Benign Paroxysmal Positional Vertigo

Padmaja Sudhakar M.B.B.S.
Sachin Kedar M.B.B.S., M.D.

Basic Information

Definition

Benign paroxysmal positional vertigo (BPPV) is a labyrinthine disorder and is the most common cause of vertigo. It is characterized by paroxysms of brief spinning sensation accompanied by nystagmus that usually lasts less than a minute. These paroxysms are generally induced by changes in head position with respect to gravity.

Synonyms

BPPV

ICD-10 CM CODES
H81.1	Benign paroxysmal vertigo

Epidemiology & Demographics

Higher prevalence seen in elderly and women.

Incidence

Incidence increases with advancing age. Unrecognized BPPV can be found in about 10% of certain geriatric populations, and there is a cumulative incidence of nearly 10% by age 80 yr.

Prevalence

Lifetime prevalence is 2.4%. Reported prevalence is 10.7 and 64 cases per 100,000 population. BPPV is by far the most common type of vertigo.

Predominant Sex and Age

Female (2:1 to 3:1 ratio); peak onset: 50-60 years.

Genetics

Unknown

Risk Factors

Head trauma, inner ear surgery, viral labyrinthitis, Ménière’s disease, migraine. The majority are idiopathic.

Physical Findings & Clinical Presentation

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Brief paroxysms of vertigo and nystagmus with certain head positions are seen in 70%.
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Episodes are typically triggered by head position changes such as while getting in or out of bed, rolling over in bed, forward head tilt, or bending forward.
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Episodes are brief, usually lasting 30 to 40 seconds but can recur for several days or months.
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Usually no hearing abnormalities are present.
•

Direction of nystagmus depends on the canal affected with reversal of direction being seen while sitting up, and fatigability with repeated testing.
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Rarely persistent vertigo and disequilibrium may be seen.

Posterior semicircular canal (PSC)

While posterior, horizontal or superior semicircular canal can be affected as isolated or in different combinations, PSC involvement is commonest (60%-90%) and will be discussed in the following sections. Nystagmus is up-beating and torsional and can be elicited by the Dix Hallpike maneuver.

Dix-Hallpike Maneuver

With head turned to one side at an angle of 45 degrees, patient is moved from sitting to supine position with head hanging below the end of the table at an angle of 15-20 degrees. The posterior semicircular canal comes into the sagittal plane and the free floating otolith debris moves down and away from the ampulla. An up-beating and torsional nystagmus will be seen with the top poles of the eye beating towards the lower ear.

Horizontal Semicircular Canal

Involvement may be underestimated as it may remit spontaneously. It produces either geotropic nystagmus beating towards the ground or apogeotropic nystagmus beating towards the ceiling when the head is turned to either side in the supine position. The nystagmus beats stronger towards the affected ear.

Head Roll Test for the Right Horizontal Semicircular Canal (Inducing Geotropic Nystagmus)

Patient is moved from sitting to supine position, then head is rolled 90 degrees to the left. The otolithic debris moves away from the cupula of horizontal semicircular canal, a left beating geotropic nystagmus (towards the ground) is seen. Next the head is turned 90 degrees to the right—a right-beating stronger geotropic nystagmus is seen as otolithic debris moves towards the cupula of the right horizontal semicircular canal.

Supine Head Roll Test for the Right Horizontal Semicircular Canal (Inducing Apogeotropic Nystagmus)

Patient is moved from sitting to supine position, then head is rolled 90 degrees to the left. This induces deflection of the cupula of the right horizontal semicircular canal due to otolithic debris near or attached to the cupula. A strong, right-beating apogeotropic nystagmus (towards the ceiling) is induced. Next, the head is turned 90 degrees in the opposite direction. Now the right horizontal semicircular canal cupula is deflected in the opposite direction and a weak, left-beating apogeotropic nystagmus results.

Anterior Semicircular Canal

Involvement is rare as it is located uppermost in the labyrinth and so otolithic debris is unlikely to become trapped. A downbeat and torsional nystagmus where the top poles of the eye beat towards the lower ear is seen. Evaluating for central lesions is a must in these cases.

Etiology

The fundamental pathologic process is believed to be the movement of otolithic debris in the endolymph of the inner ear. The debris may be present in the cupula (cupulolithiasis) or free floating within the semicircular canal near the cupula (canalithiasis). Static head position changes with respect to gravity, causing the debris to move within the semicircular canal and creating a false sense of rotation.

Diagnosis

Elicitation of a typical nystagmus with Dix-Hall pike is the standard for diagnosing posterior canal BPPV. However, 25% of symptomatic patients may not exhibit nystagmus. Appropriate referral to a neurologist or neuro-otologist should be considered in these cases.

