ABSTRACT
Treatment of the panic disorder patient has traditionally focused on blocking panic attacks, diminishing anticipatory or generalized anxi ety, and reversing phobic avoidance while recognizing and treating comorbid conditions. The current medical model of panic disorder em phasizes qualitative differences between a panic attack and other types of anxiety. According to this view, panic disorder is seen as reflecting a specific genetically influenced neurochemical dysregulation (5-7). Thus, a rational pharmacological treatment intervention would target the neurobiological pathways associated with maladaptive and overreactive fear and alarm mechanisms (see Chapter 3). Putative sites of this dysregulation have included the locus ceruleus and the noradrener gic system (8,9), the serotonergic system (10,11), and the central GABA-benzodiazepine receptor complex (12). Other studies suggest roles for various other factors in the neurobiology of panic disorder. Among them are cortisol-releasing factor, adenosine (13), and a variety of neuropeptides, including cholecystokinin (14). Support for the neu robiological illness model also stems from experimental panic induc tion from biological challenges (e.g., C 0 2 inhalation, lactate infu sion, yohimbine), and the success of treatment with pharmacological agents.
