Environmental chemical pollutants can induce an equilibrium disorder, but the mechanism of such a disorder remains unclear for most chemicals. We demonstrate herein that representative chemicals are associated with balance impairment. Some Yusho patients, a toxic accident due to dioxin and PCBs, had dizziness without any vestibular disorder but with the impairment of the peripheral nerves. Farmers using pesticides are likely to have dizziness. The organophosphate that inhibits cholinesterase may induce equilibrium impairment with a vestibular disorder. Other pesticides including pyrethroid and carbamate may also cause dizziness. However the mechanism underlying the dizziness has not been understood in detail. Further research is needed in order to resolve equilibrium disorders due to environmental chemical pollutants.

　Cerebrospinal fluid leakage is associated with several symptoms, such as headache, nausea, photophobia, diplopia and lassitude. In our practice, dizziness is a frequent presenting symptom in patients with this disorder. However, the mechanism and features of dizziness are unclear.
　In this report, we examined two patients with cerebrospinal fluid leakage with dizziness, exhibiting in particular flutter-like oscillations. Ocular flutter is characterized by intermittent bursts of horizontal saccades lacking an intersaccadic interval. Although the precise mechanisms are unknown, ocular flutter is often observed in cerebellar or brainstem lesions. In patients such as ours, ocular flutter may indicates that a central nervous system disorder may be present in cerebrospinal fluid leakage with dizziness.

　Objective: To investigate the background of hospitalized patients with vestibular neuritis over a ten-year period
.　Methods: A retrospective study was conducted in the medical records of patients with vestibular neuritis who were hospitalized in our hospital between January 2001 and December 2010.
　Results: Forty-nine patients with vertigo attacks were hospitalized during this period, with ages ranging from 22 to 82 years. The age distribution showed a peak at 60 years. The proportion of 65 years and older was 34.7%. There was no significant difference in the length of hospitalization between under 65 y.o. and 65-and-over patients. The high onset season was spring and summer but there were no significant differences. The duration of the spontaneous nystagmus, the symptoms of dizziness and of the bed rest were 5.5±2.2, 3.0±1.5 and 3.8±1.5 days respectively. The prevalence of diabetes mellitus and hypertension was 10.4% and 27.1%, respectively. Enhanced regions of the vestibular nerve were not detected in 16 cases among those who examined with gadolinium-enhanced MRI. Cases of preceding upper respiratory infection only accounted for 7 patients. Only 2 patients showed an increased level of CRP in the blood test at the time of admission. The duration of bed rest and hospitalization in the corticosteroids treatment group were shorter than in the nonsteroid treatment group.
　Conclusion: In this study, there was no trend associated with aging in hospitalized patients with vestibular neuritis. The number of cases of preceding upper respiratory infection was small. No enhanced regions were detected with Gd-enhanced MRI in all cases so examined. Our findings suggest that corticosteroids contribute less to symptomatic recovery of vestibular function in the acute phase of VN. It is useful to investigate the background of hospitalized patients in order to understand the pathology of vestibular neuritis.

　A 57-year-old woman presented at our outpatient clinic with the recent and frequent experience of paroxysmal positional vertical vertigo similar to the sensation of a somersault, especially changing position from sitting to lying supine, accompanied with spells of nausea and blackout. On examination, we observed prominent downbeat nystagmus in the primary eye position and lateral gaze. MRI disclosed prominent cerebellar cortical atrophy, especially in the vermal regions. The patient had a family history of spinocerebellar ataxia type 6 (SCA6) and had herself received a definitive diagnosis of the same phenotype disease from genetic studies. The points of the ENG findings were as follows: (1) downbeat nystagmus was prominent in the primary eye position and was combined with gaze nystagmus in the lateral gaze; (2) both horizontal & vertical rebound nystagmus were noted; and (3) impairment of both horizontal & vertical smooth pursuit were seen. In horizontal and upward pursuit, catch-up saccades (lower gain) were intermingled. In contrast, backup-saccades (higher gain) were intermingled in downward pursuit. Furthermore, (4) Horizontal saccades were hypometric, though vertical saccades were hypermetric (overshoot); (5) In both horizontal and vertical OKN, the slow phase of OKN was severely impaired. Finally, (6) vestibular caloric nystagmus was well induced bilaterally. Both sides of visual suppression of caloric nystagmus were severely impaired.
　Most of present results are well explainable with the pure cerebellar cortical atrophy as the typical pathological finding of SCA6. However, two important findings should be mainly discussed and stressed here. One, the gain of the horizontal smooth pursuit was lower, while the gain of the downward pursuit was higher. It seemed to be inconsistent that a single part of the cerebellum would simultaneously modulate decreasing gain of the horizontal and increasing gain of vertical smooth pursuit systems. Therefore, this finding suggested that several parts, not a single part, of the cerebellum would be simultaneously engaged in the gain modulation of the smooth pursuit system. Second, the severe impairments of both horizontal and vertical OKN implied disturbances of both the pursuit and the velocity storage systems. In Cohen & Raphan's model, the slow phase of OKN is composed of the “direct pathway” and the “indirect pathway.” The “direct pathway” utilizes the ocular pursuit system in the flocculus/paraflocculus, while the “indirect pathway” is mediated through the velocity storage system in the medial vestibular nuclei/prepositus hypoglossi nuclei or the interstitial nuclei of Cajal in the brainstem. Consequently, the present results of OKN strongly suggested that the neural circuits related to the velocity storage integrator in the brainstem would also be perturbed, together with the disturbance of the ocular pursuit system in the cerebellum.

