Normally, movement of the head at a rate of one to two cycles per second does not cause blurring of vision because of the rapidity with which the VOR accomplishes compensatory eye movements. Dynamic visual acuity is a term applied to testing by having the patient read an eye chart while the head is rotated back-and-forth. A substantial drop in acuity occurring with head movements at this speed is indicative of failure of the VOR. Zee has described yet another means of testing the VOR in which the examiner observes the optic nerve head while the patient rotates the head back and forth. With a normal VOR, the optic disc does not appear to move since the eye’s position in space has remained unchanged. However, if the VOR is impaired, the optic nerve head appears to oscillate.
Visual Fixation Reflex (Suppression of the Vestibuloocular Reflex)
The ability to suppress the VOR by visual fixation provides considerable information and may be tested by rotating the patient in a chair while he fixates on the thumb of his outstretched hand. There should be no loss of fixation at moderate rotational speed. Nystagmus during this maneuver, reflecting the inability to suppress the VOR and maintain fixation, is an abnormal finding. As a result of inability to suppress the VOR, the patient experiences a feeling of instability. Impaired suppression of the VOR occurs with various disorders affecting cerebellar and brainstem circuits that maintain gaze stability; progressive supranuclear palsy and multiple sclerosis are two examples where this finding can be prominent.
Testing the Near Response (Accommodative Triad)
Combined convergence and accommodative movements are tested by asking the patient to look at his thumbnail, the examiner’s finger, or object as it is brought toward the eyes. However, these fusional movements are frequently impaired in the elderly and in confused or inattentive patients and should not be interpreted as the result of disease in the ocular motor pathways. Otherwise, the absence or impairment of these movements should suggest a lesion in the rostral midbrain as a component of the Parinaud syndrome. Convergence spasm, which may mimic bilateral sixth nerve palsy, and retraction nystagmus may accompany paralysis of vertical gaze from a dorsal midbrain lesion. However, when such convergent spasms occur alone, they are usually nonorganic. Cycloplegic eye drops that abolish accommodation and pupillary miosis will sometimes abort psychogenic convergence spasm.
Impairment of Conjugate Gaze
Strictly speaking, gaze palsy refers to a complete loss of both saccadic and pursuit movements to one side. Gaze paresis would then refer to an incomplete loss of the same capacities. Gaze palsies may be overcome by reflexive mechanisms, referring mainly to the VOR, when the disturbance affects the supranuclear inputs to the pontine gaze centers. In contrast, nuclear and infranuclear lesions cause an insurmountable impairment of gaze that cannot be overcome except perhaps by physically moving the globes (forced ductions).
As a rule, the horizontal gaze palsies of cerebral and pontine origin are readily distinguished by the side of an accompanying hemiparesis. When there is a tonic deviation of the eyes ipsilateral to a cerebral lesion, the eyes look toward the lesion and away from the hemiparesis. The opposite pertains to brainstem gaze palsies, that is, gaze is impaired toward the side opposite the lesion, and if there is gaze deviation, the eyes are turned toward a hemiparesis. Palsies of pontine origin need not have an accompanying hemiparesis but are associated with other signs of pontine disease, particularly peripheral facial palsies and internuclear ophthalmoplegia on the same side as the paralysis of gaze. Pontine gaze palsies tend to be longer lasting than those of cerebral origin. Also, in the case of a cerebral lesion (but not a pontine lesion), the eyes may turn to the paralyzed side if they are fixated on a target and the head is rotated passively to the opposite side (i.e., by utilizing the VOR).