factors was about 30 percent (Kendler, Myers,Prescott, & Neale, 2001; Kendler et al., 1992b). Neverthe-less, both studies suggest that an even larger proportion of

Infants and young children who are fearful and easily distressedby novel people or situations are sometimes high on thetemperamental variable called behavioral inhibition. Suchinfants show an increased risk of developing social phobia inadolescence.

variance in who develops social phobia is due to nonsharedenvironmental factors, which is consistent with a strongrole for learning.

The most important temperamental variable is behav-ioral inhibition. Behaviorally inhibited infants who areeasily distressed by unfamiliar stimuli and who are shy andavoidant are more likely to become fearful during child-hood and, by adolescence, show increased risk of develop-ing social phobia (Hayward et al., 1998; Kagan, 1997). Forexample, children classified as behaviorally inhibited whenthey are toddlers had higher rates of social anxiety by age13 than children who were not behaviorally inhibited astoddlers (Schwartz et al., 1999). Another longitudinalstudy found that children who reported that they had beenbehaviorally inhibited as children were four times morelikely to develop social phobia in adolescence than wereadolescents who were not behaviorally inhibited as chil-dren (Hayward et al., 1998).

PERCEPTIONS OF UNCONTROLLABILITY AND UNPRE-DICTABILITY Being exposed to uncontrollable andunpredictable stressful events (such as Paul finding hisfiancee in bed with his best friend) may play an importantrole in the development of social phobia (Barlow, 2002a;Mathew, Coplan, & Gorman, 2001; Mineka & Zinbarg,1995, 2006). Perceptions of uncontrollability and unpre-dictability often lead to submissive and unassertive behav-ior, which is characteristic of socially anxious or phobicpeople. This kind of behavior is especially likely if the per-ceptions of uncontrollability stem from an actual social

defeat, which is known in animals to lead to both increasedsubmissive behavior and increased fear (Mineka & Zinbarg,1995,2006). Consistent with this, people with social phobiahave a diminished sense of personal control over events intheir lives (Leung & Heimberg, 1996). This diminishedsense of personal control may develop, at least in part, as afunction of having been raised in families with somewhatoverprotective (and sometimes rejecting) parents (Liebet aI., 2000).

COGNITIVE VARIABLES Cognitive factors also playarole in the onset and maintenance of social phobia. Beckand Emery (1985) suggested that people with social phobiatend to expect that other people will reject or negativelyevaluate them. This leads to a sense of vulnerability whenthey are around people who might pose a threat. Clark andWells (1995; Wells & Clark, 1997) also argued that thesedanger schemas of socially anxious people lead them to

expect that they will behavein an awkward and unac-ceptable fashion, resultingin rejection and loss of sta-tus. Such expectations leadto their being preoccupiedwith bodily responses andwith negative self-images insocial situations, and tooverestimating how easilyothers will detect their anxi-ety (Hirsch, Meynen, &Clark, 2004). Such intenseself-preoccupation duringsocial situations, even to thepoint of attending to theirown heart rate, interfereswith their ability to interactskillfully (Hirsch, Clark,Mathews, & Williams, 2003;Pineles & Mineka, 2005). Avicious cycle may evolve:

Social phobics' inward attention and somewhat awkwardbehavior may lead others to react to them in a less friendlyfashion, confirming their expectations (Clark, 1997; Clark& McManus, 2002).

People with social phobiainterpret ambiguous socialevents (such as a dinnercompanion's briefdistraction) to be negative,and mildly negative socialevents (such as a dinnercompanion's apparentdisinterest) as catastrophic.

Treating Social PhobiasThere are very effective forms of behavior therapy, and ofcognitive-behavioral therapy, for social phobia. As for spe-cific phobias, behavioral treatments were developed firstand generally involve prolonged and graduated exposure tosocial situations that evoke fear. More recently, as researchhas revealed the underlying distorted cognitions that char-acterize social phobia, cognitive techniques have beenadded to the behavioral techniques, generating a form ofcognitive-behavioral therapy. The therapist attempts tohelp clients with social phobia identify their underlying

negative automatic thoughts ("I've got nothing interestingto say" or"No one is interested in me"). After helping clientsunderstand that these automatic thoughts often involvecognitive distortions, the therapist helps the clients changethese inner thoughts and beliefs through logical reanalysis.The process of logical reanalysis might involve asking one-self questions to challenge the automatic thoughts: "Do Iknow for certain that I won't have anything to say?" "Doesbeing nervous have to lead to or equal looking stupid?" Inaddition, in one highly effective version of such treatments,the client may receive videotaped feedback to help modifyher or his distorted self-images. Such techniques have nowbeen very successfully applied to the treatment of socialphobia (Clark, Ehlers, et al., 2003; Heimberg, 2002).

An example of successful combined treatment can beseen in the case of Paul, the surgeon described earlier whohad social phobia.

Since the onset of his social phobia 13 years earlier, Paulhad taken a tricyclic antidepressant at one point. Thedrug had helped stop his panic attacks, although he con-tinued to fear them intensely and still avoided social sit-uations. Thus there was little effect on his social phobia.He had also been in supportive psychotherapy, whichhelped his depression at the time but not his social pho-bia or his panic. When he went for treatment at an anxi-ety clinic, he was not on any medication or in any otherform of treatment. Treatment consisted of 14 weeks ofcognitive-behavioral therapy. By the end of treatment,Paul was not panicking at all and was quite comfortablein most social situations that he had previously avoided.He was seeing old friends whom he had avoided foryears because of his anxiety, and he was beginning todate. Indeed, he even asked his female therapist for adate during the last treatment session! Although such arequest was clearly inappropriate, it did indicate howmuch progress he had made.

Unlike specific phobias, social phobias can alsosometimes be treated with medications. The most effec-tive and widely used medications are several categoriesof antidepressants (including the monoamine oxidaseinhibitors and the selective serotonin reuptake inhibitorsdiscussed in Chapters 7 and 17; Blanco et aI., 2002; Roy-Byrne & Cowley, 2002). In some studies the effects ofthese medications have been comparable to those seenwith cognitive-behavioral treatments. However, in onerecent study a new version of cognitive-behavior ther-apy produced much more substantial improvementthan did medication (Clark, Ehlers, et aI., 2003). More-over, the medications must be taken over a long period

of time to help ensure that relapse does not occur(Blanco et aI., 2002; Hayward & Wardle, 1997). A dis-tinct advantage of behavioral and cognitive therapiesover medications, then, is that they generally producemuch more long-lasting improvement, with very lowrelapse rates; indeed, clients often continue to improveafter treatment is over.

In ReVIew~ What are the primary diagnostic criteria for

social phobia and for the subtype ofgeneralized social phobia?

~ Identify the psychosocial and biologicalcausal factors of social phobia, and explainhow they interact.

~ Describe the major treatment approachesused for social phobias.

PANIC DISORDER WITHAND WITHOUTAGORAPHOBIA

Diagnostically, panic disorder is defined and characterizedby the occurrence of "unexpected" panic attacks that oftenseem to come "out of the blue." According to the DSM -IV-TR definition (see the DSM tables), the person must haveexperienced recurrent unexpected attacks and must havebeen persistently concerned about having another attackor worried about the consequences of having an attack(e.g., of "losing control" or "going crazy") for at least amonth. For such an event to qualify as a full-blown panicattack, there must be abrupt onset of at least 4 of 13 symp-toms, most of which are physical although three are cogni-tive: (1) depersonalization (a feeling of being detachedfrom one's body) or derealization (a feeling that the exter-nal world is strange or unreal), (2) fear of dying, or (3) fearof "going crazy" or "losing control." Panic attacks are briefand intense, with symptoms developing abruptly and usu-ally reaching peak intensity within 10 minutes; the attacksusually subside in 20 to 30 minutes and rarely last morethan an hour. Periods of anxiety, by contrast, do not usu-ally have such an abrupt onset and are more long-lasting.

Panic attacks are often "unexpected" or "un cued" inthe sense that they do not appear to be provoked by identi-fiable aspects of the immediate situation. Indeed, theysometimes occur in situations in which they might be least

A discrete period of intense fear in which four or more of thefollowing symptoms develop abruptly and reach a peak within10 minutes:

1. Palpitations or pounding heart.

2. Sweating.

3. Trembling or shaking.

4. Sensations of shortness of breath or being smothered.

5. Feeling of choking.

6. Chest pain or discomfort.

7. Nausea or abdominal distress.

8. Feeling dizzy, Iightheaded, or faint.

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

10. Fear of losing control or going crazy.

11. Fear of dying.

12. Paresthesias (numbness or tingling sensations).

13. Chills or hot flushes.


Criteria for Panic Disorder withoutAgoraphobia

A. Both (1) and (2):

(1) Recurrent, unexpected panic attacks.

(2) At least one of the attacks followed by 1 month ormore of

(a) Concern about having another one.

(b) Worry about consequences of an attack ("heartattack").

B. Absence of agoraphobia.

C. Panic attack not due to physiological effects of asubstance or medical condition.

D. Panic attacks not better explained by another mentaldisorder such as social or specific phobia.


expected, such as during relaxation or during sleep(known as nocturnal panic). In other cases, however, thepanic attacks are said to be "situationally predisposed;'occurring only sometimes while the person is in a particu-lar situation such as while driving a car or being in a crowd.

Because the majority of the 13 symptoms of a panicattack are physical, is not surprising that as many as 85 per-cent of people having a panic attack may show up repeat-edly at emergency rooms or physicians' offices for whatthey are convinced is a medical problem-usually cardiac,respiratory, or neurological (White & Barlow, 2002).Unfortunately, a correct diagnosis is often not made foryears, in spite of normal results on numerous costly med-ical tests. Prompt diagnosis and treatment is also impor-tant because panic disorder causes approximately as muchimpairment in social and occupational functioning as thatcaused by major depression (Hirschfeld, 1996) andbecause panic disorder can contribute to the developmentor worsening of a variety of medical problems (White &Barlow, 2002).

The case of Mindy Markowitz is typical of someonewho has panic disorder without agoraphobia.

Mindy Markowitz is an attractive ... 25-year-old art direc-tor ... who comes to an anxiety clinic... seeking treatmentfor "panic attacks" that have occurred with increasing fre-quency over the past year, often two or three times a day.These attacks begin with a sudden, intense wave of"horri-ble fear" that seems to come out of nowhere, sometimesduring the day, sometimes waking her from sleep. Shebegins to tremble, is nauseated, sweats profusely, feels asthough she is choking, and fears that she will lose controland do something crazy, like run screaming into the street.

Mindy remembers first having attacks like this whenshe was in high school. She was dating a boy her parentsdisapproved of, and had to do a lot of "sneaking around"to avoid confrontations ... she was under a lot of pressureas the principal designer of her high school yearbook, and[she] was applying to IvyLeague colleges. She remembersthat her first panic attack occurred just after the yearbookwent to press and she was accepted by Harvard,Yale,andBrown_The attacks lasted only a few minutes, and shewould just "sit through them." She was worried enough tomention them to her mother; but ... she did not seektreatment.

Mindy has had panic attacks intermittently over the8 years since her first attack, sometimes not for manymonths, but sometimes, as now, several times a day.There have been extreme variations in the intensity of theattacks, some being so severe and debilitating that shehas had to take a day off from work.

Mindy has always functioned extremely well inschool, at work, and in her social life, apart from her panicattacks .... She is a lively,friendly person who is respectedby her friends and colleagues .... Mindyhas never limitedher activities, even during the times that she was havingfrequent, severe attacks, although she might stay homefromwork for a day because she was exhausted from mul-tiple attacks. She has never associated the attacks withparticular places. She says ... she is as likely to have anattack at home in her own bed as on the subway, so thereis no point in avoiding the subway. Whether she has anattack on the subway, in a supermarket, or at home by her-self, she says, "I just tough it out." (Spitzer et aI., 2002,pp.201-2.)

Source: Reprinted with permission from the DSM-IV-TR Casebook(Copyright 2000.) American Psychiatric Publishing, Inc.

AgoraphobiaHistorically, agoraphobia was thought to involve a fear ofthe "agora"-the Greek word for public places of assem-bly (Marks, 1987). In agoraphobia the most commonlyfeared and avoided situations include streets andcrowded places such as shopping malls, movie theaters,and stores. Standing in line can be particularly difficult.See Table 6.2 for a description of situations commonlyavoided by agoraphobics. What is the common themethat underlies this seemingly diverse cluster of fears?Today we think that agoraphobia usually develops as acomplication of having panic attacks in one or more suchsituations. Concerned that they may have a panic attackor get sick, people with agoraphobia are anxious about

CrowdsTheatersShopping mallsCars and busesBridgesEscalatorsBeing home alone

Standing in lineRestaurantsSports arenasTrains and airplanesTunnelsElevatorsBeing far away fromhomeSauna bathsSexual activity

Aerobic exerciseGetting angryWatching exciting orscary movies

being in places or situations from which escape would bephysically difficult or psychologically embarrassing, or inwhich immediate help would be unavailable if somethingbad happened (see DSM table). Typically people withagoraphobia are also frightened by their own bodily sen-sations, so they also avoid activities that will createarousal such as exercising, watching scary movies, drink-ing caffeine, and even engaging in sexual activity.

As agoraphobia first develops, people tend to avoidsituations in which attacks have occurred, but usually theavoidance gradually spreads to other situations whereattacks might occur. In moderately severe cases, people

A. Anxiety about being in places from which escape might bedifficult/embarrassing, or in which help may not beavailable in the event of a panic attack.

B. Situations are avoided or endured with marked distress oranxiety about having a panic attack.

C. Anxiety or avoidance not better accounted for by anotheranxiety disorder.

Source:Adapted with permission from the DiagnosticandStatistical Manualof Mental Disorders,FourthEdition,TextRevision(Copyright 2000). American Psychiatric Association.

Criteria for Panic Disorder withAgoraphobia

A. Both (1) and (2):

(1) Recurrent, unexpected panic attacks.

(2) At least one of the attacks followed by 1 month ormore of

(a) Concern about having another one.

(b) Worry about consequences of an attack ("heartattack").

B. Presence of agoraphobia.

C. Panic attack not due to physiological effects of asubstance or medical condition.

D. Panic attacks not better explained by another mentaldisorder such as social or specific phobia.

Source:Adapted with permission from the DiagnosticandStatisticalManualof Mental Disorders,FourthEdition,TextRevision(Copyright 2000). American Psychiatric Association.

with agoraphobia may even be anxious when venturingoutside their homes alone. In very severe cases, agorapho-bia is an utterly disabling disorder in which a person can-not go beyond the narrow confines of home-or evenparticular parts of the home.

The case of John D. is typical of panic disorder withagoraphobia.

] John D.

John D. was a 45-year-old married Caucasian man withthree sons. Although well-educated and successful ...John had been experiencing difficulties with panic attacksfor 15 years ... experiencing two to five panic attacks permonth. The previous week John had had a panic attackwhile driving with his family to a computer store. He rec-ollected that before the panic attack, he might have been"keyed up" over the kids making a lot of noise in the backseat; the attack began right after he had quickly turnedaround to tell the kids to "settle down." Immediatelyafter he turned back to look at the road, John felt dizzy. Assoon as he noticed this, John experienced a rapid andintense surge of other sensations including sweating,accelerated heart rate, hot flushes, and trembling. Fear-ing that he was going to crash the car, John quickly pulledto the side of the road. He jumped out and walked aroundto the passenger's side. He lowered himself into a squat-ting position and tried to gain control over his breathing.

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 anotherpanic attack at any time. Indeed, John had developedextensive apprehension or avoidance of driving, airtravel, elevators, wide-open spaces, taking long walksalone, 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 around1:00 A.M., after returning from a night of drinking withsome of his friends. Just after awakening at 4:30, John feltstomach pains and a pulsating sensation in the back ofhis neck. All of a sudden, John noticed that his heart wasracing, too .... Although he did not know what he wassuffering from, John was certain that he was dying.

John remembered having a second panic attackabout a month later. From then on, the panic attacksbegan to occur more regularly. When the panic attacksbecame recurrent, John started to avoid situations inwhich the panic attacks had occurred, as well as situa-tions in which he feared a panic attack was likely to occur.On three occasions during the first few years of his panicattacks, John went to the emergency room of his local hos-pital because he was sure that his symptoms were a signof a heart attack. (Adapted from Brown & Barlow, 2001,PP·19-22.)

