Benign paroxysmal position vertigo (BPPV) is a peripheral perception of motion in the absence of movement disorder characterized by a brief, sensation of swaying, tilting, spinning, or feeling unbalanced current bouts of vertigo characteristic vertigo and nystagmus associated with postural changes were linked to the otolithic organs. Individuals often feel as if the room is moving or spinning and they can lose their balance and have difficulty standing or walking. During the vertigo spells, affected individuals often have abnormal eye movements as well (nystagmus). BPPV is most often triggered by changes in head position. The severity of the disorder varies. In some people, it only causes mild symptoms, while in others it can potentially cause more severe, even debilitating symptoms. BPPV may disappear but sometimes it persists recurrently for many months. Most affected individuals can be easily and effectively treated by non-invasive methods such as canalith (or sialolith) repositioning maneuvers. However, BPPV may recur even after being effectively treated. BPPV is believed to be caused by the displacement of small calcium carbonate crystals within the inner ear. These tiny crystals originate from the gravity and acceleration sensing structures and become inappropriately located in one of three semicircular canals, which are tiny, interconnected, looped tubes that serve to detect movements of the head and play a role in helping the body maintain balance. The exact, underlying cause of this displacement is not always known (idiopathic). Recurrences are possible because additional calcium can become dislodged. The treatment maneuvers move the calcium particles back to the main vestibule, the chamber from which they originated. This stops vertigo. However, the maneuvers do not prevent the shedding of additional calcium crystals in the future.
Benign paroxysmal positional vertigo is a common disorder of the inner ear that should be suspected in all patients with a history of positionally provoked vertigo. The condition appears to be caused by free-floating debris in the posterior semicircular canal.
Introduction
BPPV has been identified as a clinical entity since the late 1800s. The term benign means that the disorder is not progressive and is not considered serious. Although labeled benign, BPPV can disrupt a person’s daily activities and affect the quality of life. The term paroxysmal means that episodes arise suddenly and often unpredictably. The term positional means the disorder is contingent on a change of the position of the head. BPPV is one of the most common causes of vertigo.
Symptoms
The onset of an episode of BPPV is usually sudden following changes in head position. Often, ordinary movements such as turning over on one’s side, lying down, looking up, stooping, or bending over can cause an episode. The severity of the disorder can vary greatly from one person to another. Factors that may affect the severity include the speed of head movement, the volume of calcium crystals that are moved, and a person’s innate sensitivity to motion. For some people, only a slight positional change of the head can cause symptoms. In such cases, this extreme sensitivity can cause near frequent sensations of tilting or dizziness. In other individuals, the disorder may only produce mild symptoms despite a rapid change of head position. In some affected individuals, symptoms may only be caused by very precise, specific movements. The duration of symptoms of BPPV may also vary and can potentially persist recurrently for days, weeks, or months or become recurrent over many years.
Vertigo in individuals with BPPV usually lasts less than 30 seconds. Vertigo can lead to unsteadiness and a loss of balance. Additional symptoms can develop including lightheadedness, dizziness, nausea, vomiting, and blurred vision. Nausea or a feeling of queasiness can persist for a short time even after the sensation of vertigo has passed.
A common associated finding with BPPV is nystagmus, an eye movement disorder characterized by rapid, involuntary movements of the eye. The eyes may be described as jumping or twitching in certain directions. Nystagmus associated with BPPV is fatigable meaning that if one repeats the position change that induced original vertigo and nystagmus after time nystagmus lessens in severity.
The type of nystagmus, defined by the direction of the abnormal eye movements, depends upon which of the three semicircular canals of the inner ear is involved. The three canals are known as the posterior, horizontal (lateral), and anterior (superior) canals. Thus BPPV can be classified as posterior canal BPPV, horizontal canal BPPV or anterior canal BPPV based on the specific canal involved. Most cases of BPPV involve the posterior canal which accounts for around 80% of cases.
