Relationship of Static and Dynamic Mechanisms in Vestibuloocular Reflex Compensation

Newlands, Shawn D.; Dara, Sarita; Kaufman, Galen D.

doi:10.1097/01.mlg.0000154718.80594.2e

Cited by 26 publications

(30 citation statements)

References 56 publications

(122 reference statements)

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“…Compared to labyrinthectomy, we found that postoperative disequilibrium in patients after semicircular canal plugging compensated quickly and completely [1]. This finding was consistent with previous studies in animals [2,3,4]. …”

Section: Introductionsupporting

confidence: 90%

“…In gerbils, however, a clear difference in both the time course and degree of recovery was observed between UCP and UL. The UCP group compensated faster and more completely, particularly with rotation toward the lesion (ipsilateral side) [4]. This subtly different pattern of behavioral recovery following UCP and UL might indicate that different molecular mechanisms occurred during compensation in the vestibular nuclei.…”

Section: Discussionmentioning

confidence: 99%

“…These changes were reported to be temporally related to the appearance and development of vestibular compensation in the rat [8]. Compensation in patients and animals after UCP and UL is generally similar, but subtle differences may include differential Fos expression patterns in the models [2,3,4]. However, to date, no systematic study of Fos expression in the central vestibular system after UCP has been conducted.…”

Section: Introductionmentioning

confidence: 99%

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Fos Expression in the Rat Vestibular Nucleus Complex after Plugging the Three Semicircular Canals

Chen

Yu²,

Chen³

et al. 2009

Audiol Neurotol

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Hypothesis: Differential compensation after unilateral semicircular canal plugging (UCP) and unilateral labyrinthectomy (UL) may involve different expression patterns of fos mRNA and Fos protein in the vestibular nucleus complex. Background: The expression of Fos protein in the vestibular nuclei underwent spatiotemporal changes related to the compensation process following surgical UL and chemical UL. These changes were temporally related to the appearance and development of vestibular compensation in the rat. Methods: Spatiotemporal changes in both fos mRNA and protein levels in the rat brain after UCP were observed. The Fos expression pattern after UCP was compared to that after UL. Results: Greater fos mRNA and Fos protein expressions were detected in bilateral medial vestibular nuclei (MVNs) after UL than after UCP. The changes were relatively long-lived after UL compared to those following UCP. Conclusion: Differences in the expression pattern of fos mRNA and Fos protein in bilateral MVNs between UCP and UL may explain differences in compensation after UCP and UL.

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Section: Introductionsupporting

confidence: 90%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Fos Expression in the Rat Vestibular Nucleus Complex after Plugging the Three Semicircular Canals

Chen

Yu²,

Chen³

et al. 2009

Audiol Neurotol

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“…It can be argued that since peripheral lesions decrease both the aVOR gain and time constant (Fetter and Zee 1988;Hain and Buettner 1990;Wade et al 1999), the reason that labyrinthine-defective subjects are less prone to motion sickness is that fewer impulses are generated by the partially damaged peripheral vestibular end organs. The fact that the high frequency gains return to normal levels in the labyrinthinedefective subjects is not uncommon after bilateral labyrinthine lesions (Baloh et al 1984;Black et al 2001;Galiana et al 2001;Palla and Straumann 2004;Newlands et al 2005) and may be accomplished either centrally or peripherally (Palla and Straumann 2004).…”

Section: Possible Mechanisms For Reduction Of Motion Sickness Susceptmentioning

confidence: 99%

“…A common feature of these lesions is a reduction in the high frequency aVOR gain and a reduction in the vestibular time constant (Wade et al 1999). The reduction in the aVOR gain tested at frequencies of 2-6 Hz, can recover to normal range over about 1 year, but the time constant and low frequency aVOR gain may never recover (Fetter and Zee 1988;Black et al 2001;Palla and Straumann 2004;Newlands et al 2005).…”

mentioning

confidence: 98%

Labyrinthine lesions and motion sickness susceptibility

2007

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The angular vestibulo-ocular reflex (aVOR) has a fast pathway, which mediates compensatory eye movements, and a slow (velocity storage) pathway, which determines its low frequency characteristics and orients eye velocity toward gravity. We have proposed that motion sickness is generated through velocity storage, when its orientation vector, which lies close to the gravitational vertical, is misaligned with eye velocity during head motion. The duration of the misalignment, determined by the dominant time constant of velocity storage, causes the buildup of motion sickness. To test this hypothesis, we studied bilateral labyrinthine-defective subjects with short vestibular time constants but normal aVOR gains for their motion sickness susceptibility. Time constants and gains were taken from rotational responses. Motion sickness was generated by rolling the head while rotating, and susceptibility was assessed by the number of head movements made before reaching intolerable levels of nausea. More head movements signified lower motion sickness susceptibility. Labyrinthine-defective subjects made more head movements on their first exposure to roll while rotating than normals (39.8 ± 7.2 vs 13.7 ± 5.5; P < 0.0001). Normals were tested eight times, which habituated their time constants and reduced their motion sickness susceptibility. Combining data from all subjects, there was a strong inverse relationship between time constants and number of head movements (r = 0.94), but none between motion sickness susceptibility and aVOR gains. This provides further evidence that motion sickness is generated through velocity storage, not the direct pathway, and suggests that motion sickness susceptibility can be reduced by reducing the aVOR time constant.

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Vestibular compensation: the neuro-otologist’s best friend

2016

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Why vestibular compensation (VC) after an acute unilateral vestibular loss is the neuro-otologist’s best friend is the question at the heart of this paper. The different plasticity mechanisms underlying VC are first reviewed, and the authors present thereafter the dual concept of vestibulo-centric versus distributed learning processes to explain the compensation of deficits resulting from the static versus dynamic vestibular imbalance. The main challenges for the plastic events occurring in the vestibular nuclei (VN) during a post-lesion critical period are neural protection, structural reorganization and rebalance of VN activity on both sides. Data from animal models show that modulation of the ipsilesional VN activity by the contralateral drive substitutes for the normal push–pull mechanism. On the other hand, sensory and behavioural substitutions are the main mechanisms implicated in the recovery of the dynamic functions. These newly elaborated sensorimotor reorganizations are vicarious idiosyncratic strategies implicating the VN and multisensory brain regions. Imaging studies in unilateral vestibular loss patients show the implication of a large neuronal network (VN, commissural pathways, vestibulo-cerebellum, thalamus, temporoparietal cortex, hippocampus, somatosensory and visual cortical areas). Changes in gray matter volume in these multisensory brain regions are structural changes supporting the sensory substitution mechanisms of VC. Finally, the authors summarize the two ways to improve VC in humans (neuropharmacology and vestibular rehabilitation therapy), and they conclude that VC would follow a “top-down” strategy in patients with acute vestibular lesions. Future challenges to understand VC are proposed.

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Relationship of Static and Dynamic Mechanisms in Vestibuloocular Reflex Compensation

Cited by 26 publications

References 56 publications

Fos Expression in the Rat Vestibular Nucleus Complex after Plugging the Three Semicircular Canals

Fos Expression in the Rat Vestibular Nucleus Complex after Plugging the Three Semicircular Canals

Labyrinthine lesions and motion sickness susceptibility

Vestibular compensation: the neuro-otologist’s best friend

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