Neurologic Manifestations of Benign Positional Vertigo

Updated: Jul 23, 2018
Author: John C Li, MD; Chief Editor: Robert A Egan, MD 



Benign paroxysmal positional vertigo (BPPV) is probably the most common single cause of vertigo in the United States. Estimates indicate that at least 20% of all patients who present to the physician complaining of vertigo have benign paroxysmal positional vertigo. However, because benign paroxysmal positional vertigo is misdiagnosed frequently, this figure may not be completely accurate and is probably an underestimation. As benign paroxysmal positional vertigo can occur concomitantly with other inner ear diseases (eg, a patient may have Ménière disease and BPPV concurrently), statistical analysis may be skewed toward lower numbers.

Benign paroxysmal positional vertigo was described first by Ménière in 1921. The characteristic nystagmus and vertigo[1] associated with positioning changes were at that time attributed to the otolithic organs. Dix and Hallpike in 1952 became the namesakes for the provocative positional test still used today to identify benign paroxysmal positional vertigo. They further defined the classic nystagmus and went on to localize the pathology to the affected ear during provocation.


Defining benign paroxysmal positional vertigo is complex because, as our understanding of its pathophysiology has evolved, so has its definition. As more interest is focused on benign paroxysmal positional vertigo, new types of positional vertigo have been discovered. What was previously lumped together as benign paroxysmal positional vertigo is now subclassified on the basis of the offending semicircular canal (posterior semicircular canal vs lateral semicircular canal). These groups are divided further into canalithiasis and cupulolithiasis depending on pathophysiology. Benign paroxysmal positional vertigo is defined as an abnormal sensation of motion that is elicited by certain critical provocative positions. The provocative positions usually trigger specific eye movements (eg, nystagmus). The character and direction of the nystagmus is specific to the part of the inner ear affected and the underlying pathophysiology.

Although some controversy exists regarding the 2 pathophysiologic mechanisms, canalithiasis and cupulolithiasis, agreement is growing that the 2 entities actually coexist and account for different subtypes of benign paroxysmal positional vertigo. However, classic benign paroxysmal positional vertigo is best explained by canalithiasis. In canalithiasis (literally, canal rocks) the particles reside in the canal portion of the semicircular canals (in contradistinction to the ampullary portion). These densities are considered to be free-floating and mobile, and to cause vertigo by exerting a force. Cupulolithiasis (literally, cupula rocks), on the other hand, refers to densities adhering to the cupula of the crista ampullaris. Cupulolith particles reside in the ampulla of the semicircular canals and are not free-floating.

Classic benign paroxysmal positional vertigo is the most common variety of benign paroxysmal positional vertigo. It involves the posterior semicircular canal and is characterized by the following: geotropic nystagmus with the problem ear down, predominantly rotatory, fast phase toward undermost ear, latency (ie, a few seconds), and limited duration.

For related information, see the Medscape Reference article Dizziness, Vertigo, and Imbalance.


To understand the pathophysiology of benign paroxysmal positional vertigo, we must first understand the anatomy and physiology of the semicircular canals. The 3 semicircular canals in each inner ear are oriented in 3 perpendicular planes that mediate spatial orientation. Each canal consists of a tubular arm (ie, crura) that sprouts from a large barrellike compartment similar to how the handle of a coffee mug sprouts from the mug. Each of these arms has a dilated (ie, ampullary) end located near the top or front portion that houses the crista ampullaris (nerve receptors). The crista ampullaris has a saillike tower (the cupula) that detects the flow of fluid within the semicircular canal. For example, 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 ampullipetally). This deflection is translated into a nerve signal, which confirms that the head is rotating to the right.

In simple terms, the cupula acts as a 3-way switch which, 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, Dr Harold Schuknecht proposed the cupulolithiasis (heavy cupula) theory as an explanation for benign paroxysmal positional vertigo. Via photomicrographs, he discovered basophilic particles or densities that were adherent to the cupula. He postulated that the posterior semicircular canal was rendered sensitive to gravity by these abnormal dense particles attached to, or impinging on, the cupula. This 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 prone to moving easily from one side to the other depending on the direction the pole 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 also explains the dizziness when a patient tilts the head backward.

