A Glutamatergic Model of ECT-induced Memory Dysfunction

Abstract

Electroconvulsive therapy (ECT) is an efficacious treatment for a variety of neuropsychiatric conditions including major depression, mania, catatonia, Parkinson's disease, and neuroleptic malignant syndrome. However, ECT-induced memory dysfunction complicates the treatment and is a major concern for both patients and providers. We briefly review ECT-induced memory dysfunction and propose a glutamatergic model for it. (Articles examined were retrieved by a Medline search on the terms electroconvulsion and glutamate, with language limited to English.) Specifically, we hypothesize that ECT-induced memory dysfunction results from neuronal insults due to excessive release of excitatory amino acids and activation of their receptors, which produce cation and water flux and reversible oxidative stress. This model offers multiple testable hypotheses; exploring them may help to identify the risk factors for this significant side effect of ECT treatment and may thus yield effective agents for its prevention and treatment.

Using thiamine to reduce post‐ECT confusion

“…The authors concluded that despite occasional encouraging preliminary results from animal models, good quality data from large-scale, controlled, clinical human trials for any agent are lacking. More recently, a glutamatergic theory of ECT-induced dysmnesia has been proposed by Chamberlain and Tsai (1998), based on a recognition that glutamatergic overactivity may be a common pathological mechanism underlying a variety of neuronal insults. This hypothesis remains untested.…”

Memory and cognitive effects of ECT: informing and assessing patients†

“…Other theories focus on ECT's effects on brain metabolism and neurochemistry: breach of the blood-brain barrier and increased cerebral blood pressure (Bolwig et al, 1977;Taylor et al, 1985); regional increases in T2 relaxation times (Diehl et al, 1994); disturbance of the long-term potentiation mechanism (Sackeim, 2000;Rami-Gonzalez et al, 2001); excessive release of excitatory amino acids and activation of their receptors (Chamberlin & Tsai, 1998;Rami-Gonzalez et al, 2001), and decreased cholinergic transmission (Khan et al, 1993;RamiGonzalez et al, 2001). Even temporary alterations in any of these may have permanent effects on the brain.…”

Kognitive Störungen und Elektrokrampftherapie

“…Dabei gäbe es sehr viele Hypothesen zu überprüfen; z. B. weiß man um die Zunahme der glutamatergen Ausschüttung in den praefrontalen und medialen temporalen Regionen und dessen Zusammenhang mit mnestischen Ausfällen [60]. Mit der Anwendung des NMDA-Antagonisten Ketamin als Anästhetikum anstatt der üblichen kurzwirksamen Barbiturate könnte man selektiv und damit protektiv in diesen Mechanismus eingreifen [61].…”