Benign Paroxysmal Positional Vertigo

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Topic is covered under following heads

• Brief Anatomy and Physiology• Introduction• Aetio pathogenesis• Symptoms• Types and clinical features• Differential diagnosis• Investigations• Treatment modalities

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Anatomy of the vestibular system

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Physiology

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Benign Paroxysmal Positional Vertigo (BPPV)

• Benign: not a very serious or progressive condition

• Paroxysmal: sudden and unpredictable in onset

• Positional: comes with a change in head position

• Vertigo: causing a sense of dizziness.

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Introduction

• BPPV – One of the commonest Vestibular End organ disorders

• 17-25% of all vestibular disorders

• Most common aural cause of vertigo

• Chronic, Incapacitating, Affecting day to day functioning

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Introduction

• Hallmark of the disease is the onset of brief (seconds) spells of often severe vertigo that are experienced only with specific movements of the head with respect to gravity.

• Typical Precipitating movements- – Turning in bed,

– Getting In and Out of bed,

– Bending and straightening

– Extending the neck to look up and back• “TOP SHELF VERTIGO”

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History

• 1921 - First described by Barany

• 1952 - Dix-Hallpike reported this entity in a large number of patients and described important features of nystagmus

• 1962, Dr Harold Schuknecht proposed the cupulolithiasis (heavy cupula) theory.

• 1980, Brandt and Daroff proposed positional exercises based on the canalolithiasis hypothesis even before the theory was described

• 1980 – Hall, Ruby and McClure described the theory of canalolithiasis

• 1991 - Free floating deposits demonstrated in Endolymph of PSSC–Parnes, McClure

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Benign positional vertigo -epidemiology• Incidence: 1:20 in general practice

3:20 in ENT OPD• U.S. study – incidence 64 per 100,000. Av 10-64 / lakh• Incidence in general population is higher in persons older

than 40 years.• Elderly patients – incidence approximately 8%. • 20% of all falls that result in hospitalization for serious

injuries in the elderly are due to vertigo of end-organ origin (most often related to BPPV).

• Average age of onset 51 years. M=F, some studies show a slight predilection for women.

• Rarely seen in persons younger than 35 years without a history of antecedent head trauma.

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• Idiopathic – 48%

• Head trauma

• Viral neuronitis

• Middle ear infection

• Surgical damage to the labyrinth

• Prolonged bed rest

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BPPV- AETIOLOGY

PATHOPHYSIOLOGY OF BPPV

• Vertigo originates in Posterior Semi circular canal in majority of cases

• Rarely in Lateral Semi circular Canal and still rarer in Superior semi circular Canal

• “Cupulolithiasis” – Schucknect

• “Canalithiasis” –Hal, Ruby, McClure, Parnes, Epley

• Free Floating particles in endolymph of Posterior Semi circular Canal

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Theories of BPPV

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Cupulolithiasis • In 1962, Dr Harold Schuknecht proposed the cupulolithiasis

(heavy cupula) theory. • Discovered basophilic particles or densities that were

adherent to the cupula.• He postulated that the PSC was rendered sensitive to gravity

by these abnormal dense particles attached to, or impinging on, the cupula.

• This produces persistent nystagmus and also explains the dizziness when a patient tilts the head backward.

• Cupulolithiasis – possible role in atypical BPPV

Theories of BPPV Canalolithiasis :

– Hall, Ruby and McClure – 1980

– Free floating deposits demonstrated in Endolymph of PSSC–Parnes, McClure-1991

• The most widely accepted theory of the pathophysiology of BPV

• Otoliths (calcium carbonate particles) are normally attached to a membrane inside the utricle and saccule

• Otoliths may become displaced from the utricle to enter the posterior semicircular duct since this is the most dependent of the 3 ducts

• Changing head position relative to gravity causes the free Otoliths to gravitate longitudinally through the canal.

• The concurrent flow of endolymph stimulates the hair cells of the affected semicircular canal, causing vertigo.

• Explains all features of typical nystagmus

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Canalolithiasis

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Symptoms

• Discrete episodes of vertigo induced by specific head motions of duration less than 1 min.

• Single bouts clustered in time with remissions lasting months or more.

