Recovery of Vestibulo-Ocular Reflex Symmetry After an Acute Unilateral Peripheral Vestibular Deficit

Allum, J.H.J.; Cleworth, Taylor W.; Honegger, F.

doi:10.1097/mao.0000000000001054

Cited by 21 publications

(18 citation statements)

References 31 publications

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“…A/ there is immediately after lesion either a central component of the vestibular compensation phenomenon (Allum and Ledin 1999;Fetter and Dichgans 1990) or a peripheral component with the otolith system (Maire and van Melle, 2000). However this hypothesis is not supported by Metcalfe and Gresty (1992), who did not find immediate central compensation phenomenon in their unilateral patients after complete vestibular nerve section.…”

Section: Vir Is Correct In Acucp Ipsilateralmentioning

confidence: 99%

“…The vestibulo-ocular reflex (VOR) keeps gaze stabilized in space during head movements. This apparently simple reflex (Collewijn 1989) has been extensively investigated, for example with patients suffering and recovering from vestibular disorders (Allum and Ledin 1999, Fetter and Dichgans 1990, Maire and Van Melle 2000. Vestibular input contributes directly to the VOR but also to non-reflexive perceptual responses including body orientation (Guedry 1974, Young 1981.…”

Section: Introductionmentioning

confidence: 99%

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Effects of vestibular disorders on vestibular reflex and imagery

et al. 2017

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The aim of this study was to establish the effect of vestibular lesion on vestibular imagery. Subjects were required to estimate verbally their passively travelled rotation angles in complete darkness, i.e., to activate vestibular imagery. During motion, the vestibulo-ocular reflex (VOR) was measured. Thus, we examined the coherence between the vestibulo-ocular reflex and self-rotation imagery, with vestibular-lesioned patients and healthy participants. Unilateral acute and chronic patients, bilateral patients, and healthy subjects were compared. The stimulus was a sequence of eight successive passive rotations, with four amplitudes (from 90° to 360°) in two directions. The VOR gain was lower in patients with unilateral lesions, for ipsilateral rotations. The healthy subjects had the highest gain and the bilateral group the lowest, on both rotation sides. Thanks to vestibular compensation after acute unilateral neuritis, the VOR gain increased in lesion side and decreased in healthy side, resulting in a similar gain in both sides. A deficit of vestibular imagery was found exclusively in patients with bilateral hyporeflexia, on both sides. The performance in vestibular imagery was good in the control group and correct in the unilateral patients. Finally, we found a significant correlation between the efficiency of the VOR and that of vestibular imagery, exclusively in the bilateral patients. The present study shows the complex relationship between vestibular imagery and the VOR. This imagery test contributes to another assessment of the spatial handicap of vestibular patients. It seems particularly interesting for patients with bilateral canal paresis and could be used to confirm this diagnosis.

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Section: Vir Is Correct In Acucp Ipsilateralmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Effects of vestibular disorders on vestibular reflex and imagery

et al. 2017

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“…The peripheral recovery can be determined for the lateral canal using caloric tests. Thus, in cases of remaining pathological canal paresis, a range of vHIT gains are obtained in the post-acute stage depending on the amount of central compensation ( 12 ). Correspondingly, these cases with central compensation but pathological canal paresis result in normal vHIT gains which reduce the sensitivity of the vHIT for vestibular loss to 74% ( 12 ).…”

Section: Introductionmentioning

confidence: 99%

“…Secondly, we examined whether these compensation processes could account for differences in roll, pitch and yaw asymmetries reported by Aw et al ( 4 ). Our estimate of the period with fastest amount of compensation was based on our exponential modeling ( 12 ) of the improvement time course of the lateral canal gain after diagnosis of UVN. This modeling led to an estimate of 5.9 weeks for the time constant of gain improvement.…”

Section: Introductionmentioning

confidence: 99%

Improvement of Asymmetric Vestibulo-Ocular Reflex Responses Following Onset of Vestibular Neuritis Is Similar Across Canal Planes

Allum

Honegger

2020

Front. Neurol.

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Background: We examined whether, after onset of acute unilateral vestibular neuritis (aUVN), initial disease effects, subsequent peripheral recovery and central compensation cause similar changes in vestibular ocular reflex (VOR) gains in all 3 semi-circular canal planes. Methods: 20 patients, mean age 56.5 years, with pathological lateral canal video head impulse test (vHIT) VOR gains due to aUVN, were subsequently examined with vHIT in all 3 canal planes on average 4.3 and 36.7 days (“5 weeks”) after aUVN onset. Results: Lateral and anterior deficit side (DS) average gains equaled 0.41 at aUVN onset. Non-deficit, normal, side (NS) gains were 0.88 and 0.81, respectively. Mean posterior DS gain was similar at onset, 0.43, provided only gains lower than 0.6 (lower limit of healthy controls) were considered. NS posterior mean gain at onset (0.68) was less ( p ≤ 0.0006) than lateral and anterior NS gains. After 5 weeks, DS lateral, anterior and posterior canal gains increased ( p ≤ 0.05), on average, to 0.65, 0.59, and 0.58, respectively. NS gains increased to 0.91, 0.87, and 0.76 ( p = 0.007), respectively. At 5 weeks deficit-lateral/normal-lateral canal plane gain asymmetries were significantly ( p < 0.0008) reduced from 36.9 to 19.4%, deficit-anterior/normal-posterior asymmetry decreased from 28.6 to 18.1%, while deficit-posterior/normal-anterior asymmetry changed from 29.7 to 21.4%, all to circa 20%. Roll plane asymmetries decreased slightly over 5 weeks (28.6–18.1%) but pitch plane asymmetries remained significantly less ( p = 0.001), not different from 0% regardless of initial DS posterior canal vHIT gain. Yaw plane asymmetry changes are identical to those of the lateral canals (36.7–19.4%). Conclusions: These results indicate that, at onset, aUVN of the superior vestibular nerve has a similar effect on lateral and anterior deficit DS VOR gains, and on posterior DS canal VOR gains if the inferior nerve was also affected at onset. The significant improvements to equal 5 week levels of DS gains and slightly greater posterior NS gain improvements, compared to lateral and anterior NS gains, yielding a common canal plane gain asymmetry of 20% at 5 weeks, suggest similar neural compensation mechanisms were active along VOR pathways. Unexpectantly, canal plane improvement was not replicated in pitch plane asymmetries.

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“…Alternatively, she could be complaining of further but less severe, vertigo attacks; if the attacks are spontaneous, it might be that she actually has MD; if the attacks are positional, it might be PC BPV as a result of the vestibular neuritis [8, 116]. After acute vestibular neuritis, only some patients recover canal function—as judged by vHIT or by caloric test or rotational testing [117, 118]. If the vHIT is still impaired on one side, the diagnosis of vestibular neuritis can be safely made in retrospect, but some patients do recover vestibular function—it probably has nothing to do with steroid treatment [119]—and have a normal vHIT (and caloric), so that the distinction between recovered (as opposed to simply compensated) vestibular neuritis [118, 120] and cerebellar infarction cannot now be made clinically, and will need MRI.…”

Section: Video Head Impulse Testingmentioning

confidence: 99%