loss of peripheral vestibular function or disruption of central vestibular pathways. Reduced input to the ocular muscles from the lesioned side results in a slow conjugate eye deviation (slow phase) toward the side of the lesion, and a fast corrective movement (fast phase) away from the side of the lesion. For example, the presence of nystagmus with a vestibular lesion on the right would be seen as a conjugate horizontal jerking motion of the eyes, starting with a drift of the eyes off the visual target toward the right, followed by an immediate quick correction toward the left back onto the target. The direction of the nystagmus is named for the fast phase of eye movement (not the lesioned side). In this example, this would be defined as left- beating nystagmus . To further clarify, recall the pathways of the horizontal VOR, where decreased firing response from the canal results in inhibition of ocular muscles on the opposite side of the head movement. Two types of physiological, or normal, nystagmus are optokinetic and post-rotary nystagmus. Optokinetic nystagmus is induced by looking at a moving visual stimulus, such as watching a moving train while standing on the train platform. Visual responses for gaze fixation will cause the eye to re-establish fixation on the target as the target moves, resulting in a lateral nystagmus. Post-rotary nystagmus can be seen after a patient is subjected to continuous rotary motions, such as spinning in a chair, or that famous teacup ride in the amusement park, stimulating semicircular canal responses. Upon abrupt cessation of the spinning motion, the patient will exhibit a short duration of nystagmus until the endolymph flow and cupula of the semicircular canals return to resting state. Nystagmus that occurs in the absence of visual or vestibular stimulus is found in peripheral and central vestibular pathology. Spontaneous nystagmus is observed while the patient is in a stationary position, without head movement. Acute loss of unilateral peripheral vestibular function, such as with vestibular neuritis or postoperative vestibular schwannoma resection, results in spontaneous nystagmus due to the asymmetry in baseline firing from semicircular canals, which is interpreted by the CNS as head movement. The presence of nystagmus due to acute unilateral vestibular loss will resolve within 1 to 2 weeks without intervention due to spontaneous compensation in the CNS, which rebalances tonic firing rates even when CN VIII does not undergo recovery (Mantokoudis et al., 2013; Smith & Curthoys, 1989). However, spontaneous nystagmus due to CNS lesion is persistent. Three features of nystagmus differentiate peripheral vestibular from central causes. First, nystagmus caused by peripheral vestibular dysfunction can be suppressed by visual fixation, while centrally mediated nystagmus will not diminish or abate when the patient fixates on a target. Second, the direction of nystagmus is quite differentiating, with a peripheral lesion demonstrating movement in a mixed plane, usually horizontal with a torsional component, and central lesions demonstrating nystagmus in a single plane with either a torsional or a vertical direction. Finally, the effect of gaze also distinguishes peripheral versus central causes of nystagmus. With peripheral vestibular lesions, the intensity of the nystagmus will increase when the patient looks into the direction of the quick phase, and decrease when the patient looks into the direction of the slow phase. This phenomenon is known as Alexander’s law (Leigh & Zee, 2006). With centrally mediated nystagmus, direction of gaze will have no effect or will elicit a change in the direction of the nystagmus (direction-changing nystagmus) in that right-beating nystagmus will occur with gaze to the right, changing to left-beating nystagmus with gaze to the left (see Table 1). In acute stages of peripheral lesions, spontaneous nystagmus can be seen with center gaze, as well as gaze to the right and left. This is called third-degree nystagmus . Within the first few days of recovery, nystagmus will be seen only at center gaze and gaze away from the side of the lesion – in the direction of the
fast phase (second-degree nystagmus). As recovery continues over the course of a week or so, nystagmus can be seen only during gaze away from the side of the lesion (first-degree nystagmus). As nystagmus can be suppressed with visual fixation in the patient with peripherally mediated nystagmus, the use of Frenzel lenses or infrared goggles during examination will help the examiner appreciate the presence of the nystagmus. Pressure-induced nystagmus should also be assessed. In this test, the examiner looks for drift of the eyes or the presence of mixed vertical and torsional nystagmus while pressure is induced in three ways: The patient puts pressure against the tragus of the ears (with his or her fingers) and exerts an external pressure (Hennebert’s sign), the patient closes his or her glottis and bears down (valsalva), or the patient attempts to blow out through pinched nostrils. A positive Hennebert’s sign demonstrates conjugate eye movement away from the affected ear with positive pressure (pressure against tragus), and conjugate eye movement away from the affected ear with negative pressure. Positive findings are suggestive of perilymphatic fistula, and sometimes Ménière’s disease. Table 1: Peripheral Versus Centrally Mediated Nystagmus Peripheral Mediated Centrally Mediated Visual Fixation Decreased No change or increase Direction Horizontal and torsional Either torsional or vertical Gaze Increased w/gaze to fast phase No change or reverses direction Smooth pursuit, saccadic eye movements, and vergence Once baseline ocular motility and alignment have been established, the examiner assesses smooth pursuit and saccadic eye movements as well as vergence. Smooth pursuit testing assesses the quality of eye movement while the patient tracks a slowly moving target in all directions. The smooth pursuit system is used to maintain a moving target on the fovea of the retina during head movement at low velocities. While the vestibular system acts to maintain gaze at higher velocities, this system is driven by cortical regions in addition to the cerebellum and brainstem (Leigh & Zee, 2006). The examiner asks the patient to track a discrete target (pencil, finger) from 18 to 24 inches away. The object should move 30° from center in each direction at a speed of about 20° per second while the patient maintains a stationary head position. The examiner is looking for a smooth trajectory of oculomotor motion in all directions (lateral, vertical, diagonal). Saccadic eye movement is rapid conjugate eye movement to place the fovea on a target. The examiner holds two discrete targets within the patient’s peripheral field of vision and asks the patient to look quickly between the two targets while keeping the head in a stationary position. If the patient’s eyes do not meet the target and a refixation on the target is observed, this is called a corrective saccade . The patient should normally be able to reach the target in one movement. Abnormal findings in saccadic and smooth pursuit eye movements are indicative of lesions in the brainstem or cerebellum and would warrant referral to a physician for further diagnostic consultation. To examine vergence, the examiner holds a discrete object (finger, pencil) 2 feet away from the patient’s nose and slowly brings it toward the bridge of the nose until the target becomes double. The eyes should converge and the pupils should constrict. Normal convergence occurs at about 4 inches. Patients having difficulty with convergence will experience double vision of the target when it is farther than 4 inches from the bridge of the nose.
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