This study is aimed at exploring how the subjective visual vertical (SVV) might vary depending on the method used to determine the vertical positions. Original equipment devised by the author was used in this study (hereafter, SVV investigation equipment). Study participants spun a wheel in order to determine the vertical position of an axis presented to them as an illuminated pillar in a dark room. Participants were asked to perform the task six times during the study. The results reflect their averages, with a + indicating the results that tilted towards the right. In 20 healthy participants, the results of the SVV test obtained with the subjects using their dominant hands to adjust the angle were compared with those obtained with the subjects using their non-dominant hands. In 23 healthy participants, the results of SVV test obtained with the subjects using their hands to adjust the angle were compared with those obtained with having the subjects answer yes/no to the presented angle (12 different patterns of tilted markers from 0 to ±5 degrees). In another 20 healthy participants, the results of the SVV test obtained with the subjects performing the test with both eyes open were compared with those obtained with the subjects performing the test using either eye. All the results obtained by the different methods were correlated with each other. There was also no difference in the actual measured angle between the test methods except for that between the tests conducted with the patient using the dominant and non-dominant hands. Our present study indicates that, the characteristics of SVV deviation can be estimated correctly even if the measurement method varies slightly, although it is better not to change the method when performing quantitative or temporal evaluation.

We investigated the risk factors for vertigo from the results of health checkups conducted in Yakumo town.

It is known that a certain percentage of cases among vertigo patients with apparent peripheral disturbances actually suffer from central vertigo. Especially, vertigo caused by infarction of the posterior inferior cerebellar artery (PICA) territory may sometimes be difficult to diagnose because of the lack of central neurological signs. We encountered a patient with infarction of the area supplied by the PICA who was diagnosed by CT as having peripheral vertigo , but was then eventually definitively diagnosed as a case of infarction of the PICA territory by MRI.

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.

Recent advances in high-resolution MRI have enabled clear visualization of each nerve (cochlear nerve, vestibular nerve and facial nerve) in the internal auditory canal (IAC). Cochlear nerve deficiency (CND) is one of the known causes of bilateral or unilateral hearing loss in children. Although a narrow IAC was thought to be the cause of CND before the emergence of high-resolution MRI, recent studies have reported cases of CND associated with a normal IAC size as assessed by MRI; thus, CND is not able to diagnose by only existing a narrow IAC. There have been a few reports of CND associated with vestibular nerve deficiency, and most such cases were found to have a narrow IAC. However, there are only a few reports of assessment of vestibular function in patients with CND. In this paper, we report a rare case of a patient with CND and vestibular nerve hypoplasia, without a narrow IAC.

In cases of “heavy cupula”, the adhesive strength of the otoconia to the cupula or the adhesive side of the cupula is often unclear. To investigate this further, the course after treatment and the natural course were investigated in 31 cases of heavy cupula that we encountered at our clinic over a one-year period. First, the cases were divided into two groups by the responses to the affected-ear-down 135° maneuver; the group with the lateral canal BPPV-canalolithiasis apogeotropic variant (: L-BPPV-Can-a), in which the otoconia came in contact with the cupula on the canal side, and the group with the lateral canal BPPV-cupulolithiasis (: L-BPPV-Cup), in which the otoconia adhered to the cupula. In the L-BPPV-Can-a group, rolling the head and trunk from the affected-ear-down 135° to the supine position caused detachment of the otoconia from the canal side of the cupula and moved them further in the posterior direction. The maximum slow-phase velocity of nystagmus in the healthy-ear-down position to that in the affected-ear-down position (H/A) was examined in both groups. In the L-BPPV-Cup group, the affected-ear-up lateral decubitus method was employed. Sleeping in the affected-ear-up lateral decubitus position all through the night could detach the otoconia from the utricular side of the cupula and restore them back into the utriculus. The H/A in the L-BPPV-Can-a group was significantly greater than that in the L-BPPV-Cup group (P<0.005). Use of the ratio of 2.5 as the cutoff point to distinguish between the two groups was associated with a sensitivity of 0.8 and specificity of 0.8. The affected-ear-up lateral decubitus method was effective in 58% of the cases. The results suggest that among the 31 cases of heavy cupula, there were 13 with the L-BPPV-Can-a variant and 18 with the L-BPPV-Cup, including 4 with the otoconia adhering to the cupula on the canal side, 12 with the otoconia adherent to the cupula on the utricular side, and 2 undetermined.

Vertical nystagmus is an important sign of central nervous system disorder. Herein, we report a case of upbeat nystagmus, in a case of as the initial symptom of clinically isolated syndrome. The patient was a 45-year-old male who developed dizziness on November 7 and visited our hospital on November 12. We observed upbeat nystagmus in the gaze of all direction and primary and all positions and adduction failure of the right eye. The patient was hospitalized because MRI revealed a high-intensity area on the posterior aspect of the pons and medulla oblongata on T2-weighted and FLAIR MRI imaging. The patient was started on anticoagulant therapy as infarction was suspected, but no improvement of the symptoms was noted. A review of the second MRI revealed another high-intensity area in the right superior cerebellar peduncle, and we started steroid pulse treatment for the patient under the suspicion of multiple sclerosis. The patient's symptoms completely resolved with this treatment, and he was discharged from the hospital on November 26. We suspected that the upbeat nystagmus in this case was mainly caused by disorder of the central vestibuloocular reflex pathway in the pitch plane and area of the nucleus prepositus hypoglossi as the neural integrator. We think that the upbeat nystagmus was a very important symptom for early diagnosis and treatment in this case.