Holmes, M., & Newman, M. G. (2006). Generalized Anxiety Disorder. In M. Hersen & 1. C. Thomas (Series Eds.), & F. Andrasik (Vol. Ed.), Comprehensive Handbook of Personality and Psychopathology: Vol. II. Adult Psychopathology (pp. 101-120). New York: John Wiley & Sons.

CHAPTER 7

Generalized Anxiety Disorder MARILYN HOLMES AND MICHELLE G. NEWMAN

DESCRIPTION OF THE DISORDER AND CLINICAL PICTURE

separate from somatic anxiety (Deffenbacher, 1986; Deffenbacher & Hazaleus, 1985). When worry is induced, participants show an absence of change in heart rate (Borkovec & Hu, 1990; York, Borkovec, Vasey, & Stem, 1987). Craske (1999) suggests that worry may be a cognitive planning stage in response to anticipated threat during which arousal is reduced. Worry, however, is unlikely to occur without anxiety, despite the fact that the two can be separated. Andrews and Borko~ec (1988) found that by experimentally inducing a state of worry, a state of anxiety followed. Therefore, although theoretically there could be an adaptive function for worry (planning in order to cope with threat), Borkovec (1994) makes a distinction between preparatory coping and worry. Successful cognitive planning can be described as preparatory coping, but the anxiety-filled process of worrying does not involve effective, active problem solving or coping techniques (Borkovec et aI., 1983). In fact, worry lengthens decision-making times (Metzger, Miller, Cohen, Sofka, & Borkovec, 1990) due to heightened evidence requirements (Tallis, Eysenck, & Mathews, 1991) and serves to incubate negative thought intrusions (Butler, Wells, & Dewick, 1995; Wells & Papageorgiou, 1995). It is as yet unclear, however, whether worry without anxiety exists in nature as a coping device. Perhaps the most surprising finding from the research into worry, however, is that neither the process nor the effects of worry differ between normal and pathological worriers. For example, studies comparing the major topic areas of worry between those with GAD and controls, find that they do not differ (Craske, Rapee, Jackel, & Barlow, 1989; Roemer, Molina, & Borkovec, 1997). Similarly, studies show that when asked to worry, such worrying has the same physiological effect on non worriers as it does on worriers. What then, distinguishes the worry found in GAD from normal worry? The major point of departure of pathological worry from normal worry comes with the frequency and uncontrollability of worry in GAD. Borkovec et al. (1983) found that in a college sample those with GAD reported that their worries were sig-

Generalized anxiety disorder (GAD) has often been described as the "basic" anxiety disorder. This conceptualization is due in part to its early onset, persistent course, and resistance to change, as well as its gateway status to other anxiety disorders (Brown, Barlow, & Liebowitz, 1994). Furthermore, GAD's central and defining feature of uncontrollable worry is the primary element of anxiety. Individuals with GAD worry excessively about diverse subjects without a persistent focus on anyone thing. It is the pervasive, uncontrollable quality of worry that makes it the hallmark of GAD and the true distinguishing feature of this disorder. Such constant, diffuse worrying leads to chronic feelings of anxiety. GAD might therefore be conceived as the absolute expression of high trait anxiety. In order to understand GAD, then, it is important to understand the definition and nature of worry. By exploring the history of research into worry, a more complete picture of its meaning can be painted. In the 1970s, research into test anxiety first identified separate parts of the anxious experience. Cognitive and physiological aspects of anxiety were distinguished from one another. It was suggested that worry was the cognitive element of anxiety, and researchers defined worry as "a chain of thoughts and images, negatively affectladen and relatively uncontrollable" (Borkovec, Robinson, Pruzinsky, & DePree, 1983). These authors argued that worry is closely tied to the fear process, as it involves attempts to mentally solve a problem when the outcome is uncertain and includes one or more negative possibilities. This view led to the conceptualization of worry as an attempt to evade perceived threat through cognitive avoidance (Borkovec, Metzger, & Pruzinsky, 1986). In the wake of this conceptualization, researchers proceeded to investigate further the cognitive nature of worry and its distinction from anxiety. Research confirmed the cognitive quality of worry by demonstrating that it is functionally 101

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nificantly more uncontrollable than those of nonanxious controls. In another study comparing worry between individuals with GAD and controls, those with GAD also reported significantly more difficulty controlling, stopping, and preventing their worries (Craske et aI., 1989). Although these studies identified GAD participants based on DSM-III-R criteria, research indicates that individuals who meet criteria for GAD by DSM-III-R standards usually meet criteria according to DSM-IVas well (Abel & Borkovec, 1995). Results based on DSM-III-R criteria can therefore be considered generalizable to the current definition of GAD. Various associated cognitive features common in GAD help to further illuminate the nature and function of worry in this disorder. Individuals with GAD generally view the world as a dangerous place, and in order to avoid possible danger, or to plan for ways to deal with the occurrence of danger, they feel that it is necessary to constantly scan their environment for cues of possible threat (Beck, Emery, & Greenberg, 1985). Because there is no actual present moment or physical danger, and the threat exists only in the future and in the mind, no behavioral avoidance is possible, and worry becomes the only conceivable coping strategy (Borkovec & Newman, 1998). Indeed, individuals with GAD tend to view worry as an adaptive coping strategy. They believe that worrying will help them problem solve and get ready for the negative event that they fear, and they often hold the superstitious belief that worrying about a negative event will help to prevent its occurrence (Borkovec & Roemer, 1995). Worry may, in fact, be negatively reinforced by alleviating perceptions of unpredictability and uncontrollability in the world and replacing them with feelings of readiness for any possibility (Craske, 1999). Perhaps due to this constant, heightened state of vigilance, or perhaps contributing to it, individuals with GAD tend to interpret ambiguous or neutral stimuli as negative or threatening and also show a bias toward threat cues, even when these cues are presented outside awareness (Mathews, 1990; Mathews & MacLeod, 1994). Various physiological factors are associated with GAD as well. For example, GAD is associated with chronic vigilance, scanning, and muscle tension (Hoehn-Saric & McLeod, 1988; Lyonfields, Borkovec, & Thayer, 1995; Thayer, Friedman, & Borkovec, 1996). In addition, unlike other anxiety disorders, physiological activation is not a typical feature of GAD. In fact, whereas other anxiety disorders are associated with increased autonomic activation, people with GAD show a distinct pattern of autonomic inflexibility, i.e., a lack of autonomic reactivity (Hoehn-Saric, McLeod, & Zimmerli, 1989; Thayer et aI., 1996). For example, Lyonfields, Borkovec, and Thayer (1995) found that analogue participants showed a lower baseline vagal tone and restricted variation in both vagal tone and

