Purpose of review: This article reviews recent studies that have provided experimental evidence for mechanisms of neural and synaptic plasticity in the brain during vestibular compensation, the behavioural recovery that takes place following peripheral vestibular lesions.
Recent findings: First, experimental evidence from animal studies indicates that an unbalanced vestibular commissural system is a fundamental cause of the syndrome of oculomotor and postural deficits after unilateral labyrinthectomy. Second, recent studies suggest the involvement of both GABAergic and glycinergic commissural neurons. In addition gliosis and reactive neurogenesis in the ipsilesional vestibular nuclei appear to be involved in compensation. Third, evidence from cerebellar-deficient mutant mice demonstrates an important role for cerebellum-dependent motor learning in the longer term. Factors such as stress steroids and neuromodulators such as histamine influence these plasticity mechanisms and may thus contribute to the development of compensation in patients.
Summary: Vestibular compensation involves multiple, parallel plastic processes at various sites in the brain. Experimental evidence suggests that adaptive changes in the sensitivity of ipsilesional vestibular neurons to the inhibitory neurotransmitters GABA and glycine, changes in the electrophysiological excitability of vestibular neurons, changes in the inhibitory control of the brainstem vestibular networks by the cerebellum, gliosis and neurogenesis in the ipsilesional vestibular nuclei, and activity-dependent reorganization of the synaptic connectivity of the vestibular pathways are mechanisms involved in compensation.