Ipsilateral primary motor cortex and behavioral compensation after stroke: a case series study
Arm motor recovery after stroke is mainly attributed to reorganization of the primary motor cortex (M1). While M1 contralateral to the paretic arm (cM1) is critical for recovery, the role of ipsilateral M1 (iM1) is still inconclusive. Whether iM1 activity is related to recovery, behavioral compensation, or both is still far from settled. We hypothesized that the magnitude of iM1 activity in chronic stroke survivors will increase or decrease in direct proportion to the degree that movements of the paretic arm are compensated. Movement kinematics (VICON, Oxford Metrics) and functional MRI data (3T MR system) were collected in 11 patients before and after a 4-week training designed to improve motor control of the paretic arm and decrease compensatory trunk recruitment. Twelve matched controls underwent similar evaluations and training. Relationships between iM1 activity and trunk motion were analyzed. At baseline, patients exhibited increased iM1 activity (p = 0.001) and relied more on trunk movement (p = 0.02) than controls. These two variables were directly and significantly related in patients (r = 0.74, p = 0.01) but not in controls (r = 0.28, p = 0.4). After training, patients displayed a significant reduction in iM1 activity (p = 0.008) and a trend toward decreased trunk use (p = 0.1). The relationship between these two variables remained significant (r = 0.66, p = 0.03) and different from controls (r = 0.26, p = 0.4). Our preliminary results suggest that iM1 may play a role in compensating for brain damage rather than directly gaining control of the paretic arm. However, we recommend caution in interpreting these results until more work is completed.
KeywordsSubcortical stroke Chronic hemiparesis Ipsilateral motor cortex Behavioral compensation fMRI Movement kinematics
We thank Andrew Apostol for assistance with data analysis.
Compliance with ethical standards
Confict of interest
This study was funded by American Heart Association (0860041Z to Dr. Cirstea). The Hoglund Brain Imaging Center is supported by a generous gift from Forrest and Sally Hoglund and National Institutes of Health (P30 AG035982, UL1 RR033179). There are no financial benefits to the authors. The authors declared that they have no conflict of interest.
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