heart rate between rest, aversive imagery, and worry states. Nonanxious participants on the other hand demonstrated a decrease in vagal tone from rest to imagery and a greater decrease with worry. Thayer and colleagues (1996) replicated these findings in GAD clients and controls using states of self-relaxation and worry. The persistent deficiency in vagal tone and the resulting autonomic inflexibility found in GAD are likely linked to chronic worrisome thinking, as demonstrated by the findings that worry physically reduces vagal tone in nonanxious controls. Interestingly, autonomic inflexibility has also been found in behaviorally inhibited children (Kagan & Snidman, 1990), which has been discussed as an associated childhood risk factor for GAD. Low vagal tone and autonomic nonreactivity are likely interrelated with information processing difficulties found in GAD. For example, low vagal tone has been found to be related to poor concentration and distractibility in infants and adults (Porges, 1992; Richards, 1987). Several studies have also shown that worry strains the resources of working memory (Borkovec & Inz, 1990; Rapee, 1993). Furthermore, an inflexible information processing style is characteristic in those with GAD, especially in emotional processing. GAD and worry are also associated with other informationprocessing dysfunctions. For example, individuals with GAD are more likely than nonanxious controls to interpret ambiguous information as threatening (Butler & Mathews, 1983). In addition, GAD participants show a bias for attending to threat cues, suggesting that they are hypervigilant about scanning their environment for potential danger (Mathews & MacLeod, 1985). Anxious children are also more likely to consider ambiguous cues as threatening and to rate the possible occurrence of threatening events more likely than nonanxious children (Chorpita, Albano, & Barlow, 1996). Further, individuals with GAD show a likely cognitive avoidance of threat words while at the same time demonstrating extensive processing of these words. This is reflected in their ability to recall fewer threat words than controls when using an attentional memory task, yet recall more threat words than controls when using an implicit, or automatic, memory task (Mathews, 1990; Mathews & MacLeod, 1994; Mathews, Mogg, May, & Eysenck, 1989; Mogg, Mathews, & Weinman, 1987). Consistent with these data, another study had people with GAD monitor their daily worry predictions and the rate at which their predicted outcomes actually occurred. The outcomes turned out better than expected 84 percent of the time. Of the remainder, clients coped better than expected in 78 percent of the cases. Thus, for only 3 percent of all worries did the core feared event ("The predicted bad event will occur, and I won't be able to cope with it") actually happen (Borkovec, Hazlett-Stevens, & Diaz, 1999). This suggests

Personality Development and Psychopathology

that GAD clients often fail to process the evidence that the world offers them.

PERSONALITY DEVELOPMENT PSYCHOPATHOLOGY

AND

Several studies have examined personality correlates of GAD. Research suggests that children with GAD tend to be perfectionists, often redoing tasks if their performance is less than perfect. They may seek excessive approval and need disproportionate reassurance regarding their worries as well. Children with GAD may also be overly conforming and self-conscious and may have a negative self-image. Moreover, they are likely to report a high rate of such somatic complaints as feeling shaky and heart palpitations (Beidel, Christ, & Long, 1991; Masi, Mucci, Favilla, Romano, & Poli, 1999). Anxious children are described by parents and teachers as lacking social skills, shy, withdrawn, and lonely (Strauss, Lease, Kazdin, Dulcan, & Last, 1989). They are less liked by their peers and have trouble making friends (Strauss, Lahey, Frick, Fram, & Hynd, 1988). It is unclear whether these personality characteristics lead to GAD or whether they arise after the disorder is acquired. It is likely, however, that the relationship between these personality characteristics and the disorder exist in a cycle of interaction, each augmenting the other. In fact, several theorists have suggested that fear and negative expectations about social situations can lead to problematic interpersonal behavior. Such behavior may pull for others to respond in ways that reinforce negative expectations and ultimately maintain a psychological disorder (Bandura, 1977; Safran & Segal, 1990; Strupp & Binder, 1984; Wachtel, 1994). For example, an individual who habitually worries that others will think badly of him may act overly intellectual in an attempt to gain self-confidence. His self-presentation might alienate others by appearing condescending, selfabsorbed, or emotionally aloof, making others less interested in interacting with him in the future, hence confirming his fears. These patterns have been labeled negative interpersonal cycles by Safran and Segal (1990). Indirect evidence suggests that negative interpersonal cycles may occur with GAD individuals thus leading to the maintenance of interpersonal worries. For example, there is extensive evidence that GAD patients fear and expect negative responses from others. The content of worry for GAD clients is more frequently about interpersonal fears than any other topic (Breitholtz, Johansson, & Ost, 1999; Roemer et aI., 1997). Trait worry is also correlated more highly with social fears than with nonsocial fears (Borkovec et aI., 1983; Ladouceur, Freeston, Fournier, Dugas, & Doucet, 2002). In

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addition, social anxiety disorder is the most frequent comorbid anxiety disorder to GAD (Borkovec, Abel, & Newman, 1995; Brawman-Mintzer et aI., 1993; Brown & Barlow, 1992) and GAD is the most frequent comorbid disorder to social phobia (Turner, Beidel, Borden, Stanley, & Jacob, 1991). Experimental evidence also shows that GAD participants have a bias to social threat cues (MacLeod, Mathews, & Tata, 1986; Mathews & MacLeod, 1985; Mogg, Mathews, & Eysenck, 1992) and greater vigilance for and orientation to threatening faces relative to neutral faces compared to controls (Bradley, Mogg, White, Groom, & de Bono, 1999) and to controls or depressed participants (Mogg, Millar, & Bradley, 2000). A more recent experimental study found that compared to non-GAD participants, people with GAD had a more biased perception of their impact on other people, tending to either overestimate or underestimate the extent of their negative impact (Erickson & Newman, 2002). In addition to data showing that GAD participants expect and worry about negative responses from others, studies suggest that they are likely to act on these fears using dysfunctional interpersonal behavioral patterns. For example, Axis II pathology (primarily characterized by chronic maladaptive relationship patterns) predicted greater odds of GAD in an epidemiological survey (Nestadt, Romanoski, Samules, Folstein, & McHugh, 1992). In addition, studies show a higher rate of personality pathology and lower social functioning in GAD than in panic disorder participants (Blashfield et al., 1994; Dyck et aI., 2001) or compared to most other anxiety disorders (Reich et aI., 1994; Sanderson, Wetzler, Beck, & Betz, 1994). Also, in a national comorbidity sample as well as a sample of more than 10,000 Australian subjects, GAD predicted increased odds of being separated or divorced (Hunt, Issakidis, & Andrews, 2002; Wittchen, Zhao, Kessler, & Eaton, 1994). There is also evidence that such marital problems are somewhat specific to GAD relative to other anxiety disorders. Wives with GAD have been found to be more dissatisfied with their marriages than wives with other anxiety disorders (McLeod, 1994), and spouses with GAD reported more conflictual marriages than spouses with agoraphobia (Friedman, 1990). Moreover, in a sample of 4,933 married couples, marital discord was independently and more strongly associated with GAD than major depression, mania, dysth ymia, social phobia, simple phobia, agoraphobia, panic disorder, and alcohol dependence after controlling for demographic variables, comorbid disorders, and quality of other relationships (Whisman, Sheldon, & Goering, 2000). The latter study also found that GAD strongly predicted a lack of close friendships. Additional studies show that, compared to non-GAD participants, GAD women have more difficulty with emotional and interpersonal intimacy (Dutton, 2002)

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and that people with GAD approach their relationships with elevated hypervigilance, suspiciousness, and a tendency to feel easily slighted (Gasperini, Battaglia, Diaferia, & Bellodi, 1990). Further, parents with GAD had significantly higher rates of dysfunctional relationships with their spouses and children compared to parents without GAD (Ben-Noun, 1998). Moreover, Pincus and Borkovec (1994) found that compared to non-GAD persons, those with GAD had significantly greater interpersonal distress and interpersonal rigidity across different situations. They also found that mean scores of GAD individuals on five of eight Inventory of Interpersonal Problems Circumplex Scales (IIP-C; Alden, Wiggins, & Pincus, 1990) were significantly higher than psychiatric norms (based on 200 psychiatric clients of mixed diagnoses). Given that people with GAD worry predominantly about their relationships, their objective difficulty sustaining healthy relationships is likely to reinforce and maintain these worries. Taken together, fmdings suggest that relationship difficulties may contribute to the development or maintenance of GAD. As such, it is possible that changes in relationship difficulties may increment GAD treatment outcome. Evidence exists that temperament may also playa role in the development of GAD. Kagan and coresearchers (Kagan, Snidman, & Arcus, 1998) have classified children as young as 21 months as behaviorally inhibited or uninhibited. Uninhibited children have adventure-seeking dispositions, whereas inhibited children show timidity and avoidance of novel and unfamiliar events. An inhibited temperament style could theoretically lead to hyperarousal to environmental stimuli, which could contribute to conditioned anxiety responses and make avoidance of such stimuli more reinforcing (Frick & Silverthorn, 2001). Research supporting this suggestion has revealed that infants showing behavioral inhibition to the unfamiliar are more likely to develop an anxiety disorder later in life (Hirshfeld et al" 1992).