AGORAPHOBIA WITHOUT PANIC Although agorapho-bia is a frequent complication of panic disorder, it can alsooccur without prior full-blown panic attacks. When thishappens, there is usually a gradually spreading fearfulnessin which more and more aspects of the environment out-side the home become threatening. Cases of agoraphobiawithout panic are extremely rare in clinical settings, andover half the time when they are seen, there is a history ofwhat are called "limited symptom attacks" (with fewerthan four symptoms), or of some other unpredictablephysical ailment such as epilepsy or colitis that makes theperson afraid of being suddenly incapacitated (McNally,1994; White & Barlow, 2002). The most recent estimate ofthe lifetime prevalence of agoraphobia without panic fromthe National Comorbidity Survey-Replication is 1.4 per-cent (e.g., Kessler, Berglund, et aI., 2005b).

Prevalence, Gender, and Age ofOnset of Panic Disorder with andwithout AgoraphobiaMany people suffer from panic disorder with and withoutagoraphobia. The National Comorbidity Survey-Replica-tion found that approximately 4.7 percent of the adultpopulation has had panic disorder with or without agora-phobia at some time in their lives (Kessler, Berglund, et aI.,2005b). Another study found that the prevalence of panicdisorder (and of social phobia) seems to be increasing inyounger generations (Magee et aI., 1996), which is consis-tent with an increase in lifetime prevalence estimates from1994 to 2005 of 3.5 to 4.7 percent (Kessler et aI., 1994;Kessler, Berglund, et aI., 2005b).

The usual age of onset for panic disorder with or with-out agoraphobia is between 15 and 24, especially for men,but it can also begin when people, especially women, are intheir thirties and forties (Eaton et aI., 1994; Hirschfeld,1996). The median age of onset has been estimated at 24years. Once panic disorder develops, it tends to have achronic and disabling course, although the intensity ofsymptoms often waxes and wanes over time (Keller et aI.,1994; White & Barlow, 2002). Panic disorder is about twiceas prevalent in women as in men (Eaton et aI., 1994; White& Barlow, 2002). Agoraphobia also occurs much more fre-quently in women than in men, and the percentage ofwomen increases as the extent of agoraphobic avoidanceincreases. Among people with severe agoraphobia, approx-imately 80 to 90 percent are female (Bekker, 1996; White &Barlow, 2002). Table 6.3 on page 198 outlines gender dif-ferences in the prevalence of anxiety disorders.

The most common explanation of the pronouncedgender difference in agoraphobia is a sociocultural one. Inour culture (and many others as well), it is more acceptablefor women who experience panic to avoid the situationsthey fear and to need a trusted companion to accompanythem when they enter feared situations. Men who experi-ence panic are more prone to "tough it out" because ofsocietal expectations and their more assertive instrumental

People with severe agoraphobia are often fearful of venturing outof their homes into public places. in part because of their fear ofhaving a panic attack in a place in which escape might provephysically difficult or psychologically embarrassing. They mayeven become housebound unless accompanied by a spouse ortrusted companion.

approach to life (Bekker, 1996). Although there is very lit-tle research on this topic, one study consistent with thisidea was conducted by Chambless and Mason (1986), whoadministered a sex-role scale to both male and female ago-raphobics and found that the less "masculine" one scoredon the scale, the more extensive the agoraphobic avoid-ance, for both males and females. In addition, some evi-dence indicates that men with panic disorder may be morelikely to self-medicate with nicotine or alcohol as a way ofcoping with and enduring panic attacks, rather than devel-oping agoraphobic avoidance (White & Barlow, 2002).

Comorbidity with Other DisordersMore than 50 percent of people with panic disorder withor without agoraphobia have one or more additional diag-noses. These include generalized anxiety, social phobia,specific phobia, PTSD, depression, and substance-usedisorders (Kessler, Chiu, et aI., 2005c; Magee et aI., 1996). Itis estimated that 30 to 50 percent of people with panic dis-order will experience a serious depression at some point intheir lives (Gorman & Coplan, 1996). They may also meetcriteria for dependent or avoidant personality disorder(see Chapter 11; White & Barlow, 2002). The issue ofwhether people with panic disorder show an increased risk

Gender Differences in the'Aindety', Di'sofders:: ·.':::'>,':j~.;t..~;, .':. j "j' '~:Ji~~1Lifetime Prevalence Estimates' . :,:,," ":'. " ... ;',¥~~;':::';,,:=::~ , . ,/:-;:1

~ ~ ~ " ~_ ~ .." , v ~;..... -- < " i .."'i<r.:~'" • . ~ .•..~~" ~ •..•••..•.

Prevalence in Women (%)

15.715.5

5.06.62.9

10.4

DisorderSpecific phobiasSocial phobiaPanic disorderGeneralized anxiety disorderObsessive-compulsive disorderPost-traumatic stress disorder

Prevalence in Men (%)

6.7ILl2.03.62.05

Ratio2.341.4

2.51.81.45

2.08

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

of suicidal ideation and suicide attempts has been contro-versial. Several reviews have concluded, however, that thereis little evidence that panic disorder, by itself, increases therisk for suicide; however, it may do so indirectly by increas-ing people's risk for depression and substance use, both ofwhich are risk factors for suicide (Vickers & McNally, 2004;White & Barlow, 2002).

The Timing of a First Panic AttackAlthough panic attacks themselves appear to come "out ofthe blue," the first one frequently occurs following feelingsof distress or some highly stressful life circumstance suchas loss of a loved one, loss of an important relationship,loss of a job, or criminal victimization (see Barlow, 2002a;Falsetti et al., 1995, for reviews). Indeed, approximately 80to 90 percent of clients report that their first panic attackoccurred after one or more negative life events.

Nevertheless, not all people who have a panic attackfollowing a stressful event go on to develop full-blownpanic disorder. Current estimates are that 7 to 30 percentof adults have experienced at least one panic attack in theirlifetimes, but most have not gone on to develop full-blownpanic disorder. People who have other anxiety disordersand/or major depression often experience occasional panicattacks (Barlow, 2002a; Brown, 1996). Given that panicattacks are much more frequent than panic disorder, thisleads us to an important question: What causes full-blownpanic disorder to develop in only a subset of these people?Several very different prominent theories about the causesof panic disorder have addressed this question.

Biological Causal FactorsGENETIC FACTORS According to family and twin stud-ies, panic disorder has a moderate heritable component(e.g., Kendler et al., 1992b, 1992d, 2001; Mackinnon &Foley, 1996). 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. Somestudies have suggested that this heritability is at least partlyspecific for panic disorder (rather than all anxiety disor-ders; e.g., see Barlow, 2002a, for a review), but a largefemale twin study suggests that there is overlap in thegenetic vulnerability factors for panic disorder and pho-bias (Kendler, Walters, et al., 1995).

BIOCHEMICAL ABNORMALITIES Several decades ago,Klein (1981) and others (Sheehan, 1982, 1983) argued thatpanic attacks are alarm reactions caused by biochemicaldysfunctions. This hypothesis initially appeared to be sup-ported by numerous studies over the past 40 years, show-ing that people with panic disorder are much more likelyto experience panic attacks when they are exposed to vari-ous biological challenge procedures than are normal peopleor people with other psychiatric disorders. For example,infusions of sodium lactate, a substance resembling thelactate our bodies produce during exercise (e.g., Gormanet al., 1989), or inhaling carbon dioxide (e.g., Woods et al.,1987), or ingesting caffeine (e.g., Uhde, 1990) producepanic attacks in panic disorder clients at a much higherrate than in normal subjects (see Barlow, 2002a, forreview). There is a broad range of these so-called panicprovocation agents, and some of them are associated withquite different and even mutually exclusive neurobiologi-cal processes. Thus no single neurobiological mechanismcould possibly be implicated (Barlow, 2002a). This obser-vation originally led biologically oriented theorists to spec-ulate that there are multiple different biological causes ofpanic (Krystal, Deutsch, & Charney, 1996). Alternatively,others believe there are simpler biological and psychologi-cal explanations for this pattern of results. These alterna-tive explanations stem from the observation that what allthese biological challenge procedures have in common isthat they put stress on certain neurobiological systems,which in turn produce intense physical symptoms (such asincreased heart rate, respiration, and blood pressure).

At present, two primary neurotransmitter systems aremost implicated in panic attacks-the noradrenergic andthe serotonergic systems. Noradrenergic activity in certainbrain areas can stimulate cardiovascular symptoms associ-ated with panic (Gorman et al., 2000). Increased seroton-ergic activity also decreases noradrenergic activity. This fitswith results showing that the medications most widelyused to treat panic disorder today (the SSRIs-selectiveserotonin reuptake inhibitors) seem to increase serotoner-gic activity in the brain but also decrease noradrenergicactivity. By decreasing noradrenergic activity, these med-ications decrease many of the cardiovascular symptomsassociated with panic that are ordinarily stimulated bynoradrenergic activity (Gorman et al., 2000). Recently theinhibitory neurotransmitter GABA has also been impli-cated in the anticipatory anxiety that many people withpanic disorder have about experiencing another attack.GABA is known to inhibit anxiety and has been shown tobe abnormally low in certain parts of the cortex in peoplewith panic disorder (Goddard, Mason, et al., 2001, 2004).

PANIC AND THE BRAIN One relatively early prominenttheory about the neurobiology of panic attacks implicatedthe locus coeruleus in the brain stem (see Figure 6.1) and aparticular neurotransmitter-norepinephrine-that iscentrally involved in brain activity in this area. For exam-ple, Redmond (1985) showed that electrical stimulation ofthe locus coeruleus in monkeys leads to a constellation ofresponses that strongly resembles a panic attack; moreover,destruction of this area left the monkeys seemingly unable

to experience fear even in the presence of real danger. Suchresearch led to the idea that abnormal norepinephrineactivity in the locus coeruleus may playa crucial causal rolein panic attacks (e.g., Goddard et al., 1996). However,today it is recognized that it is increased activity in theamygdala that plays a more central role in panic attacksthan does activity in the locus coeruleus. (See Figure 6.1.)The amygdala is a collection of nuclei in front of the hip-pocampus in the limbic system of the brain that is criticallyinvolved in the emotion of fear. Stimulation of the centralnucleus of the amygdala is known to stimulate the locuscoeruleus, as well as the other autonomic, neuroendocrine,and behavioral responses that occur during panic attacks(e.g., Gorman et al., 2000; LeDoux, 2000).

Recently, some research has suggested that the amyg-dala is the central area involved in what has been called a"fear network," with connections not only to lower areas inthe brain like the locus coeruleus but also to higher brainareas like the prefrontal cortex (e.g., Gorman et al., 2000).According to this view, panic attacks occur when the fearnetwork is activated, either by cortical inputs or by inputsfrom lower brain areas. So according to this theory, panicdisorder is likely to develop in people who have abnor-mally sensitive fear networks that get activated too readilyto be adaptive. Abnormally sensitive fear networks mayhave a partially heritable basis but may also develop as aresult of repeated stressful life experiences, particularlyearly in life (e.g., Gorman et al., 2000; Ladd et al., 2000).

But panic attacks are only one component of panic dis-order. People with panic disorder also become anxious

Cingulate gyrusFornix

Limbic Stria terminalis Hypothalamussystem Thalamus

AmygdalaMidbrainHippocampus

Pons BrainPrefrontal stemcortex

Medullaoblongata

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

about the possibility of another attack, and those with ago-raphobia also engage in phobic avoidance behavior (e.g.,Gorman et a1.,1989,2000). Different brain areas are proba-bly involved in these different aspects of panic disorder. Thepanic attacks themselves arise from activity in the amyg-dala, either by cortical inputs (e.g., evaluating a stimulus ashighly threatening) or by activity coming from more down-stream areas like the locus coeruleus. For people who haveone or more panic attacks and who go on to develop signif-icant conditioned anxiety about having another one in par-ticular contexts, the hippocampus (a part of the limbicsystem, below the cortex, that is very involved in the learn-ing of emotional responses) generates this conditionedanxiety (e.g., Charney, Grillon, & Bremner, 1998; Gray &McNaughton, 1996), and is probably also involved in thelearned avoidance associated with agoraphobia (Gormanet al., 2000). Finally, the cognitive symptoms that occurduring panic attacks (fears of dying or of losing control)and overreactions to the danger posed by possibly threaten-ing bodily sensations are likely to be mediated by highercortical centers (see Gorman et a1.,2000).

Behavioral and CognitiveCausal FactorsCOMPREHENSIVE LEARNING THEORY OF PANIC DIS-ORDER One early psychological hypothesis about theorigins of agoraphobia was the "fear of fear" hypothesis.The idea was that through a process of interoceptive condi-tioning, initial internal bodily sensations of anxiety orarousal effectively become conditioned stimuli (CSs) asso-ciated with higher levels of anxiety or arousal (Goldstein &Chambless, 1978). For example, heart palpitations mayoccur at the beginning of a full-blown attack, and becausethey become predictors of the rest of the attack, they maythemselves acquire the capacity to provoke panic attacks.

Since 1978 researchers have made many advances inunderstanding the relationship between agoraphobia andpanic disorder, and the differences between anxiety andpanic as distinct emotional states. Building on these, aswell as on advances in the study of classical conditioning,investigators have recently proposed a comprehensivelearning theory of panic disorder that accounts for most ofthe known findings about panic disorder (Bouton,Mineka, & Barlow, 2001). According to this theory, initialpanic attacks become associated with initially neutralinternal (interoceptive) and external cues through a condi-tioning process (e.g., Forsyth & Eiffert, 1998). One pri-mary effect of this conditioning is that anxiety becomesconditioned to these CSs, and the more intense the panicattack, the more robust the conditioning that will occur(Forsyth, Daleiden, & Chorpita, 2000). This conditioningof anxiety to the internal or external cues associated withpanic thus sets the stage for the development of two of thethree components of panic disorder: anticipatory anxiety,and agoraphobic fears. Specifically, when people experi-ence their initial panic attacks (which are terrifying emo-

tional events replete with strong internal bodily sensa-tions), conditioning can occur to multiple different kindsof cues, ranging from heart palpitations and dizziness toshopping malls. Because anxiety becomes conditioned tothese CSs, anxious apprehension about having anotherattack, particularly in certain contexts, may develop, asmay agoraphobic avoidance of contexts in which panicattacks might occur.

However, another important effect is that panicattacks themselves (the third component of panic disor-der) are also likely to be conditioned to certain internalcues. This leads to the occurrence of panic attacks thatseemingly come out of the blue when people uncon-sciously experience certain internal bodily sensations(CSs). For example, one young man with panic disorderwho was particularly frightened of signs that his heart wasracing experienced a surprising and unexpected panicattack after hearing that his favorite presidential candidatehad won. The panic attack thus occurred when he washappy and excited (which is what made it so surprising forhim). However, from the standpoint of this theory, theattack was actually not surprising. Because the man wasexcited, his heart was racing, which probably served as aninternal CS that triggered the panic (Mineka & Zinbarg,2006). This theory also underscores why not everyone whoexperiences an occasional panic attack goes on to developpanic disorder. Instead, people with certain genetic, tem-peramental, or cognitive-behavioral vulnerabilities willshow stronger conditioning of both anxiety and panic(Bouton et al., 2001).

THE COGNITIVE THEORY OF PANIC An earlier cogni-tive theory of panic proposed that panic clients are hyper-sensitive to their bodily sensations and are very prone togiving them the direst possible interpretation (Beck &Emery, 1985; D. M. Clark, 1986, 1997). Clark referred tothis as a tendency to catastrophize about the meaning oftheir bodily sensations. For example, a person who devel-ops panic disorder might notice that his heart is racing andconclude that he is having a heart attack, or that he is dizzy,which may lead to fainting or to the thought that he mayhave a brain tumor. These very frightening thoughts maycause many more physical symptoms of anxiety, whichfurther fuel the catastrophic thoughts, leading to a viciouscircle culminating in a panic attack (see Figure 6.2). Theperson is not necessarily aware of making these cata-strophic interpretations; rather, the thoughts are often justbarely out of the realm of awareness (Rapee, 1996). Theseautomatic thoughts, as Beck calls them, are in a sense thetriggers of panic. Although it is not yet clear how the ten-dency to catastrophize develops, the cognitive model pro-poses that only people with this tendency to catastrophizego on to develop panic disorder (e.g., D. M. Clark, 1997).

