Les Surdites Brusques Idiopathiques Facteurs Pronostiques

Moalla, J; Mnejja, Malek; Hasnaoui, Mehdi; Fakhfekh, W; Chakroun, A.; Charfeddine, I; Ghorbel, Abdelmonem

doi:10.4314/jtdorl.v18i1.42037

Cited by 3 publications

(1 citation statement)

References 15 publications

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“…A massive release of glutamate during sustained ischemia or prolonged excitotoxic conditions could cause massive synapse uncoupling and pronounced retraction that would further delay, and ultimately prevent, any possibility of regrowth and reconnection. Such a situation might reflect the clinical tableau sometimes encountered in humans in cases of complete vestibular areflexia as a result of conditions diagnosed as labyrinthitis or vestibular neuritis, or in cases of cophosis encountered in sudden sensory hearing loss conditions (Moalla et al, 2007). Further quantitative analysis will be needed to precisely establish the capacity for plasticity of vestibular synapses exposed to different traumatic conditions.…”

Section: Discussionmentioning

confidence: 99%

Correlation between afferent rearrangements and behavioral deficits after local excitotoxic insult in the mammalian vestibule: an animal model of vertigo symptoms?

Gaboyard-Niay

Travo

Saleur

et al. 2016

Disease Models &Amp; Mechanisms

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Damage to inner ear afferent terminals is believed to result in many auditory and vestibular dysfunctions. The sequence of afferent injuries and repair, as well as their correlation with vertigo symptoms, remains poorly documented. In particular, information on the changes that take place at the primary vestibular endings during the first hours following a selective insult is lacking. In the present study, we combined histological analysis with behavioral assessments of vestibular function in a rat model of unilateral vestibular excitotoxic insult. Excitotoxicity resulted in an immediate but transient alteration of the balance function that was resolved within a week. Concomitantly, vestibular primary afferents underwent a sequence of structural changes followed by spontaneous repair. Within the first two hours after the insult, a first phase of pronounced vestibular dysfunction coincided with extensive swelling of afferent terminals. In the next 24 h, a second phase of significant but incomplete reduction of the vestibular dysfunction was accompanied by a resorption of swollen terminals and fiber retraction. Eventually, within 1 week, a third phase of complete balance restoration occurred. The slow and progressive withdrawal of the balance dysfunction correlated with full reconstitution of nerve terminals. Competitive re-innervation by afferent and efferent terminals that mimicked developmental synaptogenesis resulted in full re-afferentation of the sensory epithelia. By deciphering the sequence of structural alterations that occur in the vestibule during selective excitotoxic impairment, this study offers new understanding of how a vestibular insult develops in the vestibule and how it governs the heterogeneity of vertigo symptoms.

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Section: Discussionmentioning

confidence: 99%