Hostname: page-component-586b7cd67f-rcrh6 Total loading time: 0 Render date: 2024-11-25T23:31:05.069Z Has data issue: false hasContentIssue false
  • English
  • Français

ECT and neuroprotection: a review and proposed study

Published online by Cambridge University Press:  24 June 2014

M Pigot  and
C Loo
M Pigot
Affiliation:
School of Psychiatry, University of New South Wales, Sydney, Australia
C Loo
Affiliation:
School of Psychiatry, University of New South Wales, Sydney, Australia
Rights & Permissions [Opens in a new window]

Abstract

An abstract is not available for this content. As you have access to this content, full HTML content is provided on this page. A PDF of this content is also available in through the ‘Save PDF’ action button.
Type
Abstracts from ‘Brainwaves’— The Australasian Society for Psychiatric Research Annual Meeting 2006, 6–8 December, Sydney, Australia
Information
Acta Neuropsychiatrica , Volume 18 , Issue 6 , December 2006 , pp. 303
Copyright
Copyright © 2006 Blackwell Munksgaard

Background:

Electroconvulsive therapy (ECT) is a highly effective treatment for depression but its use is limited by associated cognitive side-effects. Several theories have been proposed for the mechanisms underlying cognitive impairment with ECT: excito-toxic damage through influx of intracellular calcium or excessive glutamatergic transmission, alteration in opioid receptor density and induction of inflammatory processes (Krueger et al. 1992; Bazan et al. 2005). Several neuroprotective agents have been proposed to reduce ECT-related cognitive effects, leading to some trials in animal and human subjects.

Method:

A comprehensive literature review (PubMed, Medline) identified animal and human clinical research trials of various agents proposed to have a neuropro-tective effect on ECT-induced cognitive impairments.

Results:

Several agents have been shown to reduce memory impairment after electroconvulsive shock (ECS) in rats, for example, calcium channel blockers, opioid receptor antagonists and glucocorticoid antagonists. However, results from clinical trials in humans have been less promising. There are early suggestions that ketamine anesthesia may be associated with fewer cognitive side-effects after ECT (McDaniels et al. 2006).

Conclusions:

Strong evidence from ECS models of neuroprotective strategies have to date not been confirmed in human clinical trials. However, clinical trials have been sparse, with small sample sizes and confounding methodological issues. We propose a randomized sham-controlled study to assess the effect of several neuroprotective agents on ECT-induced cognitive impairment.