Several lines of evidence are consistent with the cogni-tive theory of panic. For example, people with panic disor-der are much more likely to interpret their bodilysensations in a catastrophic manner (e.g., see D. M. Clark,

Trigger stimulus(internal or external)

iPerceived( 'h''''\

Interpretation of Apprehension or worrysensations as (e.g., about having acatastrophic panic attack or about

any distressing situation)

~ Bodysensations

Trigger stimulus(internal or external)

(e.g., exercise, excitement, anger, sexual arousal,coffee, psychoactive drugs)

The Panic CircleAny kind of perceived threat may lead to apprehension or worry,which is accompanied by various bodily sensations. According tothe cognitive model of panic, if a person then catastrophizesabout the meaning of his or her bodily sensations, this will raisethe level of perceived threat, thus creating more apprehensionand worry, as well as more physical symptoms, which fuel furthercatastrophic thoughts. This vicious circle can culminate in apanic attack. The initial physical sensations need not arise fromthe perceived threat (as shown at the top of the circle), but maycome from other sources (exercise, anger, psychoactive drugs,etc., as shown at the bottom of the circle). (Adapted from Clark,1986, 1997.)

1997, for a review). The model also predicts that changingtheir cognitions about their bodily symptoms shouldreduce or prevent panic. Evidence that cognitive therapyfor panic works is consistent with this prediction (D. M.Clark et al., 1994, 1999; see below). In addition, a briefexplanation of what to expect in a panic provocation studycan apparently prevent panic (D. M. Clark, 1997). Peoplewith panic disorder either were given a brief but detailedexplanation of what physical symptoms to expect from aninfusion of sodium lactate, and why they should not worryabout these symptoms, or were given a minimal explana-tion. The people with the cognitive rationale about what toexpect were significantly less likely to say that they had hadthe subjective experience of a panic attack in response tothe lactate (30 percent) than were control individuals(90 percent).

PSYCHOLOGICAL EXPLANATIONS OF RESULTS FROMPANIC PROVOCATION STUDIES Earlier we noted thatthere are simpler psychological explanations that provide acommon mechanism for understanding how so many var-ied panic provocation agents can all provoke panic at highrates in people with panic disorder. Because these agentsproduce arousal, they mimic the physiological cues thatnormally precede a panic attack or may be taken as a signof some other impending catastrophe (Barlow, 2002a;Bouton et al., 2001; Margraf, Ehlers, & Roth, 1986a,1986b). People with panic disorder already start at a higherlevel of arousal than others and are very familiar with theseearly warning cues. Thus, according to the cognitive the-ory, people with panic attacks frequently misinterpretthese symptoms as the beginning of a panic attack or aheart attack, which in turn induces the vicious circle ofpanic described above; this would not happen in controlswho do not have the same tendency to catastrophize. Alter-natively, according to the learning theory of panic, it wouldbe only those with panic disorder for whom these cuesmight serve as interoceptive CSs that can trigger anxietyand panic because of their prior associations with panic.

The key difference between these two theories inexplaining the results of panic provocation studies lies inthe great importance that the cognitive model places onthe meaning that people attach to their bodily sensations;they will experience panic only if they make catastrophicinterpretations of certain bodily sensations. Such cata-strophic cognitions are not necessary with the interocep-tive conditioning model, because anxiety and panicattacks can be triggered by unconscious interoceptive (orexteroceptive) cues (Bouton et al., 2001). Thus the learn-ing theory model is better able to explain the occurrenceof the panic attacks that often occur without any preced-ing negative (catastrophic) automatic thoughts, as well asthe occurrence of nocturnal panic attacks that occur dur-ing sleep; the occurrence of both of these kinds of attacksare difficult for the cognitive model to explain (seeDevelopments in Research 6.1 on p. 202).

ANXIETY SENSITIVITY AND PERCEIVED CONTROLOther cognitive and behavioral explanations of panic andagoraphobia have looked at a number of different factorsthat can generally be explained within either the condi-tioning or the cognitive perspective. For example, severalresearchers have shown that people who have high levels ofanxiety sensitivity are more prone to developing panicattacks and perhaps panic disorder (Cox, 1996; McNally,2002). Anxiety sensitivity is a trait-like belief that certainbodily symptoms may have harmful consequences. Such aperson would endorse statements such as, "When I noticethat my heart is beating rapidly, I worry that I might have aheart attack." In one important study, Schmidt, Lerew, andJackson (1997) followed over 1,400 young adults undergo-ing basic military training for 5 weeks. Schmidt and col-leagues found that high levels of anxiety sensitivitypredicted the development of spontaneous panic attacks

.1SZllthough the majority of panic attacks

experienced by people with panic disor-der occur during waking hours, approxi-mately 50 to 60 percent of people reportthat they have experienced a panic attack

during sleep at least once (Barlow, 2002a; O'Mahoney &Ward, 2003). Nocturnal panic refers to waking from sleepin a state of panic. It seems to occur with some regularity inabout 20 to 40 percent of people with panic disorder(Craske, Lang, et aI., 2002). Although one might think thatsuch panic attacks occur in response to nightmares, con-siderable research shows that this is not the case. Sleephas five stages that occur in a fairly invariant sequencemultiple times throughout the night: one stage called REMsleep (rapid eye movement sleep) when vivid dreamingoccurs, and four stages of non-REM sleep (Stages 1-4)when vivid dreams do not occur. If nocturnal panic attacksoccurred in response to dreams, we would expect them tooccur during REM sleep, but in fact they occur during Stage2 and early Stage 3 sleep, usually a few hours after fallingasleep.

It is important to note that nocturnal panic attacks aredifferent from "sleep terrors" or "night terrors," which usu-ally occur during Stage 4 sleep. Night terrors are usuallyexperienced by children who often scream and then fearthat someone or something is chasing them around theroom; however, they do not wake up (Barlow, 2002a). Noc-turnal panic attacks also differ from isolated sleep paraly-sis, which can sometimes occur during the transition fromsleep to waking. It involves a stark sense of terror (resem-bling that during a panic attack) and an inability to move,which seems to occur because the individuals are wakingfrom REM (dream) sleep, when there is suppression of

during this highly stressful period. For example, of thetrainees scoring in the top 10 percent on a scale measuringanxiety sensitivity, 20 percent experienced at least onepanic attack during the 5 weeks of basic training; only 6percent of the remaining study participants had a panicattack in the same time period. Several other studies exam-ining the same issues have obtained very similar results,thus boosting confidence in the reliability of anxiety sensi-tivity as a predictor of panic attacks (e.g., Hayward et a!',2000; Li & Zinbarg, submitted).

In addition, several important studies have shown thatsimply having a sense of perceived control-for instance,over the amount of carbon-dioxide-altered air that isinhaled (a panic provocation procedure known frequentlyto bring on anxiety and panic)-reduces anxiety and even

muscle activity below the neck. Isolated sleep paralysisoccurs much more commonly among African-Americansthan among other ethnic groups, for reasons that are stillunclear (Barlow, 2002a; McNally, 1994).

Although early research suggested that people whoexperience nocturnal panic attacks as well as daytimeattacks may show overall higher levels of psychopathol-ogy, recent research has been showing otherwise, withfew differences being reported (e.g., Craske et aI., 2002;O'Mahoney & Ward, 2003). Similarly, biological modelshave hypothesized that nocturnal panic stems from dysreg-ulation of the respiratory system, but there is no good evi-dence to support this idea. One reason nocturnal panicattacks have been of interest from a theoretical standpointis that they appear to be very difficult for any strong versionof the cognitive theory of panic to explain, in part becauseit is hard to see how the catastrophic cognitions that areposited to be necessary for the occurrence of a panic attackcould occur during Stage 2 or 3 sleep. On the other hand,the learning theory of panic disorder can explain theiroccurrence because internal bodily sensations occurringduring sleep that have been previously conditioned to elicitpanic can do so without the person being consciouslyaware of them (Bouton et aI., 2001). Consistent with this,one recent study has shown that panic attacks are lessstrongly related to catastrophic cognitions in people whosometimes experience nocturnal panic than in people whoexperience only daytime panic. Moreover, individuals whosometimes experience nocturnal panic show higher levelsof anxiety sensitivity than do individuals without nocturnalpanic (O'Mahoney & Ward, 2003). Because anxiety sensitiv-ity involves fears of bodily sensations, this finding is moreconsistent with the learning theory of panic disorder.

blocks panic (e.g., Sanderson, Rapee, & Barlow, 1989;Zvolensky et a!', 1998, 1999). In addition, if a person withpanic disorder has a "safe" person with her or him whens/he undergoes a panic provocation procedure, s/he is likelyto show reduced distress, lowered physiological arousal,and reduced likelihood of panic, relative to someone whocame alone (without a "safe" person; Carter et a!', 1995).Moreover, people high in anxiety sensitivity may be pro-tected against having panic attacks during stressful periodsif they have a sense of perceived control and predictabilityover their life situation (Schmidt & Lerew, 2002).

SAFETY BEHAVIORS AND THE PERSISTENCE OF PANICWhy do people who have developed panic disorder continueto have panic attacks in spite of the fact that their direst pre-

dictions rarely, if ever, come true? Some people with panicdisorder may, for example, have three or four panic attacks aweek for 20 years; each time they may believe they are hav-

ing a heart attack, and yetthey never do. After expe-riencing hundreds orthousands of panic attackswithout having a heartattack, one would think,from the cognitive per-spective, that this cata-strophic thought wouldhave been proven wrongso many times that itwould finally go away.However, evidence sug-gests that such disconfir-mation does not occurbecause people withpanic disorder frequentlyengage in "safety behav-iors" (such as breathingslowly) before or duringan attack. They then mis-takenly tend to attributethe lack of catastrophe totheir having engaged inthis safety behavior ratherthan to the idea that panic

attacks actually do not lead to heart attacks. Similarly, peo-ple who think they may faint will tend to lean against solidobjects (Clark, 1997; Salkovskis et aI., 1996). Research sug-gests that it is important during treatment to identify thesesafety behaviors so that the person can learn to give themup and finally see that their feared catastrophe still doesnot occur.

Many people experiencing apanic attack mistake theirsymptoms (for example, chestpain and shortness of breath)for another medical problem-most often, a heart attack.

COGNITIVE BIASES AND THE MAINTENANCE OF PANICFinally, many studies have shown that people with panic dis-order are biased in the way they process threatening infor-mation. Such people not only interpret ambiguous bodilysensations as threatening (Clark, 1997) but also interpretother ambiguous situations as more threatening than docontrols. People with panic disorder also seem to have theirattention automatically drawn to threatening informationin their environment such as words that represent thingsthey fear, such as palpitations, numbness, or faint (see Math-ews & MacLeod, 2005; Mineka et al., 2003, for reviews). Arecent study using fMRI techniques demonstrated that peo-ple with panic disorder showed greater activation to threatwords than did normals in brains areas involved in memoryprocessing of threatening material (Maddock, Buonocore,Kile, & Garrett, 2003). Whether these information-processing biases are present before the disorder begins andhelp to cause it is as yet unclear, but these biases are certainlylikely to help maintain the disorder once it has begun. Forexample, having one's attention automatically drawn to

threatening cues in the environment is likely to provokemore attacks.

In summary, research into both biological and psy-chological factors involved in panic disorder has providedimportant insights into this disorder since it was first iden-tified as a distinct disorder in 1980. It seems unlikely thatresearch from either tradition alone will ever provide acomplete account of this disorder, and we eagerly awaitmore attempts at synthesizing these findings into a biopsy-chosocial theory of this disorder.

Treating Panic Disorder andAgoraphobiaMEDICATIONS Many people with panic disorder (withor without agoraphobia) are prescribed minor tranquiliz-ers from the benzodiazepine category such as alprazolam(Xanax) or clonazepam. These people frequently showsome symptom relief with these minor tranquilizers (alsoknown as anxiolytics, or anti-anxiety medications), andmany can function more effectively. One major advantageof these drugs is that they act very quickly (in 1/2 to 1 hour)and so can be useful in acute situations of intense panic oranxiety. However, these anxiolytic medications can alsohave quite undesirable side effects such as drowsiness andsedation, which can lead to impaired cognitive and motorperformance. Moreover, they are potentially quite addic-tive, which means that with prolonged use, most peopleusing moderate to high doses develop physiologicaldependence on the drug, which results in withdrawalsymptoms when the drug is discontinued (e.g., nervous-ness, sleep disturbance, and dizziness). Withdrawal fromthese drugs can be very slow and difficult, and it precipi-tates relapse in a very high percentage of cases (Ballenger,1996; Roy-Byrne & Cowley, 2002).

The other categories of medication that are useful inthe treatment of panic disorder and agoraphobia are theantidepressants (including primarily the tricyclics and theSSRIs-selective serotonin reuptake inhibitors). Thesemedications have both advantages and disadvantagescompared with anxiolytics. One major advantage is thatthey are not addictive. However, it takes about 4 weeksbefore they have any beneficial effects, so they are not use-ful in an acute situation where a person is having a panicattack. Troublesome side effects (such as dry mouth, con-stipation, and blurred vision with the tricyclics, and inter-ference with sexual arousal with the SSRIs) mean that largenumbers of people refuse to take the medications or dis-continue their use (White & Barlow, 2002). Moreover,relapse rates when the drugs are discontinued are quitehigh (although not as high as with the benzodiazepines).

Today the SSRIs are more widely prescribed than thetricyclics because the SSRIs are generally better toleratedby most patients. In addition, some (but not all) compara-tive studies have shown that the SSRIs may be even slightlymore effective than the tricyclic antidepressants (Roy-Byrne & Cowley, 2002).

.2 Cognitive-BehavioralTherapy for PanicDisorder

The cognitive and conditioning models of panicdisorder have contributed to the formulation ofnew treatments that have been shown to behighly effective in dozens of different studies inmany countries around the world (see Ruhm-

land & Margraf, 2001; White & Barlow, 2002). Although thetreatments vary somewhat, each is a form of behavioral orcognitive-behavioral therapy. In one widely used version ofthe "Panic Control Treatment" developed by Barlow andcolleagues, several different cognitive and behavioral tech-niques are combined in a program that typically lasts for 12

to 15 sessions (Barlow & Craske, 2000; Craske, Barlow, &Meadows, 2000).

There are three aspects to Panic Control Treatment.First, clients are taught about the nature of anxiety andpanic and how the capacity to experience both is adaptive.

By learning about the nature of the fight-or-flight responseexperienced during panic, clients come to understand thatthe sensations they experience during panic are normaland harmless. Clients are also taught to self-monitor theirexperiences with anxiety and panic through daily diaries.

The second part of treatment involves teaching peo-ple with panic disorder to control their breathing. First theyare asked to hyperventilate, or overbreathe. Hyperventila-tion is known to create a variety of unpleasant physicalsensations (such as lightheadedness, dizziness, and tight-ness of the chest) that often occur during panic attacks.(Youcan see this for yourself by breathing very fast anddeeply for 1 to 2 minutes.) By then learning how to controltheir breathing, they master a new coping tool that willreduce the likelihood that they themselves will createsome of the symptoms they are so frightened of.

Not all statistically significantchanges are of sufficient magnitudeto be clinically significant. Clinicalsignificance reflects how large theeffects of a particular treatment orintervention are with respect tohow much meaningful change theyprovide in a person's level offunctioning or well-being.

BEHAVIORAL AND COGNITIVE-BEHAVIORAL TREAT-MENTS The original behavioral treatment for agora-phobia from the early 1970s involved prolonged exposureto feared situations, often with the help of a therapist orfamily member. The idea was to make people graduallyface the situations they feared and learn that there wasnothing to fear. Such exposure-based treatments werequite effective, and helped about 60 to 75 percent of peoplewith agoraphobia show clinically significant improvement.These effects were generally well maintained at 2- to 4-yearfollow-up. But this left approximately 25 to 40 percent notimproved to a clinically significant degree (Barlow, Raffa,& Cohen, 2002; McNally, 1994).

