Benign paroxysmal positional vertigo (BPPV

Background
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 Mnire disease and BPPV at once), statistical analysis may be skewed toward lower numbers. 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 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). 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.

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. [1] 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.

History
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
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.

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% Mnire disease - 7% Otosclerosis - 4% Sudden sensorineural hearing loss - 2% CNS disease - 11% Vertebral basilar insufficiency - 9% Acoustic neuroma - 2% Cervical vertigo - 2%

Differential Diagnoses
Inner Ear, Meniere Disease, Medical Treatment Inner Ear, Meniere Disease, Surgical Treatment Labyrinthitis Ossificans

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
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.

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. o 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. o

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

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

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.[2]

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 Mnire disease, they seem to have no value in the treatment of benign paroxysmal positional vertigo (BPPV).

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: o 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. o 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. o 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%.

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

References
1. Epley JM. New dimensions of benign paroxysmal positional vertigo. Otolaryngol Head Neck Surg. Sep-Oct 1980;88(5):599-605. [Medline]. 2. Shim DB, Kim JH, Park KC, Song MH, Park HJ. Correlation between the head-lying side during sleep and the affected side by benign paroxysmal positional vertigo involving the posterior or horizontal semicircular canal. Laryngoscope. Feb 16 2012;[Medline]. 3. [Guideline] Fife TD, Iverson DJ, Lempert T, Furman JM, Baloh RW, Tusa RJ, et al. Practice parameter: therapies for benign paroxysmal positional vertigo (an evidencebased review): report of the Quality Standards Subcommittee of the American Academy of Neurology. Neurology. May 27 2008;70(22):2067-74. [Medline]. [Full Text]. 4. [Guideline] Bhattacharyya N, Baugh RF, Orvidas L, Barrs D, Bronston LJ, Cass S, et al. Clinical practice guideline: benign paroxysmal positional vertigo. Otolaryngol Head Neck Surg. Nov 2008;139(5 Suppl 4):S47-81. [Medline]. [Full Text]. 5. Epley JM. The canalith repositioning procedure: for treatment of benign paroxysmal positional vertigo.Otolaryngol Head Neck Surg. Sep 1992;107(3):399-404. [Medline]. 6. Fung K, Hall SF. Particle repositioning maneuver: effective treatment for benign paroxysmal positional vertigo. J Otolaryngol. Aug 1996;25(4):243-8. [Medline]. 7. Herdman SJ, Tusa RJ, Zee DS, et al. Single treatment approaches to benign paroxysmal positional vertigo.Arch Otolaryngol Head Neck Surg. Apr 1993;119(4):450-4. [Medline]. 8. Li JC. Mastoid oscillation: a critical factor for success in canalith repositioning procedure. Otolaryngol Head Neck Surg. Jun 1995;112(6):670-5. [Medline]. 9. Li JC, Epley J. The 360-degree maneuver for treatment of benign positional vertigo. Otol Neurotol. Jan 2006;27(1):71-7. [Medline]. [Full Text].

10. Massoud EA, Ireland DJ. Post-treatment instructions in the nonsurgical management of benign paroxysmal positional vertigo. J Otolaryngol. Apr 1996;25(2):121-5. [Medline]. 11. Roberts RA. Efficacy of a new treatment maneuver for posterior canal benign paroxysmal positional vertigo. 12. Roberts RA. Efficacy of a new treatment maneuver for posterior canal benign paroxysmal positional vertigo. 13. Smouha EE, Roussos C. Atypical forms of paroxysmal positional nystagmus. Ear Nose Throat J. Sep 1995;74(9):649-56. [Medline]. 14. Weider DJ, Ryder CJ, Stram JR. Benign paroxysmal positional vertigo: analysis of 44 cases treated by the canalith repositioning procedure of Epley. Am J Otol. May 1994;15(3):321-6. [Medline].

New epidemiological finding on BPPV

J Neurol Neurosurg Psychiatry. 2007 July; 78(7): 663.