Causes
Benign paroxysmal positional vertigo occurs due to the displacement of calcium-carbonate crystals or otoconia within the fluid-filled semicircular canals of the inner ear. These otoconia are essential to the proper functioning of the utricle of the otolithic membrane by helping deflect the hair cells within the endolymph, which relays positional changes of the head, including tilting, turning, and linear acceleration.[rx]
Approximately 50% to 70% of BPPV cases occur with no known cause and are referred to as primary or idiopathic BPPV.[rx] The remaining cases are called secondary BPPV and are often associated with an underlying pathology, such as head trauma, vestibular neuronitis, labyrinthitis, Ménière disease, migraine, ischemia, and iatrogenic causes. The commonest cause of secondary BPPV is a head injury, accounting for 7% to 17% of BPPV cases.[rx][rx] Trauma to the head may lead to the release of many otoconia into the endolymph; perhaps that is why most of these patients have bilateral BPPV. Viral labyrinthitis or vestibular neuronitis accounts for up to 15% of BPPV cases.
In some patients, the exact underlying cause of BPPV is unknown. Researchers believe that most cases of BPPV are caused by abnormalities affecting the inner ear. The inner ear contains the cochlea, which converts sound pressure from the outer ear into nerve impulses that are sent to the brain via the auditory canal. The inner ear also contains a vestibular apparatus for balance that includes the semicircular canals. Fluid moves through these canals enabling the brain to detect turning movements of the head.
Two additional structures found in the inner ear are the utricle and saccule (otolith organs). The utricle and saccule are fluid-filled sacs or cavities that detect acceleration movements of the head including gravity. The utricle and saccule contain small calcium carbonate crystals. For unknown reasons, in individuals with BPPV, these crystals may partially erode and small pieces of the crystals fall off and end up in one of the adjoining semicircular canals. Within the canals, these crystals may stimulate a specialized sensing organ of the inner ear tubes that are called the cupula. This results in the body being sensitive to certain head position changes that normally would not cause dizziness. The brain is sent powerful asymmetric nerve signals that resemble the kind of asymmetry associated with spinning. This gives a patient the same sensation that would occur with spinning.
Two specific theories proposed regarding the underlying cause of BPPV are the canalithiasis and cupulolithiasis theories. These proposed mechanisms are not mutually exclusive and there is scientific evidence that both occur, but that canalithiasis is more common than cupulolithiasis. Canalithiasis refers to calcium crystals that are freely mobile within the semicircular canals and, whenever the head changes position, these crystals move through the canal. As these crystals move, they are believed to drag the fluid within the canals, known as endolymph, behind them. As the endolymph moves through the canals, it stimulates the hair cells of the cupula causing vertigo and nystagmus. When the head is not moving, the crystals (and therefore the endolymph) do not move as well. Consequently, there is no stimulation of the cupula and no associated vertigo or nystagmus. It is believed that these crystals eventually dissolve or fall back into the vestibule (the cavity at the entrance to one of the canals). Canalithiasis appears to best explain most cases of BPPV.
Cupulolithiasis refers to crystals that have become stuck or attached to the cupula in one of the three semicircular canals, usually the posterior canal. BPPV caused by cupulolithiasis is believed to account for the more persistent cases of BPPV that do not respond as well to positioning treatments.
Neither the canalithiasis nor the cupulolithiasis theories address why the crystals become dislodged. There are many different theories as to what conditions can cause crystals to become dislodged and enter the semicircular canals. Such conditions include head trauma, surgery, chronic middle ear infections (otitis media), a severe cold or infection, or vestibular neuritis. There are some possible associations with osteoporosis.
Additional factors that may predispose individuals to BPPV include alcoholism, inactivity, age, and certain central nervous system disorders. In many cases, no such precipitating cause can be identified.
Diagnosis
A diagnosis of BPPV is based upon the identification of characteristic symptoms, detailed patient history, and a thorough clinical evaluation. Affected individuals usually have a history of episodes of vertigo.
