ABSTRACT
Gorman et al (2000) have proposed an attractive hypothesis, in the form of their neuroanatomical model, to incorporate the diverse evidence for the aetiology of panic disorder outlined above. Drawing from pre-clinical animal work with conditioned fear, a fear circuit has been suggested (Figure 8). The focus of this model, is the central nucleus of the amygdala, which serves as a relay station between the higher centres (sensory thalamus, prefrontal cortex and sensory motor cortex) and the brain-stem efferent nuclei. The flow of information in the higher centres is in both directions to and from the amygdala, and also between these higher centres themselves. This model therefore proposes that the amygdala receives not only afferent sensory information but also afferents from the higher centres representing cognitive processing of that information. Abnormalities in this cognitive processing could form the basis of the catastrophic thinking, detailed by Clark (1988), in his cognitive model of panic disorder. Other factors that could influence the response to perceived threat include a genetic predisposition to fearfulness exacerbated by overcritical/controlling parenting styles (Shear et al 1993). Preclinical experiments also implicate structures known to be part of the proposed fear network. In conditioned-fear experiments rats display contextual learning, which is dependent on an intact connection between the hippocampus and the amygdala. Thus, a rat trained to associate a tone with an electric shock will also learn to associate the cage in which the experiment was performed with the noxious stimulus. However, if the tract linking the hippocampus and amygdala is severed, the rat no longer displays fear when confronted by the cage, although it continues to do so with the tone. If the amygdala is lesioned, the rat responds to the cage but not to the tone (Kim and Fanselow 1992).