H S Cohen
Author information Copyright and License information

Short abstract
In this issue of JNNP, von Brevern and colleagues1 describe an excellent population based survey of benign paroxysmal positional vertigo (BPPV) that represents a turnaround in our understanding of the disorder (see page 710). One hundred years ago, BPPV was unknown; even in the 1950s and 1960s, most specialists were not aware of it (Bobby R Alford, personal communication). The development of noninvasive, easily used and highly effective repositioning exercises and manoeuvres2,3 has prompted increased interest in BPPV. The many papers in the literature since 1990 suggest that the disorder is now widely recognised, which is fortunate because von Brevern et al1 show that BPPV is fairly common in the population. Despite recent advances and increased interest by many investigators, however, questions still remain. von Brevern et al1 describe initial age of onset in middle age and increasing incidence with advancing age, so that the prevalence is high in the elderly population. Their description of a disappointingly low rate of appropriate diagnostic testing and treatment for BPPV indicates the need for better training about vertigo for primary care and specialty physicians, as well as nurse practitioners, occupational therapists and physical therapists who support specialty care practices, particularly practices with older adults. Most studies of BPPV, using convenience samples of patients who present themselves for care at academic medical centres, show approximately twice as

many female as male patients. This might be considered an artefact of the recruitment procedures in clinical studies but for a similar finding by von Brevern et al.1 They suggest that history of migraine, which is also more common in females, explains the finding. Many women do not have migraine but do have BPPV, so other factors are probably involved. Further research is needed to learn why it is more common in women and to elucidate the relationship among comorbid factors and BPPV. The population of patients with BPPV may be composed of several subgroups with different pathophysiologies, such as head trauma, viral labyrinthitis, vestibular neuronitis and age related changes in otoconia,4,5,6 as well as migraine. von Brevern et al1 report previously unknown relationships to hyperlipidaemia, hypertension and stroke. Perhaps some of these comorbid conditions, and others previously reported in the literature, have some common underlying causes. For example, intubation, diabetes and advanced age may all cause microvascular changes that may affect the peripheral vestibular pathways. This important study should spur future research into these problems.

References
1. von Brevern M, Radtke A, Lezius F. et al Epidemiology of benign paroxysmal positional vertigo: a population based study. J Neurol Neurosurg Psychiatry 2007. 78710715.715. [PMC free article][PubMed] 2. Brandt T, Steddin S, Daroff R B. Therapy for benign paroxysmal positioning vertigo, revisited.Neurology 1994. 44796800.800. [PubMed] 3. Cohen H S, Kimball K T. Effectiveness of treatments for benign paroxysmal positional vertigo of the posterior canal. Otol Neurotol 2005. 261034 1040.1040. [PubMed] 4. Baloh R W, Honrubia V, Jacobson K. Benign positional vertigo: clinical and oculographic features in 240 cases. Neurology 1987. 37371378.378. [PubMed] 5. Gacek R R. Pathology of benign paroxysmal positional vertigo revisited. Ann Otol Rhinol Laryngol2003. 112574582.582. [PubMed] 6. Jang Y S, Hwang C H, Shin J Y. et al Agerelated changes on the morphology of the otoconia.Laryngoscope 2006. 1169961001.1001. [PubMed]

BPPV IS THE MOST COMMON VESTIBULAR DISORDER.

Benign paroxysmal positional vertigo (BPPV) is the most common disorder of the inner ears vestibular system, which is a vital part of maintaining balance. BPPV is benign, meaning that it is not life-threatening nor generally progressive. BPPV produces a sensation of spinning called vertigo that is both paroxysmal and positional, meaning it occurs suddenly and with a change in head position.

WHY DOES BPPV CAUSE VERTIGO?

The vestibular organs in each ear include the utricle, saccule, and three semicircular canals. The semicircular canals detect rotational movement. They are located at right angles to each other and are filled with a fluid called endolymph. When the head rotates, endolymphatic fluid lags behind because of inertia and exerts pressure against the cupula, the sensory receptor at the base of the canal. The receptor then sends impulses to the brain about the heads movement. BPPV occurs as a result of otoconia, tiny crystals of calcium carbonate that are a normal part of the inner ears anatomy, detaching from the otolithic membrane in the utricle and collecting in one of the semicircular canals. When the head is still, gravity causes the otoconia to clump and settle (Figure 1). When the head moves, the otoconia shift. This stimulates the cupula to send false signals to the brain, producing vertigo and triggering nystagmus (involuntary eye movements).

