The cause of vertigo/dizziness varies. We may reduce vertigo/dizziness with a nutritional approach involving the circadian rhythm and chrononutrition. We can avoid hypoglycemia-mediated vertigo/dizziness by modulating the glucose intake. We can prevent anemia-mediated vertigo/dizziness through dietary supplementation with iron, copper, and vitamin C. Supplementary calcium and zinc are effective for the prevention of psychogenic vertigo/dizziness. In addition, it is effective to enforce a low salt diet at breakfast and lunch. The effective intake-time of calcium is about 1.5 hours before sleep. It is necessary to regulate one's lifestyle, and to prevent diabetes, high blood pressure, dyslipidemia and obesity. We can reduce vertigo/dizziness by preventing edema. A genetic investigation in conjunction with obesity is also necessary. A nutritional approach based on the results of a genetic analysis can be effective for prevention of obesity. Controlled eating habits through nutrition/dietetics can help in the prevention of vertigo/dizziness.

　Generally, the prognosis of vestibular neuronitis is considered favorable due to vestibular compensation. In cases where semicircular canal function is not restored, however, a floating sensation during body motion can persist for a long period. Cases of bilateral vestibular loss are especially intractable. The onset and course of bilateral vestibular neuronitis is similar to that of sequential type idiopathic bilateral vestibular hypofunction with multiple episodes of vertigo. In this study, we experienced a case of suspected bilateral vestibular neuronitis, with onset first in the left ear and then in the right. The patient was a 55-year-old man who visited our hospital with a chief complaint of a floating sensation persisting for more than 2 months after experiencing rotational vertigo. The patient showed direction-fixed right-beating horizontal nystagmus in all head positions without cochlear symptoms. According to the caloric test, a higher rate of decline in the vestibular function of the left ear was observed. Based on these findings, the patient was diagnosed as having left vestibular neuronitis. Although vestibular function in the left ear improved after vestibular rehabilitation, vestibular hypofunction appeared in the right ear approximately 4 years later, and we thought that bilateral vestibular neuronitis had developed in our patient. Oscillopsia was observed in the early stage, but disappeared after rehabilitation at the hospital. According to posturography findings, improvement was observed. Vestibular rehabilitation is considered important in order to recover vestibular function and promote compensation of the core function of the impaired vestibule.

　This study was aimed at investigating the morphological change and plasticity of the cupula and other vestibular cells in a model of mechanical rupture of the membranous labyrinth.
　Ten bullfrogs were used as study subjects. As in our previous reports, mechanical rupturing was accomplished by inserting a fine needle into the center of the saccule. The morphological change of the vestibular organs originated in an inflammatory change, and/or mixture of endolymph and perilymph which might be caused by rupturing. The vestibular membranous labyrinths were sectioned on 1-28 days after insult, and the degrees of cupula change were observed with the stereoscopic microscope. After the fixation and preparation of specimens for transmission electron microscopy (TEM), the ampullary and utricular sensory epithelium and ampullary dark cells were evaluated and compared with cupular changes. As controls, the vestibular organs on the opposite side were observed.
　Sensory epithelia and dark cells were impaired in the early stage, and those tended to recover thereafter. Morphologically, the epithelia recovered in 14 days after the insult, whereas dark cells needed 28 days for recovery. The cupulae did not change significantly within 3 days after insults. In the lateral semicircular canals, the cupulae were highly affected, and those of the posterior semicircular canals were less affected. As for the dark cells, there were no obvious differences between each canal.
　Morphological variations and possibilities of plasticity were seen in the vestibular organs with TEM observations, however, no obvious relationship between changes in the cupulae and vestibular cells was found. It is considered that the time lag of the damage development and recovery phase in each cell and cupula are responsible for this phenomenon. The change and plasticity of the cupula might be influenced by not only the anatomical features of the canals but also the degree of ampullary epithelial change.

