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Article
March 1960

Electroconvulsive Therapy (With and Without Atropine): Effect on Electronically Analyzed Electroencephalogram

Author Affiliations

St. Louis
This study was supported in part by a research grant from the National Institute of Mental Health of the National Institutes of Health, U.S. Public Health Service, and by a grant from the Institute of Medical Education and Research, St. Louis City Hospital.
The assistance of Dr. Jack Hartstein, ophthalmology consultant, is gratefully acknowledged.
Department of Psychiatry and Neurology, Washington University School of Medicine, and the Malcolm A. Bliss Mental Health Center. Senior Author now at U.S. Navy Medical Neuropsychiatric Research Unit, San Diego.

AMA Arch Gen Psychiatry. 1960;2(3):324-336. doi:10.1001/archpsyc.1960.03590090080012
Abstract

Despite the introduction and wide use of psychopharmacologic agents, electroconvulsive therapy (ECT) still is used extensively as the treatment of choice for depressive reactions. This use of ECT is entirely empirical and is not based upon any conclusive data as to the cause of such illness or as to the site of action of ECT. Acceptable evidence is lacking for most of the 50-odd theories of ECT action. One theory that has seemed amenable to investigation is that relating to the importance of the electrocortical response to ECT. This theory states that slow-wave activity is a requisite for ECT to be effective. To date, the data generally have not supported this belief .1-3,11 However, Fink and Kahn6 have reawakened interest in the therapeutic importance of slow waves by their report of a positive correlation between the degree of EEG slowing and improvement. In

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