One limitation of these original treatments was thatthey did not specifically target panicattacks. In the mid-1980s, two new tech-niques were developed as clinicalresearchers increasingly recognized theimportance of panic attacks to mostpeople with agoraphobia. One newtechnique involves a variant on expo-sure known as interoceptive exposure,which means deliberate exposure tofeared internal sensations. As we havenoted, people with panic disorder haveprominent fears of their bodily sensa-tions, and panic attacks may be condi-tioned responses to interoceptive

conditioned stimuli. The idea is thatfear of these internal sensations shouldbe treated in the same way that fear of external agorapho-bic situations is treated-namely, through prolonged

exposure to those internal sensations so that the fear mayextinguish. Thus people with panic disorder in treatmentare asked to do a variety of exercises (such as hyperventi-lating, running in place, holding their breath, ingestingcaffeine, etc.) that bring on the physical sensations theymay fear. Whichever exercises bring on the symptoms thatmost resemble those they experience during panic arethen targeted for practice to promote extinction of theanxiety for these physical sensations.

The second set of techniques that were developed arecognitive techniques, in recognition that catastrophicautomatic thoughts may help maintain panic attacks.Developments in Practice 6.2 illustrates one kind ofintegrative cognitive-behavioral treatment for panic disor-

der. This approach targets both agora-phobic avoidance and panic attacks.Generally, this integrative treatmentproduces better results than the originalexposure-based techniques that focusedexclusively on exposure to external situa-tions (Clark, 1997; White & Barlow,2002). However, results of a quantita-tive review of 51 studies showed thatintensive exposure-based treatment thatinvolves both intensive interoceptive andexteroceptive exposure may be just aseffective as the integrative treatment(Ruhmland & Margraf, 2001). Indeed, inmany of the studies conducted using oneof the variants on these treatments, 75 to

95 percent of people with panic disorder were panic-free atthe end of 8 to 14 weeks of treatment, and gains were well

Third, clients are taught to identify the automaticthoughts they have during panic attacks, as well as duringanxiety-provoking situations. They are then taught aboutthe logical errors that people who have panic are prone tomaking and learn to subject their own automatic thoughtsto a logical reanalysis. For example, a person who fearshaving a heart attack at the first sign of heart palpitationsis asked to examine the evidence that this might be true.(When did the doctor last tell him or her that his or herheart was perfectly healthy? What is the likelihood of hav-ing a heart attack at age 30?) In later sessions the cogni-tive part of the treatment is focused on teaching peoplehow to decatastrophize-that is, to learn how to thinkthrough what the worst possible outcome might be if theydid have a panic attack (e.g., if they had a panic attackwhile driving, they might have to pull their car over to theside of the road until the attack subsided). The entireexperience of panic usually becomes less terrifying oncethey learn to decatastrophize.

Finally, another part of the treatment involves expo-sure to feared situations and feared bodily sensations.

Because of the importance of interoceptive fears (fears ofbodily sensations), clients are asked to do a variety of exer-cises with the therapist that bring on different bodily sen-sations. These include hyperventilating, breathing througha straw, shaking one's head from side to side, jogging inplace, holding one's breath for a minute, and the like. Aftereach exercise, clients describe the sensations produced,discuss how similar these sensations are to those that theyexperience during panic, and evaluate how scary thosesensations are. Whichever exercises produce the symp-toms most similar to their own during panic attacks are tar-geted for practice. The idea is that if clients practiceinducing these sensations, their anxiety about the sensa-tions will gradually extinguish. Later, clients who also haveextensive agoraphobic avoidance begin to expose them-selves to their feared situations for long enough that theiranxiety diminishes. This part of the treatment is delayeduntil clients have learned a variety of coping skills (cogni-tive techniques as well as breathing skills).

maintained at 1- to 2-year follow-up (D. M. Clark, 1996;White & Barlow, 2002). Overall, the magnitude of improve-ment is greater with these cognitive and behavioral treat-ments than with medications (Barlow et al., 2002a).

What about the combination of medication andcognitive-behavioral therapy? In the short term, such com-bined treatment may sometimes produce a slightly supe-rior result, compared to either type of treatment alone.However, in the long term after medication has beentapered, clients who have been on medication (with orwithout cognitive or behavioral treatment) seem to show agreater likelihood of relapse (Barlow et a1., 2002a; Markset a1., 1993). Perhaps this is because they have attributedtheir gains to the medication rather than to their personalefforts (Ba~oglu et a1., 1994).

In ReVIew~ Describe the major diagnostic features of

both panic disorder and agoraphobia, andexplain how they are thought to be related.

~ What biological causal factors have beenimplicated in panic disorder?

~ Compare and contrast the learning theoryand cognitive models of panic disorder.

~ Describe the major treatment approaches forpanic disorder and their relative advantagesand disadvantages.

GENERALIZED ANXIETYDISORDERMost of us worry and get anxious occasionally, and anxietyis an adaptive emotion that helps us plan for and preparefor possible threat. But for some people, anxiety and worryabout many different aspects of life (including minorevents) becomes chronic, excessive, and unreasonable. Inthese cases, generalized anxiety disorder (GAD) may bediagnosed (formerly known as free-floating anxiety).DSM-IV-TR criteria specify that the worry must occurmore days than not for at least 6 months and that it mustbe experienced as difficult to control (see DSM table). Theworry must be about a number of different events or activ-ities, and its content cannot be exclusively related to theworry associated with another concurrent Axis I disordersuch as the possibility of having a panic attack. The subjec-tive experience of excessive worry must also be accompa-nied by at least three of six other symptoms listed in thetable. Frequently people with GAD also show marked vig-ilance for possible signs of threat in the environment andengage in certain subtle avoidance activities such as pro-crastination, checking, or calling a loved one frequently tosee if he or she is safe.

The general picture of people suffering from generalizedanxiety disorder is that they live in a relatively constantfuture-oriented mood state of anxious apprehension,

Criteria for Generalized AnxietyDisorder

A. Excessive anxiety and worry occurring more days than notfor at least 6 months about a number of events oractivities

B. Person finds it difficult to control the worry

C. Anxiety and worry associated with 3 or more of following6 symptoms for more days than not:

(1) restlessness or feeling keyed up

(2) being easily fatigued

(3) difficulty concentrating

(4) irritability

(5) muscle tension

(6) sleep disturbance

D. Anxiety and worry not confined to features of anotherAxis I disorder

E. Symptoms cause clinically significant distress orimpairment in functioning

chronic tension, worry, and diffuse uneasiness. Theyattempt to be constantly ready to deal with upcoming neg-ative events and have a strong sense of lacking control overthe worry process (Barlow, 2002a; Barlow et aI., 1996).Such anxious apprehension is also part of other anxiety dis-orders (for example, the person with agoraphobia is anx-ious about future panic attacks and about dying, and theperson with social phobia is anxious about possible nega-tive social evaluation). But this apprehension is the essenceof GAD, leading Barlow and others to refer to GAD as the"basic" anxiety disorder (Roemer, Orsillo, & Barlow, 2002;Wells & Butler, 1997).

The nearly constant worries of people with general-ized anxiety disorder leave them continually upset, uneasy,and discouraged. In one study, their most common spheresof worry were found to be family, work, finances, and per-sonal illness (Roemer, Molina, & Borkovec, 1997). Notonly do they have difficulty making decisions, but afterthey have managed to make a decision, they worry end-lessly, even after going to bed, over possible errors andunforeseen circumstances that may prove the decisionwrong and lead to disaster. They have no appreciation ofthe logic by which most of us conclude that it is pointlessto torment ourselves about possible outcomes over whichwe have no control.

The following case is fairly typical of generalized anx-iety disorder.

Muscle tension, chronic overarousal, restlessness, and difficultyconcentrating are 01/symptoms that people with generalizedanxiety disorder may have. Such individuals also worry excessivelyand are hypervigilant for possible signs of threat in theirenvironment.

A Graduate Studentwith GAD

John was a 26-year-old single graduate student in thesocial sciences at a prestigious university. Although hereported that he had had problems with anxiety nearly allhis life, even as a child, the past 7 to 8 years since he hadleft home and gone to an Ivy League college had beenworse. During the past year his anxiety had seriouslyinterfered with his functioning, and he worried about sev-eral different spheres of his life. He was very concernedabout his own health and that of his parents. During oneincident a few months earlier, he had thought that hisheart was beating more slowly than usual and he hadexperienced some tingling sensations; this led him toworry that he might die. In another incident he had heardhis name spoken over a loudspeaker in an airport andhad worried that someone at home must be dying. Hewas also very worried about his future, because his anxi-ety had kept him from completing his master's thesis ontime. John also worried excessively about getting a badgrade, even though he had never had one either in col-lege or in graduate school. In classes he worried exces-sively about what the professor and other studentsthought of him, and he tended not to talk unless the classwas small and he was quite confident about the topic.Although he had a number of friends, he had never had agirlfriend because of his shyness about dating. He had noproblem talking or socializing with women as long as itwas not defined as a dating situation. He worried that heshould date a woman only if he was quite sure, from theoutset, that it could be a serious relationship. He also

worried excessively that if a woman did not want to datehim, it meant that he was boring.

In addition to his worries, John reported muscle ten-sion and easily becoming fatigued. He also reportedgreat difficulty concentrating and a considerable amountof restlessness and pacing. When he couldn't work, hespent a great deal of time daydreaming, which worriedhim because he didn't seem able to control it. At times hehad difficulty falling asleep if he was particularly anxious,but at other times he slept excessively, in part to escapefrom his worries. He frequently experienced dizzinessand palpitations, and in the past he had had full-blownpanic attacks. Overall, he reported frequently feeling par-alyzed and unable to do things.

Both of John's parents were professionals; hismother was also quite anxious and had been treated forpanic disorder. John was obviously extremely bright andhad managed to do very well in school in spite of his life-long problems with anxiety. But as the pressures of fin-ishing graduate school and starting his career loomedbefore him, and as he got older and still had never dated,the anxiety became so severe that he sought treatment.

Prevalence and Age of OnsetGeneralized anxiety disorder is a relatively common con-dition; current estimates from the National ComorbiditySurvey- Replication are that approximately 3 percent of thepopulation suffers from it in any I-year period and 5.7 per-cent at some point in their lives (Kessler et al., 1994;Kessler, Chiu et a!', 2005c, Kessler, Berglund, et a!., 2005b).GAD is approximately twice as common in women as inmen (a somewhat less dramatic difference than is seenwith many specific phobias or severe agoraphobia; seeTable 6.3 on p. 198 for summaries of gender differences inthe different anxiety disorders). Although GAD is quitecommon, most people with this disorder manage to func-tion in spite of their high levels of worry and low perceivedwell-being (Stein, Heimberg, & Stein, 2004). They are lesslikely to go to clinics for psychological treatment than arepeople with panic disorder or major depression, which arefrequently more debilitating conditions. However, peoplewith GAD do frequently show up in physicians' officeswith medical complaints (such as muscle tension orfatigue) and are known to be overusers of health careresources (similar to people with panic disorder; Green-berg et a!., 1999; Roy-Byrne & Katon, 2002).

Age of onset is often difficult to determine because 60to 80 percent of people with GAD remember having beenanxious nearly all their lives, and many others report aslow and insidious onset (Roemer et a!., 2002; Wells &Butler, 1997). However, recent research has also docu-mented that GAD often occurs in older adults where it isthe most common anxiety disorder (e.g., Roemer et a!',2002; Stein, 2004).

Comorbidity with Other DisordersGeneralized anxiety disorder often co-occurs with otherAxis I disorders, especially other anxiety and mood disor-ders such as panic disorder, social phobia, specific phobia,and PTSD (Brown, Campbell, et a!', 2001; Kessler, Chiu,et a!., 2005c). In addition, many people with GAD (likeJohn) experience occasional panic attacks without qualify-ing for a diagnosis of panic disorder (Barlow, 1988, 2002a).Many of these people are mildly to moderately depressedas well as chronically anxious, which is not surprisinggiven their generally gloomy outlook on the world (Roe-mer et a!', 2002; Stein et aI., 2004). Nor is it surprising thatexcessive use of tranquilizing drugs, sleeping pills, andalcohol often complicates the clinical picture in general-ized anxiety disorder.

Psychosocial Causal FactorsTHE PSYCHOANALYTIC VIEWPOINT According to thisviewpoint, generalized or free-floating anxiety results froman unconscious conflict between ego and id impulses thatis not adequately dealt with because the person's defensemechanisms have either broken down or have never devel-oped. Freud believed that it was primarily sexual andaggressive impulses that had been either blocked fromexpression, or punished upon expression, that led to free-floating anxiety. Defense mechanisms may become over-whelmed when a person experiences frequent and extremelevels of anxiety, as might happen if expression of idimpulses were frequently blocked from expression (e.g.,under periods of prolonged sexual deprivation). Accord-ing to this view, the primary difference between specificphobias and free-floating anxiety is that in phobias, thedefense mechanisms of repression and displacement actu-ally work, whereas in free-floating anxiety these defensemechanisms do not work, leaving the person anxiousnearly all the time. Unfortunately this viewpoint is nottestable and has therefore been largely abandoned amongclinical researchers.

THE ROLE OF UNPREDICTABLE AND UNCONTROL-LABLE EVENTS Uncontrollable and unpredictable aver-sive events are much more stressful than controllable andpredictable aversive events, so it is perhaps not surprisingthat the former create more fear and anxiety (Barlow,2002a; Craske & Waters, 2005; Mineka, 1985a; Mineka &Zinbarg, 1996). Conversely, experience with controllingaspects of one's life may immunize one against developinggeneral anxiety (Chorpita, 2001; Mineka & Kelly, 1989).

This has led researchers to hypothesize that peoplewith GAD may have a history of experiencing many impor-tant events in their lives as unpredictable and/or uncontrol-lable. For example, having a boss or spouse who hasunpredictable bad moods or outbursts of temper for seem-ingly trivial reasons might keep a person in a chronic stateof anxiety. Although the unpredictable and uncontrollable

events involved in GAD are generally not as severe andtraumatic as those involved in the origins of PTSD, there issome evidence that people with GAD may be more likely tohave had a history of trauma in childhood than individualswith several other anxiety disorders (Borkovec et al., 2004).Moreover, people with GAD clearly have far less tolerancefor uncertainty than nonanxious controls (Dugas, Buhr, &Ladoucer, 2004), which suggests that they are especially dis-turbed by not being able to predict the future (as none of uscan; Roemer et al., 2002).

In addition, perhaps some of these people's intolerancefor uncertainty, as well as their tension and hypervigilance

(the sense of always lookingfor signs of threat), stemsfrom their lacking safety sig-nals in their environment. Ifa person mostly experiencespredictable stressors (e.g.,on Mondays the boss isalways in a bad mood and islikely to be highly critical),he or she can predict whensomething bad is likely tohappen by paying attentionto this signal (e.g., Mondaysat work). Such a person thenfeels safe when that signal ismissing (a safety signal)(e.g., Tuesdays through Fri-days at work). But ifanother person has experi-enced many unpredictableor unsignaled stressors (e.g.,the boss or one's parent is ina bad mood and highly crit-ical on random days of the

week), she or he will not have developed safety signals forwhen it is appropriate to relax and feel safe, and this uncer-tainty may lead to chronic anxiety (Mineka, 1985a; Mineka& Zinbarg, 1996; Seligman & Binik, 1977). Thus a relativelack of safety signals may help explain why people withGAD feel constantly tense and vigilant for possible threats(Rapee,2001).

It is possible that some of the chronictension and hypervigi/ance thatindividuals with generalized anxietydisorder experience stem from theirlacking safety signals in theirenvironment. Without such safetysignals, such as knowing when theirboss or spouse will or will not beangry with them, they may never beable to relax and feel safe.

