findings that do not characterize vestibular pathology. The differential assessment process should provide the clinician with enough evidence to determine whether to treat the patient or refer him or her to a more appropriate specialist for further diagnostic workup and management.
antihistamines (such as meclizine, Antivert) to dampen symptoms of dizziness, nausea, and vomiting; these medications will blunt the patient’s responses on vestibular testing, reducing the diagnostic value of findings on clinical examination. Furthermore, the patient with non-vestibular- related symptoms will demonstrate a pattern of clinical Oculomotor system Examination of the oculomotor system establishes baseline function of eye muscles and central oculomotor pathways. Since the vestibular system mediates head-eye coordination, it is important to determine whether full active ocular movement is present in order to accurately interpret findings on vestibular testing. Furthermore, abnormalities seen on oculomotor testing indicate the possibility of a centrally mediated disorder; these tests assess the function of central oculomotor pathways that are independent of the vestibular system. The components of the oculomotor examination are observation of ocular motility and alignment, presence of nystagmus, tests of smooth pursuit and saccade, and vergence. Ocular motility and alignment The examination should start with observation of ocular motility and alignment. The patient is asked to actively look up, down, side to side, and across the diagonal, with the head stationary, to assess motor function of the medial and lateral rectus, trochlear, and superior and inferior oblique ocular muscles. Any abnormalities in resting alignment of the eyes in the orbits should also be appreciated. Observation of differences in vertical alignment of the eyes is called skew deviation . Skew deviation is a vertical misalignment of the eyes. Although typically a sign of CNS lesion, vertical skew deviation at rest can be seen in acute unilateral vestibular loss. The loss of utricular inputs on the side of the lesion results in the ipsilateral eye resting lower in the orbit, and the contralesional eye appearing higher in the orbit due to the loss of inhibitory input from the opposite (lesioned) side. If this finding is associated with acute peripheral vestibular dysfunction, resolution of skew deviation alignment will occur within 3 to 14 days due to spontaneous rebalancing of the tonic firing rate (Herdman & Clendaniel, 2014). Most often, skew deviation is caused by a centrally mediated lesion, typically in the cerebellum or brainstem. Further assessment of underlying skew deviation is achieved through the Cross-Cover Test, also called the Cover-Uncover or Alternate Cover Test . The examiner alternately covers one eye and then the other, looking for changes in ocular position. In most cases of skew deviation, the covered eye will migrate either up or down, and when rapidly uncovered a vertical correction (corrective saccade) will be observed. This correction repositions the eye in the center of the orbit as aided by visual fixation once the eye is uncovered. The skew is named for the side that is elevated (migrates downward with visual fixation), with the other side being the side of the CNS lesion. Nystagmus Assessing the presence of nystagmus is another important component of the oculomotor examination. Nystagmus is a rapid repetitive involuntary movement of the eyes that occurs under both normal and pathological conditions. Under normal conditions, nystagmus is elicited through vestibular or visual stimuli. It is seen in central or peripheral vestibular pathology due to an imbalance in vestibular outputs caused by a unilateral 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
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