Abstract

Stable unilateral vestibular deficit (vestibular neuronitis being the most common example in clinical practice) causes an imbalance in the information reaching the two vestibular nuclei at the level of the brain stem. This inequality of in­for­ma­tion arriving from the inner ear or the vestibular nerve is interpreted by the central vestibular structures as a rotation towards the ear from which it receives more in­for­ma­tion, generating the natural balancing reactions – nys­tag­mus and vertigo, postural and walking imbalance. The phy­sio­lo­gical mechanism involved in the healing of such an injury is represented by the phenomenon of central ves­ti­bu­lar compensation, an expression of the plasticity of the cen­tral vestibular structures. This natural recovery pattern begins in the first days after the acute injury and is a long-last­ing process that allows good but incomplete recovery of dynamic deficits secondary to peripheral vestibular in­jury. This therapeutic window of the first week after onset should not be missed – initiation of phar­ma­co­lo­gical treat­ment (betahistine) from the first days and vestibular reha­bi­li­ta­tion pro­grams, both of which have been shown to facilitate and accelerate central vestibular compensation and en­su­ring ma­xi­mum patient’s recovery.

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