A SENSE OF MASTERY: THE POSSIBILITY OF IMMU-NIZING AGAINST ANXIETY Although we cannot studywhether controlling different aspects of our lives mayimmunize us from developing generalized anxiety bydirectly manipulating the controllability and predictabilityof our life experiences over prolonged periods of time, wecan learn a lot from laboratory analogue studies in ani-mals. One longitudinal experiment with infant rhesusmonkeys supports the hypothesized role of experienceswith control in immunizing individuals against fear andanxiety (Mineka, Gunnar, & Champoux, 1986). In this

experiment, two groups of infant monkeys called "Master"monkeys were reared in peer groups (without their moth-ers) in which they gained extensive experience with controland mastery by pressing bars and pulling chains to obtainreinforcers like food, water, and treats. Two other groups ofmonkeys called "Yoked" monkeys were reared in identicalenvironments but had no control over their reinforcers;instead, they received reinforcers when a member of theMaster group exerted control. The Master and Yokedgroups had equal exposure to reinforcers; they differedonly in whether they controlled access to the reinforcers.

Between 7 and 11 months of age, all monkeys weretested for their responses to several fear- and anxiety-provoking situations. Master monkeys habituated morerapidly to frightening and stressful experiences than didYoked monkeys, and the Master monkeys were also bolderand more willing to enter and explore a novel, somewhatfrightening playroom situation. Finally, Master monkeysalso coped better when they were separated from theirpeers and placed as an intruder in the Yoked group thanYoked monkeys did when placed in the Master group. Thusit appears that early experiences with control and masterycan immunize the individual to some extent against theharmful effects of exposure to stressful situations-and, byanalogy, perhaps against the development of generalizedanxiety (see also Chorpita, 2001; Craske, 2003; Mineka &Zinbarg, 1996, in press). In human children, experienceswith control and mastery often also occur in the context ofthe parent-child relationship and so parents' responsive-ness to their children's needs directly influences their chil-dren's developing sense of mastery (e.g., Craske, 2003;Mineka et al., 1986).

THE CENTRAL ROLE OF WORRY AND ITS POSITIVEFUNCTIONS The worry process is now considered thecentral feature of GAD and has been the focus of muchresearch in recent years. Here we will first consider thenature and functions of worry. Next, we will consider whyworry comes to be such a self-sustaining process in somepeople and why it may be perceived to be uncontrollable.

Borkovec (1994) and colleagues (2004) investigatedboth what people with GAD think the benefits of worryingare and what actual functions worry serves. The five bene-fits that people with GAD most commonly think derivefrom worrying are:

1. Superstitious avoidance of catastrophe ("Worryingmakes it less likely that the feared event will occur").

2. Actual avoidance of catastrophe ("Worrying helps togenerate ways of avoiding or preventing catastrophe").

3. Avoidance of deeper emotional topics ("Worryingabout most of the things I worry about is a way todistract myself from worrying about even moreemotional things, things that I don't want to thinkabout").

4. Coping and preparation ("Worrying about apredicted negative event helps me to prepare for itsoccurrence").

5. Motivating device ("Worrying helps to motivate meto accomplish the work that needs to be done";Borkovec, 1994, pp. 16-17; Borkovec et aI., 2004).

In addition, exciting new discoveries about the nlllc-tions that worry actually serves help reveal why the worryprocess is so self-sustaining. When people with GADworry, their emotional and physiological responses toaversive imagery are actually suppressed. This suppressionof emotional and aversive physiological responding mayserve to reinforce the process of worry (that is, to increaseits probability; Borkovec et aI., 2004). Because worry sup-presses physiological responding, it also insulates the per-son from fully experiencing or processing the topic that isbeing worried about, and it is known that such full pro-cessing is necessary if extinction of that anxiety is to occur.Thus the threatening meaning of the topic being worriedabout is maintained (Borkovec, 1994; Borkovec et aI.,2004). Finally, Borkovec also believes that the worryprocess is further reinforced superstitiously, because mostthings that people worry about never happen.

THE NEGATIVE CONSEQUENCES OF WORRY In spiteof these positive functions that worry serves, some of itseffects are negative (Mineka, 2004; Mineka, Yovel, & Pine-les, 2002). For example, worry itself is certainly not anenjoyable activity and can actually lead to a greater sense ofdanger and anxiety because of all the possible catastrophicoutcomes that the worrier envisions. In addition, peoplewho worry about something tend subsequently to havemore negative intrusive thoughts than people who do notworry. For example, Wells and Papageorgiou (1995) hadpeople watch a gruesome film. Following the film, somewere told to relax and settle down, some were told to imag-ine the events in the film, and some were told to worry inverbal form about the film. Over the next several days, peo-ple in the worry condition showed the most intrusiveimages from the film. Wells and Butler (1997, p. 167) con-cluded, "Individuals who are prone to worry ... are likely toengage in an activity that pollutes the stream of conscious-ness with an increasing frequency of intrusive thoughts."

Finally, there is now considerable evidence thatattempts to control thoughts and worry may paradoxicallylead to increased experience of intrusive thoughts andenhanced perception of being unable to control them(Abramowitz et aI., 2001; Wells, 1999; Wells & Butler,1997). Somewhat paradoxically, these intrusive thoughtscan then serve as further trigger topics for more worry, anda sense of uncontrollability over worry may develop inpeople caught in this cycle that occurs in GAD. As we havenoted, perceptions of uncontrollability are also known tobe associated with increased anxiety, so a vicious circle of

anxiety, worry, and intrusive thoughts may develop(Mineka, 2004; Mineka et aI., 2002).

COGNITIVE BIASES FOR THREATENING INFORMA·TION Not only do people with GAD have frequentfrightening thoughts, they also process threatening infor-mation in a biased way. Many studies have shown that gen-erally anxious people tend to preferentially allocate theirattention toward threatening cues when both threat andnon threat cues are present in the environment. Non-anxious people show, if anything, the opposite bias (seeMathews & MacLeod, 1994, 2005; J. M. Williams et aI.,1997, for reviews). Moreover, this attentional vigilance forthreat cues occurs at a very early stage of information pro-cessing, even before the information has entered the per-son's conscious awareness. If a person is already anxious,having her or his attention automatically focused on threatcues in the environment would seem only to maintain theanxiety or even make it worse. Moreover, recent evidencealso strongly supports the idea that such attentional biasesplay a causal role in anxiety as well (e.g., Mathews &MacLeod, 2002; MacLeod et aI., 2004). Generally anxiouspeople are also more likely than nonanxious people tothink that bad things are likely to happen in the future(A. K. MacLeod, 1999), and they have a much stronger ten-dency to interpret ambiguous information in a threateningway. For example, when clinically anxious subjects read aseries of ambiguous sentences (e.g., "The doctor examinedlittle Emma's growth" or "They discussed the priest's con-victions"), they are more likely than nonanxious controlsto remember the threatening interpretation of the sen-tences (Eysenck et al., 1991; see also MacLeod et aI., 2004;Richards, 2004).

In summary, several psychosocial variables seem topromote the onset of generalized anxiety as well as itsmaintenance. Experience with unpredictable and/oruncontrollable life events may create a vulnerability toanxiety and promote current anxiety. People also believethat worry serves a number of important functions, and itmay actually be reinforced because it dampens physiologi-cal arousal. But worry also has some negative consequence,including the fact that worry begets further worry and cre-ates a sense of perceived uncontrollability over the worryprocess, which further enhances anxiety. Finally, anxiety isassociated with an automatic attentional and interpretivebias toward threatening information.

Biological Causal FactorsGENETIC FACTORS Although evidence for genetic fac-tors in GAD is mixed, it does seem likely that there is amodest heritability, although perhaps smaller than formost other anxiety disorders (Hettema, Prescott, &Kendler, 2001; Kendler et aI., 1992a; Plomin et aI., 2001).Part of the problem for research in this area has been the

evolving nature of our understanding of GAD and whatits diagnostic criteria are. Several large twin studies revealexactly how heritability estimates vary as a function ofone's definition of GAD (Hettema et al., 2001; Kendleret al., 1992a). The largest and most recent of these twinstudies estimates the heritability of GAD at about 15 to 20percent.

The evidence is increasingly strong that GAD andmajor depressive disorder (to be discussed in Chapter 7)have a common underlying genetic predisposition(Kendler, 1996; Kendler et al., 1992d). What determineswhether individuals with a genetic risk for GAD and/ormajor depression develop one or the other disorder seemsto depend entirely on the specific environmental experi-ences they have (nonshared environment). This commongenetic predisposition for GAD and major depression isbest conceptualized as the basic personality trait com-monly known as neuroticism, a proneness to experiencenegative mood states (e.g., 1. A. Clark et al., 1994; Het-tema, Prescott, & Kendler, 2004; Mineka, Watson, &Clark,1998).

A FUNCTIONAL DEFICI ENCY OF GABA In the 1950s cer-tain drugs called the benzodiazepines were found toreduce anxiety. This discovery was followed in the 1970s bythe finding that the drugs probably exert their effects bystimulating the action of gamma aminobutyric acid(GABA), a neurotransmitter now strongly implicated ingeneralized anxiety (Barlow, 2002a; Davis, 2002; LeDoux,2002). It appears that highly anxious people have a kind offunctional deficiency in GABA, which ordinarily plays animportant role in the way our brain inhibits anxiety instressful situations. The benzodiazepine drugs appear toreduce anxiety by increasing GABA activity in certain partsof the brain implicated in anxiety, such as the limbic sys-tem, and by suppressing the stress hormone cortisol.Whether the functional deficiency in GABA in anxiouspeople causes their anxiety, or occurs as a consequence ofit, is not yet known, but it does appear that this functionaldeficiency promotes the maintenance of anxiety.

More recently, researchers have discovered thatanother neurotransmitter-serotonin-is also involved inmodulating generalized anxiety (Glitz & Balon, 1996;Goodman, 2004). At present, it seems that GABA, sero-tonin, and perhaps norepinephrine all playa role in anxi-ety, but the ways in which they interact remain largelyunknown (LeDoux, 2002).

THE CORTICOTROPHIN-RELEASING HORMONE SYS-TEM AND ANXIETY An anxiety-producing hormonecalled corticotrophin-releasing hormone (CRH) has alsobeen strongly implicated as playing an important role ingeneralized anxiety (and depression). When activated bystress or perceived threat, CRH stimulates the release ofACTH (adrenocorticotrophic hormone) from the pitu-

itary gland, which in turn causes release of the stress hor-mone cortisol from the adrenal gland (Thompson, 2000);cortisol helps the body deal with stress. The CRH hormonemay play an important role in generalized anxiety throughits effects on the bed nucleus of the stria terminalis (anextension ofthe amygdala; see Figure 6.1 on p. 199), whichis now believed to be an important brain area mediatinggeneralized anxiety (e.g., Lang, Davis, & Ohman, 2000).

NEUROBIOLOGICAL DIFFERENCES BETWEEN ANXI-ETY AND PANIC As we noted at the beginning of thischapter, contemporary theorists are drawing several fun-damental distinctions between fear, or panic, and anxiety,including their neurobiological bases. Fear and panicinvolve activation of the fight-or-flight response, and thebrain areas and neurotransmitters that seem moststrongly implicated in these emotional responses are theamygdala (and locus coeruleus) and the neurotransmit-ters norepinephrine and serotonin. Generalized anxietyor anxious apprehension is a more diffuse emotionalstate involving arousal and a preparation for possibleimpending threat, and the brain area, neurotransmitters,and hormones that seem most strongly implicated are thelimbic system (especially the bed nucleus of the stria ter-minalis, an extension of the amygdala), GABA, and CRH(Lang et al., 2000). Although serotonin may playa role inboth anxiety and panic, it probably does so in somewhatdifferent ways.

Treating GeneralizedAnxiety DisorderMany clients with generalized anxiety disorder consultfamily physicians, seeking relief from their "nerves" or anx-ieties and/or their various functional (psychogenic) physi-cal problems. Most often in such cases, medications fromthe benzodiazepine (anxiolytic) category such as Valiumare used-and misused-for tension relief, reduction ofother somatic symptoms, and relaxation. Their effects onworry and other psychological symptoms are not as great.Moreover, they can be quite habit forming and difficult totaper. A newer medication called buspirone (from a differ-ent medication category) also seems effective, and it is nei-ther sedating nor addictive. However, it may take severalweeks to show results (Glitz & Balon, 1996; Roy-Byrne &Cowley, 2002). Several categories of antidepressant med-ications are also useful in the treatment of GAD, and theyseem to have a greater effect on the psychological symp-toms than do the benzodiazepines (Goodman, 2004; Roy-Byrne & Cowley, 2002).

Cognitive-behavioral therapy (CBT) for generalizedanxiety disorder has also become increasingly effective asclinical researchers have refined the techniques used. Itusually involves a combination of behavioral techniquessuch as training in applied muscle relaxation, and cogni-

tive-restructuring techniques aimed at reducing distortedcognitions and information-processing biases associatedwith GAD, as well as reducing catastrophizing about minorevents (Borkovec, Newman, et aI., 2002; Roemer et aI.,2002). GAD initially appeared to be among the most diffi-cult of the anxiety disorders to treat, and to some extentthis is still true. However, advances have been made, and aquantitative review of 13 controlled studies showed thatCBT approaches resulted in large changes on most symp-toms measured (Borkovec & Ruscio, 2001).

[ '.":.-. I CBTlo. John's GAD

The case of John, the graduate student with GAD dis-cussed earlier, serves as an example of the success ofcognitive-behavioral therapy with this condition. Beforereceiving cognitive-behavioral therapy, John had seensomeone at a student counseling center for severalmonths, but he hadn't found the "talk therapy" very use-ful. He had heard that cognitive-behavioral therapy mightbe useful and had sought such treatment. He was in treat-ment for about 6 months, during which time he foundtraining in deep muscle relaxation helpful in reducing hisoverall level of tension. Cognitive restructuring helpedreduce his worry levels about all spheres of his life. Hestill had problems with procrastinating when he haddeadlines, but this too was improving. He also begansocializing more frequently and had tentatively begundating, when treatment ended for financial reasons. Hecould now see that if a woman didn't want to go out withhim again, this did not mean that he was boring but sim-ply that they might not be a good match.

In ReVIew~ What are the key characteristics of GAD, and

what is its typical age of onset?

~ Describe the various cognitive factors thatmay be involved in GAD, and indicate whatfunctions worry may serve for those with GAD.

~ What are the major biological causal factorsin GAD?

~ Compare and contrast the biological andcognitive-behavioral treatments for GAD.

OBSESSIVE-COMPULSIVEDISORDER ---' __Diagnostically, obsessive-compulsive disorder (OCD) isdefined by the occurrence of unwanted and intrusiveobsessive thoughts or distressing images; these are usu-ally accompanied by compulsive behaviors performed toneutralize the obsessive thoughts or images or to preventsome dreaded event or situation (see DSM table). Morespecifically, according to DSM -IV -TR, obsessionsinvolve persistent and recurrent intrusive thoughts,images, or impulses that are experienced as disturbingand inappropriate. People who have such obsessions tryto resist or suppress them, or to neutralize them withsome other thought or action. Compulsions can involveeither overt repetitive behaviors (such as hand washing,checking, or ordering) or more covert mental acts (suchas counting, praying, or saying certain words silently). A

Criteria for Obsessive-CompulsiveDisorder

A. Either obsessions or compulsions

Obsessions as defined by (all 4 required)

(1) recurrent and persistent thoughts, impulses or imagesthat are experienced at some time as intrusive andcause marked anxiety

(2) thoughts, impulses, or images are not simplyexcessive worries about real life problems

(3) person attempts to ignore or suppress or neutralizethem with some other thought or action

(4) person recognizes they are a product of his or herown mind

Compulsions as defined by (1 and 2)

(1) repetitive behaviors (hand washing, ordering,checking) or mental acts (praying, counting, etc.) theperson feels driven to perform in response to anobsession, or according to rigid rules

(2) behaviors or mental acts aimed at preventing orreducing distress or preventing some dreaded event orsituation

B. At least at some point person recognizes the obsessionsor compulsions are excessive or unreasonable

C. Obsessions or compulsions cause marked distress, aretime-consuming (more than 1 hour a day) or interferesignificantly with normal functioning

person with OCD usually feels driven to perform thiscompulsive ritualistic behavior in response to an obses-

sion, and there are often veryrigid rules regarding how thecompulsive behavior shouldbe performed. The compul-sive behaviors are performedwith the goal of preventing orreducing distress or prevent-ing some dreaded event orsituation.

