eMedicine Specialties > Neurology > Neuro-otology

Benign Positional Vertigo

Author: John C Li, MD, Private Practice in Otology and Neurotology; Medical Director, Balance Center
Contributor Information and Disclosures

Updated: Apr 27, 2009

Introduction

Background

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 vertigo¹ 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.

Definition

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 eMedicine's article Dizziness, Vertigo, and Imbalance.

Pathophysiology

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.

Frequency

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.

Mortality/Morbidity

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.

Race

Little information has been published concerning racial predilection.

Sex

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

Age

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.

Clinical

History

• 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.

Physical

• 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.

Causes

• 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

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