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[橄榄体脑桥小脑萎缩中的交叉性小脑-大脑失联络]

[Crossed cerebello-cerebral diaschisis in olivopontocerebellar atrophy].

作者信息

Deguchi K, Takeuchi H, Yamada A, Touge T, Nishioka M

机构信息

Third Department of Internal Medicine, Kagawa Medical School.

出版信息

Rinsho Shinkeigaku. 1994 Aug;34(8):851-3.

PMID:7994998
Abstract

We reported a case of crossed cerebello-cerebral diaschisis (CCCD) in olivopontocerebellar atrophy (OPCA). A 49-year-old male was admitted with complaints of titubation, dysarthria and tremor. Examination on admission revealed exaggerated triceps, patella and achilles tendon reflexes on both sides and rigidity in left wrist. Ocular movements were slightly saccadic and speech was scanning or explosive. Finger-nose and heel-knee coordination was poor on both sides (left dominant). Cardiovascular reflex tests showed abnormal findings, suggesting insidious autonomic dysfunction. Brain CT and magnetic resonance imaging (MRI) revealed mild atrophy of the pons and cerebellum. Brain single photon emission computed tomography (SPECT) showed reduced cerebellar N-isopropyl-P-(123I) iodoamphetamine (IMP) uptake more prominent on the left than on the right side. A reduction of 123I-IMP uptake was more striking in the right thalamus, basal ganglia and frontal lobe than on the left side. The cerebellar sign which was left dominant and the left extrapyramidal sign were consistent with the side where reduction of 123I-IMP uptake was more prominent. We suggest that CCCD in our case resulted from transneuronal deactivation in the classic anatomical (cerebello-thalamo-cortical) pathway and dopaminergic (cerebello-basal ganglia-cortical) pathway. There is a possibility that CCCD reflects the development of pathological changes in OPCA.

摘要

我们报告了一例橄榄体脑桥小脑萎缩(OPCA)伴交叉性小脑-大脑失联络(CCCD)的病例。一名49岁男性因头部震颤、构音障碍和震颤入院。入院检查发现双侧肱三头肌、髌腱和跟腱反射亢进,左手腕僵硬。眼球运动稍有扫视,言语呈断续性或爆发性。双侧指鼻试验和跟膝试验协调性差(左侧更明显)。心血管反射试验结果异常,提示存在隐匿性自主神经功能障碍。脑部CT和磁共振成像(MRI)显示脑桥和小脑轻度萎缩。脑单光子发射计算机断层扫描(SPECT)显示小脑N-异丙基-P-(123I)碘安非他明(IMP)摄取减少,左侧比右侧更明显。右侧丘脑、基底神经节和额叶的123I-IMP摄取减少比左侧更显著。以左侧为主的小脑体征和左侧锥体外系体征与123I-IMP摄取减少更明显的一侧相符。我们认为,本例中的CCCD是由经典解剖学(小脑-丘脑-皮质)通路和多巴胺能(小脑-基底神经节-皮质)通路中的跨神经元失活所致。CCCD有可能反映了OPCA中病理变化的发展。

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