Temporal Bone Studies of the Human Peripheral Vestibular System

Tsuji, Kojiro; Velázquez-Villaseñor, L; Sd, Rauch; Rj, Glynn; Wall, Conrad; Sn, Merchant

doi:10.1177/00034894001090s505

Cited by 103 publications

(47 citation statements)

References 10 publications

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“…There is also anatomic support for the notion of preserved vestibular function in ears that have longstanding Me Ânie Áre's disease. Tsuji et al (2000) examined temporal bones from 24 patients with Me Ânie Áre's disease. While the loss of type II hair cells and Scarpa's ganglion cells were greater than expected for age, they rarely observed >50% reduc- tion in either type of hair cell or the afferent neurons.…”

Section: Discussionmentioning

confidence: 99%

Changes in the Three-Dimensional Angular Vestibulo-Ocular Reflex following Intratympanic Gentamicin for Ménière's Disease

Carey

Minor

Peng

et al. 2002

JARO - Journal of the Association for Research in Otolaryngolog

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The 3-dimensional angular vestibulo-ocular re¯exes (AVOR) elicited by rapid rotary head thrusts were studied in 17 subjects with unilateral Me Ânie Áre's disease before and 2±10 weeks after treatment with intratympanic gentamicin and in 13 subjects after surgical unilateral vestibular destruction (SUVD). Each head thrust was in the horizontal plane or in either diagonal plane of the vertical semicircular canals, so that each head thrust effectively stimulated only one pair of canals. The AVOR gains (eye velocity/head velocity during the 30 ms before peak head velocity) for the head thrusts exciting each individual canal were averaged and taken as a measure of the function of that canal. Prior to intratympanic gentamicin, gains for head thrusts that excited canals on the affected side were 0.91 0.20 (horizontal canal, HC), 0.78 0.20 (anterior canal, AC), and 0.83 0.10 (posterior canal, PC). The asymmetries between these gain values and those for head thrusts that excited the contralateral canals were <2%. In contrast, caloric asymmetries averaged 40% 32%. Intratympanic gentamicin resulted in decreased gains attributable to each canal on the treated side: 0.40 0.12 (HC), 0.35 0.14 (AC), 0.31 0.14 (PC) (p < 0.01). However, the gains attributable to contralateral canals dropped only slightly, resulting in marked asymmetries between gains for excitation of ipsilateral canals versus their contralateral mates: HC: 34% 12%, AC: 24% 25%, and PC: 42% 13%. There was no difference in the AVOR gain for excitation of the ipsilateral HC after gentamicin in patients who received a single intratympanic injection (0.39 0.11, n = 12) in comparison to those who received 2±3 injections (0.42 0.15, n = 5, p = 0.7). Gain decreases attributed to the gentamicintreated HC and AC were not as severe as those observed after SUVD. This ®nding suggests that intratympanic gentamicin causes a partial vestibular lesion that may involve preservation of spontaneous discharge and/or rotational sensitivity of afferents.

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Section: Discussionmentioning

confidence: 99%

Changes in the Three-Dimensional Angular Vestibulo-Ocular Reflex following Intratympanic Gentamicin for Ménière's Disease

Carey

Minor

Peng

et al. 2002

JARO - Journal of the Association for Research in Otolaryngolog

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“…Possible insults to vestibular hair cells include aminoglycoside toxicity, inner ear diseases, viral infections, and aging [2][3][4][5]. Clinical features of vestibular hair cell loss vary, with typical symptoms including dizziness, vertigo, and oscillopsia.…”

Section: Introductionmentioning

confidence: 99%

Spatial and Age-Dependent Hair Cell Generation in the Postnatal Mammalian Utricle

Gao

Kelly

et al. 2015

Mol Neurobiol

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Loss of vestibular hair cells is a common cause of balance disorders. Current treatment options for bilateral vestibular dysfunction are limited. During development, atonal homolog 1 (Atoh1) is sufficient and necessary for the formation of hair cells and provides a promising gene target to induce hair cell generation in the mammals. In this study, we used a transgenic mouse line to test the age and cell type specificity of hair cell induction in the postnatal utricle in mice. We found that forced Atoh1 expression in vivo can induce hair cell formation in the utricle from postnatal days 1 to 21, while the efficacy of hair cell induction is progressively reduced as the animals become older. In the utricle, the induction of hair cells occurs both within the sensory region and in cells in the transitional epithelium next to the sensory region. Within the sensory epithelium, the central region, known as the striola, is most subjective to the induction of hair cell formation. Furthermore, forced Atoh1 expression can promote proliferation in an age-dependent manner that mirrors the progressively reduced efficacy of hair cell induction in the postnatal utricle. These results suggest that targeting both cell proliferation and Atoh1 in the utricle striolar region may be explored to induce hair cell regeneration in mammals. The study also demonstrates the usefulness of the animal model that provides an in vivo Atoh1 induction model for vestibular regeneration studies.

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“…For example, it seems that in MD the caloric is impaired but the vHIT is not [48, 96, 124]. One explanation for this discrepancy is that since MD preferentially causes loss of type II vestibular hair cells [151], it will preferentially impair tonic (responsible to caloric responses) rather than phasic canal signals (responsible for impulsive responses). An alternative explanation is that the caloric impairment is a hydrodynamic effect from the swelling of the endolymphatic compartment abolishing the possibility of thermal convection—the main proposed mechanism of caloric stimulation [48].…”

Section: Video Head Impulse Testingmentioning

confidence: 99%