EPIDEMIOLOGY Precise prevalence estimates for GAD have been difficult to obtain, most likely due to definitional variations, considerable DSM criteria changes, and varying methods of assessment. Nevertheless, several studies examining prevalence are noteworthy, as they employ large representative samples and likely approximate actual prevalence rates. Using DSM-III criteria with no diagnostic exclusions, the Epidemiologic Catchment Area study found an estimated one-year prevalence rate for GAD of 3.8 percent and a lifetime prevalence rate of 4.0 percent (Blazer, Hughes, George, Swartz, & Boyer, 1991). The National Comorbidity Study

(NCS) used DSM-III-R criteria and found the prevalence rates for GAD to be 1.6 percent current and 5.1 percent lifetime. Twelve-month GAD prevalence rates from this study were near 3 percent (Kessler et aI., 1994; Wittchen et aI., 1994). The figures from the NCS most likely provide a close representation of prevalence estimates for GAD according to DSM-IV criteria as well because, as noted previously, most clients who meet DSM-III-R criteria also meet DSM-IV criteria for GAD (Abel & Borkovec, 1995). Finally, using DSMIV criteria, the Australian National Survey of Mental Health and Well-Being found similar prevalence rates to the NCS, with 1 month at 2.8 percent and 12 months at 3.6 percent for GAD (Hunt et aI., 2002). The NCS prevalence estimates also reveal that GAD is somewhat more common in the general population than panic disorder, yet less common than social and simple (specific) phobia (Kessler et aI., 1994). Moreover, GAD has been found to be among the most common comorbid conditions for other anxiety and mood disorders (Brown & Barlow, 1992). Neverthe less individuals with GAD report for mental health services relatively less often than do those with most other anxiety disorders, comprising only about 10 percent of anxiety disorder clients seeking such treatment (Kennedy & Schwab, 1997; Roy-Byrne, 1996). Indeed the NCS findings show that approximately half of its participants reported to primary care settings rather than mental health facilities when they sought treatment for GAD, and only about 12 percent of those patients were referred for psychotherapy treatment (Wittchen et al., 2002). Tellingly, among high medical utilizers in primary care settings, GAD prevalence rates rise to 22 percent (current) and 40 percent (lifetime; Katon et aI., 1990). To date, examinations of the association between sociodemographic features and an increased incidence of GAD have found gender to be the most highly correlated characteristic. As with many other anxiety disorders, GAD is much more common in women than in men. In both clinical (Woodman, Noyes, Black, Schlosser, & Yagla, 1999; Yonkers, Warshaw, Massion, & Keller, 1996) and community samples (Wittchen et aI., 1994), GAD rates were found to be approximately double in women. Other characteristics have also been established to be risk factors for GAD. The NCS found higher rates of GAD among homemakers and others not working outside the home and among those living in the Northeast as opposed to other regions of the country. However, no differences in the occurrence of GAD were found to be significantly linked to race, education, income, religion, and rural versus urban living. The Australian National Survey found being separated, di-

Etiology

vorced, or widowed and being unemployed were associated with GAD (Hunt et aI., 2002). GAD prevalence rates and associated sociodemographic considerations have also been studied in children. Overanxious disorder (the childhood version of GAD prior to DSMIV) was found to have prevalence rates ranging from 3 percent to 12 percent in a review by Silverman and Ginsberg (1998) encompassing 10 studies published between 1987 and 1993. Surprisingly, despite a high correlation between gender and GAD in adults, no such reliable relationship has been found in children. For example, in a large community sample of children, Cohen et al. (1993) found no significant gender difference. And perhaps even more strikingly, other research has identified a greater incidence of childhood GAD in males-the exact opposite trend from that seen in adults (Anderson, Williams, McGee, & Silva, 1987).

ETIOLOGY As is true for so many psychological disorders, no one simple pathway exists that leads to the emergence of GAD. Instead, a complex interlace of multiple factors-genetic, biological, environmental, and psychological--contributes to the development of this disorder. Perhaps the most straightforward examination of the etiology of any disorder comes from looking at genetic influence. Twin studies have revealed that GAD is moderately regulated by genetic factors, with about 30 percent of the variance due to heritability (Kendler, Neale, Kessler, Heath, & Eaves, 1992; Kendler et aI., 1995). Research suggests that heritable traits (accounting for 30 percent to 50 percent of the variance) such as neuroticism, negative affectivity, and anxiety significantly correlate with anxiety and anxiety disorders (Brown, Chorpita, & Barlow, 1998; Clark, Watson, & Mineka, 1994; Trull & Sher, 1994; Zinbarg & Barlow, 1996). Furthermore, family studies have demonstrated that having a first-degree relative with GAD increases the likelihood of having the disorder (Noyes, Clarkson, Crowe, Yates, & McChesney, 1987), although caution in interpreting family studies is advisable, because it is impossible to tease out all environmental factors from genetic factors. Research examining genetic contributions to GAD suggests not that genetic factors specifically lead to GAD, but that heritability contributes to a general biological vulnerability to anxiety, upon which other factors act to manifest a distinct disorder (Barlow, 2002; Kendler, 1996; Kendler et al" 1995). The underlying genetic susceptibility for anxiety emerges as GAD only under circumstances in which biological, psychological, and environmental elements converge in appropriate patterns. Specifically, recent research indicates that dysfunc-

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tions in the areas of physiology, information processing, and interpersonal functioning interact in the development of GAD. In addition to theories regarding the biological determinants of GAD, a review of the past decades of research into the development of anxiety disorders (Menzies & Clarke, 1995) found that much of the focus has been on conditioning and learning. Classical conditioning theory would suggest that a child would respond fearfully to a conditioned stimulus (CS) when it has been consistently paired with an aversive unconditioned stimulus (UCS). The CS then produces anxiety in the child, as he or she expects it to lead to that aversive event. By avoiding the CS, anxious behavior is reinforced (Mowrer, 1939). Furthermore, operant conditioning may be at work in the development and maintenance of anxiety, as parents have been shown to reward anxious behavior with extra attention, reassurance' and assistance with avoidant behavior, thus positively reinforcing the anxiety (Ayllon, Smith, & Rogers, 1970). Social modeling may also be a strong contributing factor to learned anxious behavior (Bandura & Menlove, 1968). In fact, studies do show that children of parents with an anxiety disorder are more likely to be anxious compared to children of nonanxiety disordered parents (Muris, Steememan, Merckelbach, & Meesters, 1996; Rosenbaum et al., 1988). Although learning theories provide an important potential insight into the development and maintenance of anxiety disorders, attachment may playa role as well. In fact, Bowlby (1982) explicitly hypothesized that anxiety may be the direct result of certain aspects of an insecure attachment. He suggested that when an attachment figure is habitually unavailable to a child, the result is an insecure foundation from which the child approaches the world. Thus, the child develops mental models of the world as an unpredictable, uncontrollable, and dangerous place, tends to overestimate the likelihood and negativity of feared events, and underestimates his or her ability to cope with these events. Indeed, Bowlby's proposed model is consistent with what is known about the mental models of the world present in adults with GAD. Research to date has provided support for the theory put forth by Bowlby (1982) that an insecure attachment is associated with anxiety disorders. For example, a prospective study found that anxious attachment in babies predicted the later development of anxiety disorders (Warren, Huston, Egeland, & Sroufe, 1997) and a retrospective study showed that anxious patients reported less parental care and more overprotection than matched controls (Parker, 1981). Moreover, participants classifying their parents as higher on protection and lower on care demonstrated significantly higher trait anxiety scores than those not classifying their parents in this man-