　Biofeedback is a technique in which individuals can use to learn to control their body functions and develop changes in behavior. Feedback intervention connected to electrical sensors provides patients with additional sensory information and leads to enhanced body performance. Based on the detected performance, visual, auditory, electrotactile and vibrotactile biofeedback could be provided to substitute for vestibular information and enhance balance control.
　The present clinical study investigated the effect of electrotactile biofeedback training with a vestibular substitution tongue device (VSTD) on refractory postural imbalance in 16 patients with unilateral vestibular loss. The VSTD transmits information on the head position to the brain through the tongue as substitutes for the lost vestibular information. The device's electrode array was placed on the tongue, and subjects were trained to maintain a centered body position by ensuring the electrical signals were sited in the center of their tongue. All subjects completed 10 minute training sessions two or three times per day for eight weeks and were followed-up over two years after the cessation of the training program to evaluate the long-term effect of the training.
　Balance functions involving postural stability and gait improved after the 8-week training period in all subjects. These improvements were maintained for up to 2 years even after the termination of the training program. Thus, short-term training with VSTD had beneficial long-term effects.
　It is suggested that a sensory substitution system using a human-machine interface which substitutes for diminished vestibular input can provide patients with additional sensory input to promote central compensation during the exercise.
　VSTD biofeedback training might be a useful rehabilitation therapy in subjects with persistent balance disorders and might lead to long-term improvements in their balance performance and ability to perform daily and social activities.

　Vestibular rehabilitation (VR) has been performed to improve the symptoms and function of patients with dizziness. However, autonomic symptoms such as nausea, sweating, shortness of breath, fatigue, flushing and anxiety during the rehabilitation process make it awkward for some patients to continue with rehabilitation. Anti-emetic or anti-anxiety drugs have been applied to dizzy patients to reduce the symptoms. However such drugs have been reported to delay vestibular compensation. Recently an approach involving heart rate variability biofeedback therapy (HRV-BF therapy) has been proved to be useful in cases of asthma, hypertension, anxiety disorder and post-traumatic stress disorder by strengthening autonomic function homeostasis including the vagal afferent pathway and baroreceptors. We therefore performed vestibular rehabilitation combined with HRV-BF therapy (VR with HRV-BF) in four dizzy patients with a unilateral vestibular disorder and with a high scores on the Dizziness Handicap Inventory (DHI) and Nijmegen Questionnaire for hyperventilation (NQH). VR with HRV-BF promptly reduced the subjective dizzy symptoms and improved the DHI and NQH scores. We believe that HRV-BF therapy may enhance the efficiency of VR for some patients with chronic dizziness.

　The peripheral vestibular organs sense angular and linear accelerations of the head, and help to maintain gaze and posture during head movements through the vestibulo-ocular and vestibulo-spinal reflexes. Bilateral vestibular dysfunction causes persistent imbalance and oscillopsia while moving the body or the head, and so far no effective treatments have been found for this condition except vestibular rehabilitation. We used noisy galvanic vestibular stimulation (noisy GVS), which was delivered as zero-mean current noise, of an imperceptible amplitude to improve postural performance in patients with bilateral vestibular dysfunction. We demonstrated that the application of noisy GVS for 30 sec significantly improved postural performance as measured by stabilometry in patients with bilateral vestibulopathy. We then examined the effect of noisy GVS on locomotion, and showed that it significantly increased the gait velocity and stride length, but significantly decreased the stride time in patients with vestibulopathy. Furthermore, to examine the effect of noisy GVS on vestibular function, we examined the effects of noisy GVS on ocular vestibular evoked myogenic potentials (oVEMP) in response to bone-conducted vibration (BCV). The noisy GVS increased the amplitude of oVEMP responses without affecting the latencies of oVEMP responses, suggesting that noisy GVS improves static and dynamic postural stability by enhancing the function of the vestibular afferents. Finally, we tested the long-term effects of noisy GVS on postural stability in elderly adults, and showed that noisy GVS can lead to a postural stability improvement that lasts for several hours after the cessation of the stimulus, probably via neuroplasticity. This newly discovered effect could contribute to an increase in the application of noisy GVS in appropriate patients.