History
A detailed history and physical are imperative to evaluating vertigo since differentiating vestibular versus central, potentially life-threatening processes is of critical importance. Ask open-ended questions to obtain the best possible description of symptoms. Ask regarding the timing of symptoms and context, as well as exacerbating and alleviating factors. Inquire about recent viral infections due to association with labyrinthitis and about trauma, recent neurosurgery, and medications that may be ototoxic, as this may suggest an alternate diagnosis.[rx] Relapses are common, so a history of recurrent vertiginous spells suggests BPPV. Due to age-related degeneration of the otolithic membrane, BPPV frequently occurs in the elderly population, though there must be close consideration for central causes of vertigo, which also correlate with increasing age and cerebrovascular disease. Patients with mood disorders have a propensity to develop BPPV.[27]
The severity of each episode covers a wide spectrum. For instance, in extreme cases, even the slightest head movement could result in nausea and vomiting. Patients with BPPV do not have dizziness all the time. The attacks of severe dizziness only occur when there is head movement. Between episodes, patients have few or no symptoms at rest. However, occasionally patients present with the complaint of an ongoing “foggy or cloudy” sensorium.
An episode of BPPV is usually set off by a sudden movement from the erect to the supine position keeping the head at an angle of 45 degrees toward the side of the involved ear. For an episode of BPPV to occur, the head actually must turn to the offending position, and it will not be enough to just be in the provocative position. Once the provocative pose is reached, the symptoms appear after a few seconds. When BPPV gets triggered, patients suddenly feel having been thrown into a rolling spin, tumbling toward the affected ear. The spell is violent at the outset and usually disappears within 20 to 30 seconds. The same spell strikes again upon sitting erect; however, this time, the nystagmus is reversed.
Physical Examination
The physical examination in patients with BPPV is usually unremarkable. The Dix-Hallpike maneuver is the only standard clinical test of great clinical significance in BPPV.[rx] The pathognomonic sign of BPPV is the rotatory nystagmus with latency and short duration. However, a negative test does not signify anything except that there is no active canalithiasis at the moment the test is performed.
In the Dix-Hallpike maneuver, the patient is rapidly moved from a sitting to the supine posture with the head turned 45 degrees to the right. After 20 to 30 seconds, the patient is brought back to the sitting position. If there is no nystagmus, the same procedure is repeated on the left side. While performing the Dix-Hallpike maneuver, some important tips to be mindful of are:
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The head should not be turned 90 degrees as this can bring about an illusion of bilateral influence.
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The briskness with which the Dix-Hallpike test is performed should be individualized to each patient.
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The Epley modification – The test should be performed from behind the patient as it is easier to pull the outer canthus in the superolateral direction to observe the eyeball rotation.
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The axis of the nystagmus is near the undermost canthus. It is useful to direct the patient gaze toward the anticipated axis to minimize suppression.
In a study, Yetiser and Ince reported that the most effective way to diagnose lateral canal BPPV was the head-roll maneuver. This was in comparison to the lying-down and head-bending tests. The study found that the head-roll maneuver located 75% of cases with apogeotropic nystagmus and 95.6% of cases with geotropic nystagmus.[rx]
The following are some important points to remember regarding the history and physical examination of the patients with BPPV:
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A central disorder is likely responsible if vertigo has no relation with movements. Labyrinthitis or vestibular neuronitis may mimic BPPV; however, unlike BPPV, movement in any plane can trigger a spell that will usually persist for days.
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BPPV often lasts for more than 30 seconds. In contrast, vertigo associated with other disorders is of longer duration, such as an episode of Meniere disease could last for hours, vestibular neuronitis or viral labyrinthitis persists for days, migraines have a variable duration, and the rest of the central disorders may be constant.
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BPPV has an episodic nature. In posterior canal BPPV, the spells repeat over weeks to months. In lateral or horizontal canal BPPV, the episodes repeat over days to weeks.
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An isolated attack should not be taken as BPPV unless the Dix-Hallpike maneuver is positive.
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Vertigo associated with BPPV is usually intense, specifically in the lateral canal type. If vertigo is mild, other causes, particularly central, should be considered.
