12 I ACNR • VOLUME 5 NUMBER 3 • JULY/AUGUST 2005

Benign Paroxysmal Positional Vertigo (BPPV):Diagnosis and Physical TreatmentAbstractBenign paroxysmal positional vertigo (BPPV) is one of themost common causes of vertigo. It is easily diagnosed andtreated. BPPV is due to the presence of otoconial debris with-in the semicircular canals, usually the posterior canal. Thevertigo is intense but brief, usually triggered by seating, lyingdown and turning over in bed. The diagnosis can only bemade by observing the typical nystagmus during positionalmanoeuvres such as the Hallpike manoeuvre or equivalent.The nystagmus occurs when the affected ear is in the sidedown position and is mostly torsional (rotatory) beatingtowards the undermost ear. On observing the typical nystag-mus in a patient with a typical history one can proceed imme-diately to physical treatment with one of the repositioningmanoeuvres. The Semont manoeuvre is described here,essentially consisting of one big swing whereby the patient istaken from one end of the couch (the ear down side) to theother (the eye down side). These manoeuvres ‘reposition’ thedebris back to the utricle and cure patients of their currentBPPV in 70-90% of cases. Links to a webpage showing videosof the diagnostic and treatment manoeuvres are provided.

Introduction Up to 10 or 20 years ago the diagnosis of vertigo was just anacademic exercise. Identification of the various causes of ver-tigo was largely irrelevant as all patients ended up with thesame antivertiginous drugs and with little benefit. Physicaltherapy and rehabilitation have been at the centre of arefreshing change in dizziness treatment.

We now understand that the centre piece for the treatmentof the patient with a single episode of vertigo (eg vestibularneuritis or ‘labyrinthitis’) and the patient with long termdizzy symptoms is rehabilitation.1 Setting up a vestibularrehabilitation service does not require complex equipmentor prolonged training. A physiotherapist, particularly aneuro-physiotherapist, or an audiologist, particularly onewith an interest in vestibular disorders, can quickly acquirethe necessary skills. Indeed, a recent study has shown that aGP practice nurse, with an appropriate one-day training ses-

sion, can make a significant difference to the outcome ofdizzy patients in primary care.2

In this review, however, we will concentrate on the diag-nosis and physical treatment of one specific condition,benign paroxysmal positional vertigo or BPPV. BPPV isone of the most common causes of vertigo. Both the diag-nosis and treatment are straight forward and yet manypatients have many drugs and expensive investigationsinstead of what they really need, namely a Hallpikemanoeuvre for diagnosis and an Epley or Semontmanoeuvre for treatment.

SymptomsBPPV is by far the most common cause of positional vertigo,accounting for about 90% of patients. Moreover, BPPV is thenumber one vestibular disorder, causing 20-30% of referrals tospecialised dizziness clinics.3,4 The prevalence of BPPV increas-es with advancing age; women are affected almost twice asoften as men. BPPV may involve each semicircular canal, withBPPV of the posterior canal being by far the most commonvariant.All subtypes of BPPV can be diagnosed on the basis ofclinical observation during the positional manoeuvre.

Patients with BPPV complain of brief episodes (<1 min)of vertigo that appears in specific head positions, e.g. on lyingdown or sitting up, after turning in bed from one side toanother, with head extension or bending forward.Frequently, however, the positional and brief nature of thevertigo is not recognised by the patient, even after directquestioning. Therefore, positional tests should be performedin all patients with recurrent or episodic vertigo.

Patients are usually aware that certain head movementsprecipitate attacks of vertigo. They often develop strategies toavoid vertiginous attacks, e.g. sleeping upright or holdingtheir neck stiff, which may lead to immobility and prolonga-tion of the natural course of the disease. Indeed many BPPVpatients with stiff neck and head movement-induced vertigoare often told that the problem originates in the neck – themyth of ‘cervical vertigo’.5 Another presentation is the patientwith BPPV who, due to the terrifying nature of the vertigo inBPPV, develops a secondary anxiety disorder – the myth ofthe ‘it’s all in your mind’ syndrome.

