Repeated ECT and prolactin release in depressed patients

Abstract

Whereas sham electroconvulsive therapy (ECT) increases the blood concentration of prolactin (PRL) up to two-fold after 15 m~n, real ECT increases PRL concentration several fold (Deakin et al 1983). Sequential study of the effects of electrode placement has established that bilateral ECT releases 25% (Swartz and Abrams 1984)-50% (Papakostos et al 1986) more PRL than does unilateral ECT which may demonstrate a greater hypothalan,ic-stimulating effect of bilateral ECT (Swartz and Abrams 1984). Electroencephalographic (EEG) study of the relationship between the length of cerebral seizure activity and PRL release has been inconclusive (Abrams and Swartz 198~b; Robin et at .~985), as has been the study of the relationship betw~,~ :, PRL release and recovery from depression (Deakin et al 1983; Abrams and Swartz 1985a). It has been suggested that the study of pituitary hormone release over a course of ECT may provide important information about alterations in central monoaminergic transmission in depressed patients. (Whalley et al 1982; Aperia et al 1985). The major role of the hypothalamus in the regulation of PRL release is inhibitory through the tuberoinfundibular dopaminergic system. A PRL releasing factor, such as thyrotropin releasing hormor ~ or vasoactive intestinal l~eptide, may be involved in stimulating PRL release and this may involve serotonin (5HT) (Leong et al 1983). After ECT, PRL release has been reported to be significantly reduced later on in a course of treatment for depression as compared to the first treatment (Deakin et al 1983; Abrams and Swartz 1985a; Aperia et al 1985; Cooper et al 1989), suggesting an increase in the responsiveness of post-synapuc dopamine receptors (Abrams and Swartz 1985a; Aperia et al 1985). This finding has not always been confirmed (Whalley et al 1982; Linnoila et al 1984; Haskett et al 1985). The intake of neuroleptic drugs increases both basal and ECl'-induced PRL release (Swartz 1985a; Aperia et a! 1985), but only one report concerned depressed patients free of neuroleptic drugs in the 2 weeks before ECT (Abrams and Swartz 1985a). O~:r aim was to study PRL release over a course of ECT in depressed patients who had not takeL', neuroleptic drugs during their index illness. ECT was monitored by 6-channel EEG because the ~gpatial distribution of epileptic seizures in hum,ms influences PRL release in that generalized se~ :ures release more PRL than focal seizures (Spc.ding et al 1986).