Timmermann L, Gross J, Butz M, Kircheis G, Haussinger D, Schnitzler A
Department of Neurology and Gastroenterology, University Hospital Düsseldorf, Germany.
Neurol Clin Neurophysiol. 2004 Nov 30;2004:26.
Whole-head MEG-systems and modern spatial-filter-based analysis tools recently provided new possibilities to analyze non-invasively cerebral networks of human tremor syndromes. We compared tremor syndromes in Parkinsonian patients with a typical resting tremor as well as in patients with hepatic encephalopathy (HE) with a postural tremor called "mini-asterixis". In 6 patients with idiopathic Parkinson's disease (PD) we found strong coherence between the electromyography (EMG) of forearm muscles and activity in the contralateral primary motor cortex (M1) at tremor frequency but also at double tremor frequency. Furthermore, significant coherences were observed between M1 and medial wall areas (CMA/SMA), lateral premotor cortex, diencephalon, SII cortex, posterior parietal cortex and the contralateral cerebellum at tremor and, stronger, at double tremor frequency. In contrast, in 6 patients with "mini-asterixis" and HE due to chronic liver cirrhosis excessive corticomuscular coherence occurred at the individual tremor frequency between EMG and M1 activity. Interestingly, thalamus-M1 coupling was significantly altered towards lower frequencies matching the individual frequency of the mini-asterixis. Cerebro-muscular or cerebro-cerebral coupling at double tremor frequency was not observed. Therefore, "mini-asterixis" reflects most likely a pathologically decelerated and augmented synchronized rhythmical motor cortical output. This could be due to functional alterations in the M1-basal-ganglia-thalamo-cortical loops in severe HE. In summary, tremor syndromes in PD as well as in patients with HE and "mini-asterixis" are characterized by pathological oscillatory activity within cerebral networks of motor areas. However, the present study shows different mechanisms of tremor generation in PD and HE patients.
全头型脑磁图(MEG)系统和基于现代空间滤波的分析工具最近为无创分析人类震颤综合征的脑网络提供了新的可能性。我们比较了帕金森病患者典型的静止性震颤以及肝性脑病(HE)患者的姿势性震颤“微扑翼样震颤”。在6例特发性帕金森病(PD)患者中,我们发现前臂肌肉的肌电图(EMG)与对侧初级运动皮层(M1)在震颤频率以及两倍震颤频率时的活动之间存在强相干性。此外,在震颤频率以及更强的两倍震颤频率时,观察到M1与内侧壁区域(中央前运动区/辅助运动区)、外侧运动前皮层、间脑、第二躯体感觉皮层(SII)、顶叶后皮层以及对侧小脑之间存在显著相干性。相比之下,在6例因慢性肝硬化导致“微扑翼样震颤”和HE的患者中,EMG与M1活动在个体震颤频率时出现了过度的皮质-肌肉相干性。有趣的是,丘脑-M1耦合向更低频率显著改变,与微扑翼样震颤的个体频率相匹配。未观察到两倍震颤频率时的脑-肌肉或脑-脑耦合。因此,“微扑翼样震颤”很可能反映了病理性减慢和增强的同步节律性运动皮层输出。这可能是由于严重HE中M1-基底神经节-丘脑-皮层环路的功能改变所致。总之,PD患者以及HE和“微扑翼样震颤”患者的震颤综合征的特征是运动区脑网络内的病理性振荡活动。然而,本研究显示了PD和HE患者震颤产生的不同机制。