Panic Disorder: Etiology

Etiology

Cognitive Models – The Vicious Cycle

There are several contemporary cognitive models of panic disor-der which, for the most part, are based on variations of the “fear of anxiety” construct. Goldstein and Chambless (1978) proposed that fear of anxiety arises through the association of interocep-tive cues with panic attacks. In other words, people with panic disorder are thought to learn to fear the recurrence of aversive panic episodes and thereby develop a fear of panic-related symp-toms. Refuting the premise that fear of anxiety develops from the experience of panic attacks, Clark (1986) posited that panic attacks are the product of a tendency catastrophically misinter-pret to autonomic arousal sensations that occur in the context of nonpathological anxiety (as well as physical illness, exercise and ingestion of certain substances). Reiss and colleagues (Re-iss, 1999; Reiss and McNally, 1985), incorporating components of the Goldstein and Chambless and Clark models, proposed that panic attacks arise as a consequence of both

·        a predispositional tendency to catastrophically misinterpret and respond with fear to the benign arousal sensations, and

·        a learned fear of anxiety that is maintained by the experience of panic episodes

Most recently, Bouton, Mineka and Barlow (2001) have described a variant of the original fear of anxiety model, suggesting that panic disorder develops when exposure to panic attacks condi-tions a person to respond with anticipatory anxiety (and some-times with panic) to internal arousal and contextual cues.

The vicious cycle model makes several assumptions. First, while recognizing that initial panic attacks may be caused by other factors (e.g., drug-related autonomic surges), it assumes that people prone to panic disorder have an enduring tendency cata-strophically to misinterpret benign arousal sensations. Secondly, it assumes that misinterpretations can occur at the conscious and unconscious level. Thirdly, the cycle can be entered into at any point. For example, the cycle can be initiated by a contextual trigger or simply by having catastrophic thoughts about bodily sensations. Fourthly, physiological changes are viewed as one of several components in a process, rather than as a pathogenic mechanism.

Cognitive models can also account for agoraphobia. Agoraphobia has long been regarded as a product of operant conditioning. As noted above, it most often develops as a conse-quence of panic attacks. These attacks typically occur in particu-lar situations (e.g., when in line at a shopping mall, when driv-ing) and motivate the person to avoid or escape these situations. The avoidance and escape behaviors are negatively reinforced by the reduction of aversive autonomic arousal and other anxiety-related sensations. Cognitive factors such as expectations that an attack will be imminent and harmful and that coping will be ineffective play a significant role by influencing and maintaining avoidance behavior.

A growing body of literature supports the vicious cycle model. Thoughts of imminent catastrophe have been identified as triggers of panic attacks. Patients with panic disorder relative to healthy and patient controls have been shown to be:

·        characterized by strategic and automatic information process-ing (i.e., memory, attention) biases for physical threat cues;

·        more accurate, in some instances, at detecting body sensa-tions;

·        more likely to report fear of somatic sensations and beliefs in their harmful consequences; and

·        more susceptible to the influence of instructional manipula-tions of control in response to pharmacological panic provo-cation challenges, panicking less often under the illusion of greater control in some (but not all cases).

Research shows that treatments stemming from the cognitive model are effective.

Biological Models

Evidence suggests that several neurotransmitter systems, in-volving neurotransmitters or neuromodulators such as serot-onin, noradrenalin, adenosine, gamma-aminobutyric acid and cholecystokinin-4, play a role in panic disorder. Various brain structures in the limbic system and associated regions have also been implicated. Contemporary biological models of panic have grown in number and complexity in recent years in an effort to integrate and explain these findings. Recent emphasis has fo-cused on the amygdala, a limbic structure that appears to be in-volved in coordinating the different neurotransmitters involved in anxiety disorders (Goddard and Charney, 1997). Today, there is no single, leading biological model of panic. However, there are a number of useful models that guide research and clinical practice. Among the most promising is the neuroanatomical hypothesis recently revised by Gorman and colleagues (2000). This hypothesis is useful for several reasons. First, it integrates a wide range of findings, including animal research and studies of humans. Secondly, it provides a unifying framework for un-derstanding why panic disorder is associated with so many bio-logical dysregularities such as abnormalities in neurotransmit-ter systems and irregularities on various indices of autonomic functioning. Thirdly, the model accounts for treatment-outcome data, which show that both pharmacological and psychological therapies are effective treatments for panic disorder.