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ner (Parker, 1979). In regard to GAD per se, studies show that GAD persons score higher than non-GAD persons on rolereversed/enmeshed relationships (Cassidy, 1995; Cassidy & Shaver, 1999). These individuals may view the world as a dangerous place and as a result may feel that they have to anticipate and control danger for themselves and their parents. Persons with GAD were also more likely to report greater unresolved feelings of anger toward and vulnerability surrounding their primary caregivers when compared to individuals without GAD (Cassidy, 1995; Cassidy & Shaver, 1999). Some evidence also exists for the specificity of such attachment difficulties to GAD: a logistic regression found that retrospective reports of prior attachment difficulties predicted higher odds ratios for GAD than for panic disorder (Silove, Parker, Hadzi-Pavlovic, Manicavasagar, & Blaszczynski, 1991). A possible factor that contributes to the maintenance of worry and GAD may be associated with its inflexible physiology described earlier. Borkovec has theorized that one of the functions of worrying by GAD individuals is to avoid uncomfortable emotions (Borkovec, Alcaine, & Behar, 2004). The theory further hypothesizes that such avoidance is enabled via the abstract verbal linguistic nature of worry and concomitant reduced imagery. As avoidance of a feared stimulus is likely to strengthen its anxious meaning (Fehr & Stem, 1970), such avoidance may be negatively reinforcing, thereby strengthening the associated fear and avoidance behavior. Experimental evidence indeed shows that GAD and its cardinal characteristic of worry involve a predominance of verbal-linguistic thought and reduced imagery (Borkovec & Inz, 1990; East & Watts, 1994). During relaxation, nonanxious participants report a predominance of imagery whereas persons with GAD report equal amounts of thought and imagery. When participants shift to worrying, both GAD and nonanxious controls show a predominance of thought activity. Increased left cortical activation in GAD and control participants during worry compared to relaxation as well as greater activation in GAD participants compared to controls provides objective evidence of a predominance of thought (Carter, Johnson, & Borkovec, 1986; Heller, Nitschke, Etienne, & Miller, 1997). In addition to evidence for the verbal-linguistic nature of worry and GAD, studies suggest that worrisome thought is more abstract and less concrete than nonworrisome thought in both nonclinical and GAD participants (StOber & Borkovec, 2002; Stober, Tepperwien, & Staak, 2000). When thought content is less concrete, concomitant imagery is less vivid and requires more effort to produce (Paivio, 1986). The predominance of abstract thought over imagery is important to emotional processing because imagery is more closely tied to efferent command and to affect than is thought

(Lang, 1985). Further, abstract verbal thought about feared stimuli leads to fewer and less salient images, which induce a much lower cardiovascular response than does a predominance qf salient feared imagery (Vrana, Cuthbert, & Lang, 1986; Vrana, Cuthbert, & Lang, 1989). According to Foa and Kozak's (1986) emotional processing theory, such a lowered cardiovascular response to feared stimuli means that the full fear structure was not accessed and thus full emotional processing did not take place. In the absence of emotional processing, fear is maintained. Experimental studies of the emotional impact of worrisome thought show inhibited emotional processing. Anxious participants who worry just prior to imaginal exposure to feared material show no cardiovascular response to that material. Those who think relaxing or neutral thoughts before imaginal exposure show strong cardiac arousal. Also, thinking relaxing thoughts prior to imaginal exposure leads to habituation over repeated images, whereas worrying before exposure does not (Borkovec & Hu, 1990; Peasley-Miklus & Vrana, 2000). A study of brain activity also showed that experimental manipulation of worry led to the suppression of affect at the level of the amygdala (Hoehn-Saric, Lee, McLeod, Resnik, & Wong, 2003). Further, the degree to which participants engage in worrisome thoughts, rather than thinking per se, predicts the degree of inhibited emotional processing (Borkovec, Lyonfields, Wiser, & Diehl, 1993; Freeston, Dugas, & Ladouceur, 1996). Moreover, although imagery of an aversive (unconditioned) stimulus can enhance a feared response to a previously conditioned stimulus (Davey & Matchett, 1994; Jones & Davey, 1990), worrying before imagining an aversive stimulus mitigates the impact of subsequent unconditioned stimulus imagery on skin conductance responses (Davey & Matchett, 1994), suggesting that worrying dampens emotional learning. Thus, it is possible that people with GAD use worrisome thinking as a means to maintain a distance from emotionally evocative material. In fact, there is evidence that verbal linguistic thought is used spontaneously by people to avoid emotional arousal associated with emotionally evocative stimulus materials (Tucker & Newman, 1981). Moreover, when GAD, nonworried anxious, and control participants were asked why they worried, in two separate studies the only item that discriminated the GAD group from the other two groups was "worry helps distract me from more emotional topics" (Borkovec & Roemer, 1995; Freeston, Rheaume, Letarte, Dugas, & Ladouceur, 1994). Higher levels of worry are also associated with less emotional clarity and more ditliculty identifying and describing emotions (Turk, Heimberg, Luterek, Mennin, & Fresco, in press).

Clinical Course, Complications, and Prognosis

CLINICAL COURSE, COMPLICATIONS, PROGNOSIS

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GAD, like many anxiety disorders, follows a chronic course, often quietly lingering even after successful treatment (Noyes et al., 1992; Yonkers et al., 1996). Many individuals with GAD cannot remember a time when they were not anxious and feel that they have had symptoms all of their lives. GAD does not usually appear out of the blue, but instead involves a slow, subtle, stealthy building of anxious symptoms. Individuals with the disorder generally report a gradual, insidious onset (Anderson, Noyes, & Crowe, 1984; Rapee, 1985) and an unremitting course (Noyes et aI., 1992). Perhaps in part due to this progressive beginning to the disorder, estimates of average age of onset are controversial and suggest a possible bimodal distribution. Some research has found that GAD has an earlier age of onset than other anxiety disorders (e.g., Noyes et aI., 1992; Woodman et aI., 1999). In the Epidemiological Catchment Area Study (using DSM-III criteria), GAD was most common among the youngest age group (Blazer et al., 1991). In keeping with this finding, earlier studies report that onset is usually in the midteens or early twenties (Anderson et aI., 1984; Barlow, Blanchard, Vermilyea, Vermilyea, & Di Nardo, 1986; Rapee, 1985). In further support of early GAD onset, overanxious disorder (considered the childhood form of GAD) has relatively high prevalence estimates (Anderson et aI., 1987). The early age of onset and chronic course of GAD have led many to speculate that GAD is a lifelong disorder. In fact, Rapee (1991) suggests that GAD might be considered a stable psychological trait or even a personality disorder, rather than a discreet disorder within an individual. Other evidence, however, shows that there may be a second subgroup of GAD identified by late onset. The NCS found conflicting results compared to the Epidemiological Catchment Area Study, with estimates showing GAD having the highest prevalence ratings in those older than 45 years of age and the lowest prevalence ratings among those ages 15 to 24 (Wittchen et aI., 1994). Brown (1999) suggests that the more stringent diagnostic criteria employed in DSM-III-R and DSM-IV studies removes the subclinical GAD diagnoses related to the disorder's gradual onset that earlier studies may have captured. Recent research has further explored the possibility that there are two distinct subgroups of GAD specified by age of onset and the corresponding implications for course and treatment. Several studies have found confirming evidence that two subgroups of GAD are distinguishable based on age of onset and have examined differential effects on the course of the disorder. In a clinical sample of individuals with GAD,