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BPPV is sudden in origin, while central causes present gradually.[rx]
Clinical Testing and Work-Up
Affected individuals will undergo a Dix-Hallpike test. During this test, an affected individual sits down, with legs extended, on an examination table. The doctor will rotate the head approximately 30 to 45 degrees and then help the person quickly lie on his or her back (supine position). In individuals with BPPV, this will prompt a characteristic episode of nystagmus and/or vertigo. The timing and appearance of the eye movements will help a physician determine the cause of vertigo. The Dix-Hallpike test can differentiate vertigo caused by a problem in the brain from vertigo caused by a problem in the inner ear. The specific pattern of nystagmus will tell a physician which of the three semicircular canals of the inner ear is involved in an individual case.
When the diagnosis is in doubt, affected individuals may undergo a test such as magnetic resonance imaging (MRI) to rule out other conditions. An MRI uses a magnetic field and radio waves to produce cross-sectional images of particular organs and bodily tissues such as the brain or ear.
In some cases, a physician may use a test called videonystagmography (VNG) or videonystagmography (VNG), which records the voluntary and involuntary movements of the eyes. During this exam, electrodes are placed around the eyes (ENG) or goggles with cameras are placed over the eyes (VNG). Both techniques record eye movements following different stimuli such as staring at a light, moving the head to different positions, and stimulating the inner ear and nearby tissue, usually by cold or warm water (or air). The information can then be analyzed by a computer and this can determine if there is a disturbance in the normal functioning of the inner ear balance.
Treatment
Individuals with BPPV may be treated with canalith repositioning maneuvers, in which the head is put through a series of specific movements designed to shift the crystals (otoliths) out of the semicircular canals and back into the vestibule. Once the crystals are back in the vestibule, they are usually reabsorbed in a matter of days. The maneuvers may need to be repeated. Different maneuvers are required depending upon which of the three semicircular canals is involved. Canalith repositioning maneuvers are often highly effective in treating BPPV, although the condition can recur often within one year. Canalith repositioning maneuvers are initially performed at a physician’s office, but affected individuals may be taught the maneuvers to perform them at home. During therapy, crystals may occasionally move from one semicircular canal to another, which is referred to as a canal switch.
Antihistamines address vertigo by suppressing labyrinth excitability and vestibular end-organ receptors. The antihistamine best supported in the literature for vertigo is meclizine, 25 mg to 100 mg daily.
The Epley maneuver is a common canalith repositioning maneuver. The Epley maneuver is a five-position cycle that is repeated until no signs of nystagmus are observed. Patients are placed in a sitting position on an examination table with their heads turned 45 degrees toward the affected ear. Patients are then tilted back onto the table with their heads hanging off the end. The head is then slowly rotated toward the unaffected ear. Patients are then rolled onto their side and the head is rotated back toward the affected ear. The patient is then brought back to a sitting position. Canalith repositioning maneuvers like the Epley maneuver are relatively simple, non-invasive, and effective therapy for individuals with BPPV. Treatment for right-sided typical BPPV can be viewed on YouTube at: http://www.youtube.com/watch?v=ZqokxZRbJfw. Other canal repositioning maneuvers used to treat individuals with BPPV include the Semont liberatory maneuver and for the less common horizontal canal variant of BPPV, the Lempert or Gufoni maneuver. These maneuvers may have slight variations as well and some of these treatments may be viewed on YouTube at: http://www.youtube.com/watch?v=hq-IQWSrAtM.
Some affected individuals may be referred for vestibular rehabilitation therapy (VRT). VRT is the use of specific exercises that are designed to compensate for inner ear deficiencies. While this technique may coincidentally improve BPPV, it is intended to promote adaptation by the brain to loss of balance function related to the inner ear on one side. A physical or occupational therapist will develop a treatment plan tailored to an individual based upon a thorough examination. Affected individuals will perform a series of exercises or postures that over time will lessen their symptoms. Initially, the exercises may temporarily worsen symptoms. However, if affected individuals persist with their instructions, VRT often leads to a decrease in symptom severity or complete disappearance of symptoms. In some cases, no other therapy is necessary.