Each single BPPV attack lasts a few seconds but after aseries of attacks, patients may complain of prolonged dizzi-ness and imbalance lasting from hours to days. Typically,BPPV manifests itself with symptomatic episodes lastingfrom a few days to several months, which are interspersed byasymptomatic intervals of several months to years duration.Most cases of BPPV are idiopathic, but about 25% developafter head trauma or on the background of a pre-existinglabyrinthine disorder such as vestibular neuritis orMenière´s disease. Bilateral BPPV is more common in post-traumatic patients.

ExaminationConventional clinical examination as performed by GPs, neu-rologists or ENT surgeons is negative in BPPV. Provocation ofvertigo by positional testing and observation of typical nys-tagmus is the only way to make a diagnosis of BPPV. Patientsmust have this clearly explained to them before the position-al manoeuvres. Positional vertigo is terrifying but brief - if thepatient closes his/her eyes in response to the vertigo the exam-iner will not be able to make a diagnosis.

The most popular test for provocation and confirmationof BPPV is the Hallpike manoeuvre (Figure 1A). With thisprocedure the head is rotated with respect to gravity in theplane of the affected posterior canal. Alternatively, a lateral

Adolfo Bronstein is Professor ofClinical Neuro-otology at ImperialCollege London and a ConsultantNeurologist at Charing CrossHospital and at the NationalHospital for Neurology andNeurosurgery, Queen Square,London. He heads the Departmentof Movement and Balance in theDivision of Neuroscience at ImperialCollege and is the lead Editor of thefirst and second (2004) edition of thebook ‘Clinical Disorders of Balance,Posture and Gait’.www.imperial.ac.uk/medicine/dizziness

Correspondence to:Prof Adolfo M Bronstein MDPhD FRCP,Professor of Clinical Neuro-otology and ConsultantNeurologist,Head, Department of Movement& Balance,Division of Neuroscience &Psychological Medicine,Imperial College London,Charing Cross Hospital,London W6 8RF.Tel: 020 8846 7285,Fax: 020 8846 7577,Email: a.bronstein@imperial.ac.uk

Review Article

A B

Figure 1: Two positional manoeuvres for eliciting positional vertigo andnystagmus. In this case the right ear is being investigated. Bothmanoeuvres are equally successful in inducing positional nystagmus andshould be conducted briskly. Note how the clinician can help the patientkeep the eyes open for full visibility of a positional nystagmus. A: theHallpike manoeuvre in which the head finishes in a head hangingposition. B: a trunk-sideways positional manoeuvre.

Clinical Disorders of Balance, Posture and Gait

A Bronstein, T Brandt, H Woollacott, J Nutt

This is the second editionof this text, covering allclinical aspects of humanlocomotion and its disorders.

Seewww.hoddereducation.com

for more information

tilt of the trunk and head from a sitting positioncan be performed with the head turned 45° to theopposite side, which positions the head with thelateral aspect of the occiput onto the couch (Figure1B). This latter manoeuvre is the only one that canbe performed when the couch is placed betweenwalls or cupboards and the patient’s head cannotreach the head hanging position. In any case, withboth manoeuvres, the final position of the posteri-or semicircular canal is identical (compare Figures1A & B). The patient is instructed to keep theireyes open, to watch the examiner’s forehead oreyes and to stay in the final position even if verti-go occurs. It is useful to help the patient keep theireyes open with your own fingers, as some patientsfind it difficult to keep their eyes open when thevertigo develops. Frenzel´s glasses are not neces-sary for observation of the nystagmus.

The nystagmus in posterior canal BPPV ismostly torsional (often called ‘rotatory’), with theupper pole of the eye beating towards the under-most ear (Figure 2). In addition, there is a smallervertical skewing upbeating nystagmus compo-nent, most prominent on the uppermost eye.Typically, nystagmus and vertigo start a few sec-onds after the precipitating head position isreached (latency). Nystagmus intensity increasesrapidly and then decays (adaptation), usually last-ing 10 to 20 seconds. On returning to the sittingposition, a transient nystagmus of lesser intensitybeating in the opposite direction can be observed(reversal). With repeated testing, vertigo and nys-tagmus decrease with repeated positioning inmost cases (fatigability).