Canalithiasis theory

In 1980, Epley published his canalithiasis theory.[2] He believed that the symptoms of benign paroxysmal positional vertigo were more consistent with free-moving densities (canaliths) in the posterior semicircular canal rather than fixed densities attached to the cupula. While the head is upright, the particles sit in the posterior semicircular canal at the most gravity-dependent position. When the head is tilted back supine, the particles are rotated up to about 90 degrees along the arc of the posterior semicircular canal. 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 (by sitting up again) causes reversal of the cupular deflection and thus dizziness with nystagmus beating in the opposite direction.

This model suggests that the particles behave like 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 the sensation of dizziness. Reversal of the rotation obviously causes reversal of the flow and reversal of the dizziness direction.

As compared with cupular densities, canal densities better explain the delay (ie, latency), transient nystagmus, and reversal on return to upright position. This supports canalithiasis, rather than cupulolithiasis, as the mechanism for classic benign paroxysmal positional vertigo. The canalithiasis theory was corroborated further by Parnes and McClure in 1991 with the discovery and photo documentation of free densities in posterior semicircular canal during surgery.[3]

In summary, classic benign paroxysmal positional vertigo seems to be better explained by the theory of posterior canal canalithiasis than by cupulolithiasis. Particles in the canal take time to start to move, which explains the latency of onset of nystagmus. The particles eventually stop moving once they have gravitated to the most dependent portion of the canal; this explains the "fatigability" of the symptoms. The cupulolithiasis theory does not explain these 2 features. Some particularly unusual cases of nonclassic benign paroxysmal positional vertigo that present with nonfatiguing nystagmus, however, are better explained by the cupulolithiasis theory.



United States

In one study, the age- and sex-adjusted incidence was 64 per 100,000. The incidence of benign paroxysmal positional vertigo in the general population seems to be higher in persons older than 40 years. In a study of a group of elderly patients, the incidence was found to be approximately 8%. Other studies corroborate this finding. However, in the author's experience, the incidence seems to be much higher. This increase may be due to the recent focus in recognition.


Benign paroxysmal positional vertigo is generally not thought of as a life-threatening event. However, it may represent a health hazard, particularly to the elderly population. Estimates suggest that approximately 20% of all falls that result in hospitalization for serious injuries in the elderly are due to vertigo of end-organ origin. A substantial proportion of these end-organ vertigo complaints may be related to benign paroxysmal positional vertigo.

  • The diagnosis of benign paroxysmal positional vertigo depends on taking a careful history. Typically, the vertigo is frank rotatory vertigo; it most commonly occurs when the patient is in bed and rolls from one side to the other or changes positions of the head in the yaw plane, as in looking up at the showerhead or reaching upward for an object placed on a high shelf while standing on a ladder. The vertigo lasts for only seconds. Most conspicuously, neurologic signs are absent; the patient should be questioned about the following: weakness, numbness, sensory hallucinations, amaurosis fugax, and syncope. If any of these are present, the differential diagnosis broadens to include cerebrovascular insufficiency, vertebrobasilar insufficiency, and cardiac rhythm disorders.

  • Treatment of benign paroxysmal positional vertigo is primarily through the Epley maneuver. Less than 1% of patients have persistent, or recurrent, incapacitating vertigo due to benign paroxysmal positional vertigo, and in these situations surgery may be offered for relief of symptoms. This surgery involves sectioning the semicircular canals under appropriate conditions and has a high risk for sensorineural hearing loss.


Little information has been published concerning racial predilection.


The sexual distribution is approximately equal between men and women, although some studies show a slight predilection for women (64%).


Benign paroxysmal positional vertigo seem to have a predilection for the older population, with the average age of onset 51 years. It is rarely seen in persons younger than 35 years without a history of antecedent head trauma.




Benign paroxysmal positional vertigo typically has a sudden onset. Many patients wake up with it, noticing the vertigo while trying to sit up suddenly. Thereafter, propensity for positional vertigo may extend for days to weeks and occasionally to months or years. In many, the symptoms periodically clear and then recur.

