نقش موثر نگرانی در تولید احساسات و اختلال در نظم در اختلال اضطراب فراگیر
|کد مقاله||سال انتشار||مقاله انگلیسی||ترجمه فارسی||تعداد کلمات|
|35013||2007||18 صفحه PDF||سفارش دهید||12241 کلمه|
Publisher : Elsevier - Science Direct (الزویر - ساینس دایرکت)
Journal : Behaviour Research and Therapy, Volume 45, Issue 8, August 2007, Pages 1735–1752
The role of worry in generalized anxiety disorder (GAD) has been posited to serve as an avoidance of emotional experience, and emotion regulation deficits in GAD have been found in several previous studies. It remains unclear whether those with GAD experience more dysregulated emotions during periods of euthymia and positive affect or whether these deficits occur only during periods of worry. Individuals with GAD (with and without co-occurring dysphoria) and non-anxious controls were randomly assigned to receive a worry, neutral, or relaxation induction. Following the induction, all participants viewed a film clip documented to elicit sadness. Intensity of emotions and emotion regulation were examined following the induction period and film clip. The results revealed that, regardless of co-occurring dysphoria, individuals with GAD in the worry condition experienced more intense depressed affect than GAD participants in the other conditions and controls participants. In contrast, presence of worry appeared to have less impact on indices of emotion dysregulation, which were greater in participants with GAD compared to controls, but largely insensitive to contextual effects of worry or of relaxation. Following film viewing, both GAD participants with and without dysphoria displayed poorer understanding, acceptance, and management of emotions than did controls. However, acceptance and management deficits were most pronounced in individuals with both GAD and co-occurring dysphoria. Implications for the role of emotions in conceptualization and treatment of GAD are discussed.
Generalized anxiety disorder (GAD) is a common, chronic, and disabling condition. Nearly 5% of individuals in the United States will qualify for a diagnosis of GAD at some point in their lives (Kessler et al., 1994). Despite this comparatively high rate, it has received considerably less empirical and theoretical attention than other anxiety disorders (Dugas, 2000). Much of this lack of attention has come from misconceptions about the nature and treatment of GAD, even amongst mental health professionals. For example, a commonly held misconception about GAD is that the disorder is relatively innocuous and does not cause significant distress or impairment (Persons, Mennin, & Tucker, 2001). Actually, GAD is associated with high levels of disability and absenteeism from work (Olfson et al., 1997), increased health care utilization (Roy-Byrne & Katon, 1997), as well as marked impairments in role functioning (Wittchen, Zhao, Kessler, & Eaves, 1994). Further, individuals with GAD often experience significant symptoms of the disorder for as long as 20 years, and less than 40% of individuals experience remission after 5 years (Keller, 2002). Thus, its not surprising that GAD is one of the most difficult to treat anxiety disorders (Gould, Safren, Washington, & Otto, 2004). Recent years have seen considerable advances in conceptualizing and treating GAD (cf. Borkovec, Alcaine, & Behar, 2004). Particularly instrumental in this progress has been the establishment of worry as the pathognomonic characteristic of GAD (American Psychiatric Association, 2000), and the empirical delineation of worry's avoidance function. Avoidance mechanisms in anxiety represent the hallmark of our understanding of anxiety disorders (Mowrer, 1947) and have led to improvements in treatment through the development of exposure-based therapies (e.g., Barlow, Craske, Cerny, & Klosko, 1989; Foa et al., 1999). However, whereas most anxiety disorders are characterized by overt behavioral avoidance, GAD typically does not display consistent behavioral markers and has not responded as well to traditional forms of exposure therapy as the other anxiety disorders (e.g., Gould et al., 2004). Increased focus on the avoidance function of worry and its centrality in GAD has underscored the cognitive aspects of this disorder. For example, in GAD, fear is organized around future threats or catastrophes that may occur as opposed to objects or people in the present environment. Borkovec et al. (2004) posited that worry in GAD is associated with avoidance of emotional experience. Evidence for this conceptualization of worry in GAD has been found in a number of studies. The verbal-linguistic, as opposed to imagery-based, nature of worry provides initial evidence of worry's avoidant functions. During periods of relaxation, non-anxious participants experience a predominance of imagery-based mentation, whereas individuals with GAD experience equal amounts of thought and imagery. During subsequent worry, both control and GAD participants demonstrate increases in the experience of thought-based mentation (Borkovec & Inz, 1990). Subsequent investigations confirm that worry is experienced phenomenologically as primarily verbal-linguistic thought as opposed to imagery (Freeston, Dugas, & Ladouceur, 1996). The verbal-linguistic, as opposed to imaginal, nature of worry has important implications for understanding the avoidant function of worry. It has been demonstrated that thinking about anxious material produces less cardiovascular response than does imagining the same anxious material (Vrana, Cuthbert, & Lang, 1986). Furthermore, worrying before repeated presentations of a phobic image precludes autonomic response to those images (Borkovec & Hu, 1990; Borkovec, Lyonfields, Wiser, & Deihl, 1993). The avoidance of anxiety-related imagery strengthens the worry process through negative reinforcement, because the aversive autonomic arousal associated with anxious images is decreased or eliminated during worry. In line with this conceptualization, decreased parasympathetic nervous system activity (vagal tone) has been found to occur in GAD and in the state of worry (Thayer, Friedman, & Borkovec, 1996). The assertion that