Comparison of Vestibular Compensation after Vestibular Neurectomy, Labyrinthectomy and Triple Semicircular Canal Plugging in the Cat

2021 ◽  
Author(s):  
Yafeng Lyu ◽  
Yuechen Han ◽  
Yongdong Song ◽  
Ligang Kong ◽  
Xiaofei Li ◽  
...  
2021 ◽  
Author(s):  
Guillaume Rastoldo ◽  
Emna Marouane ◽  
Nada El Mahmoudi ◽  
David Pericat ◽  
Isabelle Watabe ◽  
...  

AbstractUnilateral vestibular lesions induce a vestibular syndrome, which recovers over time due to vestibular compensation. The therapeutic effect of L-Thyroxine (L-T4) on vestibular compensation was investigated by behavioral testing and immunohistochemical analysis in a rat model of unilateral vestibular neurectomy (UVN). We demonstrated that an acute L-T4 treatment reduced the vestibular syndrome and significantly promoted vestibular compensation. Thyroid hormone receptors (TRα and TRβ) and type II iodothyronine deiodinase (DIO2) were present in the vestibular nuclei (VN), supporting a local action of L-T4. We confirmed the T4-induced metabolic effects by demonstrating an increase in the number of cytochrome oxidase-labelled neurons in the VN three days after the lesion. L-T4 treatment modulated glial reaction by decreasing both microglia and oligodendrocytes in the deafferented VN three days after UVN and increased cell proliferation. The survival of newly generated cells was not affected, but neuronal differentiation was altered by the L-T4 treatment.


2020 ◽  
Vol 163 (3) ◽  
pp. 557-559
Author(s):  
Soumit Dasgupta ◽  
Marco Mandala ◽  
Enis Alpin Guneri

Although vestibular anatomy was described in the Renaissance period, research in vestibular physiology began in the 1820s and was spearheaded by Purkinje and Flourens. This was subsequently expanded by Ménière, Helmholtz, Goltz, Mach, Breuer, Ewald, and Hogyes, who are regarded as the early pioneers in research on vestibular physiology in the 19th century. The relationship of endolymphatic flow and semicircular canal function is termed the Mach-Breuer hypothesis. What is less well known is that a Scottish chemist, Alexander Crum Brown, arrived at similar conclusions as Mach and Breuer at the same time quite independently. In fact, he pioneered several concepts in vestibular physiology that included pairing of semicircular canals for function, the vestibular pathway, optic fixation elimination in vestibular experimentation, the theory of motion intolerance, and study in deaf mutes for insights into vestibular pathology and vestibular compensation. This article is a tribute to this forgotten pioneer in vestibular research.


Neurology ◽  
2004 ◽  
Vol 62 (12) ◽  
pp. 2294-2296 ◽  
Author(s):  
N. Lehnen ◽  
S. T. Aw ◽  
M. J. Todd ◽  
G. M. Halmagyi

1988 ◽  
Vol 98 (2) ◽  
pp. 138-143 ◽  
Author(s):  
Herbert Silverstein ◽  
Horace Norrell ◽  
Eric Smouha ◽  
Thomas Haberkamp

The singular canal transmits the posterior ampullary nerve between the inferior part of the internal auditory canal (IAC) and ampulla of the posterior semicircular canal. The anatomy of the singular canal was studied in temporal bone dissections, in surgical dissections, and in high-resolution computerized tomography scans. Measurements were taken for distances between the origin of the singular canal in the IAC, the porus acousticus, the vestibule, and posterior canal ampulla. The location and importance of the singular canal are demonstrated for retrosigmoid-IAC vestibular neurectomy, retrosigmoid acoustic neuroma surgery, and transcochlear cochleovestibular neurectomy. The main purpose for the use of the retrosigmoid approach to the internal auditory canal during vestibular neurectomy and excision of acoustic neuromas is preservation of hearing. A major concern when the contents of the internal auditory canal are exposed through this approach is fenestration of the labyrinth, which results in sensorineural hearing loss. In the retrosigmoid approach, the singular canal has been found to be a vital landmark in prevention of fenestration during surgery of the internal auditory canal.


2018 ◽  
Vol 32 (2) ◽  
pp. 58-59
Author(s):  
Nathaniel W. Yang

A 62-year-old man consulted for recurrent episodes of vertigo lasting from seconds to several minutes. The vertigo was variably described as spinning, lateral swaying, and a feeling of being “unsure of his position in space.” These episodes were noted to have begun when the patient was still in his 20’s. Standard pure tone audiometry revealed a mild-to-moderate downsloping mixed hearing loss in the left ear. Bithermal caloric testing indicated the presence of a significant left-sided peripheral vestibular loss. Due to the fact that the vertigo episodes presented relatively early in life, the possibility of a congenital inner ear malformation was considered as a cause for his symptoms.  Computerized tomographic (CT) imaging of the temporal bone was performed. This clearly showed the left horizontal semicircular canal lacking a central bony island. (Figure 1 and 2) The cochlea, superior and posterior semicircular canals, vestibular and cochlear aqueducts, and ossicular chain were grossly normal. A malformation of the horizontal or lateral semicircular canal is one of the most common inner ear malformations, as it is the last vestibular structure to be formed during inner ear embryogenesis. As such, it may occur in isolation or may be associated with other vestibular, cochlear, or middle ear malformations.1,2  Although vertigo and dizziness are symptoms to be expected in such a condition, existing data indicates that it may be totally asymptomatic, or it may also present as a sensorineural, conductive, or mixed type of hearing loss.1,3   Radiologic imaging is of prime importance in diagnosing such conditions, especially when auditory and/or vestibular symptoms manifest early in life. This case perfectly illustrates the need for such studies, as the patient went undiagnosed for more than forty years!             No definitive statements can be gleaned from existing medical literature with respect to treatment. However, in patients with debilitating vestibular symptoms, management with modalities that selectively target the vestibular system, but spare the auditory system, such as vestibular neurectomy and trans-tympanic aminoglycoside therapy appear to be reasonable options.   References   Johnson J, Lalwani AK. Sensorineural and conductive hearing loss associated with lateral semicircular canal malformation. Laryngoscope 2000 Oct;110(10):1673–1679. DOI:10.1097/00005537-200010000-00019 PMID: 11037823   Casselman JW, Delanote J, Kuhweide R, van Dinther J, De Foer B, Offeciers EF. Congenital malformations of the temporal bone. In: Lemmerling M, De Foer B, editors. Temporal bone imaging. Berlin Heidelberg: Springer-Verlag; 2015, pp. 120-154.   Kim CH, Shin JE, Lee YJ, Park HJ. Clinical characteristics of 7 patients with lateral semicircular canal dysplasia. Res Vestib Sci 2012;11(2):64-68.