The severity covers a wide spectrum. In extreme cases, the slightest head movement may be associated with nausea and vomiting. In other cases, despite significant nystagmus, the patient seems relatively unfazed.

People who have benign paroxysmal positional vertigo do not usually feel dizzy all the time. Severe dizziness occurs when head movements trigger the attack. At rest and between episodes, patients usually have few or no symptoms.

However, some patients complain of an incessant foggy or cloudy sensorium.

Classic benign paroxysmal positional vertigo usually is triggered by the sudden action of moving from the erect position to the supine position while angling the head 45 degrees toward the side of the affected ear. Merely being in the provocative position is not enough to trigger an attack. The head must actually move to the offending position. After reaching the provocative position, the person experiences a lag period of a few seconds before the vertigo strikes again.

When benign paroxysmal positional vertigo is triggered, patients feel as though they are suddenly thrown into a rolling spin, toppling toward the side of the affected ear. The symptoms start very suddenly and usually dissipate within 20-30 seconds. This sensation is triggered again upon sitting erect; however, the direction of the nystagmus is reversed.


The physical examination findings in patients afflicted with benign paroxysmal positional vertigo are generally unremarkable. With one exception, the Dix-Hallpike maneuver, the entire neuro-otologic examination findings may be normal. However, the presence of neuro-otologic findings does not preclude the diagnosis of benign paroxysmal positional vertigo.

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

This test is done by moving the patient rapidly from a sitting to a supine position with the head turned 45 degrees to the right. After waiting for about 20–30 seconds, the patient is returned to the sitting position. If no nystagmus is seen, the procedure is then repeated on the left side.

Dix-Hallpike tips:

  • Do not turn head to 90 degrees as it can produce an illusion of bilateral involvement.

  • Tailor the briskness of the test to the individual patient. Sudden vigorous movements may be harmful to older patients with frail necks. Severely affected individuals can be tested slowly.

  • The Epley modification, performed from behind the patient, is easier; the outer canthus can be pulled superolaterally to visualize the eyeball rotation.

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

  • Classic posterior semicircular canal benign paroxysmal positional vertigo produces geotropic rotatory nystagmus. The top pole of the eyes rotates toward the undermost (ie, affected) ear.

  • Purely horizontal nystagmus would indicate horizontal canal involvement.

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


One of the most common causes of benign paroxysmal positional vertigo is head trauma. Although the true mechanisms are not exactly certain, the concussive forces presumably cause particles that reside in the vestibule to become displaced to the canal. Other factors that predispose individuals to benign paroxysmal positional vertigo include inactivity, acute alcoholism, major surgery, and CNS disease.

Many patients have concomitant ear pathology, which underscores the importance of a complete neuro-otologic examination.

The frequencies of various causes are as follows:

  • 39% idiopathic

  • 21% trauma

  • 29% ear diseases

  • 9% chronic otitis media

  • 7% vestibular neuronitis

  • 7% Ménière disease

  • 4% otosclerosis

  • 2% sudden sensorineural hearing loss

  • 11% CNS disease

  • 9% vertebrobasilar insufficiency

  • 2% acoustic neuroma

  • 2% cervical vertigo



Diagnostic Considerations

The differential diagnosis of benign paroxysmal positional vertigo can be divided into 3 main areas of pathology—labyrinthine, vestibular nerve, and central. These are further subdivided as follows:

  • Alcohol intoxication: This can cause positional nystagmus that is persistent in a given position and varies according to the position of the head.

  • Brainstem syndromes

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

  • Cervical disk syndromes

  • Cervical vertigo or head-extension vertigo: A somewhat ill-defined entity of symptoms that arise with head extension, this could be a manifestation of vascular compression (eg, vertebral arteries).

  • Inner ear concussion: This may cause transient positional vertigo and nystagmus, which can be confused with benign paroxysmal positional vertigo.

  • Labyrinthitis: The nystagmus is spontaneous, persistent, predominantly linear-horizontal, and minimally affected by head position. Caloric testing often reveals unilateral hypofunction.

