Anxiety Disorders Research Paper

Separation Anxiety Disorder

Separation anxiety disorder (SAD) is the most common anxiety disorder experienced by children, accounting for approximately one-half of children seen for mental health treatment of anxiety disorders (Bell-Dolan, 1995). SAD has also been associated with later risk of anxiety disorders such as panic disorder in adolescence and adulthood (Lease & Strauss, 1993). The key feature of SAD is excessive anxiety and fear concerning separation from home or from those to whom the child is attached. Such anxiety must be inappropriate given the age and expected developmental level of the child. Although separation anxiety has been recognized and studied as a characteristic of normal development for many years (Bowlby, 1970; Freud, 1958) it was not treated as a distinct clinical diagnostic category until the 1980 publication of the DiagnosticandStatisticalManualofMentalDisorders–Third Edition (DSM-III), which described SAD as one of three distinct anxiety disorders of childhood.

Clinical Presentation

Separation anxiety is well recognized as one of the normal, developmentally related fears that arise and dissipate at reasonably predictable times during childhood (Pianta, 1999). Separation fears are said to peak between the ages of 9 and 13 months, and occur among children all over the world (Barlow, 2002; Marks, 1987b). For most children, separation anxiety begins to decrease after about 2 years 6 months of age. This typically occurs through a process of experiencing progressively longer and gradual separation experiences that are not accompanied by aversive consequences (Bernstein & Borchardt, 1991). Given that separation anxiety is a normal developmental phenomenon in infancy and toddlerhood, the SAD diagnosis is given only if the child’s level of anxiety during separation is inappropriate considering the child’s age and developmental level, and significantly interferes with the child’s healthy functioning.

The defining feature of SAD is an excessive and unrealistic fear of separation from an attachment figure, usually a parent. This anxiety reaction must persist for a period of 2 weeks and mustbewellbeyondthatnormallyseeninotherchildrenofthe child’s developmental level (American Psychiatric Association [APA], 1994, p. 113). This fear is expressed through excessive and persistent worry about separation, behavioral and somatic distress when faced with separation situations, and persistent avoidance of or attempts to escape from such situations (Albano, Chorpita, & Barlow, 1996; Bell-Dolan, 1995). Children’s separation worries include worries that a parent will leave and never return, or worries that they themselves will be lost, kidnapped, or killed. In younger children, repeated nightmares containing themes of separation are common (Francis, Last, & Strauss, 1987).

Young children with SAD often display disruptive, oppositional behaviors as well as avoidance behaviors that cause significant interference in child and family functioning and in normal social development (Tonge, 1994). It is not uncommon for young children with SAD to begin to avoid social situations that involve separation from a caregiver, such as playing with friends or going to birthday parties. Young children may be very clingy with parents, often refusing to play in a different room of the house or outside unless a parent is present. Young children may become desperate in their attempts to contact parents. Academic performance may be compromised by repeated requests to leave class or a refusal to attend school, or by the child’s preoccupation with separation concerns. In addition, young children with SAD often display disruptive behaviors at bedtime, including refusing to sleep in their own rooms, begging to sleep with a parent, and crying and pleading to have siblings sleep with them. For older children, the avoidance of separation may cause them to refuse to engage in appropriate peer activities (e.g., sports, clubs, sleepovers) without a parent present (Albano et al., 1996).

Children diagnosed with SAD are more likely to report somatic complaints than children diagnosed with phobic disorders (Last, 1991). Children often complain of physical symptoms, such as headaches or gastrointestinal upset, and display disruptive behaviors such as temper tantrums, crying, or pleading. These physical symptoms and somatic complaints can lead to secondary consequences that further complicate matters for the child and family. Frequent visits to the family doctor occur and often lead to costly medical investigations. In a review of 95 children admitted to a psychiatry inpatient unit, children with SAD reported a significantly greater number of medically unexplained physical symptoms than those with other diagnoses (Livingstone, Taylor, & Crawford, 1988). Reports of abdominal pain and heart palpitations were significantly more likely in children with separation anxiety than in children with other psychopathological disorders. Pediatric headache, which is often associated with a high state of general arousal and muscle tension in the head and neck (Tonge, 1994), is another symptom often seen in children with SAD. These physical symptoms often lead to immediate care and attention from the parent, which results in positive reinforcement and secondary gain that may further perpetuate the problem.

Prevalence and Demographics

In the past 10 years there have been a number of epidemiological studies reporting the prevalence rates of various anxiety disorders in nonreferred young children. These studies indicate that anxiety disorders are probably one of the most common (if not the most common) categories of childhood disorder (Bernstein & Borchardt, 1991; Eisen, Engler, & Geyer, 1998). SAD has been said to be the most common anxiety disorder seen in children and adolescents, with epidemiological studies reporting that as many as 41% of children experience separation concerns, while between 5% and 10% show a clinical level of separation anxiety (Costello & Angold, 1995). Most clinical researchers agree that it is quite common for even very young children (aged 3 years and older) to experience excessive separation distress that causes significant interference in social, academic, and family functioning.

Comorbidity

Children with SAD often report a variety of specific fears in addition to their separation fears. These include fears of monsters, animals, and insects, fear of the dark, and fear of getting lost, although such fears may or may not be of phobic proportion (Last, Francis, & Strauss, 1989). In addition, there is considerable evidence of a high level of comorbidity between SAD and depression (Werry, 1991). For example, Werry (1991) indicated that one-third of children with SAD presented with a comorbid depressive disorder that developed several months following the onset of SAD. In more severe cases, children with SAD may threaten to harm themselves in attempts to escape or avoid separation situations (Last, 1991).

Cultural Influences

There has been relatively little research conducted about the possible influences of ethnic and cultural factors on the development and phenomenology of SAD in children, and some of these studies have had conflicting results. For example, one study found that children with SAD were primarily Caucasian (Last, Hersen, Kazdin, Finkelstein, & Strauss, 1987), yet other studies have reported that anxiety symptoms are more common in black than white childern. Such findings may have been biased, however, by the demography of the area served by the clinic, and the extent to which various ethnic groups used clinical services.

Other research has shown that children all over the world have reported feelings of anxiety upon separation (e.g., Chiland & Young, 1990). However, for some children who are raised in cultures that have extended families living together, it is possible that these children would have less opportunity to be left alone, or to have to separate from a primary caregiver. It is possible children from certain cultures may have the opportunity to develop secure attachments with several caregivers. For children whose schooling is conducted in or close to the home, there may be fewer opportunities for children to develop such separation fears. Overall, very little research has been conducted to date on the influence of culture on the epidemiology, symptom presentation, or progression of anxiety disorders in children, leaving the area relatively uncharted and open to future research.

Developmental Changes and Course

Although SAD first presents in the preschool child, the mean age of presentation of the disorder to a clinical setting has been reported to be around 9 years (Last, Francis, Hersen, & Kazdin, 1987). SAD has also been found to be more prevalent in prepubertal children than in adolescents (Geller, Chestnut, Miller, Price, & Yates, 1985). There are a number of developmental differences in the presentation and phenomenology of SAD. Francis et al. (1987) evaluated 45 children and adolescents (aged 5–16) with SAD and found no gender differences on each of the symptom criteria for the disorder. However, there were age differences with regard to which criteria were most frequently endorsed. Young children (aged 5–8) endorsed the greatest number of symptoms, and were most likely to report fears of unrealistic harm, nightmares about separation, or school refusal; older children (aged 9–12) endorsed excessive and severe distress at the time of separation; adolescents (aged 13–16) most often endorsed somatic complaints and school refusal.

Etiology

Role of Temperament

There are no empirically validated theories on the development of SAD. Because separation anxiety is normal and adaptive for infants and small children, SAD has been conceptualized as a failure to transition from this developmental stage. However, recent research about the development of SAD indicates that its onset is most likely due to the interaction of environmental events and stresses, temperamental characteristics, developmental experiences of care and attachment, and various biological vulnerabilities. Studies by Kagan and colleagues (Kagan, 1989; Kagan, Reznick, & Snidman, 1987) have carefully demonstrated the persistence of the temperamental characteristic of behavioral inhibition from early childhood to the age of 7 years. It has been suggested that this behavioral inhibition might indicate anxiety proneness. Specific temperamental characteristics such as behavioral inhibition have not yet been associated with the specific development of SAD, and this hypothesis remains to be explored.

Attachment

Developmental theorists have identified the period of early childhood as a critical period for the development of attachment, and the organization of the child-caregiver system during this period will set the stage for later development (Hofer, 1994; Thompson, 1991). Thus, developmentally oriented theories of psychopathology highlight the importance of targeting the child-caregiver dyadic system in assessment and intervention of early childhood disorders (Lieberman, 1992; Sroufe, 1985). Child-parent relationships are frequently identified as predictors and correlates of childhood adjustment or psychopathology (Pianta, 1999).According to attachment theory, an early attachment pattern characterized by consistency, responsiveness, and warmth is considered an antecedent to healthy development (Campbell, 1989; Greenberg, Speltz, & DeKlyen, 1993). Thus, common and successful treatment regimens for the period of early childhood frequently involve rearranging dyadic caregiving interactions or family interactions to promote secure, healthy attachment between parents and children (e.g., Kazdin, 1992; Schuhmann, Foote, Eyberg, Boggs, &Algina, 1998).

Main, Kaplan, and Cassidy (1985) have reported a strong relation between security of infant attachment and separation anxiety at 6 years of age. Children in this study who were securely attached as infants responded to the question of what they would do during a 2-week separation from their parents, with answers indicating effective behavior directed toward others (e.g., express disappointment to the parents, persuade them not to leave), thus showing a working model of accessibility pertaining to the attachment figures. Main et al. (1985) suggested that such an internal sense would help the child deal with real separations. Children in the study who were insecurely attached infants, however, indicated that they did not know what they would do during a 2-week separation from their parents, although some children gave responses characterized by fears of harm on themselves or their parents.

Parenting Style and Family Factors

Evidence is accumulating that problems also exist in the family relationships of children with anxiety disorders. Research indicates that parenting styles characterized by high control and low warmth are more prevalent in families with anxious children than in families in which the child does not have a psychiatric diagnosis (Hudson & Rapee, 2000; Siqueland, Kendall, & Steinberg, 1996). Compared to the parents of children without psychiatric disorders, parents of anxious children tend to grant less psychological autonomy and evidence less warmth and acceptance. This parental overcontrol and lack of warmth may contribute to the child’s experience of diminished control, leading to greater anxiety in the child (Barlow, 2000; Chorpita & Barlow, 1998). It has been suggested that child anxiety researchers begin to integrate parent-child interaction strategies and incorporate interventions that attempt to directly alter this parenting style and promote warmth, acceptance, and positive interactions between parents and children.

Aconsiderable number of studies have produced evidence that familial factors are involved in the etiology of childhood anxiety disorders. One of the research approaches that have been pursued in this area has been to assess the children of adults with an anxiety disorder; the other has been to assess the mental state and psychiatric history of parents of children with anxiety disorders. Turner, Beidel, and Costello (1987) studied the children of parents with an anxiety disorder, using a semistructured interview to derive a DSM-III diagnosis, and compared their children with the offspring of parents with dysthymia and parents without a psychiatric disorder. They found that in the group of parents with an anxiety disorder, 25–30% of their children had SAD. This study demonstrated a significantly increased risk of anxiety disorder in children with either anxious or dysthymic parents compared to normal controls, but there was no difference between the two patient groups.

Another, larger study (Tonge, 1994) examined the lifetime psychiatric histories of mothers of a group of 58 children with SAD and compared them with a group of nonanxious psychiatric controls. The study revealed that the mothers of anxiety-disordered children had a much higher lifetime rate of anxiety disorders (83%) than the control-group mothers (40%). They also found that 57% of the mothers of the anxious children were currently suffering from an anxiety disorder compared to 20% of the mothers from the control group. These findings show a surprisingly high level of mother-child linkage. In sum, it seems quite likely that familial factors are involved in the development of childhood anxiety disorders, including SAD, although there is not yet any convincing evidence that specific childhood anxiety disorders such as SAD are associated with specific types of psychiatric disorders in the parents. The field awaits twin and adoption studies to determine whether a hereditary component is present.

Learned Behavior

Another theory on the development of SAD incorporates a learned behavior model in which the child’s behaviors are reinforced through the parent’s reaction to the separation anxiety. For example, certain types of parental child-management patterns have also been discussed in the literature as being associated with fearful and anxious behaviors (e.g., Bush, Melamed, Sheras, & Greenbaum, 1986; Melamed, 1992). Melamed, for example, described how parental use of positive reinforcement, modeling, and persuasion have been associated with low levels of child fear. However, parental reinforcement of dependency has been associated with higher levels of child fear. It is possible that parents who have inadequate parenting or child-management skills may use inappropriate methods to manage their children’s fearful displays or avoidant behaviors, using physical punishment, force, or shame. Other parents, through repeatedly overprotecting their children and providing extra attention during their children’s episodes of separation distress inadvertently reinforce their children’s behavior, and thus, the fearful behavior increases.

Obsessive-Compulsive Disorder

Obsessive-compulsive disorder (OCD) is an anxiety disorder characterized by intrusive and distressing thoughts, urges, and images as well as repetitive behaviors aimed at decreasing the discomfort caused by these obsessive thoughts. Although most people experience occasional intrusive thoughts or engage in repetitive compulsive rituals from time to time, these occasional thoughts and behaviors do not pose a significant problem. In contrast, persons suffering from OCD experience obsessions and compulsions that cause significant distress and interference across many life domains (Antony, Roth, Swinson, Huta, & Devins, 1998). OCD is substantially more common in children, adolescents, and adults than was previously believed. Although clinicians and researchers have long been interested in the features of OCD, knowledge about this disorder has increased exponentially over the past few decades (Antony, Downie, & Swinson, 1998), and as a result, there have been great advances in the area of OCD and its treatment.

Clinical Presentation

In the DSM-IV (APA, 1994), the hallmark of OCD is the presence of obsessions or compulsions. Obsessions are defined as persistent thoughts, images, or impulses that occur repeatedly and are experienced as intrusive, inappropriate, and distressing. Some examples include fears of contamination, doubts about one’s actions, and aggressive impulses. Since obsessions provoke anxiety, a person with OCD attempts to ignore or suppress these obsessions or try to neutralize them with another thought or action (i.e., acompulsion). Obsessions are not simply worries about real-life problems, and according to the DSM-IV, individuals with OCD recognize that their obsessions are products of their own minds.

Compulsions are defined as repetitive behaviors, such as washing, cleaning, or repeating, or mental acts, such as counting or checking, that an individual feels compelled to perform in response to an obsession or according to certain rigid rules. Typically, compulsions are carried out to reduce discomfort or to prevent a dreaded event. However, they are clearly excessive and unconnected in a realistic way to the event they are aimed to prevent. Adults with OCD must recognize at some point during the course of the disorder that the obsessions or compulsions are unreasonable or excessive. In addition to these primary symptoms, other affective symptoms of fear, anxiety, chronic worry, and depression most usually accompany OCD. Individuals with OCD may be irritable, angry, and demanding. Not surprisingly, OCD symptoms often cause significant distress and functional impairment in patients’ lives and family functioning.

Manifestation of the symptoms of OCD in childhood is similar to that in adults. Common childhood obsessions include fears of contamination, fears of harm to self or others, and urges related to a need for symmetry or exactness. These obsessions are typically followed by compulsions of cleaning, checking, counting, repeating, touching, and straightening (Swedo et al., 1989). Children may also demonstrate hoarding, self-doubt, mental rituals such as counting or praying, and concerns of things being out of order. Some children have displayed excessive religious concerns (scrupulosity), such as worries that they have sinned. These symptoms often change over time, with no clear pattern or progression, and many children report having more than one OCD symptom at a time. By the end of adolescence, many children will have experienced many of the classic OCD symptoms (Rettew, Swedo, Leonard, Lenane, & Rappaport, 1992). It is rare for children to report only obsessions or only compulsions (Geffken, Pincus, & Zelikovsky, 1999). In addition, as many as 50–60% of children receiving diagnoses of OCD experience severe impairment in their social, personal, and academic functioning (Last & Strauss, 1989; Whitaker et al., 1990). Unlike adults, children may not recognize their obsessions and compulsions to be problematic.

Prevalence and Demographics

The prevalence of OCD is now estimated to be about 2.5% (Karno, Golding, Sorensen, & Burnam, 1988). The average age of onset of the disorder ranges from early adolescence to the mid-20s, and it typically occurs earlier in males (peak onset at 13–15 years of age) than in females (peak onset at 20–24 years of age). The onset of OCD is usually gradual, but acute onset has been reported in some cases. The disorder tends to be chronic, with symptoms waxing and waning in severity. However, episodic and deteriorating courses have been observed in about 10% of patients (Rasmussen & Eisen, 1989). Many individuals with OCD suffer for years before seeking treatment.The disorder may cause severe impairment in functioning, resulting in job loss and disruption of marital and other interpersonal relationships. A number of studies have examined gender differences in the prevalence rates for particular types of obsessions and compulsions (Castle, Deale, & Marks, 1995; Hanna, 1995). Lensi, Cassano, Correddu, Ravagli, and Kunovac (1996) found that men reported more sexual obsessions than women (27.0% vs. 12.7%), more obsessions concerning symmetry and exactness (28.6% vs. 8.0%), and more odd rituals (34.8% vs. 22.1%). Women reported more aggressive obsessions (26.2% vs. 15.3%) and cleaning rituals (59.6% vs. 43.7%) than did men.

March and Mulle (1998) report that approximately 1 in 200 children and adolescents, or approximately 3–4 children in elementary school and up to 20 teenagers in most averagesized high schools, have OCD. Leonard, Lenane, Swedo, and Rettew (1993) have suggested that these numbers are probably low due to the secrecy manifested by patients with this disorder. OCD has been referred to as the hidden epidemic because it is largely underdiagnosed and undertreated due to factors such as patient secrecy, lack of patient access to treatment resources, and health care providers’lack of familiarity with proven treatments.

