Benign paroxysmal positional vertigo (BPPV) causes discrete episodes of vertigo provoked with gravitational changes in position such as rolling from a supine position and sagittal plane movements of the head (e.g., tipping head up or down). Symptoms of general imbalance when standing and walking are also common. The cause of BPPV is the displacement of otoconia (i.e., canaliths) from the utricle that becomes trapped in the semicircular canal (SCC) system. As discussed in Chapter 1, the SCCs are not gravity sensitive structures; however, with BPPV head and body movements (e.g., lying down) cause the otoconia to move, stimulating the SCC. Based on Ewald’s laws (see Chapter 1), BPPV causes eye movements that occur in the plane of the SCC being stimulated, and in the pattern of endolymph flow. BPPV may impact any SCC. However, 85–95% of cases involve the posterior SCC, followed by the horizontal canal (5–15%) and rarely the anterior canal or multiple canals (Bhattacharyya et al., 2017).
The detachment of otoconia may be the result of head injury, vestibular disorders (e.g., vestibular neuritis and vestibular migraine), central nervous system (CNS) disease (e.g., multiple sclerosis) or aging (Bhattacharyya et al., 2017). It is the most common vestibular disorder across the lifespan; however, it is more prevalent in older adults and women (Neuhauser & Lempert, 2009). Delays in diagnosis and treatment have significant implications on quality of life and health care burden (Bhattacharyya et al., 2017). Patients with BPPV are at an increased risk of falling (Ganança et al., 2010).
DIAGNOSIS OF VERTICAL CANAL BPPV
Posterior and anterior semicircular canal BPPV may be diagnosed using the Dix-Hallpike maneuver (Dix & Hallpike, 1952; Figure 4–1) or an alternative maneuver for patients with cervical restrictions or back problems called the side-lying maneuver (Figure 4–2). The goal of these screening maneuvers is to identify provoked nystagmus patterns corresponding to the vertical SCC being stimulated due to the displaced otoconia (Table 4–1). Frenzel lenses or video-oculography (VOG) goggles are recommended to observe the nystagmus characteristics properly. The screening maneuver should be repeated with the opposite ear down if the initial maneuver is negative (Bhattacharyya et al., 2017). Anterior canal BPPV may also be diagnosed with the straight-back head-hanging maneuver (Yacovino, Hain, & Gualtieri, 2009; Figure 4–3).
Figure 4–1. Right Dix-Hallpike maneuver. The patient sits upright with their head turned 45° to the right (not shown). The clinician stands to the side (illustrated) or at the head of the examination table and quickly moves the patient into a supine position with head extended downward and rightward. The clinician monitors for symptoms/nystagmus. After 60 seconds, the clinician assists the patient to the sitting position with head still turned rightward 45°. Again, the clinician monitors for symptoms/nystagmus. Semicircular canal illustration shows otoconia moving downward (arrow) within long arm of right posterior canal (medium gray) causing ampullofugal endolymph flow and corresponding excitatory up-beating and rightward torsional nystagmus consistent with right posterior canal BPPV. Note: The patient’s eyes should remain open throughout the maneuver. (Reprinted with permission, Cleveland Clinic Center for Medical Art & Photography © 2020. All Rights Reserved.)
Figure 4–2. Schematic of side-lying maneuver to the right. The patient sits on examination table and the clinician (not shown) rotates the patient’s head 45° to the left (away from ear being assessed). The clinician assists the patient into a right side-lying position with head turned toward ceiling. The clinician monitors for symptoms/nystagmus. After 60 seconds, the clinician assists the patient to the sitting position with head still turned leftward 45°. Again, the clinician monitors for symptoms/nystagmus. Note: The patient’s eyes should remain open throughout the maneuver. (Reprinted with permission, Cleveland Clinic Center for Medical Art & Photography © 2020. All Rights Reserved.)
Table 4–1. Vertical Canal BPPV Diagnostic Criteria
Note: Eye movements should be reported in relation to the patient’s right and left and concerning the beat of the response. Changing the patient’s line of gaze may enhance the direction of the torsional (looking toward the floor) or vertical (looking toward the ceiling) nystagmus components.
Figure 4–3. Straight-back head-hanging maneuver. The patient sits on the examination table with the head in a neutral (center) position. The clinician stands at the head of the table to assist moving the patient into the supine position with head extended downward ~45–50°. The clinician monitors for symptoms/nystagmus. After 60 seconds, the clinician returns the patient to the sitting position, continuously monitoring for symptoms/nystagmus. Note: The patient’s eyes should remain open throughout the maneuver. (Reprinted with permission, Cleveland Clinic Center for Medical Art & Photography © 2020. All Rights Reserved.)
