Dizziness and imbalance are amongst the most common complaints in older people, and are a growing public health concern since they put older people at a significantly higher risk of falling. Although the causes of dizziness in older people are multifactorial, peripheral vestibular dysfunction is one of the most frequent causes. Benign paroxysmal positional vertigo is the most frequent form of vestibular dysfunction in the elderly, followed by Meniere's disease. Every factor associated with the maintenance of postural stability deteriorates during aging. Age-related deterioration of peripheral vestibular function has been demonstrated through quantitative measurements of the vestibulo-ocular reflex with rotational testing and of the vestibulo-collic reflex with testing of vestibular evoked myogenic potentials. Age-related decline of vestibular function has been shown to correlate with the age-related decrease in the number of vestibular hair cells and neurons. The mechanism of age-related cellular loss in the vestibular endorgan is unclear, but it is thought that genetic predisposition and cumulative effect of oxidative stress may both play an important role. Since the causes of dizziness in older people are multi-factorial, management of this disease should be customized according to the etiologies of each individual. Vestibular rehabilitation is found to be effective in treating both unilateral and bilateral vestibular dysfunction. Various prosthetic devices have also been developed to improve postural balance in older people. Although there have been no medical treatments improving age-related vestibular dysfunction, new medical treatments such as mitochondrial antioxidants or caloric restriction, which have been effective in preventing age-related hearing loss, should be ienvestigated in the future.

Vestibular dysfunction causes postural instability, which is prevalent in the elderly. We previously showed that an imperceptible level of noisy galvanic vestibular stimulation (nGVS) can improve postural stability in patients with bilateral vestibulopathy during the stimulus, presumably by enhancing vestibular information processing. In this study, we investigated the after-effects of an imperceptible long-duration nGVS on body balance in elderly adults. Thirty elderly participants underwent two nGVS sessions in a randomised order. In Session 1, participants received nGVS for 30 min twice with a 4-h interval. In Session 2, participants received nGVS for 3 h. Two-legged stance tasks were performed with eyes closed while participants stood on a foam rubber surface, with and without nGVS, and parameters related to postural stability were measured using posturography. In both sessions, the postural stability was markedly improved for more than 2 h after the cessation of the stimulus and tended to decrease thereafter. The second stimulation in Session 1 caused a moderate additional improvement in body balance and promoted the sustainability of the improvement. These results suggest that nGVS can lead to a postural stability improvement in elderly adults that lasts for several hours after the cessation of the stimulus, probably via vestibular neuroplasticity.

Patients with bilateral vestibulopathy (BV) suffer from persistent postural imbalance, leading to a marked decrease in quality of life and a higher risk of falls. However, so far, the effective treatments for BV are very limited. We examined whether long-term noisy galvanic vestibular stimulation (nGVS) keeps improving body balance after the cessation of the stimulus in BV patients. Thirteen BV patients received nGVS for 30 min with a lower intensity than the intensity at which they feel any cutaneous sensations, and their postural movement was monitored for 6 h after the stimuli. The same session was repeated at 14-day intervals. Stance tasks on two legs were performed with eyes closed. The velocity of the center of pressure (COP) movement, the area enclosed by the COP movement, and the root mean square of the displacement of the COP were measured. The power spectrum of the COP movement was assessed. Subjective improvement of body balance was graded as worsened (−2), slightly worsened (−1), unchanged (0), slightly improved (+1) and improved (+2) in comparison with that without nGVS. In each session, the velocity of the COP movement was significantly improved for 6 h after the stimulus had ceased (P < 0.01). Concomitantly, the mean frequency of the COP power spectrum was significantly reduced in the anterior-posterior axis (P < 0.05). Subjective symptoms of imbalance were improved during the post-stimulation effect (P < 0.05). nGVS leads to an improvement in body balance that lasts for several hours after the end of the stimulus in BV patients with a reduction in the high-frequency components of their postural movement. This trial was registered with the University Hospital Medical Information Network (UMIN) Clinical Trials Registry (UMINCTR: UMIN000028054).

Idiopathic sudden hearing loss (ISHL) is commonly defined as a severe sensorineural hearing loss of sudden onset and unknown etiology. The annual incidence of ISHL is estimated at approximately 10 cases/100 000 population.¹ Although a number of different pathologic processes might result in sudden hearing loss, it is widely believed that viral infection,² vascular obstruction,³ and cochlear membrane breaks⁴ account for most ISHL cases. Of these, a viral cause is thought to be the most common.

Individual primary vestibular afferents exhibit spontaneous activity the regularity of which can vary from regular to irregular. Different aspects of vestibular responsiveness have been associated with this dimension of regularity of resting discharge. Isolated rat vestibular ganglion cells (VGCs) showed heterogeneous intrinsic firing properties during sustained membrane depolarization: some neurons exhibited a strong adaptation generating just a single or a few spikes (phasic type), whereas other neurons showed moderate adaptation or tonic firing (tonic type). Tonic discharging VGCs were rare at postnatal days 5–7 and increased up to ∼60% of neurons during postnatal 2–3 wk. To explore the major factors responsible for the discharge regularity of primary vestibular afferents, we investigated the contribution of K⁺channels to the firing properties of isolated rat VGCs. Phasic firing became tonic firing in the presence of 4-aminopyridine or α-dendrotoxin, indicating that Kv1 potassium channels control the firing pattern of the phasic VGCs. Tetraethylammonium decreased the number of spikes during step current stimuli in all types. Blockade of Ca²⁺-activated K⁺channels decreased the number of spikes in tonic VGCs. Our results suggest that Kv1 channels are critical both in determining the pattern of spike discharge in rat vestibular ganglion neurons and in their proportional change during maturation.