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Abstract

Panic disorder was first defined by Spitzer, Endicott, and Robbins (1975) in the early editions of their research diagnostic criteria (RDC). It wa’s later included in the Diagnostic and Statistical Manual, third edition (DSM-III), of the American Psychiatric Association (APA, 1980). Whereas the early definition of panic disorder required at least six panic attacks within a 6-week period for a definite diagnosis to be made, the DSM-III modified these criteria to require only three panic attacks within any 3-week period. Each of these attacks was required to have at least 4 of 12 characteristic symptoms. Though the condition itself had existed long before the DSM-III, it was given separate status as a diagnostic entity based on the research findings of Donald Klein (1964, 1967). Klein’s central observation in these papers was that there was a type of anxiety disorder that was particularly sensitive to imipramine, a tricyclic antidepressant. This tricyclic-sensitive anxiety disorder was characterized by spontaneous panic attacks and often failed to respond to minor tranquilizers. Such observations led the DSM-III committee to make a distinction between panic disorder and generalized anxiety disorder. The underlying assumption in making this distinction was that panic disorder is responsive to tricyclic antidepressants and not to minor tranquilizers, whereas generalized anxiety disorder is sensitive to minor tranquilizers but not to tricyclics. This observation was reinforced by a study by McNair and Kahn (1981), which found that imipramine tended to be more effective than chlordiazepoxide in the treatment of agoraphobia. Subsequently, Sheehan (1982a) and Chouinard, Annable, and Fontaine (1982) independently reported that alprazolam, a triazolobenzodiazepine, was effective in the treatment of panic disorder. This finding suggested that benzodiazepines as a class might be effective in the treatment of panic disorder and at the same time offered a treatment for this condition that was quicker, safer, and easier to tolerate than the earlier recommended treatments with tricyclic antidepressants and monoamine oxidase inhibitors. The finding of a quicker and safer treatment for this condition proved to be a significant stimulus to research on this disorder over the following several years and gave rise to the World Wide Panic Project sponsored by the Upjohn Company, from which many new findings and more precise descriptions of panic disorder emerged. Further, Sheehan (1982b) articulated the emerging idea in the panic disorder literature that we should revise our view of panic disorder as a psychological problem in favor of a medical-illness model for this disorder. He suggested that, in contrast to stress-related situational anxiety, panic disorder appears to be associated with biological abnormalities in the central nervous system to which there is a genetic vulnerability. This new view (which was a logical outcome of the earlier work of Klein) had important implications for treatment and research. Attempts to test the strengths and weaknesses of this hypothesis guided much of the research effort in panic disorder in the 1980s.

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Sheehan, D.V., Raj, B.A. (1990). Panic Disorder. In: Thase, M.E., Edelstein, B.A., Hersen, M. (eds) Handbook of Outpatient Treatment of Adults. Springer, Boston, MA. https://doi.org/10.1007/978-1-4899-0894-0_9

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