Benign Paroxysmal Positional Vertigo (BPPV) is a disease characterized by recurrent episodes of rotational vertigo triggered by otoconia (calcium carbonate crystals) that have migrated into the semicircular canals, causing endolymph flow during head position changes. It accounts for 17.1% of all vertigo cases, and in the elderly, approximately 50% of vertigo is attributed to BPPV 5). It is characterized by the absence of hearing loss or neurological symptoms, which is reflected in the term “benign.”
Lifetime prevalence is 2.4%, 1-year prevalence 1.6%, and annual incidence 0.6% 4)5), with a cumulative lifetime risk of 10% in the general population 10). Prevalence is reported as 11–64 per 100,000 people 8). It is more common in women in their 60s; pediatric BPPV accounts for only 1% of cases, and prevalence increases with age 2)4).
For ophthalmologists, its importance lies in the central role of evaluating oscillopsia, blurred vision, and positional nystagmus. Additionally, the characteristics of nystagmus observed during the Dix-Hallpike test or supine head roll test are key to differentiating it from central disorders (cerebellar or brainstem lesions).
BPPV is the most common peripheral vestibular disorder among vertigo diseases. Its lifetime prevalence is 2.4%, and the cumulative incidence in the general population reaches 10% 10), accounting for approximately 50% of vertigo in the elderly 5).
The main symptom of BPPV is recurrent brief episodes of rotational vertigo triggered by specific head movements.
The nature of positional nystagmus is central to diagnosis. The characteristics of nystagmus differ depending on the affected semicircular canal.
Posterior semicircular canal type
Provocative test: Dix-Hallpike test (affected side down)
Nystagmus direction: Upbeat-torsional nystagmus
Latency: 2–20 seconds
Duration: Usually less than 1 minute, increases then disappears
Fatigability: Nystagmus decreases with repeated testing
Return to sitting position: The direction of nystagmus may reverse when the head is returned to the neutral position.
Horizontal semicircular canal type
Provocation test: Supine roll test
Direction of nystagmus: Horizontal nystagmus (geotropic or apogeotropic)
Latency: Shorter than posterior canal type, or almost absent
Duration: May exceed 60 seconds
Attenuation: Present in geotropic but poor in apogeotropic
Pseudo-spontaneous nystagmus (PSN): Persistent horizontal nystagmus may occur even in the sitting position6)
Differentiation between canalolithiasis (CAN) and cupulolithiasis (CUP) affects treatment selection.
| Differentiating point | Canalolithiasis (CAN) | Cupulolithiasis (CUP) |
|---|---|---|
| Attack duration | Less than 60 seconds | More than 60 seconds |
| Latency | 2–5 seconds present | None to short |
| Decaying | Present | Absent |
Approximately 50% of BPPV cases are idiopathic, and age-related degeneration of the utricular macula is considered the main cause5)10). The remaining cases are secondary, with the following known causes.
Main causes of secondary BPPV
Main risk factors
Post-COVID-19 BPPV (PC-BPPV) has been reported. It is presumed that microthrombus formation and hypercoagulability caused by COVID-19 lead to microcirculatory disorders in the inner ear, resulting in otolith detachment 5). All reported cases resolved with the Epley maneuver.
This is a standard examination method used for diagnosing posterior canal BPPV.
Procedure: From a seated position with the head rotated 45 degrees toward the affected side, quickly move to a supine position while lowering the head 30 degrees. Observe for the appearance of upbeating torsional nystagmus.
Diagnostic criteria: Upbeating torsional nystagmus after a latency (lasting less than 30 seconds), with fatigability on repetition, is considered positive.
Test accuracy: Sensitivity 79%, specificity 75% in adults2). If horizontal nystagmus appears, consider horizontal canal BPPV and add the supine roll test.
With the patient supine, rapidly rotate the head to the left and right.
The main diseases to differentiate from BPPV are listed below.
| Disease | Duration | Main Features |
|---|---|---|
| Meniere’s disease | Minutes to hours | Tinnitus, low-frequency hearing loss, ear fullness |
| Vestibular neuritis | Days to weeks | Dizziness even at rest, viral prodrome |
| Vestibular migraine | Seconds to hours | Associated with migraine, frequent recurrence |
| Central positional vertigo | Persistent | Downbeat nystagmus, ocular muscle palsy, lack of rotatory component |
Central positional vertigo: In cerebellar lesions, downbeat nystagmus appears persistently, in contrast to the transient upbeating-torsional nystagmus of BPPV. Pure vertical nystagmus without a torsional component also suggests a central cause.
Vestibular paroxysmia: Caused by vascular compression of the vestibular nerve, lasting seconds to minutes. It is differentiated by its response to carbamazepine or oxcarbazepine.
Superior semicircular canal dehiscence syndrome: Differs from BPPV in that loud sounds, Valsalva maneuver, or pressure changes trigger vertigo.
PPPD (Persistent Postural-Perceptual Dizziness): Characterized by floating sensation, unsteadiness, and visual hypersensitivity lasting more than 3 months. BPPV can trigger and transition into it.
Orthostatic hypotension: Symptoms occur only upon standing and are differentiated by blood pressure measurement.
