Diagnosis of Single- or Multiple-Canal Benign Paroxysmal Positional Vertigo according to the Type of Nystagmus

Hindawi Publishing Corporation International Journal of Otolaryngology Volume 2011, Article ID 483965, 13 pages doi:10.1155/2011/483965 Review Article Diagnosis of Single- or Multiple-Canal Benign Paroxysmal Positional Vertigo according to the Type of Nystagmus Dimitris G. Balatsouras,1 George Koukoutsis,1 Panayotis Ganelis,1 George S. Korres,2 and Antonis Kaberos1 1 ENT Department, Tzanio General Hospital of Piraeus, Afentouli 1 and Zanni, 18536 Piraeus, Greece 2 ENT Department, University General Hospital Attikon, 1 Rimini Street, Haidari, 12462 Athens, Greece Correspondence should be addressed to Dimitris G. Balatsouras, Received 15 February 2011; Accepted 7 May 2011 Academic Editor: Paolo Vannucchi Copyright © 2011 Dimitris G. Balatsouras et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Benign paroxysmal positional vertigo (BPPV) is a common peripheral vestibular disorder encountered in primary care and specialist otolaryngology and neurology clinics. It is associated with a characteristic paroxysmal positional nystagmus, which can be elicited with specific diagnostic positional maneuvers, such as the Dix-Hallpike test and the supine roll test. Current clinical research focused on diagnosing and treating various types of BPPV, according to the semicircular canal involved and according to the implicated pathogenetic mechanism. Cases of multiple-canal BPPV have been specifically investigated because until recently these were resistant to treatment with standard canalith repositioning procedures. Probably, the most significant factor in diagnosis of the type of BPPV is observation of the provoked nystagmus, during the diagnostic positional maneuvers. We describe in detail the various types of nystagmus, according to the canals involved, which are the keypoint to accurate diagnosis. 1. Introduction Of all the inner ear disorders that can cause dizziness or vertigo, benign paroxysmal positional vertigo (BPPV) is by far the most common [1]. Additionally, it is a condition that in most instances may be easily diagnosed and treated, with a simple office-based procedure [2]. Since the initial description by Bárány in 1921 [3], there have been major advances in the understanding of this common condition. Recently, modern clinical research focused on diagnosing and treating various types of BPPV, according to the semicircular canal involved and according to the implicated pathogenetic mechanism. Multiple-canal BPPV has been specifically investigated, as the main source of various atypical forms of the disease, which until now were resistant to treatment with standard canalith repositioning procedures (CRPs) [4, 5]. The purpose of this paper is to present the data regarding the various types of nystagmus produced during the diagnostic maneuvers of BPPV, which in conjunction with the patient’s history and symptoms, will help in obtaining accurate diagnosis and appropriate treatment. In all subsequent discussions, the various types of nystagmus will be described according to their fast phase, relative to the patient’s perspective (e.g., as horizontal nystagmus with a fast phase beating towards the patient’s right ear is termed rightward horizontal nystagmus and a rightward torsional nystagmus, which is beating towards the patient’s right ear, is a counterclockwise nystagmus, as seen by the observer). 2. Unilateral Posterior Canal BPPV This is the most common type of BPPV, accounting for up to 90% of the patients [6]. The Dix-Hallpike provoking maneuver is used to diagnose the disease by moving the patient rapidly from a sitting position to a position of head hanging with each ear alternately undermost. Posterior semicircular canal involvement is proved from the type of the visually observed paroxysmal positioning nystagmus, which is beating towards the undermost and affected ear, with a torsional component clockwise when following leftward movement, or counterclockwise, when following rightward movement 2 [7]. Typically an upbeating nystagmus component is superimposed, resulting in a mixed torsional-vertical eye movement. Intense vertigo in conjunction with this pattern of nystagmus and the additional characteristics of a short latency, limited duration, intensity characterized by crescendo and decrescendo element, reversal on returning to the upright position, and fatiguability on repetitive provocation may easily establish the diagnosis of posterior canal BPPV. Canalolithiasis is the implicated pathogenetic mechanism for this disorder, characterized by the presence of free floating debris within the posterior semicircular canal, detached from the otoconial layer by degeneration or head trauma [8]. The otoconia gravitates into the posterior canal, where it forms a plug floating in its nonampullary branch. In the provoking Dix-Hallpike position the endolymph pulls on the cupula, because the free-floating otoconia falls under the influence of gravity. In the vertical canals, ampullofugal deflection produces an excitatory response. This would cause an abrupt onset of vertigo and the typical nystagmus described previously. Nystagmus latency is explained by inertia of the clot. The cupula deflection ends when the clot reaches its lowest position and accounts for the limited duration of the nystagmus. Fatigue is due to dispersion of the clot particles and reactivation after bedrest is caused by renewed clot formation. An alternative pathogenetic theory, the cupulolithiasis of the posterior canal, may account for a small rate of cases with posterior canal BPPV [7, 8]. According to this, otoconia with a specific gravity greater than endolymph from a degenerating utricular macula settle on the cupula of the posterior canal, rendering it sensitive to gravity. Certain head movements may then produce inappropriate endolymphcupula displacement, causing nystagmus and vertigo, which in this case is of longer duration. The latency before the onset of nystagmus reflects the inertia of the otoconial mass and the cupula, and the fatiguability is presumably due to dispersal of the debris attached to the cupula or even to central vestibular adaptation. The previously described profile of nystagmus correlates with the known neuromuscular pathways that arise from stimulation of the posterior canal ampullary nerves in animal models and humans [9, 10]. It should be noticed that the character of nystagmus changes with the direction of gaze, which is explained by contraction of the ipsilateral superior oblique and contralateral inferior rectus, following the stimulation of the posterior canal. When the patient lies in the lateral head hanging position, if he looks towards the uppermost unaffected ear, the axes of these two extraocular muscles nearly coincide, resulting in movement of the eyes in a vertical plane with predominan (...truncated)