A clinical synthesis based on the most recent recommendations and meta-analyses (the AAO-HNS guideline, the Bárány Society criteria, the Cochrane review of the Epley manoeuvre). Every reference has been checked individually on PubMed.

🌀 What are the fundamentals to know about BPPV?

Benign paroxysmal positional vertigo (BPPV) is one of the most common reasons for consulting about vertigo, and yet one of the most under-diagnosed and under-treated. For the physiotherapist as much as for the informed patient, understanding its fundamentals (what it is, who it happens to, and by what mechanism) is the essential prerequisite for evidence-based management. It is a mechanical disorder of the inner ear, peripheral, benign in its course, and most often resolved by simple repositioning manoeuvres.

Definition: a positional and paroxysmal syndrome

BPPV is a syndrome characterised by brief episodes of vertigo triggered by rapid changes of head position ¹. Every word of its name carries a precise clinical meaning: positional, because the attacks are provoked by specific head movements (lying down, turning over in bed, looking up, bending forwards); paroxysmal, because the vertigo comes in brief bursts, typically from a few seconds to less than a minute; benign, because it reflects neither a central lesion nor a serious progressive disease; and vertigo in the strict sense, that is to say an illusion of rotatory movement.

BPPV now has consensus operational diagnostic criteria, drawn up by the Classification Committee for Vestibular Disorders of the Bárány Society, which structure the diagnosis and distinguish established syndromes from emerging ones ². This international classification is the common frame of reference and reflects the current state of knowledge on the clinical aspects and the pathomechanisms of the disease.

BPPV is the most frequent cause of vertigo worldwide ³.

Epidemiology: frequent, female, and age-related

BPPV accounts for a major share of the vertigo seen in practice. According to the AAO-HNS clinical practice guideline, between 17 % and 42 % of patients consulting for vertigo eventually receive a diagnosis of BPPV ⁴. In the adult general population, the reference epidemiological study finds a lifetime prevalence of 2.4 %, a 1-year prevalence of 1.6 % and a 1-year incidence of 0.6 % ⁵.

Two demographic trends dominate. First, a clear female predominance: prevalence and incidence are consistently higher in women than in men, lifetime prevalence reaching 3.2 % in women against 1.6 % in men ⁵. Second, a strong age effect: the mean age of onset is 49.4 years, and prevalence rises considerably with age, in people over 60, the 1-year prevalence is nearly seven times that of the 18-39 group ⁵.

Finally, BPPV is a recurring condition: 56 % of affected people have recurrent episodes (44 % reporting only one), with a recurrence rate estimated at around 15 % a year ⁵. This recurring character has direct implications for follow-up and for patient education.

A real impact, treatment too rare

The benign in the name must not lead anyone to underestimate the impact of the disease. In 86 % of affected people, BPPV led to a medical consultation, an interruption of daily activities or time off work ⁵. And yet, despite its treatable nature, only 8 % of affected people received effective treatment ⁵. This contrast between a major functional impact and massive under-treatment underlines what is at stake: a correct positional diagnosis, rather than further tests that are often useless, and access to repositioning manoeuvres, whose effectiveness is now well established.

Pathophysiology: otoconia, canalithiasis and cupulolithiasis

BPPV is a mechanical disorder of the inner ear. Normally, crystals of calcium carbonate, the otoconia (or otoliths), are anchored in the utricular macula of the vestibule and take part in detecting linear acceleration and gravity. In BPPV, this debris comes loose: the otoconia responsible for the disease come from detachment of the neuroepithelium of the utricular macula, secondary to a degenerative process ⁶. Once freed, they migrate abnormally into the semicircular canals, which are devoted to detecting angular acceleration, where their presence makes the canal sensitive to gravity and causes positional vertigo.

Two pathophysiological mechanisms account for the disease ⁶ :

• Canalithiasis : debris/otoliths float freely in the lumen of the semicircular canal. On a change of position, these particles move under gravity and set up an endolymphatic current that stimulates the cupula. It is the most frequent mechanism; it accounts for the brief and delayed (latent) character of the nystagmus.
• Cupulolithiasis : debris/otoliths attach directly to the cupula, making it sensitive to gravity. The nystagmus is then typically more persistent.

This distinction is not merely theoretical: in posterior canal BPPV, a nystagmus lasting less than 1 minute on the Dix-Hallpike manoeuvre suggests canalithiasis, whereas one lasting more than 1 minute points to cupulolithiasis ⁷.

The canals involved: the posterior canal above all

The otoconia can reach any of the three semicircular canals of each ear, but their involvement is very unevenly distributed, largely because of anatomy and gravity. The posterior semicircular canal, sitting in the most dependent part of the labyrinth, is by far the most frequently affected, followed by the horizontal (or lateral) canal; involvement of the anterior canal is rare ⁷.

In a cohort of 481 patients diagnosed according to the Bárány Society criteria, the distribution of the canalithiasis forms was as follows ⁷ :

The posterior canal is therefore the compulsory starting point of clinical reasoning: it is diagnosed with the Dix-Hallpike manoeuvre, which provokes vertigo with an upbeating torsional nystagmus, the upper pole of the eyes beating towards the affected ear, with frequent reversal of the nystagmus on sitting up again ⁴⁷. When the Dix-Hallpike manoeuvre shows a horizontal nystagmus or none at all in a patient whose history is compatible, a supine roll test must then be performed to assess lateral canal BPPV ⁴.

🔍 How do you diagnose BPPV with certainty?

Benign paroxysmal positional vertigo (BPPV) is the most frequent cause of vertigo ³, and on its own accounts for a major share of consultations for this complaint: between 17 % and 42 % of patients who consult for vertigo eventually receive a diagnosis of BPPV ⁴. And yet it remains largely under-diagnosed and under-treated, in a large general population study, only 8 % of affected people had received effective treatment ⁵. This paradox rests largely on a reassuring fact: the diagnosis of BPPV depends neither on imaging nor on sophisticated tests, but on a focused history and positional manoeuvres performed at the bedside. They still have to be carried out methodically, and the nystagmus that makes the diagnosis has to be recognised.

