Benign paroxysmal positional vertigo

INTRODUCTION — 

Benign paroxysmal positional vertigo (BPPV) is a common form of vertigo, accounting for nearly one-half of patients with peripheral vestibular dysfunction. It is most commonly attributed to calcium debris within the posterior semicircular canal, known as canalithiasis. While symptoms can be troublesome, the disorder usually responds to treatment with particle-repositioning maneuvers, an office-based procedure and one that patients can be taught to perform at home.

BPPV will be reviewed here. Other causes of vertigo and an overview of the approach to the patient with vertigo are discussed separately. (See "Causes of vertigo" and "Evaluation of the patient with vertigo".)

EPIDEMIOLOGY — 

In a population-based survey, the lifetime prevalence of BPPV was 2.4 percent [1]. The one-year prevalence of BPPV increased with age and was seven times higher in those older than 60 years, compared with those aged 18 to 39 years. Others have also noted a higher incidence in older patients [2]. BPPV was more common in women than men in all age groups, with a reported ratio of 2:1 to 3:1 [1,3]. Other risk factors, which may be pathogenic, are discussed in the next section.

PATHOGENESIS

●Pathophysiology – BPPV is commonly attributed to canalithiasis (ie, calcium debris within the semicircular canal) [4]. This debris likely represents loose otoconia (calcium carbonate crystals) originating from the utricular sac. In one study, these were identified intraoperatively in 8 of 26 patients undergoing surgery for refractory BPPV and in none of 73 patients undergoing labyrinthine surgery for other indications [5].

The semicircular canals normally detect angular head accelerations. Heavy debris in the canal causes inappropriate movement of the endolymph with linear accelerations, such as gravity, and causes the erroneous sensation of spinning when the head shifts with respect to gravity. (See "Overview of nystagmus", section on 'Basic clinical vestibular physiology'.)

The posterior semicircular canal is the most common site of canalithiasis. Less common are diseases of the anterior (superior) and horizontal semicircular canals; these also have slightly different clinical manifestations. (See 'Anterior canal BPPV' below and 'Horizontal canal BPPV' below.)

●Potential mechanisms – A higher frequency of BPPV has been reported in patients with giant cell arteritis (GCA) than in matched controls, suggesting that some cases of BPPV could be caused by ischemic complications of GCA [6]. A population-based survey study found that BPPV was independently associated with age, migraine, hypertension, hyperlipidemia, and stroke, also suggesting a potential vascular mechanism for at least some cases of BPPV [1].

Another theory proposes that bone loss might be the source of the calcium carbonate particles that comprise the canalithiasis. In one study of 209 patients with idiopathic BPPV, bone density was lower and the prevalences of osteopenia and osteoporosis were higher in patients compared with controls [7]. A large, prospective, population-based study found that osteoporosis but not osteopenia was associated with an odds ratio of 1.51 for BPPV, but only in females over age 60 years [8]. Osteoporosis and vitamin D deficiency may increase the likelihood of recurrence of BPPV as well, but this is uncertain [9-12]. (See 'Prognosis' below.)

●Causes of posterior canal BPPV – Posterior canal BPPV is idiopathic in 35 percent of cases. Prior head trauma, which can be relatively minor, or whiplash injuries are present in approximately 15 to 30 percent [13-16]. (See "Sequelae of mild traumatic brain injury", section on 'Benign paroxysmal positional vertigo'.)

In the remainder of patients, BPPV is a residual effect of a variety of vestibular pathologies, most commonly Meniere disease (30 percent), where BPPV may be found in approximately 15 percent of patients [17], but also of vestibular neuronitis, ear surgery, herpes zoster oticus, and inner ear ischemia/sudden sensorineural hearing loss [13,18,19]. Patients with deletions of the STRC gene that codes for stereocilin protein can have hearing loss with early-onset BPPV [20].

BPPV has also been reported as an unusual complication of surgery to elevate the floor of the maxillary sinus, possibly through transmission of vibratory or percussive forces [21]. On rare occasions, decompression sickness may cause a similar positional vertigo, possibly due to nitrogen bubbles in the semicircular canals [22].

●Causes of horizontal canal BPPV – Most cases of horizontal canal BPPV (HC-BPPV) are idiopathic or due to minor head trauma [23]. This problem is occasionally a complication of the maneuvers used to treat posterior canal BPPV. (See 'Office-based treatment' below.)

