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Hypothesis-generating for cholinergic effects in convulsive therapy; leaves open clinical relevance pending controlled data.
Recent investigations of convulsive therapy have emphasized EEG delta activity as the neurophysiologic basis for the induced behavioral change.¹⁻⁵Little study, however, has been given to the biochemical effects of this therapy, except in the course of investigations of head injuries. In investigations of head trauma significance has been ascribed to changes in the acetylcholine-cholinesterase systems both for the behavioral and for the electroencephalographic effects. An increase in free acetylcholine⁶and an alteration of the ratio of cholinesterases⁷in the spinal fluid have been positively correlated with the degree of EEG abnormality and degree of neurologic deficit. The EEG patterns were "blocked," and some improvement in clinical status was reported following the administration of atropine.⁷,⁸In convulsive therapy, atropine and scopolamine were observed to block the appearance of delta activity,⁹although the systemic effects of the large doses of these agents were marked. Recent reports
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Max Fink (1958) studied this question.
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