Although research on OCD has increased, very little is known about this disorder in the elderly (Calamari, Faber, Hitsman, & Poppe, 1994). In general, much more attention has been given to depression in the elderly than to anxiety disorders. A number of studies have noted that the rate of OCD tends to decline somewhat as individuals age (Nestadt, Bienvenu, Cai, Samuels, & Eaton, 1998). In general, additional research is needed to determine the symptom presentation of OCD in elderly populations.

Comorbidity

There is a high comorbidity of OCD with other anxiety disorders. In one sample of OCD patients, 15–30% of patients had a comorbid anxiety or depressive disorder (Karno et al., 1988; Rasmussen & Tsuang, 1986). Approximately 40% of patients report sleep disturbance in conjunction with their symptoms of OCD. In addition to these disorders, there is some evidence supporting a relationship between OCD and eating disorders. Approximately 10% of women with OCD had a history of anorexia nervosa (Kasvikis, Tsakiris, Marks, Basoglu, & Noshirvani, 1986), and more than 33% of individuals with bulimia report a history of OCD (Hudson, Pope, Yurgelun-Todd, Jonas, & Frankenburg, 1987). Lastly, tic disorders such as Tourette’s syndrome also appear related to OCD. Estimates of the comorbidity of Tourette’s and OCD range from 36% to 52% (Leckman & Chittenden, 1990).

Comorbid psychiatric disorders occur in 62–74% of children and adolescents with OCD, with anxiety disorders the most prevalent and mood disorders less prevalent than reported in adults (Last & Strauss, 1989). Similar to the rates among adults, high rates of tics and Tourette’s syndrome have been associated with this population.

Cultural Influences

Recent epidemiological studies show some consistent differences in the prevalence of OCD in different ethnic groups. In one community sample of 819 individuals, Nestadt, Samuels, Romanowki, and Folstein (1994) found the prevalence of obsessions and compulsions to be 2.1% among Caucasians and 0.5% among non-Caucasians. These findings were consistent with those in other studies (e.g., Karno et al., 1988), which showed that OCD tends to be relatively rare in Hispanic and African American individuals relative to Caucasian individuals.

Relatively little is known about the impact of ethnicity on the expression of OCD. Researchers have just recently begun to study the nature and prevalence of anxiety disorders across ethnic groups. Studies are needed to elucidate the ways in which ethnic diversity relates to the types of obsessions and compulsions experienced, as well as the usefulness of the established assessment and treatment methods in ethnically diverse groups.

Developmental Changes

Most (if not all) children display normal, age-dependent obsessive-compulsive behaviors and rituals that appear to dissipate with time (March & Mulle, 1998). For example, young children frequently like things done just so or insist on elaborate bedtime rituals. Such behaviors can often be understood in terms of developmental issues involving mastery and control and are usually replaced by collecting, hobbies, and focused interests in middle childhood. Clinically, normal childhood obsessive-compulsive behaviors can be discriminated from OCD on the basis of timing, content, and severity. Developmentally sanctioned obsessive behaviors occur early in childhood, are rare during adolescence, are common to large numbers of children, and are associated with mastery of important developmental transitions. In contrast, clinically significant OCD behaviors occur somewhat later, appear bizarre to adults and to other children, and produce disruption of the child or adolescent’s life.

Common obsessions and compulsions seen in pediatric OCD patients are fear of contamination, fear of harm to oneself and to others, and urges for symmetry or exactness. Most children develop washing and checking rituals at some time during the course of the illness. OCD symptoms change over time, often with no clear pattern of progression, and many children will have experienced almost all the classic OCD symptoms by the end of adolescence. Children who have only obsessions or compulsions are extremely rare.

Etiology

Behavioral Influences

There are several theoretical accounts of the etiology and maintenance of OCD. Mowrer’s (1939) two-stage theory for the acquisition and maintenance of fear and avoidance behavior has been commonly adopted to explain phobias and OCD. This theory’s first stage proposes that a neutral event comes to elicit fear after being experienced along with an event that causes distress. Distress can be conditioned to mental events as well as to physical events. Once fears are acquired, escape or avoidance patterns (i.e., compulsions) develop to reduce fear and are maintained by the negative reinforcement of fear reduction. Thus, in the second stage of this model, the escape or avoidance responses are developed to reduce the anxiety or discomfort evoked by the various conditioned stimuli and are maintained by the success of those responses. Dollard and Miller (1950) adopted Mower’s two-stage theory to account for phobias and obsessive-compulsive neurosis. For persons with OCD, active avoidance patterns in the form of ritualistic behaviors are developed and are maintained by their success in alleviating the person’s distress and anxiety. Thus, obsessions give rise to anxiety and discomfort, and compulsions reduce this discomfort.

Cognitive Influences

Cognitive theorists argue that OCD is founded in ideas of exaggerated negative consequences (Carr, 1974; McFall & Wollersheim, 1979). Specifically, Carr proposed that obsessive-compulsives have unusually high expectations of negative outcome, and that they overevaluate the negative consequences for a variety of actions. Carr’s explanation of OCD suggests that the cognitive processes and distortions are similar to individuals with generalized anxiety disorder, agoraphobia, and social phobia.

McFall and Wollersheim (1979) suggest that persons with OCD hold erroneous beliefs such as the belief that failure to live up to ideals should be punished and that certain magical rituals can prevent catastrophes. These mistaken beliefs lead to erroneous perceptions of threat, which in turn provoke anxiety. Persons with OCD tend to devalue their ability to deal adequately with such threats, which results in feelings of uncertainty, discomfort, and helplessness. Foa and Kozak (1985) proposed that in addition to the pathological content of the cognitions of persons with OCD, such persons have impairments in their information-processing abilities. Specifically, OCD patients have difficulty making inferences about harm, and erroneously conclude that a situation is dangerous based on the absence of evidence of safety. As a result, these patients make inductive leaps and must perform rituals to reduce the likelihood of harm.

Biological Influences

The prevailing biological account of OCD hypothesizes that abnormal serotonin metabolism is expressed as OCD symptoms. The efficacy of selective serotonin reuptake inhibitors (SSRIs) for OCD as compared with nonserotonergic compounds and to a pill placebo (PBO) has provided a compelling argument for this hypothesis (Zohar & Insel, 1987). Significant correlations between clomipramine plasma levels and improvement in OCD have led researchers to suggest that serotonin function mediates obsessive-compulsive symptoms, lending further support to the serotonin hypothesis. However, inconsistent with the serotonin hypothesis is the finding that clomipramine, a nonselective serotonergic medication, appears to produce greater OCD symptom reduction than do such SSRIs as fluoxetine, fluvoxamine, and sertraline (Franklin & Foa, 1998). Numerous studies also suggest that there may be a neuroanatomical basis to OCD. For example, some studies have indicated that individuals with OCD have some deficits in frontal lobe functioning (e.g., Head, Bolton, & Hymas, 1989), but other studies have failed to support these findings. Results of several studies using positron emission tomography (PET) to assess metabolic activity in the brain suggest that persons with OCD show increased metabolic rates in the prefrontal cortex. Currently, OCD is understood as a disorder of the neural circuitry involving the corticostriatothalamocortical (CSTC) pathways.

Specific Phobia

Specific phobias are irrational and persistent fears of certain objects or animals (Merckelbach, de-Jong, Muris, & van den Hout, 1996). Although descriptions of phobic behavior have remained remarkably consistent throughout history, theories explaining this behavior have changed dramatically, and during the past decades our understanding of the origins of specific phobias has steadily increased. It is now well recognized that learning mechanisms, developmental processes, and cognitive processes all contribute to the etiology and maintenance of phobic symptoms.

Clinical Presentation

The central features of specific phobias listed in the DSM-IV (APA, 1994) can be summarized as follows: (a) Fear and anxiety are directed at a limited set of stimuli; (b) contact with these stimuli elicits intense fear, anxiety, and avoidance behavior; and (c) fear and anxiety are unreasonable and excessive to the degree that they interfere in a person’s daily functioning. Fears are nonrandomly distributed, and in the general population, some fears are far more prevalent than others. The DSM-IV differentiates among four highly prevalent types of specific phobia: animal type (e.g., spider phobia), natural environment type (e.g., phobia of dark or heights), blood-injection-injury type (e.g., dental phobia), and situational type (e.g., elevators).Although most adult patients with intense phobias are able to admit that their fears are excessive and irrational, this is not always the case with children.

Because fears are a normal response to a threat of harm, fears can serve an adaptive function by facilitating avoidance of dangerous situations. Since genuine threats are plentiful during childhood, it is not surprising that specific fears are common in infancy and throughout childhood. When asked, most children will readily identify multiple fears (Ollendick, 1983). Typically, such fears are mild and transient, and follow a predictable developmental sequence (Marks, 1987b). However, some children experience fears that persist, interfere with daily functioning, and are not age appropriate. When these fears are excessive, and not associated with an actual threat, they suggest a clinical level of fear, or a phobic disorder. Similar to adults, the characteristic feature of phobic disorders in children is the presence of excessive fear or anxiety that leads to avoidance of a feared object, event, or situation, and the experience of extreme levels of fear and anxiety when confronted with the perceived threat. With only minor exceptions, the same criteria areused to classifyphobic disorders in adults and in children.

Prevalence and Demographics

Epidemiological evidence indicates that phobias may affect more than 12.5% of the general U.S. population (e.g., Regier et al., 1988). This indicates that phobias are the most common of the mental disorders. Kessler et al. (1994) found lifetime and 12-month prevalence rates of 11.3% and 8.8%, respectively.

All recent epidemiological studies show very high rates of prevalence for specific phobia; Epidemiologic Catchment Area (ECA) data, for example, indicate a lifetime prevalence rate ranging from 7.8% to 23.3% across three different sites (Robins et al., 1984) and 11.25% overall (Eaton et al., 1989). Thus, the prevalence of specific phobias is quite high. The 30-day prevalence rate for specific phobia is 5.5%, making it more common than social phobia (4.5%) or agoraphobia (2.3%). Among the various specific phobias, Fredrikson, Annas, Fischer, and Gustav (1996) found that situational and environmental phobias had the highest point-prevalence rate (13.2%), followed by animal phobias and blood-injectioninjury phobias (7.9% and 3.0%, respectively). Additionally, studies indicate that most specific phobias are diagnosed more often in women than in men (Chapman, Fyer, Mannuzza, & Klein,1993;Fredriksonetal.,1996).Despitetheprevalenceof specific phobia in the population, relatively few persons seek treatment.

Recent epidemiological surveys suggest that between 2 and 4% of children in the general population have clinical levels of fear that would qualify as a specific phobia (Bird et al., 1988). Phobias are not a frequent reason for seeking psychological services, accounting for fewer than 7% of the referrals for mental health services for children (Graziano & De Giovanni, 1979; Silverman & Kearney, 1992). The prognosis for children with specific phobias (without comorbidity) is excellent. Most phobias dissipate over time, even without treatment. It appears that those children who are brought to clinics for treatment often have additional anxietyrelated disorders (Last et al., 1989). These more severe problems may prompt parents to seek treatment.

Cultural Influences

Assessments of the excessiveness of fears, worries, or concerns about the dangerousness of situations or objects must be made within the cultural context of the individual’s reference group.Thecontentofphobiasaswellastheirprevalencevaries with culture and ethnicity. Many important phobic responses in other cultural groups may not be contained in the DSM-IV or may present themselves differently across cultures. For example, in certain cultures, apprehension or vigilance toward magic or spirits or a concern with being possessed or bewitched could be seen, in most cases, as a symptom of anxiety or a specific phobia rather than a sign of a thought disorder. Although ethnic comparisons within the United States have not identified major symptom differences for specific phobias between persons of different ethnicities, cross-cultural studies have indicated that there may be significant differences in the ways phobias and fears are described and, potentially, experienced (Guarnaccia, 1997). Both psychiatric researchers and clinicians need to develop a more complex understanding of culture and itsrelationship to the expression of emotion and experience of fear of specific stimuli.Although physiological reactions underlying anxiety and fear appear to be universal, culture may define the situations that arouse anxiety and fear and determine how it is expressed and reacted to by the individual and his or her group (Al-Issa & Oudji, 1998).

Developmental Changes

Childhood fears are common and usually transient, adaptive, age-appropriate behaviors with no long-lasting sequelae. Numerous studies have shown that most children experience multiple fears of mild to moderate severity that appear to be age related, following a progression associated with cognitive development (King, Hamilton, & Ollendick, 1988). These specific fears appear to follow a predictable course. For example, Wenar (1990) described the period of infancy as characterized by fear reactions in response to loud noise, pain, falling, and sudden, unexpected movement, while middle childhood is characterized by an increase in realistic fears (e.g., fears of bodily injury from traffic accidents or fires) accompanied by a decrease in fantasy-based fears (e.g., fears of ghosts and imaginary creatures). These findings are consistent with previous research (Bauer, 1976). Interestingly, both the number and the intensity of fears experienced by children and adolescents have been shown to decrease steadily with age, and thus, childhood fears are usually considered normal, short lived, adaptive reactions to either real or perceived threatening stimuli. Yet in some cases, fears persist and become debilitating and disruptive to the child and family. In general, specific phobias seem to have an early onset, with a substantial proportion of phobias beginning in childhood. For example, Ost (1987) reported mean onset ages of 7 and 9 years for animal and blood-injury-injection phobias, respectively, and a similar early onset for natural environmental phobias. Studies evaluating specific fears in children have generally found that girls report more fears than boys, yet there are also indications that gender differences are modulated by age (Ollendick & King, 1991a).

Etiology

The etiology of normal, age-appropriate fears has been conceptualized from several different theoretical perspectives. The past 40 years have produced a substantial shift away from psychoanalytic and phenomenological theorizing toward more behavioral conceptualizations (Morris & Kratochwill, 1983).

Behavioral Influences

For years, it was widely assumed that all phobias were learned through simple traumatic conditioning. As weaknesses in this model became apparent a number of modifications were proposed, inducing two-factor theory (Mowrer, 1947), observational learning (Bandura, 1969), and preparedness (Seligman, 1971). At present, we are aware of a number of psychosocial pathways to fear acquisition, with traumatic fear conditioning representing only one path.

According to the work of Pavlov (1927), Skinner (1953), and Mowrer (1939), fear is considered to be learned, as a function of conditioning history. Multiple fears are thought to be learned separately, each having its own environmental contingencies and conditions. Fears are considered to be situation specific, caused by the environment, with unconscious factors playing no essential role. Thus, behavioral perspectives on the etiologies of fears can be thought of as being based primarilyonrespondent-conditioning,operant-conditioning,and vicarious-conditioning principles.

Other behavioral theorists have expanded on this perspective. Rather than being rooted in one particular conditioning history, several theorists have attributed the emergence, persistence, and dissipation of fears to multiple sources. Rachman’s (1977) theory of fear acquisition identified three main pathways by which fears develop and are transmitted. The first pathway is traumatic conditioning, the second is through vicarious or observational learning, and the third is through informational transmission. While Rachman’s theory proposes that there are three separate possible pathways of fear, recent research (Ollendick & King, 1991a) indicates that these three pathways are unlikely to be independent but rather are integrative and interactive, thus pointing to a theory of fear acquisition in which a particular fear is multiply determined. Some studies support a role for direct or indirect conditioning (King, Clowes-Hollins, & Ollendick, 1997), but other studies find less empirical support for conditioning theories (McNally & Steketee, 1985). For example, in a classic study, di Nardo, Guzy, and Bak (1988) found that 50% of dog phobics could report having had a frightening encounter with a dog. However, 50% of a matched control group without phobia reported similar experiences with dogs.

Nonassociative Theories of Fear Acquisition

In contrast to the conditioning theories of fear acquisition, the nonassociative account suggests that evolutionarily relevant fears emerge in the absence of associative learning (Menzies & Clark, 1995). Indeed, retrospective reports of associativelearning events have been found to be extremely rare in studies examining the acquisition of evolutionarily relevant fears, including fear of heights (Menzies & Clark, 1993b, 1995), water (Menzies & Clark, 1993a), and spiders (Jones & Menzies, 1995). Pury and Mineka (1997) also reported that, regardless of their blood-injection-injury fear levels, humans show an associative bias to associate blood-injection-injury stimuli selectively with adverse outcomes, suggesting a predisposition to more readily acquire fears of stimuli that may have once posed a threat to our early ancestors. This covariation bias has been widely replicated (e.g., Tomarken, Sutton, & Mineka, 1995). These data support the preparedness theories of etiology in some phobias (e.g., Seligman, 1971). In general, many studies examining the etiology of specific phobias have found that at least a sizeable minority of people with specific phobias report a history of direct conditioning experiences, although many additional subjects fail to report any clear-cut psychosocial antecedents of their fear. In addition, most investigators reporting direct experiences have found that a relatively large number of phobic subjects also report either a history of vicarious experiences with the phobic stimulus, or having received negative information regarding the stimulus. Ollendick and King (1991b) have concluded that the three pathways of fear acquisition may be interactive rather than independent, with fear more likely to occur when two or more sources of fear acquisition are combined.

Biological Influences

Research examining anxiety disorders suggests that there is a proneness to experience both anxiety and fear that may be at least partially heritable (Barlow, 1988; Biederman et al., 1990). Genetic predisposition also appears to play an important role in the acquisition of many irrational fears and specific phobias. Specifically, researchers have reported greater concordance among monozygotic than dizygotic twins for a variety of fears, including specific fears of animals or mutilation, and social fears (Rose & Ditto, 1983). Similarly, in a genetic analysis of twin data derived from the Fear Survey Schedule for Children–Revised (FSSC-R), Stevenson, Batten, and Cherner (1992) reported significant heritabilities for the Fear of the Unknown, Fear of Injury and Small Animals, Fear of Danger, and Total Fear Score. Interestingly, they found no evidence of enhanced heritability at more extreme levels of fearfulness. Kendler and colleagues (Kendler et al., 1995) conducted an epidemiologically based study of psychiatric disorders in female twins. Both genetic factors and phobia-specific environmental events were implicated in the development of specific phobias. There are also some other data indicating that specific phobia is familial (Fyer et al., 1990). For instance, in a retrospective study of parental history and experiential factors in the development of snake and spider phobias, Fredrikson, Annas, and Wik (1997) found that a history of indirect fear exposures was more common among phobic women who also reported having a phobic parent compared with those who did not. Such family studies do not isolate the role of genetic factors in the etiology of specific phobias, and the specific pathways of familial transmission are still unclear.

