Panic disorder. Pathophysiology and drug treatment.

Abstract

Advances over the past 2 decades in our understanding of the biology of panic disorder have paralleled a remarkable increase in the development of new pharmacological agents with antipanic effects. Although we can not presently use biological tests to help with our choice of therapeutic agent for individual patients, we can use this biological understanding in the development of overall pharmaco-therapeutic strategies. Current evidence does not support the hypothesis that panic disorder is associated with a primary disorder in one neurotransmitter system. Rather, the data suggest that the biological aetiology of panic disorder is related to abnormalities in the function of a variety of neurotransmitters including serotonin (5-hydroxytyrptamine; 5-HT), noradrenaline (norepinephrine), gamma-aminobutyric acid (GABA), dopamine, and cholecystokinin. It is likely, however, that panic disorder is a biologically heterogeneous condition and that biological subtypes may exist in which the primary abnormality may involve one or a few neurotransmitter systems. Currently, the data best support the hypothesis that pharmacotherapeutic agents with primary action at sites within the GABA and serotonin systems are the most effective in the treatment of panic disorder. Nevertheless, some patients will respond well to drugs with predominant activity in other systems, or may require pharmacotherapy designed to affect the function of more than 1 neurotransmitter. As our understanding of the biological aetiology of panic disorder evolves, the pharmacotherapeutic agents and strategies used in the treatment of this disorder will continue to evolve as well.