Hirono N, Kameyama M, Mezaki T, Abe K
Department of Neurology, Sumitomo Hospital.
Rinsho Shinkeigaku. 1990 Jan;30(1):73-7.
A sixty-year-old man was admitted to our hospital on January, 1989. He had suffered a hemorrhage in the right side of pontine tegmentum on April, 1988. He had been in deep coma for about a week, and then he had showed diplopia, mild right deafness, right facial palsy, left hemiparesis, dysarthria, dysphagia, and urinary disturbance. He showed slight improvement of these symptoms and signs, but had developed thereafter extremity myorhythmia on the left side. On admission, rightward slow eye movement (absence of saccadic eye movement and preservation of pursuit eye movement of both eyes) was present. MRI revealed a hypointensity lesion with a hyperintensity spot on T2-weighted images showing an old hemorrhage in the right pontine tegmentum and a hyperintensity lesion on T2-weighted images showing an olivary pseudohypertrophy on the right. We concluded that the extremity myorhythmia in this patient was caused by the damage of the right central tegmental tract followed by right olivary pseudohypertrophy. The rightward slow eye movement was considered to be due to the damage of the right paramedian pontine reticular formation and/or its afferent fibers in the pontine tegmentum.
一名60岁男性于1989年1月入院。他在1988年4月时脑桥被盖右侧出血。他曾深度昏迷约一周，之后出现复视、轻度右耳聋、右面神经麻痹、左侧偏瘫、构音障碍、吞咽困难及排尿障碍。这些症状和体征稍有改善，但此后左侧肢体出现肌阵挛。入院时，存在向右的慢眼动（双眼无扫视眼动且保留追随眼动）。MRI显示在T2加权像上有一个低信号病变伴一个高信号点，提示右脑桥被盖陈旧性出血，且在T2加权像上有一个高信号病变，提示右侧橄榄体假肥大。我们得出结论，该患者的肢体肌阵挛是由右侧中央被盖束受损继发右侧橄榄体假肥大所致。向右的慢眼动被认为是由于右侧脑桥旁正中网状结构及其在脑桥被盖中的传入纤维受损。