Figure 1: Inner ear anatomy. Otoconia migrate from the utricle, most commonly settling in the posterior semicircular canal (shown), or more rarely in the anterior or horizontal semicircular canals. The detached otoconia shift when the head moves, stimulating the cupula to send false signals to the brain that create a sensation of vertigo. Vestibular Disorders Association. Image adapted by VEDA with permission from T. C. Hain.

TYPES OF BPPV
Subtypes of BPPV are distinguished by the particular semicircular canal involved and whether the detached otoconia are free floating within the affected canal (canalithiasis) or attached to the cupula (cupulothiasis). BPPV is typically unilateral, meaning it occurs either in the right or left ear, although in some cases it is bilateral, meaning both ears are affected. The most common form, accounting for 81% to 90% of all cases, is canalithiasis in the posterior semicircular canal.1

SYMPTOMS
In addition to vertigo, symptoms of BPPV include dizziness (lightheadedness), imbalance, difficulty concentrating, and nausea. Activities that bring on symptoms can vary in each person, but symptoms are precipitated by changing the heads position with respect to gravity. With the involvement of the posterior semicircular canal in classic BPPV, common problematic head movements include looking up, or rolling over and getting out of bed.

BPPV may be experienced for a very short duration or it may last a lifetime, with symptoms occurring in an intermittent pattern that varies by duration, frequency, and intensity. It is not considered to be intrinsically life-threatening. However, it can be tremendously disruptive to a persons work and social life, as well as pose a health hazard due to an increased risk of falls associated with dizziness and imbalance.

CAUSES
BPPV is the most common vestibular disorder; 2.4% of all people will experience it at some point in their lifetimes.1 BPPV accounts for at least 20% of diagnoses made by physicians who specialize in dizziness and vestibular disorders, and is the cause of approximately 50% of dizziness in older people. 2 The most common cause of BPPV in people under age 50 is head injury and is presumably a result of concussive force that displaces the otoconia. In people over age 50, BPPV is most commonly idiopathic, meaning it occurs for no known reason, but is generally associated with natural age-related degeneration of the otolithic membrane. BPPV is also associated with migraine3 and ototoxicity. Viruses affecting the ear (such as those causing vestibular neuritis) and Mnires disease are significant but unusual causes. Occasionally BPPV follows surgery as a result of the trauma on the inner ear during the procedure combined with a prolonged supine (laying down face-up) position.4 BPPV may also develop after long periods of inactivity.

Figure 2a: Canalith repositioning procedure (CRP) for right-sided BPPV. Steps 1 & 2 of CRP are identical to the Dix-Hallpike maneuver used to elicit nystagmus for diagnosis. The patient is moved from a seated supine position; her head is then turned 45 degrees to the right and held for 15-20 seconds.

DIAGNOSIS

BPPV is diagnosed based on medical history, physical examination, the results of vestibular and auditory (hearing) tests, and possibly lab work to rule out other diagnoses. Vestibular tests include the Dix-Hallpike maneuver (see Figure 2a) and the Supine Roll test. These tests allow a physician to observe the nystagmus elicited in response to a change in head position. The problematic semicircular canal can be identified based on the characteristics of the observed nystagmus. Frenzel goggles, especially of the type using a TV camera, are sometimes used as a diagnostic aid in order to magnify and illuminate nystagmus.If electronystagmography (ENG) is employed to observe nystagmus with position changes, it is important that the equipment used is capable of measuring vertical eye movements. A physician may also order radiographic imaging such as a magnetic resonance imaging scan (MRI) to rule out other problems such as a stroke or brain tumor, but such scans are not helpful in diagnosing BPPV.5 In addition, a physician may order auditory tests to help pinpoint a specific cause of BPPV, such as Mnires disease or labyrinthitis. Treating BPPV with in-office particle repositioning head maneuvers Recommended treatment for most forms of BPPV employs particle repositioning head maneuvers that move the displaced otoconia out of the affected semicircular canal. These maneuvers involve a specific series of patterned head and trunk movements that can be performed in a health care provi ders office in about 15 minutes.