1. The history: a brief and strictly positional vertigo

The first step, often the most discriminating, is the history. BPPV is defined as a syndrome characterised by brief episodes of vertigo triggered by rapid changes of head position ¹. Two features must be actively sought:

• Brevity : the episodes are fleeting, typically lasting from a few seconds to less than a minute, and not a continuous vertigo lasting hours or days.
• The positional character : the vertigo is triggered by a head movement, lying down, turning over in bed, bending forwards, looking up at a shelf. It is the change of position, and not the position held, that provokes the attack.

The history also establishes the background, which raises the pre-test probability. The mean age of onset is 49.4 years, and prevalence rises sharply with age: in people over 60, the 1-year prevalence is nearly seven times that of the 18–39 group ⁵. BPPV is more frequent in women (lifetime prevalence 3.2 % against 1.6 % in men) and readily recurs: 56 % of affected people report recurrent episodes, with a recurrence rate of around 15 % a year ⁵. A history of stereotyped episodes that resolve and then return is therefore a strong argument from the history.

Understanding the pathophysiology illuminates the examination. BPPV results from the presence, in a semicircular canal, of otoconial debris (otoliths) detached from the neuroepithelium of the utricular macula through a degenerative process ⁶. This debris floats freely in the canal (canalithiasis) or adheres to the cupula (cupulolithiasis) ⁶. On changes of position, its movement under gravity creates an abnormal endolymphatic flow that stimulates the canal: this is what generates both the vertigo and a nystagmus whose direction betrays the canal responsible.

2. The Dix-Hallpike manoeuvre: the reference test for the posterior canal

The posterior semicircular canal is by far the most frequently affected. In a cohort of 481 patients diagnosed according to the Bárány Society criteria, posterior canal canalithiasis accounted for 33.1 % of cases, against 14.6 % for the horizontal canal and only 4.0 % for the anterior canal ⁷. It is therefore the posterior canal that is tested first, using the Dix-Hallpike manoeuvre.

Performing it: The manoeuvre consists in bringing the patient from sitting to lying, the head turned 45° to one side and the neck extended about 20°, the suspected ear facing down ⁴. The position is held while the eyes are watched for nystagmus, then the operation is repeated on the other side.

The characteristic nystagmus: The diagnosis of posterior canal BPPV is made when the Dix-Hallpike provokes vertigo with an upbeating torsional nystagmus ⁴. More precisely, it is an upbeating vertical nystagmus, with or without a torsional component, whose upper eye pole beats towards the affected ear ⁷. Three semiological features confirm its peripheral, canal origin:

• A latency of a few seconds between taking up the position and the appearance of the nystagmus;
• A paroxysmal and transient character, the nystagmus dying away on its own;
• A reversal of the direction of the nystagmus on sitting up again ⁷.

The duration of the nystagmus further points to the mechanism: a duration of less than 1 minute suggests canalithiasis, a duration of more than 1 minute cupulolithiasis ⁷. This upbeating torsional nystagmus, stereotyped and fatigable, is what distinguishes peripheral BPPV from central causes ⁴.

A brief positional vertigo with an upbeating torsional nystagmus on the Dix-Hallpike is enough to make the diagnosis of posterior canal BPPV, with no imaging at all.

3. The supine roll test: the lateral canal

A Dix-Hallpike that does not reproduce the upbeating torsional nystagmus does not rule out BPPV: it may be lateral (horizontal) canal involvement, the second most frequent site. The AAO-HNS guideline is explicit: when the Dix-Hallpike shows a horizontal nystagmus or no nystagmus in a patient whose history is compatible, the clinician should perform a supine roll test to assess lateral semicircular canal BPPV ⁴.

Performing and interpreting it: With the patient lying on their back, the head is turned quickly to one side and then the other. Horizontal canal BPPV shows itself through a horizontal nystagmus ⁷, whose direction makes it possible to locate the affected side:

The diagnostic sequence is therefore tiered: the Dix-Hallpike first (posterior canal), then the supine roll test if the first is negative or atypical (lateral canal). This approach alone covers the great majority of BPPV, the posterior canal (33.1 %) remaining more frequent than the horizontal canal (14.6 %) ⁷.

4. The Bárány Society criteria: the consensus frame of reference

These manoeuvres are not mere examination tricks: they sit within a formalised diagnostic framework. The operational diagnostic criteria for BPPV were established by the Classification Committee for Vestibular Disorders of the Bárány Society ². They are the international consensus frame of reference, whose classification reflects current knowledge of the clinical aspects and the pathomechanisms of BPPV, and distinguishes established syndromes (including posterior canal BPPV) from emerging ones ².

In practice, making the diagnosis « with certainty » means assembling a coherent set: a history of brief, recurrent positional vertigo, and a positive positional manoeuvre reproducing the nystagmus characteristic of the canal concerned, of the expected type and direction. It is the concordance between the history and the provoked nystagmus, and not a further test, that makes the diagnosis.

5. The very limited place of imaging

Faced with vertigo, the reflex to image is frequent but, in typical BPPV, unjustified. The AAO-HNS recommendation is categorical: the clinician should not obtain radiographic imaging, nor order vestibular testing, in a patient who meets the diagnostic criteria for BPPV in the absence of additional signs or symptoms inconsistent with BPPV ⁴. Imaging is therefore legitimate only if atypical features, red flags, raise the fear of another cause, in particular a central one ⁴.

This principle of diagnostic economy has major practical reach. BPPV is frequent ⁵, benign and treatable, but massively under-treated ⁵. Piling up useless tests delays care when a correct positional diagnosis allows immediate treatment: the repositioning manoeuvre (Epley) more than quadruples the odds of complete resolution ¹, and the conversion of a positive Dix-Hallpike to negative after treatment ¹ also confirms the usefulness of the Dix-Hallpike as a verification test after the manoeuvre.

High-level evidence The « no imaging in typical BPPV » approach rests on a strong recommendation based on concordant data ⁴.

6. When to suspect a central cause: the red flags

The counterpart of a clinical diagnosis is vigilance: some presentations require a central cause to be ruled out, first among them stroke. The AAO-HNS guideline recommends differentiating BPPV from other causes of imbalance, dizziness and vertigo before any treatment ⁴. What should raise the alarm: a non-positional or continuous vertigo, an atypical nystagmus (non-fatigable, purely downbeating vertical, direction-changing), associated neurological signs, or a positional examination whose semiology fits no expected canal pattern ⁴.