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about two thirds of patients reported an early onset of symptoms (15 percent before age 10 and 85 percent between ages 10 and 19), whereas the rest of the patients reported a late onset (Hoehn-Saric, Hazlett, & McLeod, 1993). In a recent study attempting to clarify the age of onset and its correlates in GAD, Campbell, Brown, and Grisham (2003) found that most patients in their large clinical sample reported an onset of GAD by early adulthood, whereas a smaller number reported a later onset. These researchers found that early versus late onset had different meanings in several associated areas. Most patients with earlier-onset GAD reported that their symptoms arose without any precipitating stressors (however, a subgroup of the early-onset patients did report severe stressors surrounding the emergence of their disorder). Late-onset patients on the other hand were most likely to report that their GAD emerged during stressful times (Campbell et aI., 2003; Hoehn-Saric et aI., 1993). Early-onset GAD was also found to be associated with greater severity and higher levels of comorbidity in this study. Other research has associated earlyonset GAD with a worse course of the disorder (Woodman et aI., 1999); childhood problems with inhibited behavior, social and academic deficiencies, and difficult home environments; and current interpersonal difficulties and depression (Hoehn-Saric et al., 1993). However, as Brown (1999) points out, studies focusing on the impact of early versus late onset do not usually take into account duration of the disorder or the individual's current age. Even without regard for onset subgroups, GAD is associated with high levels of comorbidity. In a study examining five different anxiety disorders, GAD was more often connected with a comorbid diagnosis than the four other disorders (Goisman, Goldenberg, Vasile, & Keller, 1995). Depressive disorders and anxiety disorders are the most commonly occurring comorbid diagnoses, specifically major depressive disorder (MDD), panic disorder, social phobia and simple phobia (Borkovec et al., 1995; Brawman-Mintzer et aI., 1993; Noyes, 2001; Okasha et aI., 1994; Sanderson, Beck, & Beck, 1990). The National Comorbidity Survey and the Midlife Development in the United States survey found that the majority of respondents who met criteria for GAD also met criteria for major depression (Kessler, DuPont, Berglund, & Wittchen, 1999). Interestingly, GAD is often temporally primary in relation to comorbid disorders, and most individuals with comorbid major depression report that their GAD preceded their depression (Kessler, Keller, & Wittchen, 2001). In a naturalistic study using a large sample, 39 percent of GAD patients had a comorbid diagnosis of depression at intake, a figure that increased to 74 percent at the eight-year followup. Of those with a singular diagnosis of GAD at intake, all but 1 of 20 patients went on to develop a comorbid disorder (Bruce, Machan, Dyck, & Keller, 2001).

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Comorbidity correlates with greater impairment and worse prognosis when comparing GAD with and without comorbid diagnoses (Noyes, 2001). Nevertheless, results on the effects of comorbidity on prognosis of GAD have been mixed, perhaps in part due to the high incidence of co morbidity, leading to restricted variability. Some studies have found that Axis I comorbidity does not predict treatment outcome (e.g., Durham, Allan, & Hackett, 1997; Newman, Przeworski, & Borkovec, 2001; Yonkers, Dyck, Warshaw, & Keller, 2000). Specifically, comorbid social phobia, PTSD, and alcohol! substance abuse have not been found to predict treatment outcome (Bruce et al., 2001; Yonkers et aI., 2000). Others, however, have found that comorbid diagnoses of MDD or panic disorder decrease the likelihood of remittance (Bruce et aI., 2001). Noyes (2001) also found that comorbid diagnoses lead to a poorer response to both psychological and pharmacological treatments. Importantly, however, research has demonstrated that successful treatment of GAD leads to a reduction of comorbid disorders (Borkovec et aI., 1995; Newman et al., 2001). Clearly further research into the connections between GAD and its frequent comorbid conditions would enhance our understanding of the disorder and its course. Regardless of comorbid conditions, prognosis in general for GAD is not good. In a longitudinal study, the probability of naturalistic remission was only .15 at one year and .25 at two years (Yonkers et al., 1996). After participating in drug treatment studies, only 18 percent of those with GAD were in full remission at the five-year follow-up, compared with 45 percent of those with panic disorder (Woodman et al., 1999).

ASSESSMENT

AND DIAGNOSIS

GAD is notoriously difficult to diagnose due to complexities in the interpretation of DSM criteria, symptom overlap with other disorders, questions regarding diagnostic threshold, and patient variability in reporting symptoms (e.g., Brown, Di Nardo, Lehman, & Campbell, 2001). Of all the anxiety disorders GAD is one of the least reliably diagnosed (Brown et al., 2001; Di Nardo, Moras, Barlow, Rapee, & Brown, 1993). In fact, some recommend the use of two independent structured interviews in order to obtain an accurate diagnosis (Borkovec & Newman, 1998; Borkovec & Whisman, 1996). In this section the diagnostic criteria for GAD and various assessment measures are discussed. Since the initial inclusion of GAD in the third edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-III; American Psychiatric Association, 1980), research

into worry has led to several important changes in the criteria for diagnosing GAD. In its third edition, the DSM divided the previously single category of anxiety neurosis into panic disorder and GAD. GAD at this point was simply a residual category, a diagnosis to be given only if no other anxiety disorder were diagnosed. GAD was defined by global anxiety and its associated symptoms of apprehensive expectation, vigilance, physical tension, and autonomic overactivity. At this early stage, however, there were apparent problems with the criteria for the disorder: Interrater reliability of GAD diagnosis (kappa = .47; Di Nardo, O'Brien, Barlow, Waddell, & Blanchard, 1983) was only fair, the one-month duration criterion resulted in overdiagnosis, and the residual status of the disorder led to confusion in diagnoses (Barlow, 2002). The DSM-III-R (American Psychiatric Association, 1987) altered diagnostic criteria in response to these difficulties. GAD became a primary diagnosis, and worry (apprehensive expectation) was now its central defining feature. Its remaining symptoms were relegated to an 18-item list and recognized as associated symptoms. Nevertheless diagnostic reliability remained only fair (kappa = .57; Di Nardo et al" 1993). Several further diagnostic revisions have followed. Comprehensive reviews of the empirical literature on GAD (e.g., Borkovec, Shadick, & Hopkins, 1991) led to the current DSM-N defInition. The earlier list of 18 associated symptoms has been reduced to 6 in recognition of Marten et al.'s (1993) research into the most reliably associated symptoms of GAD, and further research has supported the specific relevance of these 6 symptoms to GAD (Abel & Borkovec, 1995; Brawman-Mintzer et aI., 1994; Brown, Marten, & Barlow, 1995). Perhaps most notably, the associated symptoms were changed so as to reflect central nervous system rather than autonomic nervous system activity, and recent research has indeed demonstrated that GAD is associated with reduced physiological arousal (Borkovec & Hu, 1990). Finally, and of central importance, the diagnostic criteria were further revised for the fourth edition to require that worry in GAD be perceived as difficult to controL A diagnosis of GAD, according to the current DSM-N criteria (American Psychiatric Association, 1994), requires excessive worry surrounding a number of events or situations, more days than not, lasting at least six months. The individual must experience the worry as difficult to control and must report at least three of six listed symptoms during most of their period of worrying. These symptom groups (restlessness, muscle tension, fatigue, difficulty concentrating, irritability, and sleep disturbance) are primarily associated with excessive psychophysiological arousal. Furthermore, in order for GAD to be diagnosed the DSM-N requires that the associated worry must not be limited to aspects of another

