Benign Paroxysmal Positional Vertigo

Also known as: BPPV

Brief episodes of vertigo provoked by changes in head position relative to gravity, caused by displaced otoconia within the semicircular canals. It is the commonest cause of vertigo, accounting for around 20 to 30 percent of all presentations to dizziness clinics, and it is curable in a single consultation, which makes failure to diagnose it a significant clinical failure.

Mechanism

Calcium carbonate otoconia detach from the utricular macula and enter a semicircular canal.

Canalolithiasis: free floating particles within the canal lumen. Head movement causes them to fall under gravity, dragging endolymph and deflecting the cupula. Latency of 1 to 5 seconds reflects the time for particles to begin moving; the nystagmus crescendos then decays over 10 to 60 seconds as they settle; fatigability occurs on repetition.
Cupulolithiasis: particles adherent to the cupula, making it gravity sensitive. Nystagmus begins immediately without latency, persists as long as the position is maintained, and does not fatigue.

Canal involvement

Posterior canal in 80 to 90 percent, because it is the most dependent canal in the upright and supine positions.
Horizontal or lateral canal in 5 to 15 percent, subdivided into geotropic canalolithiasis and apogeotropic cupulolithiasis.
Anterior or superior canal in 1 to 3 percent, which is rare because its position makes spontaneous clearance likely, and which requires exclusion of a central cause because downbeat nystagmus is its hallmark.

Causes

Idiopathic in 50 to 70 percent, particularly in older women.
Head trauma, including minor trauma, which produces multicanal and bilateral disease more often.
Vestibular neuritis and labyrinthitis, from utricular damage.
Ménière disease.
Prolonged supine positioning, including after surgery and dental procedures.
Osteoporosis and vitamin D deficiency, which are associated with recurrence, and reduced serum vitamin D is a modifiable recurrence risk factor.
Migraine.

Brief rotational vertigo lasting seconds, characteristically under 60 seconds, provoked by rolling over in bed, lying down, sitting up, looking up to a high shelf, or bending forward.
Attacks come in clusters over days to weeks, often worst on waking.
Nausea, and occasionally vomiting, disproportionate to the brief vertigo.
Persistent low grade unsteadiness and light headedness between attacks, which patients often report as the dominant symptom and which can obscure the positional pattern.
No hearing loss, tinnitus or aural fullness. Their presence points to another diagnosis.
No loss of consciousness, no focal neurological symptoms.

Features that indicate a central cause and require imaging

Downbeat or purely vertical nystagmus that does not fit the expected canal pattern.
Nystagmus without latency, without fatigue, and not matching any canal plane.
Vertigo without nystagmus on positioning.
Associated diplopia, dysarthria, dysphagia, limb ataxia or sensory symptoms.
Severe headache, particularly occipital, of sudden onset.
Failure to respond to correctly performed repositioning after several attempts.

The diagnosis is made at the bedside by provoking and observing the nystagmus. Use Frenzel glasses or video goggles where available, since visual fixation suppresses the nystagmus and causes false negatives.

Dix Hallpike manoeuvre for the posterior and anterior canals

Seated with the head turned 45 degrees to the test side, the patient is laid rapidly supine with the head extended 20 to 30 degrees below the horizontal, and held for at least 30 seconds.
Posterior canal canalolithiasis: upbeating torsional nystagmus with the top pole of the eye beating toward the dependent ear, after a latency of 1 to 5 seconds, lasting under 60 seconds, with reversal on sitting up and fatigue on repetition.
Anterior canal: downbeating nystagmus with a torsional component toward the affected ear. Because downbeat nystagmus is also a central sign, anterior canal disease should not be diagnosed without careful exclusion of central pathology.

Supine roll test for the horizontal canal

Performed when the Dix Hallpike is negative but the history is convincing.

Supine with the head flexed 30 degrees, the head is turned rapidly 90 degrees to one side, held, returned to centre, then turned to the other side.
Geotropic nystagmus beating toward the ground on both sides indicates canalolithiasis, with the affected side being the one producing the stronger nystagmus.
Apogeotropic nystagmus beating away from the ground indicates cupulolithiasis, with the affected side being the one producing the weaker nystagmus.

Additional assessment

Full neurological and cerebellar examination.
Head impulse test, spontaneous nystagmus assessment and test of skew.
Otoscopy and audiometry where any auditory symptom is present.
Magnetic resonance imaging is not required for typical benign paroxysmal positional vertigo and should not be ordered routinely. It is indicated for atypical nystagmus, central signs, or failure of repositioning.
Consider vitamin D and bone density assessment in recurrent disease.

Particle repositioning is the treatment and is effective in the great majority at the first or second attempt.

Posterior canal: Epley manoeuvre

From the Dix Hallpike position with the affected ear down, hold for 30 seconds or until the nystagmus stops.
Rotate the head 90 degrees to the opposite side, hold 30 seconds.
Roll the patient onto the shoulder with the head turned a further 90 degrees so the face is directed toward the floor, hold 30 seconds.
Sit the patient up with the chin tucked.
Success rate is 80 to 90 percent after one manoeuvre and above 95 percent after repeated treatments.
Repeat the manoeuvre in the same session if nystagmus persists.