worry in GAD is associated with avoidance of arousing fear-related imagery is thus well supported (see Borkovec et al., 2004 for a comprehensive review of evidence for this theory). A key contributor to the avoidant function of worry may be the perceived aversive nature of the evaded emotional experience. When asked about reasons for worrying, individuals with GAD were distinguished from non-anxious controls by the greater likelihood to endorse that they engaged in worry to avoid thinking about more emotional topics (Borkovec & Roemer, 1995). An important question then is why individuals with GAD want to avoid emotional experience. One possibility may result from the nature of how emotions are generated and regulated ( Gross, 2001). Mennin and colleagues ( Mennin, Heimberg, Turk, & Fresco (2002) and Mennin, Heimberg, Turk, & Fresco (2005)) argue that individuals with GAD have difficulties in four areas of emotion. Specifically, individuals with GAD reported experiencing emotions with heightened intensity compared to persons without GAD. Second, individuals with GAD experience marked difficulties identifying, describing, and clarifying their emotional experiences (i.e., poor understanding). Third, they are prone to greater negative reactivity to emotions by holding catastrophic beliefs about the consequences of both negative and positive emotions. Fourth, individuals with GAD struggle to manage or soothe themselves when they experience negative emotions (i.e., maladaptive management). Within this model, maladaptive emotion management strategies in GAD can be classified both as difficulties modulating or tempering emotional experiences (often due to their increased emotional intensity) or as attempts to control or suppress emotional experience (often through the avoidant process of worry). Mennin and colleagues have provided preliminary evidence for this emotion dysregulation model of GAD in a series of studies. Participants with self-reported GAD (Study 1) and treatment-seeking patients with clinician-assessed GAD (Study 2) have reported greater deficits in these four areas as compared to control participants (Mennin et al., 2005). Further, GAD participants, but not control participants, who underwent a negative mood induction showed increases in negative emotions as well as difficulties in their ability to regulate the negative mood, particularly with respect to their understanding of and willingness to accept the emotional experience (Study 3; Mennin et al., 2005). Also, individuals with self-reported GAD have reported greater emotional intensity and greater negative reactivity to depressive moods, than individuals with self-reported social anxiety disorder individuals and controls (Turk, Heimberg, Luterek, Mennin, & Fresco, 2005). Finally, a composite emotion regulation score derived from measures assessing each of the four branches of the emotion regulation model successfully predicted GAD after controlling for worry, anxiety, and depression (Mennin et al., 2005) and was more associated with a diagnosis of GAD than social anxiety disorder (Turk et al., 2005). As such, intensity of emotional reactions to negative stimuli and inability to manage these reactions appears to characterize GAD. However, the contexts in which individuals with GAD may react and manage their emotions differently than those without the disorder remain unclear. Given the centrality of worry in the experience of GAD individuals, it is important to determine what role worry might play in emotion dysregulation. In the emotion dysregulation model of GAD, worry is viewed primarily as a maladaptive emotion management strategy; specifically, worry is conceptualized as a strategy used in attempts to control or suppress emotional experience (Mennin, Heimberg, Turk, & Fresco (2002) and Mennin, Heimberg, Turk, & Fresco (2005)). Because worry is considered to be a response to dysregulated emotions, intense or under-regulated emotions are experienced prior to the occurrence of worry within this model. For example, an individual with GAD may experience a loss and feel sadness. Because the individual holds negative beliefs about the consequences of feeling sad, they engage in worry as an attempt to avoid feeling sad. However, it may be that worry also plays a role in the generation of dysregulated emotional experience in GAD. Individuals with GAD spend large amounts of time engaging in worry. Higher levels of worry are found in GAD than in any of the other anxiety disorders (Brown, Antony, & Barlow, 1992), and individuals with the disorder report that their worries are more pervasive (Roemer, Molina, & Borkovec, 1997) and less controllable (Borkovec, Shadick, & Hopkins, 1991; Craske, Rapee, Jackel, & Barlow, 1989) than individuals without the disorder. One study found that those with GAD reported worrying and feeling anxious 50% of the time (Sanderson & Barlow, 1990). Worry has been demonstrated to create both anxious and depressed affect (Andrews & Borkovec, 1988; Borkovec, Robinson, Pruzinsky, & DePree, 1983) and is associated with information processing biases that favor the processing of threatening information (e.g., MacLeod, Mathews, & Tata, 1986). Given that worry in GAD is pervasive, uncontrollable, and aversive, it seems likely that individuals with the disorder may experience greater difficulty managing their emotional reactions to events in the environment during or immediately following periods of worry. As such, the role of worry in emotion dysregulation in GAD may be bidirectional: worry may serve as a response to dysregulated emotional experience as an attempt to control or avoid such experience, but worry may also lead to increased intensity of emotional reactions to environmental events and a decreased ability to effectively manage those emotions. This latter conceptualization is consistent with the notion of experiential avoidance wherein control strategies such as worry beget more aversive emotional experiences (see Hayes, Strosahl, & Wilson, 2004). The primary goal of the present study was to determine the role of worry in inducing negative emotional reactions and dysregulation