Abstract

Background: Spasticity can prevent productive practice of skilled movement that should occur during neurorehabilitation of coordinated arm movements after stroke. Studies showed that spasticity could be reduced following an intervention that inhibited activation of the contralesional primary motor region (M1) using non-invasive transcranial magnetic or electric stimulation. However, there is little understanding of how the mitigation of spasticity might be controlled by the multiple sensorimotor control brain regions. Therefore, the aim of this study was to evaluate the change in activation patterns of multiple sensorimotor regions that predict the mitigation of spasticity, in response to intensive upper limb neurrehabiltiation. Methods: Twenty three stroke subjects (>6 months after stroke) with persistent arm motor deficits were treated with intensive upper extremity rehabilitation (5 hours/day, 5 days/week for 12 weeks). Baseline and post-rehab evaluation consisted of three measures: 1) functional magnetic resonance imaging (fMRI) during a shoulder/elbow reach task for the paretic arm, 2) a skilled motor function (Arm Motor Assessment test (AMAT)), and 3) spasticity (Modified Ashworth Scale(MAS)). Volume of brain activation (voxel count) during the reach task was calculated for sensory and motor control regions using SPM05 (London, UK) and in-house software in MATLAB (Natick, MA). Paired t-test analysis was conducted for pre- vs post-treatment comparisons. Multiple linear regression analysis was conducted, where post-rehab AMAT was the dependent variable, the co-variate was pre-rehab score, and the predictors were change from pre- to post-rehab in voxel count in bilateral M1, somatosensory (SS), posterior parietal (PP), lateral premotor (LPM) and supplementary motor (SMA) areas. Results: Subject characteristics were as follows: mean age, 56.3 ±12.8years; 41%, female; and 1.8±1.1 years after first ever stroke. Change in the activation pattern in a number of regions significantly predicted mitigated spasticity (R2=.86). Specifically, in response to treatment, increased activation, in ipsilesional SMA (p=.002) and contralesional M1 (p=.002), predicted mitigated spasticity. Reduction in activation volume, in ipsilesional PP region (p=.0009), contralesional SS (p=.008) and SMA (p=.006), predicted mitigated spasticity. AMAT score improved from 1636.63±668.41 to 1213.67±6643.79 seconds (p<.0001) and MAS scores improved from 6.81±2.75 to 1.86±1.49 (p<.0001). Conclusions: A specific pattern of functional brain change across multiple regions predicted mitigation of spasticity following neurorehabilitation; skill functional recovery occurred, as well. This information could be used in constructing study design for future research that would investigate brain training to mitigate spasticity and improve skilled functional task performance.

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