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.

The semicircular canals are biomechanical sensors responsible for detecting and encoding angular motion of the head in 3D space. Canal afferent neurons provide essential inputs to neural circuits responsible for representation of self-position/orientation in space, and to compensatory circuits including the vestibulo-ocular and vestibulo-collic reflex arcs. In this work we derive, to our knowledge, a new 1D mathematical model quantifying canal biomechanics based on the morphology, dynamics of the inner ear fluids, and membranous labyrinth deformability. The model takes the form of a dispersive wave equation and predicts canal responses to angular motion, sound, and mechanical stimulation. Numerical simulations were carried out for the morphology of the human lateral canal using known physical properties of the endolymph and perilymph in three diverse conditions: surgical plugging, rotation, and mechanical indentation. The model reproduces frequency-dependent attenuation and phase shift in cases of canal plugging. During rotation, duct deformability extends the frequency bandwidth and enhances the high frequency gain. Mechanical indentation of the membranous duct at high frequencies evokes traveling waves that move away from the location of indentation and at low frequencies compels endolymph displacement along the canal. These results demonstrate the importance of the conformal perilymph-filled bony labyrinth to pressure changes and to high frequency sound and vibration.

Third window syndrome describes a set of vestibular and auditory symptoms that arise when a pathological third mobile window is present in the bony labyrinth of the inner ear. The pathological mobile window (or windows) adds to the oval and round windows, disrupting normal auditory and vestibular function by altering biomechanics of the inner ear. The most commonly occurring third window syndrome arises from superior semicircular canal dehiscence (SSCD), where a section of bone overlying the superior semicircular canal is absent or thinned (near-dehiscence). The presentation of SSCD syndrome is well characterized by clinical audiological and vestibular tests. In this review, we describe how the third compliant window introduced by a SSCD alters the biomechanics of the inner ear and thereby leads to vestibular and auditory symptoms. Understanding the biomechanical origins of SSCD further provides insight into other third window syndromes and the potential of restoring function or reducing symptoms through surgical repair.

The present study examined the efficacy of 5 MHz low-intensity focused ultrasound (LiFU) as a stimulus to remotely activate inner ear vestibular otolith organs. The otolith organs are the primary sensory apparati responsible for detecting orientation of the head relative to gravity and linear acceleration in three-dimensional space. These organs also respond to loud sounds and vibration of the temporal bone. The oyster toadfish, Opsanus tau, was used to facilitate unobstructed acoustic access to the otolith organs in vivo. Single-unit responses to amplitude-modulated LiFU were recorded in afferent neurons identified as innervating the utricle or the saccule. Neural responses were equivalent to direct mechanical stimulation, and arose from the nonlinear acoustic radiation force acting on the otolithic mass. The magnitude of the acoustic radiation force acting on the otolith was measured ex vivo. Results demonstrate that LiFU stimuli can be tuned to mimic directional forces occurring naturally during physiological movements of the head, loud air conducted sound, or bone conducted vibration.

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Background Non-invasive measurement of somatosensory-evoked potentials (SEP) in a large animal model is important to translational cognitive research. We sought to develop a methodology for neurophysiological recording via a transcranial electroencephalography (EEG) cap under an effective sedative regimen with dexmedetomidine, midazolam, and butorphanol that will produce sedation instead of anesthesia while not compromising data quality. Results Pigs received intramuscular dexmedetomidine, midazolam, and butorphanol for SEP assessment with peroneal nerve stimulation. Semi-quantitative sedation assessment was performed after the animal was sufficiently sedated and 30 min later, during the transcranial SEP recording. SEP data were analyzed with commercial software. Binary qualitative analysis of the recording was categorized by an experienced neurophysiologist. All four animals had adequate surface SEP recordings. Animals received 43 [21–47] mcg/kg of dexmedetomidine, 0.3 [0.2–0.3] mg/kg of midazolam, and 0.3 [0.3–0.3] mg/kg of butorphanol IM. All treatments resulted in moderate to deep sedation (Baseline median sedation score 11.5 [11–12]; median score at 30 min: 11.5 [10.5–12]). Heart rate (median [range]) (55 [49–71] beats per minute), respiratory rate (24 [21–30] breaths per minute), and hemoglobin oxygen saturation (99 [98–100]%) and body temperature (37.7 [37.4–37.9] °C) remained within clinically acceptable ranges. There were no undesirable recovery incidents. Conclusions In this pilot study, we demonstrate the feasibility of SEP recording via a transcranial EEG cap under an effective sedative regimen in pigs. Our approach will expand the use of a large animal model in neurotranslational research.