Yokota J, Kosaka K, Yoshimoto Y, Amakusa T
Department of Neurology, Amakusa Hospital, Saitama, Japan.
No To Shinkei. 1999 Dec;51(12):1055-60.
A 60-year-old hypertensive woman had a pontine hemorrhage that caused slight right hemiplegia, deep sensory disturbance on her right side and dysarthria. Three months after the stroke, she was transferred to our hospital for rehabilitation. Approximately 6 months later, she gradually began to complain of the visual oscillation. Continual, unceasing conjugate vertical/rotatory eye movements were observed. Fixation was momentary at best because of an inability to dampen the spontaneous eye movements. Electrooculography (EOG) showed bilateral vertical/rotatory sinusoidal eye movements of 2.5 Hz frequency and 10- to 35-degree amplitude. Both vertical and horizontal optokinetic nystagmus were absent. Caloric stimulation did not evoke any responses bilaterally. There were no rhythmical movements at similar frequencies in other parts of the body such as palatal myoclonus. MRI revealed not only hematoma mainly at the dorsal pontine tegmentum but also hypertrophy of the inferior olive nucleus, suggesting disruption of the central tegmental tract. Lesions of this tract may be one cause of pendular nystagmus. Several drug therapies were investigated for the nystagmus. There was no response to baclofen 15 mg. Trihexyphenidyl 4 mg was discontinued because of drug-induced hallucinations. Tiapride 600 mg and phenobarbital 90 mg were each slightly effective in reducing both frequency and amplitude of nystagmus. Treatment with clonazepam 1 mg resulted in the striking disappearance of nystagmus. She was aware of this and no longer experienced oscillopsia. Despite the visual benefit, however, the patient did not wish to continue this drug because of drowsiness and muscle relaxation. The potential long-term therapeutic application of clonazepam should be further investigated. To our knowledge, there have been no reports of successful treatment in acquired pendular nystagmus with clonazepam. Therefore, based on this favorable experience, it is suggested that clonazepam should be added to the list of potential therapies for pendular nystagmus.
一名60岁的高血压女性发生脑桥出血,导致轻度右侧偏瘫、右侧深部感觉障碍和构音障碍。中风三个月后,她被转到我院进行康复治疗。大约6个月后,她逐渐开始抱怨视觉振荡。观察到持续不断的共轭垂直/旋转眼球运动。由于无法抑制自发眼球运动,注视最多只能是瞬间的。眼电图(EOG)显示双侧垂直/旋转正弦眼球运动,频率为2.5Hz,幅度为10至35度。垂直和水平视动性眼震均未引出。冷热刺激双侧均未引起任何反应。身体其他部位如腭肌阵挛没有类似频率的节律性运动。MRI显示不仅血肿主要位于脑桥背侧被盖部,而且下橄榄核肥大,提示中央被盖束中断。该束的病变可能是摆动性眼震的原因之一。对眼震研究了几种药物治疗方法。15mg巴氯芬治疗无效。4mg苯海索因药物性幻觉而停药。600mg硫必利和90mg苯巴比妥在降低眼震频率和幅度方面均有轻微效果。1mg氯硝西泮治疗使眼震明显消失。她意识到了这一点,不再有视振荡。然而,尽管有视觉益处,但患者因嗜睡和肌肉松弛而不愿继续使用这种药物。氯硝西泮潜在的长期治疗应用应进一步研究。据我们所知,尚无氯硝西泮成功治疗后天性摆动性眼震的报道。因此,基于这一良好经验,建议将氯硝西泮列入摆动性眼震的潜在治疗方法清单。