In addition, the personmust recognize that the obses-sion is the product of his or herown mind rather than beingimposed from without (asmight occur in schizophrenia).However, there is a continuumof "insight" among obsessive-compulsives about exactly howsenseless and excessive theirobsessions and compulsionsare (Foa & Kozak, 1995; Steke-tee & Barlow, 2002). In aminority of cases, this insight isabsent most of the time.

The following is a fairlytypical case of severe obsessive-compulsive disorder.

People who suffer from oeD oftenexhibit repetitive behaviors that arestructured around rigid rules forperformance. For example, thisperson turns the key in the lock aset number of times every time sheleaves the house.

Obsessions aboutConfessing and CompulsiveChecking

Mark was a 28-year-old single male who, at the time heentered treatment, suffered from severe obsessivethoughts and images about causing harm to others suchas running over pedestrians while he was driving. He alsohad severe obsessions that he would commit a crimesuch as robbing a store of a large amount of money orpoisoning family members or friends. These obsessionswere accompanied by lengthy and excessive checking rit-uals. For example, one day when he drove, he beganobsessing that he had caused an accident and hit apedestrian at an intersection, and he felt compelled tospend several hours driving and walking around all partsof that intersection to find evidence of the accident.

At the time Mark went to an anxiety disorder clinic,he was no longer able to live by himself, after having livedalone for several years since college. He was a very brightyoung man with considerable artistic talent. He had fin-ished college at a prestigious school for the arts and hadlaunched a successful career as a young artist when the

obsessions began in his early twenties. At first they werefocused on the possibility that he would be implicated insome crime that he had not committed; later they evolvedto the point where he was afraid that he might actuallycommit a crime and confess to it. The checking rituals andavoidance of all places where such confessions mightoccur eventually led to his having to give up his careerand his own apartment and move back in with his family.

At the time he presented for treatment, Mark'sobsessions about harming others and confessing tocrimes (whether or not he had committed them) were sosevere that he had virtually confined himself to his roomat his parent's house. Indeed, he could leave his roomonly if he had a tape recorder with him so that he wouldhave a record of any crimes he confessed to out loud,because he did not trust his memory. The clinic was sev-eral hours' drive from his home; his mother usually had todrive because of his obsessions about causing accidentswith pedestrians or moving vehicles, and because theassociated checking rituals could punctuate any trip withseveral very long stops. He also could not speak at all onthe phone for fear of confessing some crime that he had(or had not) committed, and he could not mail a letter forthe same reason. He also could not go into a store aloneor into public bathrooms, where he feared he might writea confession on the wall and be caught and punished.

Prevalence, Age of Onset, andComorbidityObsessive-compulsive disorder is much more prevalentthan it was once thought to be (see Antony, Downie, &Swinson, 1998). Specifically, the average I-year prevalencerate of OCD in the National Comorbidity Survey-Replication was 1 percent, and the average lifetime preva-lence was 1.6 percent (Kessler, Berglund, et a1., 2005b,2005c), although estimates from the earlier Epidemiologi-cal Catchment Area study were slightly higher (1.6 oneyear, and 2.5 lifetime; Robins & Regier, 1991). These latterfigures appear to be similar in other cultures that have beenstudied (Steketee & Barlow, 2002). Over 90 percent ofthose people with OCD who come for treatment experi-ence both obsessions and compulsions (Foa & Kozak,1995). When mental rituals and compulsions such ascounting are included as compulsive behaviors, this figurejumps to 98 percent.

Divorced (or separated) and unemployed people areusually somewhat overrepresented among people withOCD (Kamo et a1., 1988), which is not surprising given thedifficulties this disorder creates for interpersonal andoccupational functioning. The results of the ECA studyshowed little or no gender difference in adults, whichmakes OeD quite different from most of the rest of theanxiety disorders. Although the disorder generally beginsin late adolescence or early adulthood, it is not uncommon

Many of us show some compulsive behavior, but people withobsessive-compulsive disorder feel compelled to performrepeatedly some action in response to an obsession, in order toreduce the anxiety or discomfort created by the obsession_Although the person may realize that the behavior is excessiveor unreasonable, he or she does not feel able to control the urge.Obsessive-compulsive hand washers may spend hours a daywashing, and may even use abrasive cleansers to the point thattheir hands bleed.

in children, where its symptoms are strikingly similar tothose of adults (March & Leonard, 1998; Steketee & Bar-low, 2002). Childhood or early adolescent onset is morecommon in boys than in girls and is often associated withgreater severity. In most cases the disorder has a gradualonset, but once it becomes a serious condition, it tends tobe chronic, although the severity of symptoms usuallywaxes and wanes over time (e.g., Mataix-Cols, Rauch,et aI., 2002; Stewart, Geller, et aI., 2004).

Like all the anxiety disorders, obsessive-compulsivedisorder frequently co-occurs with other mood and anxi-ety disorders. Depression is especially common, and esti-mates are that at least one-third of people with OCD mayexperience major depression at some time in their lives,and as many as 80 percent may experience significantdepressive symptoms (Steketee & Barlow, 2002). Given thechronic and debilitating nature of this disorder, it may notbe surprising that many develop depression at least partlyin response to having OCD. The anxiety disorders withwhich OCD most often co-occurs include social phobia,panic disorder, GAD, and PTSD (Kessler, Berglund, et aI.,200Sc). The personality disorders (see Chapter 11) mostcommonly found in people with OCD are dependent andavoidant.

Another related disorder that has been studied exten-sively only in the past 15 years-body dysmorphic disorder(BDD)-also co-occurs rather commonly with OCD. In

one large study, 12 percent of patients with OCD also hadbody dysmorphic disorder, which many researchersbelieve to be a closely related disorder (e.g., Phillips, 2000,2005; Simeon et aI., 1995; see Chapter 8 for a discussion ofbody dysmorphic disorder).

Most of us have experienced minor obsessive thoughts,such as whether we remembered to lock the door or turnthe stove off. In addition, most of us occasionally engage inrepetitive or stereotyped behavior, such as checking thestove or the lock on the door or stepping over cracks on asidewalk. With OCD, however, the thoughts are excessiveand much more persistent and distressing, and the associ-ated compulsive acts interfere considerably with everydayactivities. Nevertheless, research indicates that normal andabnormal obsessions and compulsive behaviors exist on acontinuum, differing primarily in the frequency and inten-sity of the obsessions and in the degrees to which theobsessions and compulsions are resisted and are troubling(Salkovskis & Kirk, 1997; Steketee & Barlow, 2002).

TYPES OF OBSESSIVE THOUGHTS Obsessive thoughtsconsist most often of contamination fears, fears of harm-ing oneself or others, and pathological doubt. Other fairlycommon themes are concerns about or need for symme-try, sexual obsessions, and obsessions concerning religionor aggression. These themes are quite consistent cross-culturally and across the life span (Gibbs, 1996; Steketee &Barlow, 2002).

Obsessive thoughts involving themes of violence oraggression might include a wife being obsessed with theidea that she might poison her husband or child, or adaughter constantly imagining pushing her mother downa flight of stairs. Even though such obsessive thoughts areonly very rarely carried out in action, they remain a sourceof often excruciating torment to a person plagued withthem. This pattern is particularly well illustrated in a clas-sic case described by Kraines (1948) of a woman who

complained of having "terrible thoughts." When shethought of her boyfriend she wished he were dead;when her mother went down the stairs, she "wishedshe'd fall and break her neck"; when her sister spoke ofgoing to the beach with her infant daughter, the patient"hoped that they would both drown." These thoughts"make me hysterical. I love them; why should I wishsuch terrible things to happen? It drives me wild, makesme feel I'm crazy and don't belong to society; maybe it'sbest for me to end it all than to go on thinking such ter-rible things about those I love." (p. 183)

TYPES OF COMPULSIONS People with OCD feelcompelled to perform acts repeatedly that often seempointless and absurd even to them and that they in some

.3 Compulsive Hoarding:Is It a Subtype of OCD?

Compulsive hoarding is a fascinating conditionthat has received less attention than otherforms of OCD. Shirley, a 24-year-old woman,described her classic hoarding symptoms asfollows:

For the past 7 years, I have saved virtually everythingthat has come into my ownership with the exception ofused Kleenexes, gum wrappers, torn movie tickets ...I save receipts, even ones for low-cost items, paperbags, boxes, newspapers, magazines, notes and liststo myself ... advertisements, empty ... bottles ... andjars, old TV guides, catalogs clothing I don't wearanymore and know I never will The worst is my mail.For the past 7 years, I have kept 99 percent of all themail I've received. Most of it I ... don't even open,because you can see that it is junk mail ... Even afterI read my personal mail, I save it. I save it all! .because ... I feel compelled to save everything Mybedroom at home is a monumental junk heap of allmy collections. Strewn and piled and boxed everywherein the most disorderly fashion are all the items I men-tioned. There is a narrow path from my bedroom door tomy bed and even there I walk on mail and newspapers.Aside from this path, there is no other place for me towalk .... And there are piles of my stuff in other parts ofthe apartment too, growing larger and larger every day.(Rapoport, 1989, pp. 190-91.)

Compulsive hoarding is a symptom seen in approxi-mately 10 to 30 percent of people diagnosed with OCD(Steketee & Frost, 2004). Many have other OCD rituals aswell, although some show only compulsive hoarding. Suchindividuals both acquire and fail to discard many posses-sions that seem useless or of very limited value. In addi-tion, their living spaces are very cluttered and disorganizedto the point of interfering with normal activities that wouldotherwise occur in those spaces, such as cleaning, cook-ing, and walking through the house. On average they aremore disabled than people with OCD without compulsivehoarding (Frost, Steketee, Williams, & Warren, 2000), and

they may be at risk for fire, falling, poor sanitation, andhealth risks (Frost, Steketee, & Williams, 2000).

Compulsive hoarding has only recently been the sub-ject of significant research, in part because of increasingrecognition that these individuals have a much poorerprognosis for treatment than do people without hoardingsymptoms (Steketee & Frost, 2004). Medications usuallyused to treat OCD are usually not effective in treating peo-ple with compulsive hoarding symptoms. Traditionalbehavioral therapy using exposure and response preven-tion is also less effective than in other forms of OCD,although there are some promising new behavioral treat-ments that may be more effective.

Other recent neuroimaging research has found thatpeople diagnosed with OCD who have compulsive hoard-ing symptoms also show patterns of brain activation in cer-tain areas when their symptoms are provoked differentfrom those of people diagnosed with OCD who do not havehoarding symptoms (Mataix-Cols, Wooderson, et aI., 2004;Saxena, Brody, et aI., 2004). This has led some to suggestthat people with compulsive hoarding may be a neurologi-cally distinct subgroup or variant of OCD (Saxena et aI.,2004). This conclusion would also be consistent with find-ings of lack of responsiveness to the same medicationsthat are often successful in reducing the severity of other

forms of OeD.But another possibility is that at least some people

with compulsive hoarding actually have a form of psy-chopathology distinct from OCD (Steketee & Frost, 2004).This would be consistent with findings that a substantialnumber of people with hoarding symptoms do not showother obsessive-compulsive symptoms. This possibilitywould also be consistent with another marked differencebetween people with compulsive hoarding and with otherforms of OCD: Compulsive hoarding symptoms are gener-ally not experienced as repugnant and are not resisted inthe same way that other obsessive-compulsive symptomsare (Steketee & Frost, 2004). Only further research will beable to help resolve this debate in the literature about therelationship of compulsive hoarding to other forms of OeD.

sense do not want to perform. There are of five primarytypes of compulsive acts: cleaning, checking, repeating,ordering/arranging, and counting (Antony et aI., 1998),and many people show multiple kinds of rituals. For asmaller number of people, the compulsions are to per-form various everyday acts (such as eating or dressing)extremely slowly (primary obsessional slowness), and for

others the compulsions are to have things exactly sym-metrical or "evened up" (Rasmussen & Eisen, 1991; Steke-tee & Barlow, 2002). Hoarding is another form ofcompulsive behavior that is only recently receiving researchattention (see Developments in Research 6.3).

Washing rituals vary from relatively mild ritual-likebehavior such as spending 15 to 20 minutes washing one's

hands after going to the bathroom, to more extremebehavior such as washing one's hands with disinfectantsfor hours every day to the point wherethe hands bleed. Checking rituals alsovary from relatively mild such as check-ing all the lights, appliances, and lockstwo or three times before leaving thehouse, to very extreme such as goingback to an intersection where onethinks one may have run over a pedes-trian and spending hours checking forany sign of the imagined accident,much as Mark did. Both cleaning andchecking rituals are often performed aspecific number of times and thus alsoinvolve counting. The performance ofthe compulsive act or the ritualizedseries of acts usually brings a feeling ofreduced tension and satisfaction, aswell as a sense of control, although thisanxiety relief is typically fleeting, whichis why the same rituals need to berepeated over and over (Rachman &Hodgson, 1980; Steketee & Barlow,2002).

(1947). According to this theory, neutral stimuli becomeassociated with frightening thoughts or experiences

through classical conditioning andcome to elicit anxiety. For example,touching a doorknob or shakinghands might become associated withthe "scary" idea of contamination.Once having made this association,the person may discover that the anx-iety produced by shaking hands ortouching a doorknob can be reducedby hand washing. Washing his or herhands extensively reduces the anxiety,and so the washing response is rein-forced, which makes it more likely tooccur again in the future when othersituations evoke anxiety about conta-mination (Rachman & Shafran,1998). Once learned, such avoidanceresponses are extremely resistant toextinction (Mineka, 2004; Mineka &Zinbarg, 1996; Salkovskis & Kirk,1997). Moreover, any stressors thatraise anxiety levels can lead to aheightened frequency of avoidanceresponses in animals or compulsiverituals in humans.

Several classic experiments con-ducted by Rachman and Hodgson(1980) supported this theory. Theyfound that for most people withOCD, exposure to a situation that

provoked their obsession (e.g., a doorknob or toilet seatfor someone with obsessions about contamination) didindeed produce distress, which would continue for amoderate amount of time and then gradually dissipate. Ifthe person was allowed to engage in the compulsive ritualimmediately after the provocation, however, her or hisanxiety would generally decrease rapidly (although onlytemporarily) and therefore reinforce the compulsive rit-ual. This model predicts, then, that exposure to fearedobjects or situations should be useful in treating OCD ifthe exposure is followed by prevention of the ritual,enabling the person to see that the anxiety will subsidenaturally in time without the ritual (see also Rachman &Shafran, 1998).

This is indeed the core of the most effective form ofbehavior therapy for OCD (see Developments in Practice6.4 on p. 219). Thus the early behavioral model has beenvery useful in helping us understand what factors maintainobsessive-compulsive behavior, and it has also generatedan effective form of treatment. However, it has not been sohelpful in explaining why people with OCD develop obses-sions in the first place and why they have such abnormalassessments of risk.

-..,.... ~ .. - '« • . •..0: .~ .... '0:"•........ . ... '~ .i..1.•. '

~. '

Howard Stern, as with other people whohave suffered from oeD, found relief in acompulsive act or ritualized series ofacts to bring about a feeling of reducedtension as well as a sense of control. Inhis book Miss America, Stern describesbehaviors such os turning pages inmagazines only with his pinky finger,walking through doors with the rightside of his body leading, and {lippingthrough television stations in aparticular order before turning the setoff. Obsessive-compulsive disorder ismore prevalent than it was oncethought to be and its prevolence rateshows little or no difference acrosscultures and between men and women.

CONSISTENT CHARACTERISTICSGiven its many variations, OCD is insome ways more homogeneous thanone might expect (Rasmussen & Eisen,1991). Certain characteristics seemconsistent across nearly all the differentclinical presentations: (1) Anxiety is the affective symptom(except with primary obsessional slowness). (2) Compul-sions usually reduce the anxiety to some degree, at least inthe short term. (3) Nearly all people afflicted with OCDfear that something terrible will happen to themselves orothers for which they will be responsible.

This latter consistent characteristic has led some todescribe OCD as a "what if" illness (Rasmussen & Eisen,1991). Most people with obsessive-compulsive disorderare continually worried about the possibility that some-thing terrible will happen-e.g., "The very fact that it iswithin the realm of possibility, however unlikely, that Iwill stab my baby, or poison my child, is enough to terrifyme so that I can think of nothing else no matter how hardI try" (Rasmussen & Eisen, 1991, p. 37). This tendency tojudge risks unrealistically seems to be a very importantfeature of OCD.