CLINICAL MANIFESTATIONS

Symptoms — Patients with BPPV present with recurrent episodes of vertigo that last one minute or less. Episodes are provoked by specific types of head movements, such as looking up while standing or sitting, lying down or getting up from bed, and rolling over in bed. The vertigo may be associated with nausea and vomiting but is not sustained.

Hearing loss or symptoms are typically absent [24]. Patients with BPPV usually have no other neurologic complaints. Some patients have evidence of prior inner ear damage. Approximately half of patients complain of imbalance between attacks, even after successful treatment [1], and some clinicians have noted subtle abnormalities of gait in between attacks [25,26].

Episodes recur periodically for weeks to months without therapy [27]. In one study, the median duration of BPPV recurrences was two weeks; a subset of these patients was treated [1].

Some case series report that some patients with unsteadiness, imbalance, and/or falls (but not vertigo) test positive for BPPV [28,29]. However, it remains unproven that these patients actually have BPPV. Studies in healthy volunteers have shown that some asymptomatic patients can have nystagmus with provoking maneuvers tests, although they lack other features that define BPPV [30].

Response to provoking maneuvers — Observing nystagmus during a provoking maneuver solidifies the diagnosis of BPPV in patients with a typical history and identifies the side and the specific canal affected. These features help direct appropriate treatment.

Caution is recommended in using these tests in patients without typical symptoms, as false positives can occur [30].

Posterior canal BPPV — The Dix-Hallpike maneuver (figure 1) will usually provoke paroxysmal vertigo and nystagmus when the affected ear is turned downward during the maneuver [31]. In one study, the affected side could be predicted in 80 percent of patients by determining from the history the provoking position at the onset of vertigo [32]. That is, if the patient's onset of vertigo coincides with head-turning to the right when lying down, the right side was most likely to be the side affected as assessed by the Dix-Hallpike maneuver.

With the patient sitting, the neck is extended and turned to one side. The patient is then placed supine rapidly, so that the head hangs over the edge of the bed. The patient is kept in this position until 30 seconds has passed if no nystagmus occurs. The patient is then returned to upright, observed for another 30 seconds for nystagmus, and the maneuver is repeated with the head turned to the other side. A video demonstrating this maneuver can be viewed online.

Diagnostic criteria employing the Dix-Hallpike maneuver have been proposed for posterior canal BPPV (figure 1) [33]:

●Nystagmus and vertigo usually appear with a latency of a few seconds and last less than 30 seconds

●Nystagmus has a typical trajectory, beating upward and torsionally, with the upper poles of the eyes beating toward the ground

●After nystagmus stops and the patient sits up, the nystagmus will recur but in the opposite direction

●The patient should then have the maneuver repeated to the same side; with each repetition, the intensity and duration of nystagmus will diminish

The latency, transience, and fatigability, coupled with the typical mixed upbeat/torsional direction, establish this as a peripheral vertigo. Variation in these features may occur, but if present, one should consider a central lesion (table 1). The reported sensitivity of the Dix-Hallpike maneuver in patients with BPPV ranges from 50 to 88 percent [34]; however, these studies are older and difficult to verify in the absence of a gold standard.

Sometimes patients have typical symptoms of posterior canal BPPV but no nystagmus visualized during the Dix-Hallpike maneuver. The use of Frenzel glasses or other specialized techniques may improve the sensitivity of this test, but they are not routinely used. If symptoms are otherwise typical of posterior canal BPPV, the patient may have so-called "subjective" BPPV and still respond to treatment. (See 'Diagnosis' below.)

Positional nystagmus can be elicited in some healthy individuals who do not have BPPV. Differentiating features include low velocity, a purely vertical (rather than mixed vertical and torsional) trajectory, and no associated vertigo [35,36].

Horizontal canal BPPV — Horizontal canal BPPV (HC-BPPV) is provoked by turning the head while lying down, sometimes by head turns while upright, but not by getting in or out of bed or by extending the neck [23]. Some suggest that it is more common than previously thought, perhaps accounting for 45 percent of BPPV cases [37].

The nystagmus is elicited by a lateral head turn in the supine position (sometimes called the head-roll, log-roll, or supine-head-yaw test). This may induce geotropic or apogeotropic nystagmus:

●In geotropic HC-BPPV, vertigo along with horizontal nystagmus beating toward the floor begins after one to eight seconds of turning the affected ear down; it lasts approximately one minute, and after a few seconds of inactivity may be followed by a reversal of the nystagmus, which also lasts up to one minute [23,38]. A milder nystagmus is seen with the normal ear down, again beating toward the ground. This distinction between the normal versus the affected ear is important for treatment.

