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Brain Advance Access originally published online on May 25, 2005
Brain 2005 128(7):1511-1524; doi:10.1093/brain/awh504
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© The Author (2005). Published by Oxford University Press on behalf of the Guarantors of Brain. All rights reserved. For Permissions, please email: journals.permissions@oupjournals.org

Torsional optokinetic nystagmus after unilateral vestibular loss: asymmetry and compensation

Christophe Lopez1, Liliane Borel1, Jacques Magnan2 and Michel Lacour1

1 Laboratoire de Neurobiologie Intégrative et Adaptative, Université de Provence–CNRS and 2 Service d'Oto-rhino-laryngologie et Chirurgie Cervico-faciale, Hôpital Nord, Marseille, France

Correspondence to: Liliane Borel, Laboratoire de Neurobiologie Intégrative et Adaptative, UMR 6149, Université de Provence–CNRS, Pôle 3C Case B, Centre de Saint-Charles 3, Place Victor Hugo, F-13331 Marseille Cedex 3, France E-mail: borel{at}up.univ-mrs.fr

The aim of this study was to analyse torsional optokinetic nystagmus (tOKN) in 17 patients with Menière's disease before and after (1 week, 1 month and 3 months) a curative unilateral vestibular neurotomy (UVN). The tOKN was investigated during optokinetic stimulations around the line of sight directed towards either the lesioned or the healthy side, at various constant angular velocities. Dynamic properties of tOKN and static ocular cyclotorsion were analysed using videonystagmography. Patients' performances were compared with those of 10 healthy subjects. The results indicate that, in the acute stage after UVN, patients exhibited drastic impairment of tOKN velocity that depended on the direction of stimulation: tOKN velocity increased for ipsilesional stimulations and decreased for contralesional stimulations. These changes were responsible for a dramatic tOKN asymmetry, with ipsilesional directional preponderance of torsional slow-phase eye velocity. The changes were associated with static ocular cyclotorsion towards the operated side. Despite progressive compensation of tOKN deficits over time, tOKN velocity still differed from that recorded preoperatively, and tOKN asymmetry remained uncompensated 3 months after UVN. A static ocular cyclotorsion remained up to 3 months after lesion. These results are the first description of tOKN deficits and recovery after unilateral vestibular loss. They show that vestibular cues contribute to gaze stabilization during optokinetic stimulation around the line of sight. They also strongly suggest that tOKN impairment could be part of the long-term asymmetrical functions reported after unilateral loss of vestibular functions.

Key Words: gaze stabilization; roll optokinetic stimulation; static ocular cyclotorsion; unilateral vestibular neurotomy; functional recovery

Abbreviations: CCW = counterclockwise; CW = clockwise; D – 1 = tests carried out one day before neurotomy; D + 7 = tests carried out one week after neurotomy; D + 30 = tests carried out one month after neurotomy; D + 90 = tests carried out three months after neurotomy; IDP = index of directional preponderance; OKN = optokinetic nystagmus; tOKAN = torsional optokinetic afternystagmus; tOKN = torsional optokinetic nystagmus; UVN = unilateral vestibular neurotomy

Received December 6, 2004. Revised February 22, 2005. Accepted March 15, 2005.


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