Abstract
Background: A battery of stance and gait tasks can be used to quantify functional deficits and track improvement in balance control following peripheral vestibular loss. An improvement could be due to at least 3 processes: partial peripheral recovery of sensory responses eliciting canal or otolith driven vestibular reflexes; central compensation of vestibular reflex gains, including substitution of intact otolith responses for pathological canal responses; or sensory substitution of visual and proprioceptive inputs for vestibular contributions to balance control.Results: We describe the presumed action of all 3 processes observed for a case of sudden incapacitating acute bilateral peripheral loss probably due to vestibular neuritis. Otolith responses were largely unaffected. However, pathological decreases in all canal-driven vestibular ocular reflex (VOR) gains were observed. After 3 months of vestibular rehabilitation, balance control was normal but VOR gains remained low.Conclusions: This case illustrates the difficulty in predicting balance control improvements from tests of the 10 vestibular end organs and emphasizes the need to test balance control function directly in order to determine if balance control has improved and is normal again despite remaining vestibular sensory deficits. This case also illustrates that the presence of residual otolithic function may be crucial for balance control improvement in cases of bilateral vestibular hypofunction.
Highlights
It is an open question whether any improvement in balance control following an acute bilateral peripheral vestibular loss (BVL) uses the same neural processes to improve function as when the acute peripheral vestibular loss is unilateral (UVL)
It is assumed that this improvement is due to central compensation, that the crossed intact side input contributing to the vestibular ocular reflex (VOR) for head rotations to the deficit side is enhanced [3,4,5]
The question arises when there is no recovery of peripheral vestibular function bilaterally, as indicated by absent caloric responses, and abnormally low canal-elicited video head impulse test (vHIT) responses at acute onset, that is a gain below 0.6 bilaterally, [see Strupp et al for a consensus definition of BVL [6]] whether there can be any improvement in VOR gains and balance control
Summary
It is an open question whether any improvement in balance control following an acute bilateral peripheral vestibular loss (BVL) uses the same neural processes to improve function as when the acute peripheral vestibular loss is unilateral (UVL). The question arises when there is no recovery of peripheral vestibular function bilaterally, as indicated by absent caloric responses, and abnormally low canal-elicited vHIT responses at acute onset, that is a gain below 0.6 bilaterally, [see Strupp et al for a consensus definition of BVL [6]] whether there can be any improvement in VOR gains and balance control. In this situation, there is no normal side response to aid central compensation. An improvement could be due to at least 3 processes: partial peripheral recovery of sensory responses eliciting canal or otolith driven vestibular reflexes; central compensation of vestibular reflex gains, including substitution of intact otolith responses for pathological canal responses; or sensory substitution of visual and proprioceptive inputs for vestibular contributions to balance control
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