Gerloff Christian, Braun Christoph, Staudt Martin, Hegner Yiwen Li, Dichgans Johannes, Krägeloh-Mann Ingeborg
Cortical Physiology Research Group, Hertie Institute for Clinical Brain Research, Department of General Neurology, Eberhard-Karls University, Tuebingen, Germany.
Hum Brain Mapp. 2006 Oct;27(10):789-98. doi: 10.1002/hbm.20220.
Coherent oscillations of neurons in the primary motor cortex (M1) have been shown to be involved in the corticospinal control of muscle activity. This interaction between M1 and muscle can be measured by the analysis of corticomuscular coherence in the beta-frequency range (beta-CMCoh; 14-30 Hz). Largely based on magnetoencephalographic (MEG) source-modeling data, it is widely assumed that beta-CMCoh reflects direct coupling between M1 and muscle. Deafferentation is capable of modulating beta-CMCoh, however, and therefore the influence of reafferent somatosensory signaling and corresponding neuronal activity in the somatosensory cortex (S1) has been unclear. We present transcranial magnetic stimulation (TMS) and MEG data from three adult patients suffering from congenital hemiparesis due to pre- and perinatally acquired lesions of the pyramidal tract. In these patients, interhemispheric reorganization had resulted in relocation of M1 to the contralesional hemisphere, ipsilateral to the paretic hand, whereas S1 had remained in the lesioned hemisphere. This topographic dichotomy allowed for an unequivocal topographic differentiation of M1 and S1 with MEG (which is not possible if M1 and S1 are directly adjacent within one hemisphere). In all patients, beta-CMCoh originated from the contralesional M1, in accordance with the TMS-evoked motor responses, and in contrast to the somatosensory evoked fields (SEFs) for which the sources (N20m) were localized in S1 of the lesioned hemisphere. These data provide direct evidence for the concept that beta-CMCoh reflects the motorcortical efferent drive from M1 to the spinal motoneuron pool and muscle. No evidence was found for a relevant contribution of neuronal activity in S1 to beta-CMCoh.
初级运动皮层(M1)中神经元的相干振荡已被证明与肌肉活动的皮质脊髓控制有关。M1与肌肉之间的这种相互作用可以通过分析β频率范围(β-CMCoh;14 - 30Hz)内的皮质肌肉相干性来测量。很大程度上基于脑磁图(MEG)源建模数据,人们普遍认为β-CMCoh反映了M1与肌肉之间的直接耦合。然而,去传入能够调节β-CMCoh,因此,来自体感皮层(S1)的再传入体感信号和相应神经元活动的影响尚不清楚。我们展示了三名因锥体束在产前和围产期受损而患有先天性偏瘫的成年患者的经颅磁刺激(TMS)和MEG数据。在这些患者中,半球间重组导致M1重新定位到对侧半球,即患侧手的同侧,而S1仍留在受损半球。这种地形二分法使得通过MEG能够明确区分M1和S1的地形(如果M1和S1在一个半球内直接相邻则无法做到)。在所有患者中,β-CMCoh起源于对侧M1,这与TMS诱发的运动反应一致,与体感诱发电场(SEFs)相反,SEFs的源(N20m)位于受损半球的S1。这些数据为β-CMCoh反映从M1到脊髓运动神经元池和肌肉的运动皮层传出驱动这一概念提供了直接证据。未发现S1中的神经元活动对β-CMCoh有相关贡献的证据。