CBT For Anxiety Disorders

A Practitioner Book

Gregoris Simos, Stefan G. Hofmann

• Editore: Wiley-Blackwell
• Anno: 2013
• ISBN:
  9781118316764
• Edizione: 1
• Argomento: Psychology
• Categoria: Cognitive Behavioral Therapy (CBT)

CBT for Anxiety Disorders presents a comprehensive overview of the latest anxiety disorder-specific treatment techniques contributed by the foremost experts in various CBT approaches.

• Summarizes the state-of-the-art CBT approaches for each of the DSM anxiety disorders
• Represents a one-stop tool for researchers, clinicians, and students on CBT for anxiety disorders
• Features world leading CBT authors who provide an up to date description of their respective treatment approaches in a succinct, and clinician-tailored, fashion

1

Panic Disorder and Agoraphobia

Michelle G. Craske1 and Gregoris Simos2

1UCLA, Los Angeles, CA, USA
2University of Macedonia, Thessaloniki, Greece

Overview

The current diagnostic criteria for panic disorder, according to the Diagnostic and Statistical Manual of Mental Disorders, 4th edition (DSM-IV, American Psychiatric Association, 1994), are comprised of recurrent unexpected panic attacks, and anxiety about future panic attacks or their consequences, or a significant behavioral change because of the panic attacks. The additional anxiety about panic, combined with catastrophic cognitions about panic sensations, contributes to the differentiation between the person with panic disorder and the person with occasional panic attacks (e.g., Telch, Lucas, and Nelson, 1989). Agoraphobia refers to avoidance or endurance with dread of situations from which escape might be difficult or help unavailable in the event of a panic attack, or in the event of developing symptoms that could be incapacitating and embarrassing, such as loss of bowel control or vomiting. Typical agoraphobic situations include shopping malls, waiting in line, movie theaters, traveling by car or bus, crowded restaurants, and being alone.

In the general population, the 12-month prevalence estimate for panic disorder across the United States and several European countries is about 2% in adults and adolescents (Goodwin, Fergusson, and Horwood, 2005; Kessler et al., 2005b). Lower estimates have been reported for some Asian, African, and Latin American countries, ranging from 0.1 to 0.8% (Lewis-Fernandez et al., 2010). Across all studies, females are more frequently affected than males at a rate of approximately 2 : 1 (Kessler et al., 2005b). Although panic attacks occur in children, the overall prevalence of panic disorder is low prior to 14 years of age (<0.4%) (Craske et al., 2010). The rates of panic disorder show a gradual increase during adolescence, particularly in girls, and possibly following the onset of puberty (Craske et al., 2010). The modal age of onset is late teenage years and early adulthood (Kessler et al., 2005a), although treatment is usually sought at a much later age, around 34 years (e.g., Noyes et al., 1986). The prevalence rates decline in older individuals, possibly reflecting diminishing severity to subclinical levels (Wolitzky-Taylor et al., 2010). In general, differences in prevalence across gender, culture, and age groups may be due to a variety of factors, including the expression of the disorder, underlying physiology or biology, varying degrees of concern about the dangerousness of symptoms of autonomic arousal and mental symptoms of anxiety, and sensitivity of instrumentation for diagnosing panic disorder.

Panic disorder and agoraphobia tend to be chronic conditions, with severe financial and interpersonal costs; that is, only a minority (30%) of untreated individuals remit without subsequent relapse, although a similar number experience notable improvement, albeit with a waxing and waning course (35%) (Katschnig and Amering, 1998; Roy-Byrne and Cowley, 1995). Also, panic disorder is associated with high levels of social, occupational, and physical disability, considerable economic costs, and the highest number of medical visits among the anxiety disorders, although the effects are strongest with the presence of agoraphobia (Wittchen et al., 2010).

