Norman T R, Burrows G D, Judd F K, McIntyre I M
Department of Psychiatry, University of Melbourne, Heidelberg, Victoria, Australia.
Int J Clin Pharmacol Res. 1989;9(2):151-7.
The revision of psychiatric diagnostic criteria by DSM-III has emphasised the central importance of panic attacks for the diagnosis of anxiety disorders. Since the introduction of this classification, there has been a re-evaluation of the role of major neurotransmitters as causal factors in anxiety disorders. The evidence for serotonergic hyperactivity in panic disorders is supported by the efficacy of specific serotonin reuptake blockers and 5HT2 receptor antagonists in the treatment of the condition. In addition neuroanatomical studies and positron-emission transaxial tomographic scanning are also consistent with a key role for serotonin in panic disorder. Clinical evidence of serotonin dysfunction has been sought using the blood platelet, a putative model of central serotonergic neurons. Studies of 3H-imipramine binding in platelets are equivocal, but most find no difference between patients and controls. On the other hand platelet serotonin uptake is significantly elevated in panic patients compared to controls. The reasons for the difference between two reputed markers of presynaptic serotonergic function is explored. The prolactin response to intravenous tryptophan administration is regarded as a functional correlate of central serotonergic neurons. Panic disorder patients and controls were not different in one study using this test. Serotonin concentrations in panic patients may be abnormal compared with appropriate controls. Replication of these preliminary data are necessary to confirm serotonergic dysfunction and to elucidate the interaction with other neurotransmitters, with clear implications for pharmacotherapy.
