To develop and validate a simple questionnaire for the diagnosis of Benign Paroxysmal Positional Vertigo (BPPV) and also to accurately predict the involved side in BPPV. Patients (N = 148) who presented with dizziness to the ENT department were asked to fill out a questionnaire which was formulated to diagnose BPPV and the affected side. Five questions were part of the questionnaire. The fifth question was set to ascertain the affected side in BPPV. All the patients underwent a detailed neuro-otological examination and the findings were noted. The findings of the examination were correlated with the questionnaire findings. The mean age of the patient group was 54.72 years of age. The sensitivity of the questionnaire in detecting BPPV was 94.5%, though in 12.79% (n = 11) the side was not predicted correctly. The specificity of the questionnaire was 91.22%. The positive predictive value of the questionnaire in detecting BPPV was assessed at 94.5%.The questionnaire can be effectively used in predicting BPPV amongst patients presenting with dizziness and thus helps in avoiding unnecessary imaging and referrals to higher centres in view of suspicion of central causes of dizziness.

Carexduanensis Z.C.Lu, Y.F.Lu & X.F.Jin, a new species in limestone areas of Guangxi, China, was discovered and described. The morphology showed that C.duanensis is similar to C.calcicola, but differs in having culms central, leaf blades 3-5.5 mm wide, bracts longer than spikes, utricles 4-5 mm long, shorter, and nutlets abruptly contracted into an erect beak at apex. SEM microphotographs of utricles and nutlets are provided for the new and related species, C.calcicola.

Tmc1 and Tmc2 are essential pore-forming subunits of mechanosensory transduction channels localized to the tips of stereovilli in auditory and vestibular hair cells of the inner ear. To investigate expression and function of Tmc1 and Tmc2 in vestibular organs, we used quantitative polymerase chain reaction (qPCR), fluorescence in situ hybridization - hairpin chain reaction (FISH-HCR), immunostaining, FM1-43 uptake and we measured vestibular evoked potentials (VsEPs) and vestibular ocular reflexes (VORs). We found that Tmc1 and Tmc2 showed dynamic developmental changes, differences in regional expression patterns, and overall expression levels which differed between the utricle and saccule. These underlying changes contributed to unanticipated phenotypic loss of VsEPs and VORs in Tmc1 KO mice. In contrast, Tmc2 KO mice retained VsEPs despite the loss of the calcium buffering protein calretinin, a characteristic biomarker of mature striolar calyx-only afferents. Lastly, we found that neonatal Tmc1 gene replacement therapy is sufficient to restore VsEP in Tmc1 KO mice for up to six months post-injection.

One-sided vestibular disorders are common in clinical practice; however, their models have not been fully established. We investigated the effect of unilateral or bilateral deficits in the vestibular organs on the vestibulo-ocular reflex (VOR) and optokinetic reflex (OKR) of zebrafish using in-house equipment. For physical dislodgement of the otoliths in the utricles of zebrafish larvae, one or both utricles were separated from the surrounding tissue using glass capillaries. The video data from VOR and OKR tests with the larvae was collected and processed using digital signal processing techniques such as fast Fourier transform and low-pass filters. The results showed that unilateral and bilateral damage to the vestibular system significantly reduced VOR and OKR. In contrast, no significant difference was observed between unilateral and bilateral damage. This study confirmed that VOR and OKR were significantly reduced in zebrafish with unilateral and bilateral vestibular damage. Follow-up studies on unilateral vestibular disorders can be conducted using this tool.

Nestin expression is associated with pluripotency. Growing evidence suggests nestin is involved in hair cell development. The objective of this study was to investigate the morphology and role of nestin-expressing cells residing in the early postnatal murine inner ear. A lineage-tracing nestin reporter mouse line was used to further characterize these cells. Their cochleae and vestibular organs were immunostained and whole-mounted for cell counting. We found Nestin-expressing cells present in low numbers throughout the inner ear. Three morphotypes were observed: bipolar, unipolar, and globular. Mitotic activity was noted in nestin-expressing cells in the cochlea, utricle, saccule, and crista. Nestin-expressing cell characteristics were then observed after hair cell ablation in two mouse models. First, a reporter model demonstrated nestin expression in a significantly higher proportion of hair cells after hair cell ablation than in control cochleae. However, in a lineage tracing nestin reporter mouse, none of the new hair cells which repopulated the organ of Corti after hair cell ablation expressed nestin, nor did the nestin-expressing cells change in morphotype. In conclusion, Nestin-expressing cells were identified in the cochlea and vestibular organs. After hair cell ablation, nestin-expressing cells did not react to the insult. However, a small number of nestin-expressing cells in all inner ear tissues exhibited mitotic activity, supporting progenitor cell potential, though perhaps not involved in hair cell regeneration.

The biochemistry of diabetes mellitus results in multi-system tissue compromise that reduces functional mobility and interferes with disease management. Sensory system compromise, such as peripheral neuropathy and retinopathy, are specific examples of tissue compromise detrimental to functional mobility. There is lack of clarity regarding if, when, and where parallel changes in the peripheral vestibular system, an additional essential sensory system for functional mobility, occur as a result of diabetes. Given the systemic nature of diabetes and the plasticity of the vestibular system, there is even less clarity regarding if potential vestibular system changes impact functional mobility in a meaningful fashion. This commentary will provide insight as to when we should employ diagnostic vestibular function tests in people with diabetes, where in the periphery we should look, and why testing may or may not matter. The commentary concludes with recommendations for future research and clinical care.

