Finding
The therapeutic effect “is due to seizure activity and not, or only slightly, to the other effects of the c~ r ren t . ”~ The memory disturbance is to a great extent accounted for by the effects of the electrical stimulation other than the seizure.
Paper
Mechanisms of Action
Abstract
The mechanism of action of convulsive therapy has been questioned and investigated since the first therapeutic use of induced seizures by Meduna in 1935.’ Meduna believed that biological antagonism existed between the process that produces epilepsy and the process that produces schizophrenia. Thus, he thought that an induced convulsion in man would change brain chemistry in a therapeutic manner. When, in 1938, Cerletti and Bini introduced the use of electrically induced convulsions: they believed that the seizure was the fundamental therapeutic factor while the electricity was only the epileptogenic stimulus. In 1960, Ottosson and associates reported on a series of studies in which energy of electrical stimulation and cerebral seizure activity were systematically and independently manipulated experimentally to carefully delineate the specific effects of the electrical stimulation and seizure activity.’ They concluded that the therapeutic and cognitive effects of electroconvulsive therapy (ECT) arise through different mechanisms. The therapeutic effect “is due to seizure activity and not, or only slightly, to the other effects of the c~ r ren t . ”~ The memory disturbance is to a great extent accounted for by the effects of the electrical stimulation other than the seizure. Over the years of extensive ECT usage, a variety of theories or explanations have been forthcoming to attempt to ascribe the therapeutic effect of ECT to other causes including the occurrence of structural brain changes and psychological theories focusing on fear, punishment, amnesia, denial, repression, and ego adaptation.‘ No evidence is available supporting any of these theories. However, primacy of the generalized seizure itself has been confirmed clearly and repeatedly over the last 10 years in a series of controlled clinical trials comparing ECT and sham ECT (simulated ECT in which all elements of the treatment, including general anesthesia and muscle relaxant, are given except for the electrical Contemporary clinical therapy and most research on ECT have been guided by these basic assumptions. In recent years, basic and clinical scientists have intensified research efforts to better understand the mechanism of action of ECT by delineating the specific alterations in brain biological functioning brought about by a series of electrically induced generalized seizures that serve to relieve depression in man. As a result, a wealth of information is available on the effects of ECT on brain biological function from a multitude of vantage points including the neurophysiology, neuroendocrinology, neurochemistry, and neuroreceptorology. Much of this work, which has been presented earlier in this volume, has been based on basic studies employing electroconvulsive shocks in rodents. Human clinical studies attempting to clarify the
Authors
J. Blaine, S. Malitz
Journal
Annals of the New York Academy of Sciences