1

Introduction

Benign paroxysmal positional vertigo (BPPV) is a disorder of the inner ear characterized by repeated episodes of vertigo, relative to gravity. The terms paroxysmal and benign emphasize its rapid onset and its usual favorable outcome.

BPPV is the most common cause of peripheral vertigo, accounting for approximately 17% to 42% of cases , with a lifetime prevalence in the region of 2.4%. It is more common in older individuals, mostly affecting the 50- to 70-year age group .

Although half of all BPPV cases are idiopathic in origin , a significant proportion is associated with preceding traumatic events including innocuous head trauma , dental treatment , and ear surgery .

The underlying pathophysiology of BPPV was first addressed by Schuknecht in 1969 who introduced the hypothesis of cupulolithiasis or deposition of utricular otoconia on the cupula of the posterior semicircular canal (SCC). This explanation has been largely superseded by the more accepted model of canalithiasis, whereby particulate matter becomes free floating within the lumen of the SCC . Most commonly, this involves the posterior canal where these canaliths exert a plunger-like effect on canal endolymph flow . Their movement is influenced by gravity and head position change, leading to delayed vertigo and nystagmus, even after head movement ceases. Lateral SCC involvement is less commonly seen , whereas anterior or bilateral SCC involvement have also been reported.

Diagnosis of BPPV involves careful attention to the history of vertigo associated with head position change. However, the Dix-Hallpike (DH) maneuver is considered to be the criterion-standard diagnostic test . This provocative test culminates in nystagmus after stimulating the posterior SCC of the inner ear. The patient is placed in a supine position with the head turned laterally to 45 degrees to the side of testing, with slight extension beyond the edge of the examination couch. The test is deemed positive when there is upbeating rotatory nystagmus toward the dependent ear. Other criteria include a latency of onset for the nystagmus of not more than 15 seconds, with a total duration of less than 60 seconds. Test fatigability also occurs when this test is repeated.

Treatment of BPPV includes patient reassurance as well as head position exercises such as the Epley and Sermont maneuvers , which work by moving canaliths from the posterior SCC to the vestibule by means of a series of head position changes.

We describe a case of BPPV in a healthy young individual with no known risk factors to this condition. Although vertigo is not uncommonly encountered in decompression sickness (DCS), we are not aware of any previous report associating these 2 conditions.

2

Case report

A 32-year-old recreational diver presented to our unit with a 3-day history of episodic vertigo. This was precipitated by head movement with each episode lasting approximately 10 seconds. There was no associated vomiting or tinnitus, and his hearing was not impaired. He was a nonsmoker with an uneventful medical history.

His symptoms became evident 2 hours after a lake dive where he descended to 32 m, using air from his scuba equipment. After 5 minutes of bottom time, he encountered a problem with his air supply and was forced to make an uncontrolled ascent to the surface, thereby missing his decompression safety stop.

On examination, he was apyrexial, normotensive with normal cardiovascular and respiratory findings. Otoscopic inspection revealed normal tympani membranes. Neurologic examination was also normal with no demonstrable spontaneous nystagmus. DH maneuver on right gaze was positive, consistent with a diagnosis of BPPV.

His DCS was treated with an extended Royal Navy Table 62 hyperbaric protocol. At full compression pressure (equivalent to 18 m of sea water), the diver reported partial resolution of his symptoms. At the end of the 6-hour treatment protocol, his symptoms resolved completely, with subsequent Hallpike testing becoming negative.

Patient review on the next day and after 6 weeks showed him to be asymptomatic and fully recovered.

2

Case report

A 32-year-old recreational diver presented to our unit with a 3-day history of episodic vertigo. This was precipitated by head movement with each episode lasting approximately 10 seconds. There was no associated vomiting or tinnitus, and his hearing was not impaired. He was a nonsmoker with an uneventful medical history.

His symptoms became evident 2 hours after a lake dive where he descended to 32 m, using air from his scuba equipment. After 5 minutes of bottom time, he encountered a problem with his air supply and was forced to make an uncontrolled ascent to the surface, thereby missing his decompression safety stop.

On examination, he was apyrexial, normotensive with normal cardiovascular and respiratory findings. Otoscopic inspection revealed normal tympani membranes. Neurologic examination was also normal with no demonstrable spontaneous nystagmus. DH maneuver on right gaze was positive, consistent with a diagnosis of BPPV.

His DCS was treated with an extended Royal Navy Table 62 hyperbaric protocol. At full compression pressure (equivalent to 18 m of sea water), the diver reported partial resolution of his symptoms. At the end of the 6-hour treatment protocol, his symptoms resolved completely, with subsequent Hallpike testing becoming negative.

Patient review on the next day and after 6 weeks showed him to be asymptomatic and fully recovered.