Abstracts
Résumé
Les mouvements oculaires ont pour objectifs complémentaires mais antagonistes de changer rapidement l’image sur la rétine, au moyen des saccades, et de stabiliser cette nouvelle image, par différents mouvements oculaires lents. L’analyse sémiologique des principales paralysies oculomotrices permet de localiser le siège des lésions, en particulier dans le tronc cérébral. Les atteintes peuvent être infranucléaires (nerfs) ou nucléaires, touchant aussi bien les saccades que les mouvements oculaires lents (dont le réflexe vestibulo-oculaire), ou supranucléaires, touchant alors sélectivement les saccades ou les mouvements oculaires lents. Les mouvements latéraux sont organisés dans le pont et les mouvements oculaires verticaux dans les pédoncules cérébraux. Parmi les nombreux mouvements oculaires anormaux, les nystagmus sont les plus fréquents et sont en général dus à une atteinte vestibulaire périphérique ou centrale. Enfin, les mouvements oculaires peuvent servir de modèle moteur pour mieux connaître le fonctionnement cérébral. En effet, l’enregistrement de ces mouvements permet de détecter des anomalies légères et d’étudier les mécanismes neuropsychologiques qui préparent ces mouvements, tels que l’attention spatiale, l’inhibition motrice, la prédiction motrice, l’intégration visio-spatiale, la mémoire spatiale, l’apprentissage moteur, la programmation motrice et la motivation ou l’intention.
Summary
Eye movements serve vision, which has two different aims: changing images using saccades, i.e. rapid eye movements, and stabilizing new images on the retina using slow eye movements. Eye movements are performed by ocular motor nuclei in the brainstem, on which supranuclear pathways - originating in the cerebral cortex, cerebellum and vestibular structures - converge. It is useful for the neurologist to know the clinical abnormalities of eye movements visible at the bedside since such signs are helpful for localization. Eye movement paralysis may be nuclear or infranuclear (nerves), involving all types of eye movements, i.e. saccades as well as the vestibulo-ocular reflex (VOR), or supranuclear, in which case the VOR is usually preserved. Lateral eye movements are organized in the pons, with paralysis of adduction (and preservation of convergence) when the lesion affects the medial longitudinal fasciculus (internuclear ophthalmoplegia), paralysis of conjugate lateral eye movements when the lesion affects the abducens nucleus (VI) and the «one-and-a-half» syndrome when both these structures are involved. Vertical eye movements are organized in the midbrain, with ipsilateral oculomotor (III) paralysis and contralateral paralysis of the superior rectus muscle when the third nerve nucleus is unilaterally damaged, supranuclear upward gaze paralysis when the posterior commissure is unilaterally damaged and supranuclear downward gaze paralysis (often coupled with upward gaze paralysis) when the mesencephalic reticular formations are bilaterally damaged. Numerous types of abnormal eye movements exist, of which nystagmus is the most frequent and usually due to damage to peripheral or central vestibular pathways. Cerebral hemispheric or cerebellar damage results in subtle eye movement abnormalities at the bedside, in general only detected using eye movement recordings, because of the multiplicity of eye movement pathways at these levels and their reciprocal compensation in the case of a lesion. Lastly, eye movements can also help the neuroscientist to understand the organization of the brain. They are a good model of motricity allowing us, using eye movement recordings, to study the afferent pathways of the cortical areas that trigger them, and thus to analyze relatively complex neuropsychological processes such as visuo-spatial integration, spatial memory, motivation and the preparation of motor programs.
Appendices
Références
- 1. Tourbah A, Schaison-Cusin M, Bakchine S, et al. Manifestations ophtalmologiques des atteintes du système nerveux. Encycl Med Chir (Elsevier, Paris) 1999; 21-540-A-10: 1-21.
- 2. Pierrot-Deseilligny C. Paralysies oculomotrices par lésions du tronc cérébral. Rev Prat(Paris) 1990; 40: 1197-202.
- 3. Leigh RJ, Zee DS. The neurology of eye movements. New York: Oxford University Press, 1999: 646p.
- 4. Bhidayasiri R, Plant GT, Leigh RJ. A hypothetical scheme for the brainstem control of vertical gaze. Neurology 2000; 54: 1985-93.
- 5. Schon F, Hodgson TL, Mort D, Kennard C. Ocular flutter associated with a localized lesion in the paramedian pontine reticular formation. Ann Neurol 2001; 50: 413-6.
- 6. Pierrot-Deseilligny C, Rivaud S, Gaymard B, et al. Cortical control of saccades. Ann Neurol 1995; 37: 557-67.
- 7. Höllinger P, Zenhaüsern R, Schroth G, Mattle HP. MR findings in Balint's syndrome following intrathecal methotrexate and cytarabine therapy in adult acute lymphoblastic leukemia. Eur Neurol 2001; 41: 166-7.
- 8. Pierrot-Deseilligny C, Müri RM, Ploner C, et al. Cortical control of saccadic eye movements in humans: a model for motricity. Prog Brain Res 2003; 142: 3-17.
- 9. Milea D, Napolitano N, Déchy N, et al. Complete bilateral horizontal gaze paralysis revealing multiple sclerosis. J Neurol Neurosurg Psychiatr 2001; 70: 252-5.
- 10. Vidailhet M, Rivaud S, Gouider-Khouja N, et al. Eye movements in parkinsonian syndromes. Ann Neurol 1994; 35: 420-6.