Background/Objectives: The vestibular labyrinth is classically viewed as a sensor of low-frequency head motion—linear acceleration for the otoliths and angular velocity/acceleration for the semicircular canals. However, there is now substantial evidence that air-conducted sound (ACS) can also activate vestibular receptors and afferents in mammals and other vertebrates. This sound sensitivity underlies sound-evoked vestibular-evoked myogenic potentials (VEMPs), sound-induced eye movements, and several clinical phenomena in third-window pathologies. The cellular and biophysical mechanisms by which a pressure wave in the cochlear fluids is transformed into a vestibular neural signal remain incompletely integrated into a single framework. This study aimed to provide a narrative synthesis of how ACS activates the vestibular labyrinth, with emphasis on (1) the anatomical and biophysical specializations of the maculae and cristae, (2) the dual-channel organization of vestibular hair cells and afferents, and (3) the encoding of fast, jerk-rich acoustic transients by irregular, striolar/central afferents.
Methods: We integrate experimental evidence from single-unit recordings in animals, in vitro hair cell and calyx physiology, anatomical studies of macular structure, and human clinical data on sound-evoked VEMPs and sound-induced eye movements. Key concepts from vestibular cellular neurophysiology and from the physics of sinusoidal motion (displacement, velocity, acceleration, jerk) are combined into a unified interpretative scheme.
Results: ACS transmitted through the middle ear generates pressure waves in the perilymph and endolymph not only in the cochlea but also in vestibular compartments. These waves produce local fluid particle motions and pressure gradients that can deflect hair bundles in selected regions of the otolith maculae and canal cristae. Irregular afferents innervating type I hair cells in the striola (maculae) and central zones (cristae) exhibit phase locking to ACS up to at least 1–2 kHz, with much lower thresholds than regular afferents. Cellular and synaptic specializations—transducer adaptation, low-voltage-activated K
+ conductances (K
LV), fast quantal and non-quantal transmission, and afferent spike-generator properties—implement effective high-pass filtering and phase lead, making these pathways particularly sensitive to rapid changes in acceleration, i.e., mechanical jerk, rather than to slowly varying displacement or acceleration. Clinically, short-rise-time ACS stimuli (clicks and brief tone bursts) elicit robust cervical and ocular VEMPs with clear thresholds and input–output relationships, reflecting the recruitment of these jerk-sensitive utricular and saccular pathways. Sound-induced eye movements and nystagmus in third-window syndromes similarly reflect abnormally enhanced access of ACS-generated pressure waves to canal and otolith receptors.
Conclusions: The vestibular labyrinth does not merely “tolerate” air-conducted sound as a spill-over from cochlear mechanics; it contains a dedicated high-frequency, transient-sensitive channel—dominated by type I hair cells and irregular afferents—that is well suited to encoding jerk-rich acoustic events. We propose that ACS-evoked vestibular responses, including VEMPs, are best interpreted within a dual-channel framework in which (1) regular, extrastriolar/peripheral pathways encode sustained head motion and low-frequency acceleration, while (2) irregular, striolar/central pathways encode fast, sound-driven transients distinguished by high jerk, steep onset, and precise spike timing.
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