Tsuzuki S, Indo T, Aiba I, Takahashi A
Department of Neurology, Kasugai City Hospital.
Rinsho Shinkeigaku. 1990 Nov;30(11):1238-42.
Metabolic depression in the cerebellar hemisphere contralateral to supratentorial stroke termed "Crossed Cerebellar Diaschisis" (CCD) was first described by Baron and coworkers and now interpreted as a transneuronal deactivation resulted from loss of excitatory afferent inputs. Among the cerebrocerebellar pathways possibly involved, the corticopontocerebellar pathway is considered to be the most important to induce CCD. According to the hypothesis that CCD results from the destruction of the corticopontocerebellar pathway, any lesion wherever located in the corticopontocerebellar pathway may induce CCD. Little is known, however, about CCD after the brainstem lesion. Our case presented here showed that a brainstem lesion actually induced CCD and that CCD resulted from transneuronal deactivation. An 80-year-old female was admitted to the neurological department of Kasugai City Hospital because of left-sided hemiparesis of sudden onset on March 19, 1989. On admission and 5 days after admission CT scan of the brain was performed, but no stroke lesion was found. Magnetic resonance imaging of the brain disclosed a localized lesion in the right peduncle and tegmentum of the midbrain. Single photon emission computerized tomography of the brain using N-isopropyl-P-(123I) iodoamphetamine (IMP) performed about a month after admission disclosed decreased blood flow in the left hemisphere of the cerebellum compared with the right one and the findings of CCD were observed.
幕上卒中对侧小脑半球的代谢抑制被称为“交叉性小脑失联络”(CCD),最初由巴伦及其同事描述,现在被解释为由于兴奋性传入输入丧失导致的跨神经元失活。在可能涉及的脑桥小脑通路中,皮质脑桥小脑通路被认为是诱导CCD最重要的通路。根据CCD是由皮质脑桥小脑通路破坏引起的这一假设,皮质脑桥小脑通路中任何部位的病变都可能诱发CCD。然而,关于脑干病变后的CCD却知之甚少。我们在此报告的病例显示,脑干病变实际上诱发了CCD,且CCD是由跨神经元失活所致。一名80岁女性因1989年3月19日突然出现左侧偏瘫入住春日井市立医院神经科。入院时及入院后5天进行了脑部CT扫描,但未发现卒中病变。入院约1个月后使用N-异丙基-P-(123I)碘安非他明(IMP)进行的脑部单光子发射计算机断层扫描显示,与右侧相比,左侧小脑半球血流减少,观察到了CCD的表现。