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Although benign paroxysmal positioning vertigo (BPPV) is a common finding that is relatively easy to diagnose and treat, there are causes of positional nystagmus and positional vertigo that are a result of either abnormalities within the central nervous system or other peripheral vestibular conditions. These conditions will not respond to the conservative measures described for the treatment of BPPV. The goal of this appendix is to help the clinician identify the signs and symptoms of positional nystagmus and positional vertigo that are not consistent with BPPV and are suggestive of other disorders.

Central Positional Nystagmus

Two types of central positional nystagmus have been identified: central positional nystagmus without vertigo (CPN) and central positional nystagmus with vertigo (CPV).1,2 Central positional nystagmus without vertigo is characterized by nystagmus that persists as long as the head is held in the provoking position.1 The nystagmus is typically in one direction (vertical, horizontal, or torsional), unlike the mixed vertical torsional nystagmus seen in posterior and anterior semicircular canal BPPV. Central positional nystagmus may be seen in elderly patients when they are in supine. The elicited nystagmus is typically vertical. In the absence of other findings on the examination, the CPN is thought to be benign. In other individuals, the CPN may be seen in conjunction with either upbeating or downbeating spontaneous nystagmus while the patient is seated. The CPN in these cases is typically greater than the spontaneous nystagmus observed in sitting.

The downbeating spontaneous nystagmus and CPN have been associated with a variety of central disorders including Chiari malformation, multiple sclerosis, olivopontocerebellar atrophy, and brainstem infarction.3 These patients had other oculomotor signs such as impaired smooth pursuit and impaired VOR cancellation. The actual pathophysiology causing the downbeating nystagmus is not well understood at this point, but it is thought that the downbeating nystagmus results from an imbalance between the anterior and posterior semicircular canal pathways. Recall that the semicircular canal inputs are separated at the level of the vestibular nuclei into vertical (pitch), horizontal (yaw), and roll pathways. A lesion that causes either an increase in the central anterior semicircular canal pathways or a decrease in the central posterior semicircular canal pathways would lead to downbeating nystagmus.

The upbeating spontaneous nystagmus and CPN have been associated with central disorders such as tumor, stroke, and multiple sclerosis affecting brachium conjunctivum or the ventral tegmental tract.4 Many of these patients also had findings of abnormal smooth pursuit. The presumed pathophysiology for the upbeating nystagmus is thought to be the opposite of that for the downbeating nystagmus. The upbeating nystagmus is caused by a higher level of neural activity in the central posterior semicircular canal pathways relative to the central anterior semicircular canal pathways.

Given the lack of symptoms of vertigo with the positional tests, the unidirectionality of the positional nystagmus, and the other oculomotor findings, ...

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