Skip Navigation

This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Search for citing articles in:
ISI Web of Science (43)
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by REULEN, J. P. H.
Right arrow Articles by HOGENHUIS, L. A. H.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by REULEN, J. P. H.
Right arrow Articles by HOGENHUIS, L. A. H.
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Brain, Vol. 106, No. 1, 121-140, 1983
© 1983 Oxford University Press


research-article

EYE MOVEMENT DISORDERS IN MULTIPLE SCLEROSIS AND OPTIC NEURITIS

J. P. H. REULEN, E. A. C. M. SANDERS and L. A. H. HOGENHUIS

Department of Medical Physics, Vrije Universiteit, 1081 BT Amsterdam, the Department of Neurology, Academisch Ziekenhuis, Leiden and the Department of Neurology, De Goddelijke Voorzienigheid, Sittard The Netherlands

Horizontal saccadic and smooth pursuit eye movements were studied in 84 patients with multiple sclerosis (MS) and 21 patients with optic neuritis (ON). The MS patients were clinically classified as ‘definite’, ‘probable’, or ‘possible’; subclinical eye movement disorder was found in 80 per cent of the definite, 74 per cent of the probable and 60 per cent of the possible category. Five of the ON patients (25 per cent) showed a subclinical eye movement deficit; these 5 were young patients with a recent history of ON. In a group of 27 MS patients with symptoms of spinal cord involvement only, 14 showed subclinical oculomotor disorder indicating the involvement of cerebral structures in the demyelination process. A study of the correlation between specific eye movement parameters and results of visual evoked response (VER) tests revealed that saccadic latency or smooth pursuit abnormalities are not correlated with prolonged VER latencies (P-100 peak latency). This indicates that lesions beyond the primary visual pathway contribute substantially to both parameters of oculomotor dysfunction.

A significant correlation was found between prolonged saccadic latency and smooth pursuit deficit. An explanation for this finding based on functional aspects of the saccadic and smooth pursuit systems and their mutual interaction is presented. The occurrence of internuclear ophthalmoplegia (INO) is significantly related to an increase of saccadic latency. This finding indicates that demyelination in the patients manifesting INO may not be restricted exclusively to one or both medial longitudinal fasciculi, but may extend to other brainstem structures which are functionally involved in the programming of saccades.

The findings confirm the value of standardized objective examination of eye movements in the detection and clarification of subclinical lesions in the central nervous system of patients with an early diagnosis of MS or ON.

Received June 1, 1982. Revised August 24, 1982.
Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
Arch NeurolHome page
O. Meienberg, R. Muri, and P. A. Rabineau
Clinical and Oculographic Examinations of Saccadic Eye Movements in the Diagnosis of Multiple Sclerosis
Arch Neurol, May 1, 1986; 43(5): 438 - 443.
[Abstract] [PDF]


Home page
Arch NeurolHome page
R. M. Muri and O. Meienberg
The Clinical Spectrum of Internuclear Ophthalmoplegia in Multiple Sclerosis
Arch Neurol, September 1, 1985; 42(9): 851 - 855.
[Abstract] [PDF]



Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.