MANEUVERS FOR POSTERIOR CANAL BPPV

Particle repositioning head maneuvers are considered to be more effective than medication or other forms of exercise-based therapy6 in treating posterior canal BPPV. However, even with successful treatment with such maneuvers, BPPV recurs in about one-third of patients after one year, and in about 50% of all patients treated after five years.7,8,9 The canalith repositioning procedure (CRP) is the most common and empirically proven treatment for posterior canal BPPV.1 Also called the Epley maneuver or the modified liberatory maneuver, CRP involves sequential movement of the head into four positions, with positional shifts spaced roughly 30 seconds apart (Figure 2a and 2b). Differing opinions exist about the benefits of using mastoid vibration during CRP,10 with a recent evidence-based research review suggesting that it probably does not benefit patients.1 Occasionally, when CRP is being performed, neurological symptoms (e.g., weakness, numbness, and visual changes other than vertigo) occur, caused by compression of the vertebral arteries.11 In this case, persisting with the maneuver can lead to stroke.

However, medical professionals can modify the exercises or use special equipment so that the positions are attained by moving body and head simultaneously, thereby avoiding the problematic compression. The Semont maneuver involves a procedure whereby the patient is rapidly moved from lying on one side to lying on the other. Although many physicians have reported success treating patients with the Semont maneuver12 and support its use, more studies are required to determine its effectiveness.1

Figure 2b: Canalith repositioning procedure (CRP) for right-sided BPPV (continued). In Step 3 of the CRP, the head is turned 90 degrees until the unaffected left ear is facing the floor. The patient turns her body to follow her head, and the position is held for 15-20 seconds; afterwards, she returns to a seated position. The mirror image of these maneuvers can be performed for left-sided BPPV.

MANEUVERS FOR HORIZONTAL CANAL BPPV

Because of the relative rarity of horizontal canal BPPV, there are no best practices established for treatment maneuvers; however, the most widely studied is the Lempert maneuver.1 This maneuver entails moving the head through a series of 90 angles and pausing between each turn for 10 to 30 seconds. Other techniques such as the Gufoni maneuver and the Vannucchi-Asprella liberatory maneuver have also been used to treat horizontal canal BPPV, but additional well-supported clinical studies are needed to assess their effectiveness.1

MANEUVERS FOR ANTERIOR CANAL BPPV

There is no definitive treatment for anterior canal BPPV and no controlled studies of it have yet been completed. However, there is a logical modified maneuver for the anterior canal that is essentially a deep (exaggerated) Dix-Hallpike.13 Other proposed treatments employ reverse versions of the maneuvers used for posterior canal BPPV; for example, the reverse Semont (starting nose down and turned to the unaffected side), or the reverse Epley (again starting nose down). These treatments are geometrically reasonable, but require additional study to prove their efficacy.

POST-TREATMENT CONSIDERATIONS

After successful treatment with particle repositioning maneuvers, residual dizziness is often experienced for up to three months. Whether post-treatment activity restrictions are useful has not been adequately studied.1 Nevertheless, many physicians recommend that their patients sleep in an elevated position with two or more pillows and/or not on the side of the treated ear, wear a cervical collar as a reminder to avoid quick head turns, and avoid exercises that involve looking up or down or head rotation (such as freestyle lap swimming). Such precautions are thought to help reduce the risk that the repositioned debris might return to the sensitive back part of the ear before it either adheres or is reabsorbed.

OTHER BPPV TREATMENT OPTIONS

If head maneuvers dont work, other t reatment options include home-based exercise therapy, surgery, medication, or simply coping with the symptoms while waiting for them to resolve.