Rarely does the diagnosis of panic disorder, with or without agoraphobia, occur in isolation. Commonly co-occurring Axis I conditions include specific phobias, social phobia, dysthymia, generalized anxiety disorder, major depressive disorder, and substance abuse (e.g., Brown et al., 2001; Kessler et al., 2005b). Also, from 25 to 60% of persons with panic disorder also meet criteria for a personality disorder, mostly avoidant and dependent personality disorders (e.g., Chambless and Renneberg, 1988). However, the nature of the relationship between panic disorder/agoraphobia and personality disorders remains unclear, especially as some “personality disorders” remit after successful treatment of panic disorder/agoraphobia (e.g., Latas et al., 2000; Marchesi et al., 2005; Ozkan and Altindag, 2005).

Cognitive Behavioral Model

Several independent lines of research (Barlow, 1988; Clark, 1986; Ehlers and Margraf, 1989) converged in the 1980s on the same basic conceptualization of panic disorder as an acquired fear of bodily sensations, particularly sensations associated with autonomic arousal. Psychological (i.e., temperament, such as negative affectivity) and biological (i.e., genetic) predispositions are believed to enhance the vulnerability to acquire such fear. Fear conditioning, avoidant responding, and information processing biases are believed to perpetuate such fear. It is the perpetuating factors that are targeted in the cognitive behavioral treatment approach.

The temperament most associated with anxiety disorders, including panic disorder, is neuroticism (Eysenck, 1967; Gray, 1982) or proneness to experience negative emotions in response to stressors. A closely linked construct is “negative affect,” or the tendency to experience a variety of negative emotions across a variety of situations, even in the absence of objective stressors (Watson and Clark, 1984). Neuroticism predicts the onset of panic attacks in adolescents (Hayward et al., 2000; Schmidt, Lerew and Jackson, 1997, 1999), and “emotional reactivity” at age 3 was a significant variable in the classification of panic disorder in 18- to 21-year-old males (Craske et al., 2001). Numerous multivariate genetic analyses of human twin samples consistently attribute approximately 30–50% of variance in neuroticism to additive genetic factors (Eley, 2001; Lake et al., 2000). In addition, anxiety and depression appear to be variable expressions of the heritable tendency toward neuroticism (Kendler et al., 1987). Symptoms of panic (i.e., breathlessness and heart pounding) may be additionally explained by a unique source of genetic variance that is differentiated from symptoms of depression and anxiety (Kendler et al., 1987) and neuroticism (Martin et al., 1988).

Another temperament is anxiety sensitivity, which refers to the trait of believing that anxiety and associated symptoms may cause deleterious physical, social, and psychological consequences that extend beyond any immediate physical discomfort during an episode of anxiety or panic (Reiss, 1980). Anxiety sensitivity is elevated across most anxiety disorders, but it is particularly elevated in panic disorder, especially the physical concerns subscale (Zinbarg, Barlow, and Brown, 1997). Anxiety sensitivity is believed to comprise a specific psychological vulnerability for panic disorder because it primes fear reactivity to bodily sensations. In support, several longitudinal studies indicate that high scores on the anxiety sensitivity index predict the onset of panic attacks over 1- to 4-year intervals in adolescents (Hayward et al., 2000), college students (Maller and Reiss, 1992), and community samples with specific phobias or no anxiety disorders (Ehlers, 1995). In addition, anxiety sensitivity index scores predicted spontaneous panic attacks, and worry about panic (and anxiety more generally), during an acute military stressor (i.e., 5 weeks of basic training), even after controlling for history of panic attacks and trait anxiety (Schmidt, Lerew and Jackson, 1999). Finally, panic attacks themselves elevate anxiety sensitivity over a 5-week period in adults (Schmidt Lerew, and Jackson, 1999), and over a 1-year period in adolescents, albeit to a lesser extent (Weems et al., 2002).

However, Bouton, Mineka, and Barlow (2001) noted that the relationship between anxiety sensitivity and panic attacks in these studies was relatively small, not exclusive to panic, and was weaker than the relationship between panic and neuroticism. Furthermore, these studies have evaluated panic attacks and worry about panic but have not evaluated prediction of diagnosed panic disorder. Thus, the causal significance of anxiety sensitivity for panic disorder remains to be fully understood.

