Vestibular Implant Imaging.

Analogous to hearing restoration via cochlear implants, vestibular function could be restored via vestibular implants that electrically stimulate vestibular nerve branches to encode head motion. This study presents the technical feasibility and first imaging results of CT for vestibular implants in 8 participants of the first-in-human Multichannel Vestibular Implant Early Feasibility Study. Imaging characteristics of 8 participants (3 men, 5 women; median age, 59.5 years; range, 51-66 years) implanted with a Multichannel Vestibular Implant System who underwent a postimplantation multislice CT (n = 2) or flat panel CT (n = 6) are reported. The device comprises 9 platinum electrodes inserted into the ampullae of the 3 semicircular canals and 1 reference electrode inserted in the common crus. Electrode insertion site, positions, length and angle of insertion, and number of artifacts were assessed. Individual electrode contacts were barely discernible in the 2 participants imaged using multislice CT. Electrode and osseous structures were detectable but blurred so that only 12 of the 18 stimulating electrode contacts could be individually identified. Flat panel CT could identify all 10 electrode contacts in all 6 participants. The median reference electrode insertion depth angle was 9° (range, -57.5° to 45°), and the median reference electrode insertion length was 42 mm (range, -21-66 mm). Flat panel CT of vestibular implants produces higher-resolution images with fewer artifacts than multidetector row CT, allowing visualization of individual electrode contacts and quantification of their locations relative to vestibular semicircular canals and ampullae. As multichannel vestibular implant imaging improves, so will our understanding of the relationship between electrode placement and vestibular performance.

Combined ionic direct current and pulse frequency modulation improves the dynamic range of vestibular canal stimulation.

BACKGROUND: Vestibular prostheses emulate normal vestibular function by electrically stimulating the semicircular canals using pulse frequency modulation (PFM). Spontaneous activity at the vestibular nerve may limit the dynamic range elicited by PFM. One proposed solution is the co-application of ionic direct current (iDC) to inhibit this spontaneous activity. OBJECTIVE: We aimed to test the hypothesis that a tonic iDC baseline delivered in conjunction with PFM to the vestibular semicircular canals could improve the dynamic range of evoked eye responses. METHODS: Gentamicin-treated chinchillas were implanted with microcatheter electrodes in the vestibular semicircular canals through which pulsatile and iDC current was delivered. PFM was used to modulate vestibulo-ocular reflex (VOR) once it was adapted to a preset iDC and pulse-frequency baseline. Responses to stimulation were assessed by recording the evoked VOR eye direction and velocity. RESULTS: PFM produced VOR responses aligned to the stimulated canal. Introduction of an iDC baseline lead to a small but statistically significant increase in eye response velocity, without influencing the direction of eye rotation. CONCLUSIONS: Tonic iDC baselines increase the dynamic range of encoding head velocity evoked by pulsatile stimulation, potentially via the inhibition of spontaneous activity in the vestibular nerve.

Sound abnormally stimulates the vestibular system in canal dehiscence syndrome by generating pathological fluid-mechanical waves.

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.

Penlight-cover test: a new bedside method to unmask nystagmus.

BACKGROUND: Most patients with acute vestibular syndrome have vestibular neuritis or labyrinthitis. Some harbour strokes that can only be differentiated on the basis of subtle eye movement findings, including nystagmus. Peripheral nystagmus should be enhanced by removal of visual fixation. Current bedside methods for removing fixation require expensive equipment or technical skill not routinely available. We sought to test a new method for blocking fixation. METHODS: Proof-of-concept study for a new bedside oculomotor diagnostic test using an established physiological measurement of eye movements (electro-oculography (EOG)) as the reference standard. We sampled unselected patients undergoing caloric testing (surrogate model for neuritis) in an academic vestibular clinic. During the brief (30-60 s) decay phase of caloric-induced peripheral vestibular nystagmus, we shone a penlight in the left eye while intermittently occluding the right. We assessed nystagmus intensity (slow-phase velocity) clinically in all subjects and quantified change in two exemplar cases. RESULTS: Caloric responses frequently decayed before the test was complete, and artefacts rendered many EOGs uninterpretable during the short decay period. A clinically evident increase in nystagmus was seen 18 times in 10 patients and corroborated by EOG in 15. In quantified cases, slow-phase velocity increased as expected (mean change +42%) with fixation blocked. CONCLUSION: The penlight-cover test could offer a low-cost, simple means of disrupting visual fixation in clinical settings where differentiating peripheral from central vestibular disorders is crucial, such as the emergency department. Prospective studies are needed to determine the test's utility for excluding dangerous central causes among patients with suspected peripheral lesions.

Development of a biophysical model for vestibular prosthesis research.

Physiologic properties of primary vestibular neurons are compared and contrasted with properties of primary auditory neurons. The differences and similarities suggest possible coding strategies for a vestibular implant. The degree of spike rate variability, or coefficient of variation (CV), is a prominent physiological property of vestibular neurons with undetermined functional significance. At the very least, CV is highly correlated with threshold to electrical stimulation in the intact vestibular labyrinth. If CV is also important for vestibular coding, then electrical stimulation strategies should be designed to restore relatively physiologic patterns of CV. Simulations using a stochastic model of primary afferent vestibular neurons reveal that this should be possible using combinations of low and high-rate pulsatile stimulation. They also demonstrate that differences in the number and independence of synaptic inputs can significantly affect CV.