Fig. E1 shows a diagnostic algorithm for vertigo and dizziness.

FIG.E1

Diagnostic algorithm for dizziness and vertigo. *BPPV*, benign paroxysmal positional vertigo.

From Marx JA, et al.: *Rosen’s emergency medicine: concepts and clinical practice*, ed 7, Philadelphia, 2010, Elsevier.

Differential Diagnosis

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Vestibular neuritis
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Vestibular migraine
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Ménière’s disease
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Stroke
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Box 1 lists causes of vertigo with and without hearing loss.
BOX 1Causes of Vertigo With and Without Hearing Loss

Hearing Loss

CONDUCTIVE
1. •
  
  Otitis media with effusion
2. •
  
  Chronic suppurative otitis media or cholesteatoma should be considered
SENSORINEURAL
1. •
  
  Perilymphatic fistula
2. •
  
  Tumor
3. •
  
  Ménière’s disease
4. •
  
  Migraine headache
5. •
  
  Genetic syndromes
6. •
  
  Temporal bone fracture
7. •
  
  Vestibular concussion
No Hearing Loss

ACUTE VERTIGO
1. •
  
  Perilymphatic fistula
2. •
  
  Benign positional vertigo
3. •
  
  Seizure
4. •
  
  Labyrinthitis
RECURRENT OR CHRONIC VERTIGO
1. •
  
  Acoustic neuroma
2. •
  
  Multiple sclerosis
From Marx JA, et al.: Rosen’s emergency medicine: concepts and clinical practice, ed 7, Philadelphia, 2010, Elsevier.

•

Table 1 describes the differential diagnosis of true vertigo.

TABLE1 Differential Diagnosis of Patients with True VertigoFrom Marx JA, et al.: Rosen’s emergency medicine: concepts and clinical practice, ed 7, Philadelphia, 2010, Elsevier.

Cause	History	Associated Symptoms	Physical
Peripheral
1. Benign paroxysmal positional vertigo	Short-lived, positional, fatigable episodes	Nausea, vomiting	Single position can precipitate vertigo. Horizontorotary nystagmus often can be induced at bedside.
2. Labyrinthitis
• Serous	Mild to severe positional symptoms. Usually coexisting or antecedent infection of ear, nose, throat, or meninges	Mild to severe hearing loss can occur	Usually nontoxic patient with minimal fever elevation
• Acute suppurative	Coexisting acute exudative infection of the inner ear. Severe symptoms	Usually severe hearing loss, nausea, vomiting	Febrile patient showing signs of toxicity. Acute otitis media
• Toxic	Gradually progressive symptoms: Patients on medication causing toxicity	Hearing loss that may become rapid and severe, nausea and vomiting	Hearing loss. Ataxia common feature in chronic phase
3. Ménière’s disease	Recurrent episodes of severe rotational vertigo usually lasting hours. Onset usually abrupt. Attacks may occur in clusters. Long symptom-free remissions	Nausea, vomiting, tinnitus, hearing loss	Positional nystagmus not present
4. Vestibular neuronitis	Sudden onset of severe vertigo, increasing in intensity for hours, then gradually subsiding over several days. Mild positional vertigo often lasts weeks to months. Sometimes history of infection or toxic exposure that precedes initial attack. Highest incidence is found in third and fifth decades	Nausea, vomiting. Auditory symptoms do not occur	Spontaneous nystagmus toward the involved ear may be present.
5. Acoustic neuroma	Gradual onset and increase in symptoms. Neurologic signs in later stages. Most occur in women between 30 and 60	Hearing loss, tinnitus. True ataxia and neurologic signs as tumor enlarges	Unilateral decreased hearing. True truncal ataxia and other neurologic signs when tumor enlarges. May have diminution or absence of corneal reflex. Eighth cranial nerve deficit may be present.
Central
1. Vascular disorders
• Vertebrobasilar insufficiency	Should be considered in any patient of advanced age with isolated new-onset vertigo without an obvious cause. More likely with history of atherosclerosis. Initial episode usually seconds to minutes	Often headache. Usually neurologic symptoms including dysarthria, ataxia, weakness, numbness, double vision. Tinnitus and deafness uncommon	Neurologic deficits usually present, but initially neurologic examination can be normal.
• Cerebellar hemorrhage	Sudden onset of severe symptoms	Headache, vomiting, ataxia	Signs of toxicity. Dysmetria, true ataxia. Ipsilateral sixth cranial nerve palsy may be present.
• Occlusion of posterior inferior cerebellar artery (Wallenberg’s syndrome)	Vertigo associated with significant neurologic complaints	Nausea, vomiting, loss of pain and temperature sensation, ataxia, hoarseness	Loss of pain and temperature sensation on the side of the face ipsilateral to the lesion and on the opposite side of the body, paralysis of the palate, pharynx, and larynx. Horner’s syndrome (ipsilateral ptosis, miosis, and decreased facial sweating)
• Subclavian steal syndrome	Classic picture is syncopal attacks during exercise, but most cases present with more subtle symptoms.	Arm fatigue, cramps, mild light-headedness may be only other symptoms than vertigo	Diminished or absent radial pulses in affected side or systolic blood pressure differentials between the two areas occur in most patients.
2. Head trauma	Symptoms begin with or shortly after head trauma. Positional symptoms most common type after trauma. Self-limited symptoms that can persist weeks to months	Usually mild nausea	Occasionally, basilar skull fracture
3. Neck trauma	Usual onset 7–10 days after whiplash injury. Symptoms may last weeks to months. Episodes seconds to minutes when turning head	Neck pain	Neck tenderness, pain on movement, and positional nystagmus and vertigo when head is turned to side of the whiplash
4. Vertebrobasilar migraine	Vertigo almost always followed by headache. Patient has usually had similar episodes in past. Most patients have a family history of migraine. Syndrome usually begins in adolescence	Dysarthria, ataxia, visual disturbances, or paresthesias usually precede headache	No residual neurologic or otologic signs are present after attack.
5. Multiple sclerosis	Vertigo presenting symptoms in 7%–10% and appears in the course of the disease in a third. Onset may be severe and suggest labyrinth disease. Disease onset usually between ages 20 and 40. Often history of other attacks with varying neurologic signs or symptoms	Nausea and vomiting, which may be severe	May have horizontal, rotary, or vertical nystagmus. Nystagmus may persist after the vertiginous symptoms have subsided. Bilateral internuclear ophthalmoplegia and ataxic eye movements suggest multiple sclerosis.
6. Temporal lobe epilepsy	Can be initial or prominent symptom in some patients with the disorder	Memory impairment, hallucinations, trancelike states, seizures	May have aphasia or convulsions
7. Hypoglycemia	Should be considered in diabetics and any other patient with unexplained symptoms	Sweating, anxiety	Tachycardia, mental status change may be present.