In the particular context of an acute vestibular syndrome (acute, prolonged, spontaneous vertigo with nystagmus and unsteadiness), the bedside oculomotor examination performs better than early imaging. The HINTS examination in three parts (Head Impulse, Nystagmus, Test of Skew) has remarkable discriminating value: the presence of a normal horizontal head impulse test, of a direction-changing nystagmus on eccentric gaze, or of a skew deviation (vertical ocular misalignment) is 100 % sensitive and 96 % specific for stroke ⁸. These three signs are so many central red flags calling for imaging and an urgent opinion.

A crucial and counter-intuitive point: a normal early MRI is not enough to reassure. Diffusion-weighted MRI (MRI-DWI) performed early missed 12 % of strokes, all in the first 48 hours after symptom onset ⁸. In other words, a falsely negative diffusion MRI can wrongly reassure, which underlines the value of the clinical oculomotor examination. The message is twofold: in typical BPPV, imaging is useless; in a suspect acute vestibular syndrome, the HINTS examination takes precedence, and a normal early MRI does not rule out stroke.

In practice, diagnosing BPPV « with certainty » therefore needs neither a scan nor a complex vestibular work-up: it needs a rigorous history (brief, positional, recurrent vertigo), well-conducted positional manoeuvres (Dix-Hallpike then supine roll test), recognition of the characteristic canal nystagmus within the Bárány Society criteria, and exclusion of the central red flags which alone justify imaging.

🚩 How do you avoid missing a serious cause (red flags)?

Benign paroxysmal positional vertigo (BPPV) is the most frequent cause of vertigo ³, and its very ordinariness is precisely the trap: between 17 % and 42 % of patients consulting for vertigo eventually receive this diagnosis ⁴. Faced with a patient whose world is spinning, the reflex must never be « it is surely crystals » but « is this really a picture of BPPV, and nothing else? ». The great majority of positional vertigo is benign and is treated in the clinic in a few minutes with a repositioning manoeuvre ¹, but a minority is a neurological emergency, first among them a posterior fossa stroke. The American Academy of Otolaryngology guideline explicitly recommends differentiating BPPV from other causes of imbalance, dizziness and vertigo before any treatment ⁴. This section describes how to do that without piling up useless tests.

The bedrock of the reasoning: BPPV is positional, brief and stereotyped

BPPV is, by definition, a syndrome made of brief episodes of vertigo triggered by rapid changes of head position ¹ : turning over in bed, bending down, looking up at a shelf. Between the episodes, the patient has no continuous rotatory vertigo. Its diagnostic signature is not a symptom recounted but a provoked nystagmus, reproducible on positional examination.

For the posterior semicircular canal (by far the most affected, around 33 % of cases against 15 % for the horizontal canal and 4 % for the anterior ⁷), the Dix-Hallpike manoeuvre provokes vertigo with an upbeating torsional nystagmus, the upper pole of the eyes beating towards the affected ear ⁴⁷. Three features make this nystagmus reassuring, because it is typically peripheral :

• A latency then brevity : in canalithiasis (debris floating freely in the canal), the nystagmus lasts less than a minute; beyond a minute, cupulolithiasis is the more likely ⁷.
• A reversibility : the nystagmus often reverses on sitting up again ⁷.
• A torsional + vertical combination consistent with the anatomy of the canal stimulated.

When the Dix-Hallpike shows a horizontal nystagmus or none at all in a patient whose history remains compatible, the conclusion is not atypical BPPV: a supine roll test (supine roll test) is performed to look for lateral (horizontal) canal involvement first of all ⁴⁷. In other words, a nystagmus that « does not fit » has a peripheral vestibular explanation to rule out first, but if it fits no BPPV pattern at all, it becomes a warning signal (see below).

Continuous vertigo: think « acute vestibular syndrome » and do a HINTS

When the vertigo is not positional but continuous (an acute vestibular syndrome, prolonged rotatory vertigo, nausea, unsteadiness, intolerance of head movement), the question is no longer « which canal? » but « peripheral or central? ». A peripheral disorder (vestibular neuritis type) is benign; a brainstem or cerebellar stroke can present in exactly the same way, with no frank motor deficit. That is where the bedside oculomotor examination makes the difference.

The HINTS examination combines three manoeuvres: Head Impulse (head impulse), Nystagmus, Test of Skew (looking for a vertical ocular deviation). Its most important result is counter-intuitive: in an acute vestibular syndrome, the presence of at least one of the following three signs points to a stroke ⁸ :

1. A NORMAL horizontal head impulse test (no catch-up saccade): paradoxically worrying in this context, because neuritis « damages » the vestibulo-ocular reflex;
2. A nystagmus that changes direction on eccentric gaze (direction-changing);
3. A skew deviation (vertical ocular misalignment).

This combination is 100 % sensitive and 96 % specific for stroke in the acute vestibular syndrome ⁸. Better still: this clinical triad has proved more sensitive than early MRI.

A normal early diffusion MRI is not enough to rule out a stroke: it missed 12 % of strokes, all in the first 48 hours ⁸. The bedside oculomotor examination therefore keeps its full value.

This is decisive in practice: sending a patient away reassured because « the MRI is normal » is a mistake if the imaging was done early and the clinical examination suggested a central cause. Conversely, a « peripheral » HINTS consistent with the picture supports the benign diagnosis without routine recourse to imaging.

The red flags to know by heart

Some features must halt any repositioning manoeuvre and trigger an urgent neurological opinion. For the AAO-HNS guideline, they correspond to the « additional signs or symptoms inconsistent with BPPV » which alone justify imaging ⁴.

On the nystagmus in particular: posterior canal BPPV produces a torsional nystagmus combined with a vertical component, transient and reversible ⁷. Conversely, a purely vertical nystagmus, a nystagmus that does not fatigue on repetition of the manoeuvre, or a nystagmus that changes direction with the direction of gaze ⁸ correspond to no BPPV canal pattern: these are « inconsistent » signs that take the case out of the benign frame and justify imaging and a specialist opinion ⁴.

