Positional vertigo and nystagmus may occur when inputs from the semicircular canals and otolithic organs are mismatched, and when this mismatch originates from central dysfunction it is called central positional vertigo and nystagmus (CPVN)....
Clinicians should consider velocity-storage mechanism dysfunction when a patient presents with positional nystagmus or vertigo that does not fit typical benign paroxysmal positional vertigo (BPPV) patterns, as it may signal a central nervous system cause requiring further neurological workup.
Distinguishing central from peripheral positional vertigo is clinically critical; a refined mechanistic framework based on velocity-storage may improve diagnostic accuracy and reduce missed central pathology.
- 01Central positional vertigo is re-examined through the velocity-storage mechanism, a key brainstem balance-processing pathway.
- 02Central dysfunction causes mismatch between semicircular canal and otolith (gravity-sensing) inputs, producing atypical nystagmus.
- 03The framework may help differentiate central from benign peripheral positional vertigo (BPPV) at the bedside.
- 04Review published in Journal of Neurology (PMID 42334619).
- 05No new clinical trial data; this is a conceptual/mechanistic review.
Central positional vertigo and nystagmus can result from dysfunction of the velocity-storage mechanism causing semicircular canal and otolith input mismatch.
opinionpartially supported- PMID
- 42334619
- DOI
- 10.1007/s00415-026-13940-9.
- Journal
- Journal of Neurology
- Publication type
- review
- Evidence level
- 5
- Population
- Not applicable — mechanistic/conceptual review of central positional vertigo literature
- Intervention
- Velocity-storage mechanism framework applied to central positional vertigo and nystagmus
Primary outcomes
Mechanistic explanation of central positional vertigo via velocity-storage dysfunction; Differentiation of central versus peripheral positional nystagmus patterns