Internuclear ophthalmoplegia (INO) is characterized by inability to adduct one eye, combined with nystagmus of the other, abducted eye (dissociated nystagmus), on attempted lateral gaze. It is due to a lesion of the medial longitudinal fasciculus (MLF) on the side of the nonadducting eye and at a level between the nuclei of CN III and CN VI. Bilateral MLF lesions cause bilateral INO. Both eyes can adduct normally during convergence. More rostral lesions lead to convergence paresis without nystagmus; more caudal lesions lead to paresis of the lateral rectus muscle. Multiple sclerosis and vascular disorders are the most common causes of INO. Unilateral pontine lesions cause ipsilateral gaze palsy (the gaze points away from the side of the lesion) but leave vertical eye movement largely intact. Co-involvement of the MLF leads to one-and-a-half syndrome (ipsilateral pontine gaze palsy + INO), e. g., paresis of conjugate gaze to the left and impaired adduction of the left eye on looking to the right.
Supratentorial lesions. Extensive cortical or subcortical hemispheric lesions produce contralateral gaze palsy (patient gazes toward the side of the lesion). Slow reflex movements of the eyes in all directions are still possible because the optokinetic reflex is not affected. In occipital lesions, the optokinetic reflex is absent; voluntary eye movements are preserved, but the eyes can no longer follow slowly moving objects. Abnormal, diffuse elevation of activity within a hemisphere (e. g., because of an epileptic seizure) causes contralateral gaze deviation. For further information on horizontal and vertical gaze palsy, see page 70.
Complete right oculomotor palsy
(looking straight ahead)
Right trochlear palsy (looking straight ahead)
Abducens palsy (looking straight ahead)
- Nucleus praepositus hypoglossi (lateral gaze)
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