Assessment and Diagnosis

Axis I disorder. For example, worry about being contaminated by germs (as in obsessive-compulsive disorder), would not be counted toward a diagnosis of GAD. Finally, the symptoms must cause clinically significant distress or functional impairment and not be due to the direct physiological effects of a substance or a general medical condition. In a departure from earlier editions (DSM Ill, DSM-IlI-R; American Psychiatric Association, 1980, 1987), the DSM-IV (American Psychiatric Association, 1994) subsumes the childhood diagnosis of Overanxious Disorder under the category of Generalized Anxiety Disorder (GAD). The criteria for GAD are thought to describe adequately the disorder in children as well as adults (Tracey, Chorpita, Douban, & Barlow, 1997). Taken separately, several of these criteria have substantial diagnostic overlap with other anxiety and mood disorders. The listed psychophysiological symptoms, for example, are not unique to GAD and are commonly reported in other anxiety disorders as well (Barlow et al., 1986). Moreover, the associated symptoms of GAD are almost identical to symptoms associated with depression. This symptom criterion alone cannot distinguish individuals with a diagnosis of GAD from those with depressive disorders (Brown et al., 1995). Only in conjunction with the other criteria do these symptoms signify GAD specifically. GAD's worry criterion has some overlap with other disorders as well. Naturally, worry regarding specific events, activities, or situations occurs in other anxiety and mood disorders (Barlow, 1988, 2002). Clearly, there are subtleties in the diagnostic criteria and symptom picture of GAD that need to be taken into consideration during assessment. Useful assessment tools for GAD include both those designed to diagnose according to DSM criteria and those aimed more at appraising and understanding associated symptoms, features, and characteristics. Also, although not reviewed here, measures designed to assess for comorbid disorders are especially important when a diagnosis of GAD is determined, as evidenced by fmdings discussed earlier. Commonly used assessment tools for diagnosing GAD and examining its associated features discussed in the following paragraphs include interview-based instruments and self-report measures. The Anxiety Disorder Schedule for DSM-N (ADIS-IV; Brown, Di Nardo, & Barlow, 1994) and the Lifetime Version of this scale (ADIS-IV-L; Di Nardo, Brown, & Barlow, 1994) are the most widely used interview tools for assessment of GAD. Along with determining current and lifetime GAD, the ADIS-IV-L also assesses GAD onset, remission, and temporal sequence of comorbid anxiety disorders. Moreover it provides diagnoses of other anxiety, mood, and substance abuse disorders that often co-occur with GAD. In a departure

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from standard DSM-N diagnostic methods, both the ADISIV and ADIS-IV-L examine symptom intensity for associated and core features of GAD, even when diagnostic criteria are not fully met, in an assumption that emotional disorders exist along a continuum (cf. Brown et aI., 1998; Brown et aI., 2001; Ruscio, Borkovec, & Ruscio, 2001). Assessing for dimensional severity not only captures subclinical levels of a disorder, but is also useful for assessing change in treatment outcome studies (Borkovec, Newman, Pincus, & Lytle, 2002; Brown & Barlow, 1995). Interrater reliability of the ADISIV diagnoses for GAD (kappa = .67; Brown et aI., 2001) is good. The Structured Clinical Interview for DSM-N Axis I Disorders (SCID-IV; First, Spitzer, Gibbon, & Williams, 1996) is a second widely used diagnostic interview used to assess for GAD along with other Axis I disorders. However, unlike the ADIS-IV, its scope is limited strictly to assessing DSMN criteria. Although many self-report measures have been designed to assess different aspects of GAD, few exist with the function of diagnosing this disorder. One such diagnostic selfreport tool is the Generalized Anxiety Disorder Questionnaire IV (GADQ-IV; Newman, Zuellig, et al., 2002). This 21-item, Likert-scaled measure screens for GAD based on DSM-N criteria as standardized against the ADIS-IV (Brown, Di Nardo, et al., 1994). The GADQ-IV has good psychometric properties, with a specificity of 89 percent, a sensitivity of 83 percent, 92 percent of participants maintaining a stable diagnosis for two-week test-retest reliability, and a good rate of agreement between the GADQ-IV and the ADIS-IV (kappa = .65; Newman, Zuellig, et al., 2002). As suggested by its designers, this measure is particularly useful as an initial screening device for GAD, in order to rule out those not meeting criteria before a more costly structured interview is administered. Although not specifically intended to be diagnostic, the Penn State Worry Questionnaire (PSWQ; Meyer, Miller, Metzger, & Borkovec, 1990) is a widely used measure designed to determine the frequency and intensity of pathological worry. Because it measures a traitlike tendency to worry, the PSWQ is often used as a screening device for GAD. Factor analysis shows that this 16-item self-report device measures a unidimensional construct (Meyer et aI., 1990). The PSWQ also has high internal consistency (ex = .91), good test-retest reliability, and sensitivity to change in response to psychotherapy (Borkovec & Costello, 1993; Meyer et al., 1990). Molina and Borkovec (1994) provide a review of the strong psychometric properties of the PSWQ in both clinical and nonclinical populations. This measure also shows discriminant ability between GAD and PTSD and among pres-

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ence, absence, and subthreshold DSM-III-R GAD criteria (Meyer et aI., 1990). Other reliable and valid measures in common use include those for assessing different aspects of worry and anxiety. For example, the Meta-Cognitions Questionnaire (MCQ; Cartwright-Hatton & Wells, 1997) examines positive and negative beliefs about worry. Similarly, the Why Worry Scale (Freeston et al., 1994) assesses reasons people worry, and the Consequences of Worrying Questionnaire (CWQ; Davey, Tallis, & Capuzzo, 1996) assesses the consequences of worrying. The Reactions to Relaxation and Arousal Questionnaire (RRAQ; Heide & Borkovec, 1983) measures anxiety associated with relaxation, and the Intolerance of Uncertainty Scale (IU; Freeston et al., 1994) measures attempts to control the future, difficulty dealing with uncertainty, and reactions to ambiguous events. More general measures of anxiety are also used to assess different aspects of GAD. For example, the State-Trait Anxiety Inventory (STAI; Spielberger, Gorsuch, Lushene, Vagg, & Jacobs, 1983) is often used to examine changes in trait anxiety in GAD treatment outcome studies. In its Tension! Stress subscale, the Depression, Anxiety, and Stress Scales (Lovibond & Lovibond, 1995) assesses anxious arousal, problems relaxing, irritability, and becoming agitated quickly. Individuals with GAD have been shown to have significantly higher scores on this subscale compared to those with panic disorder, social phobia, and specific phobia (Brown, Chorpita, Korotitsch, & Barlow, 1997).