• Dizziness with rapid head movements. (Cupulolithiasis)• Disequilibrium worse in the morning or after day time

naps.• Nausea and vomiting

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NYSTAGMUS IN BPPV …

• Nystagmus : characterization and types – Rt / Lt , vertical / horizontal , changing– Tortional = Rotational – clockwise /

counterclockwise– Geotropic- toward the earth– Ageotropic – opposite

DIRECTION OF NYSTAGMUS

Destructive lesion of the vestibular end organ or the vestibular nerve will produce transient horizontal nystagmus with its quicker phase towards the opposite side.

Unilateral cerebellar lesion will produce vertigo with its quicker phase to the same side

Paretic lesion of labyrinth the nystagmus is towards healthy side

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Nystagmus

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  Appearance Latency Duration Fatigability Localisation

Central  Pure vertical, usually downbeat

Unusual Persistent Unusual Brainstem or cerebellum

PeripheralPostr SCC

Torsional towards the downward eye, vertical 

upbeat, geotropic

Usual (seconds)

Brief(<1 min)

Usual Posterior  semi-circular canal

PeripheralLat SCC

Horizontal, geotropic or ageotropic

Usual (seconds)

Brief (<1 min)

Less susceptible than PSCC

Horizontal semi-circular canal

I. Classic BPPV

• Involves the Posterior SCC – Canalilithiasis of Posterior SCC – most frequent

cause– Reversal upon return to upright position– Response decline upon repetitive provocation

Types of BPPV

II. Lat. SCC BPPV

• Most common atypical BPPV• 3-9% of cases• Paroxysmal horizontal direction changing nystagmus –beats

towards ground (geotropic) when head turned to side while patient lies supine - Canalilithiasis

• Ageotropic – Nystagmus away from the dependent affected ear - Cupulolithiasis

• Nystagmus lasts 1 minute, minimal latency and no fatigability. • Occurs with head to either side but stronger on one side.

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III. Ant. SCC BPPV

• Rare – 2%• Down-beating /torsional NG for the opposite ear

on Dix-Hallpike maneuver• Torsional downbeating nystagmus during

Hallpike test induced when the abnormal anterior canal (which lies at right angles to posterior) is uppermost.

• Repositioning maneuver starts with abnormal ear uppermost moving across to opposite head hanging position.

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BPPV - D.D

• Meniere’s disease• Vestibular migraine• Recurrent vestibulopathy• Vestibular Labyrinthitis – Lasting days

• Inner ear fistula• Inner ear trauma• Superior SCC dehiscence syndrome• Central origin : Stroke , MS , cerebellar degeneration• Vertebral artery insufficiency• Cervical vertigo

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Minutes to hours

Variable duration

HISTORY:

Confirmation of dizziness

Associated symptoms•Otalgia, otorrhoea, Tinnitus, headache,•Aural fullness, head injury, acoustic

trauma, ototoxic drug intake, DM, HTN, •TB, CVA, IHD•H/o Ear surgery•Difficulty in speaking/walking•Diplopia/dysarthria, loss of consciousness

points to brain stem dysfunction 26

EVALUATION AND DIAGNOSIS

Pattern Of Vertigo Onset, duration, continuous/ paroxysmalPeriod of complete reliefPostural

Preliminary tests Of Balance

Degree Of Vertigo – Is there nausea/vomiting

(I) Finger Pointing(II) Rapid Alternate Movements Of Hand(III)Gait(IV)Tandem Walk(V) Rhombergs test(VI)Unterbergers test

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Ears-EAC-FB/WAX -TM for perforation, AOM/OME -Cholesteatoma Hearing tests -TFT -PTA -FFH -Impedance Audiometry

Otological examination

Detailed clinical examination General Systemic

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Ocular Examination PtosisPupillary reactivityOcular alignmentEye movementsConvergence

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Labyrinthine Function tests (I) Caloric tests to look for nystagmus

(II) Dix Hallpike tests for positional vertigo

(III) ENG

(IV) VNG

DIX-HALL PIKE TESTS 

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RECENT ADVANCES IN EVALUATIONVIDEO NYSTAGMOGRAPHY (VNG)

•VNG – Video images of the eyes are obtained without direct contact using high resolution cameras with infrared illumination. Setup is fast & as easy using Frenzel glasses. The eyes are visualized, enabling simultaneous subjective evaluation while eye movements are analyzed by digital image processing to obtain vertical and horizontal eyeposition. Can be used for teaching purpose.