　The study was conducted from April 19, 2016 ―three days after the occurrence Kumamoto earthquake― to May 14, 2016. The subjects were divided into three groups. Seventy-four subjects who reported dizziness that exacerbated after the earthquake and visited the hospital for a repeat checkup before the scheduled date were designated as the dizziness exacerbated group (+) after the earthquake group. Thirty-four subjects who had no previous history of dizziness and first experienced it after the earthquake were designated as dizziness developed after the earthquake group. Further, one-hundred and six subjects who did not show any exacerbation of dizziness after the earthquake and visited the hospital for dizziness checkup as scheduled, were designated as the dizziness exacerbated (-) after the earthquake group. The relationship between dizziness after the earthquake and kinetosis (motion sickness experienced in childhood or after becoming an adult) was studied. The results revealed that in the dizziness exacerbated (-) after the earthquake group a significant difference (P<0.001) was observed with respect to being less prone to motion sickness on reaching adulthood. The relationship between the susceptibility to motion sickness after becoming an adult, and dizziness exhibited after the earthquake was also studied. In a comparison between the dizziness exacerbated (-) after the earthquake group and dizziness exacerbated (+) after the earthquake group, the latter showed a significant difference (0.02<P<0.05) with respect to being susceptible to motion sickness after becoming an adult. Similarly, a comparison between the dizziness exacerbated (-) after the earthquake group and dizziness developed after the earthquake group, in the latter a significant difference (P<0.01) was observed with respect to being susceptible to motion sickness on reaching adulthood. The results suggested that the number of subjects who were susceptible to motion sickness in childhood and continued to be susceptible after becoming an adult was higher in the dizziness exacerbated (+) after the earthquake group and the dizziness developed after the earthquake group. The results also suggested that, more often than not, subjects who could not adapt well to vestibular stimulation, even after becoming adults, were more susceptible to developing dizziness after the earthquake.
　Various psychological tests were conducted on subjects to assess their psychological status on developing dizziness after the occurrence of the earthquake. In the dizziness exacerbated (+) after the earthquake group, the subjects exhibited neurosis (39.1%), autonomic imbalance (44.6%), psychosomatic disorders (31.1%), and depression (17.6%). Moreover, in the dizziness developed after the earthquake group the subjects exhibited neurosis (41.1%), autonomic imbalance (58.8%), psychosomatic disorders (29.4%), and depression (23.5%). The State-Trait Anxiety Inventory (STAI) test revealed that the state anxiety (64.9%) was significantly higher (0.001<p<0.01) than trait anxiety (40.5%) in dizziness exacerbated (+) after the earthquake group. However, in the dizziness developed after the earthquake group there was no significant difference between the state anxiety and the trait anxiety measures. With respect to dizziness after the earthquake and living environment, in both the dizziness exacerbated (+) after the earthquake group and dizziness developed after the earthquake group, it was observed that a significant number of subjects were living in cars or evacuation centers rather than living at home. The above results suggest that with respect to neurosis, autonomic imbalance, psychosomatic disorders, depression, and tendency of anxiety, appropriate counseling and drug therapy are necessary.
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　Middle ear overpressure treatment is one of the therapeutic methods for the patients with intractable Meniere's disease (MD). Based on the Japanese Clinical Guidelines for Meniere's Disease in 2011, when the medical treatment is not effective to improve vertiginous attacks in MD patients, the middle ear overpressure treatment is recommended before surgical and/or vestibular deafferentation treatment. There are two types of middle ear overpressure treatment; the transtympanic membrane massage (TMM) device and the Meniett device. In the middle ear overpressure treatment with the Meniett system, the tympanic membrane ventilation tube is indispensable, but it is unnecessary when treating with the TMM device. Most of the MD patients prefer the TMM device because it is less invasive. In this study, we presented a case in which the TMM device was not effective to cure the vertiginous attacks. On the other hand, the Meniett device was effective, suggesting that this might demonstrate a new idea of a step-wise procedure for middle ear overpressure treatment.

　Benign paroxysmal positional vertigo (BPPV) is caused by either canalolithiasis or cupulolithiasis. It is usually caused by involvement of the posterior and/or horizontal semicircular canal. The movement of otoconial debris in the semicircular canal causes vertigo and positional nystagmus when patients with BPPV move their head. In regard to the location of debris in the affected semicircular canal, by sequential movement of the patient's head during the canalith repositioning procedure (CRP) the debris moves from the semicircular canal to the utricle. Although BPPV resolves spontaneously, in patients with BPPV positional vertigo in patients treated with CRP was resolved more quickly than that in untreated patients. BPPV in the bilateral canals is difficult to be resolved because CRP for one side would move debris to the cupula in the other canal. In the occasional patient who has unremitting BPPV despite conservative treatment, semicircular canal occlusion may be effective in eliminating symptoms. In patients with posterior canal type of BPPV and in patients with lateral canal type of BPPV, head movement in the sagittal plane in both cases triggers vertigo. Therefore, to decrease movement in sagittal plane in daily life for patients with intractable BPPV, we should basically educate them how to avoid movement in sagittal plane. To avoid such movement when putting on shoes, the patients should avoid wearing shoes which require laces. When looking down, the patients should squat down, not bend at the waist and lower their head. When moving, e.g., when turning to look at something, the patients should move with their whole body, not move only their head.

