Benign paroxysmal positional vertigo (BPPV) is a common cause of vertigo. We describe a case of a woman presenting acutely with a severe episode of disabling positional vertigo. Although she had no known etiologic risk factors, this attack followed 12 hours of continuously wearing digital noise-canceling headphones. This is the first such reported association between BPPV and the use of this gadget. We also provide a short review of BPPV and speculate on the possible pathogenic mechanisms involved.
Benign paroxysmal positional vertigo (BPPV) is a disorder of the inner ear involving repeated episodes of vertigo, relative to gravity. It is characterized by recurrent positional vertigo associated with torsional, vertical, or horizontal nystagmus. The term benign emphasizes its favorable prognosis in comparison with other forms of serious vestibular conditions. Its paroxysmal nature reflects a tendency to rapid and sudden onset of attacks.
Benign paroxysmal positional vertigo is the most common cause of peripheral vertigo, accounting for about 17% to 42% of cases of acutely vertiginous cases with lifetime prevalence in the region of 2.4%. It is more common in older individuals and mostly afflicts the 50- to 70-year-old age group .
Although half of all BPPV cases are of idiopathic origin , a significant proportion is associated with preceding traumatic events including head trauma , dental treatment , and ear surgery . Other conditions such as viral vestibular neuritis, suppurative otitis media, Ménière disease, and migraine have also been implicated.
In 1969, Schuknecht first raised the hypothesis of cupulolithiasis or deposition of utricular otoconia on the cupula of the posterior semicircular canal (SCC). This was later superseded by the more acceptable model of canalithiasis . Free-floating or luminal particulate matter exerts a plunger-like effect on the canal endolymph and therefore becomes more influenced by gravity. Vertigo appears when head position is altered and continues even after head movement has ceased. The posterior SCC is most commonly involved in BPPV, but there have also been reports of lateral , anterior and, less commonly, bilateral SCC involvement . Dan-Goor et al described a case of reversible decompression illness in a sea diver and suggested that nitrogen bubbles may act in the same way as canaliths in obstructing SCC endolymphatic flow.
Diagnosing BPPV relies on a characteristic history of acute vertigo associated with head position change. The Dix-Hallpike maneuver (DHM) is considered to be the criterion standard diagnostic test, where nystagmus is provoked on head tilting. The patient is placed in a supine position, and the head, supported by the examiner, is projected beyond the edge of the couch. It is then mildly extended and turned laterally by 45° to the side of testing. A positive result is when there is upbeating rotatory nystagmus toward the dependent ear, an onset of nystagmus no later than 15 seconds, and total nystagmus duration of less than 60 seconds. Fatiguability also occurs when the maneuver is repeated.
Differential diagnosis of other peripheral vestibular dysfunction includes vestibular neuritis, which is often viral in origin. In contrast to BPPV, the associated vertigo is usually severe and sustained, lasting days to weeks. Hearing loss or tinnitus also occurs if there is associated cochlear involvement . In Ménière disease, vertigo often lasts for hours, is not usually related to head movement, and involves an element of hearing loss, aural pressure, or tinnitus .
In general, BPPV is usually self-limiting and typically resolves spontaneously so that by 1 week, half of untreated cases revert to negative DHM testing, whereas 80% resolve at 1 month . Particle repositioning exercises such as the Epley and Sermont maneuvers can be highly successful in treating posterior SCC cases , especially if the etiology is idiopathic in origin. These procedures are thought to dislodge canaliths from the canal to the vestibule through a series of head position changes. In the longer term, symptoms of BPPV are more likely to recur in traumatic cases such as those involving road traffic accidents, falls, or whiplash .
A 45-year-old woman developed acute and severe positional vertigo upon waking up after continuously using electric noise-canceling headphones for the previous 12 hours of sleep.
She had been well previously and did not complain of associated tinnitus, hearing loss, or aural pressure. She enjoyed excellent health and denied recent ear infections, dental treatment, or head trauma.
On examination, she was normotensive with normal otoscopy, tuning fork audiological testing, and had no neurologic findings. The DHM was positive to right gaze, confirming acute BPPV affecting the right posterior SCC. After recuperating with rest, her condition improved, allowing her to mobilize after a week. At 6 weeks review, her positional vertigo had almost fully resolved.