Transcranial Magnetic Stimulation (TMS) as a tool for stroke motor recovery: What are we targeting? (P5.164)

PUBLICATION:

Meeting Abstract

Authors:

Muhammed Gunduz, Katherine Nearing, Douglas Labar, Tsagaris Zoe, Gary Thickbroom, Mar Cortes, Matthew Fink and Dylan Edwards

Year Published:

2015

Publisher:

67th AAN Annual Meeting; 2015 April; Washington, DC, United States. AAN Enterprises, Inc; c2015. Neurology April 6, 2015 vol. 84 no. 14 Supplement P5.164

Abstract on Neurology

Abstract

OBJECTIVE: We aim to improve our understanding of contralateral cortical activity during stroke recovery as a target of TMS-based therapy.

BACKGROUND: TMS is being widely investigated as a tool to improve outcomes after stroke. Inhibition of the unaffected hemisphere causes disinhibition of the affected hemisphere and improved functionality. However, there is wide variability between subjects. We seek to identify those who will benefit most. We start by investigating the hyperexcitability of the unaffected hemisphere following stroke and its relationship to lesion anatomy and clinical presentation.

DESIGN/METHODS: Eight adults (5 females, 3 males, mean age=62.38) were enrolled with the following criteria: first clinical stroke within the past 3-12 months resulting in moderate hemiparesis involving the hand. Subjects were assessed neurophysiologically with navigated single pulse TMS and functionally with the Fugl-Meyer Assessment (FMA), a detailed measure of hand strength and coordination, and NIH Stroke Scale (NIHSS). TMS was used to map primary cortex corresponding to the Abductor Pollicis Brevis (APB) and the Extensor digitorum (EDC) muscles and to determine motor threshold.

RESULTS: We show that motor threshold (low values being a marker of elevated excitability) of unaffected hemisphere M1 is not always excessively low, and may relate to severity of hemiparesis depending on whether the stroke lesion involves the cerebral cortex. We demonstrate that motor evoked potentials in the affected hemisphere are often small or absent. CONCLUSIONS: Our data suggest that lesion location may be indicative of whether contralesional M1 is hyper-excitable and therefore warrant targeted de-excitatory brain stimulation as a therapeutic strategy. These findings are important to clinical trials underway that presently do not assess contralesional excitability or stratify patients according to lesion location. We also suggest that transcallosal and intracortical excitability measures can be invalid in the affected hemisphere if evoked potentials are small or absent.