Psychosocial Causal FactorsTHE BEHAVIORAL VIEWPOINT The dominant behav-ioral view of obsessive-compulsive disorder derived fromO. H. Mowrer's two-process theory of avoidance learning

OCD AND PREPAREDNESS Just as the preparednessconcept has us consider specific and social phobias in ~heevolutionary context of fears that may have been adaptivefor our early ancestors, we have also enlarged our under-standing of obsessive-compulsive disorder by looking atit in an evolutionary context (e.g., De Silva, Rachman, &Seligman, 1977; Rapoport, 1989). For example, thoug~tsabout dirt and contamination associated with compulSIvewashing are so common as to make their occurrenceseem nonrandom. The overall consensus seems to be thathumans' obsessions with dirt and contamination and cer-tain other potentially dangerous situations did not ariseout of a vacuum but rather have deep evolutionary roots(Mineka & Zinbarg, 1996,2006).

In addition, some theorists have argued that the dis-placement activities that many species of animals engagein under situations of conflict or high arousal resemble thecompulsive rituals seen in obsessive-compulsive disorder(Craske, 1999; Mineka & Zinbarg, 1996; Rapoport, 1989;Winslow & Insel, 1991). Displacement activities ofteninvolve grooming (such as a bird preening his feathers) ornesting under conditions of high conflict or frustration.They may therefore be related to the distress-inducedgrooming (such as washing) or tidying rituals seen in peo-ple with OCD, which are often provoked by obsessivethoughts that provoke anxiety.

THE EFFECTS OF ATTEMPTING TO SUPPRESS OBSES-SIVE THOUGHTS When normal people attempt to sup-press unwanted thoughts (for example, "Don't think aboutwhite bears"), they may experience a paradoxical increasein those thoughts later (Abramowitz et al., 2001; Wegner,1994). In addition, two studies showed that if thought sup-pression occurs during a negative mood, a connection isproduced between the thought and the negative mood.When the negative mood occurred again later, the thoughtwas more easily experienced, or when the thought was laterexperienced, the mood returned (Wenzlaff, Wegner, &Klein, 1991).

As already noted, people with normal and abnormalobsessions differ primarily in the degree to which theyresist their own thoughts and find them unacceptable.Thus a major factor contributing to the frequency ofobsessive thoughts and negative moods may be theseattempts to suppress them (similar to what was discussedearlier about the effects of attempts to control worry inpeople with generalized anxiety disorder). For example,when people with OCD were asked to record intrusivethoughts in a diary, both on days when they were told totry to suppress those thoughts and on days withoutinstructions to suppress, the people with OCD reportedapproximately twice as many intrusive thoughts on thedays when they were attempting to suppress them(Salkovskis & Kirk, 1997). In addition, some other researchsuggests that thought suppression leads to a more general

increase in obsessive-compulsive symptoms beyond justthe frequency of obsessions (Purdon, 2004).

APPRAISALS OF RESPONSIBILITY FOR INTRUSIVETHOUGHTS Salkovskis (e.g., 1989), Rachman (1997),and others have distinguished between obsessive or intru-sive thoughts per se and the negative automatic thoughtsand catastrophic appraisals that people have about them.For example, people with OCD often seem to have aninflated sense of responsibility, possibly encouraged dur-ing childhood if parents instill extremely high standards orshow excessive criticism. In turn, this inflated sense ofresponsibility can in some vulnerable people be associatedwith beliefs that having a thought about doing something(e.g., hitting a pedestrian) is equivalent to actually ~av~ngdone it (e.g., having hit the pedestrian), or that thmkmgabout committing a sin is as bad as doing so (Steketee &Barlow, 2002). This is known as thought-action fusion (seeShafran & Rachman, 2004, for a review). This inflatedsense of responsibility for the harm they may cause adds tothe "perceived awfulness of any harmful consequences"(Salkovskis et al., 2000, p. 348), and also motivates com-pulsive behaviors such as compulsive washing and check-ing to try to reduce the likelihood of anything harmfulhappening. Part of what differentiates normal people whohave obsessions and can ordinarily dismiss them (withouta perception of responsibility) from people with OCD isthis sense of responsibility that makes the thought so"awful."

COGNITIVE BIASES AND DISTORTIONS Cognitivefactors have also been implicated in obsessive-compulsivedisorder. Research on people with OCD has shown thattheir attention is drawn to disturbing material relevant totheir obsessive concerns, much as occurs in the other anxi-ety disorders (see McNally, 2000, for a review). People withOCD seem to have difficulty blocking out negative irrele-vant input or distracting information, so they may attemptto suppress negative thoughts stimulated by this informa-tion (Enright & Beech, 1993a, 1993b; McNally, 2000). Aswe have noted, trying to suppress negative thoughts mayparadoxically increase their frequency. These people alsohave low confidence in their memory ability, which maycontribute to their repeating their ritualistic behaviors overand over again (Dar et aI., 2000; McNally, 2000).

Biological Causal FactorsIn the past 25 years there has been an explosion of researchinvestigating the possible biological basis for obsessive-compulsive disorder, ranging from studies about itsgenetic basis, to studies about brain and neurotransmitterabnormalities. The evidence accumulating from all threekinds of studies suggests that biological causal factors are

Basal GangliaI

IPutamen andGlobus pallidus

ICaudate Cerebralnucleus cortex

Cingulategyrus

Frontalcortex

/Thalamus Orbital frontal

cortexCorpuscallosum

Neurophysiological Mechanisms for Obsessive-Compulsive DisorderThe orbital frontal cortex and the basal ganglia (especially the caudate nucleus) are the brain structures most often implicated in OCO.Increased metabolic activity has been found in both the orbital frontal cortex and the caudate nucleus in people with OCO.

perhaps more strongly implicated in the causes of OCDthan in any of the other anxiety disorders.

GENETIC INFLUENCES Genetic studies have includedboth twin studies and family studies. Evidence from twinstudies reveals a moderately high concordance rate formonozygotic twins and a lower rate for dizygotic twins.One review of 14 published studies included 80 monozy-gotic pairs of twins, of whom 54 were concordant for thediagnosis of OCD, and 29 pairs of dizygotic twins, ofwhom 9 were concordant. This is consistent with a moder-ate genetic heritability (Billett, Richter, & Kennedy, 1998).Most family studies have also found substantially higherrates of OCD in first-degree relatives of OCD clients thanwould be expected from current estimates of the preva-lence of OCD (Hettema et al., 2001; Pauls et al., 1995).

Finally, the most compelling evidence of a geneticcontribution to some forms of OCD is for a form of OCDthat often starts in childhood and is characterized bychronic motor tics (Lochner & Stein, 2003). This form oftic-related OCD is linked to Tourette's syndrome, a disordercharacterized by severe chronic motor and vocal tics that issuspected to have a substantial genetic basis (see Chapter16). For example, one study found that 23 percent of first-degree relatives of people with Tourette's syndrome haddiagnosable OCD (Pauls et al., 1986, 1991, 1995). Overall,it seems that there is probably a moderate genetic contri-bution to OCD, although it may be a rather nonspecific

"neurotic" predisposition (Hanna, 2000; MacKinnon &Foley, 1996).

ABNORMALITIES IN BRAIN FUNCTION The search forabnormalities in the brains of people with OCD has beenintense in the past 20 years as advances have been made inbrain-imaging techniques. Findings from at least half adozen studies using PET scans have shown that peoplewith OCD have abnormally active metabolic levels in thecaudate nucleus, the orbital frontal cortex, and the cingu-late cortex. The caudate nucleus is part of the basal ganglia,which are a set of large nuclei lying just below the cerebralcortex; they in turn surround the thalamus (see Figure6.3). Moreover, activity in some of these areas is furtherincreased when symptoms are provoked by relevant pho-bic stimuli (see Evans, Lewis, & lobst, 2004; Rauch & Sav-age, 2000, for reviews). Some of these studies have alsoshown partial normalization of at least some of theseabnormalities with successful treatment through eithermedication or behavior therapy (Baxter et al., 2000; Sax-ena, Brody, et al., 2002).

Exactly how these areas are implicated is still unclear,although several different theories are currently beingtested. For example, Baxter and colleagues (1991, 2000)have speculated that part of the primary dysfunction inOCD may be in an area of the brain called the corpus stria-tum (which includes the caudate nucleus). The corpusstriatum/caudate nucleus (part of a set of structures called

the basal ganglia) is part of an important neural circuitlinking the orbital frontal cortex to the thalamus, which isan important relay station that receives nearly all sensoryinput and passes it back to the cerebral cortex. The orbitalfrontal cortex seems to be where primitive urges regardingsex, aggression, hygiene, and danger come from (the "stuffof obsessions"; Baxter et aI., 1991, p. 116). These urges areordinarily filtered by the caudate nucleus, allowing onlythe strongest to pass on to the thalamus.

This cortico-basal-ganglionic-thalamic circuit is nor-mally involved in the preparation of complex sets of inter-related behavioral responses used only in specificsituations such as those involved in territorial or socialconcerns. Baxter et ai. cite evidence that when this circuit isnot functioning properly, inappropriate behavioralresponses may occur, including repeated sets of behaviorsstemming from territorial and social concerns (e.g., check-ing and aggressive behavior) and from hygiene concerns(e.g., cleaning). Thus the overactivation of the orbitalfrontal cortex, combined with a dysfunctional interactionamong the corpus striatum/caudate nucleus, the orbitalfrontal cortex, and the thalamus (which is downstreamfrom the corpus striatum) may be the central componentof the brain dysfunction in OCD. This in turn preventspeople with OCD from showing the normal inhibition ofsensations, thoughts, and behaviors that would occur if thecircuit were functioning properly. In this case, impulsestoward aggression, sex, hygiene, and danger that most peo-ple keep under control with relative ease "leak through" asobsessions and distract people with OCD from ordinarygoal-directed behavior.

In summary, in people with OCD there seems to beoveractivation of the orbital frontal cortex, which deliversthe "stuff of obsessions" (Baxter et aI., 1991, p. 116). More-over, there is also a dysfunction of the cortico-basal-ganglionic-thalamic circuit, which leads to inappropriatebehavioral responses that are not inhibited as they ordi-narily would be. Considering these problems, we can beginto understand how the prolonged and repeated bouts ofobsessive-compulsive behavior in people with OCD mayoccur (Baxter et aI., 1991, 1992,2000).

THE ROLE OF SEROTONIN Pharmacological studies ofcausal factors in obsessive-compulsive disorder intensifiedwith the discovery in the 1970s that a drug called Anafranil(clomipramine) is often effective in the treatment of OCD.Clomipramine is closely related to other tricyclic antide-pressants (see Chapter 7) but is more effective in the treat-ment of OCD (Pigott & Seay, 2000). Research shows thatthis is because it has greater effects on the neurotransmit-ter serotonin, which is now strongly implicated in OCD(Pogarell, Hamann, Popper!, et aI., 2003). Moreover, sev-eral other antidepressant drugs from the SSRI categorythat also have relatively selective effects on serotonin, suchas fluoxetine (Prozac), have also been shown to be about

equally effective in the treatment of OCD (Dougherty,Rauch, & Jenike, 2002; Pigott & Seay, 2000).

The exact nature of the dysfunction in serotonergicsystems in OCD is unclear (see Gross, Sasson, Chopra, &Zohar, 1998; Murphy et aI., 1996). Current evidence sug-gests that increased serotonin activity and increased sensi-tivity of some brain structures to serotonin are involved inOCD symptoms. In this view, long-term administration ofclomipramine or fluoxetine causes a down-regulation ofcertain serotonin receptors, causing a functional decreasein availability of serotonin (Dolberg et aI., 1996a, 1996b).That is, although the immediate short-term effects ofclomipramine or fluoxetine may be to increase serotoninlevels (and exacerbate OCD symptoms too), the long-termeffects are quite different. This is consistent with the find-ing that these drugs must be taken for at least 6 to 12 weeksbefore significant improvement in OCD symptoms occurs(Baxter et aI., 2000; Dougherty et aI., 2002). However, it isalso becoming clear that dysfunction in serotonergic sys-tems cannot by itself fully explain this complex disorder.Other neurotransmitter systems also seem to be involvedalthough their role is not yet well understood (Baxter et aI.,2000; Hollander et aI., 1992).

In summary, there is now a substantial body of evi-dence implicating biological causal factors in OCD. Thisevidence comes from genetic studies, from studies of brainstructure and functioning, and from psychopharmacolog-ical studies. Although the exact nature of these factors andhow they are interrelated is not yet understood, majorresearch efforts that are currently under way are sure toenhance our understanding of this very serious and dis-abling disorder.

Treating Obsessive-CompulsiveDisorderA behavioral treatment that combines exposure andresponse prevention may be the most effective approachto obsessive-compulsive disorders (e.g., Franklin & Foa,1998, 2002; Steketee & Barlow, 2002). This treatmentinvolves having the OCD clients repeatedly expose them-selves to stimuli that will provoke their obsession (such as,for someone with compulsive washing, touching the bot-tom of their shoe or a toilet seat in a public bathroom) andthen preventing them from engaging in their compulsiverituals, which they ordinarily would engage in to reducethe anxiety/distress provoked by their obsession. Prevent-ing the rituals is essential so that they can see that the anx-iety created by the obsession will dissipate naturally if theyallow enough time to pass. This treatment is examined inmore detail in Developments in Practice 6.4.

This treatment tends to help clients who stick with thetreatment, most of whom show a 50 to 70 percent reduc-tion in symptoms (Steketee, 1993). About 50 percent aremuch improved or very much improved, and another 25

.4 Exposure and ResponsePrevention as Treatmentsfor Obsessive-Compulsive Disorder

rr: oa and Franklin (2001, pp. 241-48; see alsoSteketee & Foa, 1985) presented the follow-ing case as an illustration of their recom-mended approach to the behavioraltreatment of obsessive-compulsive disor-

ders. The patient, June, was a 26-year-old, recently marriednursing graduate who complained of washing and cleaningproblems so severe that she was unable to seek work inher profession. On initial evaluation she was agitated anddistressed, feeling helpless to control her need to take atleast two 45-minute showers daily (each with a lot ofcounting and ordering rituals) and to wash her hands some20 times a day for 5 minutes or more. She also spent agreat deal of time wiping various objects with alcohol.Inquiry soon determined that she was terrified of becoming"contaminated," particularly by "dog dirt" and bathroomgerms mostly coming from human feces, and she tookgreat pains to avoid anything that could have had contactwith either dog dirt or bathroom germs. She also had prob-lems with garbage and with dead animals on the road. Pre-vious treatments had been ineffective. Her relationshipwith her husband was very stressed because of her hus-band's frustration with her excessive cleanliness.

Exposure TreatmentThe therapist and patient worked together to create a hier-archy of upsetting stimuli, rating them on a scale of 1through 100 according to their capacity to evoke disgust andthe impulse to wash. For example, the patient gave ratingsof 100 to touching "dog dirt" (if unable to wash immedi-ately), 90 to automobile tires (which might have contacted adead animal), 90 to garbage cans outdoors (but only 50 togarbage in her own sink), and 40 to the outside doorknob ofa public bathroom (the inside doorknob rated 80 and a pub-lic toilet seat 95). Subsequently, in treatment sessions fivetimes weekly, June was instructed to expose herself deliber-ately to these stimuli either in guided fantasy or directly,beginning with those rated relatively low in the hierarchyand moving gradually to the more severely threateningones. Systematic exposure continued until the patientappeared at ease with a particular confrontation and herdiscomfort rating of it dropped to the range of 40 to 50.

In addition to the exposures conducted during ther-apy sessions, "homework" was liberally assigned. Subjec-

tive ratings of discomfort were carefully monitored duringthese encounters. On one occasion well into treatment, thetherapist drove with the patient to a place where she hadobserved a dead cat on the roadside and insisted that thepatient approach the "smelly" corpse, touch it with thesole of her shoe, and then touch her shoe. A pebble lyingclose by and a stick with which she had touched the catwere presented to the patient with the instruction that shekeep them in her pocket and touch them frequentlythroughout the day. The patient was also told to drive hercar past the spot on subsequent days.

