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Benign Paroxysmal Positional Vertigo
(Benign Postural or Positional Vertigo)
In benign paroxysmal positional vertigo (BPPV), short (< 60 sec) episodes of vertigo occur with certain head positions. Nausea and nystagmus develop. Diagnosis is clinical. Treatment involves canalith repositioning maneuvers. Drugs and surgery are rarely, if ever, indicated.
BPPV is the most common cause of relapsing otogenic vertigo. It affects people increasingly as they age and can severely affect balance in the elderly, leading to potentially injurious falls.
The condition is thought to be caused by displacement of otoconial crystals (Ca carbonate crystals normally embedded in the saccule and utricle). This displaced material stimulates hair cells most commonly in the posterior semicircular canal (and rarely in the superior semicircular canal), creating the illusion of motion. Etiologic factors include spontaneous degeneration of the utricular otolithic membranes, labyrinthine concussion, otitis media, ear surgery, recent viral infection (eg, viral neuronitis), head trauma, prolonged anesthesia or bed rest, previous vestibular disorders (eg, Meniere disease), and occlusion of the anterior vestibular artery.
Vertigo is triggered when the patient’s head moves (eg, when rolling over in bed or bending over to pick up something). Acute vertigo lasts only a few seconds to minutes; episodes tend to peak in the morning and abate throughout the day. Nausea and vomiting may occur, but hearing loss and tinnitus do not.
Diagnosis is based on characteristic symptoms, on nystagmus as determined by the Dix-Hallpike maneuver (a provocative test for positional nystagmus—see Nystagmus), and on absence of other abnormalities on neurologic examination. Such patients require no further testing. Patients with nystagmus suggesting a CNS lesion undergo gadolinium-enhanced MRI. Unlike the positional nystagmus of BPPV, the positional nystagmus of CNS lesions lacks latency, fatigability, and severe subjective sensation and may continue for as long as the position is maintained. Nystagmus caused by a CNS lesion may be vertical or change direction and, if rotary, is likely to be in the unexpected direction.
BPPV usually subsides spontaneously in several weeks or months but may continue for months or years. Because the condition can be long-lasting, drug treatment (like that used in Meniere disease—see Meniere Disease : Treatment) is not recommended. Often, the adverse effects of drugs worsen dysequilibrium.
Because BPPV is fatigable, one therapy is to have the patient perform provocative maneuvers early in the day in a safe environment. Symptoms are then minimal for the rest of the day.
Canalith repositioning maneuvers (Epley maneuver [see see Figure: The Epley maneuver.] and Semont maneuver) involve moving the head through a series of specific positions intended to return the errant canalith to the utricle. After performing these maneuvers, the patient should remain erect or semi-erect for 1 to 2 days. Both maneuvers can be repeated as necessary.
For the Semont maneuver, the patient is seated upright in the middle of a stretcher. The patient’s head is rotated toward the unaffected ear; this rotation is maintained throughout the maneuver. Next, the torso is lowered laterally onto the stretcher so that the patient is lying on the side of the affected ear with the nose pointed up. After 3 min in this position, the patient is quickly moved through the upright position without straightening the head and is lowered laterally to the other side now with the nose pointed down. After 3 min in this position, the patient is slowly returned to the upright position, and the head is rotated back to normal.
Vertigo occurs due to displacement of otoconial crystals into a semicircular canal; symptoms are triggered by head movement.
There is usually nausea and vomiting but no tinnitus or hearing loss.
Diagnosis is clinical, but some patients require MRI to rule out other conditions.
Treatment is with canalith-repositioning maneuvers.
Drugs rarely help and may worsen symptoms.
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