Objective: To critically synthesize the available evidence on the pathophysiological variants of horizontal semicircular canal benign paroxysmal positional vertigo (HSC-BPPV) and to propose an integrative model based on otoconial location and cupular dynamics to explain their clinical presentation and therapeutic implications. Methods: A scoping review was conducted through a search of PubMed/MEDLINE, Scopus, and the Cochrane Library for studies published between January 1996 and May 2026. Studies describing pathophysiological variants, biomechanical mechanisms, nystagmus patterns, or therapeutic maneuvers in HSC-BPPV were included. A total of 26 studies met the inclusion criteria and underwent qualitative analysis. Results: Six principal mechanical configurations of horizontal canal positional vertigo were identified: long-arm canalolithiasis, short-arm canalolithiasis, canal-side cupulolithiasis, utricular-side cupulolithiasis, canalith jam, and light cupula. The available evidence suggests that these variants represent different mechanical states determined by otoconial location, otoconia-cupula interaction, canal obstruction, or alterations in cupula-endolymph density. This model explains the direction, intensity, and duration of positional nystagmus, the findings observed during the supine roll test and the bow and lean test, as well as the variability in response to repositioning maneuvers. A practical classification integrating pathophysiology, clinical findings, and treatment is proposed. Conclusions: HSC-BPPV may be more appropriately understood as a spectrum of mechanical states in which the configuration of otoconial debris and its interaction with the cupula influence the nystagmus pattern, clinical presentation, and therapeutic response. This integrative model may improve diagnostic accuracy and guide treatment selection, although prospective validation is required.

Vestibular short-latency evoked potentials (VsEPs) provide an objective measure of otolith-driven vestibular nerve activity but remain technically challenging to record when compared with cochlear evoked responses. This difficulty arises from the location of the vestibular system, in close proximity to the cochlea, which generates large biopotentials to similar stimuli. In experimental animal models, VsEPs are commonly recorded using far-field (FF) scalp electrodes, however the extent to which this approach faithfully reflects near-field (NF) recordings remains unclear. Here, we directly compare simultaneous NF facial nerve canal (FNC) VsEPs and FF scalp responses in vivo in the guinea pig in response to interaural bone-conducted vibration (BCV). NF VsEPs were recorded from within the FNC adjacent to the vestibular nerve bundle, while FF responses were recorded from the scalp. NF FNC VsEPs exhibited amplitudes roughly 20-fold larger, with SNR values approximately 10-15 dB higher than FF scalp responses across animals. NF responses revealed a ∼90% reduction during transient hypoxia and an almost complete abolition following tetrodotoxin application to the otolithic macula. In contrast, FF scalp VsEPs underestimated vestibular hypofunction and retained residual responses following neural blockade and death, consistent with non-neural origins. Micro-CT imaging of the guinea pig temporal bone confirmed the close anatomical proximity of the utricular macula to the FNC, providing the anatomical basis for the superior signal amplitude recorded at this site. Together, these findings demonstrate that NF FNC recordings provide a more sensitive and selective measure of peripheral vestibular nerve activity than FF scalp electrodes in the guinea pig, demonstrating the important need for optimising recording location and experimental controls when recording vestibular evoked potentials.

Following severe injury, most cells in the vestibular sensory epithelium undergo cell death, whereas the surviving epithelial cells initiate a repair program that leads to the formation of a flat epithelium (FE). However, the mechanisms underlying FE formation remain unclear. In this study, we combine in vivo and in vitro approaches to investigate the role of TGF-β signaling in this process. Our findings reveal dynamic changes in the expression of epithelial-mesenchymal transition (EMT) markers during FE formation, and a rapid activation of the TGF-β signaling pathway following injury. In vitro experiments show that exogenous application of TGF-β1 accelerates wound closure, whereas inhibition of TGF-β signaling with SB431542 delays wound healing. Mechanistically, we demonstrate that suppression of TGF-β signaling reduces the number of α-SMA-positive cells and downregulates the expression of mesenchymal markers. Conversely, activation of TGF-β signaling enhances the expression of EMT-associated transcription factors and mesenchymal markers. These results suggest that TGF-β signaling plays a critical role in regulating FE formation following severe damage to the utricular sensory epithelium, likely through the modulation of EMT.

The rat vestibular system plays a critical role in anti-gravity responses such as the tail-lift reflex and the air-righting reflex. In a previous study in male rats, we obtained evidence that these two reflexes depend on the function of non-identical populations of vestibular sensory hair cells (HC). Here, we caused graded lesions in the vestibular system of female rats by exposing the animals to several different doses of an ototoxic chemical, 3,3'-iminodipropionitrile (IDPN). After exposure, we assessed the anti-gravity responses of the rats and then assessed the loss of type I HC (HCI) and type II HC (HCII) in the central and peripheral regions of the crista, utricle and saccule. As expected, we recorded a dose-dependent loss of vestibular function and loss of HCs. The relationship between hair cell loss and functional loss was examined using non-linear models fitted by orthogonal distance regression. The results indicated that both the tail-lift reflex and the air-righting reflexes mostly depend on HCI function. However, a different dependency was found on the epithelium triggering the reflex: while the tail-lift response is sensitive to loss of crista and/or utricle HCIs, the air-righting response rather depends on utricular and/or saccular integrity.