Objective: To examine the effect of an imperceptible level of galvanic vestibular stimulation (GVS), delivered as zero-mean current noise (noisy GVS), on postural performance in healthy subjects as well as in patients with bilateral peripheral vestibular dysfunction. Methods: White noise GVS with an amplitude ranging from 0 to 1,000 μA was applied in 21 healthy subjects and 11 patients with bilateral vestibular dysfunction. Two-legged stance tasks were performed with the eyes closed during a 60-second period, which consisted of a baseline period without stimulation and a stimulation period with GVS. We examined 3 parameters: the velocity, the envelopment area, and the root mean square (RMS) of the center of pressure. Results: White noise GVS improved all 3 parameters in 76% of healthy subjects. The amplitude of the optimal stimulus was 281 ± 40 μA, and it improved the velocity, area, and RMS by 18.4% ± 2%, 37.9% ± 3.5%, and 20.4% ± 2.2%, respectively (p < 0.01). The GVS improved all 3 parameters in 91% of patients. The amplitude of the optimal stimulus was 456 ± 82 μA, and it improved the velocity, area, and RMS by 29.4% ± 4.9%, 45.6% ± 4.7%, and 22% ± 3.3%, respectively (p < 0.01). Conclusions: Noisy GVS is effective in improving postural stability in healthy subjects as well as in patients with bilateral vestibular dysfunction. Classification of evidence: This study provides Class IV evidence that in patients with bilateral vestibular dysfunction, an imperceptible level of noisy GVS may improve postural stability.

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.

Although it is well known that injury induces the generation of a substantial number of new olfactory sensory neurons (OSNs) in the adult olfactory epithelium (OE), it is not well understood whether olfactory sensory input influences the survival and maturation of these injury-induced OSNs in adults. Here, we investigated whether olfactory sensory deprivation affected the dynamic incorporation of newly generated OSNs 3, 7, 14, and 28 d after injury in adult mice. Mice were unilaterally deprived of olfactory sensory input by inserting a silicone tube into their nostrils. Methimazole, an olfactotoxic drug, was also injected intraperitoneally to bilaterally ablate OSNs. The OE was restored to its preinjury condition with new OSNs by day 28. No significant differences in the numbers of olfactory marker protein-positive mature OSNs or apoptotic OSNs were observed between the deprived and nondeprived sides 0–7 d after injury. However, between days 7 and 28, the sensory-deprived side showed markedly fewer OSNs and mature OSNs, but more apoptotic OSNs, than the nondeprived side. Intrinsic functional imaging of the dorsal surface of the olfactory bulb at day 28 revealed that responses to odor stimulation were weaker in the deprived side compared with those in the nondeprived side. Furthermore, prevention of cell death in new neurons 7–14 d after injury promoted the recovery of the OE. These results indicate that, in the adult OE, sensory deprivation disrupts compensatory OSN regeneration after injury and that newly generated OSNs have a critical time window for sensory-input-dependent survival 7–14 d after injury.

Objectives/Hypothesis: Intracellular entry of severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) depends on the interaction between its spike protein with the cellular receptor angiotensin‐converting enzyme 2 (ACE2) and depends on Furin‐mediated spike protein cleavage and spike protein priming by host cell proteases, including transmembrane protease serine 2 (TMPRSS2). As the expression of ACE2, TMPRSS2, and Furin in the middle and inner ear remain unclear, we analyzed the expression of these proteins in mouse ear tissues.Study Design: Animal Research.Methods: We performed immunohistochemical analysis to examine the distribution of ACE2, TMPRSS2, and Furin in the Eustachian tube, middle ear spaces, and cochlea of mice.Results: ACE2 was present in the nucleus of the epithelium of the middle ear and Eustachian tube, as well as in some nuclei of the hair cells in the organ of Corti, in the stria vascularis, and the spiral ganglion cells. ACE2 was also expressed in the cytoplasm of the stria vascularis. TMPRSS2 was expressed in both the nucleus and cytoplasm in the middle spaces, with the expression being stronger in the nucleus in the mucosal epithelium of the middle ear spaces and Eustachian tube. TMPRSS2 was present in the cytoplasm in the organ of Corti and stria vascularis and in the nucleus and cytoplasm in the spiral ganglion. Furin was expressed in the cytoplasm in the middle ear spaces, Eustachian tube, and cochlea.Conclusions: ACE2, TMPRSS2, and Furin are diffusely present in the Eustachian tube, middle ear spaces, and cochlea, suggesting that these tissues are susceptible to SARS‐CoV‐2 infection.Level of Evidence: NA Laryngoscope, 131:E2013–E2017, 2021