Benign Paroxysmal Positional Vertigo 

Updated: Feb 15, 2018
Author: John C Li, MD; Chief Editor: Arlen D Meyers, MD, MBA 

Overview

Practice Essentials

Benign paroxysmal positional vertigo (BPPV) is probably the most common cause of vertigo in the United States. It has been estimated that at least 20% of patients who present to the physician with vertigo have BPPV. However, because BPPV is frequently misdiagnosed, this figure may not be completely accurate and is probably an underestimation. Since BPPV can occur concomitantly with other inner ear diseases (for example, one patient may have both Ménière disease and BPPV at once), statistical analysis may be skewed toward lower numbers.[23]

BPPV was first described by Barany in 1921. The characteristic nystagmus and vertigo associated with positioning changes were attributed at that time to the otolithic organs. In 1952, Dix and Hallpike performed the provocative positional testing named in their honor, shown below. They further defined classic nystagmus and went on to localize the pathology to the proper ear during provocation.

The patient is placed in a sitting position with t The patient is placed in a sitting position with the head turned 45° towards the affected side and then reclined past the supine position.

BPPV is a complex disorder to define; because an evolution has occurred in the understanding of its pathophysiology, an evolution has also occurred in its definition. As more interest is focused on BPPV, new variations of positional vertigo have been discovered. What was previously grouped as BPPV is now subclassified by the offending semicircular canal (SCC; ie, posterior superior SCC vs lateral SCC) and, although controversial, further divided into canalithiasis and cupulolithiasis (depending on its pathophysiology). (A literature review by Anagnostou et al indicated that approximately 3% of all BPPV cases consist of the anterior canal variant of the condition.[1] )

BPPV is defined as an abnormal sensation of motion that is elicited by certain critical provocative positions. The provocative positions usually trigger specific eye movements (ie, nystagmus). The character and direction of the nystagmus are specific to the part of the inner ear affected and the pathophysiology.

Although some controversy exists regarding the 2 pathophysiologic mechanisms, canalithiasis and cupulolithiasis, agreement is growing that the entities actually coexist and account for different subspecies of BPPV. Canalithiasis (literally, "canal rocks") is defined as the condition of particles residing in the canal portion of the SCCs (in contradistinction to the ampullary portion). These densities are considered to be free floating and mobile, causing vertigo by exerting a force. Conversely, cupulolithiasis (literally, "cupula rocks") refers to densities adhered to the cupula of the crista ampullaris. Cupulolith particles reside in the ampulla of the SCCs and are not free floating.

Classic BPPV is the most common variety of BPPV. It involves the posterior SCC and is characterized by the following:

  • Geotropic nystagmus with the problem ear down

  • Predominantly rotatory fast phase toward undermost ear

  • Latency (a few seconds)

  • Limited duration (< 20 s)

  • Reversal upon return to upright position

  • Response decline upon repetitive provocation

Because the type of BPPV is defined by the distinguishing type of nystagmus, defining and explaining the characterizing nystagmus are also important.

Nystagmus is defined as involuntary eye movements usually triggered by inner ear stimulation. It usually begins as a slow pursuit movement followed by a fast, rapid resetting phase. Nystagmus is named by the direction of the fast phase. Thus, nystagmus may be termed right beating, left beating, up-beating (collectively horizontal), down-beating (vertical), or direction changing.

If the movements are not purely horizontal or vertical, the nystagmus may be deemed rotational. In rotational nystagmus, the terminology becomes a bit more loose or unconventional. Terms such as clockwise and counterclockwise seem useful until discrepancies regarding point of view arise: clockwise to the patient is counterclockwise to the observer. Right versus left terminology is poorly descriptive because as the top half of the eye rotates right, the bottom half moves left.

Rotational nystagmus also can be described as geotropic and ageotropic. Geotropic means "toward earth" and refers to the upper half of the eye. Ageotropic refers to the opposite movement. If the head is turned to the right, and the eye rotation is clockwise from the patient's point of view (top half turns to the right and toward the ground), then the nystagmus is geotropic. If the head is turned toward the left, then geotropic nystagmus is a counterclockwise rotation. This term is particularly useful in describing BPPV nystagmus because the word geotropic remains appropriate whether the right or the left side is involved.