IMPACT ON ENVIRONMENT The overall picture for GAD is one of significant psychosocial impairment, with family life, peer interactions, and work all negatively affected. In the Epidemiological Catchment Area study (ECA), 38 percent of ECA subjects with GAD and 71 percent of outpatients with GAD characterized their emotional health as only fair to poor (Massi on, Warshaw, & Keller, 1993). Other recent studies have confirmed the severe disability and poor quality of life associated with GAD (Maier, Gansicke, Freyberger, & Schnaier, 2000; Sanderson & Andrews, 2002; Stein, 2001). Such disability has been found to be comparable to disability from depression (Wittchen, Carter, Pfister, Montgomery, & Kessler, 2000). Furthermore, research shows that significant disability similar to what would be expected from chronic medical illnesses can result from cases in which chronic anxiety is not successfully treated (Fifer et aI., 1994). One area of particular distress for individuals with GAD is close personal relationships. GAD negatively affects both

peer and family relationships. The disorder is associated with high marital discord and a lack of close friendships (Pincus & Borkovec, 1994; Sanderson et aI., 1994; Whisman et aI., 2000). Also, in a national comorbidity sample as well as a sample of more than 10,000 Australian subjects, GAD predicted increased odds of being separated or divorced (Hunt et aI., 2002; Wittchen et aI., 1994). Further evidence suggests such marital problems are somewhat specific to GAD relative to other anxiety disorders. Wives with GAD have been found to be more dissatisfied with their marriages than wives with other anxiety disorders (McLeod, 1994), and spouses with GAD reported more conflictual marriages than spouses with agoraphobia (Friedman, 1990). Moreover, in a sample of 4,933 married couples, marital discord was independently and more strongly associated with GAD than major depression, mania, dysthymia, social phobia, simple phobia, agoraphobia, panic disorder, and alcohol dependence after controlling for demographic variables, comorbid disorders, and quality of other relationships (Whisman et aI., 2000). Additional studies show that compared to non-GAD participants, GAD women have more difficulty with emotional and interpersonal intimacy (Dutton, 2002). Compared to agoraphobic patients and their spouses, GAD patients and their spouses report that there is greater conflict and less cohesion in their families (Friedman, 1990). Finally, parents with GAD report significantly greater dysfunction in their families compared to those without GAD (Ben-Noun, 1998). The poor quality of peer and family relationships found in those with GAD can be associated with several personality and interpersonal problems typically found in the disorder. Given that people with GAD approach their relationships with elevated hypervigilance, suspiciousness, and a tendency to feel easily slighted (Gasperini et aI., 1990), it is not surprising that they have high levels of interpersonal problems. As noted earlier, negative interpersonal cycles may occur with GAD individuals, thus leading to the maintenance of interpersonal problems and worries. Restricted emotional expression (a common trait for those with GAD) may also contribute to the poor close relationships associated with the disorder. Research has demonstrated that high levels of emotional disclosure predict being liked and are necessary for the development of close relationships (Collins & Miller, 1994; Dindia, 2000). Yet clinical observations suggest that individuals with GAD have restricted affect, empathy, and spontaneity and avoid displaying emotional vulnerability (Newman, 2000b; Newman, Castonguay, Borkovec, & Molnar, 2004). Several lines of research also support the idea that people with GAD have difficulty expressing emotion. For example, compared to non anxious individuals, both GAD analogues and clients report a greater

Treatment Implications 111 intensity of emotional experience and greater difficulty labeling emotions (Abel, 1994; Brown, Di Nardo, et aI., 1994; Mennin, Turk, Fresco, & Heimberg, 2000; Turk et al., in press; Yamas, Hazlett-Stevens, & Borkovec, 1997). Furthermore, because worry inhibits emotional processing (Borkovec & Hu, 1990; Borkovec et aI., 1993; Peasley-Miklus & Vrana, 2000), it has been conceived as motivated avoidance of emotional imagery and associated physical sensations (Borkovec & Inz, 1990). This avoidance of emotion likely leads to the "opposite" of emotional disclosure found in those with GAD (Borkovec, Roemer, & Kinyon, 1995). Along with problems relating to close relationships, GAD also has a negative impact on work. The anxiety associated with GAD is debilitating, causing many with the disorder to be unable to go to work. For example, the ECA survey found that 27 percent of ECA subjects with GAD and 25 percent of outpatients with GAD were receiving disability payments, and only about 50 percent worked full-time. Of those who were working, 38 percent had missed at least one week of work in the past year due to their anxiety (Massion et al., 1993). It is likely that both extreme worry and the interpersonal apprehension and rigidity common to GAD lead to difficulty excelling in the workplace as well. Indeed, the ECA survey also found a strong correlation between both occupational status and income and GAD. GAD was associated with a threefold greater likelihood of working at a low occupationallevel and a more than twofold likelihood of earning less than $10,000 per year. Another recent study found that the role impairment in those with pure GAD (without comorbidity) is comparable to that of major depression (Kessler, Stang, Wittchen, Stein, & Walters, 1999).

TREATMENT IMPLICATIONS Although substantial gains in GAD treatment have been made over the years, it remains the least successfully treated of the anxiety disorders (Brown, Barlow, et al., 1994). Nevertheless, cognitive behavioral treatment (CBT) for GAD has been found to be generally effective against the disorder (for a review, see Newman, Castonguay, Borkovec, & Molnar, 2004). The symptoms of GAD are believed to arise from consistent, spiraling, rigid patterns of interaction between cognitive, imaginal, and physiological responses to continuously perceived threat (Barlow, 1988; Borkovec & Inz, 1990; Newman & Borkovec, 2002). Cognitive behavioral therapy contains elements designed to target each of these cognitive, imaginal, and physiological response systems (Newman, 1999; Newman & Borkovec, 1995). The client learns techniques in CBT with the aim of developing a more flexible and relaxed

lifestyle leading to a reduction in their anxiety. The specific interventions in CBT include self-monitoring, stimulus control, relaxation, self-control desensitization, and cognitive therapy. Several recent chapters provide a more complete review of CBT for GAD (Borkovec & Newman, 1998; Newman, 2000a; Newman & Borkovec, 2002). Clients in CBT first learn self-monitoring and early cue detection. They are taught to pay attention to internal (and, with less emphasis, external) cues that signal that they are becoming anxious. Because of the spiraling nature of anxiety in GAD, it is important for clients to learn their early warning signs and stop their worry early before it reaches uncontrollable levels. Self-monitoring helps to identify triggers and patterns specific to the anxious experience of each individual client. Once clients are aware of their anxiety cues, elements of CBT designed to intervene at early stages of anxiety and worry can be employed. Stimulus control is the next element of CBT that clients learn to utilize. GAD clients worry across numerous situations, a habit that leads to many cues (both internal and external) that trigger their anxiety. In order to lessen the association between worry and these cues, clients are asked to schedule in a specific 30-minute worry period each day and to purposefully put off worrying at other times until the appointed time. This procedure provides the client with a sense of control over their worry, thus targeting the prominent feature of uncontrollable worry indicative of GAD. The physiological aspects of GAD are also targeted in therapy. Diaphragmatic breathing and progressive muscle relaxation (PMR) are helpful methods of addressing the autonomic rigidity common to the disorder. Diaphragmatic breathing teaches clients that breathing from the chest activates the sympathetic autonomic nervous system, thus leading to physiological sensations indicating anxiety. Breathing from the diaphragm, on the other hand, stimulates the parasympathetic nervous system and produces physiological sensations of deep relaxation. Clients can actively switch to breathing from the diaphragm as soon as they detect the first cues of their anxiety. This simple breathing technique offers clients a better sense of control over their somatic anxious sensations. PMR is another helpful method of relaxation. Clients are taught to systematically tense and then release 16 distinct muscle groups. As the technique is mastered, the muscle groups are gradually reduced to only four, and finally clients are able to relax their muscles without first tensing them at all. During PMR, clients focus on a calming mantra or image in order to aide the relaxation process. The goals of relaxation are to increase adaptive behavior and to focus the client's attention on the present moment. Applied relaxation (AR) can further help clients to reach these goals by requiring them to

