The smooth-pursuit system generates smooth conjugate eye movements that maintain the image of a moving target on the fovea. Pursuit eye movements are able to track a moving target both when the head is immobile and when it is in motion. In order to perform the latter function, the pursuit system must override the VOR. For example, rightward head rotation stimulates the VOR to move the eyes in the opposite direction, toward the left. Therefore, in order to track a rightward-moving object with simultaneous rightward head rotation, the pursuit system (which tracks the object by moving the eyes toward the right) must cancel the VOR (which drives the eyes in the opposite direction, toward the left).
Pursuit movements cannot be generated without a moving target; attempts to pursue an imaginary target will result in a series of saccades. When a patient tracks an object, the moving target generates signals from the M ganglion cells in the retina that are relayed through the magnocellular layers of the lateral geniculate nucleus to the striate cortex (V1), and from there to the extrastriate cortex (V2, V3). These signals are subsequently relayed to the middle temporal (MT) area (where neurons preferentially respond to the speed and direction of moving stimuli), the medial superior temporal (MST) area, the posterior parietal cortex, and the FEF. The MT and MST areas are part of the dorsal visual processing stream, which plays an important role in detecting moving visual stimuli (see Chapter 1, Fig 1-23). The descending cortical pathways of the temporal, parietal, and frontal lobes converge and pass through the posterior limb of the internal capsule to innervate the ipsilateral dorsal lateral pontine nucleus (DLPN). The pathway that follows the DLPN comprises 2 decussations. First, the neurons in the DLPN decussate and project to the contralateral cerebellar lobe (the first decussation), which in turn innervates the medial CN VIII nucleus. Thereafter, neurons in the medial vestibular nucleus decussate and project to the contralateral CN VI nucleus (the second decussation). The CN VI nucleus initiates conjugate horizontal eye movements by innervating the ipsilateral lateral rectus muscle and, via internuclear neurons that travel in the MLF, the contralateral medial rectus muscle. Thus, the cortical regions control ipsilateral pursuit movements as a result of the double decussation pathway. Vertical pursuit movements are generated by similar pathways that ultimately stimulate CN III and CN IV.
Clinicians test pursuit eye movements by having the patient’s eyes follow a predictably slow-moving target horizontally and then vertically while the head and body are held in position. Two main types of pursuit dysfunction occur: (1) abnormal gain and (2) delayed initiation. The gain of pursuit eye movements should be 1—that is, the eyes should accurately follow the slow-moving stimulus. A low gain results in eye movements that trail the target (ie, the motor output is not commensurate with the speed of the moving target), which prompts initiation of catch-up saccades to maintain visual fixation. This combination of too-slow pursuit movements with interposed saccades is called cogwheel, or saccadic, pursuit. Conversely, a high gain causes the eyes to pursue ahead of the target, which prompts backup saccades.
The OKN drum can be used to evaluate smooth pursuit. The smooth-pursuit system generates the eye movements that follow the rotating lines on the OKN drum. Pursuit movements toward the side of drum rotation should be accurate without saccadic interruptions. The OKN drum should be rotated to each side to evaluate the symmetry of the pursuit response.
The smooth-pursuit system can also be evaluated by testing VOR cancellation. This is assessed by having the patient fixate on a target (his thumb or a near card) in his out-stretched hand while he is rotated from side to side in the examination chair. The patient’s head, the target, and the chair rotate in the same direction as a unit. If the smooth-pursuit system cancels the VOR, the patient will maintain fixation on the target during chair rotation. If the smooth-pursuit system does not cancel the VOR, the VOR will drive the eyes off target in the direction opposite of the chair rotation, followed by a corrective saccade. For example, a patient with intact VOR cancellation will maintain fixation on his thumb during rightward chair rotation. If there is inadequate VOR cancellation, the VOR will rotate the eyes off of the thumb to the left in response to rightward rotation. This will be followed by a rightward corrective saccade, which indicates low pursuit gain to the right (Fig 8-3). It is normal in such assessments for the patient to exhibit catch-up saccades during the first 4 or 5 rotations but not thereafter.
Smooth-pursuit system dysfunction
Smooth-pursuit system dysfunction is of poor localizing value. Accompanying neurological abnormalities are often required to determine the location and etiology of the lesion.
Abnormal gain is typically observed in older patients without other definable neurologic problems or secondary to use of a wide range of medications. With age, reduced gain decreases the smoothness of smooth pursuit, although obvious saccadic pursuit is pathologic.
Large cerebral lesions that involve the frontal, parietal, or temporal lobe or the underlying white matter may cause decreased pursuit gain (saccadic pursuits) when the patient fixates on an object moving toward the side of the lesion. These lesions may cause an asymmetric OKN response, with abnormal saccadic pursuits in response to drum rotation toward the side of the lesion and normal smooth pursuits when the drum is rotated away from the side of the lesion. Occipital lobe lesions do not cause OKN asymmetry.
Figure 8-3 Clinical assessment of vestibular ocular reflex (VOR) suppression. A, The patient is seated in a swivel chair, fixating on the letters of a near card held at arm’s length. B, If VOR suppression is normal (intact), the eyes maintain fixation on the target as the chair, the patient’s head and arms, and the card rotate together as a unit. C, Conversely, if VOR suppression is impaired, the eyes are dragged off target during rotation due to an inability to cancel the VOR. In this example, the chair is rotated to the patient’s right, and the VOR moves the eyes to the patient’s left, prompting a rightward saccade to regain the target; this result likely indicates right cerebellar system pathology.
(Illustration by Christine Gralapp.)
Cerebellar disease of any etiology may cause saccadic pursuits and an inability to cancel the VOR, demonstrated by the chair rotation fixation test (see Fig 8-3). Accompanying signs of cerebellar disease are often present.
Smooth-pursuit deficits are usually present in both horizontal and vertical planes, although the vertical plane may be involved selectively in patients with bilateral internuclear ophthalmoplegia or PSP.
Excerpted from BCSC 2020-2021 series: Section 5 - Neuro-Ophthalmology. For more information and to purchase the entire series, please visit https://www.aao.org/bcsc.