These 2 terms are useful only when the head is turned. If the patient is supine and looking straight up, these terms cannot be used. Fortunately, the nystagmus associated with BPPV usually is provoked with the head turned to one side. The most accurate way to define nystagmus is by terming it clockwise or counterclockwise from the patient's point of view.

Diagnosis and management

The Dix-Hallpike maneuver is the standard clinical test for BPPV. The finding of classic rotatory nystagmus with latency and limited duration is considered pathognomonic. A negative test result is meaningless except to indicate that active canalithiasis is not present at that moment.

The Dix-Hallpike maneuver is performed by rapidly moving the patient from a sitting position to the supine position with the head turned 45° to the right. After waiting approximately 20-30 seconds, the patient is returned to the sitting position. If no nystagmus is observed, the procedure is then repeated on the left side.

Treatment options for BPPV include watchful waiting, vestibulosuppressant medication, vestibular rehabilitation, canalith repositioning, and surgery. Since the benefit-to-risk ratio is so high with canalith repositioning, it appears to be the obvious first choice among treatment modalities.

Surgery is usually reserved for those in whom the canalith repositioning procedure (CRP) fails. Options include labyrinthectomy, posterior canal occlusion, singular neurectomy, vestibular nerve section, and transtympanic aminoglycoside application.

Pathophysiology

To understand pathophysiology, an understanding of normal SCC anatomy and physiology is necessary. Each inner ear contains 3 SCCs oriented in 3 perpendicular planes; the SCCs mediate spatial orientation. Each canal consists of a tubular arm (crura) that sprouts from a large barrellike compartment, much like the handle of a coffee mug sprouts from the mug. Each of these arms has a dilated (ampullary) end located near the top or front portion that houses the crista ampullaris (nerve receptors).

The crista ampullaris has a sail-like tower, the cupula, that detects the flow of fluid within the SCC. If a person turns suddenly to the right, the fluid within the right horizontal canal lags behind, causing the cupula to be deflected left (toward the ampulla, or ampullopetally). This deflection is translated into a nerve signal that confirms the head is rotating to the right.

In simple terms, the cupula acts as a 3-way switch that, when pressed one way, appropriately gives the body a sensation of motion. The middle or neutral position reflects no motion. When the switch is moved the opposite way, the sensation of motion is in the opposite direction.

Particles in the canal slow and even reverse the movement of the cupula switch and create signals that are incongruous with the actual head movements. This mismatch of sensory information results in the sensation of vertigo.

Cupulolithiasis theory

In 1962, Harold Schuknecht, MD, proposed the cupulolithiasis (heavy cupula) theory as an explanation for BPPV. Via photomicrographs, he discovered basophilic particles or densities that were adherent to the cupula. He postulated that the posterior semicircular canal (PSC) was rendered sensitive to gravity by these abnormal dense particles attached to or impinging upon the cupula.

This theory is analogous to the situation of a heavy object attached to the top of a pole. The extra weight makes the pole unstable and thus harder to keep in the neutral position. In fact, the pole is easily prone to "clunk" from one side to the other depending on the direction it is tilted. Once the position is reached, the weight of the particles keeps the cupula from springing back to neutral. This is reflected by the persistent nystagmus and explains the dizziness when a patient is tilted backward.

Canalithiasis theory

In 1980, Epley published his theories regarding canalithiasis.[2] He thought that the symptoms of BPPV were much more consistent with free-moving densities (canaliths) in the posterior SCC rather than fixed densities attached to the cupula. While the head is upright, the particles sit in the PSC at the most gravity-dependent position. When the head is tilted back supine, the particles are rotated up approximately 90° along the arc of the PSC. After a momentary (inertial) lag, gravity pulls the particles down the arc. This causes the endolymph to flow away from the ampulla and causes the cupula to be deflected. The cupular deflection produces nystagmus. Reversal of the rotation (sitting back up) causes reversal of the cupular deflection and thus dizziness with nystagmus beating in the opposite direction.

This model can be compared with pebbles inside a tire. As the tire is rolled, the pebbles are picked up momentarily and then tumble down with gravity. This tumbling triggers the nerve inappropriately and causes dizziness. Reversal of the rotation obviously causes reversal of the flow and reversal of the dizziness direction.