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use relaxation techniques throughout the day whenever they detect anxiety cues. Imaginal exposure is another important element in the treatment of GAD. Whereas worry impedes emotional processing, imagery assists the process. Self-control desensitization (SCD) uses imagery as a form of exposure to anxiety problems in which no specific phobic object exists (Goldfried, 1971). First clients use PMR to relax, and then they imagine themselves in an anxiety-provoking situation until they feel symptoms of anxiety. Next the clients imagine themselves coping effectively with the situation and thus relax the anxiety away. SCD teaches clients to use their CBT coping strategies when they notice anxious cues. Another important element of CBT is cognitive therapy (CT). CT is based on the premise that emotions depend on the wayan individual interprets different situations. People with GAD tend to negatively interpret ambiguous or neutral stimuli (Mathews, 1990; Mathews & MacLeod, 1994). They also often vastly misjudge the probability of a core feared event occurring, as evidenced by the finding in the Penn State GAD project that this event occurred in only 3 percent of all worries. Therefore, CT may be a particularly important element of treatment for GAD. Cognitive therapy teaches clients to reinterpret stimuli in a more accurate, positive light based on actual evidence from their environment. Although CBT has been shown to be effective in treating GAD, on average only about 50 percent of clients show clinically significant change at follow-up (Borkovec & Newman, 1998; Newman, 2000b). Some authors suggest that by introducing interpersonal and experiential elements into the nowstandard CBT package for GAD, more of the core elements of the disorder would be addressed, thus leading to higher rates of therapeutic change (e.g., Newman, 2000b; Newman et al., 2004). In fact, these researchers have developed a therapy that integrates present-moment awareness and interpersonal concerns into a CBT package in order to focus on these specific difficulties associated with GAD (Newman, Castonguay, & Borkovec, 2002). Pharmacological treatment has also been used effectively to treat GAD, however, its effects have not been found to be as high as those found with CBT, particularly when clients have comorbid depression (Gould, Otto, Pollack, & Yap, 1997). Three classes of drugs are commonly used to treat GAD, those being benzodiazepines, azapirones, and antidepressants. Benzodiazepines such as diazepam have historically been the most widely used medication for anxiety. They have been shown to produce short-term alleviation of GAD symptoms; however, full remission is rare, and relapse after treatment is common (Schweizer & Rickels, 1996).

Benzodiazepines target the somatic symptoms of GAD and have not been found to be particularly effective against the cognitive symptoms such as worry (e.g., Pourmotabbed, McLeod, Hoehn-Saric, Hipsley, & Greenblatt, 1996). Fur" thermore, benzodiazepines have been shown less effective when depressive symptoms are present (Gould et aI., 1997), which presents an important consideration in light of high rates of comorbidity. A further drawback of benzodiazepines includes serious side effects such as anterograde amnesia (Lucki, Rickels, & Geller, 1986), sedation (Shader & Greenblatt, 1993), and psychomotor dysfunction (Pourmotabbed et aI., 1996). Finally, benzodiazepines can be addictive (Moller, 1999) and often produce withdrawal symptoms after long-term treatment (Rickels, Case, Schweizer, Swenson, & Fridman, 1986; Schweizer & Rickels, 1998). Abecarnil, a new type of partial benzodiazepine agonist that has recently been developed, seems to produce fewer withdrawal symptoms while still reducing anxiety effectively compared to placebo in some studies (Lydiard, Ballenger, & Rickels, 1997). Further research is needed, however, as other studies have failed to show a significant difference between abecarnil and placebo (e.g., Rickels, DeMartinis, & Aufdembrinke, 2000). Azapirones such as buspirone and antidepressants such as impramine (a tricyclic antidepressant) and paroxetine (a selective serotonin reuptake inhibitor) are also used to treat GAD. These drugs have fewer side effects and dependence risk than benzodiazepines and target cognitive symptoms of anxiety rather than somatic symptoms. Although these improvements are hopeful, there is a strong likelihood of relapse once use of the drug is discontinued, and due to the chronicity and early onset of GAD, drug therapy is often problematic for this disorder (Schweizer & Rickels, 1996). Few studies to date exist regarding factors predictive of treatment outcome for GAD (Newman, Crits-Christoph, Connelly, & Erickson, in press). Expectancy ratings at the start of treatment have been found to predict outcome in some studies (Borkovec & Costello, 1993; Borkovec & Mathews, 1988) but not in others (Borkovec et aI., 2002; Ladouceur et aI., 2000). Similarly, whereas some studies found no relationship between credibility and outcome (Borkovec & Costello, 1993; Borkovec & Mathews, 1988), others found credibility ratings significantly predicted outcome (Borkovec et al., 2002). Also, Borkovec and colleagues found a negative relationship between anxiety experienced during relaxation and treatment outcome (Borkovec et aI., 1987; Borkovec & Mathews, 1988). Finally, Borkovec, Newman et al. (2002) identified several dimensions of interpersonal problems reported both at the start of treatment and at follow-up as negative predictors of outcome.

References 113 SUMMARY This chapter has provided an overview of generalized anxiety disorder (GAD), including a clinical picture of the disorder and sections on personality development, etiology, course and prognosis, epidemiology, assessment and diagnosis, impact on the environment, and treatment. The nature and function of worry were discussed, including cognitive findings regarding information processing dysfunctions such as the tendency of those with GAD to interpret ambiguous/neutral stimuli as negative. These difficulties are related to the view held by individuals with GAD that the world IS a dangerous place and the belief that worry is a positive coping strategy. Also, emotion avoidance theory was discussed based on findings of inflexible physiological characteristics of those with GAD. Worry reduces physiological arousal and thus may be negatively reinforced, with the negative consequence of precluding emotional processing. Next, personality correlates of the disorder were detailed, and development in terms of negative interpersonal cycles was discussed, along with various accounts of etiology. The development and maintenance of GAD is linked to attachment theory, the verbal-linguistic nature of worry, and emotional processing dysfunction. Prevalence of GAD and risk factors such as gender and marital status were noted in the next section. The early onset, chronic course, and the frequently comorbid nature of GAD were highlighted as well. Possibilities of a bimodal age of onset and its implications were also discussed. Current assessment and diagnosis tools such as the GADQ-IV were outlined, and diagnostic criteria were given. Finally, various treatment strategies such as cognitive behavioral techniques and pharmacological interventions were reviewed.

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