Abstract
Electroconvulsive therapy of neuropsychiatric disorders, widely used for one quarter of a century, is still acknowledged to have an obscure mechanism of action. Considerable theorizing and investigation have produced a number of postulated mechanisms for electroconvulsive therapy (ECT), among the more popular being the suggestion that therapeutic response is reflected and perhaps mediated by the autonomic nervous system [1, 2]. Increased activity in certain areas of the hypothalamic-sympathoadrenal neurohumoral complex after electric shock, particularly after a series of such applications, has been reported [3,4]. Some have claimed that therapeutic response to ECT is associated with increasing reactivity of the sympathetic nervous system [2]. A number of biological phenomena have been cited as reflecting such a response, including the ECT effect of stimulating a plasma rise of adrenal medullary amines [5, 6], the well-known glycogenolytic effects of epinephrine and anoxia, and serial changes noted in the pharmacological testing of the autonomic system [7]. A sensitive though nonspecific index of acute sympathetic system stimulation is the liberation of free fatty acids (FFA, NEFA) from what in past years had been considered relatively inert stores of body fat [8, 16, 20, 21].
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Cochran, B., Marbach, E.P., Thompson, G.N. (1962). Some Acute and Chronic Biochemical Responses to Electroconvulsive Therapy. In: Wortis, J. (eds) Recent Advances in Biological Psychiatry. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-8306-2_16
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DOI: https://doi.org/10.1007/978-1-4684-8306-2_16
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