Some individuals with BPPV may opt for watchful waiting, meaning not treating the condition and waiting for symptoms to spontaneously resolve. This is the best option for those with recent cervical spine fractures that must remain immobilized while healing, for example. For most people, however, there seems little point in waiting to be treated since treatment is so quick and easy. Furthermore, symptom resolution can take weeks or months in some individuals.
Some affected individuals may receive vestibular suppressant medications (e.g., meclizine or diazepam) that may help relieve certain symptoms of BPPV such as the spinning sensation or nausea. However, drug therapy for BPPV itself is generally ineffective and usually not recommended because canalith repositioning maneuvers are so effective.
Repositioning Maneuvers
The first-line treatment option for posterior canal BPPV is a repositioning maneuver designed to rid the affected semicircular canal of any debris. The repositioning maneuvers are efficacious in improving posterior canal BPPV.[rx][rx] There are some contraindications to their use, such as:
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Severe cervical disease
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Suspected vertebrobasilar disease
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Unstable cardiovascular disease
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High-grade carotid stenosis
There are many variants of PRM, such as the Semont or liberatory maneuver, the Epley maneuver, and the 3-position maneuver.[rx] It has been established through trials that all these maneuvers are highly efficacious. The PRM is like the Epley maneuver, except it is simpler, and sedation or mastoid vibration is not usually necessary.[rx] The PRM and Semont maneuvers are equally efficacious; however, the PRM is more widely used in North America as it is easier for the provider and patient, particularly in overweight and older patients.[rx] Post-maneuver instructions and postural restrictions are not needed.[rx][rx][rx][rx]
In a patient with right-sided BPPV, the Epley procedure will be done as follows:
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Start with the sitting position, and the head is turned in the direction of the affected side. To move the particles, a mastoid bone oscillator is kept behind the affected ear with the help of a headband.
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Position 1 – The patient reclines slowly to the supine position, with head turned 45 degrees to the affected side. The rate is altered to achieve a point of no nystagmus and no symptoms. This usually takes approximately 30 seconds.
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Position 2 – The patient lies supine, 15 degrees Trendelenburg, and head turned 45 degrees toward the affected side. The patient reclines more to the Dix-Hallpike position on the ipsilateral side. It takes around 10 seconds. Then the patient stays in the Dix-Hallpike position for another 20 seconds with the affected ear down.
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Position 3 – The patient lies supine, 15 degrees Trendelenburg, and head turned 45 degrees toward the opposite side. After this, the patient’s head is slowly turned from position 3 to the opposite side.
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Position 4 – The patient lies on the side with the opposite shoulder down, head turned 45 degrees toward the contralateral side. The body is then rolled to bring the shoulders perpendicular to the floor with the affected ear up. Next, the head is turned more so that the nose comes at an angle of 45 degrees below the horizon. This takes 40 seconds more.
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Position 5 – The patient is brought back to the sitting position, and the head is turned away from the affected side.
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Ending position – In the end, the head is brought back to the midline. At this point, the headband and the mastoid bone oscillator are removed.
There are some adverse effects of repositioning maneuvers that the providers should be aware of, such as:
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Conversion of posterior BPPV to a lateral or anterior canal BPPV during a maneuver[rx]
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Emesis[rx]
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Prolonged autonomic dysfunction
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Imbalance
Surgical Treatment
Most patients with BPPV will get better with repositioning maneuvers or resolve completely. However, surgical intervention is reserved for refractory cases. There are two surgical options for BPPV:
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Singular neurectomy
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Posterior canal occlusion
The recommended surgical option is posterior canal occlusion because it has proven to be highly effective and safe.[rx]
In rare cases, individuals with BPPV may be treated with surgery. The frequency of surgery as a treatment for BPPV has dropped in recent years. Surgery for BPPV is reserved for individuals who fail to respond to less invasive treatment options and for whom symptoms are recurrent and problematic (intractable BPPV). The most common procedure used is plugging (occluding) the posterior semicircular canal to prevent crystals from causing deflection and stimulation of the cupula. Canal plugging is used more often in rare cases that require surgical intervention. Surgical therapy is not considered for BPPV except as a last resort.
References