  • Ménière disease: Chronic benign paroxysmal positional vertigo is misdiagnosed most frequently as Ménière disease because patients fail to recognize the positional provocation. Benign paroxysmal positional vertigo can occur concomitantly with Ménière disease, thus increasing the diagnostic difficulty. Furthermore, some evidence suggests that Ménière disease may actually cause canaliths to form (unpublished data, personal communications with Gerald Gianoli, MD, Tulane University).

  • Orthostatic hypotension: Low blood volume or poor systemic arterial tone can account for hypoperfusion of the brain and cause dizziness. Symptoms are relieved by lying down and triggered by the sitting position.

  • Positional down-beating nystagmus: This often is associated with a lesion of the nodulus (which normally inhibits vertical vestibulo-ocular reflex gain) from stroke, multiple sclerosis, Arnold-Chiari malformations, cerebral ischemia, cerebellar degeneration, or intoxication.

  • Positional nystagmus of central origin: This is seldom transient, and may be down-beating, whereas benign paroxysmal positional vertigo is usually up-beating. Frequently, other CNS signs are present.

  • Vascular loop syndrome: The diagnostic criteria have been defined poorly. This diagnosis should be considered only after all other possibilities are exhausted. MRI is used to find aberrant loops of the anterior inferior cerebellar artery that may impinge upon the contents of the internal auditory canal.

  • Vertebral artery insufficiency

  • Vestibular neuronitis

Differential Diagnoses



Laboratory Studies

Since the Dix-Hallpike test is pathognomonic, laboratory tests are not required to make the diagnosis of benign paroxysmal positional vertigo. However, keep in mind that since benign paroxysmal positional vertigo is strongly associated with inner ear disease, lab workup might be needed to delineate other associated conditions.

Imaging Studies

If objective abnormalities are confirmed in the general physical or neurologic examination, or clinical history warrants it, strong consideration should be given to obtaining neuroimaging (ie, MRI of the brain) with particular attention to the brain stem and posterior fossa structures.

Other Tests

See the list below:

  • Electronystagmography (ENG): Torsional eye movement cannot be demonstrated directly. Occasionally ENG is helpful in detecting the presence and timing of nystagmus.

  • Caloric test can be normal or hypofunctional (unpublished data, personal communication from Mohammed Hamid, MD).

    • Vestibular response can be reduced secondary to the sluggishness of the particle-laden endolymph.

    • Benign paroxysmal positional vertigo can originate in the ear with an absent caloric response because the nervous and vascular supply to the horizontal canal is separate from that of the posterior semicircular canals.

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

  • Audiogram: Findings may be normal.

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



Medical Care

Since benign paroxysmal positional vertigo is benign and can resolve on its own in weeks to months, the argument has been made that simple observation is all that is needed. However, this involves weeks or months of discomfort and vertigo, with the danger of falls and other accidents or injuries that may arise out of the episodic vertigo spells.

Vestibulosuppressant medications usually do not stop the vertigo. In some cases, they may provide minimal relief; however, they do not solve the problem but only mask it. To complicate matters, they may cause grogginess and sleepiness.

Vestibular rehabilitation is a noninvasive therapy that can achieve success after lengthy periods of time. Unfortunately, it causes repeated stimulation of vertigo while performing the therapeutic maneuvers.

Particle repositioning techniques are represented by 2 major variations that developed simultaneously, yet independently, in the United States and France. These variations are the "Epley Method" and the "Semont Method." 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 more gentle, involving a reclining movement, and is described below. The author favors the Epley maneuver because it seems less violent and more physiologically sensible with respect to the presumed canalithiasis etiology.

Recently, research has been conducted on multiaxial positioning devices that can perform canalith repositioning using 360-degree rotation in the proper plane of the semicircular canals.[4] These automated repositioning chairs can help isolate the problematic semicircular canal, and they can help treat that particular canal without tremendous effect on the other canals. Furthermore, patients are securely fastened to the seats; therefore, they can be rotated more easily and can achieve the appropriate repositioning points better.