Canal densities would better explain the delay (latency), transient nystagmus, and reversal on return to upright than would cupular densities. This supports canalithiasis rather than cupulolithiasis as the mechanism for classic BPPV.

The canalithiasis theory received further corroboration by Parnes and McClure in 1991 with the discovery of free densities in PSC at surgery.

Epidemiology

Frequency

United States

In one study, the age- and sex-adjusted prevalence of BPPV was 64 per 100,000. Other studies corroborate this finding.

Race

Little published information is available on racial predilection.

Sex

The sex distribution seems to indicate a predilection for women (64%).

Age

BPPV seems to have a predilection for the older population (average age, 51-57.2 y). It is rarely observed in individuals younger than 35 years without a history of antecedent head trauma.

 

Presentation

History

See the list below:

  • The onset of benign paroxysmal positional vertigo (BPPV) is typically sudden. Many patients wake up with the condition, noticing the vertigo while trying to sit up suddenly. Thereafter, propensity for positional vertigo may extend for days to weeks, occasionally for months or years. In many, the symptoms periodically resolve and then recur.

  • The severity covers a wide spectrum. In patients with extreme cases, the slightest head movement may be associated with nausea and vomiting. Despite strong nystagmus, other patients seem relatively unfazed.

  • People who have BPPV do not usually feel dizzy all the time. Severe dizziness occurs as attacks triggered by head movements. At rest between episodes, patients usually have few or no symptoms. However, some patients complain of a continual sensation of a "foggy or cloudy" sensorium.

  • Classic BPPV is usually triggered by the sudden action of moving from the erect position to the supine position while angling the head 45° toward the side of the affected ear. Merely being in the provocative position is not enough. The head actually must move to the offending pose. After reaching the provocative position, a lag period of a few seconds occurs before the spell strikes. When BPPV is triggered, patients feel as though they are suddenly thrown into a rolling spin, toppling toward the side of the affected ear. Symptoms start very violently and usually dissipate within 20 or 30 seconds. This sensation is triggered again upon sitting erect; however, the direction of the nystagmus is reversed.

Physical

See the list below:

  • The physical examination findings in patients affected by BPPV are generally unremarkable. All neurotologic examination findings except those from the Dix-Hallpike maneuver may be normal. However, the presence of neurotologic findings does not preclude the diagnosis of BPPV.

  • The Dix-Hallpike maneuver is the standard clinical test for BPPV. The finding of classic rotatory nystagmus with latency and limited duration is considered pathognomonic. A negative test result is meaningless except to indicate that active canalithiasis is not present at that moment.

    • This test is performed by rapidly moving the patient from a sitting position to the supine position with the head turned 45° to the right. After waiting approximately 20-30 seconds, the patient is returned to the sitting position. If no nystagmus is observed, the procedure is then repeated on the left side.

    • Dix-Hallpike maneuver tips include the following:

      • Do not turn the head 90° since this can produce an illusion of bilateral involvement.

      • Tailor briskness of the Dix-Hallpike test to the individual patient.

      • Consider the Epley modification. From behind the patient, performing the maneuver is easier, since one can pull the outer canthus superolaterally to visualize the eyeball rotation.

      • In typical nystagmus, the axis is near the undermost canthus. Minimize suppression by directing the patient gaze to the anticipated axis of rotation.

  • Classic posterior canal BPPV produces geotropic rotatory nystagmus. The top pole of the eyes rotates toward the undermost (affected) ear.

  • Purely horizontal nystagmus indicates horizontal canal involvement.

  • Sustained or nonfatiguing nystagmus may indicate cupulolithiasis rather than canalithiasis.

A study by Yetiser and Ince indicated that the head-roll maneuver is the most effective positioning test for diagnosing lateral canal BPPV, in a comparison with the head-bending and lying-down positioning tests. The study, which involved 78 patients with lateral canal BPPV, found that using the head-roll maneuver, the affected side was located in 75% of patients with apogeotropic nystagmus and in 95.6% of patients with geotropic nystagmus.[3]

Causes

A few factors predispose patients to BPPV. These include inactivity, acute alcoholism, major surgery, and central nervous system (CNS) disease. A complete neurotologic examination is important because many patients have concomitant ear pathology, as follows:

  • Idiopathic pathology - 39%

  • Trauma - 21%

  • Ear diseases - 29%

  • Otitis media - 9%

  • Vestibular neuritis - 7%

  • Ménière disease - 7%

  • Otosclerosis - 4%

  • Sudden sensorineural hearing loss - 2%

  • CNS disease - 11%

  • Vertebral basilar insufficiency - 9%

  • Acoustic neuroma - 2%

  • Cervical vertigo - 2%

A study by Chang et al suggested that BPPV can be triggered by dental procedures. The study, which included 768 patients with BPPV and 1536 controls, found that within 1 month before they were diagnosed, 9.2% of the patients with BPPV had undergone dental treatment, compared with 5.5% of controls within a month before they were identified. Adjustments for demographic factors and comorbidities indicated that a positive relationship exists between recent dental procedures and BPPV.[4]

A retrospective study by Faralli et al indicated that in persons with migraine headache and BPPV, the onset of BPPV tends to occur earlier in life than it does in patients with this form of vertigo but no migraine. The investigators found that the mean age at BPPV onset for patients with migraine was 39 years, compared with 53 years for patients without migraine. In addition, highly recurrent BPPV was found in 19.4% of the migraine patients, compared with 7.3% of persons without migraine. Moreover, the frequency of atypical eye movements and Ménière-like vertigo was greater in patients with both migraine and highly recurrent BPPV. Faralli and colleagues stated, however, that it has not yet been determined whether a direct pathophysiologic association exists between migraine and BPPV.[5]

An Italian study, by Messina et al, indicated that hypertension, dyslipidemia, and preexisting cardiovascular comorbidities are risk factors for recurrent episodes of BPPV, with the odds ratios ranging from 1.84 to 2.31.[25]

 

DDx

Diagnostic Considerations

Differential diagnoses for benign paroxysmal positional vertigo (BPPV) can be divided into 3 main areas of pathology: labyrinthine, vestibular nerve, and central sites of lesions. These are subdivided further as follows:

  • Ménière disease is probably the most frequent misdiagnosis applied to chronic BPPV because patients may fail to recognize the positional provocation. It is also confusing because BPPV can occur concomitantly.

  • Inner ear concussion may cause transient positional vertigo and nystagmus and can be confused with BPPV.

  • Alcohol intoxication can cause positional nystagmus, is persistent in a given position, and varies according to head position.

  • With labyrinthitis, the nystagmus is spontaneous, persistent, predominantly linear-horizontal and affected little by head position. Caloric testing often reveals unilateral weakness.

  • For vascular loop syndrome, the diagnostic criteria have been defined poorly. This diagnosis should be considered only after all other possibilities are exhausted.

  • Positional nystagmus of central origin is seldom transient and may be down-beating, whereas BPPV is usually up-beating. Frequently, other CNS signs are present.

  • Positional down-beating nystagmus is often associated with a lesion of the nodulus (which normally inhibits vertical vestibuloocular reflex gain) from stroke, multiple sclerosis, Arnold-Chiari malformation, ischemia, cerebellar degeneration, and intoxication.

  • Central positional nystagmus may indicate a posterior fossa lesion such as acoustic neuroma or meningioma.

  • Vertebral artery insufficiency is also a differential diagnosis for BPPV.

  • Cervical vertigo, or head extension vertigo, is a somewhat ill-defined entity of symptoms that arises with head extension, quite possibly a manifestation of vascular compression (vertebral arteries).

  • With orthostatic hypotension, low blood volume or poor systemic arterial tone can account for hypoperfusion of the brain and cause dizziness. Patients feel better when lying down and are symptomatic when sitting up.

Differential Diagnoses

 

Workup

Laboratory Studies

Because the Dix-Hallpike maneuver is pathognomonic, laboratory tests are not needed to make the diagnosis of benign paroxysmal positional vertigo (BPPV). However, since a high association with inner ear disease exists, laboratory workup may be needed to delineate these other pathologies.

Imaging Studies

Imaging studies are not needed in the workup of a patient in whom BPPV is suspected.

Other Tests

See the list below:

  • The Dix-Hallpike maneuver is the standard clinical test for BPPV (see Physical).

  • Electronystagmography

    • Torsional eye movement cannot be demonstrated directly, but occasionally electronystagmography (ENG) is helpful in detecting the presence and timing of nystagmus.

    • Caloric test results can be normal or hypofunctional.

