Mechanisms of recovery following unilateral labyrinthectomy: a review

Abstract

This paper reviews the literature on the mechanisms responsible for the behavioural recovery which occurs following unilateral labyrinthectomy (UL). UL causes a syndrome of ocular motor and postural disorders, which diminish over time in a process of behavioural recovery known as vestibular compensation. Electrophysiological studies show that the VIIIth nerve does not undergo a functional recovery, therefore vestibular compensation has been attributed to CNS plasticity. However, the nature of the plasticity responsible for vestibular compensation is not understood. Single-neuron studies have demonstrated that a significant recovery of resting activity has occurred in the vestibular nuclei (VN) ipsilateral to the UL by the time symptoms such as spontaneous nystagmus and roll head tilt (static symptoms) have largely disappeared. However, many of the deficits in the response of VN neurons to head acceleration persist and may be permanent. This lack of recovery in the response of neurons to head acceleration correlates with the incomplete and sometimes poor recovery of the vestibulo-ocular and vestibulo-spinal reflex responses to head movement (dynamic symptoms). The major neuronal change in the VN during vestibular compensation appears to be the recovery of resting activity in the VN ipsilateral to the UL, although this recovery is more pronounced in the medial VN than in the lateral VN. The mechanism responsible for the regeneration of resting activity in VN neurons is unknown. In frogs, there is evidence to suggest that transcommissural synaptic input to the VN, from the contralateral (intact) labyrinth, increases in efficacy. However in mammals, the recovery of VN resting activity seems to be independent of transcommissural influences. The preand postsynaptic mechanisms responsible for this neural recovery in mammals remain to be determined.