A Diathesis-Stress Framework

The development of specific phobias may be conceptualized in terms of a diathesis-stress model (e.g., Barlow, 1988), which predicts that both high levels of the diathesis and exposure to psychosocial factors are necessary for the development of specific phobia. Thus, the major factors placing an individual at risk for specific phobia include psychosocial experiences (i.e., direct conditioning, indirect conditioning, and instruction-information) as well as a biologically influenced propensity to experience fear and anxiety.

Social Phobia (Social Anxiety Disorder)

Social fears are a universal experience. Social phobia, however, goes beyond appropriate and helpful fear reactions to social situations. Social phobia was discussed as early as 1966 (Marks & Gelder, 1966); however, it did not find its way into the diagnostic nomenclature until 1980, when the third edition of the DSM (APA, 1980) was published. In the previous version (DSM-II; APA, 1968), social fears were thought to be similar to a specific phobia of social situations, or an excessive fear reaction to being observed or scrutinized by others. This perspective was challenged when it became clear that social phobia often includes fear of multiple social situations, is more debilitating and more prevalent than initially assumed, and is often under-recognized, probably because either individuals with social phobia do not bring their fears directly to the physician’s attention or the physician does not recognize them adequately (Den-Boer & Dunner, 1999; Liebowitz, Gorman, Fyer, & Klein, 1985; Liebowitz, Heimberg, Fresco, Travers, & Stein, 2000). In 1985, social phobia was still viewed as the neglected anxiety disorder (Liebowitz et al., 1985). In 1994 an alternative term for social phobia—social anxiety disorder—was introduced into the DSM-IV to indicate how generalized and pervasive these fears can be and to indicate that the term phobia might be inappropriate to describe the disorder (Liebowitz et al., 2000).

Clinical Presentation

Individuals suffering from social phobia often fear being humiliated, embarrassed, or judged negatively in social situations. They may fear that they will behave inappropriately or possibly be scrutinized by others. Patients are often concerned about making a mistake or acting somewhat awkwardly, or that others will notice their anxiety and their physical symptoms in particular. Typical situations that are avoided or endured with distress are initiating or maintaining a conversation; speaking, performing, eating, drinking, or writing in front of people; meeting new people; attending social gatherings; and talking on the phone. When exposed to social situations, individuals with social phobia experience a range of physical symptoms that may culminate in a panic attack. Muscle twitches, blushing, heart racing, sweating, and trembling often occur as part of a fear reaction to social situations (Amies, Gelder, & Shaw, 1983). However, physical reactions need to be limited to social situations in order to qualify for a social phobia diagnosis.

Prevalence and Demographics

Social phobia is the third most common mental disorder with a lifetime U.S. prevalence of 13% (Kessler et al., 1994). In European studies the lifetime prevalence seems to be lower, from 2% (Norway; Den-Boer et al., 1999) to 7% (Italy; Faravelli et al., 2000).The prevalence of social phobia in general appears to have increased over time, although the prevalence of the fear of public speaking in particular seems to have remained consistent. (Heimberg, Stein, Hiripi, & Kessler, 2000). The disorder usually begins during late adolescence (between ages 13 and 20) and follows a chronic, unremitting course (Hazen & Stein, 1995; Ost, 1987; Wittchen, Stein, & Kessler,1999).Newcasesofsocialphobiahavebeenfoundin all age groups with an incidence rate of 4–5 per 1,000 per year (Neufeld, Swartz, Bienvenu, Eaton, & Cai, 1999). In a recent study in Norway, social phobia was found to be the most chronic anxiety disorder (Alnaes & Torgersen, 1999). In epidemiological studies, woman are more likely to receive a diagnosis of social phobia; however, in treatment samples, social phobia is equally distributed across gender (Heimberg & Juster, 1995; Turk et al., 1998).

Comorbidity

Individuals with social phobia are often very self-critical (Cox et al., 2000; Heckelman & Schneier, 1995), self-conscious (Boegels, Alberts, & de Jong, 1996; Jostes, Pook, & Florin, 1999), and self-focused in their attention (Hofmann, 1999; Mellings & Alden, 2000). They tend to evaluate their own performance as being worse than that of others (Rapee & Lim, 1992) and they generate a negative impression of how they appear to others by imagining how they look from an observer’s vantage point (Wells, Clark, & Ahmad, 1998; Wells & Papageorgiu, 1998, 1999). People with social phobia often live in social isolation and occupational maladjustment. Their quality of life is significantly reduced in a variety of areas, including education, career, friendships, and romantic relationships (Wittchen, Fuetsch, Sonntag, Mueller, & Liebowitz, 2000). Depression, increased suicidal ideation, general anxiety, and alcohol abuse have repeatedly been found to be associated with social phobia (Den-Boer et al., 1999; Kessler, Stang, Wittchen, Stein, & Walters, 1999). In adolescence, social anxiety and social phobia have also been found to beassociated with higher rates of nicotine dependence (Sonntag, Wittchen, Hoefler, Kessler, & Stein, 2000)

Avoiding a variety of social situations often leads to a significant phenomenological overlap with avoidant personality disorder (APD). Most studies support the assumption that there is no dividing line between social phobia and APD, either conceptually or diagnostically (Noyes, Woodman, Holt, & Reich, 1995; Reich, 2000). Individuals with an additional diagnosis of APD are typically characterized by greater social anxiety and greater overall psychopathology than individuals with generalized social phobia alone, who in turn show greater psychopathology than individuals with nongeneralized social phobia (Boone et al., 1999; Stemberger, Turner, Beidel, & Calhoun, 1995; Turner, Beidel, Borden, Stanley, & Jacob, 1991). Another Axis II disorder that often co-occurs with social phobia is obsessive-compulsive personality disorder (Turner et al., 1991).

It might be difficult to differentiate social phobia from other Axis I disorders at times. The focus and extensiveness of reported worries are helpful characteristics in discriminating social anxiety disorder from generalized anxiety disorder. Panic disorder and social phobia share the concern that others might notice physical symptoms. In addition, panic attacks can also occur in either disorder. However, many differences exist, including age of onset, gender distribution, help-seeking and avoidance behavior, and neurobiological and physical reactions (Reich, Noyes, & Yates, 1988; Uhde, Tancer, Black, & Brown, 1991).

Cultural Influences

Social phobia is expressed differently across cultures (e.g., Kleinknecht, Dinnel, Kleinknecht, Hiruma, & Harada, 1997; Lee & Oh, 1999). In East Asia, offensive social phobia is a common type of social anxiety disorder (Kleinknecht et al., 1997; Lee & Oh, 1999). Individuals with offensive social phobia are obsessed with embarrassing or offending others by blushing, emitting offensive odors, or staring inappropriately (taijin kyofusho; Kleinknecht et al., 1997), or they are fearful of offending other persons with certain parts of their body (taein kong po). This type seems to occur most often among Japanese and Korean individuals. It has been suggested that a submissive, collectivist social structure and the nonverbal social communication in East Asian culture favors the development of this social phobia type (Kleinknecht et al., 1997; Lee & Oh, 1999). Recently, the influence of Arab-Muslim culture on social phobia has also been reviewed (Takriti & Ahmad, 2000), but more empirical evidence is needed to come to a conclusion about the cultural influence on social anxiety disorder in this population.

Developmental Changes

Developmental variables that have been considered in relation to social phobia are shyness, neuroticism, introversion, and behavioral inhibition (Kagan, Snidman, & Arcus, 1992; Stemberger et al., 1995). In a retrospective study, 72% of individuals with social phobia reported a childhood history of shyness and indicated significantly higher neuroticism scores and lower extraversion scores than individuals without social phobia (Stemberger et al.). Similar results were obtained in previous studies (Amies et al., 1983;Watson, Clark, & Carey, 1988). Similarly, shy children with no mental disorder were more often found to have mothers with social phobia (Cooper & Eke, 1999). The onset of shyness is usually very early, is often transitory, and, in contrast to social phobia, is considered a temperament trait of social reticence and not an emotional disorder. Furthermore, although a number of individuals in epidemiological studies endorsed shyness, only a small portion met criteria for social phobia (e.g., Robins et al., 1984). This indicates that the two concepts are not interchangeable. Similarly, behavioral inhibition (BI), which is a behavioral pattern characterized by discomfort with novelty and heightened physiological arousal that can be observed at 4 months and persists until age 7 or 8 years, has been viewed as a vulnerability factor for social phobia (Kagan et al., 1987, 1992). Although some studies indicate that subsequent fear development predominantly relates to social situations (Biederman et al., 1990), children who show this behavior pattern are more likely to be anxious in general, as well. However, data on the relationship among shyness, behavioral inhibition, and social phobia are rare, and despite the remarkably similar expression of these concepts, it remains unclear whether shyness or behavioral inhibition are vulnerability factors for social phobia or if they are milder versions of social phobia (Turner, Beidel, & Townsley, 1990).

Social phobia itself expresses similarly in both childhood and adulthood (Spence, Donovan, & Brechman-Toussaint, 1999). However, different diagnostic criteria apply to childhood social phobia, specifying that the child needs to be developmentally capable of engaging in social interactions and that social-evaluative fears need to occur in interactions with peers, not only in interactions with adults. Furthermore, social anxiety in children can be expressed in tantrums, freezing, or crying in social situations. Social anxiety in childhood also seems to be associated with a reduced general facial activity, a restricted facial repertoire, and less accurate facial expression of emotions (Melfsen, Osterlow, & Florin, 2000).

Etiology

Biological Influences

Family studies of social phobia show higher prevalence of this disorder in relatives of patients with social phobia than in relatives of patients with other anxiety disorders or of participants with no mental disorder (Knowles, Mannuzza, & Fyer, 1995; M. B. Stein et al., 1998). Several twin studies suggest moderate heritability for social fears; however, no data exist for heritability of social anxiety disorder as defined by DSM-IV(APA, 1994). Differences in physiological reactions to social situations between the generalized and nongeneralized subtype (Hofmann, Newman, Ehlers, & Roth, 1995) lead to the speculation that individuals with generalized social phobia are biologically more vulnerable to developing social phobia than are individuals with nongeneralized social phobia (Zuckerman, 1999). A recent family study supports this suggestion, finding an increased risk for generalized social phobia in first-degree relatives of individuals with generalized social phobia only, not in relatives of individuals with nongeneralized social phobia (M. B. Stein et al., 1998). A high comorbidity between Parkinson’s disease and social phobia has been observed, suggesting that dopamine depletion is possibly related to the development of social phobia (Lauterbach & Duvoisin, 1991; M. B. Stein, 1998; M. B. Stein, Heuser, Juncos, & Uhde, 1990). Recent single photon emission computed tomography studies in patients with social phobia found that striatal dopamine reuptake site densities were lower in patients with social phobia than in individuals without a mental disorder (Schneier et al., 2000; Tiihonen et al., 1997), and that chronic amphetamine abuse seems to be capable of causing social phobia through dopamine depletion (Williams, Argyropoulos, & Nutt, 2000). Results from numerous pharmacotherapy studies also point to the contribution of the dopaminergic system in social phobia (e.g., Blanco, Schneier, & Liebowitz, in press); however, it remains unclear whether dopamine depletion is a cause or consequence of social phobia.

Behavioral Influences

Several researchers have discussed the role of conditioning in the development of social phobia (Hofmann, Ehlers, & Roth, 1995; D. J. Stein & Bouwer, 1997). Often, ethological considerations are integrated in this debate, providing reasons for the evolution of vulnerability to social threat (Ohman, 1986; D. J. Stein & Bouwer, 1997). Zuckerman (1999) suggested that the greater physiological reactivity of nongeneralized social phobics to specific social situations such as public speaking likely indicates conditioning processes in the development of this disorder (see also Hofmann, Ehlers, & Roth, 1995).Although traumatic experiences have been reported from speech-phobic individuals, these events often occurred after the phobia began (Hofmann et al., 1995). Similarly to public-speaking anxiety, fear of blushing has been discussed in terms of conditioning (Mulkens & Boegels, 1999). Highly fearful individuals reported more negative learning experiences with regard to blushing. Individuals with social phobia differ from healthy individuals in the classical conditioning processes of aversive emotional reactions, indicating that learning processes contribute to some extent to the development and persistence of social anxiety disorder.

Cognitive Influences

Individuals with social phobia share typical negative beliefs about themselves in social situations (e.g., “What I say sounds stupid,” “I’m boring,” “I will make a fool out of myself,” “I won’t have anything to say”). Clark and Wells (1995) assume that individuals with social phobia activate a series of negative beliefs about themselves as social subjects when they are faced with social situation. These assumptions likely cause social phobics to perceive threat in such circumstances. In particular, they overestimate the likelihood that they will behave inadequately in social situations, and they tend to believe that this behavior will result in a personal catastrophe, such as rejection or loss of worth (Clark & Wells, 1995). These thoughts elicit anticipatory anxiety and avoidance, leading to short-term anxiety reduction. This way, cognitive responses and applied strategies to control increasing anxiety result in a vicious circle that maintains social anxiety. A more detailed outline of this cognitive model can be found in Clark and Wells. The model has stimulated extensive research on the cognitive basis of social anxiety disorder (discussed later in this research paper), particularly with regard to information processes. Individuals with social phobia seem to attend selectively to socially threatening information (Amir, Foa, & Coles, 1998b; Gilboa-Schechtman, Foa, & Amir, 1999; Horenstein & Segui, 1997; Maidenberg, Chen, Craske, Bohn, & Bystritsky, 1996), and they also seem more prone to interpret and judge information in a socially threatening way (Amir, Foa, & Coles, 1998a; Foa, Franklin, Perry, & Herbert, 1996; Stopa & Clark, 2000)—for example, by overestimating the likelihood and the cost of negative social outcomes (Foa et al.) or by drawing more negative inferences from available social stimuli (Amir et al., 1998a, 1998b; Stopa & Clark; Wallace & Alden, 1997). Furthermore, individuals with social phobia show a rather unique cognitive process after facing a social situation in which they review the previous interaction in detail (post-event processing; Clark & Wells). This review seems to be dominated by negative self-perception that enhances future avoidance tendencies. For a review of information-processing biases in social phobia and their relation to Clark and Wells’cognitive model, see Heinrichs and Hofmann (2001).

Other cognitive models of social phobia focus more on expectancies (Trower & Gilbert, 1989) or on interpersonal goals that persons aim to achieve and their low confidence in their ability to achieve these goals (self-presentation model; Leary & Kowalski, 1995a, 1995b). According to this approach, individuals with social phobia are extraordinarily motivated to make desired impressions on others because of certain dispositional traits that predispose them to develop social anxiety. Most research conducted to test this model involved individuals with subclinical social anxiety (for a review see Leary & Kowalski, 1995a, 1995b).

Panic Disorder With And Without Agoraphobia

Panic disorder is a syndrome that has stimulated a significant amount of research, particularly since 1987 (McNally, 1994). Today, it is probably the most researched anxiety disorder. In DSM-III, panic disorder (PD) was classified as an anxiety neurosis that is best characterized and differentiated from other anxiety disorders by the presence of spontaneous panic attacks. Agoraphobia was conceptualized as a consequence of spontaneous panic attacks (APA, 1980; Barlow, 1988, 2002; Klein & Klein, 1989a). Three types of panic attacks are distinguished (DSM-IV; APA, 1994): unexpected or spontaneous attacks, situationally bound attacks, and situationally predisposed attacks. If panic attacks are exclusively triggered by a phobic stimulus, the attacks are situationally bound (e.g., a person experiences panic attacks if and always if faced with heights). Situationally predisposed attacks tend to occur more in some situations than in others; however, they are not inevitably experienced in those situations (e.g., in a large mall). Spontaneous panic attacks seem to occur “out of the blue,” with no evident situational trigger. This conceptualization of panic attacks reflects a dimension of predictability on which situationally bound attacks are predictable but spontaneous attacks are not.

Panic attacks occur across all anxiety disorders, and can also be found in the general population (Barlow, 2002; Katerndahl & Realini, 1993); they are not specific to PD. This knowledge was clarified in DSM-IV, which defines panic attacks separately from PD. Situationally predisposed and spontaneous attacks are most relevant to PD and agoraphobia.

Clinical Presentation

Panic attacks are defined as sudden episodes of fear accompanied by distressing physical sensations such as dizziness, heart racing, palpitations, chest pain, shortness of breath, choking sensations, sweating, or nausea. The particular symptoms of panic vary across different individuals. If a patient has 4 or more symptoms, the experience is defined as a full-blown (vs. limited-symptom) attack. During a panic attack, the individual often fears dying, losing control, or going crazy. Patients with PD worry persistently about potential adverse implications or consequences of panic attacks. As a result, they usually engage in behavioral strategies to prevent the feared consequences. Active avoidance behaviors range from subtle (e.g., unzipping one’s jacket to be able to breathe) to obvious (e.g., not going into movie theaters), and may include different forms of distraction and safety behaviors (e.g., turning up the volume on the radio, or carrying around a bottle of water). To qualify for a PD diagnosis, these worries or behavioral changes due to a panic attack need to persist for at least 1 month (APA, 1994).