    • According to Mohammed Hamid, MD, a reduced vestibular response can occur secondary to the sluggishness of the particle-laden endolymph.

    • BPPV can originate in an ear with an absent caloric response because the nervous and vascular supply to the horizontal canal is separate from that of the PSCs.

  • Infrared nystagmography: Torsional eye movement can be demonstrated directly.

  • Audiogram: The result of an audiogram may be normal.

  • Posturography: Posturography results are often abnormal but follow no predictable or diagnostic pattern.

 

Treatment

Medical Care

Treatment options include watchful waiting, vestibulosuppressant medication, vestibular rehabilitation, canalith repositioning, and surgery.

Watchful waiting

Since benign paroxysmal positional vertigo (BPPV) is benign and can resolve without treatment in weeks to months, some have argued that simple observation is all that is needed. Conversely, this involves weeks or months of discomfort and vertigo, with the danger of falls and other mishaps from the episodic vertigo spells (eg, patients who work on scaffolding may fall easily).

Vestibulosuppressant medication

This medication usually does not stop the vertigo. Although it may provide minimal relief for some patients, it does not solve the problem; it only masks the problem. Adverse effects of grogginess and sleepiness also complicate the issue of medication.

Vestibular rehabilitation

Vestibular rehabilitation is a noninvasive therapy that can have success after lengthy periods. Unfortunately, it causes repeated stimulation of vertigo while the patient is performing the therapeutic maneuvers. Patients can be instructed in Cawthorne exercises that seem to help by dispersing particles.

Canalith repositioning

Since the benefit-to-risk ratio is so high with canalith repositioning, it appears to be the obvious first choice among treatment modalities.

Particle repositioning is represented by two major maneuvers that developed simultaneously, yet independently, in the United States and France. These methods are the Epley maneuver and the Semont maneuver, and many minor variations of each of the methods exist. Both involve movements of the head to rearrange displaced particles. The Semont maneuver involves rapid and vigorous side-to-side head and body movements. The Epley maneuver is gentler and is described below. The canalith repositioning procedure (CRP) is a simple and noninvasive office treatment that is designed to cure BPPV in 1-2 sessions. See the image below. This therapy, in experienced hands, has a success rate of more than 95% for patients with BPPV.

The patient is placed in a sitting position with t The patient is placed in a sitting position with the head turned 45° towards the affected side and then reclined past the supine position.

A retrospective study by Tirelli et al indicated that patients with recurrent BPPV who undergo repeated CRP have a significantly increased dizziness recovery rate but do not have a significant difference in BPPV recurrence, compared with patients who have undergone an initial treatment with CRP but not repeated procedures.[6]

A retrospective study by Yoon et al of 1900 patients indicated that the following risk factors increase the chance that a patient with BPPV will need multiple CRPs: longer pretreatment duration of vertigo, involvement of bilateral or multiple canals, and age over 50 years.[24]

Multi-axial positioning devices

Research into multi-axial positioning devices that can perform canalith repositioning using 360º rotation in the proper plane of the semicircular canals has been conducted. The results are promising, but these devices need more study.

Epley procedure

The Epley procedure is as follows (patient with right-sided BPPV in this example):

  • Starting position (sitting, head turned 45° toward ipsilateral side): The patient begins the procedure in a sitting position with the head turned toward the affected side. A mastoid bone oscillator is applied and held in position behind the affected ear by a headband to help agitate the particles so that they move more easily.

  • Position 1 (supine, head turned 45° toward ipsilateral side): The patient is reclined slowly to the supine position of the affected side. The rate is titrated to the point of no nystagmus and no symptoms. This usually takes approximately 30 seconds.

  • Position 2 (supine, 15° Trendelenburg, head turned 45° toward ipsilateral side): The patient is reclined further to the Dix-Hallpike position of the affected side. This usually takes 10 seconds. Another 20 seconds are spent in the Dix-Hallpike position with the affected ear down.

  • Position 3 (supine, 15° Trendelenburg, head turned 45° toward contralateral side): Next, the patient's head is turned slowly from position 3 toward the opposite side.

  • Position 4 (lying on side with contralateral shoulder down, head turned 45° below horizon toward contralateral side): The body is rolled so that the shoulders are aligned perpendicularly to the floor, affected ear up. The head is then turned farther so that the nose points 45° below the plane of the horizon. This usually takes another 40 seconds.

