Benign Paroxysmal Positional Vertigo (BPPV)

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Benign paroxysmal positional vertigo (BPPV)\: inner ear disorder with recurrent brief attacks of positional vertigo; most
common cause of vertigo.
Benign\: indicates a good prognosis, peripheral cause; untreated cases may a
Paroxysmal\: sudden and rapid onset of vertigo with certain head movements.
Vertigo\: illusory sensation of motion in the absence of true motion; positional vertigo triggered by head position changes.
Anatomy of inner ear\: bony labyrinth (cochlea, vestibule, semi-circular canals) and membranous labyrinth (cochlear duct,
semi-circular ducts, utricle, saccule); balance maintained by endolymph and sensory receptors in ampulla and otoconia in
utricle and saccule.
Pathophysiology\: most commonly a
trapped in canal, stimulating hair cells and causing vertigo.
Causes\: idiopathic, head injury, vestibular neuronitis, labyrinthitis, complications of mastoid/stapes surgery.
Risk factors\: older age (40-60 years), female sex, Meniere’s disease, migraines, anxiety disorders.
Clinical features\: brief vertigo episodes (30 seconds to 1 minute), provoked by head movements; possible nausea, light-
headedness, imbalance, falls.
Di
stroke, cervical vertigo, medication-induced vertigo.
Dix-Hallpike test\: gold-standard for diagnosis; positive test shows latency, vertigo, rotatory and vertical nystagmus;
contraindicated in neck/back pathology.
Management\: self-limiting within 6 months; avoid provoking positions, counsel on recurrence risk; vestibular rehabilitation
(Epley manoeuvre, Semont manoeuvre, Brandt-Daro
Medications\: anti-emetics (prochlorperazine, cyclizine), vestibular sedatives (cinnarizine, betahistine); limited e
Surgical management\: reserved for intractable cases; options include denervation of posterior semi-circular canal or
obliteration via trans-mastoid approach.
Patient education\: avoid driving when dizzy, inform employer if vertigo poses occupational hazard.
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A comprehensive topic overview

Introduction

Benign paroxysmal positional vertigo (BPPV) is an inner ear disorder characterised by recurrent brief attacks of positional
1 2
vertigo. BPPV is the commonest cause of vertigo.
The use of the word ‘benign’ re
5
However, undiagnosed and untreated cases of BPPV may signi
reduced quality of life.
6
‘Paroxysmal’ refers to the sudden and rapid onset of vertigo with certain head movements.
3
Vertigo is an illusory sensation of motion of either oneself or the surroundings in the absence of true motion. 3
Positional
vertigo is the provoking of a spinning sensation by changes in head position in relation to gravity (e.g. rolling over in bed,
bending over and looking upward).
4Aetiology
Anatomy of the inner ear
The inner ear consists of two parts, the bony labyrinth and the membranous labyrinth (Figure 1)\:
The bony labyrinth comprises cavities in the petrosal part of the temporal bone. It holds the cochlea, vestibule and
semi-circular canals.
The membranous labyrinth sits inside the bony labyrinth. It consists of the cochlear duct, semi-circular ducts, utricle
and saccule.
The cochlea is regarded as the spiral organ for hearing. The semi-circular ducts, saccule and utricle form the vestibular
apparatus, which assists with balance.
The semi-circular ducts, within the semi-circular canals, have three individual parts that connect at the utricle (located
anteriorly to the saccule in the vestibule). The three components are named in regards to their anatomical position –
anterior, lateral and posterior semi-circular ducts.
The planes of these semi-circular canals form obtuse angles to one another. These ducts are
endolymph. They also have enlarged ends when they reach the utricle, called ampullae. The ampulla contains sensory
receptors which detect changes in the
balance control.
8,9
Figure 1. Anatomy of the internal ear, including the components of the bony labyrinth, membranous labyrinth, and vestibulocochlear
nerve
7
Another important component of the vestibular system is the otoconia. These are bio-crystals present in the utricle and
saccule (Figure 2).
They are located above the hair cells (kinocilia and stereocilia) in the macula (sensory epithelium), which is found in the
utricle and saccule. The otoconia are displaced with head movements, leading to the depolarisation of sensory hair cells.
This further generates electrical signals relayed to the CNS by the vestibular nerve. In turn, this stimulates the CNS to
respond with appropriate responses and ensures the maintenance of balance.
10Figure 2. Microanatomy of the sensory system in the utricle and saccule of the membranous labyrinth
11
Pathophysiology
The posterior canal is most commonly a
One of the most understood and accepted theories for the posterior semi-circular canal is canalolithiasis. This describes
the displacement of free-
The detached otoconial debris, in addition to the endolymph, may continue to stimulate hair cells even after head
movements have ceased. This leads to an abnormal sensation of vertigo and nystagmus when the head moves in the
plane of the a
1,2,3,12
Causes of BPPV
Most cases of BPPV are idiopathic.
Other known causes of BPPV include\:
Head injury
Vestibular neuronitis (post-viral illness)
Labyrinthitis (due to age-related degeneration of the labyrinth)
Complications of mastoid/stapes surgery