VESTIBULAR REHABILITATION HOME EXERCISES

Exercises performed at home are sometimes recommended. Brandt-Daroff exercises (Figure 3) involve repeating vertigo-inducing movements two to three times per day for up to three weeks. After receiving training from a doctor or physical therapist, a patient can perform the exercises at home, but they are more arduous than office treatments. With adherence to the prescribed schedule, Brandt-Daroff exercises have been reported to reduce vertiginous responses to head movements in 95% of cases.14 Patients performing Brandt-Daroff exercises may develop multicanal BPPV as a complication and so should note any symptom changes to their physicians. 14 Another home exercise method is daily self-administration of particle repositioning head maneuvers. One potential problem with this method is that it may cause the condition to worsen or initiate problems in another semicircular canal. Although one study15 has reported a cure rate as high as 95% for this strategy, insufficient evidence exists to recommend or refute its use. For horizontal canal BPPV that does not respond to head maneuvers, a home treatment called forced prolonged positioning may be recommended. This requires a patient to rest in bed for at least 12 hours with the head turned toward the unaffected ear, permitting the canaliths to gradually move out of the canal. Finally, some physicians suggest that after office treatment, patients might perform a daily self-canalith repositioning exercise at home to support the treatments continued ffectiveness. However, such home treatment probably does not affect the reoccurrence rate of posterior canal BPPV.16

Figure 3: Brandt-Daroff exercises. The patient sits upright, turns her head 45 degrees to the left, then lies down quickly on her right side for 10 seconds. After returning to an upright seated position, the patient turns her head 45 degrees to the right, lies down quickly on her left side for 10 seconds, then returns to an upright seated position.

SURGERY
If head maneuvers and vestibular rehabilitation exercises are ineffective in controlling symptoms, surgery is sometimes considered. The goal of surgery is to stop the inner ear from transmitting false signals about head movement to the brain. Several surgical approaches are possible; however, a procedure called posterior canal plugging, also called fenestration and occlusion of the posterior canal, is preferable to other methods. These include removing the balance organs with a labyrinthectomy; severing the vestibular portion of the vestibulo-cochlear nerve with a vestibular nerve section, thus terminating all vestibular signals from the affected side; or severing the nerve that transmits signals from an individual canal with a singular neurectomy. Canal plugging stops the movement of particles within the posterior semicircular canal with minimal impact on the rest of the inner ear. This procedure should not be considered until the diagnosis of BPPV is certain and all maneuvers or exercises have been attempted and found ineffective.17 The surgery poses a small risk to hearing; some studies show it to be effective in 85% to 90% of individuals who have had no response to any other treatment,18 although further research is recommended.1

MEDICATION
Motion sickness medications are sometimes helpful in controlling the nausea associated with BPPV and are sometimes used to help with acute dizziness during particle repositioning maneuvers. Otherwise, medications are rarely considered beneficial. Medication that suppresses vestibular function in the long term can interfere with a person making necessary adaptations to symptoms or remaining physically active because of side-effects such as drowsiness. The American Academy of OtolaryngologyHead and Neck Surgery recommends against using vestibular suppressant medications, including antihistamines and benzodiazapines, to control

BPPV.5 Likewise, the American Academy of Neurology reports that there is no evidence supporting the routine use of medication to treat the disorder. 1

WAIT-AND-SEE
Sometimes, adopting a wait-and-see approach is used for BPPV. Physicians often choose to monitor patients with BPPV before attempting treatment because it frequently resolves without intervention.1 This may also be the approach taken with rare variants of BPPV that occur spontaneously or after maneuvers and exercises. Coping strategies during this wait-and-see phase can involve modifying daily activities to help minimize symptoms. For example, this may involve using two or more pillows while in bed, avoiding sleeping on the affected side, and rising slowly from bed in the morning. Other modifications include avoiding looking up, such as at a high cupboard shelf, or bending over to pick up something from the floor. Patients with BPPV are also cautioned to be careful when positioned in a dentists or hairdressers chair, when lying supine, or when participating in sports activities.

FINDING DIAGNOSIS AND TREATMENT FOR BPPV

A list of vestibular disorder specialists is available from on our website. This provider directory is annotated to indicate those specialists who are trained to perform canalith repositioning maneuvers.

