eMedicine Specialties > Emergency Medicine > Neurology

Benign Positional Vertigo

Author: Andrew K Chang, MD, Associate Professor, Department of Emergency Medicine, Albert Einstein College of Medicine, Montefiore Medical Center
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Updated: Aug 24, 2009

Introduction

Background

Benign positional vertigo (BPV) is the most common cause of vertigo. Vertigo is an illusion of motion (an illusion is a misperception of a real stimulus) and represents a disorder of the vestibular proprioceptive system.

BPV was first described by Adler in 1897 and then by Bárány in 1922; however, Dix and Hallpike did not coin the term benign paroxysmal positional vertigo until 1952. This terminology defined the characteristics of the vertigo and introduced the classic provocative test that is still used today. Using positional testing, benign positional vertigo can readily be diagnosed in the emergency department. Benign positional vertigo is one of the few neurologic entities the emergency physician can cure at the patient's bedside by performing a series of simple and safe head-hanging maneuvers.

For further information, see Benign Positional Vertigo in the Neurology volume.

Pathophysiology

Benign positional vertigo (BPV) is caused by calcium carbonate particles called otoliths (or otoconia) that are inappropriately displaced into the semicircular canals of the vestibular labyrinth of the inner ear. These otoliths are normally attached to hair cells on a membrane inside the utricle and saccule. Because the otoliths are denser than the surrounding endolymph, changes in head movement vertically causes the otoliths to tilt the hair cells, which triggers a nerve that send a signal to the brain letting the brain know that the head is tilting up or down. 

The utricle is connected to the 3 semicircular canals. The otoliths may become displaced from the utricle by aging, head trauma, or labyrinthine disease. When this occurs, the otoliths have the potential to enter the semicircular canals. When they do, they almost always enter the posterior semicircular canal because this is the most dependent (inferior) of the 3 canals.

Frequency

United States

The incidence of benign positional vertigo (BPV) is 64 cases per 100,000 population per year (conservative estimate).¹

International

One study in Japan found an incidence of 11 cases per 100,000 population per year, but patients were counted only if examined by a subspecialist or at a referral center.

Mortality/Morbidity

The B of BPV stands for benign and designates that the cause of the vertigo is peripheral to the brainstem and, hence, likely to be benign. However, BPV can be severely incapacitating to the patient.

Sex

Women are affected twice as often as men.

Age

BPV, in general, is a disease of elderly persons, although onset can occur at any age. Several large studies show an average age of onset in the mid 50s. Vertigo in young patients is more likely to be caused by labyrinthitis (associated with hearing loss) or vestibular neuronitis (normal hearing).

Clinical

History

When asked about their dizziness, patients with benign positional vertigo (BPV) characteristically describe that the room or world is spinning. However, other descriptions, such as rocking, tilting, somersaulting, and the like, are also possible. All that matters is that an illusion of motion is caused by a misperception of a stimulus (the otoliths). Diagnosis of BPV is based on a characteristic history and a positive Hallpike test.

• Episodic vertigo may occur with the following head movements:
  • Rolling over in bed
  • Lying down
  • Sitting up
  • Leaning forward
  • Turning the head in a horizontal plane
• Symptoms of BPV are usually worse in the morning (the otoliths are more likely to clump together as the patient sleeps and exert a greater effect when the patient gets up in the morning) and mitigate as the day progresses (the otoliths become more dispersed with head movement).
• Nausea is typically present (vomiting is less common).
• A history of head trauma may be present, especially in young patients with BPV. The head trauma may dislodge the otoliths off the hair cells within the utricle, allowing them the opportunity to enter the semicircular canals.
• Eliciting that the individual episodes of vertigo in BPV last for seconds at a time is important. Patients may describe that they are having continuous vertigo, when in reality, they are having repeated episodes (with each episode typically lasting seconds or less than a minute). Patients with vestibular neuritis and labyrinthitis have continuous vertigo, often for hours to days.
• During the interview, if patient states that the "room is spinning" while the patient's head is still and prior to any manipulative tests, then it is highly unlikely that the patient has BPV because the vertigo in BPV lasts for seconds at a time and occurs only after head movement.

