Article

Cortical excitability and post-stroke recovery

Department of Neurology, David Geffen School of Medicine at UCLA, Los Angeles, CA 90095, USA.
Biochemical Society Transactions (Impact Factor: 3.24). 12/2009; 37(Pt 6):1412-4. DOI: 10.1042/BST0371412
Source: PubMed

ABSTRACT Stroke is the leading cause of adult disability. Recent studies show that the brain can engage in a limited process of neural repair after stroke: re-mapping of sensory and motor function and sprouting of new connections in peri-infarct cortex surrounding the stroke. Changes in cortical sensory and motor maps and alterations in axonal structure are dependent on patterned neuronal activity. The central cellular process in these events is alteration in neuronal response to incoming inputs--manipulations that increase neuronal firing to a given input are likely to induce changes in neuronal structure and alterations in cortical maps. Because post-stroke neural repair and recovery also involves neuronal sprouting and re-mapping of cortical sensory and motor representations, it has been assumed that changes in neuronal excitability underlie neural repair.

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    • "Changes in neuronal excitability, loss of GABAergic inhibition , enhanced glutamatergic transmission, and synaptic plasticity all contribute to neuronal reorganization after stroke. Studies that promote an increase in local brain excitability result in improved function [21, 34, 39, 45] and suggest that decreasing GABA activity within the brain could facilitate structural changes that promote functional recovery [21] [34] [45]. In particular, this enhancement of neuronal excitability involves dampening baseline levels of inhibition. "
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    • "In the present experiments, increasing TMS stimulation intensity by 10% produced changes that were reliably detected by the DI. This finding suggests that calculating the DI on repeated TMS/hd-EEG sessions may be effective in revealing rather fine modifications in cortical excitability (indexed by the response's amplitude) due to pathological alterations, i.e. stroke, epilepsy and depression [49]–[52] or therapeutic interventions, i.e. electroconvulsive therapy, rTMS, neurorehabilitation or drug administration [51], [52]. "
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