This article reviews the pathophysiology, diagnosis, and treatment of benign paroxysmal positional vertigo of the posterior and lateral semicircular canals and summarizes the evidence-based outcome data. The authors discuss this common cause of vertigo, its cause and prevalence across the life span, and efficacy of treatment through both physical repositioning maneuvers and surgery.
J.W. is a pleasant, articulate 71-year-old man describing motion-provoked, position-dependent vertigo. He states that his symptoms began suddenly 3 weeks ago after spending 2 days supervising landscapers pruning the trees in his yard looking up for hours. He reports that on rolling over in bed to turn off the alarm clock, he became vertiginous and noted that everything in the room was swirling around. He states that he tried to sit up and call to his wife for help, but fell backward onto the bed feeling very dizzy and disoriented. He indicates that he lay still for a few minutes and the symptoms subsided, only to return when he attempted to sit up again. He indicates that his wife did come to his aid and she noticed that his eyes would “jump around” every time she tried to help him sit up. Later that morning, the symptoms improved and he was able to go about his day, but only if he moved very slowly. He notes that since this time he experiences 15 to 30 seconds of true vertigo when he transitions from sitting to supine positions, rolls onto his right side in bed, or bends over. He denies associated auditory symptoms. He states that his medical history is significant for hypertension, cardiac bypass surgery 8 years ago, high cholesterol, arthritis in his knees and hands, frequent heartburn, and seasonal sinus problems.
Positional vertigo
Benign paroxysmal positional vertigo (BPPV) is one of the most common vestibular disorders with an estimated lifetime prevalence of 2.4% in the general adult population. Of the 5.6 million clinic visits per year in the United States for dizziness, it is estimated that between 17% and 42% of patients with vertigo are diagnosed with BPPV. Although this disorder affects people across their lifespan, it tends to affect individuals aged 50 to 70 years and therefore has some noteworthy societal burdens. For example, it is estimated that $2000 is spent on average to diagnose BPPV and that 86% of patients have interruption in their daily activities and lost work days because of the vertigo symptoms. Furthermore, older patients with BPPV have a greater incidence of falls and impairments to their daily activities. These falls can cause secondary injuries, including hip fractures, and can lead to additional costs from hospital and nursing home admissions. (See article by Barin and Dodson in this publication). Therefore, this disorder affects not only an individual’s quality of life but also the society.
The true incidence and prevalence of BPPV is difficult to accurately estimate. For example, a study in Japan estimated the incidence to be 0.01%, whereas one done in Minnesota estimated it to be 0.06% with an increase of 38% with each decade of life. However, it is likely that these early epidemiologic studies were underestimates because they included only those patients who presented to physicians with their acute vestibular problem and did not include those who never reported to physicians. A recent study in Germany looked at the estimated prevalence and incidence of BPPV in the general adult population. The investigators used a cross-sectional nationally representative survey of the general adult population in Germany and found a prevalence of 2.4% overall with a prevalence of 3.2% in females and 1.6% in males. The 1-year incidence was calculated at 0.6%, which is approximately 10 times higher than earlier estimates. In this study, the 1-year prevalence was also broken down by age. In patients aged 18 to 39 years, the estimated prevalence was 0.5%. From 40 to 59 years of age, the prevalence was 1.7%. Finally, for patients older than 60 years, the estimated prevalence was 3.4%.
BPPV across the lifespan
There are very few published reports of BPPV in patients younger than 18 years. However, one series of case reports by Giacomini and colleagues described 9 patients who developed BPPV after intense physical activity. Of these 9 patients, 7 were younger than 36 years. One 16-year-old girl developed BPPV after an intense dolphin stroke–style swimming activity. She was diagnosed with posterior semicircular canal (PSC) BPPV on the left. Personal communication with Giacinto Asprella-Libonati, MD, in 2010, showed that, in his experience, approximately 1% of BPPV seen per year affects the pediatric population aged 3 to 14 years. He reports that it is important to examine these children within 24 to 48 hours because BPPV was diagnosed in only 25% of those referred by pediatricians. There was a higher spontaneous resolution of BPPV in children, possibly because of their continuous head movements when playing games. PSC-BPPV was the most common form (about 80% of cases), followed by BPPV of lateral semicircular canal (LSC) (20% of cases). The BPPV cases were generally related to recent minor head trauma in the previous 24 to 48 hours (domestic injuries, sports injuries, school injuries, dental care). However, recurrent cases of BPPV usually occurred in children with a family history of migraine. These patients had more episodes of typical BPPV not preceded by head injury with involvement of multiple channels (LSC and PSC) in subsequent episodes. (Giacinto Asprella-Libonati, MD, Italy, personal communication, August 2010).
In the authors’ experience with adults aged 18 to 39 years, risk factors for BPPV include certain activities such as yoga, pounding activities such as running on pavement, working underneath objects such as cars, and repetitively reaching high up, as would be common for ceiling painters. Giacomini and colleagues also found that activities such as intense aerobic exercise, jogging, running on the treadmill, and swimming caused BPPV in this age group.