●By contrast, in apogeotropic HC-BPPV, the induced nystagmus beats toward the uppermost ear [39].

Apogeotropic HC-BPPV is thought to be associated with otolithic debris in the anterior arm of the horizontal canal or attached to the cupula, while geotropic HC-BPPV occurs with free-floating debris in the HC. Approximately 25 percent of patients with geotropic HC-BPPV also have posterior canalithiasis [23].

Another method of diagnosing HC-BPPV is the "bow and lean" test [40]. The seated patient first bends his or her head forward, aligning the horizontal canal with the gravity vector, and then leans his or her head backward, flipping the horizontal canal 180°. Right horizontal canalithiasis will cause a right beating nystagmus during the bow and a left beating nystagmus during the lean. This test may be better than the head-roll test at lateralizing the problem [41].

A third test is the upright head-roll test, in which the seated patient's head is tilted laterally to one shoulder, and then to the other, to elicit the horizontal nystagmus. One retrospective study claimed that this test achieved the correct diagnosis in 95 percent of cases, better than the supine tests [42].

Determining the provoking position at the onset of the patient's vertigo may also help in lateralization of geotropic HC-BPPV. In one study, 70 percent of patients who indicated that vertigo was provoked by rotating the head to the right were found to have involvement of the right horizontal canal during the supine head-roll test [32].

Recognizing HC-BPPV and its subtypes is important because it requires a different therapeutic maneuver. (See 'Particle repositioning maneuvers' below.)

Anterior canal BPPV — Anterior canal BPPV (also known as superior canal BPPV) has similar provoking factors as classic posterior canal BPPV, but the nystagmus is downbeat and torsional, with the top of the eye torting away from the lower ear (ie, apogeotropic) [43]. The latency, duration, and fatigability are similar [44,45]. It is rare, accounting for only approximately 1 to 2 percent of patients with BPPV, likely due to its anatomic position that makes it difficult for debris to enter [46].

Bilateral and multiple-canal BPPV — In some patients, more than one semicircular canal is affected [47,48]. In one case series, bilateral involvement of the same canal, usually the posterior, occurred in approximately 10 percent of patients. Less commonly, multiple different canals were affected, usually the horizontal and posterior canals; two-thirds of these were on the same side [48,49]. In one series, 25 percent of multiple different canal cases were caused by trauma, compared with 15 percent for single-canal and bilateral same-canal cases [48].

Diagnostic testing — Further testing is not indicated with typical posterior canal BPPV. Findings are typically normal:

●Electronystagmography (ENG) or video nystagmography (VNG), which tests caloric responses and records other eye movements, is usually normal in BPPV. ENG is indicated only if an alternative vestibular disease is suspected by history or examination. (See "Evaluation of the patient with vertigo".)

●Audiometry, if performed, is typically normal [24].

●Neuroimaging is necessary only if nystagmus does not fit the classic posterior canal BPPV profile or if the patient doesn't respond to treatment (table 1) [13], and it is likely to be normal in the absence of clinical findings suspicious for central pathology [50].

DIAGNOSIS — 

The diagnosis of BPPV is made in a patient who has recurrent, brief (<1 minute) episodes of vertigo that are provoked by specific types of head movements and is confirmed by observing nystagmus during a provoking maneuver as described above.

The diagnosis of BPPV is uncertain if no nystagmus is seen on examination. Some patients who report symptoms that suggest BPPV have symptoms but no elicitable nystagmus with provoking maneuvers; they have been suggested to have so-called "subjective" BPPV [38,51-53]. In one center, over a two-year period, 204 patients were diagnosed with BPPV and an additional 63 patients were thought to have subjective BPPV [53]. On follow-up, 18 in the latter category were given other diagnoses, emphasizing the importance of considering other disorders in these patients. Empiric treatment with liberatory maneuvers in this setting is often effective if the history is highly suggestive of BPPV [51,52]. Other diagnoses should be considered for those who do not respond to treatment within a few days.

DIFFERENTIAL DIAGNOSIS

●Postural hypotension – Postural (orthostatic) hypotension can be confused with BPPV since both cause dizziness that is provoked by a positional change. Patients with orthostatic hypotension may describe presyncopal sensation (faintness) rather than vertigo. In addition, orthostatic presyncope is not induced by rolling over in bed or lying down, while 90 percent of patients with BPPV complain that these maneuvers cause dizziness. (See "Approach to the patient with dizziness", section on 'Presyncope'.)

