Horizontal gaze palsy of cerebral origin An acute lesion of one frontal lobe, such as an infarct, usually causes impersistence or paresis of contralateral gaze (more so than an actual palsy of gaze), and the eyes may for a limited time turn involuntarily toward the side of the cerebral lesion. In most cases of acute frontal lobe damage, the gaze palsy is incomplete and temporary, lasting for a week or less. Almost invariably, it is accompanied by hemiparesis. Forced closure of the eyelids may cause the eyes to move paradoxically to the side of the hemiparesis (Cogan spasticity of conjugate gaze; although this finding is variable and of limited clinical value). Similarly, during sleep, the eyes may also deviate conjugately away from the side of the lesion toward the side of the hemiplegia. Pursuit movements away from the side of the lesion tend to be fragmented or lost. In contrast, posterior parietal lesions reduce ipsilateral pursuit movements but do not cause gaze palsy.
With bilateral frontal lesions, the patient may be unable to turn his eyes voluntarily in any direction but retains fixation and pursuit movements. Occasionally, a deep cerebral lesion, particularly a thalamic hemorrhage extending into the midbrain, will cause the eyes to deviate conjugately to the side opposite the lesion (“wrong-way” gaze); the basis for this anomalous phenomenon is not established, but interference with descending oculomotor tracts in the midbrain has been postulated by Tijssen. It should be emphasized that cerebral gaze paralysis is not attended by strabismus or diplopia, that is, gaze remains conjugate. The usual causes of gaze paresis are vascular occlusion with infarction, hemorrhage, and abscess or tumor of the frontal lobe.
A seizure originating in the frontal lobe may transiently drive the eyes to the opposite side, giving the impression of gaze palsy. In the postictal period, the direction of the gaze deviation may reverse with the eyes directed ipsilateral to the seizure focus. An unexplained phenomenon we have had the opportunity to observe is extreme deviation of the eyes to the side of induced visual hallucinations from an occipital seizure. This may also occur in a rare childhood form of occipital seizures.
A unilateral lesion in the rostral midbrain tegmentum, by interrupting the cerebral pathways for horizontal conjugate gaze before their decussation, may also cause a supranuclear paresis of gaze to the opposite side. Vestibulocerebellar lesions can cause yet another disorder of conjugate gaze that simulates a gaze palsy in which the eyes are forced, or driven to one side in a manner termed “pulsion” that prevents voluntary movement to the other side.
Midbrain lesions affecting the pretectum and the region of the posterior commissure interfere with conjugate movements in the vertical plane. Paralysis of vertical gaze is a prominent feature of the Parinaud or dorsal midbrain syndrome described earlier. Upward gaze in general is affected far more frequently than downward gaze because, as already explained, some of the fibers subserving upgaze cross rostrally and posteriorly between the riMLF and INC and are subject to interruption before descending to the oculomotor nuclei, whereas the pathways for down-gaze apparently project directly downward to oculomotor nuclei from the two controlling centers.