Evaluation and Treatment of Benign Paroxysmal Positional Vertigo
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Introduction
Benign paroxysmal positional vertigo (BPPV) is the single most common cause of vertigo. BPPV accounts for 26% of all cases of vertigo1 and was found in 9% of geriatric patients in an urban clinic.2 The incidence of BPPV increases with age.1,3 BPPV affects the quality of life of elderly patients and is associated with reduced activities of daily living scores, falls, and depression.2 The purpose of this article is to review the evaluation and treatment of BPPV.
Clinical Features of BPPV
BPPV is characterized by brief periods of vertigo triggered by a change in the position of the patient’s head relative to gravity. Brief periods of vertigo typically occur when the patient rolls in bed towards one side, gets in and out of bed (“bed-spins”), bends over and straightens up, or looks up (top-shelf syndrome).4,5 If one observes the patient’s eyes during these periods, one can sometimes observe that the eyes are jumping. The rapid, involuntary oscillation of the eyes is referred to as nystagmus. Patients with BPPV are usually most symptomatic while lying flat in bed and often adopt sleeping strategies such as propping themselves up in bed.
There are three main variants of BPPV. Each variant is characterized by a specific direction of nystagmus, and the direction is dependent on the part of the inner ear that is causing the vertigo. In the most common variant, posterior canal BPPV (PC-BPPV; see Figure 1 for the location of the posterior canal), the eyes jump upward as well as twist. In the second most common variant, horizontal canal BPPV (HC-BPPV), the eyes jump horizontally. The least common type is anterior canal BPPV (AC-BPPV), where the eyes jump downward.
Most BPPV is caused by loose particles within the inner ear. This is more formally called canalithiasis (Figure 1).6 In canalithiasis, heavy debris from another part of the ear (the utricle) becomes dislodged and enters a semicircular canal. The debris, being made of calcium carbonate (limestone), is heavier than the fluid in the canal. Thus, when the position of the head changes relative to gravity, the debris falls downward in the semicircular canal. As the debris falls, the patient experiences a brief burst of vertigo and nystagmus. Once the debris comes to rest, typically in 10-60 seconds, the nystagmus and vertigo stops. PC-BPPV is the most common because the PC is at the bottom of the inner ear, and this promotes accumulation of heavy debris.
Differential Diagnosis of BPPV
BPPV causes about 85% of all positional vertigo. Orthostatic hypotension and other conditions that cause low blood pressure also result in positional symptoms, but symptoms are triggered by standing up, and typically no symptoms are noted when the person is supine. Damage to the brainstem or cerebellum can also cause positional vertigo. Central positional vertigo is far less common than BPPV, is accompanied by other neurological signs, and also generally shows a different pattern of nystagmus on positional testing, as discussed subsequently. Low spinal fluid pressure can also cause orthostatic symptoms, but again like orthostatic hypotension, they are not prominent when lying in bed. All types of BPPV are accompanied by nystagmus, and this is the main feature that distinguishes BPPV from other types of positional vertigo. More about the nystagmus follows in the next section.
Positional Testing to Diagnose BPPV
The diagnosis of BPPV is established through two positional tests; the Dix-Hallpike maneuver7 and the supine with lateral head turns maneuver.8 Determining the canal involved is based on the direction and characteristics of the nystagmus found during the positional testing. Positional testing is best performed with an examination tool that prevents fixation, such as the patient wearing Frenzel goggles or using video-oculography.
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