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Benign paroxysmal positional vertigo (BPPV) is an inner ear disorder characterised by recurrent brief attacks of positional vertigo.1 BPPV is the commonest cause of vertigo.2
The use of the word ‘benign’ reflects the good prognosis of BPPV, as its’ cause is likely peripheral, rather than central.5 However, studies have shown that undiagnosed and untreated cases of BPPV may affect patients clinically with a risk of falls, and psychologically with quality of life issues.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.3Positional 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).4
Anatomy of the inner ear
The inner ear consists of two parts – the bony labyrinth and the membranous labyrinth (Figure 1). The bony labyrinth is comprised of cavities in the petrosal part of the temporal bone. It holds the cochlea, vestibule and the 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 together at the utricle (located anteriorly to the saccule in the vestibule) (Figure 1). 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 in relation to one another. These ducts are filled with a fluid called endolymph. They also have enlarged ends when they reach the utricle, called ampullae. The ampulla contains sensory receptors which detect changes in the flow of endolymph with head movements. This sends signals to the brain for balance control.8,9
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 to be 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.10
There are various theories to why BPPV occurs in patients, and this depends on the particular location of the problems within the semi-circular canals. The posterior canal is most commonly affected in BPPV. However, the lateral, anterior or multiple canals can be affected. One of the most understood and accepted theories for the posterior semi-circular canal is canalolithiasis. This describes the displacement of free-floating otoconia particles from the macula that then become trapped in the posterior canal. 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 affected semi-circular canal.1,2,3,12
Most cases of BPPV are idiopathic.
Other known causes of BPPV include:
Vestibular neuronitis (post-viral illness)
Labyrinthitis (due to age-related degeneration of the labyrinth)
Complications of mastoid/stapes surgery
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 disorders2
History and examination
Most common symptoms 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:
Light-headedness, imbalance (as a result, patients may present with a fall – hence, it is crucial to have vestibular dysfunction as a differential diagnosis in your fall history; see the Geeky Medics guide for the assessment of falls here.)
Currently, there are no investigations that can depict the location and movement of otoconia. The only gold-standard investigation performed to elicit BPPV is the Dix-Hallpike Test (DHT). A positive DHT will confirm posterior semi-circular canal BPPV, with its 82% sensitivity and 71% specificity.13 Only a properly trained clinician should perform DHT. See the Geeky Medics guide and video on how to conduct the DHT here.
If the test is positive, there will be:
Latency period – the onset of nystagmus after 5 to 20 seconds
Rotatory and vertical nystagmus (up-beating and towards the affected ear)
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. 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
It is important to rule out 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 differentiating features between common otologic, neurological and other diseases can be found in Table 1.
Table 1. Differential diagnoses of BPPV
Differential diagnoses of BPPV
Characteristic differentiating symptoms
Sustained vertigo, fluctuating loss of hearing, aural fullness, and tinnitus in the affected ear
Follows a viral prodrome, with hearing loss and potential tinnitus; gradual onset
Follows a viral prodrome, tinnitus may occur; gradual onset
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
History of degenerative cervical spine disease
Carbamazepine, phenytoin, antihypertensives may produce side effects of vertigo and/or dizziness
BPPV is often a self-limiting condition and symptoms may subside within 6 months of onset.3 Patients should be advised to:
Avoid positions that may provoke vertigo symptoms
Counsel that symptoms may re-occur. One study identified 36% recurrence in symptoms within 48 months of onset.14
If symptoms persist, vestibular rehabilitation should be performed. This can be done with either:
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. See the Geeky Medics guide and video on how to perform the Epley manoeuvre here.
Other techniques include the Semont manoeuvre, the Brandt-Daroff exercises and the modified Epley manoeuvre (the latter two can be performed at home by the patients once they are taught the steps).
Anti-emetics – prochlorperazine or cyclizine
Vestibular sedatives – cinnarizine or betahistine (histamine analogue)
However, the literature suggests that these medications have little effect on controlling symptoms.15 Hence, repositioning methods are the go-to for clinicians.
Surgical intervention is usually reserved for patients with intractable symptoms, which have failed to respond to repeated repositioning procedures. The two surgical options are:
Denervate the posterior semi-circular canal (by singular neurectomy)
Obliterate the posterior canal (via a trans-mastoid approach)2
It is important to also counsel on other aspects of a patient’s life:
Advise the patient to not drive when they feel dizzy or if the driving provokes the episodes.
Advise the patient to inform their employer where it may pose as an occupational hazard (e.g. working with machinery, at heights etc).
BPPV is an inner ear disorder characterised by repeated episodes of positionalvertigo
The vertigo is provoked by certain headmovements, such as rollingover in bed, lookingupward etc…
It is more common in women (2:1), and patients >40 years old
Most cases of BPPV are idiopathic; known secondary causes include head injury and vestibular neuronitis/labyrinthitis
Symptoms include vertigo, provoked by headmovements, lasting 30seconds to 1 minute, with associated nausea, light-headedness and imbalance.