The effective agent in electroconvulsive therapy: convulsion or coma?

Abstract

The ability of electrically-induced convulsions to alleviate at least some symptoms of mental illness was first reported in the literature 50 years ago; however, the cerebral mechanisms responsible for such therapeutic effects have thus far escaped elucidation. It is thus interesting to note that those seeking explanations for the therapeutic effects of electroconvulsive therapy (ECT) have focused their attention on the convulsion produced by ECT, as opposed to the coma. The present hypothesis emphasizes the coma following the convulsion as a potential explanation of the effectiveness of ECT and other convulsive therapies. It is postulated that the primary effect of the convulsion is to cause the release of adenosine (ARN) from neuronal tissue and that the subsequent depressant effect of ARN on neuronal activity results in the clinical effect observed. Thus hypothesis suggests that chemically-induced coma, particularly coma induced by benzodiazepines, may offer a safe, effective and more acceptable alternative to ECT.