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The Dix-Hallpike test

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Laboratory testsRoutine hemogram, urine examinationBlood sugarT3, T4 ,TSHSerological tests to rule out Syphilis

Radiological investigationsX-Ray Skull-Per orbital viewX-Ray mastoidsX-Ray Cervical spineCT- Temporal bone and Brain

SPECIAL TESTS

EEGBERA

Psychological Evaluation 34

To rule out other pathologies

BPPV - Treatment

• Watchful waiting• Pharmacotherapy• Canalith repositioning procedure• Vestibular rehabilitation• Surgery care

– Singular neurectomy– Post. Canal occlusion– Vestibular nerve section

Pharmacotherapy

• Directed principally at suppressing vestibular response.

• Alleviating nausea associated with vertigo.• Does not treat underlying cause.

– Low dose diazepam – used prior to CRP– Antiemetics like phenergan– Longer acting vestibular suppressants like

clonazepam for chronic disequilibrium

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Canalith Repositioning Procedure ( CRP )

• The treatment of choice for BPPV (Epley maneuver)

• The patient positioned in a series of steps so as to slowly move the otoconia particles from the Posterior SCC into the utricle.

• Takes approximately 5 minutes.

• The patient is instructed to wear a neck brace for 24 hours and to not bend down or lay flat for 24 hours after the procedure.

• Dix-Hallpike test is repeated soon after the CRP and after 1 week.

• If the patient does experience vertigo and nystagmus, then the CRP is repeated with a vibrator placed on the skull in order to dislodge the otoconia.

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The Epley Maneuver

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Epley manouevre

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CRP – Semont maneuver

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Brandt-Daroff Exercises

• Method of treating BPPV, usually used when the office treatment fails.

• These exercises should be performed

– For one week, three times per day

– For three weeks, twice per day.

• In each time, one performs the maneuver as shown five times.

• 1 repetition = maneuver done to each side in turn (takes 2 minutes)

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Brandt-Daroff Exercises

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Lampert maneuver- Lat. SCC BPPV

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Complications of CRP

• Failure – 25% (12%-56)• Recurrence – 13% in 6 months• Side effects

– Nausea ,Vomiting, Fainting, Sweating

• Worse vertigo – Lateral SCC BPPV

• “Canalith jam”

• Conversion to another canal

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Vestibular Rehabilitation Exercises (VRE)

• Reduces symptoms, Promotes Spontaneous resolution

• Safe and effective

• Cawthorne-Cooksey Exercises

• Need to be carried out regularly

– Over 12-16 Weeks before improvement is noticed

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Vestibular rehabilitaions

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Surgery• Singular neurectomy

• Posterior Canal Plugging Procedure

• Vestibular Nerve Section

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Role of Surgery

• Very limited, < 2% may need Surgery which is rarely offered

• Highly responsive to physical therapy interventions

• Only in intractable cases affecting the life style of the patient

Singular neurectomy

• Evolved by Gacek

• Section the posterior ampullary nerve that transmits information from the posterior semicircular canal ampulla toward the brain.

• Highly rational

• Technically difficult

• Can cause hearing loss in 7-17% of patients and fails in 8-12%.

• Anatomical abnormalities of singular canal

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Singular neurectomy

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Posterior Canal Plugging Procedure

• Parnes and McLure introduced this concept.

• Prevent movement of debris towards ampulla.

• Technically simpler and safer.

• Replaced the singular neurectomy.

• Less than 20% hearing loss.

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Posterior Canal Plugging Procedure

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Vestibular Nerve Section

• Done when the attacks of vertigo cannot be controlled with medication. Seems unreasonably aggressive for BPPV

• Approaches – Middle fossa, retrolabyrinthine, retrosigmoid

• The vestibular part of the nerve is cut. • The operation is done with a neurosurgeon and takes

about two hours. • The success rate (no vertigo attacks) is over 90%. • The hearing is slightly affected.

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Vestibular Nerve Section

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Bibliography

• Scott Brown Otorhinolaryngology, Head and Neck surgery, 7th edition

• Otorhinolaryngology Head & Neck Surgery,

Ballenger (17th edition)• Galsscock – Shambaugh Surgery of the Ear 5th

edition• Cumming’s otolaryngology, head and neck surgery

4th edition59

• Thank you

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