　Some patients with uncompensated vestibular hypofunction present with a long history of persistent severe problems in posture and mobility that are intractable to any treatment.
　We examined whether graded vestibular balance rehabilitation would alleviate the dizziness and balance problems, and increase the safety and independence of patients with chronic balance disorders following unilateral vestibular loss. The stepwise treatment program for vestibular balance rehabilitation developed at our clinic consists of vestibular adaptation training (Step 1), sensory reweighing training (Step 2), and vestibular substitution training (Step 3). This rehabilitation program is intended at promoting the central vestibular adaptation process, altering the vestibular, visual and somatosensory inputs, and encouraging the use of the sensory substitution system with a human (brain)-machine interface as a substitute for the diminished vestibular input, for transmitting information about the patient's head position to the tongue. Clinical trials were performed to investigate the degree to which the stepwise multimodal approach might be effective for chronic balance disorder in subjects with unilateral decompensated vestibular loss. Some interventions for rehabilitation were selected and customized for each patient in accordance with the level of their compensation for postural control and sensory dependence.
　Improvements in the balance performance were noted in 64.4% of all the subjects after the Step 1 training. Of the 31 subjects (35.6%) who failed to improve with the step 1 program, 14 (45.2%) showed improvements after the Step 2 training. All of the subjects who failed to show improvement after the Step 1 and 2 training programs showed pronounced improvements after the Step 3 training.
　These results suggest that programmatic stepwise multimodal approach to vestibular rehabilitation yields beneficial effect in patients with balance disorder secondary to vestibular decompensation.

　Headaches are a similar physical complaint to dizziness that is a functional disorder and it is difficult to ascertain any physical abnormality in such subjects. In addition, both of the symptoms may be caused by a possible fatal illness. Headaches are quite common in healthy subjects and it is a common comorbid disorder with dizziness. We found out that 163 (40%) of 403 patients with intractable dizziness complained of some type of headache. So far the relationship between headache and dizziness has not been intensively investigated. One reason for this is that the physicians who are specialized in vestibular disorders usually focus on the dizzy symptom and do not have much interest in the comorbid headache in the same patient. Recently the relationship between migraine and dizziness has attracted more interest than before and the diagnostic criteria of vestibular migraine have been proposed by the ICHD (International Classification of Headache Disorders). It is important to have basic knowledge concerning headaches to understand the vestibular migraine. Migraine and tension type headaches are important primarily headache disorders. It is well known that the patients with migraine are at a higher risk of having dizziness as a complaint. When we treat the dizzy patients with headache, it is important to identify the type of the comorbid headache. The prophylactic treatment is more important than the acute treatment. The point is to promote the life style change and pharmacotherapy. The first line of medical treatment is a Ca blocker, such as lomerizine hydrochloride, followed by valproic acid, and amitriptyline. Collaboration with headache specialists is also an important strategy.

　The elderly with dizziness and disequilibrium have a higher risk of falls in comparison with the elderly without dizziness or disequilibrium. We should not, therefore, overlook the complaint of dizziness and disequilibrium in the elderly as aging effects. Also, disequilibrium and dizziness in the elderly are often intractable. It may be due to some factors, which are an aging-related functional decline of the sensory and motor organs, deterioration of the postural control system through the central nervous system, and anxiety and depression due to aging: these factors result in the increased morbidity of orthostatic hypotension (OH) with age and, polypharmacy by five or more medications. The score of the functional items on the Dizziness Handicap Inventory (DHI) increased in the late elderly aged more than 80 years old in our department, resulting in a decreased level of activities of daily living, the so-called “frailty”. Those elderly patients with OH showed more severe asymptomatic infarction of cerebral white matter lesions (WMLs) on MRI and most of them have been treated by five or more medications for a variety of diseases. The degree of the WNLs in the elderly patients with OH was correlated with the variance of the subjective visual vertical, which was associated with the spatial cognitional function. If the elderly patients with disequilibrium are frail, or in the prefrail stage, early intervention with vestibular exercise should be considered. When elderly patients meet the criteria for OH in the Schellong test, we should check their polypharmacy and should firstly treat them with non-pharmacologic interventions for the OH. Also, psychologic disorders, such as depression due to aging, often make the disequilibrium symptoms intractable or severe. We should initiate cooperation with other physicians, psychologists, and urologists for the treatment of the elderly with intractable disequilibrium. In conclusion, a holistic treatment approach is necessary for the elderly with intractable disequilibrium.