Sasaki I, Fujii S, Ichihara N, Hatanaka Y
Department of Neurology, Takamatsu National Hospital, Kagawa-ken, Japan.
No To Shinkei. 1999 Jul;51(7):638-40.
We report a 56-year-old woman with vitamin B1 polyneuropathy, showing bilateral homolateral imitative synkinesia. Needle electromyogram revealed neurogenic changes, and the amplitude of muscle action potential was low. Sural nerve biopsy showed a marked loss of myelinated fibers, and severe axonal degeneration was diagnosed. Spinal and brain MRI revealed no abnormalities. In the literature, these synkinesias were observed in patients with parietal, thalamic, and basal ganglia lesions and with chorea. We suggest that this synkinesia is the release phenomenon in the circuit of the motor programming system due to the disturbance of peripheral nerve or funiculus posterior.
我们报告了一名56岁患有维生素B1多发性神经病的女性,其表现为双侧同侧模仿性联带运动。针极肌电图显示为神经源性改变,肌肉动作电位幅度较低。腓肠神经活检显示有髓纤维明显缺失,诊断为严重轴索变性。脊柱和脑部MRI未发现异常。在文献中,这些联带运动在患有顶叶、丘脑和基底神经节病变以及舞蹈病的患者中观察到。我们认为这种联带运动是由于周围神经或后索受干扰,在运动编程系统回路中出现的释放现象。