Primary Motor Cortex Ipsilateral to the Paretic Arm - A Potential Neural Substrate for Compensatory Trunk Use in Chronic Stroke
- *Corresponding Author:
- Carmen M. Cirstea
Department of Physical Medicine and Rehabilitation University of Missouri
One Hospital Drive, DC046.00 Columbia-65212, MO, USA
E-mail: [email protected]
Received date: March 22, 2017; Accepted date: April 10, 2017; Published date: April 12, 2017
Citation: Bani-Ahmed A, Savage C, Nudo RJ, Lee P, Choi IY, et al. (2017) Primary Motor Cortex Ipsilateral to the Paretic Arm - A Potential Neural Substrate for Compensatory Trunk Use in Chronic Stroke. Int J Phys Med Rehabil 5:400. doi: 10.4172/2329-9096.1000400
Copyright: © 2017 Bani-Ahmed A, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Objective: Arm motor recovery after stroke is primarily attributed to the primary motor cortex (M1) plasticity. While the M1 contralateral to the paretic arm (cM1) is undoubtedly critical for recovery, the role of the ipsilateral M1 (iM1) is still inconclusive. For instance, an abnormally increased activity in the iM1 is reported immediately after stroke and normalizes at the chronic stage in recovered patients. Whether persistent iM1 hyperactivity in chronic stroke reflects a less efficient type of plasticity (so-called maladaptive) is still far from settled. We investigated the functional significance of the iM1 hyperactivity with respect to compensatory behavioral strategies employed by patients suffering from chronic arm paresis.
Methods: Functional MRI and trunk kinematics data were collected during paretic arm movements in 11 patients before and after a four-week training specifically designed to improve the motor control of the paretic arm and diminish the behavioral (trunk) compensation comprising of variable practice of a reach-to-grasp task with feedback given as knowledge-of-performance. Eight age-matched healthy controls underwent similar evaluations and training. Magnitude of iM1 (and cM1) activation and anterior trunk displacement were analysed.
Results: Before training, patients exhibited significantly stronger iM1 activation, increased trunk motion, and significant positive correlations between these two variables compared to controls. After training, patients significantly decreased iM1 activation and displayed a trend toward decreased trunk use. The correlations between iM1 activation and trunk motion persisted and were different from those in controls.
Conclusion: Our preliminary data provide evidence that functional iM1 plasticity is related to behavioral compensation, suggesting a maladaptive role of the iM1 in chronic subcortical stroke. We however recommend caution in interpreting these results until more work is completed.