There are important vestibulocerebellar influences on both smooth pursuit and saccadic movements (see also Chaps. 5 and 14). The flocculus and posterior vermis of the cerebellum receive abundant sensory projections from proprioceptors of the cervical musculature (responsive to head velocity), the retinas (sensitive to target velocity), proprioceptors of eye muscles (eye position and eye velocity), auditory and tactile receptors, and the superior colliculi and PPRF. Cerebellar efferents concerned with ocular movement project onto the vestibular nuclei. The latter, in turn, influence gaze mechanisms through several projection systems: one, for horizontal movements, consists of direct projections from the vestibular nuclei to the contralateral sixth nerve nucleus; another, for vertical movements, projects via the contralateral MLF to third and fourth nerve nuclei (Figs. 13-1 and 13-2).
Lesions of the flocculus and posterior vermis are consistently associated with deficits in smooth pursuit movements and an inability to suppress the vestibuloocular reflex by fixation (Baloh et al). Floccular lesions are also an important cause of downbeat nystagmus. As indicated in Chap. 5, patients with cerebellar (floccular) lesions are unable to hold eccentric positions of gaze and must make repeated saccades to look at a target that is away from the neutral position (gaze-evoked nystagmus). This phenomenon is explained by the fact that with acute, one-sided lesions of the vestibulocerebellum, the inhibitory discharges of the Purkinje cells onto the ipsilateral medial vestibular nucleus are removed, and the eyes deviate away from the lesion. When gaze to the side of the lesion is attempted, the eyes drift back to the midline, and fixation can be corrected only by a saccadic jerk. The head and neck may also turn away from the lesion (the occiput toward the lesion and the face away). In addition, the vestibuloocular reflexes, which coordinate eye movements with head movements, are improperly adjusted (Thach and Montgomery). The interested reader can find further details concerning cerebellar influences on ocular movements in the monograph by Leigh and Zee and the review by Lewis and Zee.
Testing of Conjugate Gaze
It is apparent from the foregoing remarks that there is considerable clinical information to be obtained from an analysis of ocular movements. To fully examine the eye movements, the patient should be asked to look quickly to each side as well as up and down (saccades) and to follow a moving target (pursuit of a light, the examiner’s finger, or an optokinetic drum). A patient with stupor and coma can be examined by passively turning the head or by irrigating the external auditory canals; these are vestibular stimuli to reflex eye movement as discussed in Chaps. 14 and 16.
Most individuals make accurate saccades to a target. Alterations of saccadic movements, particularly overshooting of the eyes (hypermetria), are characteristic of a cerebellar lesion. Slowness of saccadic movements is mainly the result of disease of the basal ganglia such as Huntington and Wilson diseases, ataxia-telangiectasia, progressive supranuclear palsy, multiple system atrophy, and certain lipid storage diseases. Lesions involving the PPRF may also be accompanied by slow saccadic movements to the affected side. Hypometric, slow saccades occurring only in the adducting eye indicate an incomplete internuclear ophthalmoparesis caused by a lesion of the ipsilateral MLF. When the earliest sign of a progressive eye movement disorder is slow saccades in the vertical plane, the likely diagnosis is progressive supranuclear palsy, but the same sign may occur in Parkinson disease and several less common processes that affect the basal ganglia, as discussed further on under “Vertical Gaze Palsy.” Slow up-and-down saccades are also found in Niemann-Pick disease type C.