In 1971, Kamei et al. reported that delayed onset of episodic vertigo of the Meniere's type was caused by preexisting profound hearing loss of unknown cause from early childhood. In 1975, Wolfson and Leiberman and Nadol et al. separately described that profound hearing loss caused by viral and bacterial infections, sudden deafness, and head trauma could also be followed by delayed episodic vertigo. In 1978, Schuknecht described delayed endolymphatic hydrops (DEH) as a disease entity. He also pointed out that there were two types of DEH, namely, the ipsilateral and contralateral types. In 2017, new diagnostic criteria for DEH were proposed by the Japan Society for Equilibrium Research. Based on these criteria, patients with DEH can now apply for medical subsidy in the new system of intractable diseases specified by the Japanese government.
The present status of usage and popular usage of the popularly used drugs for dizziness and vertigo in Japan are described herein. The agents are introduced These drugs are prescribed according to the phase of the patients' symptoms (emergency, acute, subacute or chronic) and the underlying pathology, with reference to the literature as evidence. Conservative therapy for dizziness and vertigo consists of three categories; drug therapy, cognitive therapy and physical and exercise therapy. The mutual strategy using An appropriate combination of these three therapies is important for successful treatment of dizziness and vertigo. Thorough history-taking is very important for a precise diagnosis of dizziness and vertigo. Appropriate treatment is selected according to the precise diagnosis. The mainstream anti-dizziness/vertigo drugs used in Japan consists of antihistamine agents (used as anti-emetic drugs), anti-motion sickness drugs, microcirculation agents, emulgents and vitamin B12 preparations. In this manuscript, we provide a detailed description of all the anti-dizziness/vertigo drugs used currently in Japan, along with a review of the relevant literature. However, most of these drugs are already well-dated and have been traditionally used for many years. In recent years, antidepressant agents and herbal medicines have also begun to be used. There are no new drug developments in this area of vestibular pathologies. We hope that treatments for these conditions will be updated with the development of novel anti dizziness/vertigo drugs, so as to bring this area of study into the modern age of medicine.
Regimens for dysequilibrium include pharmacotherapy, surgery, and rehabilitation. Treatment is prolonged only with pharmacotherapy, and dysequilibrium may persist for a long time. Also, the indications of surgery are limited. Rehabilitation has been given for persistent dysequilibrium. While the effect of rehabilitation is well-known, no thorough evaluation has been conducted. Therefore, in this study, we report the results of evaluation of rehabilitation for dysequilibrium using stabilometry, the Kitasato method symptom evaluation list and activities of daily living rated on a subjective scale. We conducted the evaluation at admission, and then, one or two, and three months after discharge. There were no significant differences in the results of evaluation between one month after discharge and at admission, but significant differences were observed between two months after discharge and at admission. Our findings suggest that the effect of the rehabilitation appears approximately two months after the initiation of rehabilitation.
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.
A 51-year-old immunocompetent woman presented with slight fever, cough and general fatigue. After 4 days, she developed slight headache, spontaneous rotatory vertigo, nausea and vomiting. Subsequently, she gradually developed unsteadiness of gait. Two weeks after the onset of vertigo, she visited the outpatient clinic of our university hospital. Neurologic examination revealed a wide-based gait, predominantly right-sided upper/lower limb ataxia, and right dysdiadochokinesia. On cranial nerve examination, she was found to have right peripheral facial nerve palsy, which she had not recognized before. She had neither rash nor pain in her auricles. Brain MRI was normal. Laboratory data showed positive results for serum anti-varicella zoster virus (VZV) IgG, but negative results for IgM. The findings of electronystagmography (ENG) were as follows; 1) ataxic nystagmus with irregular amplitudes and frequencies on lateral gaze; 2) eye position of slow-phase nystagmus with a negative exponential time course (decreasing velocity), reflecting an unsustained eye position signal caused by an impaired neural integrator; 3) impaired smooth pursuit; 4) reduced optokinetic nystagmus; 5) impaired caloric nystagmus. These findings suggested disturbances of both the neural integrator and velocity storage systems, in addition to cerebellar (flocculus, paraflocculus) dysfunction. As for the pathophysiological mechanisms underlying the disturbances of both the neural integrators, we suspected VZV involvement of the peripheral vestibular nerve, in addition to right peripheral facial nerve involvement, rather than lesions of the brainstem (MVN, NPH). Cerebellitis associated with VZV is very rare in adults. Furthermore, it would be emphasized that it is very rare for peripheral facial palsy to be followed by cerebellitis two weeks later in cases of VZV involvement.
Ten healthy volunteers were spun passively on a revolving chair (0.5 Hz left-winded 7 rotation), asked to stand up immediately thereafter and take 30 steps with their eyes closed. The observations revealed that subjects having an anteverted posture turned to the right, whereas those with a retroverted posture turned to the left. To ascertain the reason for this directional switch, volunteers carried a 10-kg weight on their front or back while keeping their axis vertical. The front-weighted subjects turned to the right like the subjects with the anteverted posture, while the back-weighted subjects turned to the left like those with the retroverted posture. The results indicated that shifting of the center of gravity, and not the posture, was the reason for the difference. When the subjects kept their arms up forward horizontally and the legs high up as in Fukuda's stepping test, they turned to the right, because their horizontal arms and highly up legs set the weight forward. The neutral pose, with the arms hanging down along the side of the body and stepping low, was scarcely associated with any turning.
[Introduction] I conducted this experiment to examine whether virtual stare can suppress nystagmus.
[Subjects] Twelve healthy adult volunteers (total 24 ears).
[Method] The experiment was conducted as follows:
1. Subjects wearing a video-oculograhic apparatus for nystagmus
measurement underwent a caloric test, and nystagmus was recorded.
2. When the slow-phase velocity of the nystagmus reached its maximum
value, the subjects were told/asked the following: “A dim light is lit at
the same place as that in the visual suppression test. Please gaze at the
light. What color is it now?” No light was actually lit.
3. After 10 seconds, they were instructed to stop looking (unable to see
[Results] The mean slow-phase velocity of the caloric nystagmus decreased significantly during the load (stimulation) (p<0.01). The mean slow-phase velocity during the 10 seconds prior to the load (stimulation) was 12.4±3.3°/s, and that during the load (stimulation) was 8.1±2.7°/s. The nystagmus suppression rate was 33.2±18.0%.
[Summary] The study suggested that virtual stare suppressed peripheral nystagmus.