Vestibular neuritis, Ménière's disease: the other differentials

Two peripheral causes deserve to be distinguished from BPPV, without confusing them with a stroke either.

The vestibular neuritis presents as an acute vestibular syndrome: continuous, prolonged, non-positional vertigo. The reasoning to apply is therefore not that of the Dix-Hallpike but that of HINTS, whose whole purpose is to separate this benign peripheral disorder from a stroke that can mimic it feature for feature ⁸. The classic trap is to attribute to « neuritis » a continuous vertigo that is in fact central.

By contrast, Ménière's disease runs in attacks and is a differential in its own right for recurrent vertigo. It has particular reach in a patient already known to have BPPV: on multivariate analysis, Ménière's disease is the strongest independent risk factor for recurrence of BPPV (odds ratio 6.0), ahead of migraine (OR 2.5), hypertension (OR 1.5) and hyperlipidaemia (OR 1.4) ⁹. A BPPV that recurs unusually therefore invites a search for an associated comorbidity rather than indefinite repetition of the manoeuvre alone.

Do not over-investigate either: imaging has a narrow place

The corollary of vigilance is restraint: once the diagnosis of BPPV has been made on criteria, one must not multiply the investigations. The AAO-HNS guideline is a strong recommendation: in a patient who meets the diagnostic criteria for BPPV, the clinician should not obtain radiographic imaging or order vestibular testing in the absence of additional signs or symptoms inconsistent with BPPV ⁴. Imaging is justified only when a red flag is present.

This message matters all the more because BPPV remains massively under-treated : in the general population, its lifetime prevalence is 2.4 % and its 1-year prevalence 1.6 % ⁵, and it affects up to 86 % of those concerned to the point of causing a consultation, an interruption of activity or time off work, while only 8 % receive effective treatment ⁵. The problem is therefore not too much imaging but too little correct positional diagnosis. A rigorous clinical examination (Dix-Hallpike, supine roll test, HINTS if the vertigo is continuous), meets both requirements at once: spotting the minority of serious causes, and treating the great majority of BPPV in the clinic.

🎯 Which manoeuvres effectively treat BPPV?

Benign paroxysmal positional vertigo (BPPV) is a syndrome characterised by brief episodes of vertigo triggered by rapid changes of head position ¹, and it is the most frequent cause of vertigo in the world ³. Its management follows directly from its pathophysiology: otolithic debris, detached from the neuroepithelium of the utricular macula through a degenerative process, migrates and moves freely in a semicircular canal (canalithiasis) or attaches to the cupula (cupulolithiasis) ⁶. The reference treatment is therefore neither pharmacological nor surgical: it consists of repositioning manoeuvres which, through a precise sequence of head rotations, bring this debris out of the affected canal and back into the utricle, where it stops generating an aberrant signal. It is a mechanical treatment, whose effectiveness is now supported by randomised trials and meta-analyses.

This effectiveness contrasts sharply with reality on the ground. In the general population, BPPV has a lifetime prevalence of 2.4 %, a 1-year prevalence of 1.6 % and a 1-year incidence of 0.6 % ⁵. It weighs heavily on daily life (in 86 % of affected people it led to a medical consultation, an interruption of daily activities or time off work), but only 8 % of people received effective treatment ⁵. In other words, an eminently treatable condition remains massively under-treated, while the corrective procedure is simple, quick and safe.

The Epley manoeuvre: the reference treatment for the posterior canal

The posterior semicircular canal is the most frequently affected (posterior canalithiasis 33.1 % of cases in a cohort of 481 patients diagnosed according to the Bárány Society criteria), far ahead of the horizontal canal (14.6 %) and the anterior canal, which is rare (4.0 %) ⁷. It is therefore for this form, diagnosed with the Dix-Hallpike manoeuvre which provokes vertigo with an upbeating torsional nystagmus ⁴, that treatment is best codified.

The Epley manoeuvre, or canalith repositioning procedure (canalith repositioning procedure), was described in its original form by John Epley, who reported resolution of the nystagmus and of the positional vertigo in 100 % of his 30 patients ; 30 % of them had one or more recurrences, but these responded well to further treatment with the same procedure ¹⁰. These initial results have since been widely confirmed. The reference Cochrane review concludes that the Epley is a safe and effective treatment for posterior canal BPPV: complete resolution of the vertigo occurs significantly more often in the Epley group than in the sham manoeuvre or control group, with an odds ratio of 4.42 (95 % CI 2.62–7.44; 5 studies, 273 participants), the proportion of patients in resolution rising from 21 % to 56 % ¹.

A second, objective indicator confirms this effect: the conversion of a positive Dix-Hallpike test to negative clearly favours the Epley group (OR 9.62; 95 % CI 6.0–15.42; 8 studies, 507 participants) ¹. The Dix-Hallpike therefore plays a double role, diagnostic and then verifying after the manoeuvre: its becoming negative marks the success of the repositioning.

Complete resolution of the vertigo rises from 21 % to 56 % with the Epley versus a sham manoeuvre, but 36 % of patients will have a recurrence ¹.

The Semont manoeuvre: a validated alternative for the posterior canal

When the patient's position or cervical mobility makes the Epley difficult, the Semont manoeuvre (or liberatory manoeuvre) offers an alternative of equivalent value for the posterior canal. Its effectiveness rests on a class I double-blind randomised trial: at 4 days, the Semont manoeuvre produced complete resolution of symptoms in 84.62 % of the patients treated (55/65), against 14.29 % (9/63) in the control group ¹¹. The Cochrane review moreover places the results of the Epley as comparable to those of the Semont and Gans manoeuvres, and superior to the Brandt-Daroff exercises ¹. The choice between Epley and Semont is therefore more a matter of practical feasibility and of the practitioner's habit than of a difference in effectiveness.

The lateral (horizontal) canal: the Gufoni manoeuvre and rolling

The horizontal canal is the second most often responsible. Its involvement is not picked up by the Dix-Hallpike: faced with a horizontal or absent nystagmus on the Dix-Hallpike in a patient with a compatible history, the clinician should perform a supine roll test (supine roll test), which induces a geotropic (beating towards the ground) or apogeotropic horizontal nystagmus pointing to both the diagnosis and the affected side ⁴⁷.

