This weakened functional coupling may contribute to poor reaching performance and could be a consequence of a loss of common drive at the frequency bands as a result of interruption of information flow in the corticospinal pathway.
Objectives: Neuroplastic changes that drive recovery of shoulder/elbow function after stroke have been poorly understood. The purpose of this study was to determine the relationship between neuroplastic brain changes related to shoulder/elbow movement control in response to treatment and recovery of arm motor function in chronic stroke survivors.Methods: Twenty-three chronic stroke survivors were treated with 12 weeks of arm rehabilitation. Outcome measures included functional Magnetic Resonance Imaging (fMRI) for the shoulder/elbow components of reach and a skilled motor function test (Arm Motor Abilities Test, AMAT), collected before and after treatment.Results: We observed two patterns of neuroplastic changes that were associated with gains in motor function: decreased or increased task-related brain activation. Those with significantly better motor function at baseline exhibited a decrease in brain activation in response to treatment, evident in the ipsilesional primary motor and contralesional supplementary motor regions; in contrast, those with greater baseline motor impairment, exhibited increased brain activation in response to treatment. There was a linear relationship between greater functional gain (AMAT) and increased activation in bilateral primary motor, contralesional primary and secondary sensory regions, and contralesional lateral premotor area, after adjusting for baseline AMAT, age, and time since stroke.Conclusions: Recovery of functional reach involves recruitment of several contralesional and bilateral primary motor regions. In response to intensive therapy, the direction of functional brain change (i.e., increase or decrease in task-related brain recruitment) for shoulder/elbow reach components depends on baseline level of motor function and may represent either different phases of recovery or different patterns of neuroplasticity that drive functional recovery.
Purpose: Recovery of the most basic shoulder-flexion/elbow-extension components of functional reach is critical for effective arm function following stroke. In order to understand the mechanisms of motor recovery, it is important to characterize the pattern of brain activation during the reach task. Methods: We evaluated 11 controls and 23 moderately to severely impaired chronic stroke survivors (>6 months), with impaired shoulder flexion and elbow extension. Measures were acquired for Arm Motor Ability Test (AMAT) and functional Magnetic Resonance Imaging (fMRI) during the basic shoulder/elbow reach. Results: First, in controls, lateralization of fMRI signal during the reach task was less pronounced in comparison to other tasks, and even further diminished after stroke (p < 0.05). Second, for the stroke group, centroid locations, for specific ipsilesional (contralateral to working limb) motor-sensory regions and for contralesional (ipsilateral to working arm) somatosensory and SMA regions, were significantly more distant from the centroid location of average healthy controls (p < 0.05). Third, both greater activation volume and greater degree of signal intensity were correlated with better motor function in stroke survivors. Conclusions: These findings can be useful in guiding the development of more targeted brain training methods for recovery of impaired reach coordination.
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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