●Chronic unilateral vestibular hypofunction – Chronic unilateral vestibular hypofunction from any cause is associated with transient dizziness after rapid head turns, but these are fleeting, lasting only one to two seconds. By contrast, vertigo from BPPV does not require rapidity of the head turn, and it typically lasts 30 to 60 seconds. Furthermore, vertigo in posterior canal BPPV is provoked by looking up or down, whereas these maneuvers are not necessarily problematic for patients with chronic unilateral vestibular hypofunction.

●Vestibular paroxysmia – Vestibular paroxysmia refers to a syndrome of brief attacks of vertigo that last one to several seconds and recur several times a day. In some patients, attacks are unprovoked; in others, they are precipitated by head turn or other action. Magnetic resonance imaging (MRI) may reveal evidence of neurovascular compression. (See "Causes of vertigo", section on 'Vestibular paroxysmia'.)

●Vestibular migraine – Migraine is a frequent cause of episodic vertigo, and vestibular migraine, also known as migrainous vertigo, can present as an isolated positional vertigo mimicking BPPV. The duration of symptoms is a useful, but not an infallible, distinguishing feature; most episodes last a few to several hours, but a minority can last seconds to a few minutes. A migraine headache with or following the vertiginous spell makes for an easy diagnosis, but this sequence does not always occur. (See "Pathophysiology, clinical manifestations, and diagnosis of migraine in adults", section on 'Vestibular migraine'.)

A retrospective review of 362 outpatients with positional vertigo identified 10 patients with migrainous positional vertigo, which differed from BPPV by the following features [54]:

•A shorter duration of a period of recurrent episodes than BPPV (eg, recurrences happening over hours to days rather than weeks to months)

•More frequent subsequent periods of recurrent dizziness than BPPV

•Onset at a young age in some patients

•Migrainous symptoms, often subtle, during episodes with positional vertigo and/or at other times

•Positional nystagmus atypical for BPPV

Vestibular migraine is discussed in detail separately. (See "Vestibular migraine".)

●Central positional vertigo – Central positional vertigo and nystagmus may occur with lesions of the cerebellum, particularly the cerebellar vermis. The classic sign of central positional vertigo is downbeat nystagmus. In contrast with BPPV, the nystagmus is static and persists as long as the provocative position is maintained. In some patients, the downbeat nystagmus is present or increased only when lying down, more so when prone than supine [55].

The main consideration in the differential diagnosis of positional central downbeat nystagmus is the anterior canal form of BPPV [56]. In addition to the static rather than transient nature of the induced nystagmus, other clinical features may be helpful. The lack of a torsional component to the nystagmus differentiates central downbeat nystagmus from that with anterior canal BPPV. Other features that indicate central disease are a lack of latency, lack of fatigability, and the inability to suppress nystagmus with vision (table 1 and table 2).

Patients with static positional nystagmus without prior evidence of more typical BPPV should be investigated for central disease with neuroimaging. Central positional vertigo and nystagmus has been described with both cerebrovascular [57-59] and demyelinating diseases [60]. Other possible causes include Chiari malformation, idiopathic cerebellar degeneration, and spinocerebellar ataxia type 6 [55,61]. (See "Autosomal dominant spinocerebellar ataxias", section on 'SCA6'.)

●Rotational vertebral artery syndrome – The rotational vertebral artery refers to a rare but well-documented phenomenon of symptomatic vertebral artery compression by bony elements of the spine (usually at CI-C2) that occurs with physiologic head rotation. The diagnosis is suggested when symptoms begin with a rotational head turn with respect to the body and persist as long as the head is held in that position. Symptoms do not occur if both the head and the body are turned together, as when rolling over in bed. Also, it can occur with head turn whether the patient is standing or lying. While vertigo or nonspecific dizziness is most commonly described, other brainstem symptoms may occur as well. The diagnosis is made by vascular imaging that includes the neutral as well as the symptomatic position. (See "Causes of vertigo", section on 'Rotational vertebral artery syndrome'.)

TREATMENT

Particle repositioning maneuvers — BPPV is treated effectively in most cases using particle repositioning maneuvers.