Treatment calls on manoeuvres specific to the horizontal canal: first among them the Gufoni manoeuvre and the rolling manoeuvres (called « barbecue » or BBQ roll), which roll the head and the body in successive stages to clear the otoliths from the lateral canal. The effectiveness of the Gufoni manoeuvre is established by a class I double-blind randomised trial: it produced resolution of the vertigo in 75.7 % of patients at 1 hour and 83.8 % at 24 hours, against around 10 % with the sham manoeuvre (P < 0.0001) ¹².

Success rate, number of sessions and recurrence

A major feature of these manoeuvres is their high yield from the first application or two, as the table below summarises.

Most patients are relieved in one to a few sessions ; the manoeuvre is repeated in the same consultation or a few days apart until the positional verification test becomes negative. On the other hand, curing the episode does not prevent the next ones: BPPV is a recurring condition. In the general population, 56 % of affected people have had recurrent episodes, with a recurrence rate of around 15 % a year ⁵, and the Cochrane review notes a recurrence rate after treatment of 36 % ¹.

Some factors increase this risk. The 1-year recurrence rate rises in absolute terms with age (22.79 % in the 18–45 group, 23.92 % in the 45–60 group, 28.89 % beyond 60), but on multivariate analysis age is not an independent risk factor; female sex, Ménière's disease (OR 6.009), hypertension (OR 1.510), migraine (OR 2.534) and hyperlipidaemia (OR 1.419) are ⁹. On the preventive side, supplementation with vitamin D (400 IU) and calcium (500 mg twice a day for 1 year) in patients whose serum vitamin D is below 20 ng/mL reduces recurrence (0.83 vs 1.10 recurrences per person-year; incidence rate ratio 0.76; 95 % CI 0.66–0.87; p < 0.001): a class III level of evidence ¹³.

What the guidelines say

The clinical practice guideline of the American Academy of Otolaryngology–Head and Neck Surgery (AAO-HNS) frames management precisely. Recall that BPPV accounts for a major share of vertigo: between 17 % and 42 % of patients consulting for vertigo eventually receive the diagnosis ⁴. Its main therapeutic positions are as follows:

• Treat by repositioning. For posterior canal BPPV, the guideline makes a strong recommendation in favour of treatment with a canalith repositioning manoeuvre (Epley type): the clinician should treat the patient, or refer them to a practitioner able to do so ⁴.
• No postural restrictions. The guideline makes a strong recommendation against imposing postural restrictions after the manoeuvre: the classic instructions to « not bend over / sleep sitting up » are not justified ⁴.
• No routine imaging or vestibular testing. In a patient who meets the diagnostic criteria for BPPV, in the absence of additional inconsistent signs or symptoms, neither radiographic imaging nor vestibular testing should be carried out ⁴.

The all but non-existent place of drugs

The most counter-intuitive point for many patients, and sometimes for prescribers, is that BPPV is not treated with drugs. The AAO-HNS guideline advises against routine treatment of BPPV with vestibular suppressants, that is to say antihistamines and/or benzodiazepines ⁴. These drugs do not act on the mechanical cause, the displaced otoliths, and can on the contrary delay the curative procedure, increase drowsiness and the risk of falling, and mask the picture. The logical corollary of the canalithiasis pathophysiology is that only repositioning the debris resolves the vertigo durably ; pharmacotherapy has, at best, a very limited and occasional supporting place.

Finally, the only real limit of this « all-manoeuvre » strategy must be kept in mind: it assumes a correct positional diagnosis. The Brandt-Daroff exercises, long prescribed as self-rehabilitation, neither significantly reduce symptoms nor promote recovery from posterior canal BPPV compared with the Epley and Semont manoeuvres, and are only a secondary option with a low level of evidence ¹⁴. And faced with an atypical picture (a normal horizontal head impulse test, a direction-changing nystagmus on eccentric gaze, a skew deviation), it is a central cause that must be considered: these three signs of the HINTS examination are 100 % sensitive and 96 % specific for stroke, better than an early diffusion MRI (falsely negative in 12 % of cases in the first 48 hours) ⁸. Repositioning is the treatment of the right BPPV, correctly identified.

🔄 Recurrence and prevention: how do you make the result last?

Repositioning the otoliths settles the acute episode, but does not « cure » the background that allowed them to come loose. BPPV is, by nature, a recurring condition : the otoconial debris responsible comes from detachment of the neuroepithelium of the utricular macula through a degenerative process ⁶, a mechanism that does not disappear with a successful manoeuvre. In practice, a well-conducted Epley manoeuvre raises complete resolution of the vertigo from 21 % to 56 % versus a sham manoeuvre ¹, but the patient remains exposed to new episodes. Making the result last therefore consists less in « treating better » than in informing, screening for modifiable recurrence factors and organising realistic follow-up.

A real risk of recurrence: what do the figures say?

Recurrence is the rule rather than the exception. In the general population, 56 % of affected people had had recurrent episodes, with a recurrence rate of around 15 % a year ⁵ ; only 44 % reported a single episode. This figure is consistent from one study to another, the authors noting values close to 50 to 55 % in other cohorts.

Recurrence also exists after treatment with a manoeuvre. The Cochrane review reports a recurrence rate of 36 % after the Epley manoeuvre ¹ High-level evidence. From the original description of the canalith repositioning procedure, Epley himself observed that 30 % of the patients treated had one or more recurrences, but that these responded well to further treatment ¹⁰. This is a central message to pass on to the patient: a recurrence is neither a failure of the initial manoeuvre nor a sign of seriousness; it is an expected event, which is re-treated just as effectively.

A successful manoeuvre resolves the episode; it does not lock down the future. The good news: a recurrence is re-treated as well as the first episode.

Which factors increase the risk of recurrence?