Finally, common causes of BPPV in people older than 40 years include head trauma or association with other ear disorders such as vestibular neuritis or labyrinthitis. As with the 18- to 39-year-olds, certain positions are most likely to provoke vertigo, including lying back in bed, arising quickly, looking up, or reclining for dental or hairdressing procedures.
Recent work has suggested a correlation of recurrent episodes of positional vertigo with migraine, and because migraine is more prevalent in females, it may be a factor in the higher prevalence of BPPV in females. Migraine-associated vertigo may cause episodic positional nystagmus that is difficult to differentiate from BPPV. The short duration of episodes (1 to 2 days) and frequent recurrence in otherwise healthy young patients with a history of migraine meeting the International Headache Society criteria often aid in making this diagnosis. Repositioning maneuvers are usually not effective in migraine-associated vertigo. Positional vertigo nystagmus during migraine-associated vertigo attacks may also appear atypical or have central features.
BPPV across the lifespan
There are very few published reports of BPPV in patients younger than 18 years. However, one series of case reports by Giacomini and colleagues described 9 patients who developed BPPV after intense physical activity. Of these 9 patients, 7 were younger than 36 years. One 16-year-old girl developed BPPV after an intense dolphin stroke–style swimming activity. She was diagnosed with posterior semicircular canal (PSC) BPPV on the left. Personal communication with Giacinto Asprella-Libonati, MD, in 2010, showed that, in his experience, approximately 1% of BPPV seen per year affects the pediatric population aged 3 to 14 years. He reports that it is important to examine these children within 24 to 48 hours because BPPV was diagnosed in only 25% of those referred by pediatricians. There was a higher spontaneous resolution of BPPV in children, possibly because of their continuous head movements when playing games. PSC-BPPV was the most common form (about 80% of cases), followed by BPPV of lateral semicircular canal (LSC) (20% of cases). The BPPV cases were generally related to recent minor head trauma in the previous 24 to 48 hours (domestic injuries, sports injuries, school injuries, dental care). However, recurrent cases of BPPV usually occurred in children with a family history of migraine. These patients had more episodes of typical BPPV not preceded by head injury with involvement of multiple channels (LSC and PSC) in subsequent episodes. (Giacinto Asprella-Libonati, MD, Italy, personal communication, August 2010).
In the authors’ experience with adults aged 18 to 39 years, risk factors for BPPV include certain activities such as yoga, pounding activities such as running on pavement, working underneath objects such as cars, and repetitively reaching high up, as would be common for ceiling painters. Giacomini and colleagues also found that activities such as intense aerobic exercise, jogging, running on the treadmill, and swimming caused BPPV in this age group.
Finally, common causes of BPPV in people older than 40 years include head trauma or association with other ear disorders such as vestibular neuritis or labyrinthitis. As with the 18- to 39-year-olds, certain positions are most likely to provoke vertigo, including lying back in bed, arising quickly, looking up, or reclining for dental or hairdressing procedures.
Recent work has suggested a correlation of recurrent episodes of positional vertigo with migraine, and because migraine is more prevalent in females, it may be a factor in the higher prevalence of BPPV in females. Migraine-associated vertigo may cause episodic positional nystagmus that is difficult to differentiate from BPPV. The short duration of episodes (1 to 2 days) and frequent recurrence in otherwise healthy young patients with a history of migraine meeting the International Headache Society criteria often aid in making this diagnosis. Repositioning maneuvers are usually not effective in migraine-associated vertigo. Positional vertigo nystagmus during migraine-associated vertigo attacks may also appear atypical or have central features.
Pathophysiology of BPPV
Regardless of age, the pathophysiology of BPPV does not change. It is likely caused by otoconia that fall into the PSC or LSC after detaching from the utricle. The reasons for detachment are many but include increasing age, trauma, and infection. Schuknecht was the first to suggest that these basophilic deposits on the cupula of the posterior canal caused BPPV. However, further work and intraoperative observations suggest that these canaliths are likely to be floating in the PSC or LSC where they render the canal gravitationally sensitive by acting as a plunger.
Approximately 94% of BPPV cases involve the PSC-BPPV. Dix and Hallpike first observed this occurrence in 1952 when they developed the head maneuver that produces the characteristic ipsidirectional torsional nystagmus used to identify BPPV. During this maneuver, the patient’s head is turned 45° to one side while he is seated. The patient is then moved quickly to a supine position with the neck slightly extended and the head remaining turned. The characteristic ipsidirectional torsional nystagmus is seen when the undermost ear is affected. The patient is then brought back up to a sitting position, and the nystagmus is noted to reverse direction as the canaliths fall back into the canal by gravity. The characteristics of the nystagmus include onset after several seconds, a decline after 10 to 30 seconds, and diminished effect with repeated positional testing in the same sitting ( Fig. 1 ). Although the maneuver needs no special equipment, visualization of the nystagmus can be aided by the use of infrared video or optical Frenzel lenses, which eliminate visual fixation.
