Ocular vestibular evoked myogenic potentials in superior canal dehiscence.

OBJECTIVE: Patients with superior canal dehiscence (SCD) have large sound-evoked vestibular reflexes with pathologically low threshold. We wished to determine whether a recently discovered measure of the vestibulo-ocular reflex-the ocular vestibular evoked myogenic potential (OVEMP)-produced similar high-amplitude, low-threshold responses in SCD, and could differentiate patients with SCD from normal control patients. METHODS: Nine patients with CT-confirmed SCD and 10 normal controls were stimulated with 500 Hz, 2 ms tone bursts and 0.1 ms clicks at intensities up to 142 dB peak SPL. Conventional VEMPs were recorded from the ipsilateral sternocleidomastoid muscle to determine threshold, and OVEMPs were recorded from electrode pairs placed superior and inferior to the eyes. Three-dimensional eye movements were measured with scleral dual-search coils. RESULTS: In patients with SCD, OVEMP amplitudes were significantly larger than normal (p<0.001) and thresholds were pathologically low. The n10 OVEMP in the contralateral inferior electrode became particularly large with increasing stimulus intensity (up to 25 microV) and with up-gaze (up to 40 microV). Sound-evoked (slow-phase) eye movements were present in all patients with SCD (vertical: upward; torsional: upper pole away from the affected side; and horizontal: towards or away from the affected side), but began only as the OVEMP response became maximal, which is consistent with the surface potentials being produced by activation of the extraocular muscles that generated the eye movements. CONCLUSIONS: OVEMP amplitude and threshold (particularly the contralateral inferior n10 response) differentiated patients with SCD from normal controls. Our findings suggest that both the OVEMPs and induced eye movements in SCD are a result of intense saccular activation in addition to superior canal stimulation.

A sensorimotor theory of temporal tracking and beat induction.

In this paper, we develop a theory of the neurobiological basis of temporal tracking and beat induction as a form of sensory-guided action. We propose three principal components for the neurological architecture of temporal tracking: (1) the central auditory system, which represents the temporal information in the input signal in the form of a modulation power spectrum; (2) the musculoskeletal system, which carries out the action and (3) a controller, in the form of a parieto-cerebellar-frontal loop, which carries out the synchronisation between input and output by means of an internal model of the musculoskeletal dynamics. The theory is implemented in the form of a computational algorithm which takes sound samples as input and synchronises a simple linear mass-spring-damper system to simulate audio-motor synchronisation. The model may be applied to both the tracking of isochronous click sequences and beat induction in rhythmic music or speech, and also accounts for the approximate Weberian property of timing.