The apparent weight of a factor in absolute terms must be distinguished from its status as an independent risk factor on multivariate analysis. Age is the most useful illustration. Across the population, BPPV is strongly age-related: the mean age of onset is 49.4 years, and in people over 60 the 1-year prevalence is nearly seven times that of the 18–39 group ⁵. After treatment, the 1-year recurrence rate also rises in absolute terms with age (22.79 % in the 18–45 group, 23.92 % in the 45–60 group, 28.89 % beyond 60). But on multivariate analysis, age is not an independent risk factor for recurrence: « aging does not increase the recurrence risk » ⁹. In other words, it is the comorbidities that accumulate with age, more than age itself, that carry the excess risk.

In that same cohort, the independent risk factors for recurrence were female sex, Ménière's disease, hypertension, migraine and hyperlipidaemia ⁹. The female over-representation is already there in the basic epidemiology: a lifetime prevalence of 3.2 % in women against 1.6 % in men ⁵.

Risk factors for recurrence at 1 year after repositioning ⁹.

Vitamin D and calcium: the only validated background lever

This is the best-documented preventive avenue to date. In patients with a low serum vitamin D (< 20 ng/mL), supplementation with vitamin D (400 IU) and calcium (500 mg twice a day for 1 year) reduces BPPV recurrence: an annual recurrence rate of 0.83 versus 1.10 recurrences per person-year, an incidence rate ratio of 0.76 ¹³ Moderate evidence. The authors themselves call this level of evidence class III.

The pathophysiological coherence is pleasing: the otoconia are crystals of calcium carbonate, and a degraded calcium-phosphate status could weaken their anchorage. The practical approach that follows is simple and without risk: in a patient with recurrences, it is legitimate to offer a vitamin D level and, if there is a deficiency, to arrange supplementation. Beware the reach of this: the demonstrated benefit concerns the deficient population: this finding does not justify routine supplementation of every patient with BPPV.

Home self-manoeuvres and the Brandt-Daroff exercises: what place?

Patients ask frequently: « what can I do at home? ». The answer must stay honest about the levels of evidence.

The Brandt-Daroff exercises are the historical self-exercise. Their place today is that of a secondary option. The Cochrane review concludes that the results of the Epley are superior to those of the Brandt-Daroff exercises ¹, and a more recent review confirms that these exercises neither significantly reduce symptoms nor promote recovery from posterior canal BPPV compared with other interventions such as the Epley and Semont manoeuvres ¹⁴ Low quality evidence. They must therefore not replace a well-conducted repositioning manoeuvre as a first line; they can be a complement for habituation at home, in the knowledge that their own effectiveness is modest.

On the matter of everyday advice, two strong recommendations of the 2017 AAO-HNS guideline relieve the patient of useless constraints:

• A strong recommendation against imposing postural restrictions after the repositioning manoeuvre ⁴ : the patient does not have to sleep sitting up or refrain from bending over.
• A strong recommendation against the routine use of vestibular suppressants, antihistamines and/or benzodiazepines, to treat BPPV ⁴ : these drugs mask the symptoms without correcting the otoconial mechanics and expose older people in particular to the risk of falling.

A well-learnt repositioning self-manoeuvre can be useful in a clearly recurring patient, provided that a professional has first confirmed the canal and the side affected with the positional tests (Dix-Hallpike for the posterior canal, supine roll test for the horizontal canal). It never replaces the initial positional diagnosis.

Organising follow-up

Follow-up answers a twofold epidemiological finding. First, BPPV has a real impact: in 86 % of affected people it led to a consultation, an interruption of daily activities or time off work ⁵. Second, it remains massively under-treated: only 8 % of affected people had received effective treatment ⁵. Follow-up is therefore first of all an opportunity to guarantee that effective treatment has actually been delivered, and to verify it objectively.

Verifying the cure is not subjective: the conversion of a positive Dix-Hallpike test to negative clearly favours the group treated with the Epley ¹. Repeating the positional manoeuvre at the end of the session, or at the next one, objectifies success better than the patient's impression alone.

The follow-up plan can thus be structured around four steps: (1) check that the positional test has become negative after the manoeuvre; (2) educate the patient about the recurring and re-treatable nature of the condition, to defuse the anxiety of a relapse; (3) look for and arrange management of the modifiable factors (vitamin D deficiency, hypertension, hyperlipidaemia, migraine), with the GP; (4) set a clear criterion for coming back. On this last point, a safety reminder is needed: a typical positional vertigo is re-treated calmly, but central signs (a direction-changing nystagmus on eccentric gaze, a normal horizontal head impulse test, a skew deviation) are 100 % sensitive and 96 % specific for stroke in the acute vestibular syndrome ⁸ and call for urgent assessment. Any atypical presentation must lead to reconsidering the diagnosis rather than blindly repeating the manoeuvre.

📋 What do concrete clinical cases teach us?

The large epidemiological series and the controlled trials draw a statistical picture of benign paroxysmal positional vertigo (BPPV). But it is often at the bedside of a particular patient that the diagnostic and therapeutic logic makes full sense. The two cases that follow are published and verifiable, each with its PubMed identifier: a lateral canal BPPV in a young child¹⁵ and a recurring BPPV in a footballer after a head injury¹⁶. No patient has been invented for the demonstration: a case built to measure proves exactly what it was made to prove. The commentary that accompanies them stays anchored to the data presented in this article, in order to show how the evidence-based approach unfolds in practice, from the first symptom to the prevention of recurrence.

Published case no. 1: lateral canal BPPV in a young child, resolved in two manoeuvres

Presentation. Chuang and colleagues report a young girl referred to an ENT clinic for episodes of vertigo occurring when she rolled over lying down. She reported no other audio-vestibular symptom¹⁵.

Examination. The bedside Dix-Hallpike manoeuvre showed a geotropic rotatory nystagmus, marking involvement of the lateral canal¹⁵. Triggering on rolling rather than on lying down or getting up is consistent with that canal, and it is this detail of the history that guides the choice of manoeuvre.

What was done in addition, and why. Because of her young age, her limited communication and the fear of a more serious underlying condition, the authors carried out a complete neurological examination, an MRI and pure-tone audiometry¹⁵. That is the main lesson of this case: a typical positional picture does not excuse the clinician from looking for something else when the background is unusual.