Physical

• Nystagmus (an involuntary rhythmic oscillation of the eyes) is described in terms of the fast-phase component.
  • Classic nystagmus occurs when the patient's head is dependent and turned to the affected side.
  • The nystagmus is torsional or rotatory. In the head-hanging position, the fast phase should beat toward the forehead (upbeat) and in the same direction as the affected side (ipsilateral). Although some describe the fast phase in terms of being clockwise or counterclockwise, most experts avoid this terminology because it can be unclear if the clock is being viewed from the patient's or physician's perspective.
  • Nystagmus usually occurs within 10 seconds after positioning but may present as late as 40 seconds. Hence, if the history is classic, observe the patient for at least 40 seconds while he or she is in the head-hanging position during the Hallpike test.
  • Duration varies from a few seconds to a minute and parallels the sensation of vertigo.
  • Response fatigues if the patient is repeatedly placed into the provoking position (due to dispersion of the otoliths).
• Note: If the patient has a classic history of BPV (after a short delay, the room spins, but then revolves in 20-30 seconds, and then the rooms spins in the opposite direction when he or she sits back up) but no nystagmus is seen during the Hallpike test, most experts would agree to go ahead and treat the patient with the modified Epley maneuver (see Treatment).
  • Nystagmus may be blocked by fixation suppression. Most emergency physicians do not have access to Frenzel lenses or infrared nystagmography that specialists use to prevent fixation suppression.
  • One study showed that treating such patients with the Epley maneuver is still effective (despite the lack of nystagmus). Again, these patients must have a classic history.
• Perform the Hallpike test as follows (Caution: For patients with cervical spondylosis, it may not be advisable to extend the neck. However, because having the head dependent is important, the same effect can be achieved if the gurney is placed in the Trendelenburg position for such patients).
  • First, warn the patient that symptoms of vertigo will likely be reproduced but will resolve after a few seconds.
  • Seat the patient close enough to the end of the gurney so that when he or she lies supine, the head can extend backward an additional 30-45°.
  • Instruct the patient to keep his or her eyes open because you want to observe the direction of the nystagmus. The examiner may need to use his thumb to hold the eyelid open because patients may involuntarily close their eyes even when instructed to keep them open.
  • To test the left posterior canal, follow these steps:
    • Turn the patient's head 45° to the left. This position orients the head such that the left posterior semicircular canal is going to be in the same plane as the upcoming head movement (next step). This is the most provocative way to move the otoliths (if they are indeed in the posterior semicircular canal) which will result in a positive test.
    • With your hands on either side of the patient's head, lay the patient down until the head is dependent (hanging over the edge of the gurney). Note that this step does not need to be performed rapidly.
    • Check for reproduction of symptoms and nystagmus. In most cases, the fast phase of the nystagmus should be upbeat (toward the forehead) and ipsilateral (in this example, toward the patient's left).
    • Return the patient to the upright position. Nystagmus may be observed in the opposite direction, and the patient may describe that the world is spinning in the opposite direction.
  • To test the right posterior canal, repeat the Hallpike test with the head turned 45° to the right side. In general, if the patient has BPV, only one side should test positive during the Hallpike test. Although having bilateral posterior semicircular canal BPV is possible, it is unlikely and should suggest horizontal canal involvement, vestibular neuritis/labyrinthitis, or a central cause.
  • Note that almost all patients experience mild dizziness when being brought up from the head-hanging position to the sitting position. It is important not to confuse this dizziness (which is more near-syncope in character) with true vertigo.
• If the patient's head cannot be extended over the edge of the gurney, 2 additional options exist. The first is to place the patient in the Trendelenburg position if a gurney that allows this position is available. The other alternative is to use the side-lying test; the patient sits with his or her legs over one side of the gurney. To test the left posterior semicircular canal, turn the patient's head 90° to the opposite side (in this case, the right side). Then, lay the patient on his or her left side. By turning the patient's head to the right, the left posterior semicircular canal is aligned in the same plane as the sideways movement. As in the Hallpike test, this will allow the greatest chance for otoliths to move if they are indeed located in the posterior semicircular canal.
• The neurologic examination findings should be otherwise normal; if not, strongly consider alternative diagnoses.

Causes

Several disorders affecting the peripheral vestibular system may precede the onset of benign positional vertigo (BPV).

• Idiopathic (50-60%)
• Infection (viral neuronitis)
• Head trauma, especially in younger patients
• Degeneration of the peripheral end organ
• Surgical damage to the labyrinth

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