In mammals, spatial orientation is synaptically-encoded by sensory hair cells of the vestibular labyrinth. Vestibular hair cells (VHCs) harbor synaptic ribbons at their presynaptic active zones (AZs), which play a critical role in molecular scaffolding and facilitate synaptic release and vesicular replenishment. With advancing age, the prevalence of vestibular deficits increases; yet, the underlying mechanisms are not well understood and the possible accompanying morphological changes in the VHC synapses have not yet been systematically examined. We investigated the effects of maturation and aging on the ultrastructure of the ribbon-type AZs in murine utricles using various electron microscopic techniques and combined them with confocal and super-resolution light microscopy as well as metabolic imaging up to 1 year of age. In older animals, we detected predominantly in type I VHCs the formation of floating ribbon clusters, mostly consisting of newly synthesized ribbon material. Our findings suggest that VHC ribbon-type AZs undergo dramatic structural alterations upon aging.

Static high magnetic fields (MFs) interact with the vestibular system of humans and rodents. In rats and mice, exposure to MFs causes perturbations such as head movements, circular locomotion, suppressed rearing, nystagmus, and conditioned taste aversion acquisition. To test the role of otoconia, two mutant mouse models were examined, head-tilt Nox3het (het) and tilted Otop1 (tlt), with mutations, respectively, in Nox3, encoding the NADPH oxidase 3 enzyme, and Otop1, encoding the otopetrin 1 proton channel, which are normally expressed in the otolith organs, and are critical for otoconia formation. Consequently, both mutants show a near complete loss of otoconia in the utricle and saccule, and are nonresponsive to linear acceleration. Mice were exposed to a 14.1 Tesla MF for 30 min. After exposure, locomotor activity, conditioned taste aversion and c-Fos (in het) were assessed. Wild-type mice exposed to the MF showed suppressed rearing, increased latency to rear, locomotor circling, and c-Fos in brainstem nuclei related to vestibular processing (prepositus, spinal vestibular, and supragenual nuclei). Mutant het mice showed no response to the magnet and were similar to sham animals in all assays. Unlike het, tlt mutants exposed to the MF showed significant locomotor circling and suppressed rearing compared with sham controls, although they failed to acquire a taste aversion. The residual responsiveness of tlt versus het mice might reflect a greater semicircular deficit in het mice. These results demonstrate the necessity of the otoconia for the full effect of exposure to high MFs, but also suggest a semicircular contribution.

The otolith end organs inform the brain about gravitational and linear accelerations, driving the otolith-ocular reflex (OOR) to stabilize the eyes during translational motion (e.g., moving forward without rotating) and head tilt with respect to gravity. We previously characterized OOR responses of normal chinchillas to whole body tilt and translation and to prosthetic electrical stimulation targeting the utricle and saccule via electrodes implanted in otherwise normal ears. Here we extend that work to examine OOR responses to tilt and translation stimuli after unilateral intratympanic gentamicin injection and to natural/mechanical and prosthetic/electrical stimulation delivered separately or in combination to animals with bilateral vestibular hypofunction after right ear intratympanic gentamicin injection followed by surgical disruption of the left labyrinth at the time of electrode implantation. Unilateral intratympanic gentamicin injection decreased natural OOR response magnitude to about half of normal, without markedly changing OOR response direction or symmetry. Subsequent surgical disruption of the contralateral labyrinth at the time of electrode implantation surgery further decreased OOR magnitude during natural stimulation, consistent with bimodal-bilateral otolith end organ hypofunction (ototoxic on the right ear, surgical on the left ear). Delivery of pulse frequency- or pulse amplitude-modulated prosthetic/electrical stimulation targeting the left utricle and saccule in phase with whole body tilt and translation motion stimuli yielded responses closer to normal than the deficient OOR responses of those same animals in response to head tilt and translation alone.NEW & NOTEWORTHY Previous studies to expand the scope of prosthetic stimulation of the otolith end organs showed that selective stimulation of the utricle and saccule is possible. This article further defines those possibilities by characterizing a diseased animal model and subsequently studying its responses to electrical stimulation alone and in combination with mechanical motion. We show that we can partially restore responses to tilt and translation in animals with unilateral gentamicin ototoxic injury and contralateral surgical disruption.

UNASSIGNED: To review the history and pathophysiologic theories for cupulolithiasis and canalith jam in benign paroxysmal positional vertigo.
UNASSIGNED: PubMed, Google Scholar.
UNASSIGNED: Three PubMed and Google Scholar searches were performed, keywords: \"cupulolithiasis,\" \"apogeotropic [and] benign,\" and \"canalith jam,\" resulting in 187 unique full-text articles in English or with English translation. Figures-Labyrinthine photographs were obtained of fresh utricles, ampullae, and cupulae of a 37-day-old mouse.
UNASSIGNED: Freely moving otoconial masses explain most cases (>98%) of benign paroxysmal positional vertigo. Evidence that otoconia adhere strongly or persistently to the cupula is lacking. Apogeotropic nystagmus in the horizontal canal form is often attributed to cupulolithiasis; however, periampullary canalithiasis explains self-limited nystagmus, and reversible canalith jam explains prolonged apogeotropic nystagmus. Treatment-resistant cases can be explained by entrapment of particles in the canals or ampullae, but persistent adherence to the cupula remains theoretical.
UNASSIGNED: Apogeotropic nystagmus is usually due to freely moving particles and should not be used in studies of horizontal canal benign paroxysmal positional vertigo as the sole method to define entrapment or cupulolithiasis. Caloric testing and imaging may help differentiate jam from cupulolithiasis. Treatment for apogeotropic benign paroxysmal positional vertigo should include maneuvers that rotate the head through 270° to fully clear the canal of mobile particles, using mastoid vibration or head shaking if entrapment is suspected. Canal plugging can be used for treatment failures.