Symptoms and signs in superior canal dehiscence syndrome.

Patients with superior canal dehiscence (SCD) syndrome experience vertigo and oscillopsia in response to loud sounds and to stimuli that result in changes in middle ear or intracranial pressure. They may also experience hyperacusis to bone-conducted sounds. The evoked eye movements in this syndrome align with the plane of the dehiscent superior canal. The symptoms and signs can be understood in terms of the effect of the dehiscence in creation of a third mobile window into the inner ear. The SCD syndrome has been diagnosed in 28 patients who were examined in the neuro-otology clinics at the Johns Hopkins Medical Institutions from May 1995 through January 2001. The diagnosis is best established based upon the symptoms that are characteristic for the syndrome, the vertical-torsional eye movements evoked by sound or pressure stimuli noted on examination performed with Frenzel goggles, the lowered thresholds for responses to vestibular-evoked myogenic potentials, and CT imaging of the temporal bones.

Eye movements in patients with superior canal dehiscence syndrome align with the abnormal canal.

BACKGROUND: The superior canal dehiscence (SCD) syndrome consists of sound- or pressure-induced nystagmus and vertigo caused by a defect in bone overlying the superior semicircular canal. The SCD syndrome is diagnosed based upon characteristic symptoms, signs, and findings on CT imaging of the temoral bones. However, SCD syndrome is often misdiagnosed as perilymphatic fistula (PLF), and the symptoms of sound- and pressure-induced vertigo are more commonly attributed to the vestibular utricle, rather than to the superior semicircular canal. This study explored the role of the superior canal and the utricle in the pathophysiology of SCD syndrome. METHODS: Three-dimensional scleral search coils were used to record eye movements in 11 patients with SCD syndrome. RESULTS: Ten patients developed nystagmus with upward torsional slow phases characteristic of superior canal activation when loud tones were presented to the affected ear or when the patients performed a Valsalva maneuver. Visual fixation led to a suppression of the nystagmus and the appearance of a sustained torsional deviation of the eyes. Two patients also had sound-evoked head movements in the same direction as the ocular slow phases. The response of the affected superior canal to rapid head rotations was tested in nine patients. The response was diminished in those with large (>/=5 mm) defects in the bone overlying the superior canal. CONCLUSIONS: The evoked eye movements in patients with SCD syndrome arise from the superior canal, not the utricle. The syndrome is recognized by the characteristic nystagmus evoked by tones or maneuvers that change middle ear or intracranial pressure. Examination for this nystagmus should be performed under conditions that prevent visual fixation.

Multi-unit recording from regenerated bullfrog eighth nerve using implantable silicon-substrate microelectrodes.

Multi-microelectrode silicon devices were developed for extracellular recording from multiple axons in regenerated eighth cranial nerves of American bullfrogs. Each includes a photolithographically defined array of holes and adjacent metal microelectrodes. A device is implanted within a transected eighth nerve; regenerating fibers grow through the holes en route to the brainstem. Multiple spike trains were recorded from two animals at up to 21 weeks after implantation. Single units were tracked for over 8 h. Some responded to sound with tuning typical of fibers innervating the amphibian and basilar papillae. Units of vestibular origin also were recorded. Action potentials were 30-140 microV P-P amid noise of 5 10 microV RMS, an adequate signal-to-noise ratio for spike detection and sorting. Histology confirmed that bundles of myelinated fibers grew through holes near electrodes that recorded activity. The implantation success rate was low, due to surgical morbidity, device extrusion, and lack of nerve regeneration through some devices. Future designs will address these issues and incorporate transistor amplifiers on devices to increase signal-to-noise ratios. The potential of implanted silicon devices to simultaneously record from many axons offers an opportunity for multicellular studies of auditor, vestibular and seismic signal processing in the vertebrate inner ear.

Silicon-substrate microelectrode arrays for parallel recording of neural activity in peripheral and cranial nerves.

A new process for the fabrication of regeneration microelectrode arrays for peripheral and cranial nerve applications is presented. This type of array is implanted between the severed ends of nerves, the axons of which regenerate through via holes in the silicon and are thereafter held fixed with respect to the microelectrodes. The process described is designed for compatibility with industry-standard CMOS or BiCMOS processes (it does not involve high-temperature process steps nor heavily-doped etch-stop layers), and provides a thin membrane for the via holes, surrounded by a thick silicon supporting rim. Many basic questions remain regarding the optimum via hole and microelectrode geometries in terms of both biological and electrical performance of the implants, and therefore passive versions were fabricated as tools for addressing these issues in on-going work. Versions of the devices were implanted in the rat peroneal nerve and in the frog auditory nerve. In both cases, regeneration was verified histologically and it was observed that the regenerated nerves had reorganized into microfascicles containing both myelinated and unmyelinated axons and corresponding to the grid pattern of the via holes. These microelectrode arrays were shown to allow the recording of action potential signals in both the peripheral and cranial nerve setting, from several microelectrodes in parallel.