Etiology
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.
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.
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