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1 - Mechanism of action of ECT

Published online by Cambridge University Press:  02 January 2018

Ian M. Anderson
Affiliation:
Honorary Consultant Psychiatrist, Manchester Mental Health and Social Care Trust, and Professor of Psychiatry, Neuroscience and Psychiatry Unit, University of Manchester
Grace M. Fergusson
Affiliation:
Consultant Psychiatrist, Argyll and Bute Hospital, Lochgilphead
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Summary

Seventy-five years after its introduction, ECT remains the most effective treatment for severe depressive disorder (UK ECT Review Group, 2003). Nevertheless, ECT is relatively underresearched compared with other forms of treatment for mental disorders; in particular there has been a relative lack of research using newer brain imaging techniques. Possible factors for the neglect of ECT include its adverse public image, funding priorities, the interests of researchers and the practical and ethical difficulties in studying this group of severely ill patients. Here, we briefly review some of the important neurobiological effects of ECT, concentrating on those related to its use in treating affective disorders, its principal indication. For more detailed information, see the reviews by Nobler & Sackeim (2008), Pigot et al (2008), Kato (2009), Merkl et al (2009) and Scott (2011).

A frequent criticism of ECT is that its mode of action is not understood. This is scarcely surprising given that the same can be said of other biological treatments in psychiatry. For example, although we understand much about the pharmacology of antidepressant and antipsychotic drug treatments, we still do not know how these pharmacological effects bring about improvement in mood or psychosis. Similarly for ECT, we know that both the generalised seizure and the dose of electricity used are important in bringing about its therapeutic effects, and that it has multiple, varied and lasting effects on the central nervous system (Merkl et al, 2009; Scott, 2011). Nevertheless, how these are translated into clinical effects remains obscure.

In recent years, advances in neuroscience have led to the development of various models of psychiatric disorders, particularly mood disorders, which encompass biological, psychological, social and developmental aspects (Mayberg, 2002; Seminowicz et al, 2004; Ebmeier et al, 2006; Beck, 2008; Akil et al, 2010). A common feature of these models is that psychiatric disorders are the result of disruptions of neural circuits, the functional networks of neurons that mediate thought, feelings and behaviour. Key areas concerned with networks involved in mood disorders include the hippocampus and amygdala, cingulate cortex (especially sub- and pregenual regions) and other areas of the prefrontal cortex. Underlying these networks are the structural and functional attributes of neurons and their connections. It is at this level that biological treatments are thought to exert their effects.

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Publisher: Royal College of Psychiatrists
Print publication year: 2013

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