Mechanism of action of ECT in major depressive disorders: a neuroendocrine interpretation.
Electroconvulsive therapy (ECT) is often efficacious in severe depression, and it is occasionally used in the treatment of schizophrenia. The mechanism of action of ECT is still poorly understood. We evaluated thyroid-stimulating hormone (TSH) and prolactin responses to thyrotropin-releasing hormone (TRH) after a first ECT and at the end of a series of seven ECTs in eight unipolar depressed patients with blunted basal TSH/TRH response, eight unipolar depressed patients with normal TSH/TRH response, and eight schizophrenic patients. The hormone patterns obtained after the first ECT showed an increase in prolactin and a decrease in TSH in all groups of patients, suggesting a nonspecific response. At the end of the therapeutic course, TSH responses increased in both groups of depressed patients, and the elevation was more relevant in depressed patients with normal TSH/TRH. Our data suggest that the mechanism of action of ECT becomes more specific when it is performed chronically and differs according to the organic substrate underlying different mental disorders. Moreover, an aminergic activation in the two groups of depressed patients seems to take place.
D000328:Adult; D003866:Depressive Disorder / Q000378:metabolism / Q000628:therapy*; D004565:Electroconvulsive Therapy; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D011388:Prolactin / Q000378:metabolism*; D012559:Schizophrenia / Q000378:metabolism / Q000628:therapy; D013972:Thyrotropin / Q000378:metabolism*; D013973:Thyrotropin-Releasing Hormone
D013973:Thyrotropin-Releasing Hormone; D011388:Prolactin; D013972:Thyrotropin