Positioning Velocity Matters in Central Paroxysmal Positional Vertigo: Implication for the Mechanism

Abstract

Objectives: To elucidate the mechanism of paroxysmal central positional nystagmus (CPN) by determining the effects of head rotation velocity on the intensity of paroxysmal downbeat nystagmus induced during straight head hanging (SHH). Methods: We recruited 21 patients with paroxysmal downbeat CPN induced during SHH at the Dizziness Center of Seoul National University Bundang Hospital from September 2018 to July 2019. Twenty-one patients had manual SHH at two different lying velocities, the fast (routine) and slow, and they also underwent SHH at different rotation velocities of 10, 20, 30, and 40 • /s using a motorized rotation chair. Induced nystagmus was recorded using video-oculography and the maximum slow phase velocity (SPV) and time constant (TC) of the induced paroxysmal nystagmus were analyzed. Results: During manual SHH, paroxysmal downbeat nystagmus was invariably induced during routine SHH (fast lying down), but absent or minimal during slow positioning. During motorized SHH, the median of maximum intensity of downbeat nystagmus increased from 7.6 • /s (0-16.9) to 14.0 • /s (0-32.5), 16.5 • /s (0-44.6), and 19.1 • /s (0-55.2) as the rotation velocity increased from 10 to 20, 30, and 40 • /s (P < 0.001, P < 0.001, P = 0.004; linear mixed models). In contrast, the TCs of paroxysmal downbeat CPN remained unchanged (P = 0.558, P = 0.881, P = 0.384, linear mixed models). Conclusions: The dependence of nystagmus intensity on head rotation velocity supports a disinhibited and exaggerated inhibitory rebound of the canal signals as the mechanism of paroxysmal CPN.

Effects of Baclofen on Central Paroxysmal Positional Downbeat Nystagmus

“…This study documented a decrease in the maximum SPV of paroxysmal downbeat CPN with administration of baclofen, a GABA B agonist. This result supports our prior presumption that the paroxysmal CPN results from disinhibited and abnormally enhanced canal responses during positioning due to cerebellar dysfunction [2,4].…”

“…During the SHH, patients were laid from the sitting upright position onto the lying down position with the head extended about 30° below the table. This positioning was completed usually within 3 s (2-4 s), resulting in an average head rotation velocity of an approximately 40 °/s during the positioning [4]. In each testing condition, the SHH position was maintained until the positional nystagmus disappeared or at least for one minute.…”

“…Indeed, the paroxysmal CPN mostly occurs in the planes of semicircular canals that are inhibited during the positioning, and shows the features suggestive of a semicircular canal origin regarding the latency and duration [2]. Furthermore, the intensity of paroxysmal downbeat CPN induced during SHH depends on the positioning head velocity [4]. Since the lesions having caused paroxysmal CPN were mostly overlapped in the cerebellar nodulus and uvula, disruption of GABAergic inhibition over the velocity-storage mechanism (VSM) may be presumed as the mechanism of paroxysmal CPN [2,5].…”

“…Central positional nystagmus (CPN) mostly presents with apogeotropic nystagmus in the eardown position or downbeat nystagmus after lying down or straight head-hanging (SHH) [3]. In previous studies, the paroxysmal CPN has been ascribed to disinhibition and enhanced canal signals during positioning due to cerebellar dysfunction [2,4]. Indeed, the paroxysmal CPN mostly occurs in the planes of semicircular canals that are inhibited during the positioning, and shows the features suggestive of a semicircular canal origin regarding the latency and duration [2].…”

Periodic vertigo and downbeat nystagmus while supine: Dysfunction of Purkinje cells coding gravity

“…Therefore, we evaluated the modulation pattern of positional nystagmus based on the following considerations. First, to verify that the development of paroxysmal vertigo and nystagmus depended on positioning velocity, 7 we adopted two different positioning speeds: Slow and fast, with approximate durations of 15 and 2 s for lying down, respectively. Second, if cerebellar adaptation was the underlying mechanism, we expected other types of periodic vertigo and nystagmus would occur in other head positions, as the patient also showed paroxysmal upbeat nystagmus when resuming the sitting position after lying down and apogeotropic nystagmus during the supine head roll test.…”