Vestibular influences are of particular importance in stabilizing images on the retina during head and body movement. By means of the vestibuloocular reflex (VOR), a prompt short latency movement of the eyes is produced that is equal and opposite to movement of the head. During sustained rotation of the head, the VOR is supplemented by the optokinetic system, which enables one to maintain compensatory eye movements for a more prolonged period. If the VOR is lost, as occurs with disease of the vestibular apparatus or eighth nerve, the slightest movements of the head, especially those occurring during locomotion, cause a movement of images across the retina large enough to impair vision. A unilateral loss of the VOR strongly implicates a disease of the vestibular apparatus on the side toward the rotation of the head. When objects are tracked using both eye and head movements, the VOR must be suppressed, otherwise the eyes would remain fixed in space; to accomplish this, the smooth pursuit signals cancel the unwanted vestibular ones (Leigh and Zee). It follows that the inability to suppress the VOR, while viewing a target moving with the patient’s head or body, is indicative of a defect of supranuclear pursuit.
As already mentioned, the signals for volitional horizontal gaze saccades originate in the eye field of the opposite frontal lobe (area 8 of Brodmann, see Fig. 21-2) and are modulated by the adjacent supplementary motor eye field and by the posterior visual cortical areas. Leichnetz traced the cortical-to-pontine pathways for saccadic horizontal gaze in the monkey. These fibers traverse the internal capsule and separate at the level of the rostral diencephalon into two bundles, the first being a primary ventral “capsular–peduncular” bundle, which descends through the most medial part of the cerebral peduncle. This more ventral pathway undergoes a partial decussation in the low midbrain, at the level of the trochlear nucleus, and terminates mainly in the vaguely defined paramedian pontine reticular formation (PPRF) of the opposite side, neurons of which, in turn, project to the adjacent sixth nerve nucleus (Fig. 13-1). A second, more dorsal “transthalamic” bundle is predominantly uncrossed and courses through the internal medullary lamina and paralaminar parts of the thalamus to terminate diffusely in the pretectum, superior colliculus, and periaqueductal gray matter. An off-shoot of these fibers (the prefrontal oculomotor bundle) projects to the rostral part of the oculomotor nucleus and to the ipsilateral rostral interstitial nucleus of the medial longitudinal fasciculus (riMLF) and to the interstitial nucleus of Cajal (INC), which are involved in vertical eye movements, as discussed in the next section.
The pathways for smooth pursuit movements are less well defined. One probably originates in the posterior parietal cortex and the adjacent temporal and anterior occipital cortex (area MT of the monkey), descending to the ipsilateral dorsolateral pontine nuclei. Also contributing to smooth pursuit movements are projections from the frontal eye fields to the ipsilateral dorsolateral pontine nuclei. The latter, in turn, project to the flocculus and dorsal vermis of the cerebellum, which provide stability for the pursuit movements. However, for the purposes of clinical work, lesions of the posterior parietal cortex are the ones known to impair pursuit toward the damaged side. Part of the frontal eye fields have been shown experimentally to participate in pursuit eye movements, but the influence of this area on pursuit is far less than that of the parietal lobes and is insignificant clinically.