Internuclear and supranuclear disorders of eye movements: clinical features and causes

Abstract

Eye movements bring visual stimuli to the fovea and also maintain foveal fixation on a moving target and during head movements. These movements are performed by the ocular motor system that consists of ocular motor nerves and nuclei in the brainstem originating in the cerebral cortex, cerebellum, vestibular structures, and the extraocular muscles. The ocular motor system is divided according to anatomic location into infranuclear, nuclear, internuclear, and supranuclear components. It is important to distinguish supranuclear and internuclear from nuclear and infranuclear disturbances affecting cranial nerves III, IV, and VI, because the disturbances are of highly varied causes and present different clinical pictures. Internuclear ophthalmoplegia is due to a lesion of the medial longitudinal fasciculus, caused by multiple sclerosis in younger patients, particularly when the ophthalmoplegia is bilateral, and usually of vascular origin in the elderly. Eye movement abnormalities of supranuclear origin are characterized by gaze palsies, tonic gaze deviation, saccadic and smooth pursuit disorders, vergence abnormalities, nystagmus, and ocular oscillations. Supranuclear disorders result from lesions above the level of the ocular motor nerve nuclei. If oculocephalic maneuvers move the eyes appropriately, the lesion causing the gaze palsy is supranuclear. Supranuclear disorders account for almost 10% of all patients with disorders of eye movements.

Clinical Study of Twenty-One Patients with Pure Midbrain Infarction

“…MLF syndrome occurred in patients with rostral and caudal PM area infarction in this study. This finding is associated with the fact that the MLF is situated in both the rostral and caudal part of the midbrain [13]. …”

“…The MLF is situated in the ventromedial area from midbrain to medulla [12,13]. The MLF in the rostral midbrain is located at the lateral part of the oculomotor nerve nucleus.…”

Eye Movement Abnormalities in Spinocerebellar Ataxias

“…Peripheral abnormalities result from lesions in the oculomotor muscles or nerves, whereas the central disturbances are caused by lesions in the brainstem, cerebellum or other higher-level centers (Karatas, 2009). Oculomotor signs of cerebellar impairment include pathological nystagmus such as downbeat, rebound and periodic alternating nystagmus, as well as abnormal pursuit, VOR/OKR abnormalities and saccadic dysmetria (Robinson & Fuchs, 2001;Strupp et al, 2011).…”

“…Affectations in the basal ganglia can lead to reduced ability to initiate voluntary eye movements and to suppress unwanted saccades, in addition to deficits in memory-guided saccades, eye-head coordination and eye-hand coordination (Hikosaka et al, 2000;Shires et al, 2010). Frontal cortex lesions produce prolongation of saccadic latency, impaired ability to make saccades to remembered target locations and errors on the antisaccade task, as well as delayed initiation of smooth pursuit and increase of catch up saccades (Pierrot-Deseilligny et al, 2004;Thurtell et al, 2007;Karatas, 2009). …”

Vertical Gaze Palsy due to Infarct at Thalamus-Basal Ganglia

“…The ocular motor system is classified according to anatomic location into infranuclear, nuclear, internuclear, and supranuclear components [1]. Supranuclear disorders result from lesions above the level of the ocular motor nerve nuclei and account for almost 10% of all patients with disorders of eye movements [1][2][3][4]. Supranuclear disorders are characterized by gaze palsies, tonic gaze deviation, saccadic and smooth pursuit disorders, vergence abnormalities, nystagmus, and ocular oscillations [1,5].…”