Office-based treatment — So-called "particle repositioning" maneuvers have been devised to treat patients with BPPV (figure 2) [35]. These are the treatment of choice for posterior canal BPPV and include:

●The Epley maneuver [36] (figure 2) and modified Epley maneuver (figure 3A-B)

●The Semont maneuver [62] and modified Semont maneuver (figure 4)

The treatment maneuvers encourage the debris to migrate toward the common crus of the anterior and posterior canals and exit into the utricular cavity [44]. As noted above, these maneuvers may be effective when the history is highly suggestive of BPPV, even if nystagmus is not seen on examination [51,52].

●Efficacy – The efficacy of the maneuvers have been evaluated in several randomized studies [63-67]. Systematic reviews and meta-analyses have concluded that particle repositioning maneuvers are safe and effective for the treatment of posterior canal BPPV [68-73]. Treated subjects are 37 times more likely to recover than subjects undergoing sham treatments.

The Semont and Epley maneuvers appear to be equally effective [74]. A modification of the Semont maneuver based on biophysical models, the "Semont plus," requires the body to be placed below the horizontal. Comparison studies suggest that this leads to more rapid elimination of positional attacks than either the traditional Semont maneuver (1 versus 2 days on average) [75] or the Epley maneuver (2 versus 3.3 days) [76].

A large study of nearly one thousand patients found that a single maneuver was effective in 85 percent of patients, with only 2 percent requiring more than three treatments [67]. The success of the procedure can be predicted by inspection of nystagmus during the second position of the Epley maneuver; reversed nystagmus direction or no nystagmus observed at this point suggest that the procedure will not be efficacious [77].

●Additional treatment – These maneuvers can be repeated in patients who do not completely respond to or who relapse after the first attempt; subsequent treatments appear to have a similar likelihood of benefit as a first treatment [78]. Some studies suggest that patients with posttraumatic BPPV and those with BPPV following vestibular neuronitis or Meniere disease are more likely to need multiple treatments compared with those with idiopathic BPPV [17,79-81].

After successful repositioning treatment, some patients have persistent, mild imbalance and dizziness for a few weeks. This is usually but not always self-limited. (See 'Prognosis' below.)

In some patients, debris may reenter another canal, most commonly the horizontal, causing "transitional BPPV" [82]. This may resolve on its own or require treatment with the horizontal canal maneuvers below. (See 'Horizontal canal BPPV' above and 'Maneuvers for other BPPV variants' below.)

We do not routinely recommend postural restriction in our patients after treatment. Postural restriction, using a cervical collar, and maintaining an upright head position for two days after treatment has been recommended to prevent return of particles into the semicircular canal. While one study found that patients instructed to restrict head motion were less likely to require repeated treatment [83], other studies have not found a benefit for post-maneuver activity restrictions [70,84]. A meta-analysis of six studies (523 patients) found that restriction of head movement after repositioning did not appear to affect the efficacy of the maneuver [85], while another meta-analysis concluded that this added a small improvement in treatment efficacy [86].

Self-treatment — Based on the same principles, exercises for self-treatment at home have been developed: the Brandt-Daroff exercises (figure 5) [44], a modified Epley maneuver (figure 3A and figure 3B) [87], and the modified Semont maneuver (figure 4). Self-treatments are likely to be most effective when instruction includes a demonstration of the procedure as well as provision of printed directions [88]. Patients should know that the appropriate maneuver is specific to the side of the affected ear; performing the contralateral maneuver may not be effective and has the potential to worsen the condition. Video demonstration originally published by the American Academy of Neurology is available for general viewing online [89].

The modified Epley and Semont maneuvers are likely similarly effective. However, one study of 70 patients found that self-treatment with the modified Epley maneuver was more effective in abolishing vertigo than self-treatment with the modified Semont maneuver was (response rate 95 versus 58 percent), likely because patients had more difficulty performing the latter [90]. In general, Brandt-Daroff exercises are less effective than particle repositioning maneuvers [91,92]. In one study of 54 patients, vertigo resolved more often in patients who used the modified Epley maneuver compared with those using the Brandt-Daroff exercises (64 versus 23 percent) [91].

