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"Neurochemical changes underpinning the development of adjunct therapies in recovery after stroke: A role for GABA?" - Johnstone, Levenstein et al. 2017

Published Paper: Journal of Cerebral Blood Flow and Metabolism

We are pleased to announce the publication of a recent review article written by four members of our group: Ainslie Johnstone, Jacob Levenstein, Emily Hinson and Charlie Stagg.  

The review highlights the role of GABA underpinning the development of adjunct therapies in recovery after stroke.

This paper: "Neurochemical changes underpinning the development of adjunct therapies in recovery after stroke: A role for GABA?" is published in the Journal of Cerebral Blood Flow and Metabolism and can be found online here

Abstract

Stroke is a leading cause of long-term disability, with around three-quarters of stroke survivors experiencing motor problems. Intensive physiotherapy is currently the most effective treatment for post-stroke motor deficits, but much recent research has been targeted at increasing the effects of the intervention by pairing it with a wide variety of adjunct therapies, all of which aim to increase cortical plasticity, and thereby hope to maximize functional outcome. Here, we review the literature describing neurochemical changes underlying plasticity induction following stroke. We discuss methods of assessing neurochemicals in humans, and how these measurements change post-stroke. Motor learning in healthy individuals has been suggested as a model for stroke plasticity, and we discuss the support for this model, and what evidence it provides for neurochemical changes. One converging hypothesis from animal, healthy and stroke studies is the importance of the regulation of the inhibitory neurotransmitter GABA for the induction of cortical plasticity. We discuss the evidence supporting this hypothesis, before finally summarizing the literature surrounding the use of adjunct therapies such as non-invasive brain stimulation and SSRIs in post-stroke motor recovery, both of which have been show to influence the GABAergic system.