Central positional nystagmus: an update
Abstract
Clinically, central positional nystagmus (CPN) is often suspected when atypical forms of its peripheral counterpart, i.e., benign paroxysmal positional vertigo (BPPV), are observed, namely a linear horizontal nystagmus as in horizontal canal BPPV or a downwardly and torsionally beating nystagmus as in anterior canal BPPV. Pathophysiologically, CPN is caused by cerebellar and/or brainstem dysfunction. Recent work has provided further insights into the different clinical phenotypes and the underlying pathomechanisms. We performed a PubMed review focused on the findings on CPN using the key words "Central Positional Nystagmus", "Central Positional Vertigo", "Positional Nystagmus" OR "Positioning Nystagmus" OR "Positional Vertigo" OR "Positioning Vertigo" AND "Central" from January 2015 to August 2021. CPN may account for up to 12% of patients with positional nystagmus. Clinical data on CPN are mostly based on case reports or small retrospective case series. CPN is frequently associated with cerebellar and/or brainstem structural lesions, namely stroke, tumours or demyelination, or diffuse involvement of these structures due to degenerative or autoimmune/paraneoplastic diseases; it is also found in patients with vestibular migraine. CPN can be paroxysmal or persistent. The direction of the nystagmus is often downward in head-hanging or apogeotropic in lateral supine positions; combinations of both forms also occur. Clinically it is important to note that CPN is often associated…
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