As a result of their worries, individuals with recurrent panic attacks often feel vulnerable in places or situations that would be difficult to leave, or where help might not be readily available in the event of sudden need. Examples include open spaces, unfamiliar or unpopulated areas, crowds, modes of public transportation, elevators, bridges, limited-access highways, restaurants, malls, and movie theaters. If such situations are physically avoided or cause significant distress, the person is said to have agoraphobia. Severe agoraphobia can prevent individuals from leaving their homes, resulting in a variety of occupational, social, and personal disadvantages. Panic disorder and agoraphobia typically coexist, although either one can also occur separately. About 95% of individuals presenting in clinical settings with agoraphobia also have PD (APA, 2000). The development of agoraphobia in PD seems to be more closely associated with an earlier onset of PD, with a fear of losing control and with experiencing chills or hot flushes, whereas chest pain was found more often in PD alone (Langs et al., 2000). If agoraphobia occurs alone, the fear often relates to experiencing panic-like sensations. A predominant fear of embarrassment due to others’ noticing these effects (e.g., diarrhea, loss of bladder control, vomiting, excessive sweating) can sometimes make it difficult to distinguish agoraphobia from social phobia. Guidelines for a differential diagnosis of panic disorder with agoraphobia (PDA) versus other anxiety disorders can be found in Baker, Patterson, and Barlow (2002).

The core of PD is a strong fear of physical sensations, even in the absence of any noticeable sensations (fear of the fear). As a consequence, patients with PD usually avoid situations (e.g., exercising, sexual activity) that are naturally capable of eliciting physical sensations similar to those of a panic attack. Environmental factors such as humidity and hot weather may also contribute to panic attacks (Asnis, Faisal, & Sanderson, 1999).

Panic attacks can occur at any time, including at night. Awakening from sleep in a state of sudden, uncued panic is referred to as a nocturnal panic attack. Similar to daytime panic attacks, these attacks are not limited to PD but rather occur across all anxiety disorders. They are often misconceptualized as some form of a sleeping disorder (Craske & Rowe, 1997). Differential diagnoses can best be established by a focus on the time at which panic occurs (e.g., nocturnal panic attacks usually occur in Stage 2 and 3 sleep [Craske & Rowe, 1997], whereas symptoms of sleep apnea typically occur in Stage 1 or 2 sleep or during rapid eye movement [George, Millar, & Kryger, 1988]).

Patients with PD often seek medical advice for their physical sensations, and if the unexpected sensations are severe, they may seek intensive medical services such as emergency rooms (Barsky, Delamater, & Orav, 1999; Klerman, Weissman, Oullette, Johnson, & Greenwald, 1991). Quality of life is significantly reduced in patients with PD (Birehall, Brandon, & Taub, 2000; Kessler et al., 1994; Rubin et al., 2000), and patients with PD are more likely to initiate disability payments (Kouzis & Eaton, 2000). Panic disorder is therefore associated with high social and economic costs (Hofmann & Barlow, 1999).

Prevalence and Demographics

PDAis a prevalent and chronic condition: The lifetime prevalence is estimated to be 1–4% (APA, 2000). A recent survey of panic in a general practice population found a lifetime prevalence o f8.6% (Birehalletal, 2000). Women are twice as likely to have PDA than men (Katerndahl & Realini, 1993).The median age of onset is 24 years (Burke, Burke, Regier, & Rae, 1990). PDA has also been observed in children; however, there is an ongoing controversy regarding at which age PDA can occur (e.g., Klein, Mannuzza, Chapman, & Fyer, 1992; Moreau & Follet, 1993). In older adults, increasing prevalence of medical conditions and physical complaints (e.g., shortness of breath, rapid heart rate; Zarit & Zarit, 1998) make it reasonable to also assume a higher prevalence of PDA. Furthermore, in the ECA study, a second peak age of onset was found (45– 54 years; Eaton, Kessler, Wittchen, & Magee, 1994), indicating the existence of late-onset PDA. It has been stated repeatedly, however, that PD is rather uncommon in elderly, among whom agoraphobia without PD occurs more often, frequently subsequent to a traumatic event (Flint, 1998). Epidemiological studies with the elderly, however, are rare, preventing any firm conclusions on the prevalence of PDA in older adults.Two studies that analyzed sociodemographic and clinical characteristics of late-onset PD found that this PD type may be associated with less severe panic symptoms and general mental health complaints, a less likely family history of PD, more distress from sensations of choking and numbness, less utilization of mental health services, and more likely use of physical health services (e.g., family physicians; Katerndahl & Realini, 1995; Katerndahl & Talamantes, 2000; Seguietal., 2000). PDA typically takes an unremitting course. As do most other anxiety disorders, it seems to be a chronic condition with spontaneous remissions occurring rather rarely (for a recent review see Pollack & Marzol, 2000).

Comorbidity

Panic disorder also was found to be associated with and predictive of suicide risks (Clayton, 1993; Cox, Direnfeld, Swinson, & Norton, 1994). However, the suicidal risk seems to be associated with comorbid Axis I (e.g., major depression) and II (e.g., borderline personality disorder; Friedman, Jones, Chernen, & Barlow, 1992; Johnson, Weissman, & Klerman, 1990). More recent studies of PD and suicidal ideation did not find an increased suicidal risk in PD patients alone (Hornig & McNally, 1995; Starcevic, Bogojevic, Marinkovic, & Kelin, 1999). Whether patients with PD are at risk of committing suicide seems, therefore, to depend strongly on the presence of comorbid conditions. Depression often co-occurs with PDA (Roy-Byrne et al., 2000), and PDA was found less likely to precede the first depressive episode than to emerge subsequently (Fava et al., 2000).

Stein, Shea, and Uhde (1989) stated that 46% of patients with PDAhave also been diagnosed with social phobia. In our clinical setting, these disorders co-occur less often (15%; Brown, Campbell, Lehman, Grisham, & Mancill, 2001). It is unclear whether these two disorders are, in fact, so strongly associated or the association is due to differential diagnosis difficulties.

PDA often co-occurs with personality disorders (Brooks, Baltazar, & Munjack, 1989; Dammen, Ekeberg, Arnesen, & Friis, 2000). Closely associated with PD are dependent, avoidant, and histrionic personality disorders (Chambless, Renneberg, Goldstein, & Gracely, 1992; Diaferiaetal., 1993).

Several medical conditions are also associated with PD (e.g., Jeejeebhoy, Dorian, & Newman, 2000). The prevalence of PD in patients with coronary artery disease (CAD) ranges from10to50%(Fleet,Lavoie,&Beitman,2000).Asthmaand panic attacks also frequently co-occur (Feldman, Giardino, & Lehrer, 2000), and asthma has been noted as a risk factor for the development of PDA (Carr, 1998, 1999) because of the shared sensations between an asthma and a panic attack (e.g., feeling of suffocation). In most instances it is unclear whether these medical conditions are conceptually associated with PDA. A specific pathophysiological mechanism for PD has not been found (Jeejeebhoy et al., 2000). Fleet and colleagues (2000) conclude their review of the PD-CAD association by stating that PD is prevalent in CAD patients, but that there is no evidence that PD puts a patient at risk for developing CAD. This seems also true for cardiovascular problems such as mitral valve prolapse (MVP; Bowen, D’Arcy, & Orchard, 1991; Yang, Tsai, Hou, Chen, & Sim, 1997). Similarly, the presence of a direct association between pulmonary impairment and PD has been subject to debate (Ley, 1998; Spinhoven, Sterk, van der Kamp, & Onstein, 1999) with no concluding evidence that PD is associated with pulmonary impairment. Medical conditions in general are more likely to heighten body awareness and thus contribute to PDAby exacerbating symptoms.

Cultural Influences

Panic disorder seems to occur less frequently in Hispanic Americans andAsianAmericans than in Whites in the United States (Zhang & Snowden, 1999). Hispanics show aculturally bound reaction—ataques de nervios—that seems related to PD (Guarnaccia, Canino, Rubio-Stipec, & Bravo, 1993; Guarnaccia, Rubio-Stipec, & Canino, 1989). During such an attack, PD-like symptoms are experienced (e.g., palpitations, shaking, numbness, etc.). The attacks, however, are triggered by stressful life events such as funerals or accidents, and afterward there is no recollection of the attacks.Although these attacks may be related to PD, they also show some important differences (e.g., the missing recollection). Other transcultural research focusing on how cultural beliefs may influence the expression of PDA demonstrated that, in Khmer culture, PDA-related complaints have been found: Khmer refugees in a clinical setting in the United States reported sore neck attacks (Hinton, Ba, Peou, & Um, in press a, in press b). A sore neck attack is a state of autonomic arousal (e.g., heart racing, shortness of breath, sudden headaches, blurry vision, dizziness, and buzzing in the ears) that emerges as a consequence of Kyol Goeu (wind overload, which is assumed to occur if blood and wind cannot be carried through the body because important vessels in the neck are blocked).

Despite a similar clinical presentation of PD, African Americans were found to have a later age of onset for PDA than do EuropeanAmericans, and the groups differ in the coping strategies they use to face their PDA(Smith, Friedman, & Nevid, 1999). African Americans experienced more needless psychiatric hospitalizations, more frequent emergency room visits, higher incidence of childhood trauma (Friedman, Paradis, & Hatch, 1994), and higher comorbidity with posttraumatic stress disorder (PTSD; Smith et al., 1999).

Developmental Changes

Panic disorder has also been found in adolescence; however, it is assumed that the clinical presentation does not differ from that of adults. Panic disorder in childhood is extremely rare and thus not much research has been conducted (Moore & Carr, 2000). In a study investigating the prevalence of mitral valve prolapse in children with anxiety disorders, no association with PD was found; of 52 anxious children, 9.6% were diagnosed with PD (Toren et al., 1999). It has been suggested that PD and SAD may be different clinical manifestations of the same underlying disorder (e.g., Black, 1995; Black & Robins, 1990) in different developmental stages. A recent study attempted to explore childhood risk factors such as SAD for onset of panic attacks in adolescents (Hayward, Killen, Kraemer, & Taylor, 2000). Negative affectivity and anxiety sensitivity in childhood, but not SAD, were found to predict onset of panic attacks. Other studies also failed to provide reasonable evidence that SAD in childhood continues as PD in adulthood (Manicavasagar, Silove, Curtis, & Wagner, 2000).

Etiology

Different theoretical models for PD have been presented (for a balanced review of research from different perspectives see McNally, 1994, and White & Barlow, 2002). Recently, the most common models have been integrated into a biopsychosocial approach (Barlow, 2002) in which the initial panic attack is conceptualized as a misfiring of the fear system under stressful life circumstances in physiologically vulnerable individuals. The panic reaction is similar to the emergence of the biologically based mechanism of fear in response to immediate survival threat, whereas anxiety is a response to future threats. An overly reactive autonomic nervous system (biological basis) puts an individual at risk of experiencing a panic attack in response to stress. The (false) alarm reaction becomes associated with internal sensations, leading to further false alarms in response to internal sensations (behavioral basis).

Biological Influences

Biological research on panic focuses on estimating heritability, biological challenges, neuroendocrine functioning, and neuroanatomy. With respect to heritability, the tendency to panic runs in families and has a genetic component (Barlow, 2002; Scherrer et al., 2000). Zuckerman (1999) estimates a modest heritability for PD. The disorder shares a genetic factor with agoraphobia, but not with generalized anxiety disorder or depression (Kendler et al., 1995). Chromosome studies using the quantitative trait loci method showed that chromosomes 1, 12, 15 and other nearby chromosomes are associated with a tendency to be uptight and anxious (Flint et al., 1995).

Patients with PDAare more likely to experience a panic attack in response to carbon dioxide inhalation (CO₂ hypersensitivity) than patients with other anxiety disorders (Beck & Shipherd, 1997; Biber & Alkin, 1999; Schmidt, 1999; Schmidt, Trakowski, & Staab, 1997; Sinha et al., 1999). This hypersensitivity was also found to run in families (van Beek & Griez, 2000). Recent studies found evidence, however, that it is not the CO₂ sensitivity that causes exaggerated anxiety, but rather a change in breathing involving either increased CO₂ or decreased oxygen (Beck, Ohtake, & Shipherd, 1999) and that patients with predominantly respiratory symptoms may be more affected by breathing challenges than others (Biber & Alkin, 1999; Schmidt, 1999). Results from other studies suggest a biological sensitivity to sympathetic stimulation (van Zijderveld, Veltman, van Dyck, & van Doornen, 1999).

Neuroendocrine Functioning. The brain circuit involved in panic is the fight-or-flight system (FFS; Gray, 1982; Gray & McNaughton, 1996). When stimulated in animals, this circuit triggers a response that resembles panic in humans (Gray & McNaughton, 1996).

The FFS originates in the brain stem and is also connected to the limbic system. Recently, developments in the neurobiology of fear have been integrated into a comprehensive neuroanatomical hypothesis of PD (Gorman, Kent, Sullivan, & Coplan, 2000). The authors suggest that fear responses are mediated by a fear network that is centered in the amygdala, which interacts with the hippocampus and medial prefrontal cortex. These projections may account for conditioned fear responses.

Behavioral Influences

Behavioral approaches to panic (e.g., Mineka, 1985;Wolpe & Rowan, 1988) are based on classical conditioning processes assuming that an initial fear reaction (unconditioned response, or UCR) occurs in response to a dangerous or stressful situation (unconditioned stimulus, or UCS). During this response a variety of stimuli (conditioned stimuli, or CSs), both external (e.g., open spaces) and internal (e.g., cardiorespiratory symptoms such as hyperventilation, rapid heartbeat); are present and may become associated with this fear reaction. Subsequently, these cues will be able to provoke a similar fear reaction (conditioned response, or CR) despite the absence of a dangerous or stressful situations (UCS), resulting in panic attacks. The behavioral approach is based on Razran’s (1961) model of interoceptive conditioning. Furthermore, internal cues such as breathing alterations can also cause a panic attack when they are provoked by normal circumstances, including exercising, due to the associative power they acquired during the conditioning process. Near-drowning or other suffocation experiences have been emphasized as initial traumatic situations that can elicit the first panic attack and were found to precede the onset of PD in a subsample of patients with the disorder (Alkin, 1999; Bouwer & Stein, 1997). Furthermore, one year after traumatic brain injury, the rates of PD were much higher in this population than in the general population (Deb, Lyons, Koutzoukis, Ali, & McCarthy, 1999). The frequency of panic attacks in patients who had already developed PD, however, was unaffected by a traumatic event (Sasson, Zohar, Gross, Taub, & Fux, 1999).

The behavioral approach to PD was criticized because of the conceptual ambiguity of the CS, CR, and UCS in regard to internal sensations (McNally, 1990, 1994), and because the behavioral approach could explain neither why these sensations become conditioned only for PD patients nor why they do not always result in full-blown panic attacks. Answers to these puzzles have been suggested in the context of an up-todate learning-theory conceptualization of the development of PD (Barlow, 2002).

Cognitive Influences

As an alternative to the interoceptive conditioning model, Clark (1986, 1989) emphasized catastrophic misinterpretations of bodily sensations as the primary cause of PD. Typical panic-related thoughts are “I will have a heart attack,” “I will collapse,” “I will go crazy,” or “I will lose control.” Impending insanity is often associated with feelings of derealization, whereas thoughts about heart failure are often triggered by heart-related sensations such as palpitations. In his cognitive model, Clark assumes that sensations, regardless of their origins, will not lead to panic unless they are interpreted as a threat to one’s physical or mental integrity. Furthermore, stimuli related to panic concerns were found to be processed differently than stimuli that were not related to panic concerns (McNally, 1994; Pauli et al., 1997). Improvements in panic symptoms have been associated with changes in information-processing characteristics (e.g., Dengler, Wiedemann, & Pauli, 1999). Further evidence for this model comes from biological challenge studies.As discussed previously, patients with PDA are more sensitive to artificially provoked breathing alterations. Clark believes that these challenge procedures provoke sensations in all participants, but that only patients with PD experience fear in response to these sensations because they tend to misinterpret them. In fact, it has been found that challenges produce similar bodily sensations both in patients with PD and in participants without a mental disorder (Gaffney, Fenton, Lane, & Lake, 1988). Furthermore, providing safety information makes it less likely that patients with PD will panic in challenge situations (Salkovskis & Clark, 1990). In addition, physical sensations alone are not sufficient to predict panic development (Moore & Zebb, 1999). Clark’s (1989) cognitive theory was criticized several times (e.g., Klein & Klein, 1989b; Seligman, 1988) because, for example, it does not explain why catastrophic beliefs persist despite contrary information (e.g., information that one has repeatedly survived panic attacks).

Recent developments focus on the concept of sensitivity to anxiety. Catastrophic cognitions can occur at the time of the attack (i.e., they are acute) or can be more persistent. Apersistent tendency to misinterpret certain bodily sensations as catastrophic or imminently dangerous can be considered a trait called anxiety sensitivity (AS). Persons with high AS dislike intense arousal and perceive it as frightening. The concept of AS has stimulated a significant amount of research, which is summarized in Taylor (1999). Anxiety sensitivity was found to significantly predict panic symptoms after a biological challenge task in nonclinical participants (Eifert, Zvolensky, Sorrell, Hopko, & Lejuez, 1999). Other cognitive factors that contribute to panic attacks are predictability, controllability, and expectancies (see Barlow, 2002; McNally, 1990, 1994).

Generalized Anxiety Disorder

Generalized anxiety disorder (GAD) is characterized by excessive anxiety and worry about a number of events or activities. Individuals with GAD tend to find this worry difficult to control. The worry is also associated with several physical symptoms such as muscle tension, fatigue, and restlessness (APA, 1994). In comparison with other anxiety disorders, GAD has less well established theoretical understanding; and, compared with other anxiety disorders, GAD is the diagnostic category that has changed the most over the past 20 years (Campbell & Brown, 2002).

