A small maintained electrical current passed between electrodes on the skin over each mastoid (galvanic vestibular stimulation: GVS) activates the vestibular system and elicits vestibular responses, such as sensations of rotation, eye movements and postural instability. GVS has been used to test both human and animal vestibular systems. It modulates the vestibular signal by increasing the firing rate of afferents on the cathodal side and decreasing the firing rate on the anodal side, causing standing subjects to sway towards the anodal side. Although the neuronal pathways activated by GVS have been well delineated, the generated behavioral responses vary among individuals, depending critically on specific aspects of both the stimulation and recording conditions. Galvanic body sway test (GBST) provides important information for differential diagnosis between inner ear and retro-labyrinthine disorders of the vestibular system. On the other hand, interpretation of nystagmus was difficult, because precise measurement of eye movements by electronystagmography was not feasible. However, with the recent development of video-oculography (VOG), it has become possible to carry out accurate recording and evaluation of nystagmus. Recent technological developments, including the use of improved VOG, might lead to the rediscovery of GVS as a research and diagnostic tool.

　The recent advent of next-generation sequencing has led to the identification of novel gene mutations that cause non-syndromic deafness, characterized by sensorineural hearing loss with or without vertigo as the sole symptom. As the molecular function and tissue expression of these deafness genes are unique to the cochleovestibular system, studies on the vestibular symptoms associated with these deafness gene mutations have led to a better understanding of the molecular mechanisms underlying the manifestation of peripheral vertigo/dizziness. We have compiled a comprehensive list of deafness genes associated with vestibular symptoms and non-syndromic deafness by reviewing the information deposited in the English literature and in the Deafness Gene Database (Hereditary Hearing Loss Homepage, the University of Iowa). Mutations of 23 deafness genes (KCNQ4, LMX1A, COCH, MYO7A, COL11A2, MYH9, KITLG, SLC12A2, SLC26A4, STRC, OTOG, USH1C, PCDH15, GRXCR1, ESPIN, MYO6, PJVK, PTPRQ, OTOGL, CLIC5, ROR1, ESRP1, POU3F4) are reported to be associated with clinical vestibular symptoms, radiologic vestibular anomalies, and/or abnormal results of vestibular function tests, such as the caloric test and rotatory chair test. Genes such as LMX1A, KITLG, SLC12A2, OTOGL, ROR1, and ESRP1 were identified as being associated with non-syndromic deafness and vestibular symptoms by means of whole-exome sequencing after 2010, when the molecular diagnosis of deafness by next-generation sequencing was first reported in the English literature. Tissue expressions of MYO7A, MYH9, STRC, USH1C, PCDH15, GRXCR1, ESPIN, MYO6, and CLIC5 have been found in the hair cells and have been recognized as playing roles in hair cell structures, such as the stereocilia. COL11A2, OTOG and OTOGL encode extracellular proteins of the otolithic membrane and tectorial membrane. COCH protein is the most inner ear-abundant protein specific to the perilymph fluid. These non-syndromic deafness genes play important roles in vestibular functions.

　We had previously presented the case of a 67-year-old woman with Arnold-Chiari malformation (type-I), who concurrently showed three different kinds of rebound nystagmus (RN) in the dark in a single electronystagmography (ENG) study; (i) rightward (leftward) nystagmus during rightward (leftward) gaze, followed by leftward (rightward) nystagmus upon returning to the primary position, (ii) rightward (leftward) nystagmus followed by reversed nystagmus in the opposite direction while rightward (leftward) gaze was still maintained, with the reversed leftward (rightward) nystagmus persisting even after return to the primary position, and (iii) scarce or no nystagmus on leftward (rightward) gaze and marked lateral nystagmus in the direction opposite to the preexisting deviation soon after return to the primary position. There are already reports in the literature of the first two kinds of RN, that is, (i) and (ii) above; however, the third type of RN ((iii) above) had never been reported in any other case. Recently, however, we encountered two other cases with the third type of RN. One was a case of multiple lacunar infarction in the dorsal pons and another was a case of a traumatic lesion of a cerebellar hemisphere (inferior semilunar lobule). The common findings of the ENG were as follows: (1) horizontal third type of RN in the dark; (2) while the vertical (upward) pursuit was a back-up (overshoot) saccadic pursuit, the horizontal pursuit was well-preserved; (3) The peak slow phase velocity of the OKN was slightly reduced, while the frequencies of the slow phase velocity of the OKN were preserved; (4) the OKAN were within normal limits.

　In general, RN is attributed to a smooth eye movement bias that is generated by both visual sources and non-visual sources, in order to oppose gaze-evoked centripetal drift of the eyes. In our cases, such a bias could have been generated only by non-visual sources, because the RN was observed in the dark, when visual sources are not operative. Although the origin of the non-visual sources are still obscure, efference copy, such as the eye velocity signal and/or eye position signal, is considered as a possible candidate.

　It is assumed that apparently no nystagmus was observed during lateral gaze, which would be resulted from gaze nystagmus was equally offset by RN each other. Although gaze nystagmus had already disappeared by the time of return to the primary position, RN was still preserved, derived from signal processing error of the efference copy because of cerebellar dysfunction.

