Reddy H, Floyer A, Donaghy M, Matthews P M
Centre for Functional Magnetic Resonance Imaging of the Brain, Department of Clinical Neurology, University of Oxford, John Radcliffe Hospital, Headington, UK.
Exp Brain Res. 2001 Jun;138(4):484-91. doi: 10.1007/s002210100732.
We wished to contrast cortical activation during hand movements in profoundly weak patients with motor neuropathy and in normal controls using a paradigm that is behaviourally matched between the two groups. Previous work has suggested that a passive movement task could be appropriate. Using functional magnetic resonance imaging (fMRI), we first characterised patterns of brain activation during active and passive index finger movements in healthy controls (n=10). Although the relative activation differences were highly variable, there was a trend for the mean number of significantly activated voxels in the primary motor cortex contralateral to the hand moved (CMC) to be lower for the passive than for the active task (40% relative decrease, P=0.09). There was a small posterior shift in the centre of mass of the CMC (mean, 8 mm, P<0.02) and of the ipsilateral sensorimotor cortex (IMC) (mean, 11 mm, P<0.05). No activation with passive movement was found in the patients with severe distal sensory neuropathy (n=2), suggesting that activation with passive movements is dependent on sensory feedback and unlikely to be due to mental imagery alone. In contrast, patients with severe pure motor neuropathies (MN, n=2) showed substantial increases in the volumes of activation compared to controls. The relative increases in numbers of voxels activated above threshold in different regions of interest for both the active (MN/controls: CMC, 2. 1; IMC, 8.1; supplementary motor area [SMA], 5.2) and passive (CMC, 2.6; IMC, 8.0; SMA, 5.1) tasks were similar. These results confirm expansion of cortical representation for finger movement in patients with motor neuropathy and demonstrate central reorganisation as a consequence of the motor nerve loss. An expanded representation for finger movement in the primary motor cortex with peripheral weakness suggests the possibility that the primary motor cortex may encode motor unit activation rather directly.
我们希望通过一种两组行为匹配的范式，对比患有运动神经病的极度虚弱患者与正常对照组在手部运动时的皮质激活情况。先前的研究表明被动运动任务可能是合适的。我们使用功能磁共振成像（fMRI），首先对10名健康对照者在主动和被动食指运动期间的脑激活模式进行了特征描述。尽管相对激活差异变化很大，但对于被动任务，与运动手对侧的初级运动皮层（CMC）中显著激活体素的平均数量有低于主动任务的趋势（相对减少40%，P = 0.09）。CMC的质心有小幅度的向后移动（平均8毫米，P < 0.02），同侧感觉运动皮层（IMC）的质心也有小幅度向后移动（平均11毫米，P < 0.05）。在患有严重远端感觉神经病的患者（n = 2）中未发现被动运动激活，这表明被动运动激活依赖于感觉反馈，不太可能仅由心理意象引起。相比之下，患有严重纯运动神经病（MN，n = 2）的患者与对照组相比，激活体积有大幅增加。在主动（MN/对照组：CMC，2.1；IMC，8.1；辅助运动区[SMA]，5.2）和被动（CMC，2.6；IMC，8.0；SMA，5.1）任务中，不同感兴趣区域高于阈值激活的体素数量的相对增加相似。这些结果证实了运动神经病患者手指运动的皮质表征扩大，并证明了运动神经损伤导致的中枢重组。初级运动皮层中手指运动表征的扩大以及周围神经无力表明，初级运动皮层可能相当直接地编码运动单位激活。
