Vestibular Compensation

Curthoys, Ian S.; Halmagyi, G. Michael

doi:10.1159/000059059

Cited by 71 publications

(71 citation statements)

References 79 publications

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“…Presumed cellular and network mechanisms underlying the recovery of central symmetry after UL in amphibians and mammals have been discussed by a number of authors (Darlington and Smith, 1996;Ris et al, 1995Ris et al, , 2001Vibert et al, 1999;Curthoys and Halmagyi, 1999;Smith and Curthoys, 1989;Dieringer, 1995). Some of these mechanisms can be considered in relation to the lamprey.…”

Section: Discussionmentioning

confidence: 99%

Vestibular compensation in lampreys: restoration of symmetry in reticulospinal commands

Pavlova

Popova

Orlovsky

et al. 2004

Journal of Experimental Biology

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SUMMARY Removal of a vestibular organ (unilateral labyrinthectomy, UL) in the lamprey results in a loss of equilibrium, so that the animal rolls (rotates around its longitudinal axis) when swimming. Owing to vestibular compensation,UL animals gradually restore postural equilibrium and, in a few weeks, swim without rolling. Important elements of the postural network in the lamprey are the reticulospinal (RS) neurons, which are driven by vestibular input and transmit commands for postural corrections to the spinal cord. As shown previously, a loss of equilibrium after UL is associated with disappearance of vestibular responses in the contralateral group of RS neurons. Are these responses restored in animals after compensation? To answer this question, we recorded vestibular responses in RS neurons (elicited by rotation of the compensated animal in the roll plane) by means of chronically implanted electrodes. We found that the responses re-appeared in the compensated animals. This result supports the hypothesis that the loss of equilibrium after UL was caused by asymmetry in supraspinal motor commands, and the recovery of postural control in compensated animals was due to a restoration of symmetry.

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Section: Discussionmentioning

confidence: 99%

Vestibular compensation in lampreys: restoration of symmetry in reticulospinal commands

Pavlova

Popova

Orlovsky

et al. 2004

Journal of Experimental Biology

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“…Further studies investigating both, the semicircular canal function by caloric and head impulse testing as well as otolithic function by vestibular evoked myogenic potentials will allow gaining a better insight on the pattern of vestibular nerve affection and on the extent of recovery. Further possible explanations of protracted recovery include age, the percept of vestibular symptoms including visual disturbances [76] and the previous function of the vestibular system [5,77].…”

Section: The Impact Of Vc On Recoverymentioning

confidence: 99%

Neurobiological Mechanisms of Acute Vertigo

Tarnutzer

Palla

2013

Future Neurol.

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The vestibular system provides us with reflexive responses of eye movements and balance control, as well as with perceptual estimates of self-motion and gravity direction. Crucial to its proper functioning is a bilaterally balanced vestibular signal originating from the vestibular end organs in the inner ears and projecting via vestibular nerve afferents to the brainstem vestibular nuclei. Disturbances of the bilateral vestibular interplay become evident in cases of acute unilateral peripheral vestibular deafferentation. The resultant sudden imbalance of vestibular afferent tone at the level of the vestibular nuclei leads to pronounced ocular-motor and postural impairment, as well as to intensive vertigo and/or dizziness, accompanied by autonomic symptoms, such as nausea and vomiting. Subsequent compensatory mechanisms efficiently diminish these static symptoms (such as spontaneous nystagmus) within days and allow functional recovery of dynamic symptoms (such as blurred vision during fast head turns) to such a degree that most patients return to their normal daily activities within weeks. This article aims to provide an understanding about the pathophysiological changes after unilateral vestibular deafferentation and the current knowledge on the compensatory mechanisms. SummaryThe vestibular system provides us with reflexive responses of eye movement and

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“…The signs and symptoms that follow UVD have since been characterized in a range of species using a wide range of techniques, including posturography, video oculography, 3D search coil recordings of eye movements and X-ray cinematography. Although there are species differences, the nature of the vestibular deafferentation syndrome and the subsequent behavioral recovery are broadly similar in various animals from the goldfish and frog to monkey and man, indicating that the underlying processes share many commonalities [1,2,4,10] .…”

Section: Static and Dynamic Signs And Symptoms Of Unilateral Vestibulmentioning

confidence: 99%

“…Many studies have investigated the effects of unilateral vestibular deafferentation (UVD) on neurons in the VN, and possible mechanisms of deafferentation-induced plasticity in the VN and cerebellum, in various species [reviewed in ref. [1][2][3][4][5][6][7][8]. At the same time, detailed studies of the behavioral deficits that follow UVD in animals and humans have emphasized that VC is by no means a single process.…”

mentioning

confidence: 99%

“…At the same time, detailed studies of the behavioral deficits that follow UVD in animals and humans have emphasized that VC is by no means a single process. There are wide differences in the time course and ultimate level of compensation for the range of oculomotor, postural and cognitive deficits that follow UVD [1,2,5] . Thus although VC refers to the overall behavioral recovery that takes place after vestibular damage it is clear that the underlying physiological processes are diverse, with differences in the signals that initiate and drive them, their time course and end points.…”

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confidence: 99%

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Cellular Mechanisms of Vestibular Compensation

Paterson¹,

Menzies²,

Bergquist³

et al. 2004

Neuroembryol Aging

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Vestibular compensation, the behavioral recovery that takes place after unilateral vestibular deafferentation, is a complex and multifactorial process involving synaptic and neuronal plasticity in the vestibular nuclei, cerebellum and related structures. Recent experimental evidence suggests that changes in the intrinsic properties of the vestibular nucleus neurons, changes in the efficacy of their inhibitory synaptic inputs, activity-dependent rewiring of synaptic connectivity in the vestibular brainstem, and changes in the cerebellar control of the brainstem neurons are involved in the rebalancing of resting activity of the vestibular neurons after deafferentation. In this article, we review recent advances in understanding the cellular and molecular mechanisms of vestibular compensation.

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Vestibular Compensation

Cited by 71 publications

References 79 publications

Vestibular compensation in lampreys: restoration of symmetry in reticulospinal commands

Vestibular compensation in lampreys: restoration of symmetry in reticulospinal commands

Neurobiological Mechanisms of Acute Vertigo

Cellular Mechanisms of Vestibular Compensation

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