Bedside evaluation of peripheral positional downbeating nystagmus: Toward the new definition of down-beating BPPV

Abstract

Background

Positional downbeat nystagmus (pDBN) may have multiple etiologies.

Objectives

Description of a case series and further considerations about pDBN characteristics, pathogenesis, and differential diagnosis.

Methods

Descriptive study concerning 153 consecutive patients with pDBN of presumed peripheral origin that were recruited and observed. They were treated only with Brandt-Daroff Exercises.

Results

56% reported symptoms of “typical positional vertigo,” 44% described postural instability during head movements or a continuous sense of dizziness. 40% of patients were symptom- and nystagmus-free after 1 week and almost 60% after 2 weeks 5% were still affected by pDBN after 1 month. Several pathogenetic hypotheses have been advanced: otoconia in the anterior canal, an apogeotropic variant of posterior canal, or in the short arm of the posterior canal.

Conclusion

Down-beat nystagmus arising from the semicircular canals must contain a torsional component and be in “canal-plane” - presenting more torsional when gaze is towards the affected canal, and more purely vertical when directed away, whereas central causes of DBN may be “pure” down-beat. Peripheral pDBN is fatigable, often no nystagmus when returning in sitting position and, highly relevantly, it is self-limiting (95% disappears with only Brandt-Daroff Exercises), with no central signs. Patients may complain of long-term dizziness, trunk oscillation, and prolonged motion sickness. New guidelines may consider the term of Down-Beating BPPV or Down-Beating peripheral positional vertigo, even if the otoconia’s exact position is still uncertain: in our opinion pDBN might be considered as an “apogeotropic variant of PC-BPPV”.