For example, in DSM-III, the diagnostic criteria for GAD required the presence of persistent anxiety as evidenced by symptoms from at least three of four categories, including motor tension, autonomic hyperactivity, apprehensive expectation, and vigilance and scanning of the environment (APA, 1980). However, this diagnostic description of GAD made it difficult for both researchers and clinicians to distinguish between generalized and anticipatory anxiety (Brown, O’Leary, & Barlow, 1993). Accordingly, in DSM-III-R (APA, 1987), the symptom criteria were changed to specify that the worry was not due to another Axis I diagnosis. The time required to make a diagnosis of GAD was also extended from 1 to 6 months, to differentiate the disorder from transient worry due to stressful events (APA, 1987). After DSM-III-R and by the time of publication of DSM-IV, GAD was conceptualized by defining features of chronic worry and persistent somatic symptoms (Brown et al., 1993). DSM-IV stipulated that a worried individual must have at least three of six physical symptoms of anxiety for 6 months or more in order to receive a diagnosis of GAD.

In part because of the changing view of GAD, treatments developed or adapted for the disorder are less well established. In recent years, the nature of GAD has been more fully explored and effective psychological treatments have been critically evaluated. The following section will describe the clinical presentation, models of etiology, and understanding of the current treatments for GAD.

Clinical Presentation

In general, GAD tends to be a chronic condition that fluctuates with the current level of stress in the patient’s life (Brown, 1997). The majority of patients report an onset of GAD before the age of 20, although a subset of patients report that their worries began in adulthood (Brown et al., 1993). Although the results vary, several studies suggest that the age of onset for GAD may be earlier than for other anxiety disorders (Massion, Warshaw, & Keller, 1993; Woodman, Noyes, Black, Schlosser, & Yagla, 1999).

Prevalence and Demographics

Prevalence data for GAD are determined from epidemiological studies. In the United States, the National Comorbidity Survey (NCS) estimated the current prevalence rate of GAD to be 1.6% of the population (Wittchen, Zhao, Kessler, & Eaton, 1994). The NCS also found that GAD affects approximately 5.1% of the population over the course of a lifetime (Kessler et al., 1994). In the general population, GAD appears to be less common than specific or social phobia but is currently slightly more common than PD (Roemer, Orsillo, & Barlow, 2002).

Outside the United States, prevalence rates for GAD have also been estimated. In Italy, current and lifetime GAD prevalence estimates based on DSM-III-R criteria were found to be 2.8 and 5.4%, respectively (Faravelli, Degl’Innocenti, & Giardinelli, 1989). Alternately, a two-stage epidemiological study of a rural area in South Africa found a prevalence rate of 3.7% based on DSM-IV criteria (Bhagwanjee, Parekh, Paruk, Petersen, & Subedar, 1998, as cited in Roemer et al., 2002).

In general, the research suggests that GAD occurs more frequently in women. For example, GAD appears to be about twice as common for women as for men in both community and clinical samples (Wittchen et al., 1994). However, cultural factors may also play a role in determining the prevalence of GAD among different groups of individuals. For example, the epidemiological study conducted in South Africa found that men showed a higher prevalence of GAD than women (Bhagwanjee et al., 1998).

GAD is frequently comorbid with other disorders. Some symptoms of GAD, such as irritability and fatigue, overlap with other disorders, such as depression. However, research suggests that GAD is a separate diagnostic factor (Brown, Chorpita, & Barlow, 1998). At the same time, GAD commonly co-occurs with other disorders. For example, clinical data suggest 68% current and 92% lifetime comorbidity with another Axis I disorder (Brown et al., 2001). Mood disorders and social phobia seem to be the disorders most frequently diagnosed in addition to GAD (Brown et al., 2001).

It may be difficult at times for clinicians to distinguish GAD from normal worry or anxious cognitions associated with other anxiety disorders (Campbell & Brown, 2002). Borkovec, Shadick, and Hopkins (1991) describe worry as a predominantly verbal, conceptual activity aimed at problem solving. Borkovec (1994) suggests that worry is an attempt to control uncertainty and avoid the negative affect associated with a lack of control. However, the long-term consequences of avoidance may lead to the maintenance of worry. Thus, pathological worry is hypothesized to be maintained by the negative reinforcement associated with the avoidance of negative affect. Avoidance of negative affect also may inhibit the processing of emotionally threatening material, which is considered necessary in the reduction of anxiety (Brown, 1997).

Pathological worry is associated with the perception that the world is threatening and that one is unable to cope with or control uncertain future events (Brown, 1997). Pathological worry in GAD patients is distinguished from normal worry by the percentage of the day that is taken up with worry, as well as the impairment and distress caused by the worry. Additionally, some researchers suggest that the distinguishing factor between GAD and normal worry is the amount of meta-worry—that is, the concern that the worry causes the individual (Wells & Carter, 1999). This model suggests that pathological worry results from the interaction between positive beliefs concerning the advantages of worry as a coping strategy and negative appraisals of worry. For example, Wells and Carter suggest that the GAD patients’ worry is maintained by avoidance of the thoughts associated with negative beliefs regarding worry, along with the continued use of worry as a coping strategy. Both models stress the importance of avoidance and cognitions in the maintenance of GAD. A theoretical framework for understanding GAD is an important element of developing and evaluating treatment to address this disorder.

Children as well as adults with GAD manifest excessive anxiety concerning a number of different spheres, including the future, world events, school or work, and the health of themselves and their families. The clinician must distinguish between developmentally appropriate levels of anxiety and clinically significant levels of worry. Anxiety and fear naturally develop in children but become clinically significant when they begin to interfere in the child’s life. GAD should be distinguished from other anxiety disorders by the nature and specificity of the worry. For example, if the worry in different areas, such as relationships and work, is focused on one principal concern, such as the negative evaluation of others, a diagnosis of social phobia instead of GAD would better describe the individual’s anxiety (Campbell & Brown, 2002). Conversely, if the individual has diffuse and varied concerns in a number of different areas, a diagnosis of GAD may best capture the client’s anxiety.

Developmental Changes

As with other anxiety disorders, the expression of GAD changes throughout the lifetime. Because GAD emphasizes worry or uncontrollable cognitions, it is seldom diagnosed in very young children. However, children as young as 7 years of age can express their worries about a number of areas. Often parents provide information concerning the nature of their child’s worries. Interestingly, the parents of some children may provide the model and initial negative evaluation of worry for their children (Chorpita & Barlow, 1998).

Children who are overanxious may innately have the higher baselines of arousal associated with excessive worry and elevated tension. However, expression of worry does seem to change over time. For example, older and younger children report differences in their worry. Data derived from self-report inventories demonstrates significantly more state and trait anxiety, worry, and oversensitivity, and higher levels of depression in older than younger children with GAD. Children of different ages also report differences in the number of worry symptoms, displayed patterns of comorbidity, and severity of anxiety. However, GAD is equally likely to occur in younger and older age groups.

In some cases, GAD may be considered to be a chronic, lifelong illness. When GAD is diagnosed in adulthood, many patients report that GAD began during childhood (Brown, 1997). However, other individuals report that GAD began during adulthood, usually in response to a stressful life event. Brown (1997) suggests that there may be two separate pathways to the development of GAD. Interestingly, both models of GAD correctly reflect one of the separate mechanisms that may result in the expression of GAD.

Although GAD does not disappear with age, little is known about its expression in the elderly population. The NCS found that GAD was most common in the group over age 45, and least common in the youngest group (aged 15–24; Wittchen et al., 1994). Flint (1994) reported prevalence rates of GAD among older adults to be as high as 7%. More recent research revealed that 25% of older adults with depression also met criteria for GAD, and that the additional presence of symptoms of GAD was associated with a higher level of suicidality (Lenze et al., 2000, as cited in Roemer et al., 2002). However, the elder adult population seems to have been neglected by researchers for the most part (Blazer, 1997). The lack of information on GAD in the elderly may be attributed in part to difficulties associated with conducting research in this population (e.g., many of the physical symptoms associated with GAD could also be due to other medical conditions or factors associated with aging; Blazer, 1997). Thus, good assessment instruments and treatment studies are lacking for elder adults, largely due to a lack of sufficient research interest (Beck & Stanley, 1997).

Additionally, a diagnosis of GAD also requires a rule-out of medical conditions, which may be more difficult to determine in an older individual. Although some treatment techniques may be beneficial for those elderly individuals who are not cognitively impaired, no research has been conducted in this area (Blazer, 1997). As yet there is little known or understood about the expression of GAD in the elderly.

Etiology

In general, GAD is considered to develop as neurobiological and psychological vulnerabilities are activated by negative or stressful life events (Roemer et al., 2002). These neurobiological and psychological vulnerabilities are considered to develop as the result of early experience and patterns of interaction. In GAD, when an individual’s vulnerabilities are activated by life events, the attentional focus remains on these generally negative life events. This attention to the negative events distinguishes GAD from other anxiety disorders, which focus attention on discrete external events such as phobic objects, or on internal events as with panic attacks (Roemer et al., 2002). Thus, a sensitivity to relatively minor inconveniences develops. Additionally, the individual’s reaction to these events is accompanied by arousal associated with negative affect. The individual develops a sense that these events are proceeding in an unpredictable, uncontrollable fashion, reflecting a psychological diathesis arising out of early experience (Roemer et al., 2002).

Thus begins a maladaptive process of shifting the focus of attention from the task at hand to self-evaluative modes, which further increases arousal (Roemer et al., 2002). As noted previously, psychological and neurobiological vulnerabilities lead to a fundamental perception of a lack of control over potential threats. The perceived lack of control leads to distortions in information processing, as occurs with the narrowing of attention to the focus of the concern and the increasing of vigilance (Roemer et al., 2002). The process of worry becomes negatively reinforcing in an attempt to control this spiraling process.

It is hypothesized that the isolated presence of either a psychological or a neurobiological vulnerability would be insufficient to lead to the development of GAD. Rather, one would expect to see a personality style characterized by some combination of pessimism, arousability, low self-confidence, or, perhaps, no clinical manifestations (Roemer et al., 2002). However, the synergistic effect of the combination of genetic vulnerabilities and early experiences would be most likely to lead to the clinical manifestation of GAD (Roemer et al., 2002).

Conclusions

We have learned much about anxiety disorders in the last decade—but we still have much to learn. Currently, we categorize anxiety disorders based on presenting symptoms that often comprise the focus of anxiety and fear. The implication of this classification is that we need to develop individual treatments for each specific anxiety disorder as well as specific assessment strategies. It may be, however, that we categorize anxiety (and mood) disorders more parsimoniously by focusing on the commonalities rather than on the differences among them. Work is currently proceeding along these lines in anticipation of the next edition of the DSM (namely, the DSM-V). These developments may, in turn, open up a new perspective on the nature and treatment of anxiety, mood, and related disorders.

Bibliography:

