Morphologic Changes in the Vestibular Nerves and Nuclei after Labyrinthectomy in the Cat: A Case for the Neurotrophin Hypothesis in Vestibular Compensation

Abstract

Morphological changes in the vestibular nerves and superior vestibulocular neurons (SVON) after unilateral labyrinthectomy in cats revealed a progressive loss of axons in the ipsilateral vestibular nerve (35%) and synaptic profiles (SP) on ipsilateral SVON (60%) up to a 1-year survival period. Although the ipsilateral vestibular nerve showed further degeneration (45%) at 2 years post ablation, the number of SP on ipsilateral SVON increased to 60% of normal (40% loss). These SP likely represent sprouting from crossing commissural or cerebellar pathways. Contralateral vestibular nerves at 1 and 2 years post ablation revealed normal numbers and size spectrum, but the number of SP contacting the contralateral SVON at 8 weeks, 1 and 2 years paralleled the levels of SP found on ipsilateral SVON. The symmetry in adjustment of SP on the SVON of both sides of the brainstem after ablation may be explained by the neurotrophin hypothesis.

Ménière’s Disease Is a Viral Neuropathy

“…The argument that this neural degeneration may be secondary to end-organ toxicity from increased potassium levels [7] rather than a primary neuropathy is not valid because it has been shown that labyrinthectomy results in a loss of only one third of the VG [25] . The loss of VG cells in many of these TBs was greater than 50%.…”

“…First, it preserves vestibular function by targeting the specific agent responsible. By avoiding ablation methods (chemical or surgical), the central nervous system changes that follow ablation [25] are also avoided. Second, the prevention of bilateral involvement by MD or VN may be accomplished by either the repetition or maintenance of the antiviral regimen.…”

A Perspective on Recurrent Vertigo

“…These light microscopy observations are supported by transmission electron microscopy, which demonstrated fully formed viral particles in vestibular ganglion cells excised from patients with VN and MD. Treatment with acyclovir has the advantage of preserving the vestibular neural network, allowing compensation of the deficits caused by vestibular ganglion cell degeneration resulting from virus reactivation [66]. Usually this recovery is effective leaving no detectable clinical deficit.…”

Modifications of perineuronal nets and remodelling of excitatory and inhibitory afferents during vestibular compensation in the adult mouse

“…Unilateral damage to the vestibular peripheral receptors and nerve peripheral terminals (i.e. labyrinthectomy) may cause a progressive degeneration of vestibular nerve fibres, inducing a partial and gradual deafferentation of the vestibular nuclei (VN) (Gacek and Schoonmaker 1997;Lacour et al 2009). At the acute stage, neurons of deafferented VN lose their normal high resting activity, while those of the contralateral side become hyperactive.…”