Clinical examination of the supranuclear systems includes assessment of ocular fixation, vestibular-ocular reflex (VOR), optokinetic nystagmus (OKN), saccadic and pursuit eye movements, and convergence (see Table 8-1). Each of these movements is controlled by dedicated anatomical pathways, the collective goals of which are to direct and maintain the image of a target of interest on the fovea. Methods of assessing each subsystem and signs of malfunction are described in the following sections. A thorough assessment of ocular motility also requires a search for nystagmus (see Chapter 9). Videos of many of the supranuclear ocular motility disorders discussed in this chapter are available at the NOVEL (Neuro-Ophthalmology Virtual Education Library) website at http://novel.utah.edu.
Ocular Fixation System
The ocular fixation system holds the image of a stationary object on the fovea when the head is immobile. Eye movement recordings show that the eye is not completely still during ocular fixation; subclinical eye movements prevent attenuation of neuronal responses in the retina. A basic principle of all sensory systems is that any persistent, unchanging stimulus gradually produces an attenuated neural response. This phenomenon explains, for instance, why one does not attend to the constant tactile stimulus of wearing clothing or a wristwatch.
The degradation of image quality that would result if the eye were completely still is countered by microsaccadic refixation movements. These eye movements are continuous, very small amplitude (0.1°–0.2° of visual angle) square waves. The term square waves derives from the appearance of eye movement tracings, in which eye movements of equal amplitude and speed to the left and right have a brief intersaccadic interval that produces tracings in the shape of square waves (see Chapter 9). The to-and-fro movements are small enough that the image is maintained within the field of the fovea but large enough to provide a constantly changing image to photoreceptors, thereby enhancing perceptual quality. As is true for most saccadic movements, there is a slight pause (180–200 milliseconds) between movements, known as an intersaccadic interval.
The anatomic pathways that control ocular fixation include the dorsolateral prefrontal cortex, the supplementary eye field, the parietal eye field, regions V5 and V5a, the basal ganglia, and the superior colliculi. Clinical evaluation of ocular stability involves observing the patient’s ability to fixate on a target when the head and body are held stationary.
Ocular fixation dysfunction
Malfunction of other ocular motor systems may disrupt steady fixation. Saccadic eye movements that disrupt fixation are referred to as saccadic intrusions (see Chapter 9). Saccadic intrusions are of brief duration, quite rapid, and in most cases small amplitude. The most common intrusions are square-wave jerks (SWJs), which lead the eyes off and then back onto the target with symmetric movements (amplitude of 0.5°–3° of visual angle). Infrequent SWJs (4–6 per minute) may be observed in patients with normal vision. Frequent SWJs (> 15 per minute) are pathologic and occur in patients with progressive supranuclear palsy (PSP) or certain cerebellar diseases. They may also be seen in patients who smoke cigarettes. Other examples of saccadic intrusions include ocular flutter and opsoclonus.
Sustained slow eye movements that disrupt fixation characterize nystagmus, which is often caused by an imbalance of vestibular input to the ocular motor nuclei. A continuous slow eye movement that displaces the eye off fixation, followed by a corrective saccade, is referred to as a jerk nystagmus. A continuous slow eye movement that oscillates around fixation without a corrective saccade is referred to as a pendular nystagmus (see Chapter 9).
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.