A patient with a typical history of brief rotation-al vertigo on lying, seating or turning over in bedand with a transient torsional nystagmus asdescribed above does not require any further inves-tigations. One should proceed to repositioningtreatment straight away. A similar clinical historycan be due to the rarer horizontal or anterior canalvariants of BPPV. The former has horizontal nys-tagmus and the latter downbeat nystagmus with atorsional component. However, unless the clinicianis conversant with positional nystagmus, an MRI isadvisable to rule out cerebellar-brainstem diseasewhenever a positional manoeuvre induces a nys-tagmus atypical for posterior canal BPPV.

PathophysiologyBPPV appears when dislodged calcium rich par-ticles from the utricular otoconia fall into theposterior semicircular canal. These debris, due togravitational forces, move within a semicircularcanal and cause inadequate endolymph flow

after changes of head position (canalolithiasis).There are five factors predisposing to BPPV,namely advanced age, head trauma, a precedinginner ear disease, migraine, and general anaes-thesia. These predisposing factors act by a com-bination of age related or ischemic utriculardegeneration and head reclination (for intuba-tion during anesthesia).

Figure 3 shows how these otoconial debrismove within the posterior canal. Once otoconiahave entered the posterior canal they tend to sinkto the most dependent point. When the patient isupright, they are located at the base of the cupulaand do not have any effect. During the Hallpiketest, the head is rotated backwards in the plane ofthe posterior canal, inducing movement of theparticles within the canal away from the cupulaand thus activation of the canal’s hair cells. Thenystagmus subsides after the particles havereached the most dependent point of the canaland the cupula has returned to the resting posi-tion. Agglomerates of otoconia may disperse withrepeated positional manoeuvres which mayexplain BPPV fatigability. Although thecanalolithiasis concept is supported by several his-tological and intraoperative findings, the mostconvincing proof for canalolithiasis comes fromthe efficacy of positioning manoeuvres, whichclear the affected canal from mobile particles.

TreatmentThe rationale of the treatment is to redirect theotoconial particles back to the utricle where theydo not cause BPPV symptoms. First of all thepatient is informed about the benign course ofBPPV, its mechanism and rationale for reposi-tioning treatment. Patient cooperation is vitalduring the treatment as further vertigo isunavoidable during the manoeuvres. There areessentially two repositioning treatments, Epley´sand Semont´s manoeuvre. Patients should keeptheir eyes open for observation of nystagmus,since a positional nystagmus beating in the samedirection with respect to the head indicates suc-

cessive movement of the particles towards theutricle and predicts a favourable outcome to someextent. Both these therapies are highly effective interminating an acute episode of BPPV but recur-rences after several months or years are notuncommon.

Epley has introduced the canalith repositioningprocedure, in which the posterior canal is rotatedbackwards close to its planar orientation. Themanoeuvre consists of a series of successive headpositionings each of about 90° displacement andseveral reviews illustrate clearly how to carry itout3,4. My personal impression is that, unless thedoctor or therapist applies this manoeuvre fre-quently, Epley’s manoeuvre is more difficult toremember than Semont’s, so the latter will bedescribed and illustrated here.