Course. After two sessions of the Epley manoeuvre, the patient was asymptomatic. At three months of follow-up, she reported no recurrence¹⁵.

Published case no. 2: recurring BPPV in a footballer, eight months after a head injury

Presentation. Warming and colleagues report a man of 19 years with recurrent episodes of vertigo while playing football. Eight months before referral, he had been involved in a road traffic accident with a mild head injury. A diagnosis of BPPV had already been made several times¹⁶.

What the case illuminates. The aetiology of BPPV remains unknown in around half of cases, which are then called primary; secondary BPPV is the term used when a predisposing factor is identified¹⁶. Here, the head injury provides that factor, and the authors discuss the plausibility of a contribution from playing football itself¹⁶.

The practical reach. A BPPV that recurs in a young, sporting person is not a failure of the manoeuvre: it is an invitation to look for the secondary cause, head injury included, and to ask about the activity. The contrast with the previous case is instructive: the same diagnosis, once resolved in two sessions, once recurring because the cause persists.

What these cases bring out: choosing the right manoeuvre

The lesson running through these two published stories is that the therapeutic procedure depends on the canal affected, itself identified by the appropriate positional test. The table below brings together the correspondences from the confirmed data.

Markers for the posterior canal manoeuvres. The results of the Epley manoeuvre are comparable to those of the Semont and Gans manoeuvres, and superior to the Brandt-Daroff exercises ¹. The effectiveness of the Semont is likewise supported by a class I double-blind randomised trial ¹¹. Conversely, the Brandt-Daroff exercises neither significantly reduce symptoms nor promote recovery from posterior canal BPPV compared with Epley and Semont; they remain a secondary option with a low level of evidence low quality evidence ¹⁴.

Historical perspective and diagnostic caution

The robustness of these manoeuvres is not recent. In the original description of the canalith repositioning procedure, Epley reported resolution of the nystagmus and of the positional vertigo in 100 % of his 30 patients treated ; among them, 30 % had one or more recurrences, but these responded well to further treatment ¹⁰: a lesson that transfers directly to case no. 2, where the recurrence is not a failure but an expected feature of a recurring condition.

An essential reservation. These two cases describe typical positional and paroxysmal vertigo. They never excuse the clinician from ruling out a central cause when the picture does not fit: the AAO-HNS guideline requires precisely that BPPV be differentiated from other causes of imbalance, dizziness and vertigo ⁴, and imaging becomes justified again in the presence of additional signs inconsistent with BPPV ⁴. In the distinct context of an acute vestibular syndrome (continuous vertigo, and not brief positional attacks), the bedside HINTS examination (a normal horizontal head impulse test, a direction-changing nystagmus on eccentric gaze, or a skew deviation) is 100 % sensitive and 96 % specific for stroke, and proves more sensitive than early diffusion MRI, which can be falsely negative in 12 % of cases in the first 48 hours ⁸. These signs are central red flags calling for imaging: a boundary that clinical reasoning must keep in mind, even when BPPV remains, statistically, the most likely explanation.

🧭 How is this applied in practice?

BPPV is at once the most frequent cause of vertigo ³ and one of the easiest to treat, and yet it remains massively under-treated: in the reference German population study, only 8 % of affected people had received effective treatment while 86 % had consulted, interrupted their activities or taken time off work ⁵. What is at stake in practice is therefore not piling up tests, but applying a rigorous positional approach: suspect, test the right canal, treat with the appropriate manoeuvre, verify. This section offers a working decision algorithm, the key messages to hold on to in the clinic, the mistakes that make management fail, and the situations that call for referral.

Step 1: Suspect BPPV from the clinical history

BPPV is a syndrome characterised by brief episodes of vertigo triggered by rapid changes of head position ¹ : turning over in bed, lying down, getting up, tipping the head back. This brief and positional character is the first clinical filter. The pre-test probability is high: between 17 % and 42 % of patients consulting for vertigo eventually receive a diagnosis of BPPV ⁴.

Some features reinforce the suspicion and guide vigilance:

• Background. Mean age of onset 49.4 years, prevalence rising sharply with age, in people over 60, the 1-year prevalence is nearly seven times that of the 18-39 group ⁵. More frequent in women (lifetime prevalence 3.2 % vs 1.6 % in men).
• The recurring character. 56 % of affected people have recurrent episodes, with a recurrence rate of around 15 % a year ⁵ : a history of « positional vertigo » that comes back is highly suggestive.

On the pathophysiological side, it helps to have the mechanism in mind in order to understand the logic of the manoeuvres: BPPV results from otolithic debris detached from the neuroepithelium of the utricular macula by a degenerative process ⁶, either free in the canal (canalithiasis), or attached to the cupula (cupulolithiasis) ⁶. The therapeutic manoeuvre aims to bring this debris out of the canal.

Step 2: Confirm with the Dix-Hallpike, then identify the canal

The diagnosis is clinical and positional, not radiological. Posterior canal BPPV, the most frequent, is diagnosed with the Dix-Hallpike manoeuvre: the patient is brought from sitting to lying, head turned 45° to one side and neck extended 20°, the ear being tested facing down ⁴. The diagnosis is made when vertigo with an upbeating torsional nystagmus is provoked ⁴.

Reading the nystagmus closely points to the side and the mechanism ⁷ :

• An upbeating vertical nystagmus, with or without a torsional component; the upper pole of the eyes beats towards the affected ear.
• The nystagmus often reverses on sitting up again.
• Duration < 1 minute → canalithiasis; duration > 1 minute → cupulolithiasis.

If the Dix-Hallpike shows a horizontal or absent nystagmus in a patient whose history is compatible, a supine roll test must be performed (or the patient referred to a clinician who can perform it) to assess lateral/horizontal canal BPPV ⁴. Interpreting the roll test gives the side ⁷ : a horizontal geotropic nystagmus (beating towards the ground) → affected side = the one with the most intense nystagmus; an apogeotropic nystagmus → affected side = the one with the weakest nystagmus.

Expected distribution of the canals, useful for ordering the tests ⁷ :

The frame of reference is that of the operational diagnostic criteria of the Bárány Society, the international consensus reference structuring the diagnosis and distinguishing established syndromes from emerging ones ².

