Okuda B, Tachibana H, Takeda M, Kawabata K, Sugita M
Fifth Department of Internal Medicine, Hyogo College of Medicine, Nishinomiya, Japan.
Acta Neurol Scand. 1998 Jun;97(6):409-12. doi: 10.1111/j.1600-0404.1998.tb05975.x.
To clarify the underlying mechanism of limb apraxia in corticobasal degeneration (CBD), we investigated somatosensory evoked potentials in 5 patients with CBD, as compared with 12 age-matched control subjects. All patients presented with asymmetric limb apraxia, particularly of limb-kinetic type. N20 latencies were significantly prolonged following median nerve stimulation on the more apraxic side, but not on the less apraxic side. These results suggest that limb apraxia in CBD may, at least in part, be due to a disorder of somatosensory information processing involving the parietal cortex.
为阐明皮质基底节变性(CBD)中肢体失用症的潜在机制,我们对5例CBD患者的体感诱发电位进行了研究,并与12名年龄匹配的对照受试者进行了比较。所有患者均表现为不对称肢体失用症,尤其是肢体运动型。在失用症较重一侧进行正中神经刺激后,N20潜伏期显著延长,而在失用症较轻一侧则未出现这种情况。这些结果表明,CBD中的肢体失用症可能至少部分归因于涉及顶叶皮质的体感信息处理障碍。