Posterior canal alternative: Semont manoeuvre

Used where neck or back limitation makes the Epley difficult. The patient is moved rapidly from lying on the affected side to lying on the opposite side, with the head position maintained relative to the body.

Horizontal canal

Geotropic canalolithiasis: barbecue or Lempert roll, rotating the patient 360 degrees in 90 degree increments away from the affected side, holding each position 30 seconds; or the Gufoni manoeuvre, lying rapidly on the unaffected side then turning the head 45 degrees toward the floor.
Apogeotropic cupulolithiasis: Gufoni manoeuvre toward the affected side to convert cupulolithiasis to canalolithiasis, followed by treatment of the resulting geotropic form; or head shaking to dislodge particles from the cupula.
Horizontal canal disease is more resistant and often requires several sessions.

Anterior canal

Deep head hanging manoeuvre or a reverse Epley, after central pathology has been excluded.

Post manoeuvre instructions

Post procedural restrictions such as sleeping upright and avoiding head movement for 48 hours do not improve outcomes and are not required.
Warn about residual unsteadiness for a few days, which is common and does not indicate failure.
Advise caution with driving immediately after treatment.

Home exercises

Brandt Daroff exercises, performed five repetitions three times daily, are less effective than a properly performed repositioning manoeuvre and are reserved for patients with residual symptoms, for those who cannot attend for treatment, and for frequently recurrent disease where the patient can self treat.

Medication

Vestibular sedatives do not treat benign paroxysmal positional vertigo, do not shorten its course, and impair the compensation that resolves residual symptoms. They also mask the nystagmus needed for diagnosis.
A single dose of an antiemetic before a manoeuvre is reasonable for a patient who vomits severely, but routine prescription of prochlorperazine for this condition is inappropriate and is a common error.
Betahistine has no role.

Refractory and recurrent disease

Recurrence occurs in around 15 to 50 percent within 5 years. Teach self administered repositioning to frequent recurrers.
Correct vitamin D deficiency, with supplementation reducing recurrence in deficient patients.
Reconsider the diagnosis after three or four failed correctly performed manoeuvres, and image for central pathology.
Surgical posterior canal occlusion is a last resort for truly intractable, disabling, unilateral posterior canal disease, carrying a risk of sensorineural hearing loss of a few percent. Singular neurectomy is now rarely performed.

Special considerations

Elderly patients: benign paroxysmal positional vertigo is a substantial and treatable cause of falls and hip fracture. Actively screen for it in any older patient presenting with falls or dizziness, since many do not report the positional trigger.
Cervical spine disease, atlantoaxial instability, carotid stenosis, retinal detachment and recent neck surgery require modification of the manoeuvre or use of the Semont alternative.
Bilateral and multicanal disease is common after head trauma and requires treating one canal at a time, beginning with the most symptomatic.

Clinical toolsCalculators

BMI GCS EDD Parkland Formula

Corrected Sodium Corrected Calcium Anion Gap Creatinine Clearance Insulin Calculations qSOFA Wells PE Wells DVT CHA₂DS₂-VASc HAS-BLED CURB-65 Centor/McIsaac

Hyposmia

Reduced but not absent sense of smell. It is far more common than complete anosmia, affecting around 15 to 20 percent of adults and more than half of those over 65, and it is substantially underrecognised because patients adapt gradually and rarely present with it as a complaint.

Relationship to anosmia

Hyposmia and anosmia share the same causes and differ in degree. The practical distinctions are that hyposmia is more likely to be conductive and reversible, more likely to be detected only on objective testing, more likely to represent early or partial disease, and more likely to represent either the early stage of a progressive process or the recovering stage of an acute one.

Quantification

Objective testing grades severity, typically as normosmia, mild hyposmia, moderate hyposmia, severe hyposmia and anosmia, using threshold, discrimination and identification scores. Testing all three components is more informative than identification alone, since threshold reflects peripheral function and discrimination and identification reflect central processing, and the pattern helps localise the lesion.

Causes worth emphasising in the hyposmic patient

Chronic rhinosinusitis, with or without polyps, which is the commonest treatable cause and in which the fluctuating nature of the loss is a useful clue.
Allergic rhinitis, in which smell fluctuates with obstruction and season.
Post viral, particularly in the recovery phase of a previously complete loss.
Presbyosmia, which is progressive, bilateral and symmetrical, and which contributes to poor nutrition and reduced quality of life in the elderly.
Smoking, which causes a dose dependent reduction that partially recovers over years after cessation.
Neurodegenerative disease in its prodromal phase. Hyposmia is present in around 90 percent of patients with Parkinson disease and precedes motor symptoms by up to a decade. It is one of the strongest premotor markers.
Diabetes, chronic kidney disease, hypothyroidism and nutritional deficiency.
Medications, particularly in polypharmacy in the elderly.
Obstructive causes: septal deviation, turbinate hypertrophy, adenoid hypertrophy in children, and tumour.