in comparison to other contextual states such as relaxation or euthymia. The current investigation examined the impact of being in a worried, relaxed, or neutral state on emotion generation and regulation differences between individuals with GAD and non-anxious controls following a negative emotion induction. A previous experimental investigation of the emotion dysregulation model did not specifically examine the role of contexts such as worry in emotion regulation deficits in GAD (Mennin et al., 2005; Study 3). Also, in this prior study, participants with GAD did not undergo diagnostic interviews to confirm the diagnosis; rather, a self-report measure of GAD was used to identify an analog sample. In addition, music was used to induce mood rather than more evocative and well-studied film clips (e.g., Gross & Levenson, 1995). Finally, the pre-induction state of participants was not a factor examined in the analyses. Differences in baseline worry, or relaxation, may have been confounded with participant group. The current investigation seeks to build upon the first experimental investigation of the emotion dysregulation model of GAD by addressing these limitations in study design. Participants were assigned to diagnostic groups using a structured diagnostic interview, a standardized film clip was used to induce mood, and the pre-induction state of participants was controlled using thought induction procedures (to ensure that GAD and control participants were equivalent prior to the emotion induction). The target emotion elicited by our emotion induction was sadness. We chose to elicit sadness for a number of reasons. First, we wanted to examine the experience and regulation of a negative emotion, given that deficits in negative affect regulation are of theoretical and practical significance when examining emotional disorders. Secondly, sadness is a negative emotion that is an experience commonly experienced by individuals with GAD but is not as core to the diagnosis as anxiety, which supports the notion of a generalized emotion deficit in GAD, rather than one specific to anxiety (Mennin et al., 2005). Finally, sadness is a negative emotion that is experienced ubiquitously across cultures and individuals (e.g., Ekman, Sorenson, & Friesen, 1969), making it an emotion that virtually all individuals have experienced and had to manage in their everyday lives. Thus we focused on sad emotional reactions but also assessed anxiety reactions given their centrality to the disorder. Our primary goals in this study are to examine experimentally differences in emotional intensity and emotion regulation between individuals with GAD and those without the disorder and to examine the role that worry plays in contributing to differences in emotional intensity and regulation. However, it is important to note that it is difficult in any study to examine the independent effects of GAD, given the high rates of comorbidity between GAD and depression and other anxiety disorders (Brown, Barlow, & Liebowitz, 1994; Brown, Campbell, Lehman, Grisham, & Mancill, 2001; Grant et al., 2005; Kessler, Dupont, Berglund, & Wittchen, 1999). Because GAD is highly comorbid with other emotional disorders, any differences found between GAD and control participants could be due, in part, to the effects of co-occurring disorders. This concern is particularly important to address with regard to depression, as depression has the highest rates of comorbidity with GAD with lifetime comorbidity rates ranging from 50–60% (Brown, Barlow, & Liebowitz (1994) and Brown, Campbell, Lehman, Grisham, & Mancill (2001); Kessler et al., 1999) and given that recent conceptualizations of GAD have called into question the delineation of GAD from depression (Brown, Chorpita, & Barlow, 1998; Watson, 2005). The emotion regulation deficits of interest in this study have been found to occur in GAD but not in social phobia (Mennin, Holaway, Fresco, Moore, & Heimberg, in press), the anxiety disorder that is most frequently comorbid with GAD (Brown et al., 1994). However, the nature of the emotion regulation deficits of interest has not been thoroughly examined in depression. Given that we were particularly interested in the experience of sadness, we have included comparisons of subgroups of participants with GAD who did and did not have dysphoria. However, we did not anticipate that co-occurring dysphoric symptoms would impact emotional intensity or emotion regulation for individuals with GAD. Because previous research has documented that the emotion regulation deficits reviewed above are distinct (e.g., heightened intensity) or particularly elevated (e.g., maladaptive management) in GAD (Mennin et al., in press), we expected to find differences between GAD participants and controls regardless of the presence of dysphoria. Nonetheless, the role of co-occurring depressive symptoms was examined in all of our analyses to determine whether differences in dysphoria between the GAD and control group were responsible for any observed group differences in emotional intensity and regulation. We hypothesized that GAD participants (regardless of co-occurring dysphoria) in the worry condition would: (1) report experiencing more intensely negative emotions (both sadness and anxiety) across time (i.e., from baseline to the worry period to post-film clip) than non-anxious controls and GAD participants in neutral and relaxation conditions; (2) would report experiencing less awareness, understanding, and acceptance of their emotions than controls and GAD participants in neutral and relaxation conditions; and (3) would report more difficulty in effectively managing their emotions than controls and GAD participants in neutral and relaxation conditions. Because we predicted that participants with GAD would only differ from control participants in their emotional reactions, understanding of emotions, and emotion management in their response to the sad mood clip occurring after the worry induction, we expected that no differences would emerge between GAD and control participants after the neutral and relaxation inductions. Method Participants S