1. Albano, A. M., Chorpita, B. F., & Barlow, D. H. (1996). Childhood anxiety disorders. In E. J. Mash & R. A. Barkley (Eds.), Child psychopathology (pp. 196–241). New York: Guilford Press.
2. Al-Issa, I., & Oudji, S. (1998). Culture and anxiety disorders. In S. S. Kazarian & D. R. Evans (Eds.), Cultural clinical psychology: Theory, research, and practice (pp. 127–151). New York: Oxford University Press.
3. Alkin, T. (1999). Near-drowning experiences and panic disorder. American Journal of Psychiatry, 156,
4. Alnaes, R., & Torgersen, S. (1999). A 6-year follow-up study of anxiety disorders in psychiatric outpatients: Development and continuity with personality disorders and personality traits as predictors. Nordic Journal of Psychiatry, 53, 409–416.
5. (1968).Diagnosticandstatistical manual of mental disorders (2nd ed.). Washington, DC: Author.
6. (1980).Diagnosticandstatistical manual of mental disorders (3rd ed.). Washington, DC: Author.
7. American Psychiatric Association. (1987). Diagnostic and statistical manual of mental disorders (3rd ed., rev.). Washington, DC: Author.
8. (1994).Diagnosticandstatistical manual of mental disorders (4th ed.). Washington, DC: Author.
9. American Psychiatric Association. (2000). Diagnostic and statistical manual of mental disorders (4th ed., Text Revision). Washington, DC: Author.
10. Amies, P. L., Gelder, M. G., & Shaw, P. M. (1983). Social phobia: A comparative clinical study. British Journal of Psychiatry, 142, 174–179.
11. Amir, N., Foa, E. B., & Coles, M. E. (1998a). Automatic activation and strategic avoidance of threat-relevant information. Journal of Abnormal Psychology, 107, 285–290.
12. Amir, N., Foa, E. B., & Coles, M. E. (1998b). Negative interpretation bias in social phobia. Behavior Research and Therapy, 36, 945–957.
13. Antony, M. M., Downie, F., & Swinson, R. P. (1998). Diagnostic issues and epidemiology in obsessive-compulsive disorder. In R. P. Swinson, M. M. Antony, S. Rachman, & M. A. Richter (Eds.), Obsessive-compulsive disorder: Theory, research and treatment (pp. 3–32). New York: Guilford Press.
14. Antony, M. M., Roth, D., Swinson, R. P., Huta, V., & Devins, G. M. (1998). Illness intrusiveness in individuals with panic disorder, obsessive-compulsive disorder, or social phobia. Journal of Nervous and Mental Disease, 186(5), 311–315.
15. Asnis, J., Faisal, A., & Sanderson, W. (1999). Environmental factors in panic disorder. Journal of Clinical Psychiatry, 60,
16. Baker, S. L., Patterson, M. D., & Barlow, D. H. (2002). Panic disorder and agoraphobia. In M. M. Anthony & D. H. Barlow (Eds.), Handbook of assessment and treatment planning for psychological disorders (pp. 67–112). New York: Guilford Press.
17. Bandura, A. (1969). Principles of behavior modification. New York: Holt, Rinehart, & Winston.
18. Barlow, D. H. (1988). Anxiety and its disorders. New York: Guilford Press.
19. Barlow, D. H. (2000). Unraveling the mysteries of anxiety and its disorders from the perpective of emotion theory. American Psychologist, 55, 1245–1263.
20. Barlow, D. H. (2002). Anxiety and its disorders: The nature and treatment of anxiety and panic (2nd ed.). New York: Guilford Press.
21. Barsky, A. J., Delamater, B. A., & Orav, J. E. (1999). Panic disorder patients and their medical care. Psychosomatics, 40, 50–56.
22. Bauer, D. H. (1976). An exploratory study of developmental changes in children’s fears. Journal of Child Psychology and Psychiatry and Allied Disciplines, 17(1), 69–74.
23. Beck, G. J., Ohtake, P. J., & Shipherd, J. C. (1999). Exaggerated anxiety is not unique to CO₂ in panic disorder: A comparison of hypercapnic and hypoxic challenges. Journal of Abnormal Psychology, 108, 473–482.
24. Beck, G. J., & Shipherd, J. C. (1997). Repeated exposure to interoceptive cues: Does habituation of fear occur in panic disorder patients? A preliminary report. Behaviour Research and Therapy, 35, 551–557.
25. Beck,J.G.,&Stanley,M.A.(1997).Anxietydisordersintheelderly: The emerging role of behavior therapy. Behavior Therapy, 28(1), 83–100.
26. Bell-Dolan,D.(1995).Separationanxietydisorder.InR.T.Ammerman & M. Hersen (Eds.), Handbook of child behavior therapy in the psychiatric setting (pp. 217–298). NewYork:Wiley.
27. Bernstein, G. A., & Borchardt, C. M. (1991). Anxiety disorders of childhood and adolescence: A critical review. Journal of the American Academy of Child and Adolescent Psychiatry, 30(4), 519–532.
28. Biber, B., & Alkin, T. (1999). Panic disorder subtypes: Differential responses to CO₂ American Journal of Psychiatry, 156, 739–744.
29. Biederman, J., Rosenbaum, J. F., Hirshfeld, D. R., Faraone, S. V., Bolduc, E. A., Gersten, M., Meminger, S. R., Kagan, J., Snidman, N., & Reznick, S. (1990). Psychiatric correlates of behavioral inhibition in young children of parents with and without psychiatric disorders. Archives of General Psychiatry, 47, 21–26.
30. Bird, H. R., Canino, G., Rubio-Stipec, M., Gould, M. S., Ribera, J., Sesman, M., Woodbury, M., Huertas-Goldman, S., Pagan, A., Sanchez-Lacay, A., & Moscoso, M. (1988). Estimates of the prevalence of childhood maladjustment in a community survey in Puerto Rico: The use of combined measures. Archives of General Psychology, 45(12), 1120–1126.
31. Birehall, H., Brandon, S., & Taub, N. (2000). Panic in a general practice population: Prevalence, psychiatric comorbidity, and associated disability. Social Psychiatry and Psychiatric Epidemiology, 35, 235–241.
32. Black, B. (1995). Separation anxiety disorder and panic disorder. In J. S. March (Ed.), Anxiety disorders in children and adolescents (pp. 212–234). New York: Guilford Press.
33. Black, B., & Robins, D. R. (1990). Panic disorder in children and adolescents. Journal of the American Academy of Child and Adolescent Psychiatry, 29, 36–44.
34. Blanco, C., Schneier, F. R., & Liebowitz, M. R. (in press). Psychopharmacology. In S. G. Hofmann & P. M. DiBartolo (Eds.), Social phobia and social anxiety: An integration. Needham Heights, MA: Allyn & Bacon.
35. Blazer, D. G. (1997). Generalized anxiety disorder and panic disorder in the elderly: A review. Harvard Review of Psychiatry, 5, 18–27.
36. Boegels, S. M., Alberts, M., & de Jong, P. J. (1996). Selfconsciousness, self-focused attention, blushing propensity and fear of blushing. Personality and Individual Differences, 21, 573–581.
37. Boone, M. L., McNeil, D. W., Masia, C. L., Turk, C. L., Carter, L. E., Reis, B. J., & Lewin, M. R. (1999). Multimodal comparison of social phobia subtypes and avoidant personality disorder. Journal of Anxiety Disorders, 13, 271–292.
38. Borkovec, T. D. (1994). The nature, functions, and origins of worry. In G. C. Davey & F. Tallis (Eds.), Worrying: Perspectives on theory, assessment, and treatment (pp. 5–33). New York: Wiley.
39. Borkovec, T. D., Shadick, R., & Hopkins, M. (1991). The nature of normal and pathological worry. In R. M. Rapee & D. H. Barlow (Eds.), Chronic anxiety: Generalized anxiety disorder, and mixed anxiety depression (pp. 29–51). New York: Guilford Press.
40. Bouwer, C., & Stein, D. J. (1997). Association of panic disorder with a history of traumatic suffocation. American Journal of Psychiatry, 154, 1566–1570.
41. Bowen, R. C., D’Arcy, C., & Orchard, R. C. (1991). The prevalence of anxiety disorders among patients with mitral valve prolapse syndrome and chest pain. Psychosomatics, 32, 400–406.
42. Bowlby, J. (1970). Disruption of affectional bonds and its effects on behavior. Journal of Contemporary Psychotherapy, 2, 75–86.
43. Brooks, R. B., Baltazar, P. L., & Munjack, D. J. (1989). Cooccurrence of personality disorders with panic disorder, social phobia, and generalized anxiety disorder: A review of the literature. Journal of Anxiety Disorders, 3, 259–285.
44. Brown, T. A. (1997). The nature of generalized anxiety disorder and pathological worry: Current evidence and conceptual models. Canadian Journal of Psychiatry, 42, 817–825.
45. Brown, T. A., Campbell, L. A., Lehman, C. L., Grisham, J. R., & Mancill, R. B. (2001). Current and lifetime comorbidity of the DSM-IV anxiety and mood disorders in a large clinical sample. Journal of Abnormal Psychology, 110, 585–599.
46. Brown, T. A., Chorpita, B. F., & Barlow, D. H. (1998). Structural relationships among dimensions of the DSM-IV anxiety and mood disorders and dimensions of negative affect, positive affect, and autonomic arousal. Journal of Abnormal Psychology, 107, 179–192.
47. Brown, T. A., O’Leary, T. A., & Barlow, D. H. (1993). Generalized anxiety In D. H. Barlow (Ed.), Clinical handbook of psychological disorders: A step-by-step treatment manual (2nd ed., pp. 137–188). NewYork: Guilford Press.
48. Burke, K. C., Burke, J. D., Jr., Regier, D. A., & Rae, D. S. (1990). Age at onset of selected mental disorders in five community populations. Archives of General Psychiatry, 47, 511–518.
49. Bush, J. P., Melamed, B. G., Sheras, P. L., & Greenbaum, P. E. (1986). Mother-child patterns of coping with anticipatory medical stress. Health Psychology, 5(2), 137–157.
50. Calamari, J. E., Faber, S. D., Hitsman, B. L., & Poppe, C. J. (1994). Treatment of obsessive-compulsive disorder in the elderly: A review and case example. Journal of Behavior Therapy and Experimental Psychiatry, 25(2), 95–104.
51. Campbell, L. A., & Brown, T. A. (2002). Assessment of generalized anxiety disorder. In M. M.Antony & D. H. Barlow (Eds.), Handbookofassessment,treatmentplanning,andoutcomeevaluation: Empirically supported strategies for psychological disorders (pp. 147–181). New York: Guilford Press.
52. Campbell, S. B. (1989). Developmental perspectives. In T. H. Ollendick & M. Hersen (Eds.), Handbook of child psychopathology (pp. 5–28). New York: Plenum.
53. Carr, A. T. (1974). Compulsive neurosis: A review of the literature. Psychological Bulletin, 81, 311–318.
54. Carr, R. E. (1998). Panic disorder and asthma: Causes, effects and research implications. Journal of Psychosomatic Research, 44, 43–52.
55. Carr, R. E. (1999). Panic disorder and asthma. Journal of Asthma, 36, 143–152.
56. Castle, D. J., Deale, A., & Marks, I. M. (1995). Gender differences in obsessive-compulsive disorder. Australian and New Zealand Journal of Psychiatry, 29(1), 114–117.
57. Chambless, D. L., Renneberg, B., Goldstein, A., & Gracely, E. J. (1992). MCMI-diagnosed personality disorders among agoraphobic outpatients: Prevalence and relationship to severity and treatment outcome. Journal of Anxiety Disorders, 6, 193– 211.
58. Chapman, T. F., Fyer, A. J., Mannuzza, S., & Klein, D. F. (1993). A comparison of treated and untreated simple phobia. American Journal of Psychiatry, 150(5), 816–818.
59. Chiland, C., & Young, B. F. (1990). Why children reject school: Views from seven countries. New Haven, CT: Yale University Press.
60. Chorpita, B. F., & Barlow, D. H. (1998). The development of anxiety: The role of control in the early environment. Psychological Bulletin, 124(1), 3–21.
61. Clark, D. M. (1986). A cognitive approach to panic. Behaviour Research and Therapy, 24, 461–470.
62. Clark, D. M. (1989). A cognitive model of panic attacks. In S. Rachman & J. D. Maser (Eds.), Panic: Psychological perspectives (pp. 71–89). Hillsdale, NJ: Erlbaum.
63. Clark, D. M., & Wells, A. (1995). A cognitive model of social phobia. In R. G. Heimberg, M. R. Liebowitz, D. A. Hope, & F. R. Schneier (Eds.), Social phobia: Diagnosis, assessment, and treatment (pp. 69–93). New York: Guilford Press.
64. Clayton, P. I. (1993). Suicide in panic disorder and depression. Current Therapeutic Research, 54, 825–831.
65. Cooper, P. J., & Eke, M. (1999). Childhood shyness and maternal social phobia: Acommunity study. British Journal of Psychiatry, 174, 439–443.
66. Costello, E. J., & Angold, A. (1995). Epidemiology. In J. March (Ed.), Anxiety disorders in children and adolescents (pp. 109– 124). New York: Guilford Press.
67. Cox, B. J., Direnfeld, D. M., Swinson, R. P., & Norton, R. G. (1994). Suicidal ideation and suicide attempts in panic disorder and social phobia. American Journal of Psychiatry, 151, 882– 887.
68. Cox, B. J., Rector, N. A., Bagby, R. M., Swinson, R. P., Levitt, A. J., & Joffe, R. T. (2000). Is self-criticism unique for depression? A comparison with social phobia. Journal of Affective Disorder, 57, 223–228.
69. Craske, M. G., & Rowe, M. K. (1997). Nocturnal panic. Clinical Psychology: Science and Practice, 4, 153–174.
70. Dammen, T., Ekeberg, O., Arnesen, H., & Friis, S. (2000). Personality profiles in patients referred for chest pain: Investigation with emphasis on panic disorder patients. Psychosomatics, 41, 269–276.
71. Deb, S., Lyons, I., Koutzoukis, C., Ali, I., & McCarthy, G. (1999). Rate of psychiatric illness 1 year after traumatic brain injury. American Journal of Psychiatry, 156, 374–378.
72. Den-Boer, J.-A., Baldwin, D. S., Bobes, J., Katschnig, H., Westenberg, H., & Wittchen, H.-U. (1999). Social anxiety disorder: Our current understanding. International Journal of Psychiatry in Clinical Practice, 3(Suppl. 3), 3–12.
73. Den-Boer, J.-A., & Dunner, D. L. (1999). Physician attitudes concerning diagnosis and treatment of social anxiety disorder in Europe and North America. International Journal of Psychiatry in Clinical Practice, 3(Suppl. 3), 13–19.
74. Dengler, W., Wiedemann, G., & Pauli, P. (1999). Association between cortical slow potentials and clinical rating scales in panic disorder: A 1.5-year follow-up study. European Psychiatry, 14, 399–404.
75. Diaferia, G., Sciuto, G., Perna, G., Barnardeschi, L., Battaglia, M., Rusmini, S., & Bellodi, L. (1993). DSM-III-R personality disorders in panic disorders. Journal of Anxiety Disorders, 7, 153– 161.
76. diNardo, P. A., Guzy, L. T., & Bak, R. M. (1988). Anxiety response patterns and etiological factors in dog-fearful and non-fearful subjects. Behavior Research and Therapy, 26(3), 245–251.
77. Dollard, J., & Miller, N. E. (1950). Personality and psychotherapy: Ananalysisintermsoflearning,thinking,andculture.NewYork: McGraw-Hill.
78. Eaton, W. W., Kessler, R. C., Wittchen, H. U., & Magee, W. J. (1994). Panic and panic disorder in the United States. American Journal of Psychiatry, 151, 413–420.
79. Eaton,W.W.,Kramer,M.,Anthony,J.C.,Dryman,A.,Shapiro,S.,& Locke, B. Z. (1989). The incidence of specific DIS/DSM-III mental disorders: Data from the NIMH Epidemiologic Catchment area program. Acta Psychiatrica Scandinavica, 79(2), 163– 178.
80. Eifert, G. H., Zvolensky, M. J., Sorrell, J.T., Hopko, D. R., & Lejuez, C. W. (1999). Predictors of self-reported anxiety and panic symptoms: An evaluation of anxiety sensitivity, suffocation fear, heart-focused anxiety, and breath-holding duration. Journal of Psychopathology and Behavioral Assessment, 21, 293–305.
81. Eisen, A. R., Engler, L. B., & Geyer, B. (1998). Parent training for separation anxiety disorder. In J. M. Briesmeister & C. E. Schaefer (Eds.), Handbook of parent training: Parents as cotherapists for childrens’ behavior problems (2nd ed., pp. 205– 224). NewYork: Wiley.
82. Faravelli, C., Degl’Innocenti, B. G., & Giardinelli, L. (1989). Epidemiology of anxiety disorders in Florence. Acta Psychiatrica Scandinavica, 79(4), 308–312.
83. Faravelli, C., Zucchi, T., Viviani, B., Salmoria, R., Perone, A., Paionni, , Scarpato, A., Vigliaturo, D., Rosi, S., D’Adamo, D., Bartolozzi, D., Cecchi, C., & Abrardi, L. (2000). Epidemiology of social phobia: Aclinical approach. European Psychiatry, 15, 17–24.
84. Fava, M., Rankin, M. A., Wright, E. C., Alpert, J. E., Nierenberg, A. A., Pava, J., & Rosenbaum, J. F. (2000). Anxiety disorders in major depression. Comprehensive Psychiatry, 41, 97–102.
85. Feldman, J. M., Giardino, N. D., & Lehrer, P. M. (2000). Asthma and panic disorder. In D. L. Mostofsky & D. H. Barlow (Eds.), The management of stress and anxiety in medical disorders (pp. 220–239). Boston: Allyn & Bacon.
86. Fleet, R., Lavoie, K., & Beitman, B. D. (2000). Is panic disorder associated with coronary artery disease? A critical review of the literature. Journal of Psychosomatic Research, 48, 347–356.
87. Flint, A. J. (1994). Epidemiology and comorbidity of anxiety disordersintheelderly.AmericanJournalofPsychiatry,151,640–649.
88. Flint, A. J. (1998). Management of anxiety in late life. Journal of Geriatric Psychiatry and Neurology, 11, 194–200.
89. Flint, J., Corley, R., DeFries, J. C., Fulker, D. W., Gray, J. A., Miller, S., & Collins, A. C. (1995). Chromosomal mapping of three loci determining quantitative variation of susceptibility to anxiety in the mouse. Science, 268, 1432–1435.
90. Foa, E. B., Franklin, M. E., Perry, K. J., & Herbert, J. D. (1996). Cognitive biases in generalized social phobia. Journal of Abnormal Psychology, 105, 433–439.
91. Foa, E. B., & Kozak, M. J. (1985). Treatment of anxiety disorders: Implications for psychopathology. In A. H. Tuma & J. D. Maser (Eds.), Anxiety and the anxiety disorders (pp. 421–452). Hillsdale, NJ: Erlbaum.
92. Francis, G., Last, C. G., & Strauss, C. C. (1987). Expression of separation anxiety disorder: The roles of age and gender. Child Psychiatry and Human Development, 18(2), 82–89.
93. Franklin, M. E., & Foa, E. B. (1998). Cognitive-behavioral treatments for obsessive-compulsive disorder. In P. E. Nathan & J. M. Gorman (Eds.), A guide to treatments that work (pp. 339–357). New York: Oxford University Press.
94. Fredrikson, M., Annas, P., Fischer, H., & Gustav, W. (1996). Gender and age differences in the prevalence of specific fears and phobias. Behaviour Research and Therapy, 34(1), 33–39.
95. Fredrikson, M., Annas, P., & Wik, G. (1997). Parental history, aversive exposure and the development of snake and spider phobia in women. Behavior Research and Therapy, 35(1), 23–28.
96. Freud, A. (1958). Psychoanalytic study of the child. New Haven, CT: Yale University Press.
97. Friedman, S., Jones, J. C., Chernen, L., & Barlow, D. H. (1992). Suicidal ideation and suicide attempts among patients with panic disorder: Asurvey of two outpatient clinics. American Journal of Psychiatry, 149, 680–685.
98. Friedman, S., Paradis, C. M., & Hatch, M. (1994). Characteristics of African-American and White patients with panic disorder and agoraphobia. Hospital and Community Psychiatry, 45, 798–803.