Overall, studies suggest that self-treatment is effective in 65 to 90 percent of patients. Self-treatment with either a modified Epley or Semont maneuver has not been well studied in comparison with more standard particle repositioning maneuvers [70]. Self-treatment is useful for patients with frequent recurrences [91,93]. It may also serve a complementary role for initial treatment in patients who do not respond immediately to the single treatment maneuvers listed above. A randomized trial in 80 patients treated with the Epley maneuver alone versus the Epley maneuver supplemented by self-treatment with the modified Epley maneuver found that combined therapy resulted in a higher rate of symptom resolution (88 versus 77 percent) [94]. This finding was not replicated in another prospective study that found similar treatment responses with these two approaches [88].

The maneuvers are well tolerated by most patients. However, approximately 6 percent have the debris migrate into the anterior or horizontal canals, causing other variants of positional vertigo [45,94].

Daily performance of particle repositioning maneuvers does not affect either the rate of or the time to recurrence in BPPV; patients should cease performing these maneuvers at home once the symptoms of the current bout have resolved [95].

Maneuvers for other BPPV variants

●Horizontal canal BPPV – Different maneuvers are used for horizontal canal BPPV (HC-BPPV) than for posterior canal type BPPV [23,96].

One better-studied maneuver for the horizontal canal variant involves stepwise rotations of the non-tilted head in the supine position moving 360° from the affected to the unaffected ear [70,97,98]. This is performed two to four times or until nystagmus disappears. This method has been dubbed the "barbecue rotation" maneuver, and is also known as the Lempert roll maneuver. The efficacy of this maneuver may depend upon correct determination of the side of the problem, which may be improved by the "bow and lean" test [41]. (See 'Horizontal canal BPPV' above.)

Another option is the Gufoni maneuver, which can be performed in one of two ways. The first way is to have the sitting patient rapidly bend to lie on his or her unaffected ear, quickly turn his or her head to face down, stay there for two minutes, and then sit back up [99]. The second way is to have the patient lie on the affected side, then quickly turn the head to face up [39]. The treatment appears to be effective, at least in the short term [100], with one retrospective study suggesting an efficacy of approximately 70 percent after the maneuver was performed once [101]. In a randomized trial, 31 of 37 patients with HC-BPPV had recovered one day after treatment with the Gufoni maneuver, compared with 4 of 35 patients who received sham treatment [102]. Another randomized study suggested that the Gufoni maneuver was slightly more effective than the Lempert maneuver (described above) at 30 days after treatment [99]. A third small trial suggested that the Gufoni maneuver is equivalent to a head-shaking maneuver (performed with the head bent forward 30° in the sitting position for 15 seconds) [39].

An alternative treatment, Vannucchi's forced prolonged position, requires patients to lie with the unaffected ear down for 12 hours [103]. This can be helpful in patients with severe symptoms who may be reluctant to perform one of the other maneuvers. In one prospective case series, this treatment appeared to have an efficacy that was similar to the Gufoni or Lempert maneuver [104]. An evaluation of a "shortened forced position" (lying for 1 hour only instead of 12 hours) found improvement in 70 percent of patients [105].

Whether there is any difference in the efficacy of these maneuvers for the geotropic versus apogeotropic variants of HC-BPPV is not clear. Some suggest that the apogeotropic form is best treated with modified versions of the Semont or Gufoni maneuvers [3]. A randomized trial in 48 patients concluded that the Gufoni maneuver was superior to the barbecue roll maneuver for both geotropic and ageotropic forms [106].

●Anterior canal BPPV – The best treatment maneuver for this variant is uncertain. The scarcity of data is likely a consequence of the rarity of this condition.

The same liberatory maneuvers used for posterior canal BPPV have been used to treat the anterior canal variant. However, few studies have reported on the success of this treatment for anterior canal BPPV. A few small studies of patients with anterior canal BPPV have reported that vertiginous symptoms appeared to resolve as rapidly following repositioning as did posterior canal BPPV [46,107].

As an alternative approach, one study reported success using a "reverse Epley" maneuver (ie, the maneuver for a right posterior canal BPPV is used to treat a left anterior canal BPPV) in two of four patients [108]. A later study reported benefit with a "prolonged forced position" procedure (requiring hospitalization and a head-positioning pulley system) in two patients [109].

●Multiple canal BPPV – Liberatory maneuvers are still effective when multiple canals are involved, though this is more complicated. A review concluded that approximately 60 percent improved with a single session but that treatment failed in 18 percent and recurrences occurred in 30 percent [49].

●Pediatric BPPV – Maneuvers also appear to be effective and safe in children and adolescents, with an approximately 80 percent success rate with a single maneuver; however, it is less well studied in these patients [110].