The Semont manoeuvre involves a 180° swing ofthe head in the plane of the posterior canal (Figure3). The examiner guides the manoeuvre by stand-ing in front of the patient who is seated on a couchwith the head rotated 45° away from the affectedear. Then the patient is brought with a fast move-ment to a lying position on the side of the provoca-tive ear (Figure 3 - 1,2). This initial part of themanoeuvre is in fact the diagnostic phase equiva-lent to a Hallpike manoeuvre or, more precisely, thesideways variant Hallpike manoeuvre describedunder Examination and illustrated in Figure 1B. Inthis position vertigo is triggered and torsional nys-tagmus beats toward the affected (undermost) ear.After being kept in this position for approximatelya minute (so all debris falls to the bottom), thepatient is swung rapidly onto the opposite side ofthe couch (and stays there for another minute)(Figure 3 - 2,3). The manoeuvre should be execut-ed quickly in one single movement step and so, ifthe patient is frail, old or overweight, an assistantcan help the therapist achieve this from behind thepatient. In order to memorise this manoeuvre, it isuseful to think that the plane of the posterior semi-circular canal lies vertically in the head at 45degrees, midway between the sagittal and coronalplanes. In order to move the head diagonally at 45

Review Article

Figure 2: The nystagmus observed in a case of right sidedBPPV in the right ear down position. The arrows indicatethe predominant beat (fast phase) direction: torsionalbeating towards the right ear with a minor upbeatingcomponent. This nystagmus pattern is the result of theexcitation of the right posterior semicircular canal.

Figure 3: Pathophysiology and treatment of right sided BPPV. The cartoon illustrates canalolithiasis of the right posteriorcanal. On the left, the debris move down during the diagnostic positional manoeuvre (as illustrated in Figure 1B). On theright, the particles are swung out of the posterior canal back into the utricle by way of the fast head acceleration producedduring the repositioning treatment (Semont manoeuvre).

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degrees all you have to remember is to “go from one ear down to the opposite eyedown”. That is, to do a Semont manoeuvre on a patient with right BPPV (i.e. ver-tigo/nystagmus evoked by right ear down positional manoeuvre) swing thepatient from right ear down all the way to a left eye down position (Figure 3).

Vibration of the mastoid during these repositioning treatments has been rec-ommended but does not improve treatment outcome. Similarly, keepingupright for 48 hours after treatment has proven unnecessary. In a few patientswith unusual anxiety, vertigo or nausea medication with sedatives or antiemet-ics before the repositioning treatment is required.

Both the Epley and Semont manoeuvres are highly effective when performedproperly. After a single application complete recovery is achieved in approxi-mately 70% of patients and 90% after a second session.6 Randomised, controlledtrials have shown that repositioning manoeuvres are clearly more effective thana sham procedure or no treatment.7,8 For patients who do not respond to thesemanoeuvres or suffer from frequent recurrences, several useful procedures forself-treatment at home are available, eg Brandt-Daroff exercises or a modifiedEpley procedure.9 It is advisable to visit the original publications or visitWebPages illustrating these self-treatments and prepare handouts for patientswho require them.

Surgery of the posterior canal can be considered in those rare patients withlongstanding BPPV who have not responded to appropriate and repeated ther-apeutic positionings, but this is very rarely required nowadays.

Differential diagnosisPosterior canal BPPV must be differentiated from other forms of BPPV (hori-zontal and rarely anterior canal) and from central positional vertigo due to alesion of the vestibular nuclei or caudal cerebellum. The distinction is mainlybased on nystagmus features and a patient with atypical nystagmus shouldalways be imaged. A purely vertical (either downbeat or upbeat) nystagmusstrongly suggests a central positional nystagmus whereas a history of recur-rences and remissions is in favour of BPPV and against a central lesion.Migrainous vertigo is often aggravated by changes of head position and mayoccasionally present with pure positional vertigo. The following factors help todistinguish migrainous positional vertigo from BPPV: short-duration sympto-matic episodes and frequent recurrences, manifestation early in life, migrainoussymptoms during episodes with positional vertigo.10 A trial with antimigraineprophylactic agents is often required in a patient with migraine and recurrentvertigo, whether positional or not.

