Benign Paroxysmal Positional Vertigo (BPPV)

Article Author:
Renata Palmeri
Article Editor:
Anil Kumar
Updated:
10/27/2018 12:32:08 PM
PubMed Link:
Benign Paroxysmal Positional Vertigo (BPPV)

Introduction

Vertigo is the allusion of movement, a perception of motion though none exists. It is a sensation of swaying, tilting, spinning, or feeling unbalanced, which may be experienced as self-motion to some versus movement of the surrounding environment to others. Due to highly variable descriptions of the vertigo experience, it is often consolidated into the umbrella term “dizziness,” which is a very common complaint, accounting for over three million emergency department (ED) visits annually. Vertigo can be of vestibular or peripheral origin or be due to non-vestibular or central causes. With regards to peripheral vertigo, benign paroxysmal positional vertigo (BPPV) is the most common cause, accounting for over one-half of all cases. It is of great importance to identify BPPV versus other causes of vertigo as the differential diagnosis includes a spectrum of diseases processes ranging from benign to life-threatening.

Etiology

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 proper functioning of the utricle of the otolithic membrane by helping deflect the hair cells within endolymph, which relays positional changes of the head including tilting, turning, and linear acceleration.

Epidemiology

Dizziness, including vertigo, affects 15% to 20% of adults yearly based on population studies. The lifetime prevalence of BPPV specifically was found to be 2.9%, and incidence increases with age due to age-related degeneration of the otolithic membrane. Additionally, BPPV is about two to three times more common in women versus men. 

Pathophysiology

With BPPV, otoconia (also known as “otoliths” or “canaliths”) dislodge and settle within the endolymph of the semicircular canals. When the head remains static, there is no stimulus causing the hair cells to fire. With motion, however, the displaced otoconia shift within the fluid, and the subsequent stimulus is unbalanced with respect to the opposite ear, inappropriately causing symptoms of dizziness, spinning, and/or swaying. Hence, symptoms of BPPV are profound with movement but classically lessen with rest.

History and Physical

A detailed history and physical are imperative to the evaluation of 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. 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 close consideration must be made for central causes of vertigo, which also correlate with increasing age and cerebrovascular disease.

Classically, the symptoms of BPPV are sudden in onset, provoked by movement, and decreased with rest. The Dix-Hallpike test is a diagnostic maneuver that can be performed quickly and easily to evaluate for BPPV. It is based on the anatomical properties of the inner ear, which predispose displaced otoconia to settle in the posterior semicircular canal. Theoretically, otoconia may settle in the superior or lateral semicircular canals, leading to a negative test, though with a sensitivity of 79% and specificity of 75%, this maneuver does have clinical utility. The Dix-Hallpike helps localize the affected ear by exacerbating both symptoms and clinical signs such as nystagmus. Subsequently, the Epley maneuver can be performed, coercing the crystals back into the utricle and removing the disturbance from the otolithic membrane. The Epley can promptly relieve symptoms, though relapses are common. Additionally, the Epley is often not tolerated by elderly patients as well as those with active nausea/vomiting and those with profound symptoms who cannot cooperate. The Epley is contraindicated in cervical spine injury/abnormality, such as possible atlantoaxial subluxation, as well as in patients with possible carotid or vertebral artery dissection. In addition to these special tests, it is imperative to perform a full neurological exam, including cranial nerves, coordination, and gait. The neurological exam is expectedly normal in BPPV with a few exceptions. Patients with BPPV can demonstrate nystagmus, which is typically horizontal and unidirectional as well as fatigable, meaning it peaks in intensity but subsequently tapers off. Vertical, torsional, or direction-changing nystagmus should raise concern for the central cause. With BPPV, there is a latency period of 30 seconds or less between provocative head movement and onset of nystagmus. Also, the otoconia in BPPV cause aberrant impulses to be fired from the semicircular canals via cranial nerve VIII, impairing the vestibular-ocular reflex. Patients with BPPV will have issues coordinating head movement with extra-ocular movement, leading to an abnormal head impulse test. The HiNTS exam, which includes nystagmus and head impulse testing, is a sequence of tests to help discern central versus peripheral causes of dizziness. It would be of value to perform in the physical exam of patients being evaluated for possible BPPV.

Evaluation

BPPV is largely a clinical diagnosis, and often the battery of laboratory and imaging tests ordered only help rule-out other possibilities. As above, obtaining a good history and performing a thorough neurological exam is imperative. Laboratory studies are not found to be helpful. Imaging of the head in BPPV is unremarkable. Head CT and MRI are useful to rule-out infarct, hemorrhage, masses/tumors, or other pathology that would suggest alternative causes of vertigo. The Dix-Hallpike, if it can be tolerated, should be performed as a provocative test to observe for expected changes in symptoms and to localize which inner ear is involved.

Treatment / Management

After using the Dix-Hallpike maneuver to localize which side is problematic, the Epley maneuver can be performed. This series of positional changes helps dislodge otoconia from the otolithic membrane and back into the utricle, removing the disturbance and symptomatology. As aforementioned, the Dix-Hallpike and Epley are not always tolerated by patients with BPPV, in which case treatment is symptomatic. 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. Vertigo associated with BPPV is typically abrupt in onset, very brief, and truly paroxysmal, just as the name suggests, and medications may not be particularly beneficial. Hence, routine medical management with Meclizine is not indicated unless the frequency of vertigo spells is high and disruptive to daily function. Nausea and vomiting is another common complaint with BPPV and can be treated with anti-emetics as needed: ondansetron, metoclopramide, or promethazine/prochlorperazine. Patients with recurrent BPPV should be provided with ENT referral for further evaluation as there are lateral and horizontal canal variants of BPPV that require specific re-positioning maneuvers different from the Epley.

Differential Diagnosis

Vestibular neuritis, labyrinthitis, brainstem or cerebellar infarction, brainstem or cerebellar hemorrhage, traumatic vestibulopathy, cerebellopontine angle neoplasm, vestibular migraine, medication ototoxicity, herpes zoster oticus, decompression sickness, brainstem encephalitis, vertebrobasilar insufficiency, vertebral artery dissection.