ADDITIONAL RESOURCES
Some helpful documents available from VEDA:

Inner Ear Surgeries Meant to Control Vertigo/Disequilibrium Vestibular Rehabilitation: An Effective, Evidenced-Based Treatment References 1. Fife TD, Iverson DJ, Lempert T, Furman JM, Baloh RW, Tusa RJ, Hain TC, Herdman S, Morrow MJ, Gronseth GS. Practice parameter: therapies for benign paroxysmal positional vertigo (an evidencebased review): report of the Quality Standards Subcommittee of the American Academy of Neurology. Neurol. 2008;70:20672074. 2. Froehling DA, Silverstein MD, Mohr DN, Beatty CW, Offord KP, Ballard DJ. Benign positional vertigo: incidence and prognosis in a population-based study in Olmsted County, Minnesota. Mayo Clin Proc. 1991;66(6):596601. 3. 4. Ishiyama A, Jacobson KM, Baloh RW. Migraine and benign positional vertigo. Ann Otol Rhinol Laryngol. 2000;109:377380. Atacan E, Sennaroglu L, Genc A, Kaya S. Benign paroxysmal positional vertigo after stapedectomy. Laryngoscope. 2001;111:12571259.

5.

Bhattacharyya N, Baugh RF, Orvidas L, Barrs D, Bronston L, Cass S, Chalian AA, Desmond AL, Earll JM, Fife TD, Fuller DC, Judge JO, Mann NR, Rosenfeld RM, Schuring LT, Steiner RWP, Whitney SL, Haidari J. Clinical practice guideline: benign paroxysmal positional vertigo. Arch Otolaryngol Head Neck Surg. 2008;139:S47S81.

6. 7. 8. 9.

Herdman SJ, ed. Vestibular Rehabilitation. 3rd ed. Philadelphia: F.A. Davis Co.; 2007. Nunez RA, Cass SP, Furman JM. Short and long-term outcomes of canalith repositioning for benign paroxysmal positional vertigo. Arch Otolaryngol Head Neck Surg. 2000;122:647 652. Sakaida M, Takeuchi K, Ishinaga H, Adachi M, Majima Y. Long-term outcome of benign paroxysmal positional vertigo. Neurol. 2003;60(9):1532 1534. Brandt T, Steddin S, Daroff RB. Therapy for benign paroxysmal positioning vertigo, revisited. Neurol. 1994;44(5):796800.

10. Hain TC, Helminski JO, Reis I, Uddin M. Vibration does not improve results of the canalith repositioning maneuver. Arch Otolaryngol Head Neck Surg. 2000;126:617 622. 11. Sakaguchi M, Kitagawa K, Hougaku H, Hashimoto H, Nagai Y, Yamagami H, Ohtsuki T, Oku N, Hashikawa K, Matsushita K, Matsumoto M and Hori M. Mechanical compression of the extracranial vertebral artery during neck rotation. Neurol. 2003;61(6):845 847. 12. Levrat E, van Melle G, Monnier P, Maire R. Efficacy of the Semont maneuver in benign paroxysmal positional vertigo. Arch Otolaryngol Head Neck Surg. 2003;129(6):629 633. 13. Kim YK, Shin JE, Chung JW. The effect of canalith repositioning for anterior semicircular canal canalithiasis. Otorhinolaryngol Relat Spec. 2005;67:56 60. 14. Hain TC. Home treatment of BPPV: Brandt-Daroff exercises. Available at: www.dizziness-andbalance.com/disorders/bppv/bppv.html#home. Accessed Jan 26, 2009. 15. Radtke A, von Brevern M, Tiel-Wilck K, Mainz-Perchalla A, Neuhauser H, Lempert T. Self-treatment of benign paroxysmal positional vertigo: Semont maneuver vs Epley procedure. Neurol. 2004;63:150 152. 16. Helminski JO, Janssen I, Hain TC. Daily exercise does not prevent recurrence of benign paroxysmal positional vertigo. Otol Neurol. 2008;29(7):976 981. 17. Parnes LS. Update on posterior canal occlusion for benign paroxysmal positional vertigo. Otolaryngol Clin North Am. 1996;29(2):333342. 18. Shaia WT, Zappia JJ, Bojrab DI, LaRouere ML, Sargent EW, Diaz RC. Success of posterior semicircular canal occlusion and application of the dizziness handicap inventory. Otolaryngol Head Neck Surg. 2006;134(3):424430. - See more at: http://vestibular.org/understanding-vestibular-disorders/typesvestibular-disorders/benign-paroxysmal-positional-vertigo#sthash.wzxdjxQU.dpuf