Reduced intensity of smells rather than absence, often described as smells being faint or requiring effort.
Reduced flavour perception, with food described as bland.
Increased use of salt, sugar and strong seasoning, which has consequences for blood pressure and glycaemic control in patients with cardiovascular disease and diabetes.
Reduced appetite and unintended weight loss in the elderly, contributing to frailty and sarcopenia.
Difficulty detecting smoke, gas and spoiled food, though the risk is less absolute than in anosmia.
Fluctuation with nasal obstruction, allergen exposure, season and upper respiratory infection, which strongly indicates a conductive cause.
Frequently identified incidentally on testing rather than reported, particularly in older adults who attribute it to ageing and do not mention it.

Examination

Nasal endoscopy with specific attention to the olfactory cleft, which is where the relevant obstruction sits and which cannot be assessed with a speculum.
Assess for polyps, mucosal oedema, discharge, septal deviation, turbinate hypertrophy and masses.
Cranial nerve and neurological examination, including a screen for parkinsonian features: bradykinesia, rigidity, rest tremor, reduced arm swing and hypomimia. Given the strength of the association, a patient over 50 with unexplained progressive hyposmia deserves a deliberate look for these.
Cognitive screening where memory complaints coexist.
Nutritional assessment and weight in the elderly.

Objective psychophysical testing is essential, because self reported smell function correlates poorly with measured function and because grading severity guides both prognosis and management. Sniffin Sticks with threshold, discrimination and identification scoring, or the University of Pennsylvania Smell Identification Test, are the usual instruments.
Test each nostril separately.
Nasal endoscopy in every patient.
Computed tomography of the sinuses to assess the olfactory cleft and sinus disease, particularly where a conductive cause is suspected. Opacification of the olfactory cleft correlates with olfactory loss and predicts response to treatment.
Magnetic resonance imaging where the loss is unilateral, progressive without sinonasal disease, associated with neurological signs, or following trauma.
Blood tests: glucose and HbA1c, thyroid function, full blood count, vitamin B12, zinc, renal and liver function.
Medication review, which frequently identifies a contributory agent that can be substituted.
Neurology referral where parkinsonian or cognitive features are found, since olfactory testing contributes to early diagnosis.
A trial of oral corticosteroid, which distinguishes a conductive inflammatory component from a sensorineural loss and predicts the response to topical therapy and to surgery.

The higher proportion of reversible causes makes hyposmia more rewarding to treat than complete anosmia, and this justifies a systematic search for a conductive component in every patient.

Treat conductive and inflammatory causes

Chronic rhinosinusitis with polyps: high dose intranasal corticosteroid, corticosteroid delivered by irrigation or in the head down forward position, a course of oral prednisolone 0.5 mg/kg for 5 to 10 days, escalation to endoscopic sinus surgery, and biologic therapy in severe type 2 disease. Dupilumab in particular produces substantial and sustained smell recovery.
Chronic rhinosinusitis without polyps: topical steroid, high volume saline irrigation, macrolide therapy where appropriate, and surgery for failure.
Allergic rhinitis: continuous intranasal corticosteroid, antihistamine, allergen avoidance and immunotherapy.
Anatomical obstruction of the olfactory cleft: septoplasty or turbinate reduction, with honest counselling that smell improvement is variable.
Steroid delivery technique matters. Standard sprays deposit almost nothing in the olfactory cleft. Use drops in the Mygind or Kaiteki position, or high volume irrigation, where smell is the target symptom.

Olfactory training

Indicated for post viral, post traumatic and idiopathic hyposmia, and as an adjunct after treatment of a conductive cause where recovery is incomplete.
The same protocol as for anosmia: four odorants, twice daily, 20 to 30 seconds each, for at least 12 weeks and preferably 6 to 12 months, with the odorant set changed every 12 weeks.
Outcomes are better in hyposmia than in anosmia, since more residual function remains to build on.

Address modifiable contributors

Smoking cessation, with counselling that recovery is gradual over years and is proportional to the duration of abstinence.
Optimise glycaemic control, treat hypothyroidism, and correct vitamin B12 and zinc deficiency where present. Do not give zinc without documented deficiency, and never intranasally.
Review and substitute medications where feasible.
Remove occupational toxin exposure.

Management in the elderly

Address the nutritional consequences directly. Refer to a dietitian where there is weight loss.
Enhance food using texture, temperature, colour, umami rich ingredients and trigeminal stimulants such as chilli, pepper and mint, which remain perceptible.
Discourage excessive salt and sugar addition, and offer alternative flavour strategies, since this is a real cardiovascular and metabolic risk in this group.
Safety measures: smoke alarms, gas detectors, date labelling of food, and consideration of induction or electric cooking.
Screen for depression and social isolation.

Follow up

Repeat objective testing at 6 and 12 months, and after any intervention, to document change objectively.
Progressive unexplained decline in an older adult warrants neurological review, since it may be the earliest manifestation of neurodegenerative disease.
Recovery of smell after treatment of sinus disease is often reported by patients as the single most valued outcome, which is a reason to measure and pursue it rather than treating it as a secondary endpoint.

Benign Paroxysmal Positional Vertigo

Overview

Clinical Features

Diagnosis

Management

Overview

Clinical Features

Diagnosis

Management