Michikawa M, Takahashi M, Kishida S, Yano Y, Muro T
Department of Internal Medicine, Tokyo Metropolitan Komagome Hospital.
Rinsho Shinkeigaku. 1991 Jan;31(1):44-8.
We report a 54-year-old woman who revealed right hemiparesis and ataxia in her right extremities due to a lesion which was suggested to be cavernous hemangioma located in the left side of pons in 1971, and showed remarkable crossed cerebellar atrophy (CCA) by computed tomography and magnetic resonance imaging in 1985 and 1989. Angiography showed no abnormality but made iatrogenic embolism in left thalamus which developed severe pain in her right side. Single-photon-emission-computed-tomography (SPECT) with I123-IMP in 1989 showed reduction of right cerebellar hemispheric blood flow (crossed cerebellar diaschisis: CCD) and left cerebral hemispheric blood flow. Our case was thought to have revealed persisting CCD. Although there are many reports about CCD and CCA following cerebral damage, CCD and CCA due to brain stem lesion has not been described yet. This might be explained by the persisting functional depression of cerebro-ponto-cerebellar pathways at the pons' level by cavernous hemangioma. It was assumed that the left cortical hypometabolism was result from damage to thalamo-cortical pathways due to ipsilateral thalamic lesion.
我们报告了一名54岁女性,她于1971年因位于脑桥左侧的病变(提示为海绵状血管瘤)出现右侧偏瘫和右肢共济失调,并于1985年和1989年通过计算机断层扫描和磁共振成像显示出明显的交叉性小脑萎缩(CCA)。血管造影未显示异常,但在左侧丘脑进行了医源性栓塞,导致她右侧出现剧痛。1989年使用I123-IMP进行的单光子发射计算机断层扫描(SPECT)显示右侧小脑半球血流减少(交叉性小脑神经机能联系失联络:CCD)以及左侧大脑半球血流减少。我们的病例被认为显示出持续性CCD。尽管有许多关于脑损伤后CCD和CCA的报道,但尚未描述过脑干病变导致的CCD和CCA。这可能是由于海绵状血管瘤在脑桥水平持续导致脑桥-小脑通路功能抑制所致。据推测,左侧皮质代谢减退是由于同侧丘脑病变导致丘脑-皮质通路受损所致。