1995 ◽  
Vol 104 (5) ◽  
pp. 381-387 ◽  
Author(s):  
Jean-Philippe Guyot ◽  
Richard R. Gacek ◽  
Michael J. Lyon ◽  
Christine Magnin

The ultrastructural changes of the feline superior vestibular commissural neurons (CNs) were quantitatively assessed 8 weeks following ipsilateral vestibular neurectomy. Results indicated a slight degeneration of synaptic profiles (SPs; 25%) representing the primary vestibular afferent input onto CN soma. The synaptic vesicles of the remaining SPs, which likely originate from the cerebellum and the contralateral CNs, were smaller and rounder, suggesting a transition from an inhibitory to an excitatory mode of response. The SP loss had little impact on the CNs' capacity for protein synthesis and structural maintenance, since there was no change in the volume fraction of intracellular organelles. These data suggest that CNs do not degenerate and are likely functional after vestibular compensation. These findings support the role of the commissural pathway in vestibular compensation as proposed by Galiana et al, which is based on the assumption that the intervestibular commissural connections remain intact following vestibular neurectomy.


1988 ◽  
Vol 97 (1) ◽  
pp. 42-51 ◽  
Author(s):  
Richard R. Gacek ◽  
Michael J. Lyon ◽  
Joanne Schoonmaker

Vestibulo-ocular (VO) neurons in the superior vestibular nucleus were labeled retrogradely with horseradish peroxidase and studied quantitatively using electron microscopy to determine the morphologic correlates of vestibular compensation. Eleven VO neurons from three normal cats were compared to 26 VO neurons in four animals killed 8 weeks after vestibular neurectomy and 13 VO cells from two animals killed 1 year after vestibular neurectomy. The results demonstrated a marked reduction (74%) in the number of synaptic profiles (SPs) on the VO cell soma in both experimental groups. Synaptic vesicles in the remaining SPs on VO neurons were fewer, smaller, and rounder than vesicles in control animals. The residual SPs also were associated with more asymmetric synapses. The experimental VO neuron showed a significant decrease in soma and organelles associated with protein synthesis.


2021 ◽  
Vol 18 (1) ◽  
Author(s):  
Nada El Mahmoudi ◽  
Guillaume Rastoldo ◽  
Emna Marouane ◽  
David Péricat ◽  
Isabelle Watabe ◽  
...  

Abstract Background Due to their anti-inflammatory action, corticosteroids are the reference treatment for brain injuries and many inflammatory diseases. However, the benefits of acute corticotherapy are now being questioned, particularly in the case of acute peripheral vestibulopathies (APV), characterized by a vestibular syndrome composed of sustained spinning vertigo, spontaneous ocular nystagmus and oscillopsia, perceptual-cognitive, posturo-locomotor, and vegetative disorders. We assessed the effectiveness of acute corticotherapy, and the functional role of acute inflammation observed after sudden unilateral vestibular loss. Methods We used the rodent model of unilateral vestibular neurectomy, mimicking the syndrome observed in patients with APV. We treated the animals during the acute phase of the vestibular syndrome, either with placebo or methylprednisolone, an anti-inflammatory corticosteroid. At the cellular level, impacts of methylprednisolone on endogenous plasticity mechanisms were assessed through analysis of cell proliferation and survival, glial reactions, neuron’s membrane excitability, and stress marker. At the behavioral level, vestibular and posturo-locomotor functions’ recovery were assessed with appropriate qualitative and quantitative evaluations. Results We observed that acute treatment with methylprednisolone significantly decreases glial reactions, cell proliferation and survival. In addition, stress and excitability markers were significantly impacted by the treatment. Besides, vestibular syndrome’s intensity was enhanced, and vestibular compensation delayed under acute methylprednisolone treatment. Conclusions We show here, for the first time, that acute anti-inflammatory treatment alters the expression of the adaptive plasticity mechanisms in the deafferented vestibular nuclei and generates enhanced and prolonged vestibular and postural deficits. These results strongly suggest a beneficial role for acute endogenous neuroinflammation in vestibular compensation. They open the way to a change in dogma for the treatment and therapeutic management of vestibular patients.


1991 ◽  
Vol 104 (1) ◽  
pp. 14-19 ◽  
Author(s):  
Stephen P. Cass ◽  
Harry G. Goshgarian

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