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Brain, Vol. 113, No. 3, 821-846, 1990
© 1990 Guarantors of Brain


research-article

OCULOMOTOR DISTURBANCES DURING VISUAL-VESTIBULAR INTERACTION IN WALLENBERG'S LATERAL MEDULLARY SYNDROME*

WALTER WAESPE1, and WERNER WICHMANN2

1Department of Neurology Zürich, Switzerland 2Department of Neuroradiology, University Hospital of Zürich Zürich, Switzerland

Correspondence to: Correspondence to: Professor W. Waespe, Department of Neurology, University Hospital, Frauenklinikstrasse 29, CH-809I Zurich, Switzerland

Transient and lasting oculomotor disturbances during visual-vestibular interaction are described in 9 patients with Wallenberg's lateral medullary syndrome. In all patients magnetic resonance imaging (MRI) demonstrated a single focal area of pathological signal intensity in the (dorso)-lateral medulla suggesting infarction. In 2 of these 9 patients and in 3 further patients with no medullary signs, the infarction involved the cerebellar territory of the posterior inferior cerebellar artery (PICA). Acutely, all patients with Wallenberg's syndrome (except 1) had saccadic lateropulsion and spontaneous nystagmus in light with the horizontal fast component beating to the contralateral normal side. The velocity of the slow drift to the side of the lesion was dependent on eye position and induced a characteristic asymmetry of the visually and vestibularly elicited slow eye movements. In most patients smooth pursuit, optokinetic nystagmus and visual suppression of the vestibulo-ocular reflex were still impaired when this spontaneous drift was minimal or absent. The oculomotor disturbances in patients with and without cerebellar infarction are compared. The following conclusions are made. (1) The spontaneous drift that is dependent on eye position is mostly created by ‘ocular lateropulsion’, that is, a tonic bias within the oculomotor system which may have several sources. (2) The abnormalities and asymmetries of oculomotor responses during visual-vestibular stimulation cannot solely be explained by this spontaneous drift and its interaction with otherwise normal eye movements. Instead, structures and pathways are damaged in Wallenberg's syndrome which mediate visual and/or motor signals important for the cerebellar control of visually-guided slow eye movements. (3) Damage to these pathways occurs in the lateral medulla, as the MRI findings show that in most patients the cerebellum is rarely involved, but no definite conclusion can be made as to which of the fibres travelling in the inferior peduncle to the cerebellum may be interrupted.

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Received May 16, 1989. Accepted July 17, 1989.


* To Professor G. Baumgartner on his 65th birthday.


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