  • Position 5 (sitting, head turned at least 90-135° toward contralateral side): The patient is raised back to the sitting position with the head turned away from the affected side.

  • Ending position: Finally, the head is turned back to the midline. The mastoid bone oscillator is turned off, and the headband is removed.

A Dix-Hallpike test is performed immediately following the procedure. If nystagmus is observed, the procedure is repeated. After the procedure, the patient is instructed to avoid agitation of the head for approximately 48 hours while the particles settle and to return in 1 week for a follow-up examination.

The previously mentioned literature review by Anagnostou et al indicated that the anterior canal variant of BPPV can be successfully treated with the Epley and Yacovino maneuvers, as well as with various nonstandard maneuvers. The study, which included 31 citations, found a success rate of over 75% for each of these three types of maneuvers.[1]

Surgical Care

Surgery is usually reserved for those in whom CRP fails. It is not a first-line treatment because it is invasive and holds the possibility of complications such as hearing loss and facial nerve damage. Options include labyrinthectomy, posterior canal occlusion, singular neurectomy, vestibular nerve section, and transtympanic aminoglycoside application. All have a high chance of vertigo control.

Complete destruction of the affected inner ear is excessive, considering that only the posterior semicircular canal is involved. Therefore, the authors would not recommend labyrinthectomy or vestibular nerve section, except in the most extreme of cases.

Singular neurectomy, while theoretically a reasonable choice because it is directed at denervation of the offending posterior semicircular canal, is technically difficult and has only been mastered by a handful of surgeons. Furthermore, some of these patients have significant postoperative imbalance issues.

The most viable surgical option for patients who have failed CRP is posterior canal occlusion. The idea is to stop the benign positional vertigo by collapsing the posterior canal, immobilizing the movement of particles through the canal. This procedure is performed through a standard mastoidectomy approach. The offending posterior semicircular canal is isolated. The hard bone is drilled down with diamond burrs to expose the membranous labyrinth without spilling much perilymphatic fluid. The membranous labyrinth containing the endolymphatic fluid is compressed so that the flow of the length is disrupted. This keeps the particles from traveling through the endolymphatic space, thereby stopping the dizziness.

Success rates are in the 95th percentile range. Postoperative imbalance is not uncommon for a few weeks to months. This is typically treated with postoperative vestibular rehabilitation.

Activity

After CRP treatment, patients are instructed to avoid lying completely flat for 24-48 hours. Sleeping with the head elevated on a few pillows is recommended. Avoidance of jarring activities or gymnastic flips is recommended.

A correlation has been demonstrated between the head-lying side during sleep and the side affected by benign paroxysmal positional vertigo. Patients may want to adjust their sleeping positions accordingly to prevent recurrence.[7]

 

Guidelines

Guidelines Summary

In 2017, the American Academy of Otolaryngology-Head and Neck Surgery Foundation (AAO-HNSF)released an update to a 2008 guideline regarding benign paroxysmal positional vertigo (BPPV). The update included recommendations that clinicians do as follows[8, 9, 10] :

  • Diagnose posterior semicircular canal BPPV when vertigo associated with torsional, upbeating nystagmus is provoked by the Dix-Hallpike maneuver, performed by bringing the patient from an upright to a supine position with the head turned 45° to one side, the neck extended 20°, and the affected ear aimed downward
  • Treat, or refer to a clinician who can treat, patients with posterior canal BPPV with a canalith repositioning procedure
  • Not impose postprocedural postural restrictions after canalith repositioning procedure for posterior canal BPPV
  • Perform, or refer the patient to a clinician who can perform, a supine roll test to assess for lateral semicircular canal BPPV if the patient has a history compatible with BPPV and the Dix-Hallpike test results in horizontal or no nystagmus
  • Differentiate, or refer the patient to a clinician who can differentiate, BPPV from other causes of imbalance, dizziness, and vertigo
  • Assess patients with BPPV for factors that modify management, including impaired mobility or balance, central nervous system disorders, a lack of home support, and/or increased risk for falling
  • Reassess patients within 1 month after an initial period of observation or treatment to document resolution or persistence of symptoms
  • Evaluate, or refer to a clinician who can evaluate, patients with persistent symptoms for unresolved BPPV and/or underlying peripheral vestibular or CNS disorders
  • Educate patients regarding the impact of BPPV on their safety, the potential for disease recurrence, and the importance of follow-up
  • Not perform radiographic imaging in a patient who meets diagnostic criteria for BPPV in the absence of additional signs and/or symptoms inconsistent with BPPV that warrant imaging
  • Not perform vestibular testing in a patient who meets diagnostic criteria for BPPV in the absence of additional vestibular signs and/or symptoms inconsistent with BPPV that warrant testing
  • Not routinely treat BPPV with vestibular suppressant medications such as antihistamines and/or benzodiazepines
 

