A mechanism of central compensation of vestibular function following hemilabyrinthectomy.

Precht, W.; Shimazu, Hiroshi; Markham, Charles H.

doi:10.1152/jn.1966.29.6.996

Cited by 425 publications

(110 citation statements)

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“…Shimazu and Precht (1966) have shown that there are strong inhibitory influences on Type I vestibular neurons originating from the contralateral labyrinth. Type I neurons depolarize and hyperpolarize to ipsi-and contralateral rotation, respectively, and are considered to be major vestibular neurons because of their lower threshold to rotary stimulation (Precht, Shimazu, & Markham, 1966). Weak electrical stimulation of the contralateral vestibular nerve inhibits the spontaneous discharges of Type I neurons, whereas midline incisions which interrupt the commissural fibers from the contralateral labyrinth completely abolish such inhibition.…”

Section: Discussionmentioning

confidence: 99%

The effect of visual-vestibular conflict on the latency of steady-state visually induced subjective rotation

Wong

Frost

1981

Perception & Psychophysics

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Two experiments were carried out to test the hypothesis that the long onset latency of steady-state subjective rotation induced by rotating a tall striped drum around a stationary observer is the result of visual-vestibular conflict. A reduction of this conflict should, therefore, reduce the length of the latency period. In Experiment 1, visual-vestibular conflict was reduced by providing the observers with corroborating vestibular stimulation at the start of optokinetic stimulation. Onset latencies were found to be significantly shortened with corroborating vestibular stimulation, but to be unaffected by noncorroborating vestibular stimulation. In Experiment 2, testing was done on a group of patients with unilateral (right labyrinth) Meniere's disease, which produces decreased vestibular sensitivity to rightward body rotation and increased vestibular sensitivity to leftward body rotation. Visual-vestibular conflict during subjective rotation to the right should therefore be decreased, while during leftward subjective rotation it should be increased. The prediction that the latency to steadystate subjective rotation should be shorter than normal with subjective rotation to the left was supported.

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Section: Discussionmentioning

confidence: 99%

The effect of visual-vestibular conflict on the latency of steady-state visually induced subjective rotation

Wong

Frost

1981

Perception & Psychophysics

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“…In addition, there is also an increased inhibitory drive from the contralesional MVN and transmitted via the reciprocal commissural inhibitory system to ipsilesional Type I MVN neurons (see [20] for review). The firing rate of contralesional Type I MVN neurons, at the same time, either remains unchanged or increases slightly [21,22], as the inhibitory drive of contralesional Type II MVN neurons (normally provided by ipsilesional Type I neurons) on these neurons is lost [17] (see also [23,24]. Accordingly, it is this marked asymmetry at the level of the MVN neurons that is believed to cause the acute ocular motor, postural and sensory deficits and complaints.…”

Section: Pathophysiological Changes Occurring In Unilateral Vestibulamentioning

confidence: 99%

“…Immediately after UVD, a drop of normal resting discharge rate and sensitivity of ipsilesional Type I MVN neurons is observed [17][18][19], as the excitatory synaptic input from the ipsilateral vestibular afferents is lacking (see figure 2, panel B). In addition, there is also an increased inhibitory drive from the contralesional MVN and transmitted via the reciprocal commissural inhibitory system to ipsilesional Type I MVN neurons (see [20] for review).…”

Section: Pathophysiological Changes Occurring In Unilateral Vestibulamentioning

confidence: 99%

“…The principle of regaining balanced activity within the vestibular system is encountered not only at the level of the VN, but also within the commissural inhibitory pathways connecting both MVN [17,[46][47][48]. Specifically, Bergquist and colleagues [24] demonstrated in rats that the GABA release in ipsilesional MVN neurons immediately after UVD was markedly increased.…”

Section: Re-organization Of Synaptic Pathways To the Mvnmentioning

confidence: 99%

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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 recovery of these reflexes is termed "vestibular compensation," and its onset can be detected both behaviorally and electrophysiologically within 10 h post-UL (Beraneck et al 2008;Precht et al 1966;Ris and Godaux 1998;Schaefer and Meyer 1973).…”

Section: Chronic Improvement Of Vestibular Modulation Of Css and Sss mentioning

confidence: 99%

Modulated discharge of Purkinje and stellate cells persists after unilateral loss of vestibular primary afferent mossy fibers in mice

Barmack

Yakhnitsa

2013

Journal of Neurophysiology

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A mechanism of central compensation of vestibular function following hemilabyrinthectomy.

Cited by 425 publications

References 0 publications

The effect of visual-vestibular conflict on the latency of steady-state visually induced subjective rotation

The effect of visual-vestibular conflict on the latency of steady-state visually induced subjective rotation

Neurobiological Mechanisms of Acute Vertigo

Modulated discharge of Purkinje and stellate cells persists after unilateral loss of vestibular primary afferent mossy fibers in mice

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