Medications — In general, medications are not useful for the brief episodes of vertigo associated with BPPV [70]. A review of studies, including five randomized trials, concluded that there was no effect of vestibular suppressant medication on symptom resolution for BPPV [111].

However, vestibular suppressants can be used as premedication with liberatory maneuvers and may help patients who would not otherwise tolerate these maneuvers because of discomfort and nausea. In a randomized trial, patients given betahistine, 24 mg twice daily for one week, along with the Epley maneuver appeared to reduce symptoms compared with those treated with the maneuver alone [112]. (See "Treatment of vertigo".)

In addition, testing for and supplementing severe vitamin D deficiency may be beneficial for some patients with recurrent episodes of BPPV. (See 'Recurrent episodes' below.)

Vestibular rehabilitation — Vestibular rehabilitation has a limited role in the treatment of BPPV; the preponderance of evidence suggests that particle repositioning maneuvers are more effective [113].

Two studies have examined the role of the addition of vestibular rehabilitation to particle repositioning maneuvers, suggesting that patients who receive both treatments are less likely to have a recurrence and have better balance at two weeks compared with those who have repositioning maneuvers alone [114,115]. An impact on longer-term outcomes was not examined.

Refractory BPPV — BPPV is intractable in a very small number of patients. Surgical treatments may be considered in patients who are disabled by their symptoms [116]:

●Surgical occlusion of the posterior canal with bony plugs is one option; success rates of approximately 90 percent have been reported for this procedure in uncontrolled reports [35,70,117-120]. This surgery renders the posterior canal permanently nonfunctional; transient postoperative hearing loss and dizziness are very common. Persistent hearing loss occurs in less than 5 percent; hence, impaired hearing in the other ear is a contraindication to this procedure.

●An argon laser can also be used to induce ossification of the posterior canal [121,122].

●Another surgical option is transection of the posterior ampullary nerve, which has a similar reported success rate [116]. Sensorineural hearing loss occurs in 4 to 40 percent of patients; however, the better complication rates appear to be attributed to one surgeon's experience, and most surgeons favor the occlusive procedure.

●One anecdotal report of four patients suggested that intratympanic dexamethasone may lead to resolution of refractory BPPV [123]. This requires confirmation.

PROGNOSIS

Duration of illness — While the natural history of BPPV is not well studied, it is widely accepted that untreated episodes usually resolve spontaneously over days to weeks, sometimes longer [124]. In a case series of 108 patients with BPPV who did not receive canalith repositioning maneuvers, positional vertigo symptoms disappeared at a mean of 39 days for patients with posterior BPPV and a mean of 16 days for those with horizontal BPPV [125]. Patients with BPPV due to certain etiologies such as ischemia, vestibular neuronitis, or trauma may have with a more prolonged course than those with idiopathic BPPV [18,79].

Persistent symptoms — A residual nonpositional vague dizziness or imbalance can persist despite resolution of BPPV in some patients, for which age and osteoporosis appear to be risk factors [126-128]. In some, this residual dizziness may be related to persistent otolith dysfunction [129]. In others, psychogenic factors may play a role. One study found that pretreatment anxiety was the most significant predictor of residual dizziness [130]. Along these lines, others report that older patients with a long interval before diagnosis may develop secondary persistent postural perceptual dizziness [127,131].

BPPV can have a significant impact on quality of life, with restrictions on daily activities and work, social isolation, anxiety, and depression [132]. It also carries a 2.6 times increased risk for injury [133].

Recurrent episodes

●Frequency – Later recurrences of BPPV are fairly common. One study followed 50 patients with BPPV for a mean of 52 months and found that the recurrence rates at one and three years were 18 and 30 percent, respectively [134]. Other case series have reported five-year recurrence rates of 33 and 35 percent [135,136].

●Risk factors – Risk factors for recurrence have been somewhat variably observed and include older age and female sex [9,10,67,137]. Recurrence is more common with comorbid vascular risk factors such as diabetes, hypertension, and hyperlipidemia. Posttraumatic BPPV may also have a higher risk of recurrence than idiopathic BPPV does, although this is not uniformly observed [79,80,136]. Likewise, BPPV following vestibular neuronitis or Meniere disease may recur more frequently than idiopathic BPPV [9,10,17,67,81].

Some have also noted that osteoporosis and vitamin D deficiency are risk factors, although the data regarding vitamin D deficiency are conflicting [9,10,67,137,138].