Medication

Medication Summary

Vestibulosuppressant medication can be used to mitigate the severity of vertigo. Unfortunately, many times it is not effective and only masks the problem. Adverse effects of grogginess and sleepiness are also possible.

Although steroids have some beneficial effects in acute vertigo syndromes such as Ménière disease, they seem to have no value in the treatment of benign paroxysmal positional vertigo (BPPV).

 

Follow-up

Complications

Serious complications of canalith repositioning procedure (CRP) are rare.

  • Nausea/vomiting: This is usually not a problem if the procedure is performed slowly with mastoid oscillation. In severely symptomatic or anxious patients, premedication with diazepam (Valium) or prochlorperazine (Compazine) may be used.

  • Failure: Although rare, failure can occur in approximately 3-15% of patients (depending upon the series). If no effect is observed, the recommendation is to repeat the procedure. If not successful, investigate other diagnoses. Residual BPPV usually means that purging of canalithiasis was not complete; therefore, repeat the procedure.

  • Worse vertigo afterward: In the event of worsened vertigo after CRP, consider differential diagnoses as follows:

    • Canal jam occurs when the bolus of canalithiasis becomes stuck at the relatively narrower distal canal (near the apex area). Patients become vertiginous upon moving between position 5 and position 6. The recommendation is to reverse CRP back to position 3 in an attempt to unjam the canaliths.

    • Symptoms of contralateral BPPV or other forms of BPPV occur when the bolus of canaliths becomes sidetracked into another SCC. Involvement of the SCC mimics BPPV of the contralateral PSC. The topic of other canal involvement and cupulolithiasis treatment can be quite complex and is beyond the scope of this chapter.

    • Dispersion is possible. Possibly, once shaken, the canaliths are suspended into solution much like dirt in muddy water. As long as they remain suspended, the patient has no symptoms. When the canaliths finally settle, the vertigo can return.

Prognosis

Prognosis following CRP is usually good. Spontaneous remission can occur within 6 weeks, although some cases never remit. Once treated, the recurrence rate is 10-25%.

A retrospective study by Picciotti et al indicated that in individuals who have experienced BPPV, the risk of recurrence is higher in female patients, older patients, and patients with comorbidities (particularly psychiatric disorders). The persistence rate was significantly higher in persons with posttraumatic BPPV (45.2%) than in those with nontraumatic BPPV (20.5%). The study included 475 patients, including 139 (29.3%) with recurrence of BPPV.[11]

A retrospective study by Tan et al indicated that patients with hypertension comorbid with BPPV have a greater BPPV recurrence rate than do those with idiopathic BPPV.[12]

Patient Education

For patient education resources, see the Brain and Nervous System Center, as well as Benign Positional Vertigo, Vertigo, and Dizziness.

 

Questions & Answers

Overview

What is the prevalence of benign paroxysmal positional vertigo (BPPV)?

What is the historical history of benign paroxysmal positional vertigo (BPPV)?

What is benign paroxysmal positional vertigo (BPPV)?

How are the canalithiasis and cupulolithiasis forms of benign paroxysmal positional vertigo (BPPV) defined?

How is classic benign paroxysmal positional vertigo (BPPV) characterized?

How is nystagmus characterized in benign paroxysmal positional vertigo (BPPV)?

What is the standard clinical test for benign paroxysmal positional vertigo (BPPV)?

How is the Dix-Hallpike maneuver performed in the evaluation of benign paroxysmal positional vertigo (BPPV)?

What are the treatment options for benign paroxysmal positional vertigo (BPPV)?

What is the role of surgery in the treatment of benign paroxysmal positional vertigo (BPPV)?

