[Vestibular compensation. Review of the literature and clinical applications].

Vestibular compensation is an excellent model for the study of plasticity of the adult central nervous system. Therefore it has been the subject of several studies in humans and animals, which will be briefly summed up by the authors. Lesions of the labyrinth or vestibular neurectomy are immediately followed of postural and oculomotor disorders, as well as by dynamic deficits of the various vestibular reflexes (vestibulo-ocular and vestibulonucal reflexes). While the former problems always recede in all species, the restoration of the dynamic properties of vestibular reflexes largely depends upon the species considered, in particular for the vestibulo-ocular reflex. However, this function seems to recover the gain and phase it had prior to the lesion in both humans and monkeys. What is the neuronal substrate of these various deficits? Electrophysiological studies have demonstrated at the acute stage a symmetrical activity between the two vestibular nuclei: on the side of the lesion, the nucleus becomes inactive, while the resting discharge of the contralateral vestibular neurons is increased. Following compensation, symmetric activity is restored between both nuclei due to the regeneration of a new basic discharge in the deafferented neurons. The matter of vestibular compensation can therefore be formulated as follows: which mechanisms enable a central neuron inactivated du to the suppression of most of its excitatory afferences to recover a normal spontaneous activity? Several hypotheses, either pre- or postsynaptic, are currently put forward. Presynaptic hypotheses consider the role of the various afferences of the vestibular nuclei, ie. visual, proprioceptive, commissural, cerebellar and other afferences. In fact, the vestibular nuclei are not merely relays between the labyrinthine receptors and the nuclei of the oculomotor nerves, but actually form real sensorimotor integration centers. Besides the afferences from the vestibular nerve, they receive several other sorts of information, including visual and spinal proprioceptive inputs. An increase in the activity of these afferences, a sprouting of their axon collaterals, may favor the return to a normal basic discharge of the central vestibular neurons. The postsynaptic hypotheses involve either a change in the intrinsic membrane properties of the central vestibular neurons following the lesion, or an increase in the number of receptors located on their surface. More specifically, denervation supersensitivity of the glutamatergic receptors has been put forward as the possible origin of vestibular compensation.