99. Fyer, A. J., Manuzza, S., Gallups, M. S., Martin, L. Y., Aaronson, C., Gorman, J. M., Liebowitz, M. R., & Klein, D. F. (1990). Familial transmission of simple phobias and fears: A preliminary report. Archives of General Psychiatry, 47(3), 252–256.
100. Gaffney, F. A., Fenton, B. J., Lane, L. D., & Lake, C. R. (1988). Hemodynamic, ventilatory, and biochemical responses of panic patients and normal controls with sodium lactate infusion and spontaneous panic attacks. Archives of General Psychiatry, 45, 53–60.
101. Geffken, G. R., Pincus, D. B., & Zelikovsky, N. (1999). Obsessive-compulsive disorder in children and adolescents: Review of background, assessment, and treatment. Journal of Psychological Practice, 5(1), 15–31.
102. Geller, B., Chestnut, E. C., Miller, M. D., Price, O. T., & Yates, E. (1985). Preliminary data on DSM-III associated features of majordepressivedisordersin children and adolescents.American Journal of Psychiatry, 142(5), 643–644.
103. George, C. F., Millar, T. W., & Kryger, M. H. (1988). Sleep apnea and body position during sleep. Sleep, 11(1), 90–99.
104. Gilboa-Schechtman, E., Foa, E. B., & Amir, N. (1999). Attentional biases for facial expressions in social phobia: The face-in-thecrowd paradigm. Cognition and Emotion, 13, 305–318.
105. Gorman, J. M., Kent, J. M., Sullivan, G. M., & Coplan, J. D. (2000). Neuroanatomicalhypothesisofpanicdisorder,revised.American Journal of Psychiatry, 157, 493–505.
106. Gray, J. A. (1982). The neuropsychology of anxiety. New York: Oxford University Press.
107. Gray, J. A., & McNaughton, N. (1996). The neuropsychology of anxiety: Reprise. In D. A. Hope (Ed.), Perspectives on anxiety, panic and fear (The 43rd Annual Nebraska Symposium on Motivation) (pp. 61–134). Lincoln: Nebraska University Press.
108. Graziano, A. M., & De Giovanni, I. S. (1979). The clinical significance of childhood phobias: A note on the proportion of childclinical referrals for the treatment of children’s fears. Behaviour Research and Therapy, 17(2), 161–162.
109. Greenberg, M. T., Speltz, M. L., & DeKlyen, M. (1993). The role of attachment in early development of disruptive problems. Development and Psychopathology, 5(1-2), 191–213.
110. Guarnaccia, P. J. (1997). A cross-cultural perspective on anxiety disorders. In S. Friedman (Ed.), Cultural issues in the treatment of anxiety (pp. 3–20). New York: Guilford Press.
111. Guarnaccia, P. J., Canino., G., Rubio-Stipec, M., & Bravo, M. (1993). The prevalence of ataques de nervios in the Puerto Rico Disaster Study. Journal of Nervous and Mental Disease, 181, 157–165.
112. Guarnaccia, P. J., Rubio-Stipec, M., & Canino, G. J. (1989). Ataques de nervios in the Puerto Rican Diagnostic Interview Schedule: The impact of cultural categories on psychiatric epidemiology. Culture, Medicine, and Psychiatry, 13, 275–295.
113. Hanna,G.L.(1995).Demographicandclinicalfeaturesofobsessivecompulsive disorder in children and adolescents. Journal of the American Academy of Child and Adolescent Psychiatry, 34(1), 19–27.
114. Hayward, C., Killen, J. D., Kraemer, H. C., & Taylor, C. B. (2000). Predictors of panic attacks in adolescents. Journal of the American Academy of Child and Adolescent Psychiatry, 39, 207–214.
115. Hazen, A. L., & Stein, M. B. (1995). Clinical phenomenology and comorbidity. In M. B. Stein (Ed.), Social phobia: Clinical and research perspectives (pp. 3–41). Washington, DC: American Psychiatric Press.
116. Head, D., Bolton, D., & Hymas, N. (1989). Deficit in cognitive shifting ability in patients with obsessive-compulsive disorder. Biological Psychiatry, 25(7), 929–937.
117. Heckelman, L. R., & Schneier, F. R. (1995). Diagnostic issues. In R. G. Heimberg, M. R. Liebowitz, D. A. Hope, & F. R. Schneier (Eds.), Social phobia: Diagnosis, assessment, and treatment (pp. 3–20). New York: Guilford Press.
118. Heimberg, R. G., & Juster, H. R. (1995). Cognitive-behavioral treatments: Literature review. In R. G. Heimberg, M. R. Liebowitz, D.A.Hope,&F.R.Schneier(Eds.),Socialphobia:Diagnosis,assessment,andtreatment(pp.261–309).NewYork:GuilfordPress.
119. Heimberg, R. G., Stein, M. B., Hiripi, E., & Kessler, R. C. (2000). Trends in the prevalence of social phobia in the United States: A synthetic cohort analysis of changes over four decades. European Psychiatry, 15, 29–37.
120. Heinrichs, N., & Hofmann, S. G. (2001). Information processing biases in social phobia: A critical review. Clinical Psychology Review, 21(5), 751–770.
121. Hinton, D., Ba, P., Peou, S., & Um, K. (in press a). Kyol Goeu (“wind overload”): Part I. Cultural syndromes, catastrophic cognitions, and the generation of panic; or, Kyol Goeu and orthostatic panic among Khmer refugees attending a psychiatric clinic. Transcultural Psychiatry.
122. Hinton, D., Ba, P., Peou, S., & Um, K. (in press b). Kyol Goeu (“wind overload”): Part II. The prevalence of Kyol Goeu (“wind overload”) and near-Kyol Goeu episodes in a Khmer psychiatric population. Transcultural Psychiatry.
123. Hofer, M. A. (1994). Hidden regulators in attachment, separation, and loss. In A. C. Huston (Ed.), Children in poverty: Child development and public policy (pp. 1–22). New York: Cambridge University Press.
124. Hofmann, S. G. (1999). Self-focused attention before and after treatment of social phobia. Behaviour Research and Therapy, 38, 717–725.
125. Hofmann, S. G., & Barlow, D. H. (1999). The costs of anxiety disorders: Implications for psychosocial interventions. In N. E. Miller & K. M. Magruder (Eds.), Cost-effectiveness of psychotherapy: A guide for practitioners, researchers, and policymakers (pp. 224–234). New York: Oxford University Press.
126. Hofmann, S. G., Ehlers, A., & Roth, W. T. (1995). Conditioning theory: A model for the etiology of public speaking anxiety? Behaviour Research and Therapy, 33, 567–571.
127. Hofmann, S. G., Newman, M. G., Ehlers, A., & Roth, W. T. (1995). Psychophysiological differences between subgroups of social phobia. Journal of Abnormal Psychology, 104, 224–231.
128. Horenstein, M., & Segui, J. (1997). Chronometrics of attentional processes in anxiety disorders. Psychopathology, 30, 25–35.
129. Hornig, C. D., & McNally, R. J. (1995). Panic disorder and suicide attempt: A reanalysis of data from the Epidemiologic Catchment Area study. British Journal of Psychiatry, 167, 76–79.
130. Hudson, J. I., Pope, H. G., Yurgelun-Todd, D., Jonas, J. M., & Frankenburg, F. R. (1987). A controlled family history study of bulimia. Psychological Medicine, 17(4), 883–890.
131. Hudson, J. L., & Rapee, R. M. (2000). The origins of social phobia. Behavior Modification, 24, 102–129.
132. Jeejeebhoy, F. M., Dorian, P., & Newman, D. M. (2000). Panic disorder and the heart: A cardiology perspective. Journal of Psychosomatic Research, 48, 393–403.
133. Jones, M. K., & Menzies, R. G. (1995). The etiology of fear of spiders. Anxiety, Stress, and Coping: An International Journal, 8(3), 227–234.
134. Jostes, A., Pook, M., & Florin, I. (1999). Public and private selfconsciousness as specific psychopathological features. Personality and Individual Differences, 27, 1285–1295.
135. Kagan, J. (1989). Temperamental contributions to social behavior. American Psychologist, 44, 668–674.
136. Kagan, J., Reznick, J. S., & Snidman, N. (1987). The physiology and psychology of behavioral inhibition in children. Child Development, 58, 1459–1473.
137. Kagan, J., Snidman, N., & Arcus, D. M. (1992). Initial reactions to unfamiliarity. Current Directions in Psychological Science, 1, 171–174.
138. Karno, M., Golding, J. M., Sorenson, S. B., & Burnam, M. A. (1988). The epidemiology of obsessive-compulsive disorder in five U.S. communities. Archives of General Psychiatry, 45(12), 1094–1099.
139. Kasvikis,Y. G.,Tsakiris, F., Marks, I. M., Basoglu, M., & Nashirvani (1986). Past history of anorexia nervosa in women with obsessive-compulsive disorder. International Journal of Eating Disorders, 5(6), 1069–1075.
140. Katerndahl, D. A., & Realini, J. P. (1993). Lifetime prevalence of panic states. American Journal of Psychiatry, 150, 246–249.
141. Katerndahl, D. A., & Realini, J. P. (1995). Where do panic sufferers seek care? Journal of Family Practice, 40, 237–243.
142. Katerndahl, D. A., & Talamantes, M. (2000). A comparison of persons with early- versus late-onset panic attacks. Journal of Clinical Psychiatry, 61(6), 422–427.
143. Kazdin, A. E. (1992). Overt and covert antisocial behaviour: Child and family characteristics among psychiatric inpatient children. Journal of Child and Family Studies, 1(1), 3–20.
144. Kendler, K. S., Walters, E. E., Neale, M. C., Kessler, R. C., Heath, A. C., & Eaves, L. J. (1995). The structure of the genetic and environmental risk factors for six major psychiatric disorders in women. Archives of General Psychiatry, 52, 374–383.
145. Kessler, R. C., McGonagle, K. A., Zhao, S., Nelson, C. B., Hughes, M., Eshleman, S., Wittchen, H.-U., & Kendler, K. S. (1994). Lifetime and 12-month prevalence of DSM-III-R psychiatric disorders in the United States: Results from the National Comorbidity Study. Archives of General Psychiatry, 51(1), 8–19.
146. Kessler, R. C., Stang, P., Wittchen, H. U., Stein, M., & Walters, E. E. (1999). Lifetime comorbidities between social phobia and mood disorders in the US National Comorbidity Survey. Psychological Medicine, 29(3), 555–567.
147. King, N. J., Clowes-Hollins, V., & Ollendick, T. H. (1997). The etiology of childhood dog phobia. Behaviour Research and Therapy, 35(1), 77.
148. King, N. J., Hamilton, D. I., & Ollendick, T. H. (1988). Children’s phobias: A behavioral perspective. London:Academic Press.
149. Klein, D. F., & Klein, H. M. (1989a). The definition and psychopharmacology of spontaneous panic and phobia. In P. Tyrer (Ed.), Psychopharmacology of anxiety (pp. 135–162). New York: Oxford University Press.
150. Klein, D. F., & Klein, H. M. (1989b). The nosology, genetics, and theory of spontaneous panic and phobia. In P. Tyrer (Ed.), Psychopharmacology of anxiety (pp. 163–195). New York: Oxford University Press.
151. Klein, D. F., Mannuzza, S., Chapman, T., & Fyer, A. J. (1992). Child panic revisited. Journal of the American Academy of Child and Adolescent Psychiatry, 31, 112–114.
152. Kleinknecht, R. A., Dinnel, P. L., Kleinknecht, E. E., Hiruma, N., & Harada, N. (1997). Cultural factors in social anxiety: Comparison of social phobia symptoms and taijin kyofusho. Journal of Anxiety Disorders, 11, 157–177.
153. Klerman, G. L., Weissman, M. M., Ouellette, R., Johnson, J., & Greenwald, S. (1991). Panic attacks in the community: Social morbidity and health care utilization. Journal of the American Medical Association, 265, 742–746.
154. Knowles, J. A., Mannuzza, S., & Fyer, A. J. (1995). Heritability of social anxiety. In M. B. Stein (Ed.), Social phobia: Clinical and research perspectives (pp. 147–161).Washington, DC:American Psychiatric Press.
155. Kouzis,A. C., & Eaton, W. W. (2000). Psychopathology and the initiation of disability payments. Psychiatric Services, 51, 908–913.
156. Langs, G., Quehenberger, F., Fabisch, K., Klug, G., Fabisch, H., & Zapotoczky, H.-G. (2000). The development of agoraphobia in panic disorder: A predictable process? Journal of Affective Disorders, 58, 43–50.
157. Last, C. G. (1991). Somatic complaints in anxiety disordered children. Journal of Anxiety Disorders, 5(2), 125–138.
158. Last, C. G., Francis, G., Hersen, M., & Kazdin, A. E. (1987). Separation anxiety and school phobia: A comparison using DSM-III criteria. American Journal of Psychiatry, 144(5), 653–657.
159. Last, C. G., Francis, G., & Strauss, C. C. (1989). Assessing fears in anxiety-disordered children with the Revised Fear Survey Schedule for Children (FSSC-R). Journal of Clinical Child Psychology, 18(2), 137–141.
160. Last, C. G., Hersen, M., Kazdin, A. E., Finkelstein, R., & Strauss, C. C. (1987). Comparison of DSM-III separation anxiety and overanxious disorders: Demographic characteristics and patterns of comorbidity. Journal of the American Academy of Child and Adolescent Psychiatry, 26(4), 527–531.
161. Last, C. G., & Strauss, C. C. (1989). Panic disorder in children and adolescents. Journal of Anxiety Disorders, 3, 221–241.
162. Lauterbach, E. C., & Duvoisin, R. C. (1991). Anxiety disorders in familial parkinsonism. American Journal of Psychiatry, 148,
163. Leary, M. R., & Kowalski, R. M. (1995a). The self-presentation model. In R. G. Heimberg, M. R. Liebowitz, D. A. Hope, & F. R. Schneier (Eds.), Social phobia: Diagnosis, assessment, and treatment (pp. 94–112). New York: Guilford Press.
164. Leary, M. R., & Kowalski, R. M. (1995b). Social anxiety. New York: Guilford Press.
165. Lease, C. A., & Strauss, C. C. (1993). Separation anxiety disorder. In R. T. Ammerman & M. Hersen (Eds.), Handbook of behavior therapy with children and adults: A developmental and longitudinal perspective (Vol. 171, pp. 93–107). Needham Heights, MA: Allyn and Bacon.
166. Leckman, J. F., & Chittenden, E. H. (1990). Gilles de La Tourette’s syndrome and some forms of obsessive-compulsive disorder may share a common genetic diathesis. Encephale, 16(1), 321– 323.
167. Lee, S.-H., & Oh, K. S. (1999). Offensive type of social phobia: Cross-cultural perspectives. International Medical Journal, 6, 271–279.
168. Lensi, P., Cassano, G. B., Correddu, G., Ravagli, S., & Kunovac, J. J. (1996). Obsessive-compulsive disorder. Familial-developmental history, symptomatology, comorbidity and course with special reference to gender-related differences. British Journal of Psychiatry, 169(1), 101–107.
169. Leonard, H. L., Lenane, M. C., Swedo, S. E., & Rettew, D. C. (1993). Tics and Tourette’s disorder: A 2- to 7-year follow-up of 54 obsessive-compulsive children. Annual Progress in Child Psychiatry and Child Development, 402–417.
170. Ley, R. (1998). Pulmonary function and dyspnea/suffocation theory of panic. Journal of Behavior Therapy and Experimental Psychiatry, 29, 1–11.
171. Lieberman, A. F. (1992). Infant parent psychotherapy with toddlers. Development and Psychopathology, 4(4), 559–574.
172. Liebowitz, M. R., Gorman, J. M., Fyer, A. J., & Klein, D. F. (1985). Social phobia: Review of a neglected anxiety disorder. Archives of General Psychiatry, 42(7), 729–736.
173. Liebowitz, M. R., Heimberg, R. G., Fresco, D. M., Travers, J., & Stein, M. B. (2000). Social phobia or social anxiety disorder: What’s in a name? Archives of General Psychiatry, 57(2), 191–192.
174. Livingstone, R., Taylor, J. L., & Crawford, S. L. (1988). A study of somatic complaints and psychiatric diagnosis in children. Journal of the American Academy of Child and Adolescent Psychiatry, 27(2), 185–187.
175. Maidenberg, E., Chen, E., Craske, M., Bohn, P., & Bystritsky, A. (1996). Specificity of attentional bias in panic disorder and social phobia. Journal of Anxiety Disorders, 10, 529–541.
176. Main, M., Kaplan, N., & Cassidy, J. (1985). Security in infancy, childhood, and adulthood: A move to the level of representation. Monographs of the Society for Research in Child Development, 50(1-2), 66–104.
177. Manicavasagar, V., Silove, D., Curtis, J., & Wagner, R. (2000). Continuities of separation anxiety from early life into adulthood. Journal of Anxiety Disorders, 14, 1–18.
178. March, J. S., & Mulle, K. (1998). OCD in children and adolescents: A cognitive-behavioral treatment manual. New York: Guilford Press.
179. Marks,I.M.(1987a).Behavioralaspectsofpanicdisorder.American Journal of Psychiatry, 144, 1160–1165.
180. Marks, I. M. (1987b). The development of normal fear: A review. Journal of Child Psychiatry and Allied Disciplines, 28(5), 667–697.
181. Marks, I. M., & Gelder, M. G. (1966). Different ages of onset in varieties of phobia. American Journal of Psychiatry, 123, 218– 221.
182. Massion, A. O., Warsaw, M. G., & Keller, M. B. (1993). Quality of life and psychiatric morbidity in panic disorder and generalized anxiety disorder. American Journal of Psychiatry, 150(4), 600–607.
183. McFall, M. E., & Wollersheim, J. P. (1979). Obsessive-compulsive neurosis: A cognitive-behavioural formulation and approach to treatment. Cognitive Therapy and Research, 3(4), 333–348.
184. McNally, R. J. (1990). Psychological approaches to panic disorder: A review. Psychological Bulletin, 108, 403–419.
185. McNally, R. J. (1994). Panic disorder: A critical analysis. New York: Guilford Press.
186. McNally, R. J., & Steketee, G. S. (1985). The etiology and maintenance of severe animal phobias. Behavior Research and Therapy, 23(4), 430–435.
187. Melamed, B. G. (1992). Family factors predicting children’s reaction to anesthesia induction. In A. M. La Greca & L. J. Siegel (Eds.), Stress and coping in child health: Advances in pediatric psychology (pp. 140–156). New York: Guilford Press.
188. Melfsen, S., Osterlow, J., & Florin, I. (2000). Deliberate emotional expressions of socially anxious children and their mothers. Journal of Anxiety Disorders, 14, 249–261.
189. Mellings, T. M. B., & Alden, L. E. (2000). Cognitive processes in social anxiety: The effects of self-focus, rumination and anticipatory processing. Behaviour Research and Therapy, 38, 243– 257.
190. Menzies, R. G., & Clarke, J. C. (1993a). The etiology of childhood water phobia. Behaviour Research and Therapy, 31(5), 499–501.
191. Menzies, R. G., & Clarke, J. C. (1993b). The etiology of fear of heights and its relationship to severity and individual response patterns. Behaviour Research and Therapy, 31(4), 355–365.
192. Menzies, R. G., & Clarke, J. C. (1995). The etiology of phobias: A nonassociative account. Clinical Psychology Review, 15(1), 23–48.
193. Merckelbach, H., de-Jong, P. J., Muris, P., & van den Hout, M. A. (1996). The etiology of specific phobias: A review. Clinical Psychology Review, 16(4), 337–361.
194. Mineka, S. (1985). Animal models of anxiety based disorders: Their usefulness and limitations. In A. H. Tuma & J. D. Maser (Eds.), Anxiety and the anxiety disorders (pp. 199–244). Hillsdale, NJ: Erlbaum.
195. Moore, M. C., & Carr, A. (2000). Anxiety disorders. In A. Carr (Ed.), What works with children and adolescents? A critical review of psychological interventions with children, adolescents, and their families (pp. 178–202). New York: Routledge.
196. Moore, M. C., & Zebb, B. J. (1999). The catastrophic misinterpretation of physiological distress. Behaviour Research and Therapy, 37, 1105–1118.