Acute “fear of fear” (or more accurately, anxiety focused on somatic sensations) that develops after initial panic attacks is attributed to two factors: catastrophic misappraisals of bodily sensations (i.e., misinterpretation of sensations as signs of imminent death, loss of control, and so on) (Clark, 1986); and interoceptive conditioning, or conditioned fear of internal cues, such as elevated heart rate, because of their association with intense fear, pain, or distress (Razran, 1961). Specifically, interoceptive conditioning refers to low-level bodily sensations of arousal coming to serve as conditional stimuli that trigger increased autonomic arousal and fear through Pavlovian conditioning (Bouton, Mineka, and Barlow, 2001). Thus, small changes in physiological functioning lead to conditioned fear or panic as a result of prior pairings of these initial somatic sensations with full-blown panic attacks. An extensive experimental literature attests to the robustness of interoceptive conditioning (e.g., Dworkin and Dworkin, 1999), particularly with regard to early interoceptive drug onset cues becoming conditioned stimuli for larger drug effects (e.g., Sokolowska, Siegel, and Kim, 2002). In addition, interoceptive conditioned responses are not dependent on conscious awareness of triggering cues and thus have been observed under anesthesia (e.g., Block et al., 1987). As such, interoceptive conditioning accounts for what appear to be “out of the blue” panic attacks.

Evidence for extreme fear and anxiety of somatic sensations is robust across a variety of paradigms. Persons with panic disorder endorse strong beliefs that bodily sensations associated with panic attacks cause physical or mental harm (e.g., McNally and Lorenz, 1987). They are more likely to interpret bodily sensations in a catastrophic fashion (Clark et al., 1988), and to allocate more attentional resources to words that represent physical threat such as “disease” and “fatality” (e.g., Hope et al., 1990), catastrophe words, such as “death” and “insane” (e.g., Maidenberg et al., 1996), and heartbeat stimuli (Kroeze and van den Hout, 2000). Also, individuals with panic disorder show enhanced brain potentials to panic-related words (Pauli et al., 2005). In addition, they are more likely to become anxious in procedures that elicit bodily sensations similar to the ones experienced during panic attacks, including benign cardiovascular, respiratory, and audiovestibular exercises (Antony et al., 2006), as well as more invasive procedures such as carbon dioxide inhalations, compared to clients with other anxiety disorders (e.g., Perna et al., 1995; Rapee et al., 1992) or healthy controls (e.g., Gorman et al., 1994). The findings are not fully consistent, however, as clients with panic disorder did not differ from clients with social phobia in response to an epinephrine challenge (Veltman et al., 1996). Nonetheless, individuals with panic disorder also fear signals that ostensibly reflect heightened arousal and false physiological feedback (Craske et al., 2002; Ehlers et al., 1988).

Such anxiety about bodily sensations plays a central role in the perpetuation of panic disorder. First, once the bodily sensations are noticed, they elicit fear in an individual with panic disorder. This fear serves to intensify the sensations, causing an increase in fear, which further enhances the bodily sensations in a self-perpetuating cycle of fear and bodily sensations that typically results in a panic attack. Second, because bodily sensations that trigger panic attacks are not always immediately obvious, they may generate the perception of unexpected or “out of the blue” panic attacks that generates even further distress (Craske, Glover, and DeCola, 1995). Third, the perceived uncontrollability, or inability to escape from, or terminate bodily sensations again is likely to generate heightened anxiety (e.g., Maier, Laudenslager, and Ryan, 1985). Unpredictability and uncontrollability, then, are seen as enhancing general levels of anxiety about “when is it going to happen again” and “what do I do when it happens,” thereby contributing to high levels of chronic anxious apprehension. In turn, anxious apprehension increases the likelihood of panic, by directly increasing the availability of sensations that have become conditioned cues for panic and/or by increasing attentional vigilance for these bodily cues. Thus, a maintaining cycle of panic and anxious apprehension develops.

Individuals with panic disorder often engage in safety behaviors that they believe enable them to escape or avoid the feared outcome. For example, if individuals believe that they will pass out during a panic attack, they might sit down or hold on to an object for support. Engaging in safety behaviors prevents disconfirmation of cognitive misappraisals, thus contributing to the maintenance of panic disorder (Salkovskis, Clark, and Gelder, 1996). Individuals may also engage in safety behaviors designed to prevent panic, or its feared consequences, such as carrying arou...