The canalith repositioning procedure (CRP) is a simple, noninvasive, office treatment that is designed to actually cure benign paroxysmal positional vertigo in 1–2 sessions (see Media files 1-3).[5, 6, 7, 8, 9, 10] This therapy has enjoyed a success rate greater than 97% for patients with benign paroxysmal positional vertigo.[11, 2] Computer-controlled CRP is also effective for the treatment of posterior canal BPPV, with a success rate similar to those treated with the Epley maneuver, and is safe and easy to perform on patients.[12]

The procedure is conducted as follows:

  • Starting position: Patient is sitting, head turned 45 degrees toward the ipsilateral side.

    • The patient begins the procedure in a sitting position. The head is 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 can move more easily.

  • Position 1: Patient is supine, head turned 45 degrees toward the 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 about 30 seconds.

  • Position 2: Patient is supine, 15 degrees Trendelenburg, head turned 45 degrees toward the ipsilateral side.

    • The patient is reclined further to the Dix-Hallpike position of the affected side. This usually takes 10 seconds longer.

    • Another 20 seconds are spent in that Dix-Hallpike position (affected ear down).

  • Position 3: Patient is supine, 15 degrees Trendelenburg, head turned 45 degrees toward the contralateral side.

    • The patient's head is turned slowly from position 3 toward the opposite side.

  • Position 4: Patient is lying on the side with the contralateral shoulder down, head turned 45 degrees below the horizon toward the contralateral side.

    • The body is rolled so that the shoulders are aligned perpendicular to the floor (ie, affected ear up).

    • The head is turned further so that the nose points 45 degrees below the plane of the horizon. This usually takes another 40 seconds.

  • Position 5: Patient is sitting, head turned at least 90-135 degrees toward the contralateral side.

    • The patient is raised back to the sitting position with the head turned away from the affected side.

  • Position 6: Finally, the head is turned back to the midline. The mastoid bone oscillator is turned off and the headband is removed.

Dix-Hallpike test is done immediately following the procedure. If nystagmus is seen, the procedure is repeated.

After the procedure, the patient is instructed to avoid agitation of the head for about 48 hours while the particles settle, and to return within a week for follow-up examination.

The steps involved in performing left-sided canali The steps involved in performing left-sided canalith repositioning procedure (CRP). The head is positioned 30 degrees toward the affected ear (left ear in this example). Next it is brought gently back to a reclining position. Note how the labyrinthine particles gravitate.
Continuation of the canalith repositioning procedu Continuation of the canalith repositioning procedure (CRP). Once supine, the head is rotated 180 degrees (ie, away from the affected side).
Another view of the canalith repositioning procedu Another view of the canalith repositioning procedure treating the left ear.

Surgical Care

Surgery usually is reserved for those in whom canalith repositioning procedure is not successful. Surgery is not the first line of treatment because it is invasive and carries the possibility of complications (eg, hearing loss, facial nerve damage).

The options, all of which have a high chance of vertigo control, include the following:

  • Labyrinthectomy

  • Posterior canal occlusion

  • Vestibular nerve section

  • Singular neurectomy (ie, selective denervation of the posterior semicircular canal, sparing the other parts of the ear)

Of all of these options, the posterior semicircular canal occlusion seems to be gaining the most favor. This procedure has the capability of hearing preservation, without sacrifice of the entire vestibular system. Only the affected posterior semicircular canal (or horizontal semicircular canal) is ablated. The other semicircular canals, as well as the saccule and utricle, are left intact. This procedure is far easier to perform than the singular neurectomy. Ongoing studies are evaluating its effects. Some have reported 95% improvement.


Otolaryngological consultation should be considered for differentiating the associated inner ear disorders.


After treatment, patients are instructed to avoid lying down 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.



Medication Summary

Generally, medications are not recommended, as they do not seem to help. Supportive medications for vertigo include vestibulosuppressants and antiemetics. Several medications have antivertiginous properties (eg, meclizine, scopolamine, ephedrine, dimenhydrinate, diazepam) and others are useful as antiemetics (eg, promethazine, prochlorperazine). The majority of acute episodes are short-lived and self-limited.


