THE GROWTH OF THE CLINICAL PHYSIOLOGICAL LABORATORY
One clear advance has been the increase in direct, physiologically sophisticated investigations of real anxious patients (rather than surrogate sophomores) compared with each other and with normals. The past 20 years have demonstrated that systematic perturbations (challenges) provide fascinating data indicating, at physiological and genetic levels, that the anxiety disorders are distinct from each other and normal controls. Splitting rather than lumping seems to pay off.
Cognitive theorists deny that spontaneous panics are qualitatively unique. They posit that people with enduring catastrophizing attitudes misconstrue harmless endogenous sensations as dangerous, eliciting fear-associated autonomic responses which then increases these sensations. This confirms the erroneous cognition of imminent peril, sparking a psychophysiological vicious circle that culminates in panic, i.e., the apprehension of immediate total disaster.
This view seems contradicted by a range of data, including the antipanic effects of imipramine which does not dampen ordinary fear, while incurring unpleasant side effects resembling fear, such as tachycardia, sweating, dry mouth, and tremors (Klein, 1994; Klein, 1995).
An outstanding puzzling aspect of spontaneous panic attacks is the lack of HPA activation during the panic characteristic of panic disorder, which is also inconsistent with fear equivalence. A number of investigations of the HPA axis in panic disorder agree with this finding but have fairly inconsistent results concerning other aspects of HPA dysregulation. The limited evidence for chronic hypercortisolemia seems related more to anticipatory anxiety than to the panic state. Reports of blunted responses to CRH have primarily occurred in panic patients with elevated baseline cortisols. The belief that the absence of HPA axis activation in panic disorder might be due to chronic repeated stresses was challenged by several anecdotal reports of first panics occurring in normals, without HPA activation. It is also unclear if repeated stresses would not sensitize rather than blunt HPA responsiveness. It seems good scientific strategy, to me, to focus on such counter-intuitive findings since they are likely to lead to real novelties.