History and exam

Key diagnostic factors

common

presence of risk factors

Key risk factors include increasing age, female sex, head trauma, vestibular neuronitis, labyrinthitis, migraines, inner ear surgery, and Meniere's disease.

specific provoking positions

Vertigo provoked by specific head movements (e.g., looking up or bending down, getting up, turning the head, and rolling over in bed to one side).

In posterior canal BPPV, patients may identify the direction of movement that precipitates an episode, thus corresponding to the affected ear.

If vertigo is not provoked by movements, then a central disorder is considered. Labyrinthitis or vestibular neuronitis can mimic BPPV, but unlike BPPV, head movement in any plane can precipitate vertigo that will persist for days at a time.[7]

brief duration of vertigo

BPPV often lasts for <30 seconds. The vertigo of other disorders lasts much longer: Meniere's disease lasts for hours; viral labyrinthitis or vestibular neuronitis lasts for days; migraines are variable; and other central disorders can be constant.

Associated symptoms (nausea, imbalance, and lightheadedness) may persist for a longer duration. Therefore, care should be taken to specifically differentiate the duration of vertigo from the duration of other associated symptoms.[7]

episodic vertigo

BPPV is episodic. In posterior canal BPPV, the attacks occur repeatedly over weeks to months. In lateral (horizontal) canal BPPV, the attacks occur repeatedly over days to weeks. A single isolated attack is not usually suggestive of BPPV, unless confirmed with the Dix-Hallpike manoeuvre or supine lateral head turn.[7]

severe episodes of vertigo

The vertigo of BPPV is usually intense, more so in the lateral canal variant. If mild, then the differential diagnosis should be broadened and other causes (especially central) considered.[7]

sudden onset of vertigo

A gradual onset is not suggestive of BPPV and may suggest a central pathology.[37]

nausea, imbalance, and lightheadedness

May persist for a longer duration. Therefore, care should be taken to specifically differentiate the duration of vertigo from the duration of other associated symptoms.[7]

absence of associated neurological or otological symptoms

If the following symptoms occur in addition to the vertigo, alternative diagnoses to BPPV are likely: hearing loss, tinnitus, aural fullness, and other neurological symptoms. However, it is not uncommon for patients to experience associated symptoms of nausea, imbalance, and lightheadedness. BPPV commonly occurs after vestibular neuronitis and may also co-exist with other conditions.[7]

normal neurological examination

Besides a positive Dix-Hallpike manoeuvre or positive supine lateral head turn, any other neurological abnormalities suggest either another pathological process, secondary BPPV, or a co-existing disorder.[7]

positive Dix-Hallpike manoeuvre or positive supine lateral head turn

A suggestive history of BPPV combined with a positive Dix-Hallpike manoeuvre (posterior canal BPPV) or positive supine lateral head turn (lateral canal BPPV) is usually sufficient for diagnosis.[7]

normal otological examination

Any otological abnormalities suggest either another pathological process, secondary BPPV, or a co-existing disorder.[7]

Other diagnostic factors

common

age >50 years

Peak incidence is between 50 and 70 years of age.[2]

female sex

Females are almost twice as likely to be affected by BPPV.[5]

uncommon

positional vertigo in absence of nystagmus

Mild cases of BPPV may give rise to vertigo during diagnostic manoeuvres but without nystagmus, termed subjective BPPV.[7] However, the reported vertigo should follow a pattern similar to expected nystagmus: latency, a transient crescendo-decrescendo nature, and fatigability. Otherwise, there is a greater likelihood of labelling cervical problems or phobic postural vertigo as BPPV.

Risk factors

strong

increasing age

Degenerative processes occur with ageing, including vascular and metabolic pathologies that promote otoconia detachment from the utricle.[4][5][17][18]

female sex

Possibly enhanced by the association of migraines (another BPPV risk factor) with females. In addition, possible metabolic differences in females, especially post-menopausal hormonal changes, may accelerate decalcification of the utricle (similar to osteoporosis).[5][17]

head trauma

Direct damage to the utricle can dislodge otoconia from the utricle.[17][19] Head trauma is the most common cause of simultaneous bilateral BPPV.

vestibular neuronitis

Arteriolar branches of the anterior vestibular artery run alongside the superior vestibular nerve in relatively narrow and long bony channels. Inflammation and oedema in this vicinity leads to entrapment and compression of the arterioles, which results in ischaemia, damage and degeneration of the utricular end-organ, and subsequent otoconial detachment.[2][17][20][21]

labyrinthitis

Direct damage to the inner ear and utricle via inflammatory or infectious processes can displace otoconia from the utricle.[2][17]

migraines

Vasospasm of the labyrinthine arteries and possible ischaemia facilitates detachment of otoconia from the utricle.[5][22][23][24]

inner ear surgery

Direct damage to the vestibular apparatus results in otoconial debris.[7][25][26][27]

Meniere's disease

Studies have shown a strong association between Meniere's disease and BPPV. The mechanism is unclear. However, it is postulated that hydropic mechanical damage to the utricle or partial obstruction of the membranous labyrinth facilitates otoconial detachment.[7][27][28][29]

weak

otitis media

Labyrinthitis, a complication of otitis media, is associated with BPPV.[30]

hypertension

Vascular system damage; facilitates ischaemia of the vestibular apparatus.[5]

hyperlipidaemia

Vascular system damage; facilitates ischaemia of the vestibular apparatus.[5]

diabetes mellitus

Vascular system damage; facilitates ischaemia of the vestibular apparatus.[5]

vertebrobasilar insufficiency

Ischaemic changes weaken or damage the utricle; otoconial debris results.[5][17][27][31]

giant cell arteritis

Postulated that arteritis results in ischaemic damage and degeneration to the utricle, resulting in the release of otoconial debris.[32]

osteoporosis

Accelerates decalcification of the utricle, resulting in free-floating otoconia particles.[18][33]

intubation

Prolonged supine and head-reclined position assists entry of free-floating otoconia particles into the semicircular canal.[5][17]

habitual lateral head-positioning during bed rest (ipsilateral BPPV)

Facilitates adhesion of particles to the cupula and/or encourages amalgamation of a critical mass to be reached in the semicircular canal.[18][34]

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