Response PreventionAfter obtaining June's commitment to the full treatmentprocedure, the therapist instituted a no-washing rule afterthe first exposure session. Specifically, the patient was toremain completely unwashed for a period of 3 days, afterwhich she could take a 1Q-minute shower to be followed byanother wash-free 3 days. As anticipated, June was notablyupset by this proposed regimen and strongly doubted thatshe could carry it off. The therapist was encouraging butinsistent, promising support through the hard times, andthe patient was indeed successful. The transition to "nor-mal washing and cleaning behavior" was instituted shortlybefore the end of the planned 15 therapy sessions of sev-eral hours each. This plan consisted of one 1Q-minuteshower per day and 30-second hand washings not toexceed five per day at mealtimes, after bathroom use, andafter touching clearly soiled or greasy objects.

In an evaluation 9 months following the initiation oftreatment, June described herself as "definitely a lotbetter ... maybe about 80 percent better." She acknowl-edged that she still had obsessions "once every week ortwo" (most often still about dog feces), but she was nowemployed and her relationship with her husband was muchimproved. She felt she was living a "normal life."

As Foa and Franklin (2001) and Steketee and Foa(1985) have pointed out, obsessive-compulsive disordersrarely remit completely; even a successfully treated patientusually has some residual obsessive problems or rituals,as in June's case. The behavioral treatment undertakenhere was of course rigorous and demanding, but it appearsto have been the treatment of choice.

percent are moderately improved. These results are consid-ered superior to those obtained with medication (Franklin& Foa, 2002; Steketee & Barlow, 2002).

The successful use of this treatment in the case ofMark, the young artist with severe OeD, is described herebriefly.

Mark was initially treated with medication and with expo-sure and response prevention. He found the side effectsof the medication (clomipramine) intolerable and gave itup within a few weeks. For the behavioral treatment, hewas directed to get rid of the tape recorder and was givena series of exercises in which he exposed himself tofeared situations where he might confess to a crime orcause harm to others, including making phone calls, mail-ing letters, and entering stores and public bathrooms(all things he had been unable to do). Checking rituals(including the tape recorder) were prevented. Althoughthe initial round of treatment was not especially helpful,in part because of difficulty in getting to treatment, he dideventually make a commitment to more intensive treat-ment by moving to a small apartment closer to the clinic.Thereafter, he did quite well.

To date, medications that affect the neurotransmitterserotonin seem to be the primary class of medication thathas reasonably good effects in the treatment of personswith OCD. The other anxiety and mood disorders respondto a wider range of drugs (Dougherty, Rauch, & Jenike,2002; Pigott & Seay, 2000). These medications that alterfunctioning of the serotonin system, such as clomipramine(Anafranil) and fluoxetine (Prozac), appear to reduce theintensity of the symptoms of this disorder; approximately50 to 70 percent of OCD clients show at least a 25 percentreduction in symptoms (relative to 4 to 5 percent onplacebo; Iancu et aI., 2000; Pigott & Seay, 2000). Someclients may show greater improvement than this, but about30 to 50 percent do not show any clinically significantimprovement.

A major disadvantage of medication treatment forOCD, as for other anxiety disorders, is that when the med-ication is discontinued, relapse rates are generally veryhigh (as high as 90 percent) following discontinuation ofthe medication (Dolberg et aI., 1996a, 1996b; Franklin &Foa, 2002). Thus many people who do not seek alternativeforms of behavior therapy that have more long-lastingbenefits may have to stay on these medications indefinitely.Studies in adults have generally not found combiningmedication with exposure and response prevention to bemuch more effective than behavior therapy alone(Franklin & Foa, 2002; Foa, Liebowitz, & Kozak, 2005),although one recent study showed that a combinationtreatment was superior in the treatment of children andadolescents with OCD (Pediatric OCD Treatment Study,2004).

Finally, because OCD in its most severe form is such acrippling and disabling disorder, in recent years psychia-trists have begun to reexamine the usefulness of certainneurosurgical techniques for the treatment of severeintractable OCD (which may afflict as many as 10 percentof people diagnosed with OCD; Mindus, Rasmussen, &Lindquist, 1994). Before such surgery is even contem-plated, the person must have had severe OCD for at least 5years and must not have responded to any of the knowntreatments discussed so far (medication or behavior ther-apy). Several studies have shown that approximately one-third of these intractable cases respond quite well toneurosurgery designed to destroy brain tissue in one of theareas implicated in this condition (Dougherty et aI., 2002;Jenike, 2000). The results of these techniques will be dis-cussed in greater detail in Chapter 17.

In ReVIew~ Summarize the major symptoms of

obsessive-compulsive disorder.

~ How have conditioning and cognitive factorsbeen implicated in OCD?

~ What are the major biological causal factorsfor OeD?

~ Describe the major treatment approaches forOeD and their relative advantages anddisadvantages.

SOCIOCULTURAL CAUSALFACTORS FOR ALLANXIETY DISORDERSCross-cultural research suggests that although anxiety is auniversal emotion, and anxiety disorders probably exist inall human societies, there are some differences in preva-lence and in the form in which the different disorders areexpressed in different cultures (Barlow, 2002a; Good &Kleinman, 1985; Kirmayer, Young, & Hayton, 1995).Within the United States, however, prevalence rates of thedifferent anxiety disorders are quite similar across differentracial groups, including whites, African-Americans, andHispanic Americans, although phobic disorders are some-what more common among African-Americans and His-panic Americans.

However, Latin Americans from the Caribbean, andother people from the Caribbean, do show higher rates of

a variant of panic disorder called ataque de nervios (Bar-low, 2002a; Liebowitz et al., 1994) than do other groups.Most of the symptoms of ataque de nervios are the same asin a panic attack but may also include bursting into tearsand uncontrollable shouting. Other symptoms can includetrembling, verbal or physical aggression, dissociative expe-riences, and seizure-like or fainting episodes. Such attacksare often associated with a stressful event relating to thefamily (e.g., news of a death) and the person may haveamnesia for the episode (APA, DSM-IV-TR, 2000).

Looking at anxiety disorders from a cross-nationalperspective, one recent study of over 60,000 people across14 countries (8 developed and 6 less developed) by theWorld Health Organization (WHO World Mental HealthSurvey Consortium, 2004) showed that anxiety disorderswere the most common category of disorder reported inall but one country (Ukraine), but that reported preva-lence rates for all the anxiety disorders combined variedfrom 2.4 percent (Shanghai, China) to 18.2 percent(United States). Other countries with moderately highrates of reported anxiety disorders were Colombia, France,and Lebanon, and other countries with moderately lowrates were China, Japan, Nigeria, and Spain. We now turnto several examples of cultural variants on anxiety disor-ders that illustrate the range of expressions of anxiety thatare exhibited worldwide.

Cultural Differences in Sourcesof WorryIn the Yoruba culture of Nigeria, there are three primaryclusters of symptoms associated with generalized anxiety:worry, dreams, and bodily complaints. However, thesources of worry are very different than in Western soci-ety; they focus on creating and maintaining a large familyand on fertility. Dreams are a major source of anxietybecause they are thought to indicate that one may bebewitched. The common somatic complaints are alsounusual from a Western standpoint: "I have the feeling ofsomething like water in my brain," "Things like ants keepon creeping in various parts of my brain," and "I am con-vinced some types of worms are in my head" (Ebigbo,1982; Good & Kleinman, 1985). Nigerians with this syn-drome often have paranoid fears of malevolent attack bywitchcraft (Kirmayer et al., 1995). In India also there aremany more worries about being possessed by spirits andabout sexual inadequacy than are seen in generalized anx-iety in Western cultures (Carstairs & Kapur, 1976; Good &Kleinman, 1985).

Another culture-related syndrome that occurs inplaces like China is Koro, which for men involves intense,acute fear that the penis is shrinking into the body and thatwhen this process is complete, the sufferer will die. Korooccurs less frequently in women, for whom the fear is thattheir nipples are retracting and their breasts shrinking.

Koro tends to occur in epidemics-especially in culturalminority groups when their survival is threatened. Itoccurs in a cultural context where there are serious con-cerns about male sexual potency (Barlow, 2002a; Kirmayeret al., 1995).

Taijin KyofushoThere is also some evidence that the form that certain anx-iety disorders take has actually evolved to fit certain cul-tural patterns. A good example is the Japanese disordertaijin kyofusho (TKS), which is related to the Western diag-nosis of social phobia. Like social phobia, it is a fear ofinterpersonal relations or of social situations (Kirmayer,1991; Kleinknecht et al., 1997; Tseng et al., 1992). However,Westerners with social phobia are afraid of social situa-tions where they may be the object of scrutiny or criticism.By contrast, most people with TKS are concerned aboutdoing something that will embarrass or offend others(Barlow, 2002a). For example, they may fear offendingothers by blushing, emitting an offensive odor, or staringinappropriately into the eyes of another person, orthrough their perceived physical defects or imagineddeformities. This fear of bringing shame on others oroffending them is what leads to social avoidance(Kleinknecht et al., 1997). Two of the most commonsymptoms (phobias about eye contact and blushing) arenot mentioned in the DSM-IV- TR description of socialphobia (Kirmayer, 1991). Body dysmorphic disorder-the fear that some part of the body is defective or mal-formed (see Chapter 8)-also commonly occurs in TKSsufferers.

Kirmayer (1991) and colleagues (1995) have arguedthat the pattern of symptoms that occurs in taijin kyofushohas clearly been shaped by cultural factors. Japanese chil-dren are raised to be highly dependent on their mothersand to have a fear of the outside world, especially strangers.As babies and young children, they are praised for beingobedient and docile. There is also a great deal of emphasison implicit communication-being able to guess another'sthoughts and feelings and being sensitive to them. Peoplewho make too much eye contact are likely to be consideredaggressive and insensitive, and children are taught to lookat the throat of people with whom they are conversingrather than into their eyes. The society is also very hierar-chical and structured, and many subtleties in language andfacial communication are used to communicate one'sresponse to social status.

At a more general level, cross-cultural researchershave noted that recognition of the cognitive component ofmost anxiety disorders leads one to expect many cross-cultural variations in the form that different anxiety dis-orders take. Anxiety disorders can be considered, at leastin part, disorders of the interpretive process. Because cul-tures influence the categories and schemas that we use to

interpret our symptoms of distress, there are bound to besignificant differences in the form that anxiety disorderstake in different cultures (e.g., Barlow, 2002a; Good &Kleinman, 1985; Kirmayer et aI., 1995).

~ The anxiety disorders have anxiety or panic or both attheir core. They were initially considered a subset ofthe neuroses, but recent versions of the DSM-III andDSM-IV-TR have largely abandoned this term.

~ Fear or panic is a basic emotion that involvesactivation of the fight-or-flight response of theautonomic nervous system.

~ Anxiety is a more diffuse blend of emotions thatincludes high levels of negative affect, worry aboutpossible threat or danger, and the sense of beingunable to predict threat or to control it if it occurs.

~ Anxiety and panic are each associated with a numberof distinct anxiety disorder syndromes.

~ With specific phobias, there is an intense andirrational fear of specific objects or situations; whenconfronted with a feared object, the phobic personoften shows activation of the fight-or-flight response,which is also associated with panic.

~ Many sources of fear and anxiety are believed tobe acquired through conditioning or otherlearning mechanisms. However, some people(because of either temperamental or experientialfactors) are more vulnerable than others toacquiring such responses.

~ We seem to have a biologically basedpreparedness to acquire readily fears of objectsor situations that posed a threat to our earlyancestors.

~ In social phobia, a person has disabling fears of oneor more social situations usually because of fears ofnegative evaluation by others or of acting in anembarrassing or humiliating manner; in some cases a

In ReVIew~ What are some examples of cultural

differences in sources of worry?

~ How is taijin kyofusho related to socialphobia, and what kinds of cultural forcesseem to have shaped it?

person with social phobia may actually experiencepanic attacks in social situations.

~ We seem to have an evolutionarily basedpredisposition to acquire fears of social stimulisignaling dominance and aggression from otherhumans.

~ People with social phobia are also preoccupiedwith negative self-evaluative thoughts that tendto interfere with their ability to interact in asocially skillful fashion.

~ In panic disorder, a person experiences unexpectedpanic attacks that often create a sense of stark terror,which usually subsides in a matter of minutes.

~ Many people who experience panic attacksdevelop anxious apprehension aboutexperiencing another attack; this apprehension isrequired for a diagnosis of panic disorder.

~ Many people with panic disorder also developagoraphobic avoidance of situations in whichthey fear that they might have an attack.

~ The conditioning theory of panic disorderproposes that panic attacks cause theconditioning of anxiety primarily to external cuesassociated with the attacks, and conditioning ofpanic itself primarily to interoceptive cuesassociated with the early stages of the attacks.

~ The cognitive theory of panic disorder holds thatthis condition may develop in people who areprone to making catastrophic misinterpretationsof their bodily sensations, a tendency that maybe related to preexisting high levels of anxietysensitivity.

~ Other biological theories of panic disorderemphasize that the disorder may result frombiochemical abnormalities in the brain as well asabnormal activity of the neurotransmittersnorepinephrine and serotonin.

~ Panic attacks may arise primarily from the brainarea called the amygdala, although many otherareas are also involved.

~ In generalized anxiety disorder, a person has chronicand excessively high levels of worry about a numberof events or activities and responds to stress withhigh levels of psychic and muscle tension.

~ Generalized anxiety disorder may occur in peoplewho have had extensive experience withunpredictable and/or uncontrollable life events.

~ People with generalized anxiety seem to haveschemas about their inability to cope withstrange and dangerous situations that promoteworries focused on possible threats.

~ The neurobiological factor most implicated ingeneralized anxiety is a functional deficiency inthe neurotransmitter GABA, which is involved ininhibiting anxiety in stressful situations; thelimbic system is the brain area most involved.

~ Thus different neurotransmitters and brain areas areinvolved in panic attacks and generalized anxiety.

~ In obsessive-compulsive disorder, a personexperiences unwanted and intrusive distressingthoughts or images that are usually accompanied bycompulsive behaviors performed to neutralize thosethoughts or images. Checking and cleaning rituals aremost common.

~ Biological causal factors also seem to beinvolved in obsessive-compulsive disorder, with

evidence coming from genetic studies, studies ofbrain functioning, and psychopharmacologicalstudies.

~ Once this disorder begins, the anxiety-reducingqualities of the compulsive behaviors may help tomaintain the disorder.

~ Once a person has an anxiety disorder, mood-congruent information processing, such asattentional and interpretive biases, seems to helpmaintain it.

~ Many people with anxiety disorders are treated byphysicians, often with medications designed to allayanxiety or with antidepressant medications that alsohave anti-anxiety effects.

~ Such treatment focuses on suppressing thesymptoms, and some medications have addictivepotential.

~ Once the medications are discontinued, relapserates tend to be high.

~ Behavioral and cognitive therapies have a very goodtrack record with regard to treatment of the anxietydisorders.

~ Behavior therapies focus on prolonged exposureto feared situations; with obsessive-compulsivedisorder, the rituals also must be preventedfollowing exposure to the feared situations.

~ Cognitive therapies focus on helping clientsunderstand their underlying automatic thoughts,which often involve cognitive distortions such asunrealistic predictions of catastrophes that inreality are very unlikely to occur. Then they learnto change these inner thoughts and beliefsthrough a process of logical reanalysis known ascognitive restructuring.

agoraphobia (P. 195)

amygdala (P. 199)

anxiety (P. 181)

anxiety disorders (P. 180)

anxiety sensitivity (P. 201)

blood-injection-injury phobia(P. 185)

compulsions (P. 211)

fear (P. 181)

generalized anxiety disorder (GAD)(p.205)

interoceptive fears (P. 205)

neuroses (P. 180)

neurotic behavior (P. 180)

obsessions (P. 211)

obsessive-compulsive disorder(OCD) (P. 211)

panic (P. 181)

panic disorder (P. 194)

panic provocation agent (P. 198)

phobia (P. 183)

social phobia (P. 190)

specific phobia (P. 183)

006 - Chapter 6 - Panic, Anxiety, And Their Disorders

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