Benign positional vertigo, its diagnosis, treatment and mimics

Abstract

The diagnosis of benign positional vertigo (BPV) relies on a history of episodic positional vertigo and a distinctive pattern of nystagmus during provocative positional testing. The direction of the induced nystagmus is specific to the affected canal and the velocity profile reflects the underlying mechanism of canalithiasis (free-floating otoconia within the canal duct) or cupulolithiasis (otoconia adherent to the cupula). We review current theories on the pathophysiology of BPV, the clinical history and examination underlying its diagnosis, and recommended repositioning manoeuvres for each of the BPV subtypes. Disorders other than BPV which may present with a similar history and/or positional nystagmus are discussed.

Keywords: Benign paroxysmal positional vertigo; Canalithiasis; Cupulolithiasis; Positional nystagmus.

Fig. 1

Right posterior canalithiasis. In the upright position, the otoconia are positioned close to the ampulla of the right posterior canal. Only subtle spontaneous upbeat nystagmus was seen in this subject. During the right Dix-Hallpike test, the ampulla is brought to a higher gravitational point causing otoconia to gravitate away from the ampulla and generate a brief excitatory nystagmus which is upbeating with a rightward torsion. The nystagmus slow phase velocity (SPV) profile shows a brief onset latency, crescendo-decrescendo intensity pattern and short duration.

Fig. 2

Left posterior cupulolithiasis. The otoconia adhere to the cupula of the left posterior canal creating a heavy cupula. This patient had an acute vestibular syndrome and secondary BPV. In the upright position, low velocity right-beating nystgamus is seen, consistent with the left unilateral vestibular loss. During the left Dix-Hallpike test, the cupula is deflected away from the ampulla due to its increased mass, causing excitation of the left posterior canal and generating an upbeating leftward torsional nystagmus. The nystagmus slow phase velocity (SPV) profile shows an immediate onset of nystagmus that rises to a peak, gradually decays but persists for more than one minute.

Fig. 3

Right anterior canalithiasis. In the upright position, the otoconia are positioned near the cupula of the right anterior canal. There is no spontaneous nystagmus. The Dix-Hallpike position brings the ampullary end of the anterior canal to a higher gravitational point. There is an excitatory downbeat rightward torsional nystagmus as the otoconia fall away from the ampulla. The slow phase velocity (SPV) profile illustrates the paroxysmal nature of the nystagmus, the quick rise to a peak velocity, and brief duration of less than 30 s.

Fig. 4

Right lateral canalithiasis. In the upright position, the otoconia are located in the long arm of the right lateral canal at a distance from the ampulla. There was no spontaneous nystagmus in this subject. During the right roll test, otoconia descend towards the ampulla creating an intense excitatory right-beating nystagmus. During the left roll test, otoconia gravitate away from the ampulla producing a less intense inhibitory left-beating nystagmus. The slow phase velocity (SPV) profiles for both roll tests show a brief duration nystagmus with a higher peak velocity reached during the right roll test.

Fig. 5

Right lateral cupulolithiasis. The otoconia adhere to the cupula of the right lateral canal. There was no spontaneous nystagmus in this subject. During the right roll test, the cupula is deflected away from the ampulla creating an inhibitory left-beating nystagmus. During the left roll test, the cupula is deflected towards the ampulla generating an excitatory right-beating nystagmus. The slow phase velocity (SPV) profiles during both roll tests reveal persistent nystagmus, with a higher peak velocity reached during the left roll test.

Fig. 6

Horizontal eye position and slow phase velocity (SPV) during right and left roll tests in a subject with an acute attack of left-sided Meniere’s disease. This subject had right-beating spontaneous nystagmus. There was no change in nystagmus direction during the right and left roll tests. The slow phase velocity (SPV) profiles are flat and illustrate persistent right-beating nystagmus in either roll position.

Fig. 7

Horizontal eye position and slow phase velocity (SPV) during right and left roll tests in a subject with vestibular migraine. In the upright position, this subject had left-beating nystagmus. Right and left roll tests showed direction-changing horizontal nystagmus. With the right ear down, the nystagmus was right-beating. With the left ear down, the nystagmus was left-beating. The nystagmus was low velocity, persistent and did not have a crescendo-decrescendo slow phase velocity (SPV) profile, unlike lateral canalithiasis.

Fig. 8

Eye position and vertical slow phase velocity (SPV) during Dix-Hallpike tests in a subject with a cerebellar arteriovenous malformation. In the upright position, no nystagmus was observed. Dix-Hallpike tests revealed a rapid onset of downbeat nystagmus with either ear down. The nystagmus was persistent, lasting more than one minute, unlike the characteristic nystagmus of canalithiasis.