Otorhinolaryngology Clinics: An International Journal, January-April 2012;4(1):25-40 25 Benign Paroxysmal Positional Vertigo and Positional Vertigo Variants AIJOC REVIEW ARTICLE Benign Paroxysmal Positional Vertigo and Positional Vertigo Variants Giacinto Asprella Libonati 10.5005/jp-journals-10003-1085 ABSTRACT This article reviews the causes of positional vertigo and positional nystagmus of peripheral origin. Benign paroxysmal positional vertigo is described in all its variants, its diagnosis and therapy are highlighted. In addition, nonparoxysmal positional vertigo and nystagmus due to light/heavy cupula of lateral and posterior semicircular canal is focused on. The differential diagnosis between positional vertigo due to otolithic and nonotolithic causes is discussed. Keywords: Benign paroxysmal positional vertigo, Light/heavy cupula, Liberatory manoeuver, Semicircular canal, Canalolithiasis, Cupulolithiasis. How to cite this article: Asprella Libonati G. Benign Paroxysmal Positional Vertigo and Positional Vertigo Variants. Int J Otorhino- laryngol Clin 2012;4(1):25-40. Source of support: Nil Conflict of interest: None declared INTRODUCTION Benign paroxysmal positional vertigo (BPPV) is the most common cause of peripheral vertigo and is due to a mechanical labyrinthine disorder. It is characterized by brief and violent crises of spinning sensation with brisk onset and rapid decrease—paroxysmal vertigo. Each crisis usually lasts from 15 to 60 seconds and is related to head position changes with respect to gravity— positional vertigo. It usually has a favorable course and therefore is defined as ‘Benign’, however, there are very disabling variants of BPPV because of their high recurrence rate and their low response to physical therapy, such that some authors prefer to omit the term benign. BPPV can occur at any age, even in infants, but its peak of incidence occurs between 50 and 60 years of age. BPPV is uncommon in children and in our experience only 1% of BPPV seen in 1 year concerns the pediatric age group, i.e. patients aged 3 to 14 years. 1 BPPV usually occurs spontaneously, but can be associated with triggering events causing otoconial detachment. Such a causal relationship can be hypothesized with high probability in case of minor head trauma occurring within the last 24 to 72 hours (domestic injuries, sports injuries, school injuries, dental care), while only a possible or probable relationship can be assumed with viral or vascular illness. 1 BPPV pathophysiology is due to a mechanical labyrinthine disorder caused by the presence of free floating otoconial debris inside the semicircular canals— canalolithiasis, or attached to the ampullary cupula— cupulolithiasis. Both of the previous conditions transform the ampullary cupula of the involved canal from a detector of angular accelerations into a detector of liner accelerations, thus becoming gravity sensitive. According to the canalolithiasis theory the otoconial conglomerate gravitates inside the canal because of head movements and in so doing pushes the endolymphatic column. In this way, the otoconial bolus, acting as a piston, provokes a hydrodynamic drag on the endolymph, which deflects the ampullary cupula, thus generating an excitatory or an inhibitory stimulus which causes the paroxysmal vertigo. 2 According to the cupulolithiasis theory the otoliths are attached to the cupula which becomes heavier than the surrounding endolymph and gravity sensitive (heavy cupula). In our experience, cupulolithiasis is rare compared to canalolithiasis. BPPV Classification The most useful BPPV classification for clinical practice is based on the involved canal. • Posterior semicircular canal (PSC) • Lateral semicircular canal (LSC) • Anterior semicircular canal (ASC) • Multicanalar BPPV – Simultaneous involvement: Posttraumatic BPPV – No simultaneous involvement: Canalar conversion How to Diagnose BPPV? The BPPV diagnosis should be related to the evoked nystagmus and not to the maneuver which elicits it. In fact, both excitatory and inhibitory stimuli of each semicircular canal are linked to a typical nystagmus, as every vestibular stimulus triggered by each ampullary cupula deflection provokes the contraction of a couple of extrinsic ocular muscles, thus generating typical eye movement responses of a characteristic nystagmus. Therefore, there are maneuvers suggested to diagnose every single type of BPPV, but the pathognomonic nystagmus for a subtype of BPPV is sometimes evoked performing the maneuver recommended to diagnose a different BPPV subtype. So it is the evoked nystagmus and not the kind of the performed maneuver, that allows us to diagnose the involved semicircular canal. 1