Abstract
The central vestibular system operates to precisely estimate the rotational velocity and gravity orientation using the inherently ambiguous information from peripheral vestibular system. Therefore, any lesions disrupting this function can generate positional nystagmus. Central positional nystagmus (CPN) can be classified into the paroxysmal (transient) and persistent forms. The paroxysmal CPN has the features suggesting a semicircular canal origin regarding the latency, duration, and direction of nystagmus. Patients with paroxysmal CPN commonly show several different types of nystagmus classified according to the provoking positioning. The persistent form of CPN mostly appears as downbeat nystagmus while prone or supine, or apogeotropic or geotropic horizontal nystagmus when the head is turned to either side while supine. CPN may be ascribed to erroneous neural processing within the velocity-storage circuit that functions in estimating angular head velocity, gravity direction, and inertia. Paroxysmal CPN appears to be post-rotatory rebound nystagmus due to lesions involving the cerebellar nodulus and uvula. In contrast, persistent CPN may arise from erroneous gravity estimation. The overlap of lesion location responsible for both paroxysmal and persistent CPN may account for the frequent coexistence of both forms of nystagmus in a single patient.
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