PANIC DISORDER - PATHOPHYSIOLOGY AND DRUG-TREATMENT

Advances over the past 2 decades in our understanding of the biology o f panic disorder have paralleled a remarkable increase in the developm ent of new pharmacological agents with antipanic effects. Although we can not presently use biological tests to help with our choice of ther apeutic agent for individual patients, we can use this biological unde rstanding in the development of overall pharmacotherapeutic 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 disor der is related to abnormalities in the function of a variety of neurot ransmitters including serotonin (5-hydroxytryptamine; 5-HT), noradrena line (norepinephrine), gamma-aminobutyric acid (GABA), dopamine, and c holecystokinin. It is likely, however, that panic disorder is a biolog ically heterogeneous condition and that biological subtypes may exist in which the primary abnormality may involve one or a few neurotransmi tter systems. Currently, the data best support the hypothesis that pha rmacotherapeutic agents with primary action at sites within the GABA a nd 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 ou r understanding of the biological aetiology of panic disorder evolves, the pharmacotherapeutic agents and strategies used in the treatment o f this disorder will continue to evolve as well.