Workup

None; BPPV is a clinical diagnosis

Imaging Studies

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To be obtained only when stroke remains high in the differential diagnosis.

Treatment

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BPPV usually resolves without treatment in 2 to 4 weeks. Recurrences are common in the first year, and long-term recurrence rates range from 30% to 50%.
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Nausea and vomiting may be treated symptomatically with medications.
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Canalith repositioning maneuvers (Epley’s and Semont’s maneuvers for the posterior canal) are effective. They are designed to “flush” otolithic debris out of the semicircular canals into the vestibule where they are resorbed. Epley’s maneuver for BPPV of the posterior canal is recommended as standard of care by the American Academy of Neurology and American Academy of Otolaryngology-Head and Neck Surgery. When patients do not respond, it may be related to the technique, or they may be refractory. There is no clear consensus on how many times the maneuver should be performed at a single visit. Many prefer to do it two or three times if nystagmus is still present with the second maneuver. Other maneuvers such as Barbecue, Vannucchi, and Gufoni are used to reposition debris in the horizontal semicircular canal and will not be discussed here.

Epley’s Maneuver

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Head is turned 90 degrees towards unaffected side. The head and trunk are then turned an additional 90 degrees in the same direction, so that the patient lies on the unaffected side with head pointing towards the floor. The otolithic debris moves in the same direction, producing a brief nystagmus. The patient is then moved to a sitting position, which allows the debris to fall out of the canal into the utricle through the common crus.
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Each position should be maintained for 30 seconds or until the nystagmus or vertigo resolves. Sometimes nystagmus in the opposite direction is seen. It is prudent for patients to sit still in the upright position for about 15 minutes and then to walk cautiously.

Nonpharmacologic Therapy

Transection of the ampullary nerve (singular nerve) and plugging of the involved canal are rarely performed for intractable and treatment-resistant cases.

Acute General Rx

Canalith repositioning

Chronic Rx

If multiple treatments are needed, patients should be instructed to perform the maneuvers at home.

Referral

To a neuro-otologist, otolaryngologist, neurologist

Pearls & Considerations

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BPPV is a benign and self-limiting condition but can be disabling.
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Diagnosis is clinical and canalith repositioning maneuvers are effective.

Patient/Family Education

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Reassurance
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Fall precautions