Ogawa M, Nagata K, Satoh Y, Hirata Y, Hatazawa J
Department of Neurology, Institute for Brain and Blood Vessels.
Rinsho Shinkeigaku. 1994 Mar;34(3):267-9.
We report a 68-year-old right-handed male who exhibited Dejerine-Roussy syndrome including a persistent cerebellar ataxia following the left thalamic hemorrhage with special reference to the evolution of crossed cerebellar diaschisis (CCD) measured with positron emission tomography (PET). The initial PET studies performed 50 days after onset revealed a mild reduction of blood flow and glucose metabolism in the right cerebellar hemisphere in addition to the severe reduction in the left thalamus. Even in the chronic stage when the motor weakness almost disappeared, he persistently showed a cerebellar ataxia in his right extremities. The cerebellar blood flow and metabolism became normalized without laterality in the follow-up PET studies which were performed 29 months after onset, although the left thalamus and left cerebral cortices were still severely involved. The cerebellar ataxia with preserved cerebellar blood flow and metabolism following the thalamic hemorrhage was possibly associated with damage to the efferent fibers from the cerebellum, whereas the CCD observed in the early stage probably was caused by a transient involvement of the cortico-ponto-cerebellar tract at the level of the internal capsule.
我们报告了一名68岁的右利手男性,其出现了Dejerine-Roussy综合征,包括左侧丘脑出血后持续存在的小脑共济失调,并特别提及了用正电子发射断层扫描(PET)测量的交叉性小脑失联络(CCD)的演变情况。发病50天后进行的首次PET研究显示,除左侧丘脑血流和葡萄糖代谢严重降低外,右侧小脑半球也有轻度降低。即使在运动无力几乎消失的慢性期,他的右上肢仍持续存在小脑共济失调。在发病29个月后进行的随访PET研究中,小脑血流和代谢在双侧均恢复正常,尽管左侧丘脑和左侧大脑皮质仍严重受累。丘脑出血后小脑共济失调伴小脑血流和代谢保留,可能与小脑传出纤维受损有关,而早期观察到的CCD可能是由内囊水平的皮质-脑桥-小脑束短暂受累所致。