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Home > Journals > Otorinolaringologia > Past Issues > Otorinolaringologia 2005 September;55(3) > Otorinolaringologia 2005 September;55(3)155-8



A Journal on Otorhinolaryngology, Head and Neck Surgery,
Plastic Reconstructive Surgery, Otoneurosurgery

Indexed/Abstracted in: EMBASE, Scopus

Frequency: Quarterly

ISSN 0026-4938

Online ISSN 1827-188X


Otorinolaringologia 2005 September;55(3)155-8


Vestibular compensation: neurophysiological aspects

Manfrin N.

Clinica Otorinolaringoiatrica Dipartimento di Scienze Sensoriali IRCCS Policlinico San Matteo e Università di Pavia, Pavia

Vestibular compensation is a series of complex neurological processes that express themselves at many levels. In a subject that suddenly loses his vestibular functions they allow a complete return to normality. Principal events of compensation happen in the CNS structures through a change of neurological activity in vestibular nuclei. After a sudden vestibular loss, nuclear vestibular neurons ipsilateral to lesion stop their resting activity. Their functional re-establishment involves multiple neurogenetic mechanisms. At the moment it is accepted the theory that supports some processes that start up immediately and others later. Undamaged neurons present a sprouting with new synapsis with neurons liberated by axonal degeneration of damaged ones. This is a late process in compensation maintenance. Denervation hypersensitivity too is a late process. Nuclear vestibular cells denied by their afferent nerve fibres show an increased sensitivity to neurotransmitter. Other neurons (oculars, proprioceptives, etc) that contract synapsis with vestibular nucleus can release the same neurotransmitter producing an excessive reply. Neuronal adaptation is the quickest compensation process that precedes others. Acute deafferentation produces a big increment in type I neurons tonic afferent activity in contralateral vestibular nuclei in which the inhibitor tonic effect of commissural fibres is stopped. Quick adaptation of these neurons involves a progressive reduction of commissural inhibition that permits damaged neurons to re-gain their basal tonic activity.

language: Italian


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