Benign paroxysmal positional vertigo is the most common peripheral vestibular disorder. It can be defined as transient vertigo induced by a rapid head position change, associated with a characteristic paroxysmal positional nystagmus. Canalolithiasis of the posterior semicircular canal is considered the most convincing theory of its pathogenesis and the development of appropriate therapeutic
maneuvers resulted in its effective treatment. However, involvement of the horizontal or the anterior canal has been found in a significant rate.
The vestibular system plays an important role in maintaining balance and is also critical for optimal function. Among vestibular disorders, benign paroxysmal positional vertigo (BPPV) is considered the most common peripheral vestibular disorder.Most BPPV patients are idiopathic— that accounts for about 50% to 70% of all cases. The second most common cause of the BPPV is head trauma, representing 7% to 17% of all BPPV cases. The onset age of the disorder occurred mostly between aged 50 to 70 years. Patients with BPPV usually suffer from paroxysmal attacks of positional vertigo and nystagmus during specific movements. In addition, many patients also complain of lightheadedness, nausea, imbalance, and standing and walking disturbances. The most common provoking movements include rolling in bed, lying down, sitting up, extending the neck to look up, and bending forward. Various pathophysiological mechanisms have been proposed to explain paroxysmal positional vertigo. Parnes and McClure5 in 1992
hypothesized “Canalithiasis,” free-floating debris moving within a semicircular canal. Movement of the debris would cause the endolymph to move away from the cupula, causing cupular deflection and inappropriate excitation.
? Positional vertigo is defined as a spinning sensation produced by changes in head position relative to gravity.
? Benign paroxysmal positional vertigo is defined as a disorder of the inner ear characterized by repeated episodes of positional vertigo.
Traditionally, the terms benign and paroxysmal have been used to characterize this particular form of positional vertigo. In this context, the descriptor benign historically implies that BPPV was a form of positional vertigo not due to any serious CNS disorder and that the overall prognosis for recovery was favorable.The term paroxysmal in this context describes the rapid and sudden onset of the vertigo associated with an episode of BPPV.
BPPV is most commonly clinically encountered as one of two variants: BPPV of the posterior semicircular canal (posterior canal BPPV) or BPPV of the lateral semicircular canal (also known as horizontal canal BPPV).Posterior canal BPPV is more common than horizontal canal BPPV, constituting approximately 85 to 95 percent of BPPV cases.Although debated, posterior canal BPPV is most commonly thought to be due to canalithiasis. Debris (thought to be fragmented endolymph particles) entering the posterior canal becomes “trapped” and causes inertial changes in the posterior canal, thereby resulting in abnormal nystagmus
and vertigo with head motion in the plane of the canal.Lateral (horizontal) canal BPPV accounts for between 5 and 15 percent of BPPV cases.The etiology of lateral canal BPPV is also felt to be due to the presence of abnormal
debris within the lateral canal, but the pathophysiology is not as well understood as that of posterior canal BPPV. Other rare variations include anterior canal BPPV, multiple canal BPPV, and bilateral multiple canal BPPV.
In addition to the historical criteria for the diagnosis of posterior canal BPPV, the diagnosis of posterior canal BPPV is confirmed by performing the Dix- Hallpike maneuver. The nystagmus produced by the Dix-Hallpike maneuvers in posterior canal BPPV typically displays two important diagnostic characteristics. First, there is a latency period between the completion of the maneuver, and the onset of subjective rotational vertigo and the objective nystagmus. The latency period for would range from 5 to 20 seconds, although it may be as long as 1 minute in rare cases.Second, the provoked subjective vertigo and the nystagmus increase, and then resolve within a time period of 60 seconds from the onset of nystagmus.
The fast component of the nystagmus provoked by the Dix-Hallpike maneuver demonstrates a characteristic mixed torsional and vertical movement (often described as upbeating- torsional), with the upper pole of the eye beating toward
the dependent ear and the vertical component beating toward the forehead Temporally, the rate of nystagmus typically begins gently, increases in intensity, and then declines in intensity as it resolves. This has been termed crescendo-decrescendo nystagmus. The nystagmus is again commonly observed after the patient returns to the upright head position and upon arising, but the direction of the nystagmus may be reversed. Another classical feature of the nystagmus associated with posterior canal BPPV is that the nystagmus typically
fatigues (a reduction in severity of nystagmus) when the maneuver is repeated.However, repeated performance of the Dix-Hallpike maneuver to demonstrate fatigability is not recommended, because it unnecessarily subjects patients to repeated symptoms of vertigo that may be discomforting, and repeat performance may interfere with the immediate bedside treatment of BPPV.
If the patient has a history compatible with BPPV and the Dix-Hallpike test is negative, the clinician should perform a supine roll test to assess for lateral semicircular canal BPPV.
Lateral canal BPPV (also called horizontal canal BPPV) is the second most common type of BPPV.Patients with a history compatible with BPPV (ie, repeated episodes of vertigo produced by changes in head position relative to gravity) who do not meet diagnostic criteria for posterior canal BPPV should be investigated for lateral canal BPPV. In many instances, the presenting symptoms of lateral canal BPPV are indistinguishable from posterior canal BPP.
In 1980, Brandt and Daroffproposed the first effective therapy for BPPV, based on the assumption that cupulolithiasis was the underlying mechanism, consisting of a set of physiotherapeutic exercises repeated many times a day for 2 to 3 weeks. As an alternative, Semont et alin 1988, introduced a single liberatory maneuver, based on the theory of cupulolithiasis, but the major breakdown was the “canalith
repositioning procedure,” by Epleyin 1992, based on the theory of canalolithiasis.