The eye movements should be reported in relation to the patient’s right and left and concerning the beat of the response:
• The direction of the torsional nystagmus indicates the side involved
• The direction of the vertical nystagmus indicates the SCC involved
○ Posterior canal = up-beating nystagmus
○ Anterior canal = down-beating nystagmus
○ < 60 seconds suggests otoconia free-floating with the canal (canalithiasis)
○ > 60 seconds suggests otoconia on or near the cupula (cupulolithiasis)
Furman and Cass (1999) outlined additional characteristics of vertical canal BPPV including:
• brief latency (few seconds) to the onset of symptoms after the patient is placed in the screening maneuver
• crescendo-decrescendo nystagmus pattern
• reversal of nystagmus (i.e., inhibitory response) during return to sit positioning
• response often fatigues with repeat positioning
The fatigability of the BPPV response is likely due to particle displacement away from the ampulla during positioning maneuvers (Boselli, Kleiser, Bockisch, Hegemann, & Obrist, 2014); however, observation of fatigability may cause unwanted patient symptoms and thus is not a current diagnostic criterion for BPPV (Bhattacharyya et al., 2017).
Anterior canal BPPV may present as pure down-beating nystagmus with a weaker torsional component that may not be observed without the use of Frenzel lenses or video-oculography system (Crevits, 2004); however, down-beating nystagmus is common with central etiologies (e.g., Chiari malformation, cerebellar lesions or degeneration). If there are no significant changes with treatment maneuvers, the down-beating nystagmus may be an indicator of CNS disease rather than BPPV (Bhattacharyya et al., 2017).
A diagnosis of BPPV is made when there is a history of vertigo provoked with changes in position relative to gravity, and screening measures provoke nystagmus characteristic of BPPV. The diagnosis should not be based on history alone; however, it is essential to note that there are instances of false-negative responses, and reevaluation on a separate date may be necessary to confirm the presence of BPPV (Bhattacharyya et al., 2017). If BPPV screening is positive and symptoms align with the condition, then no further workup (radiographic or formal vestibular testing) is warranted (Bhattacharyya et al., 2017).
Atypical Posterior SCC Canal Variants
Atypical vertical canal variants may be observed but are extremely rare (Buki, Mandalà, & Nuti, 2014). Oas (2001) describes a posterior SCC short-arm canalolithiasis variant where otoconia are positioned close to the utricle, causing prolonged torsional nystagmus toward the involved ear. Some discrepancies are reported on the provocation of nystagmus with short arm variants. Buki et al. (2014) report prolonged down-beating or no nystagmus in the Dix-Hallpike maneuver based on otoconia location and possible body sway with the return to sit positioning.
Apogeotropic posterior SCC variant suggests otoconia positioned within the common crus (e.g., shared canal joining the anterior and posterior SCCs) causing an inhibitory response (see Chapter 1) when in the Dix-Hallpike position (Vannuchi et al., 2015). The affected side is then opposite the direction of the torsion due to inhibition of the posterior SCC. For example, down-beating and rightward torsional nystagmus suggests left posterior SCC involvement, which may be mistaken for right-sided anterior canal BPPV (see Table 4–1).
TREATMENT FOR VERTICAL CANAL BPPV
When vertical canal BPPV is identified, clinicians should treat with an appropriate particle repositioning maneuver (PRM) based on the canal involved. The gold standard maneuver for vertical canal BPPV is the Epley maneuver (Epley, 1992) that utilizes five stages of gravitational positions to move otoconia (Figure 4–4). The Semont maneuver (Semont, Freyss, & Vitte, 1988) is an alternative to the Epley maneuver that may be utilized for posterior or anterior canal BPPV (Figure 4–5), and demonstrates comparable treatment efficacy (Hilton & Pinder, 2014).
Yacovino et al. (2009) proposed an alternative PRM for anterior canal BPPV. With this maneuver, the patient first sits upright on the examination table and then lays in the straight-back head-hanging position (see Figure 4–3). This position is maintained for 30 seconds. The patient’s head is then lifted 30° (chin-to-chest) upwards and held in this position for 30 seconds. Finally, the patient returns to the sitting position with the head facing forward.