Trouillas P, Nighoghossian N, Mauguière F
Service de Neurologie B et Centre de Recherches Cliniques de l'ataxie., Faculté Alexis Carrel, Hôpital Neurologique, Lyon.
Rev Neurol (Paris). 1990;146(8-9):484-9.
A 76 year-old hypertensive man developed an acute inability to stand due to a right cerebellar ataxia. Somatosensory performances were normal, but a transient and mild weakness of the right arm and leg with Babinski's sign was observed. There was a prominent asterixis of the right hand. CT scan showed a hemorrhage of the thalamus with surrounding edema of the adjacent internal capsule. Initial median nerve somatosensory evoked potentials showed a mild reduction of left parietal responses with absent left frontal SEPs (P22 and N30). Fourty days later the cerebellar ataxia was persisting while asterixis had disappeared. A second recording of SEPs showed a complete recovery of all cortical components. MRI performed at the same time showed a left postero lateral thalamic lesion. CT, MRI and SEPs findings suggested that asterixis could result from interruption of somatosensory fibres projecting to the motor cortex.
一名76岁的高血压男性因右侧小脑共济失调而突然无法站立。躯体感觉功能正常，但观察到右侧手臂和腿部有短暂且轻微的无力，并伴有巴宾斯基征。右手有明显的扑翼样震颤。CT扫描显示丘脑出血，相邻内囊周围有水肿。最初的正中神经体感诱发电位显示左侧顶叶反应轻度降低，左侧额叶SEP（P22和N30）消失。40天后，小脑共济失调持续存在，而扑翼样震颤消失。第二次SEP记录显示所有皮层成分完全恢复。同时进行的MRI显示左侧丘脑后外侧病变。CT、MRI和SEP的结果表明，扑翼样震颤可能是由于投射到运动皮层的体感纤维中断所致。
