Greater loss in structural integrity of the ipsilesional corticospinal tract (CST) is associated with poorer motor outcome in hemiparetic stroke patients. Animal models of stroke have demonstrated that structural remodeling of white matter in the ipsilesional and contralesional hemispheres is associated with improved motor recovery. Accordingly, motor recovery in stroke patients may relate to the relative strength of CST degeneration and remodeling. This study examined the relationship between microstructural status of brain white matter tracts, indexed by the fractional anisotropy (FA) metric derived from diffusion tensor imaging (DTI) data, and motor skill of the stroke-affected hand in chronic stroke patients. Voxelwise analysis revealed that motor skill significantly and positively correlated with FA of the ipsilesional and contralesional CST in the patients. Additional voxelwise analyses showed that patients with poorer motor skill had reduced FA of bilateral CST compared to normal control subjects whereas patients with better motor skill had elevated FA of bilateral CST compared to controls. These findings were confirmed using a DTI-tractography method applied to the CST in both hemispheres. The results of this study suggest that the level of motor skill recovery achieved in hemiparetic stroke patients relates to microstructural status of the CST in both the ipsilesional and contralesional hemispheres, which may reflect the net effect of degeneration and remodeling of bilateral CST.
Previous studies have shown that unilateral finger movements are normally accompanied by a small activation in ipsilateral motor cortex. The magnitude of this activation has been shown to be altered in a number of conditions, particularly in association with stroke recovery. The site of this activation, however, has received limited attention. To address this question, functional magnetic resonance imaging (MRI) was used to study precentral gyrus activation in six control and three stroke patients during right index finger tapping, then during left index finger tapping. In each hemisphere, the most significantly activated site (P < 0.001 required) was identified during ipsilateral and during contralateral finger tapping. In the motor cortex of each hemisphere, the site activated during use of the ipsilateral hand differed from that found during use of the contralateral hand. Among the 11 control hemispheres showing significant activation during both motor tasks, the site for ipsilateral hand representation (relative to contralateral hand site in the same hemisphere) was significantly shifted ventrally in all 11 hemispheres (mean, 11 mm), laterally in 10/11 hemispheres (mean, 12 mm), and anteriorly in 8/11 hemispheres (mean, 10 mm). In 6 of 11 hemispheres, tapping of the contralateral finger simultaneously activated both the ipsilateral and the contralateral finger sites, suggesting bilateral motor control by the ipsilateral finger site. The sites activated during ipsilateral and contralateral hand movement showed similar differences in the unaffected hemisphere of stroke patients. The region of motor cortex activated during ipsilateral hand movements is spatially distinct from that identified during contralateral hand movements.
Animal studies have demonstrated that motor recovery after hemiparetic stroke is associated with functional and structural brain plasticity. While studies in stroke patients have revealed functional plasticity in sensorimotor cortical areas in association with motor recovery, corresponding structural plasticity has not been shown. We sought to test the hypothesis that chronic hemiparetic stroke patients exhibit structural plasticity in the same sensorimotor cortical areas that exhibit functional plasticity. Functional MRI during unilateral tactile stimulation and structural MRI was conducted in chronic stroke patients and normal subjects. Using recently developed computational methods for high-resolution analysis of MRI data, we evaluated for between-group differences in functional activation responses, and cortical thickness of areas that showed an enhanced activation response in the patients. We found a significant (P < 0.005) increase in the activation response in areas of the ventral postcentral gyrus (POG) in the patients relative to controls. These same ventral POG areas showed a significant (P < 0.05) increase in cortical thickness in the patients. Control cortical areas did not show a significant between-group difference in thickness or activation response. These results provide the first evidence of structural plasticity co-localized with areas exhibiting functional plasticity in the human brain after stroke.
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