めまい症状を伴った Opalski 症候群2症例の神経耳科学的検討

抄録

　Opalski's syndrome is considered to be a variant of lateral medullary infarction (Wallenberg's syndrome) with ipsilateral hemiplegia. Although dizziness/vertigo or ocular motor abnormalities commonly occur in Wallenberg's syndrome, these abnormalities are scarcely encountered in Opalski's syndrome.
　In the present study, two patients with Opalski's syndrome experiencing vertigo/dizziness were evaluated by electronystagmography (ENG). The characteristic findings of ENG were as follows: (1) horizontal nystagmus beating toward the contralateral side of the lesion, (2) tonic conjugate deviation to the side of the lesion (case 2), (3) hypometric saccade toward the side of the lesion and hypermetric saccade toward the contralateral side, (4) smooth pursuit was impaired to the ipsilateral side of the lesion, (5) slow phase peak velocities of OKN were reduced bilaterally, while the steady-state velocities were preserved, and (6) impaired visual suppression (VS) of the slow phase of caloric nystagmus on the ipsilateral side. Among these features, (3) and (4) were the most remarkable findings in our patients. In our present cases, the characteristic directional preponderance of the saccadic and smooth-pursuit eye movement disorders was just the reverse of those observed in Wallenberg's syndrome. Several lines of neurophysiological evidence suggest that in Wallenberg's syndrome, the impaired saccadic and smooth-pursuit movements are caused by dysfunction of the caudal fastigial nuclei. In contrast, after experimental lesioning of the posterior vermis (lobules VI and VII), the directional preponderance of the saccadic and smooth-pursuit eye movements is just the opposite. The findings in our cases were consistent with these observations. Consequently, the findings in our case were presumed to be originated from dysfunction of the posterior vermis. As for reduction of the bilateral slow-phase peak velocities of OKN, it appears to be derived from dysfunction of the flocculus/paraflocculus, and reduction of the ipsilateral VS may be derived from dysfunction of the flocculus or nodulus. MRI in our cases revealed lateral medullary infarction, but no lesions in the cerebellum. Therefore, it was assumed that the above ocular motor abnormalities in our cases may have been mainly derived from lesions of the inferior cerebellar peduncle disrupting the climbing fibers from the contralateral inferior olivary nuclei to the posterior vermis, flocculus/paraflocculus, and nodulus.