197. Moreau, D., & Follet, C. (1993). Panic disorder in children and adolescents. Child and Adolescent Psychiatric Clinics of North America, 2, 581–602.
198. Morris, R. J., & Kratochwill, T. R. (1983). Treating children’s fears andphobias:Abehavioralapproach.NewYork:PergamonPress.
199. Mowrer, O. H. (1939). A stimulus-response analysis of anxiety and its role as a reinforcing agent. Psychological Review, 46(1), 553–566.
200. Mowrer, O. H. (1947). On the dual nature of learning—a reinterpretation of “conditioning” and “problem-solving.” Harvard Educational Review, 17, 102–148.
201. Mulkens, S., & Boegels, S. M. (1999). Learning history in fear of blushing. Behaviour Research and Therapy, 37, 1159–1167.
202. Nestadt, G., Bienvenu, O. J., Cai, G., Samuels, J. F., & Eaton, W. W. (1998). Incidence of obsessive-compulsive disorder in adults. Journal of Nervous and Mental Disease, 186(7), 401–406.
203. Nestadt, G., Samuels, J. F, Romanowski, A. J., & Folstein, M. F. (1994). Obsessions and compulsions in the community. Acta Psychiatrica Scandinavica, 89(4), 219–224.
204. Neufeld, K. J., Swartz, K. L., Bienvenu, O. J., Eaton, W. W., & Cai, G. (1999). Incidence of DIS/DSM-IV social phobia in adults. Acta Psychiatrica Scandinavica, 100(3), 186–192.
205. Noyes, R., Woodman, C. L., Holt, C. S., & Reich, J. H. (1995). Avoidant personality traits distinguishing social phobic and panic disorder subjects. Journal of Nervous and Mental Disease, 183, 145–153.
206. Ohman, A. (1986). Face the beast and fear the face: Animal and social fears as prototypes for evolutionary analysis of emotion. Psychophysiology, 23, 123–145.
207. Ollendick, T. H. (1983). Reliability and validity of the Revised Fear Schedule for Children (FSSC-R). Behavior Research and Therapy, 21, 685–692.
208. Ollendick, T. H., & King, N. J. (1991a). Developmental factors in child behavioral assessment. In P. R. Martin (Ed.), Handbook of behavior therapy and psychological science: Vol. 164. An integrative approach (pp. 57–72). Elmsford: Pergamon.
209. Ollendick, T. H., & King, N. J. (1991b). Origins of childhood fears: An evaluation of Rachman’s theory of fear acquisition. Behaviour Research and Therapy, 29(2), 117–123.
210. Ost, L. G. (1987). Age of onset in different phobias. Journal of Abnormal Psychology, 96, 223–229.
211. Pauli, P., Dengler, W., Wiedemann, G., Montoya, P., Flor, H., Birbaumer, N., & Buchkremer, G. (1997). Behavioral and neurophysiological evidence for altered processing of anxiety-related words in panic disorder. Journal of Abnormal Psychology, 106, 213–220.
212. Pavlov, I. P. (1927). Conditioned reflexes (G. V. Anrep, Trans.). London: Oxford University Press.
213. Pianta, R. C. (1999). Early childhood. In W. K. Silverman & T. H. Ollendick (Eds.), Developmental issues in the clinical treatment of children (pp. 88–107). Needham Heights, MA: Allyn and Bacon.
214. Pollack, M. H., & Marzol, P. C. (2000). Panic: Course, complications and treatment of panic disorder. Journal of Psychopharmacology, 14(Suppl. 1), 25–30.
215. Pury, C. L. S., & Mineka, S. (1997). Covariation bias for bloodinjury stimuli and aversive outcomes. Behaviour Research and Therapy, 35(1), 35–47.
216. Rachman, S. (1977). The conditioning theory of fear acquisition: A critical examination. Behavior Research and Therapy, 15, 375– 387.
217. Rapee, R. M., & Lim, L. (1992). Discrepancy between self- and observer ratings of performance in social phobics. Journal of Abnormal Psychology, 101(4), 728–731.
218. Rasmussen, S. A., & Eisen, J. L. (1989). Clinical features and phenomenology of obsessive-compulsive disorder. Psychiatric Annals, 19(2), 67–73.
219. Rasmussen, S. A., & Tsuang, M. T. (1986). Clinical characteristics and family history in DSM-III obsessive-compulsive disorder. American Journal of Psychiatry, 143(3), 317–322.
220. Razran, G. (1961). The observable unconscious and the inferable conscious in current Soviet psychophysiology. Interoceptive conditioning, semantic conditioning, and the orienting reflex. Psychological Review, 68, 81–147.
221. Regier, D. A., Boyd, J. H., Burke, J. D., Rae, D. S., Myers, J. K., Kramer, M., Robins, L. N., George, L. K., Karno, M., & Locke, B. Z. (1988). One-month prevalence of mental disorders in the United States: Based on five epidemiologic catchment area sites. Archives of General Psychiatry, 45(11), 977–986.
222. Reich, J. H. (2000). The relationship of social phobia to avoidant personality disorder: A proposal to reclassify avoidant personality disorder based on clinical empirical findings. European Psychiatry, 15, 151–159.
223. Reich, J. H., Noyes, R., & Yates, W. (1988). Anxiety symptoms distinguishing social phobia from panic and generalized anxiety disorders. Journal of Nervous and Mental Diseases, 176(8), 510–513.
224. Rettew, D. C., Swedo, S. E., Leonard, H. L., Lenane, M. C., & Rappaport, M. (1992). Obsessions and compulsions across time in 79 children and adolescents with obsessive-compulsive disorder. Journal of the American Academy of Child and Adolescent Psychiatry, 31(6), 1050–1056.
225. Robins, L. N., Helzer, J. E., Weissman, M. M., Orvaschel, H., Gruenberg, B., Burke, J. D., Jr., & Regier, D. A. (1984). Lifetime prevalence of specific psychiatric disorders in three sites. Archives of General Psychiatry, 41(10), 949–958.
226. Roemer, L., Orsillo, S., & Barlow, D. H. (2002). Generalized anxiety disorder.InD. H.Barlow(Ed.),Anxietyanditsdisorders:Thenature and treatment of anxiety and panic (2nd ed., pp. 477–518). NewYork: Guilford Press.
227. Rose, R. J., & Ditto, W. B. (1983). A developmental-genetic analysis of common fears from early adolescence to early adulthood. Child Development, 54(2), 361–368.
228. Roy-Byrne,P.P.,Stang,P.,Wittchen,H.-U.,Ustun,B.,Walters,E.E., & Kessler, R. C. (2000). Lifetime panic-depression comorbidity intheNationalComorbiditySurvey:Associationwithsymptoms, impairment, course, and help-seeking. British Journal of Psychiatry, 176, 229–235.
229. Rubin, H. C., Rapaport, M. H., Levine, B., Gladsjo, J. K., Rabin, A., Aurbach, M., Judd, L. L., & Kaplan, R. (2000). Quality of well being in panic disorder: The assesment of psychiatric and general disability. Journal of Affective Disorders, 57(1-3), 217–221.
230. Salkovskis, P. M., & Clark, D. M. (1990). Affective responses to hyperventilation: A test of the cognitive model of panic. Behaviour Research and Therapy, 28, 51–61.
231. Sasson, Y., Zohar, J., Gross, R., Taub, M., & Fux, M. (1999). Response to missile attacks on civilian targets in patients with panic disorder. Journal of Clinical Psychiatry, 60, 385–388.
232. Scherrer, J. F., True, W. P., Xian, H., Lyons, M. J., Eisen, S. A., Goldberg, J., Lin, N., & Tsuang-Ming, T. (2000). Evidence for genetic influences common and specific to symptoms of generalized anxiety and panic. Journal of Affective Disorders, 57, 25–35.
233. Schmidt, N. B. (1999). Examination of differential anxiety sensitivities in panic disorder: A test of anxiety sensitivity subdomains predicting fearful responding in a 35% CO₂ Cognitive Therapy and Research, 23, 3–20.
234. Schmidt, N. B., Trakowski, J. H., & Staab, J. P. (1997). Extinction of panicogenic effects of a 35% CO₂ challenge in patients with panic disorder. Journal of Abnormal Psychology, 106, 630– 638.
235. Schneier, F. R., Liebowitz, M. R., Abi-Dargham, A., Zea-Ponce, Y., Lin, S.-H., & Laruelle, M. (2000). Low dopamine D₂ receptor binding potential in social phobia. American Journal of Psychiatry, 157, 457–459.
236. Schuhmann, E. M., Foote, R. C., Eyberg, S. M., Boggs, S. R., & Algina, J. (1998). Efficacy of parent-child interaction therapy: Interim report of a randomized trial with short-term maintenance. Journal of Clinical Child Psychology, 27(1), 34–45.
237. Segui, J., Salvador-Carulla, L., Marquez, M., Garcia, L., Canet, J., & Ortiz, M. (2000). Differential clinical features of late-onset panic disorder. Journal of Affective Disorders, 57, 115–124.
238. Seligman, M. E. (1971). Phobias and preparedness. Behavior Therapy, 2(3), 307–320.
239. Seligman, M. E. P. (1988). Competing theories of panic. In S. Rachman & J. D. Maser (Eds.), Panic: Psychological perspectives (pp. 321–329). Hillsdale, NJ: Erlbaum.
240. Silverman, W. K., & Kearney, C. A. (1992). Listening to our clinical partners: Informing researchers about children’s fears and phobias. Journal of Behavior Therapy and Experimental Psychiatry, 23(2), 71–76.
241. Sinha, S. S., Coplan, J. D., Pine, D. S., Martinez, J. A., Klein, D. F., & Gorman, J. M. (1999). Panic induced by carbon dioxide inhalation and lack of hypothalamic-pituitary-adrenal axis activation. Psychiatry Research, 86, 93–98.
242. Siqueland, L., Kendall, P. C., & Steinberg, L. (1996). Anxiety in children: Perceived family environments and observed family interaction. Journal of Clinical Child Psychology, 25(2), 225–237.
243. Skinner, B. F. (1953). Science and human behavior. New York: Macmillan.
244. Smith, L. C., Friedman, S., & Nevid, J. (1999). Clinical and sociocultural differences inAfricanAmerican and EuropeanAmerican patients with panic disorder and agoraphobia. Journal of Nervous and Mental Disease, 187, 549–560.
245. Sonntag, H., Wittchen, H.-U., Hoefler, M., Kessler, R. C., & Stein, M. B. (2000).Are social fears and DSM-IV social anxiety disorder associated with smoking and nicotine dependence in adolescents and young adults? European Psychiatry, 15, 67–74.
246. Spence, S. H., Donovan, C., & Brechman-Toussaint, M. (1999). Social skills, social outcomes, and cognitive features of childhood social phobia. Journal of Abnormal Psychology, 108, 211–221.
247. Spinhoven, P., Sterk, P. J., van der Kamp, L., & Onstein, E. J. (1999). The complex association of pulmonary function with panic disorder: A rejoinder to Ley (1998). Journal of Behavior Therapy and Experimental Psychiatry, 30, 341–346.
248. Sroufe, L. A. (1985). Attachment classification from the perspective of infant-caregiver relationships and infant temperament. Child Development, 56, 1–14.
249. Starcevic, V., Bogojevic, G., Marinkovic, J., & Kelin, K. (1999). Axis I and II comorbidity in panic/agoraphobic patients with and without suicidal ideation. Psychiatric Research, 88, 153–161.
250. Stein, D. J., & Bouwer, C. (1997). Blushing and social phobia: A neuroethological speculation. Medical Hypotheses, 49, 101–108.
251. Stein, M. B. (1998). Neurobiological perspectives on social phobia: From affiliation to zoology. Biological Psychiatry, 44, 1277– 1285.
252. Stein, M. B., Chartier, M. J. D., Hazen, A. L., Kozak, M. V., Tancer, M. E., Landers, S., Furer, P., Chubory, D., & Walker, J. R. (1998). A direct-interview family study of generalized social phobia. American Journal of Psychiatry, 151, 90–97.
253. Stein, M. B., Heuser, I. J., Juncos, J. L., & Uhde, T. W. (1990). Anxiety disorders in patients with Parkinson’s disease. American Journal of Psychiatry, 147, 217–221.
254. Stein, M. B., Shea, C. A., & Uhde, T. W. (1989). Social phobic symptoms in patients with panic disorder: Practical and theoretical implications. American Journal of Psychiatry, 146, 235–238.
255. Stemberger, R. T., Turner, S. M., Beidel, D. C., & Calhorn, K. S. (1995). Social phobia: An analysis of possible developmental factors. Journal of Abnormal Psychology, 104, 526–531.
256. Stevenson, J., Batten, N., & Cherner, M. (1992). Fears and fearfulness in children and adolescents: A genetic analysis of twin data. Journal of Child Psychology and Psychiatry and Allied Disciplines, 33(6), 977–985.
257. Stopa, L., & Clark, D. M. (2000). Social phobia and interpretation of social events. Behaviour Research and Therapy, 38, 273– 283.
258. Swedo, S. E., Rapoport, J. L., Leonard, H. L., & Lenane, M. (1989). Obsessive compulsive disorder in children and adolescents: Clinical phenomenology of 70 consecutive cases. Archives of General Psychology, 46(4), 335–341.
259. Takriti, A., & Ahmad, T. (2000). Anxiety disorders and treatment in Arab-Muslim culture. In I. Al-Issa et al. (Eds.), Al-Junnun: Mental illness in the Islamic world (pp. 235–250). Madison, CT: International Universities Press.
260. Taylor, S. (1999). Anxiety sensitivity: Theory, research, and treatment of the fear of anxiety. Mahwah, NJ: Erlbaum.
261. Thompson, R. A. (1991). Emotion regulation and emotional development. Educational Psychology Review, 3, 269–307.
262. Tiihonen, J., Kuikka, J., Bergstroem, K., Lepola, U., Koponen, H., & Leinonen, E. (1997). Dopamine reuptake site densities in patients with social phobia. American Journal of Psychiatry, 154, 239–242.
263. Tomarken, A. J., Sutton, S. K., & Mineka, S. (1995). Fear-relevant illusory correlations: What type of associations promote judgmental bias? Journal of Abnormal Psychology, 104(2), 312–326.
264. Tonge, B. (1994). Separation anxiety disorder. In T. H. Ollendick, N. J. King, & W. Yule (Eds.), International handbook of phobic and anxiety disorders in children and adolescents (pp. 145–167). New York: Plenum.
265. Toren, P., Eldar, S., Cendorf, D., Wolmer, L., Weizman, R., Zubadi, R., Koren, S., & Laor, N. (1999). The prevalence of mitral valve prolapse in children with anxiety disorders. Journal of Psychiatric Research, 33, 357–361.
266. Trower,P.,&Gilbert,P.(1989).Newtheoreticalconceptionsofsocial anxiety and social phobia. Clinical Psychology Review, 9, 19–35.
267. Turk, C. L., Heimberg, R. G., Orsillo, R. M., Holt, C. S., Gitow, A., Street, L. L., Schneier, F. R., & Liebowitz, M. R. (1998). An investigation of gender differences in social phobia. Journal of Anxiety Disorders, 12(3), 209–223.
268. Turner, S. M., Beidel, D. C., Borden, J. W., Stanley, M. A., & Jacob, R. G. (1991). Social phobia: Axis I and II correlates. Journal of Abnormal Psychology, 100, 102–106.
269. Turner, S. M., Beidel, D. C., & Costello, A. (1987). Psychopathology in the offspring of anxiety disorder patients. Journal of Consulting and Clinical Psychology, 55(2), 229–235.
270. Turner, S. M., Beidel, D. C., & Townsley, (1990). Social phobia: Relationship to shyness. Behaviour Research and Therapy, 28(6), 497–505.
271. Uhde, T. W., Tancer, M. E., Black, B., & Brown, T. M. (1991). Phenomenologyandneurobiologyofsocialphobia:Comparisonwith panic disorder. Journal of Clinical Psychiatry, 52(Suppl. 11), 31–40.
272. van Beek, N., & Griez, E. (2000). Reactivity to a 35% CO₂ challenge in health first-degree relative of patients with panic disorder. Biological Psychiatry, 47, 830–835.
273. van Zijderveld, G. A., Veltman, D. J., van Dyck, R., & van Doornen, I. J. P. (1999). Epinephrine-induced panic attacks and hyperventilation. Journal of Psychiatric Research, 33, 73–78.
274. Watson, D., Clark, L. A., & Carey, G. (1988). Positive and negative affectivity and their relation to axiety and depressive disorders. Journal of Abnormal Psychology, 97(3), 346–353.
275. Wells, A., & Carter, T. (1999). Preliminary tests of a cognitive model of generalized anxiety disorder. Behaviour Research and Therapy, 37, 585–594.
276. Wells, A., Clark, D., & Ahmad, S. (1998). How do I look with my minds eye: Perspective taking in social phobic imagery. Behaviour Research and Therapy, 36, 631–634.
277. Wells, A., & Papageorgiu, C. (1998). Social phobia: Effects of external attention on anxiety, negative beliefs and perspective taking. Behavior Therapy, 29, 357–370.
278. Wells, A., & Papageorgiu, C. (1999). The observer perspective: Biased imagery in social phobia, agoraphobia, and blood/injury phobia. Behaviour Research and Therapy, 37, 653–658.
279. Wenar, C. (1990). Childhood fears and phobias. In M. Lewis & S. M. Miller (Eds.), Handbook of developmental psychopathology: Perspectives in developmental psychology (pp. 281–290). New York: Plenum.
280. Werry, J. S. (1991). Overanxious disorder: A review of its taxonomic properties. Journal of the American Academy of Child and Adolescent Psychiatry, 30(4), 533–544.
281. Whitaker, A., Johnson, J., Shaffer, D., Rapoport, J., Kalikow, K., Walsh, B. T., Davies, M., Braiman, S., & Dolinsky, A. (1990). Uncommon troubles in young people: Prevalence estimates of selected psychiatric disorders in a nonreferred adolescent population. Archives of General Psychiatry, 47, 487–496.
282. White, K. S., & Barlow, D. H. (2002). Panic disorder and agoraphobia. In D. H. Barlow (Ed.), Anxiety and its disorders: The nature and treatment of anxiety and panic (2nd ed., pp. 328–379). New York: Guilford Press.
283. Williams, K., Argyropoulos, S., & Nutt, D. J. (2000). Amphetamine misuse and social phobia. American Journal of Psychiatry, 157, 834–835.
284. Wittchen, H.-U., Fuetsch, M., Sonntag, H., Muellen, N., & Liebowitz, M. R. (2000). Disability and quality of life in pure and comorbid social phobia: Findings from a controlled study. European Psychiatry, 15, 46–58.
285. Wittchen, H.-U., Stein, M. B., & Kessler, R. C. (1999). Social fears and social phobia in a community sample of adolescents and young adults: Prevalence, risk factors and comorbidity. Psychological Medicine, 29, 309–323.
286. Wittchen, H., Zhao, S., Kessler, R. C., & Eaton, W. W. (1994). DSM-III-R generalized anxiety disorder in the National Comorbidity Study. Archives of General Psychiatry, 51, 355–364.
287. Wolpe, J., & Rowan, V. C. (1988). Panic disorder: Aproduct of classical conditioning. Behaviour Research and Therapy, 26, 441– 450.
288. Woodman, C. L., Noyes, R., Black, D. W., Schlosser, S., & Yagla, S. J. (1999). A 5-year follow-up study of generalized anxiety disorder and panic disorder. Journal of Nervous and Mental Disease, 187(1), 3–9.
289. Yang, S., Tsai, T. H., Hou, Z. Y., Chen, C. Y., & Sim, C. B. (1997). The effect of panic attack on mitral valve prolapse. Acta Psychiatrica Scandinavica, 96, 408–411.
290. Zarit, S. T., & Zarit, J. M. (1998). Mental disorders in older adults: Fundamentals of assessment and treatment. New York: Guilford Press.
291. Zhang, A. Y., & Snowden, L. R. (1999). Ethnic characteristics of mental disorders in five U.S. communities. Cultural Diversity and Ethnic Minority Psychology, 5, 134–146.
292. Zohar, J., & Insel, T. R. (1987). Obsessive-compulsive disorder: Psychobiological approaches to diagnosis, treatment and pathophysiology. Biological Psychiatry, 22(6), 667–687.
293. Zuckerman,M.(1999).Vulnerabilitytopsychopathology:Abiosocial model. Washington, DC: American Psychological Association.