　Rehabilitation for vestibular dysfunction patients has been performed through group exercise or home exercise with the aid of a pamphlet. We believe, however, that an individual rehabilitation program should be performed under the supervision of a clinician, because in the United States vestibular dysfunction patients are treated by clinicians in cooperation with a physical therapist. Thus, we must establish rehabilitation of vestibular dysfunction through pre-graduate, post-graduate, and lifelong education.
　Several years ago, we proposed a combination protocol of repetitive transcranial magnetic stimulation (rTMS) and intensive occupational therapy for upper limb hemiparesis after a stroke. Furthermore, our proposed combination protocol could be a potentially safe and useful therapeutic intervention for post-stroke upper limb hemiparesis. This combination protocol demonstrated that neural activation in the lesional hemisphere plays an important role in such recovery in poststroke hemiparetic patients together with functional MRI, and upper limb motor function improvement in post-stroke patients reflects evolution of brain perfusion in single-photon emission computed tomography. In addition, this method produced significant reduction of motor neuron excitability using neurophysiological studies including F-wave parameter measurements. It is our hope that this method can play a role in the treatment of the vestibular dysfunction patient in the clinical setting.

　The head impulse test (HIT) is a safe and quick way of assessing at the bedside semicircular canal function in patients with peripheral vestibular loss, first described in 1988. This test is practical even in sick patients and needs no equipment. The clinician identifies overt (=visible) catch-up saccades back to the target after passive head rotation as a clinical sign of canal paresis. However, it is known that some patients with absence of vestibular function do not make overt saccades, but instead make covert catch-up saccades during a passive unpredictable head turn, which are extremely difficult for the clinician to detect with the naked eye.
　In 2009, a new lightweight, nonslip, high-speed video-oculography system (vHIT; video head impulse test) was developed, that measures eye velocity during head rotations. This system is easy to use in a clinical setting, provides an objective measure of the vestibulo-ocular-reflex (VOR), and detects both overt and covert catch-up saccades in patients with vestibular loss.
　This article discusses the diagnostic values of vHIT which can evaluate both horizontal and vertical semicircular canal functions in patients with a variety of vestibular diseases.

　VEMP (vestibular evoked myogenic potential) testing was first reported at 1992. Since then, it has been developed as the examination for the otolith organs including the saccule and utricle. VEMPs are applicable to evaluate the following pathological conditions; endolymphatic hydrops, BPPV, vertigo due to otolith organs and dysfunction of the inferior vestibular nerve. By first comparing the amplitude of cVEMP before and after furosemide administration, we can detect the presence of endolymphatic hydrops in Meniere's disease and even in silent ear. More than 60% of patients with benign paroxysmal positional vertigo indicated abnormal oVEMP results. Residual dizziness after successful results of physiological therapy may related to the abnormal oVEMP results. Abnormal cVEMP results have been noted in more than 80% of cases with acoustic neurinomas. Inferior vestibular neuritis, which shows normal result on caloric testing, can be diagnosed with abnormal cVEMP and video head impulse testing (vHIT) results in the posterior semicircular canal. VEMP and vHIT testing complement each other. With both examinations, we can diagnose the functions of 5 peripheral vestibular organs.

　Video head impulse testing (vHIT), which can quantitatively evaluate semicircular canal function, has been gaining popularity. However, there are multiple types of devices in use even in Japan, and evaluation methods differ between institutions. We conducted and compared vHIT measurements of the lateral semicircular canal with EyeSeeCam VOG^® (EyeSeeCam) and ICS Impulse^® (ICS).
　We conducted vHIT using EyeSeeCam and ICS on 72 patients (37 females, 35 males; average age: 52.6 years [22-76 years]), diagnosed with ailments that could lead to unilateral peripheral vestibular disorders such as vestibular neuritis or unilateral acoustic neuroma. The results were evaluated using vHIT gain values from the affected and unaffected sides, as well as vHIT gain differences (|[unaffected side vHIT gain - affected side vHIT gain]|/[unaffected side vHIT gain+affected side vHIT gain]) and vHIT gain ratios (affected side vHIT gain/unaffected side vHIT gain).
　On comparing the lateral semicircular canal vHIT measurements conducted with ICS and EyeSeeCam, we found the results to have a high degree of concordance. Although the vHIT gain for the unaffected and affected sides was larger with EyeSeeCam, vHIT gain differences and gain ratios indicated no significant differences between the device types. Furthermore, vHIT gain differences and gain ratios were strongly correlated between device types, more so than gain measurements alone.
　Considering that multiple vHIT device types are presently in use, when comparing vHIT gain across different models, comparisons based on vHIT gain differences or gain ratios may be more useful than those based on gain values alone.