"Sitting-up vertigo as an expression of posterior semicircular canal heavy cupula and posterior semicircular canal short arm canalolithiasis"

Abstract

Background: Vestibular symptoms on sitting-up are frequent on patients seen by vestibular specialists. Recently, a benign paroxysmal positional vertigo (BPPV) variant which elicits vestibular symptoms with oculomotor evidence of posterior semicircular canal (P-SCC) cupula stimulation on sitting-up was described and named sitting-up vertigo BPPV. A periampullar restricted P-SCC canalolithiasis was proposed as a causal mechanism.

Objective: To describe new mechanisms of action for the sitting-up vertigo BPPV variant.

Methods: Eighteen patients with sitting-up vertigo BPPV were examined with a pre-established set of positional maneuvers and follow-up until they resolved their symptoms and clinical findings.

Results: All patients showed up-beating torsional nystagmus (UBTN) and vestibular symptoms on coming up from either Dix-Hallpike (DHM) or straight head-hanging maneuver. Sixteen out of 18 patients presented a sustained UBTN with an ipsitorsional component to the tested side on half-Hallpike maneuver (HH). A slower persistent contratorsional down-beating nystagmus was found in eleven out 18 patients tested on nose down position (ND).

Conclusions: Persistent direction changing positional nystagmus on HH and ND positions indicative of P-SCC heavy cupula was found in 11 patients. A sustained UBTN on HH with the absence of findings on ND, which is suggestive of the presence of P-SCC short arm canalolithiasis, was found on 5 patients. All patients were treated with canalith repositioning maneuvers without success, but they resolved their findings by means of Brandt-Daroff exercises. We propose P-SCC heavy cupula and P-SCC short arm canalolithiasis as two new putative mechanisms for the sitting-up vertigo BPPV variant.

Keywords: BPPV; BPPV, benign paroxysmal positional vertigo; Benign paroxysmal positional vertigo; CRM, canalith repositioning maneuvers; DBTN, down-beating torsional nystagmus; DHM, Dix-Hallpike maneuver; HH, half-Hallpike maneuver; HYT, head yaw test; Heavy cupula; ND, nose down position; Residual dizziness; SCC, semicircular canal; SHH, straight head hanging; Short arm canalolithiasis; Sitting up vertigo; Subjective BPPV; UBTN, up-beating torsional nystagmus; Vertigo.

Fig. 1

Possible effects of right posterior semicircular canal cupula plane orientation variants in the context of a heavy cupula on Dix-Hallpike maneuver. Different scenarios could be expected. a, neutral. The plane of the posterior cupula is in the earth vertical plane on Dix-Hallpike maneuver. The cupula is not stimulated; b, a vestibulum angulated cupula (the posterior cupula plane is closer to the earth vertical in sitting position than the neutral configuration) elicits a persistent ampullofugal deflection in the context of a heavy cupula; c, a canal angulated cupula (the posterior cupula plane is farther from the earth vertical in sitting position than the neutral configuration) elicits a persistent ampullopetal deflection in the context of a heavy cupula. The red arrow represents the influence of the gravity force over the cupula.

Fig. 2

Right posterior semicircular canal cupula stimulation on different positions (upper and second row) in the context of a heavy cupulolithiasis plus short arm canalolithiasis (A) and a short-arm posterior canal canalolithiasis (B). A sustained ampullofugal deflection is expected on sitting position (a,f) and on sitting-up from Dix Hallpike maneuver (c,h) in both scenarios. A neutral deflection on Dix-Hallpike maneuver is shown in both scenarios (b,g). A maximal ampullofugal deflection on half-Hallpike position is expected on both scenarios (d,i) The nose-down position elicits an ampullopetal deflection on the heavy cupula scenario (e) but a neutral stimulation on short-arm canalolithiasis scenario (j). Red arrow, gravity force influence over cupula.

Fig. 3

Right posterior cupula deflection during sitting-up from Dix-Hallpike maneuver. A, a normal cupula is ampullopetaly deflected during positioning. When rotation stops, a transient ampullofugal deflection arises as an inertial rotation aftereffect. Gravity has no influence on the cupula. The rotation feedback mechanism of the velocity storage produces a virtual rotation that cancels the inertial rotation aftereffect. B, in a heavy cupula scenario, gravity force increases its influence until the half-Hallpike position is reached. From there until sitting position, the gravity influence is decremental but remains positive. The hypothetical cupular deflection during sitting-up mediated by the interaction between the inertial and gravity forces is depicted by the dotted line (c). An enhanced and abnormally persistent rotation aftereffect is expected given the summation influence of the inertial rotation aftereffect and the gravity force. The rotation feedback mechanism is unable to compensate for the abnormally enhanced rotation feedback. c, cupular deflection (upward ampullofugal, downward ampullopetal). g and green arrow, gravity force influence over cupula (upward ampullofugal, downward ampullopetal). RA, rotation aftereffect. RF, rotation feedback mechanism. Red arrow, influence of endolymph inertial force over cupula.