BENIGN PAROXYSMAL POSITIONAL VERTIGOAN OVERVIEW

R. BONIVER Invited Professor – Faculty of Medicine – Liege University - Belgium

Abstract:

A general review of benign paroxysmal positional vertigo and nystagmus: mainethiopathogenies, diagnosis and treatments are evoked.The author describes his experience on the subject.

Key Words:

Benign paroxysmal vertigo, ethiopathogeny, treatment, diagnosis.

1.INTRODUCTION :

Benign Positional Paroxysmal Vertigo (BPPV) has a sudden onset which is provoked by acertain position or appears in a determined position.This type of vertigo produces a nystagmus which is called

benign paroxysmal positional nystagmus

(BPPN).This disease occurs frequently and constitutes around 50% of acute vertigo complaint in my practice.Barany (1) was the first to evoke BPPV in 1921 and Dix and Hallpike (2) described thecharacteristic torsional nystagmus in response to the provocative positional testing named intheir honor in 1952. ____________________________________________________________________________ Reprint RequestProf. Raymond Boniver, 21, rue de Bruxelles, 4800 Verviers-Belgium.r.boniver@win.be

In 1998, I published a "State of the art" on this subject in the review of the Royal BelgianE.N.T. Society (3)A report was presented by Sauvage and coll (4) at the "Société française d'oto-rhinolaryngologie et de chirurgie de la face et du cou" in October 2007 and published by thissociety.In February 2008, 800 references about the subject are found in PubMed (Medline) on internet.

2.ETHIOPATHOGENY :

Several hypothesis have been evoked to explain the mechanism of these vertigo and nystagmus.

2.1.Lithiasis

Schuknecht (5) defined the « cupulolithiasis » in demonstrating basophilic deposit on thecupula of the posterior semi-circular canal.Kornhuber (6) evoked that the possibility of mechanic disturbances in a semi-circular canal may be in the origin of the BPPN: for example: blood clotting, group of desquamated cells in the endolymph or perilymphe.Hall (7), at first, proposed that fragments of otoconias floated in the endolymph to produce the BPPN: he called this pathology « canalolithiasis ».Gordon (8) evoked the possibility of an air plug floating in the semi circular canal. Thistheory is not supported by some characteristics of this nystagmus: it does not explain, for -2-

example, the direction of the nystagmus toward the higher ear when the patient reaches body rotation of 180°.Brandt and Steddin (9), have compared argumentation pro and contra canalo andcupulolithiasis.Pro cupulolithiasis (fig. 1)=============- Single histological findings of debris which seemed to be attached to the cupula.Contra cupulolithiasis===============

No BPPV attacks with slow head tilt (

6 seconds).

No typical vertigo with linear head accelerations.

Direction and intensity of induced nystagmus/vertigo do not reflect the position of « heavy » cupula relative to gravity.

Short duration of positioning nystagmus (less than 1 minute) with the head motionless.

Clinical fatigability with repetitive positioning maneuvers.

Spontaneous course with varying severity of the attacks.

Efficiency of physical therapy with unpredictable remission phases and relapses.

Incompatible with nystagmus direction in horizontal BPPV.-3-