前庭性片頭痛症例における ENG 解析

抄録

　In the present study, in order to elucidate the pathophysiology of vestibular migraine (VM), we performed electronystagmography (ENG) during the interictal period in seven patients with VM diagnosed according to the International Classification of Headache Disorders (ICHD-3β). The results of audiometry, posturography, and CT/MRI revealed no abnormalities in any of the patients. The characteristic ENG findings were as follows: 1) In the dark, lateral and vertical gaze nystagmus were recognized. 2) In the dark, abnormal eye movements, such as square wave jerks, rebound nystagmus and hypometric saccades were frequently observed. 3) In the vertical eye tracking test (ETT), saccadic pursuit was prominent, whereas horizontal smooth pursuit was preserved. 4) The peak velocity of the slow phase in optokinetic nystagmus (OKN) was markedly reduced in three VM patients (43%). 5) The optokinetic after-nystagmus (OKAN) showed the “inhibition pattern” in four patients (57%), and the “disinhibition pattern” in three patients (43%). 6) Caloric nystagmus could be normally induced in two patients. An “ataxic patterm” was observed in two patients. In contrast, the remaining two patients showed suppressed or scarce responses, which suggested peripheral vestibular dysfunction. Except in such cases with peripheral-type abnormalities, most of the aforementioned ocular motor abnormalities were suggestive of dysfunction of both the medial vestibular nuclei (MVN) and the vestibulocerebellum. Although the precise pathophysiology of VM still remains unclear, several hypotheses have been advanced. First, the vascular hypothesis suggests that VM is associated with subclinical microischemic lesions, mainly in the posterior circulation, caused by episodes of vasoconstriction during successive migraine attacks. Second, recent genetic studies have disclosed similarities between familial hemiplegic migraine, which is considered as a Ca²⁺ channelopathy, and spinocerebellar ataxia type 6 (SCA6). Although no mutations have been identified until now in the common forms of migraine, it is speculated that the Ca²⁺ channels could be functionally impaired by subtle genetic changes, such as gene polymorphisms, resulting in cortical hyperexcitability; the latter would increase the susceptibility for cortical spreading depression (CSD) over the medulla (vestibular nuclei) and vestibulocerebellum. In conclusion, VM appears to be a heterogeneous central vestibular disorder, and various pathophysiological mechanisms may be mutually involved.