Risk factors

Risk factors for the development of BPPV include\:
Older age (onset common between 40 to 60 years old).
Female sex (women are twice as likely to have BPPV compared to men)
Meniere’s disease (usually diagnosed alongside BPPV in 30% of cases)
Patients with migraines and/or anxiety disorders
2

Clinical features

HistoryTypical symptoms of BPPV include\:Brief episodes of vertigo usually lasting 30 seconds to 1 minute
Symptoms provoked by head movements such as rolling over in bed, gazing upwards (e.g. when placing an object on a
shelf), bending forward (e.g. when tying shoe laces, sitting down)
Less common symptoms include\:
Nausea
Light-headedness, imbalance (as a result, patients may present with a fall – hence, it is crucial to consider vestibular
dysfunction; see the Geeky Medics guide to the assessment of falls)
Clinical examination
Typical clinical
Dix-Hallpike test positive\: leading to rotational vertigo and nystagmus

Investigations

Currently, there are no investigations that can identify the location and movement of otoconia.
Dix-Hallpike test
The current gold-standard test to elicit BPPV is the Dix-Hallpike test (DHT). A positive DHT will con
circular canal BPPV, with its 82% sensitivity and 71% speci
13
If the test is positive, there will be\:
Latency period\: the onset of nystagmus after 5 to 20 seconds
Vertigo
Rotatory and vertical nystagmus (up-beating and towards the a
These symptoms will begin gradually with the latency period, then increase intensely and decline gradually due to
fatigability.
Once the patient returns to sitting, there is prolonged vertigo and reversal of the nystagmus. If any of these features are
absent (no latency, no vertigo and persisting nystagmus), investigate for a central cause of vertigo.
In addition, BPPV is generally unilateral. Therefore positive movements will often be in one eye. If the test is bilaterally
positive, this could suggest a lateral semi-circular canal BPPV, vestibular neuritis, or a central cause.
2
Contraindications to DHT include\:
Patients with neck- or back-related pathology (i.e. severe rheumatoid arthritis, cervical stenosis, spinal cord injury,
vertebral artery disease or carotid stenosis).
2

Di

It is important to identify any negative symptoms as these may point towards other conditions. Crucial negatives to be
established are\:
Persistent vertigo\: indicative of Meniere’s disease
Tinnitus, hearing loss or aural fullness\: indicative of Meniere’s disease, labyrinthitis
Long and gradual onset, viral prodrome\: indicative of vestibular neuronitis, labyrinthitis
Visual, speech, motor or sensory loss\: indicative of a CNS lesion
Vertical/down-beating nystagmus\: indicative of a CNS lesion
Further di
Table 1. Di
Di
Otologic diseasesMeniere’s disease
Vestibular neuronitis
Labyrinthitis
Sustained vertigo,
aural fullness, and tinnitus in the a
Follows a viral prodrome, potential tinnitus;
gradual onset
Follows a viral prodrome, hearing loss, tinnitus
may occur; gradual onset
Neurological diseases
Vestibular migraine
Brainstem/cerebellar stroke (or
transient ischaemic attack)
Symptoms may last from 5 mins to 72 hours,
current history of migraines (with other features
– e.g. headache, photophobia, visual aura etc)
Very sudden onset, other neurological
symptoms – dysarthria, dysphagia,
sensory/motor loss

Management

Conservative management
BPPV is often a self-limiting condition, and symptoms may subside within 6 months of onset. 3
to\:
Patients should be advised
Avoid positions that may provoke vertigo symptoms
Counsel that symptoms may re-occur. One study identi
14
Medical management
If symptoms persist, vestibular rehabilitation should be performed. This can be done with either\:
Repositioning techniques
One of the recommended techniques for posterior canal BPPV is the Epley manoeuvre. The aim is to reposition the
displaced otoconial particles back into the utricle from the posterior canal.
Other techniques include the Semont manoeuvre, the Brandt-Daro
latter two can be performed at home by the patients once they are taught the steps).
Medications
Medications which may be considered include\:
Anti-emetics\: prochlorperazine or cyclizine
Vestibular sedatives\: cinnarizine or betahistine (histamine analogue)
However, the literature suggests that these medications have little e
15
Surgical management
Surgical intervention is usually reserved for patients with intractable symptoms who have failed to respond to repeated
repositioning procedures. The two surgical options are\:
2
Denervate the posterior semi-circular canal (by singular neurectomy)
Obliterate the posterior canal (via a trans-mastoid approach)
Patient education
It is important to also counsel on other aspects of a patient’s life\:
Advise the patient not to drive when they feel dizzy or if the driving provokes the episodes.
Advise the patient to inform their employer where it may pose an occupational hazard (e.g. working with machinery, at
heights etc).References
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Reviewer

Ms Shadaba Ahmed and Dr Elizabeth Cotzias
Consultant ENT Surgeon and ENT Registrar

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Contents

IntroductionAetiology
Risk factors
Source\: geekymedics.com