Lateral (horizontal) canal involvement is the next most common variant of BPPV, constituting between 5% to 15% of BPPV cases. LSC-BPPV was first described by Cipparrone and colleagues and McClure in 1985 and is characterized by nystagmus provoked by supine bilateral head turns with beating toward the undermost ear. The two distinct subtypes of LSC-BPPV based on the direction of horizontal nystagmus during supine head turns are geotropic and apogeotropic. Geotropic LSC-BPPV beats toward the undermost ear on supine positional testing. The horizontal nystagmus has a short latency and prolonged duration with poor fatigability. It is thought to be caused by canaliths moving under the influence of gravity within the long arm of the LSC. This, in turn, causes stimulation of utriculopetal endolymph flow in the supine position with the affected ear down ( Fig. 2 ). Apogeotropic LSC-BPPV is characterized by a similar short latency and prolonged duration horizontal nystagmus, but the direction of beating is away from the undermost ear on supine positional testing. Apogeotropic LSC-BPPV was not reported until later by Pagnini and colleagues and Baloh and colleagues in 1995. Different factors are likely responsible for apogeotropic LSC-BPPV, which includes otoconial debris that adhere to the cupula of the lateral canal causing the cupula to become gravity sensitive (cupulolithiasis) or otoconia trapped in the proximal segment of the lateral canal near the cupula ( Fig. 3 ).
Diagnosis and treatment
Initially, BPPV treatments were exercise based and emphasized compensation and habituation. However, specific canalith repositioning maneuvers based on an improved understanding of the pathophysiology of BPPV have been developed in the last 20 years and are now the standard of treatment, including the maneuvers described by Semont and colleagues, and Epley and the particle repositioning maneuvers for PSC-BPPV, which is a modified Epley maneuver without mastoid vibration ( Fig 4 ). Vestibular suppressant medication is not as effective as repositioning maneuvers and vestibular therapy.
Although Dix-Hallpike positioning is highly effective for diagnosing PSC-BPPV, it lacks sensitivity in LSC-BPPV. For this reason, positional testing should include Dix-Hallpike positioning to head hanging right and left positions and also supine positional testing in the head centered supine, right ear down, and left ear down positions. Dix-Hallpike positional testing was entirely negative in case reports of 2 patients whose horizontal nystagmus with lateral supine head turns reached 12 degrees/second and 16 degrees/second. In 4 other patients, the horizontal nystagmus observed in Dix-Hallpike positions appeared to beat in the contralateral direction to that observed during supine positional testing (1 geotropic and 3 apogeotropic). Furthermore, in most of the other patients, the Dix-Hallpike positioning nystagmus had a lesser velocity than that seen on supine positional testing.
The identification of the involved ear in LSC-BPPV can be especially difficult because the canals are coplanar and nystagmus is seen in both lateral supine positions. Order effect and head tilt may also affect the direction of nystagmus. In geotropic LSC-BPPV, the nystagmus is worse with the affected ear down. Treatment of geotropic LSC-BPV consists of 360° roll maneuvers toward the unaffected ear at 90° increments every 30 to 60 seconds, beginning with the patient in the supine position with the head flexed 0° to 30° and laterally rotated toward the affected ear. The Gufoni maneuver is also highly effective and is performed with the patient beginning in the sitting position, lying quickly to the unaffected side, and then rotating the head 45° downwards, maintaining the position for 2 to 3 minutes, as described by Casani and colleagues.
Treatment of apogeotropic LSC-BPPV consists of a variety of maneuvers because none are universally effective. Identification of the affected ear can be more challenging in apogeotropic LSC-BPPV. Nystagmus is usually worse with the affected ear uppermost, and spontaneous nystagmus is occasionally seen in the supine position, which usually beats toward the involved side. The Lempert 360° roll maneuver toward the unaffected ear may be used first. The modified Gufoni maneuver can also be performed with the patient beginning in the sitting position and lying quickly to the affected side and then rotating the head 45° upwards, maintaining the position for 2 to 3 minutes, as described by Appiani and colleagues. The Vannucchi-Asprella maneuvers are performed with the patient rapidly moving from the sitting to the supine position, then turning the head rapidly to the unaffected side, and returning to sitting position in which the head is then returned to midline. This maneuver is repeated 5 to 8 times in rapid succession.
Finally, anterior semicircular canal BPPV is a controversial entity. Some investigators suggest that the paroxysmal nystagmus has a pure or torsional downbeat component in contrast to that seen with posterior canal involvement, which has a vertical upbeat component. Because the same maneuvers used to treat posterior canal BPPV seem effective for possible anterior canal involvement (although they may be performed on the contralateral side in some reports), the question may have more theoretical than clinical relevance.
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