In children: Exclusion of central lesions such as posterior fossa tumors is particularly important, requiring MRI and a complete neurological evaluation2).
It cannot be ruled out. In horizontal canal BPPV, the Dix-Hallpike test is negative, so a supine head roll test is separately required. There is also “subjective BPPV” where dizziness occurs during the provocative maneuver but nystagmus does not appear. The sensitivity of the test is 79% in adults 2), and if clinically suspected, repeated evaluation is necessary.
The treatment for BPPV is based on canalith repositioning maneuvers, and physical procedures are the first choice rather than drug therapy. Although it usually resolves spontaneously without treatment, early remission can be achieved with repositioning maneuvers.
Epley Maneuver
Indication: Posterior canal BPPV (most common)
Overview: Continuous sequential repositioning of the head and body moves otoconia from the posterior semicircular canal to the utricle.
Effectiveness: Many cases resolve after 1–2 sessions. Almost all case reports applying the Epley maneuver report resolution1)2)3)4)8)9).
Semont maneuver
Indication: Alternative to the Epley maneuver for posterior canal BPPV
Overview: The patient is rapidly moved from a seated position to lying on the affected side, then quickly turned to the opposite side.
Effectiveness: Effective as an alternative to the Epley maneuver, but the Epley maneuver may be more effective.
Lempert maneuver
Indication: Horizontal canal BPPV (canalolithiasis)
Overview: With the patient supine, flex the cervical spine 30 degrees, rotate the head 90 degrees toward the affected side → hold for 30 seconds → return to neutral → rotate 90 degrees to the healthy side → prone position, performing a 360-degree rotation (BBQ roll). Repeat until nystagmus and vertigo resolve7).
Efficacy: Complete remission was achieved in cases performed in the emergency department, allowing same-day discharge7).
Gufoni maneuver: Effective for cupulolithiasis (CUP) type of horizontal canal BPPV6).
The 1-year recurrence rate is 15%, and the 5-year recurrence rate reaches 37–50%10). Higher recurrence rates have been reported in post-traumatic BPPV and horizontal canal type. In cases with vitamin D deficiency, supplementation may be effective for preventing recurrence1)5).
The pathogenesis of BPPV is broadly divided into two types: canalithiasis and cupulolithiasis.
Otolith particles detached from the utricular macula aggregate near the cupula within the semicircular canal (mainly the posterior canal). During head position changes, they move within the endolymphatic duct under gravity, causing a plunger effect that deflects the cupula in the same direction. This inappropriate cupular deflection sends false rotational motion signals to the brain, triggering vertigo and transient nystagmus. It is characterized by position dependence, short duration, fatigability, and latency.
Otoliths attach directly to the cupula rather than floating in the endolymph. The specific gravity of the cupula changes, causing a sustained gravity-dependent deviation. Therefore, symptoms persist and do not decay even when the head is held in position. In the horizontal semicircular canal type, pseudo-spontaneous nystagmus (PSN) may be present even in the sitting position 6).
Schwarz et al. (2022) proposed a new mechanism for PSN in horizontal semicircular canal BPPV, where otolith attachment to the lower part of the cupula causes a sustained gravity-dependent deviation 6). In addition to the anatomical anterior 30-degree tilt of the horizontal semicircular canal and “canalith jam,” cupulolithiasis can be a cause of PSN.
Multiple mechanisms are involved in otolith detachment.
As a mechanism for the development of BPPV after COVID-19 (PC-BPPV), it has been proposed that COVID-19-specific microthrombus formation and hypercoagulable state may cause microcirculatory disorders in the inner ear 5). An increase in the incidence of BPPV during the COVID-19 pandemic has been observed, and verification through large-scale studies in the future is awaited.
Maslovara et al. (2021) reported two cases (women aged 28–41 years) who developed right posterior semicircular canal BPPV approximately one month after mild COVID-19 5). Both resolved with two sessions of the Epley maneuver, and COVID-19-specific inflammatory and microvascular mechanisms were considered as etiologies.
Research on post-traumatic and sports-related BPPV is advancing.
Warming et al. (2023) reported BPPV cases in soccer players, showing that 22% of young adult BPPV patients had a history of amateur soccer 10). In these cases, cupulolithiasis and horizontal canal involvement were common, and complete remission was achieved after 10 treatment sessions over 2 years and a 6-year follow-up.
Enhanced repositioning maneuvers (potentiated Epley maneuver, dynamic BBQ roll) using a TRV-chair (mechanical rotational chair) are being considered for post-traumatic BPPV cases resistant to standard procedures 10).
Post-concussion BPPV is often diagnosed weeks later, according to reports 9).
Bashir et al. (2023) reported post-concussion BPPV in two rugby players (ages 15–16), noting a 5–6 week delay from symptom onset to diagnosis 9). 85% of ED physicians used only medication, while only 4% chose physical maneuvers as first-line treatment, suggesting improvement through an educational program based on Gagne’s nine steps.
It has been suggested that repositioning maneuvers such as the Epley maneuver may induce epigenetic modifications (Tsai et al. 2016), and research is ongoing to elucidate the molecular mechanisms of BPPV5).