What is the pathophysiology of vertigo?

What is the cupulolithiasis theory of the pathogenesis of benign paroxysmal positional vertigo (BPPV)?

What is the canalithiasis theory of the pathogenesis of benign paroxysmal positional vertigo (BPPV)?

What is the prevalence of benign paroxysmal positional vertigo (BPPV) in the US?

What are the racial predilections o benign paroxysmal positional vertigo (BPPV)?

How does the prevalence of benign paroxysmal positional vertigo (BPPV) vary by sex?

What are the age predilections of benign paroxysmal positional vertigo (BPPV)?

Presentation

What are the signs and symptoms of benign paroxysmal positional vertigo (BPPV)?

Which physical findings are characteristic of benign paroxysmal positional vertigo (BPPV)?

How is the Dix-Hallpike maneuver performed, and which findings indicate benign paroxysmal positional vertigo (BPPV)?

What do nystagmus findings indicate in the evaluation of benign paroxysmal positional vertigo (BPPV)?

What is the most effective positioning test for diagnosing lateral canal benign paroxysmal positional vertigo (BPPV)?

What are the risk factors for benign paroxysmal positional vertigo (BPPV)?

What is the role of dental procedures in the etiology of benign paroxysmal positional vertigo (BPPV)?

What is the role of migraine headache in the etiology of benign paroxysmal positional vertigo (BPPV)?

What are the risk factors for recurrent benign paroxysmal positional vertigo (BPPV)?

DDX

Which conditions should be included in the differential diagnoses for benign paroxysmal positional vertigo (BPPV)?

What are the differential diagnoses for Benign Paroxysmal Positional Vertigo?

Workup

What is the role of lab studies in the workup of benign paroxysmal positional vertigo (BPPV)?

What is the role of imaging studies in the workup of benign paroxysmal positional vertigo (BPPV)?

Which tests are performed in the workup of benign paroxysmal positional vertigo (BPPV)?

Treatment

What are the treatment options for benign paroxysmal positional vertigo (BPPV)?

What are the limitations of watchful waiting in the treatment of benign paroxysmal positional vertigo (BPPV)?

What is the role of vestibulosuppressant medication in the treatment of benign paroxysmal positional vertigo (BPPV)?

What is the role of vestibular rehabilitation in the treatment of benign paroxysmal positional vertigo (BPPV)?

What is the role of canalith repositioning (CRP) in the treatment of benign paroxysmal positional vertigo (BPPV)?

What is the efficacy of canalith repositioning (CRP) for the treatment of benign paroxysmal positional vertigo (BPPV)?

Which factors may indicate repeated need for canalith repositioning (CRP) during treatment of benign paroxysmal positional vertigo (BPPV)?

What is the efficacy of multi-axial positioning devices in the treatment of benign paroxysmal positional vertigo (BPPV)?

How is the Epley procedure performed in the treatment of benign paroxysmal positional vertigo (BPPV)?

Which CRP maneuvers are effective in the treatment of benign paroxysmal positional vertigo (BPPV)?

When is surgery indicated in the treatment of benign paroxysmal positional vertigo (BPPV)?

Which surgical procedures are contraindicated for the treatment of benign paroxysmal positional vertigo (BPPV)?

Which is the role of singular neurectomy in the treatment of benign paroxysmal positional vertigo (BPPV)?

What is the role of posterior canal occlusion in the treatment of benign paroxysmal positional vertigo (BPPV)?

What activity modifications are needed following treatment of benign paroxysmal positional vertigo (BPPV)?

Guidelines

What are the AAO-HNSF recommendations for the treatment of benign paroxysmal positional vertigo (BPPV)?

Medications

What are the limitations of medications for the treatment of benign paroxysmal positional vertigo (BPPV)?

What is the role of steroids in the treatment of benign paroxysmal positional vertigo (BPPV)?

Follow-up

What are possible complications of canalith repositioning procedure (CRP) for the treatment of benign paroxysmal positional vertigo (BPPV)?

What is the prognosis of benign paroxysmal positional vertigo (BPPV) following canalith repositioning procedure (CRP)?

What is the risk of recurrence of benign paroxysmal positional vertigo (BPPV)?

What are some patient education resources for benign paroxysmal positional vertigo (BPPV)?