●Prevention – We suggest testing for vitamin D deficiency in older patients (>60 years) who present with recurrences of BPPV.

Vitamin D supplementation appears to reduce the recurrence rate in patients who have vitamin D deficiency [139,140]. In one trial, patients were randomized to assessment of vitamin D levels and supplementation for deficiency (vitamin D <20 ng/mL) compared with observation without vitamin D assessment or supplementation [141]. The annual recurrence rate was lower in those in the intervention group: 0.8 versus 1.1 recurrences per year (relative risk [RR] 0.76, 95% CI 0.66-0.87). The RR reduction was numerically high in the subgroup of patients with vitamin D levels <10 ng/mL (RR 0.55, 95% CI 0.39-0.77).

Supplementation of vitamin D deficiency is discussed separately. (See "Vitamin D deficiency in adults: Definition, clinical manifestations, and treatment".)

●Treatment – Recurrences can be treated with the same liberatory maneuvers at home or in the office [142]. However, in 20 percent, the recurrence may involve a different canal, requiring evaluation and a different treatment approach [143].

INFORMATION FOR PATIENTS — 

UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5^th to 6^th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10^th to 12^th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

●Basics topics (see "Patient education: Vertigo (a type of dizziness) (The Basics)" and "Patient education: Exercises (maneuvers) for benign paroxysmal positional vertigo (The Basics)")

●Beyond the Basics topics (see "Patient education: Vertigo (Beyond the Basics)")

SUMMARY AND RECOMMENDATIONS

●Epidemiology and pathogenesis – Benign paroxysmal positional vertigo (BPPV) is a common form of peripheral vertigo, attributed to canalithiasis (calcium debris within a semicircular canal). Involvement of the posterior canal is most common, followed by the horizontal canal. Anterior canal BPPV is rare. (See 'Epidemiology' above and 'Pathogenesis' above.)

●Clinical features – BPPV presents with recurrent episodes of vertigo lasting one minute or less that are provoked by specific types of head movements. (See 'Symptoms' above.)

BPPV does not cause prolonged or sustained vertigo, hearing loss, tinnitus, or neurologic deficits; these suggest an alternative diagnosis. (See "Evaluation of the patient with vertigo" and "Causes of vertigo".)

●Diagnosis – In patients with typical symptoms, perform a provoking maneuver and observe symptoms and nystagmus to confirm the diagnosis of BPPV and localize the abnormality. (See 'Response to provoking maneuvers' above.)

•The Dix-Hallpike maneuver (figure 1) is used to identify posterior canal BPPV, the most common subtype. (See 'Posterior canal BPPV' above.)

•If the Dix-Hallpike maneuver does not identify posterior canal BPPV, evaluate for other subtypes with an appropriate maneuver and consider alternative diagnoses. (See 'Response to provoking maneuvers' above and 'Differential diagnosis' above.)

●Differential diagnosis – Considerations in the differential diagnosis of BPPV are postural hypotension, chronic unilateral vestibular hypofunction, vestibular migraine, and central positional vertigo with static downbeat nystagmus. Patients with static positional nystagmus without prior evidence of more typical BPPV should be investigated for central disease with neuroimaging. (See 'Differential diagnosis' above.)

●Treatment – For patients with posterior canal BPPV, we recommend treatment with a particle repositioning maneuver (Grade 1A). The Epley maneuver (figure 3A-B) is most commonly used; the Semont maneuver (figure 4) appears similarly effective. (See 'Particle repositioning maneuvers' above.)

For other BPPV subtypes, we suggest the appropriate particle repositioning maneuver (Grade 2C). (See 'Maneuvers for other BPPV variants' above.)

Most patients respond to particle repositioning maneuvers, but some patients may require repeat treatment. Medications are not useful for most patients with BPPV. (See 'Medications' above and 'Refractory BPPV' above.)

●Recurrences – Recurrences of BPPV are fairly common and respond to self-treatment with the Epley maneuver (figure 3A-B) or Semont maneuver (figure 4). These are most effective when the procedure is first demonstrated in the office and written instructions are provided. The Brandt-Daroff maneuver (figure 5) may be less effective but is simple and can be used when the affected side is uncertain. (See 'Prognosis' above and 'Self-treatment' above.)

In patients who present with recurrent episodes of BPPV, we suggest testing for vitamin D deficiency. Supplementation is recommended for those with severe deficiency. (See "Vitamin D deficiency in adults: Definition, clinical manifestations, and treatment".)