ConclusionBPPV is one of the most common causes of vertigo. Diagnosis is straightfor-ward if clinicians develop the healthy habit of doing positional manoeuvres(Hallpike or equivalent) as the single most important step in the diagnosis ofpatients with positional and recurrent vertigo. Treatment with repositioningprocedures is effective and clinicians should get familiar with at least one ofthese manoeuvres (either Epley or Semont). The Semont manoeuvre is easilyremembered: take your patient quickly in a big swing from the symptomatic eardown to the opposite eye down. You can see videos of these manoeuvres inwww.imperial.ac.uk/medicine/dizziness

Review Article

References1. Pavlou M, Shumway-Cook A, Horak F, Yardley L, Bronstein A. Rehabilitation of balance dis-

orders in the patient with vestibular pathology. In: Bronstein A, Brandt T, Woolacott M, NuttJG, eds. Clinical Disorders of Balance and Gait Disorders. London: Edward Arnold;2004:317-43.

2. Yardley L, Donovan-Hall M, Smith HE, Walsh BM, Mullee M, Bronstein AM. Effectiveness ofprimary care-based vestibular rehabilitation for chronic dizziness. Ann Intern Med.2004;141(8):598-605.

3. Lempert T, Gresty MA, Bronstein AM. Benign positional vertigo: recognition and treatment.BMJ. 1995;311(7003):489-91.

4. Furman JM, Cass SP. Benign paroxysmal positional vertigo. N Engl J Med.1999;341(21):1590-6.

5. Brandt Th, Bronstein AM. Controversial Topics in Neurology: Cervical Vertigo. J of NeurolNeurosurg Psychiatry. 2001;71:8-12.

6. Bronstein AM. Benign paroxysmal positional vertigo: some recent advances. Curr OpinNeurol. 2003;16(1):1-3.

7. Lempert T, Wolsley C, Davies R, Gresty MA, Bronstein AM. Three hundred sixty-degree rotationof the posterior semicircular canal for treatment of benign positional vertigo: a placebo-controlledtrial. Neurology. 1997;49(3):729-33.

8. Woodworth BA, Gillespie MB, Lambert PR. The canalith repositioning procedure for benignpositional vertigo: a meta-analysis. Laryngoscope. 2004;114(7):1143-6.

9. Radtke A, Neuhauser H, von Brevern M, Lempert T. A modified Epley’s procedure for self-treatment of benign paroxysmal positional vertigo. Neurology 1999;53(6):1358-60.

10. von Brevern M, Radtke A, Clarke AH, Lempert T. Migrainous vertigo presenting as episodicpositional vertigo. Neurology 2004;62(3):469-72.

The National Hospital forNeurology and Neurosurgery,

Queen Square, London

DIZZINESSA Multi-Disciplinary Approach

Assessment, Clinical Diagnosis and Management

11th – 14th October 2005

Following the success of the previous Dizziness Courses, theDepartment of Neuro-otology has expanded its course tofour full days, which will include:

• Mechanisms of dizziness• Evidence based vestibular testing• Opportunity for ‘hands-on’ experience with the

department’s equipment• Developments in genetics and radiology• The range of medical diagnoses• Diagnostic strategy• BPPV and Particle Repositioning Manoeuvres• Role of physiotherapy• Psychological aspects including the role of cognitive

behavioural therapy• The future of pharmacological therapy• Failed management and role of surgery• Theoretical basis of vestibular compensation

The course will include three full days on the diagnosis andmanagement of balance disorders with case histories, videosand quizzes and an optional fourth practical day. There willbe a course dinner on the Wednesday evening.Cost: £125/day or £420 for 4 days.

The course will be suitable for clinicians, scientists, audiologists and therapists involved in the care of the dizzypatient and will be run by Professor Linda Luxon, Dr Rosalyn Davies, Mr Albert Coelho and Mrs Karen Cox.The faculty will include renowned national and internationalspeakers.

CME accreditation will apply and CPD points will be awarded.

For details contact:

Dr Rosalyn Davies / Mr Albert Coelho / Mrs Karen CoxDepartment of Neuro-otologyThe National Hospital for Neurology and NeurosurgeryQueen SquareLondon WC1N 3BG

Tel: 020 7837 3611 ext. 3386 or 3274Fax: 020 7829 8775