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RESEARCH SUPPORT, NON-U.S. GOV'T
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Recovery of vestibulo-ocular reflex-function in subjects with an acute unilateral peripheral vestibular deficit.

The centrally controlled compensation for a reduced horizontal vestibulo-ocular reflex (VOR) gain caused by a unilateral afferent deficit is usually studied following a selective surgical procedure which completely lesions the vestibular nerve or blocks the horizontal semicircular canal. The more common, unilateral, vestibular deficit encountered clinically, is a partial loss of peripheral vestibular function, following which peripheral recovery and/or central compensation may occur. We investigated changes of the VOR gain in response to a sudden, idiopathic, unilateral vestibular deficit in 64 subjects by examining the responses to low-frequency, whole-body, rotations about an earth vertical axis with different accelerations (5, 20 and 40 deg/sec2) during in- and out-patient visits separated by 4 months in an attempt to identify changes brought about by peripheral recovery and by central compensation processes. Peripheral function was assumed to be measured by the response to caloric irrigation. It improved some 30% on average between the two visits. VOR responses for rotations towards the deficit side also improved between the two visits. Most improvement occurred for 20 deg/sec2 accelerations. However, the correlation coefficient between rotation and caloric responses was always less than 0.6. Unlike caloric responses which improved over time, responses for rotations to the intact side did not change between the visits. For this reason, the majority of observed VOR rotation responses were nearly symmetrical at the time of the second visit, despite being below normal levels. These findings suggest that both peripheral recovery and central compensation processes help restore symmetrical VOR function for head rotations after a partial unilateral vestibular deficit. However the improvement of VOR response symmetry, particularly to slow (< 40 deg/sec2) accelerations, is largely independent of the recovery of peripheral sensitivity.

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