The otolith end organs inform the brain about gravitational and linear accelerations, driving the otolith-ocular reflex (OOR) to stabilize the eyes during translational motion (e.g., moving forward without rotating) and head tilt with respect to gravity. We previously characterized OOR responses of normal chinchillas to whole-body tilt and translation and to prosthetic electrical stimulation targeting the utricle and saccule via electrodes implanted in otherwise normal ears. Here we extend that work to examine OOR responses to tilt and translation stimuli after unilateral intratympanic gentamicin injection and to natural/mechanical and prosthetic/electrical stimulation delivered separately or in combination to animals with bilateral vestibular hypofunction after right ear intratympanic gentamicin injection followed by surgical disruption of the left labyrinth at the time of electrode implantation. Unilateral intratympanic gentamicin injection decreased natural OOR response magnitude to about half of normal, without markedly changing OOR response direction or symmetry. Subsequent surgical disruption of the contralateral labyrinth at the time of electrode implantation surgery further decreased OOR magnitude during natural stimulation, consistent with bimodal-bilateral otolith end organ hypofunction (ototoxic on the right ear, surgical on the left ear). Delivery of pulse-frequency- or pulse-amplitude-modulated prosthetic/electrical stimulation targeting the left utricle and saccule in phase with whole-body tilt and translation motion stimuli yielded responses closer to normal than the deficient OOR responses of those same animals in response to head tilt and translation alone.
Objective: To determine whether prosthetic stimulation delivered via a vestibular implant can elicit artificial sensation of head movement despite long (23-yr) duration adult-onset ototoxic bilateral vestibular hypofunction (BVH). Study Design: Case report. Setting: Tertiary care center as part of a first-in-human clinical trial. Patients: One. Interventions: Unilateral vestibular implantation with an investigational multichannel vestibular implant in a 55-year-old man with a well-documented 23-year history of aminoglycoside-induced BVH. Main Outcome Measures: Electrically evoked vestibulo-ocular reflexes (eeVOR). Results: Vestibular implant stimulation can drive stimulus-aligned eeVOR and elicit a vestibular percept 23 years after the onset of bilateral vestibulopathy. Prosthetic stimulation targeting individual semicircular canals elicited eye movements that approximately aligned with each targeted canal's axis. The magnitude of the eeVOR response increased with increasing stimulus current amplitude. Response alignment and magnitude were similar to those observed for implant recipients who underwent vestibular implantation less than 10 years after BVH onset. Responses were approximately stable for 18 months of continuous device use (24 h/d except during sleep). Conclusions: Vestibular implantation and prosthetic electrical stimulation of semicircular canal afferent nerves can drive canal-specific eye movement responses more than 20 years after the onset of ototoxic vestibular hypofunction.
Vestibular implants (VI) modulate the rate and amplitude of charge-balanced current pulses to encode head angular velocity or acceleration. When the battery of a VI becomes depleted, stimulation interruptions can cause vertigo. To avoid this, VIs can use alert signals such as vibration and beeping to remind the user to replace the battery. However, in distracting and noisy environments typical of activities of daily life, some patients may fail to hear or feel those alerts, so a physiological signal can be used as an alternate channel for signaling battery depletion. Pauses in the stimulation waveform can be delivered for this purpose, with the length of the pause long enough to be detected reliably by the patient but not so long as to induce dizziness or a vertigo attack. As a guide for the design of a physiologic battery depletion alert system, this study reports the ability of nine longterm, continuous VI users to detect stimulation pauses of various durations. We also show the effect of distraction on patients’ detection thresholds and response latencies for detected events.
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