Functional Brain Correlates of Upper Limb Spasticity and Its Mitigation following Rehabilitation in Chronic Stroke Survivors

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Functional Brain Correlates of Upper Limb Spasticity and Its Mitigation following Rehabilitation in Chronic Stroke Survivors

Svetlana Pundik,1,2 Adam D. Falchook,3 Jessica McCabe,1
Krisanne Litinas,1 and Janis J. Daly3
1 Neurology and Research Service, Cleveland VA Medical Center, 10701 East Boulevard, Cleveland, OH 44106, USA
2Department of Neurology, CaseWestern Reserve University School of Medicine, 11100 Euclid Avenue, Cleveland, OH 44106, USA
3Department of Neurology and McKnight Brain Institute, Brain Rehabilitation Research Center of Excellence,
Malcom Randall VA Medical Center, University of Florida, 1601 SWArcher Road, Gainesville, FL 32608, USA
Correspondence should be addressed to Svetlana Pundik; sxp19@cwru.edu
Received 31 March 2014; Revised 23 May 2014; Accepted 11 June 2014; Published 3 July 2014
Academic Editor: Steve Kautz
Copyright © 2014 Svetlana Pundik et al.This is an open access article distributed under theCreativeCommonsAttribution License,
which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Background.

Arm spasticity is a challenge in the care of chronic stroke survivors with motor deficits. In order to advance spasticity
treatments, a better understanding of the mechanism of spasticity-related neuroplasticity is needed. Objective. To investigate brain function correlates of spasticity in chronic stroke and to identify specific regional functional brain changes related to rehabilitation induced mitigation of spasticity. Methods. 23 stroke survivors (>6 months) were treated with an arm motor learning and spasticity therapy (5 d/wk for 12 weeks). Outcome measures included Modified Ashworth scale, sensory tests, and functional magnetic resonance imaging (fMRI) for wrist and hand movement. 
Results.  First, at baseline, greater spasticity correlated with poorer motor function (P = 0.001) and greater sensory deficits (P = 0.003). Second, rehabilitation produced improvement in upper limb
spasticity and motor function (P < 0.0001). Third, at baseline, greater spasticity correlated with higher fMRI activation in the
ipsilesional thalamus (rho = 0.49, P = 0.03). Fourth, following rehabilitation, greater mitigation of spasticity correlated with
enhanced fMRI activation in the contralesional primary motor (r = −0.755, P = 0.003), premotor (r = −0.565, P = 0.04), primary sensory (r = −0.614, 
P= 0.03), and associative sensory (r = −0.597, P = 0.03) regions while controlling for changes in motor
function.