Step 3: Do not multiply the further tests

A point often poorly applied: in a patient who meets the diagnostic criteria for BPPV, the clinician should not obtain radiographic imaging, or order vestibular testing, in the absence of additional signs or symptoms inconsistent with BPPV ⁴. Imaging is justified only if atypical red flags are present ⁴. This diagnostic restraint is consistent with the under-treatment observed: the problem is not a lack of tests, but a lack of well-conducted positional manoeuvres ⁵.

Step 4: Treat with the manoeuvre matched to the canal

For the posterior canal, the AAO-HNS guideline strongly recommends treating (or referring to a clinician who can treat) with a canalith repositioning manoeuvre, Epley type ⁴. The level of evidence is solid: high-level evidence

• The Epley manoeuvre more than quadruples the odds of complete resolution of symptoms versus sham/control: OR 4.42 (95 % CI 2.62–7.44), the proportion of patients in resolution rising from 21 % to 56 % ¹.
• It clearly converts the Dix-Hallpike from positive to negative: OR 9.62 (95 % CI 6.0–15.42), which validates the use of the Dix-Hallpike as a verification test after the manoeuvre ¹.
• In the original description, Epley reported resolution of the nystagmus and of the positional vertigo in 100 % of the 30 patients, of whom 30 % had one or more recurrences that responded well to further treatment ¹⁰.

The effective alternatives for the posterior canal, depending on the patient and the operator:

• Semont: a double-blind randomised trial: complete resolution at 4 days in 84.62 % (55/65) of the treated group vs 14.29 % (9/63) of the control group ¹¹. Results comparable to the Epley ¹.
• Gans: results comparable to the Epley ¹.

For the horizontal/lateral canal, the Gufoni manoeuvre has proved its effectiveness: a double-blind randomised trial: resolution of the vertigo in 75.7 % of patients at 1 h and 83.8 % at 24 h, against around 10 % with the sham manoeuvre (P < 0.0001) ¹².

Step 5: Check the effect and explain what comes next

The verification test is the Dix-Hallpike: its conversion to negative marks the success of the manoeuvre ¹. Two instructions after the manoeuvre, from strong AAO-HNS recommendations:

• Do not impose postural restrictions after the repositioning manoeuvre (a strong recommendation AGAINST) ⁴.
• Do not treat routinely with vestibular suppressants (antihistamines and/or benzodiazepines) ⁴.

The patient must be warned of the risk of recurrence : a recurrence rate of around 15 % a year ⁵ and a high rate after treatment ¹. Age raises the recurrence rate in absolute terms (22.79 % in the 18–45 group, 28.89 % in those > 60) but is not an independent risk factor on multivariate analysis; the independent factors are female sex, Ménière's disease (OR 6.009), migraine (OR 2.534), hypertension (OR 1.510) and hyperlipidaemia (OR 1.419) ⁹. In patients whose serum vitamin D is < 20 ng/mL, supplementation with vitamin D 400 IU + calcium 500 mg twice a day for 1 year reduces recurrence (0.83 vs 1.10 recurrences per person-year; IRR 0.76; 95 % CI 0.66–0.87; p < 0.001) ¹³. moderate evidence

Key messages in the clinic

« A brief vertigo, triggered by a change of head position, in a woman in her fifties who has had this before: we test, we treat, we check: we do not image. »

• « It is a mechanical problem of the inner ear, not your brain. » Debris detached from the utricle is floating in a canal ⁶ ; the manoeuvre repositions it.
• « It is common and very treatable. » The most frequent cause of vertigo ³, but only 8 % of affected people are effectively treated ⁵.
• « The manoeuvre works quickly and well. » Resolution rising from 21 % to 56 % vs control for the Epley ¹ ; 84.6 % at 4 days for the Semont ¹¹.
• « No restrictions, no routine drugs. » Strong AAO-HNS recommendations ⁴.
• « It can come back, and it is re-treated. » Recurrence ≈ 15 %/year ⁵, 36 % after treatment ¹, responding well to further treatment ¹⁰.

Frequent mistakes to avoid

• Ordering imaging or vestibular testing « to be sure » when the criteria for BPPV are met with no atypical sign ⁴.
• Treating without having identified the canal. A Dix-Hallpike showing a horizontal or absent nystagmus calls for a supine roll test, not an Epley straight away ⁴.
• Relying first on the Brandt-Daroff exercises. They neither significantly reduce symptoms nor promote recovery from posterior BPPV compared with Epley and Semont, and remain a secondary option with a low level of evidence ¹⁴¹.
• Imposing strict postural instructions after the manoeuvre: a strong recommendation against ⁴.
• Routinely prescribing vestibular suppressants (antihistamines, benzodiazepines) ⁴.
• Not checking the result. Without repeating the Dix-Hallpike, there is no way of knowing whether the manoeuvre has converted the test to negative ¹.
• Neglecting to explain recurrence and its risk factors (Ménière's, migraine, hypertension, hyperlipidaemia, female sex) ⁹.

When to refer on (ENT / neurology)

The 2017 AAO-HNS guideline requires that the clinician differentiate (or refer to a clinician able to differentiate) BPPV from other causes of imbalance, dizziness and vertigo ⁴. Refer on in the following situations:

• An atypical picture or signs inconsistent with BPPV : this is precisely where imaging becomes justified ⁴.
• Inability to carry out the required test or manoeuvre : the guideline explicitly allows referral to a clinician who can perform the supine roll test or the repositioning manoeuvre ⁴.
• Suspicion of a central cause: stroke red flags. In an acute vestibular syndrome, the bedside HINTS examination (Head Impulse, Nystagmus, Test of Skew) is more sensitive than early MRI for identifying a stroke: a normal horizontal head impulse, a nystagmus that changes direction on eccentric gaze or a skew deviation are 100 % sensitive and 96 % specific for stroke ⁸. These signs call for imaging and urgent neurological referral. Of note: early diffusion MRI missed 12 % of strokes, all within 48 h: a normal early MRI is not enough to rule out a central cause ⁸.
• Failure or repeated recurrences justifying a specialist work-up, particularly in the presence of risk factors such as Ménière's disease (OR 6.009) ⁹.