Abstract
Individuals suffering from Tullio phenomena experience dizziness, vertigo, and reflexive eye movements (nystagmus) when exposed to seemingly benign acoustic stimuli. The most common cause is a defect in the bone enclosing the vestibular semicircular canals of the inner ear. Surgical repair often corrects the problem, but the precise mechanisms underlying Tullio phenomenon are not known. In the present work we quantified the phenomenon in an animal model of the condition by recording fluid motion in the semicircular canals and neural activity evoked by auditory-frequency stimulation. Results demonstrate short-latency phase-locked afferent neural responses, slowly developing sustained changes in neural discharge rate, and nonlinear fluid pumping in the affected semicircular canal. Experimental data compare favorably to predictions of a nonlinear computational model. Results identify the biophysical origin of Tullio phenomenon in pathological sound-evoked fluid-mechanical waves in the inner ear. Sound energy entering the inner ear at the oval window excites fluid motion at the location of the defect, giving rise to traveling waves that subsequently excite mechano-electrical transduction in the vestibular sensory organs by vibration and nonlinear fluid pumping.
Highlights
Babylonian tablets scribed in the second millennium BC describe symptoms of vertigo, nystagmus, nausea and loss of balance – often disabling conditions attributed at the time to demonic possession rather than biology[1,2]
Simulations predict the presence of traveling waves (TW), propagating away from the location of dehiscence and toward the location of acoustic stimulation Po (See Supplemental Video 1)
Waves always traveled away from the dehiscence site and toward the pressure stimulus. This reverse propagation occurs because conservation of mass in the bony labyrinth forces the fluid displacement to be much larger near the small dehiscence relative to fluid displacement in the larger vestibule
Summary
Babylonian tablets scribed in the second millennium BC describe symptoms of vertigo, nystagmus, nausea and loss of balance – often disabling conditions attributed at the time to demonic possession rather than biology[1,2]. The third mobile window relieves pressure in the perilymph at the point of the fistula, thereby leading to a transmembrane pressure difference between endolymph and perilymph that can deform the membranous labyrinth, producing flow of endolymph that deflects sensory hair bundles in the SCC crista This mechanism likely contributes to pressure and low-frequency infrasound sensitivity[6,20], but cannot account for sustained responses of afferent neurons to auditory frequency sound, nor can it account for frequency dependence of the magnitude and direction of eye movements. In the present work we combine theory and experiment to examine the hypothesis that traveling waves in the vestibular labyrinth give rise to phase-locked afferent neural responses by vibrating sensory hair bundles cycle-by-cycle, and give rise to sustained changes in afferent discharge rate by frequency dependent pumping of endolymph. Results are consistent with mathematical analysis of nonlinear canal biomechanics and explain the origin of both sustained and transient vestibular responses in subjects suffering from Tullio phenomena
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