Class Summary

These agents prevent the histamine response in sensory nerve endings and blood vessels. They are effective in treating vertigo.

Meclizine (Antivert, Antrizine, Meni-D)

Decreases excitability of middle ear labyrinth and blocks conduction in middle ear vestibular-cerebellar pathways. These effects are associated with therapeutic effects in relief of nausea and vomiting.

Dimenhydrinate (Dimetabs, Dramamine)

A 1:1 salt of 8 chlorotheophylline and diphenhydramine thought to be useful in treatment of vertigo. Diminishes vestibular stimulation and depresses labyrinthine function through central anticholinergic effects. However, prolonged treatment may decrease rate of recovery of vestibular injuries.


Class Summary

These agents work centrally by suppressing conduction in the vestibular cerebellar pathways.

Scopolamine (Isopto)

Blocks action of acetylcholine at parasympathetic sites in smooth muscle, secretory glands, and CNS. Antagonizes histamine and serotonin action.

Transdermal scopolamine may be most effective agent for motion sickness. Its use in vestibular neuronitis is limited by its slow onset of action.


Class Summary

By binding to specific receptor sites, these agents appear to potentiate the effects of GABA and facilitate inhibitory GABA neurotransmission and other inhibitory transmitters. These effects may prevent vertigo and emesis.

Diazepam (Valium)

Depresses all levels of CNS (eg, limbic and reticular formation), possibly by increasing activity of GABA. Individualize dosage and increase cautiously to avoid adverse effects.


Class Summary

These agents are effective in treating emesis, possibly owing to effects in the dopaminergic mesolimbic system.

Promethazine (Phenergan)

Antidopaminergic agent effective in treating emesis. Blocks postsynaptic mesolimbic dopaminergic receptors in brain and reduces stimuli to brainstem reticular system.

Prochlorperazine (Compazine)

May relieve nausea and vomiting by blocking postsynaptic mesolimbic dopamine receptors, through anticholinergic effects, and by depressing reticular activating system.


Class Summary

These agents may relieve vertigo, possibly through modulating the sympathetic system.

Ephedrine (Pretz-D)

Stimulates release of epinephrine stores, producing alpha- and beta-adrenergic receptors.



Further Inpatient Care

See the list below:

  • Inpatient care usually is not required.

  • Severe cases may require supportive therapy for nausea and vomiting.


See the list below:

  • Complications of canalith repositioning procedure are rare.

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

    • Failure: Although rare, failure is seen in about 3-5% of all patients.

    • No effect: Repeating the procedure is recommended. If it is not successful, other diagnostic possibilities should be considered.

    • Residual benign paroxysmal positional vertigo: This usually indicates that purging of canalithiasis is not complete, so the procedure should be repeated.

  • If vertigo is worse after canalith repositioning procedure, the differential diagnosis is as follows:

    • Canal jam: This occurs when the bolus of canalithiasis gets stuck at the relatively narrower distal canal (near the apex area). Patients experience vertigo when moving between position 5 and position 6. Reversing canalith repositioning procedure back to position 3 is recommended. This attempts to dislodge the canaliths.

    • Symptoms of contralateral benign paroxysmal positional vertigo or other forms of benign paroxysmal positional vertigo: This occurs when the bolus of canaliths gets sidetracked into another semicircular canal. Involvement of the semicircular canal mimics benign paroxysmal positional vertigo of the contralateral posterior semicircular canal.

    • Cupulolithiasis: The loose canal particles get stuck on the cupula and cause a paradoxical nystagmus profile. This type of nystagmus does not fatigue easily, and can beat in the opposite direction. These particles have to be shaken loose, converted back to canal particles, and then repositioned properly.

    • Dispersion: Once shaken, canaliths conceivably are suspended into solution much like dirt in muddy water. As long as they remain suspended, the patients have no symptoms. When they finally settle, the vertigo can return.


See the list below:

  • Prognosis is usually good.

  • Spontaneous remission can occur within 6 weeks, although some cases never remit.

  • Once treated, benign paroxysmal positional vertigo recurrence rate is between 5% and 15%.

Patient Education

See the list below:

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