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Brain Advance Access originally published online on June 30, 2009
Brain 2009 132(8):2114-2124; doi:10.1093/brain/awp165
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© The Author (2009). Published by Oxford University Press on behalf of the Guarantors of Brain. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Anatomical correlates of ocular motor deficits in cerebellar lesions

B. Baier1, P. Stoeter2 and M. Dieterich1,3

1 Department of Neurology, Johannes Gutenberg-University, Mainz, Germany 2 Department of Neuroradiology, Johannes Gutenberg-University, Mainz, Germany 3 Department of Neurology, Ludwig-Maximilians-University, Munich, Germany

Correspondence to: Bernhard Baier, MD, PhD, Department of Neurology, University of Mainz, Langenbeckstr. 1, 55131 Mainz, Germany E-mail: baierb{at}uni-mainz.de

Humans are able to stabilize the images of moving targets on the retina by means of smooth pursuit eye movements. After the pontine level, all smooth pursuit pathways pass through the cerebellum. Previous animal studies gave evidence that two specific lesion sites within the cerebellum cause smooth pursuit disorders: those of the flocculus/paraflocculus and the vermis including lobule VI, VII, the uvula and the deep cerebellar nuclei. To date, there have been only a few lesion studies in patients with smooth pursuit disorders that do not allow direct comparison with a control group. In the present study, new lesion mapping techniques determined which cerebellar structures were involved in patients with deficits of smooth pursuit eye movements, slow phase of optokinetic nystagmus (OKN) and fixation suppression of vestibulo-ocular reflex, i.e. in eye movements that are considered to belong to the smooth pursuit system. The aim was to elucidate whether there is an anatomical and clinical link between these different eye movement disorders. Seventeen patients with acute, mainly unilateral cerebellar infarctions and an intact gain of the smooth pursuit system were compared with 11 patients with cerebellar lesions and deficient gain of sinusoidal smooth pursuit eye movements by means of lesion-mapping imaging. In addition, lesion analyses were conducted in subgroups with impaired fixation suppression of vestibulo-ocular reflex and deficient gain of the slow phase of the OKN. The uvula and partly the vermal pyramid were found to be the structures commonly damaged in patients with deficient gain of the horizontal sinusoidal smooth pursuit eye movement, of the slow phase of the OKN and impaired fixation suppression of vestibulo-ocular reflex; and were less involved in patients with intact smooth pursuit system. The present data give evidence for an anatomical link between sinusoidal smooth pursuit eye movements, fixation suppression of vestibulo-ocular reflex and the slow phases of OKN implying that the uvula and the vermal pyramid are important structures for generating slow phases within the smooth pursuit network in humans.

Key Words: smooth pursuit system; vestibulo-ocular reflex; optokinetic nystagmus; cerebellar infarctions

Abbreviations: OKN, optokinetic nystagmus; VOR, vestibular ocular reflex; VORS, suppression of the vestibulo-ocular reflex

Received December 31, 2008. Revised May 14, 2009. Accepted May 15, 2009.


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