　A 79-year-old man who was treated for malignant lymphoma presented with a history of dizziness and right ear fullness since February 2019. He developed right facial nerve palsy and visited our hospital a week later. At the time of his first consultation, his facial nerve palsy score was 4 points, according to the Yanagihara grading system, and a hearing test revealed acute right-sided mixed hearing loss. Temporal bone computed tomography revealed no obvious abnormalities, and magnetic resonance imaging revealed contrast findings enhancement in the bilateral internal auditory canals. He received a 10-day course of steroid infusion as treatment for the facial nerve palsy and acute sensorineural hearing loss. He developed dizziness and gait disorder 11 days after discharge. Cerebrospinal fluid cytology revealed central nervous system invasion by the malignant lymphoma. Caloric testing revealed bilateral loss of vestibular function. He was treated with whole-brain irradiation and intrathecal methotrexate injection three times. Post-treatment caloric testing revealed recovery of the left-sided vestibular function. Unfortunately, the patient died of progressive disease 7 months later. Whole-brain radiotherapy and intrathecal injections of anticancer drugs serve as useful palliative treatment for leptomeningeal carcinomatosis-induced balance disorder, particularly in patients with malignant lymphoma.

　Although posturography and motion capture system are useful to measure postural stability, they are difficult to transfer or setup. Because most tablet PCs are equipped with an accelerometer and storage media, they can measure and record motion in single units. In an attempt to identify a measuring system that would be excellent in portability and handiness, we investigated the usefulness of a tablet PC to measure the body stability. First, we assessed the properties of the accelerometer in four tablet PCs, as compared to an inertial sensor, the accuracy of which was known. We found that all the tablet PCs validated in this study had good accuracy, good linearity, and there were little inter-device differences. Then, we investigated whether the acceleration data obtained with the tablet PC could determine the postural stability in normal subjects. Except for 1 subject, who was an outlier, the acceleration data provided with the tablet PCs were significantly correlated with the Center of Position data. We consider that tablet PCs could be useful devices to measure the postural stability in humans.

　We report a case of chronic dizziness and frailty that improved with a combination of exercise and medical guidance.

　The patient was an elderly 77-year-old woman with a floating sensation and decreased activity due to chronic dizziness. Approximately one year after the onset of her symptoms, she was started on outpatient rehabilitation. At the beginning of the program, the VEMP (Vestibular Evoked Myogenic Potential) was unremarkable, the DHI (Dizziness Handicap Inventory) score was 54, the HADS (Hospital Anxiety and Depression Scale) score for anxiety/depression was 9/14, and the Kihon Check List (KCL) score was 11. These results suggested psychogenic dizziness and frailty.

　First, exercise therapy, including with a balance exercise assist robot (BEAR), was performed once a week for two months. BEAR is a training robot that manipulates back and forth shift and horizontal rotation by moving the center of gravity while playing a game. Previous studies have shown that BEAR exercises improve muscle strength and balance ability in frail older adults (Ozaki, 2017).

　Physical function (gait speed, muscle strength) improved after the intervention, but the dizziness and anxiety symptoms persisted. Then, medical guidance based on the Cognitive Behavioral Therapy Manual (Seki, 2016) was provided once a week for 2 months to listen to the person's thoughts and discuss how to respond. Finally, her DHI score improved to 38 points, the HADS score to 1/2, and the KCL score to 5, the dizziness and anxiety were reduced, and frailty improved.

　Improved physical functioning and reduced anxiety through exercise and medical guidance may have contributed to the improvement of the chronic dizziness and frailty in this patient. .

　We propose to continue to investigate more effective interventions and validate the indications.

　Inner ear malformations are rarely encountered, but are present in approximately 20% of the patients with congenital sensorineural hearing loss. At present, hearing aids and cochlear implantation are considered as effective treatments for hearing loss associated with inner ear malformations. Therefore, classification of inner ear malformations is based on the cochlear anatomy from a therapeutic point of view. On the other hand, few studies have reported on the vestibular functions of patients with inner ear malformations. We administered a detailed vestibular test battery to a patient with inner ear malformations, and found an occult response on the vHIT, delivered under the absence of the corresponding semi-circular canal.

　A 26-year-old female patient presented with a history of hearing loss in her left ear since childhood. MRI revealed only a hypoplastic vestibule, with no evident cochlea or semicircular canals in the left inner ear. Although impulses toward the left lateral and left posterior canals elicited reduced VOR (vestibulo-ocular reflex) gains on vHIT (video head impulse test), as expected, an impulse toward the left anterior canal triggered complete VOR gain. The discrepancies between the anatomical findings and the results of functional examination in this case are discussed.

　Vestibular function of the inner ear malformations is an important topic that needs to be clarified. With diagnostic imaging and vestibular function tests having become more and more advanced in recent years, further accumulation and study of cases of inner ear malformations are warranted in the future.

　There are two types of psychogenic dizziness, the narrowly defined type (pure) and the type with a broader definition. The narrow one refers to pure psychotic dizziness, which is a manifestation of underlying psychiatric disorders, including major depression, anxiety disorder, and somatoform disorder. The latter refers to the symptom mainly arising from vestibular dysfunction, and comorbid psychiatric disorders could modify or cause further deterioration of the severity of dizziness. There are no objective examinations for the diagnosis of psychogenic dizziness. The important steps for the diagnosis are a precise evaluation of the vestibular functions as well as a precise psychiatric evaluation. Questionnaires, including the Japanese version of the Dizziness Handicap Inventory and Japanese version of the Hospital Anxiety and Depression Scale, are useful for the psychiatric evaluation. The characteristic “tear drop” type gravichart in posturography may be useful to define the type of psychogenic dizziness. Kamikihito is one of the herbal drugs originally prescribed for patients with insomnia, anxiety, neuralgia, or anemia. Kamikihito is considered as an anxiolytic in herbal medicine. Patients with psychogenic dizziness can be treated with kamikihito. The dizzy patients who already prescribed benzodiazepines, and patients. Patients with psychogenic dizziness who show poor response to benzodiazepines are potential candidates for treatment with kamikihito. The possible indications for kamikihito are discussed in the text.