Introduction
Benign paroxysmal positional vertigo (BPPV) is known to be the most common peripheral vestibular disorder characterized by brief, recurrent episodes of vertigo provoked by changes in head position [1,2]. Typically, as the otoconia located in the utricular macule degenerate, fragments of these particles enter the semicircular canal or adhere to the cupula. As the displaced otoconial debris cannot be directly observed, the diagnosis of BPPV and the effectiveness of repositioning maneuvers rely entirely on the indirect observation of characteristic nystagmus patterns. Afferent vestibular nerve excitation is induced, leading to dizziness and nystagmus, when the otoconial debris move within the semicircular canal or directly deflect the cupula [1–3]. Characteristic nystagmus can be observed during provocative maneuvers performed in the plane of the affected canal. While BPPV is self-limiting in many cases, unresolved BPPV can restrict daily activities and increase the risk of falls in elderly patients. Although BPPV can occur in any of the three semicircular canals, it has been generally recognized that posterior canal BPPV (PC-BPPV) is the most frequent subtype, while according to recent reports, horizontal canal BPPV (HC-BPPV) also accounts for a considerable proportion of cases [4–6]. Repositioning maneuvers have been well established specific to the affected canal, which is a mainstay in the treatment of BPPV. Nevertheless, there are still patients with recurrent or residual vertigo even after the standard repositioning therapy. And there are central and peripheral disorders mimicking the presentation of BPPV, which need to be excluded in the process of diagnosis. Although the underlying causes of BPPV remain unclear, many studies have investigated risk factors for the occurrence of BPPV [1,5].
Given that the diagnosis and treatment of BPPV rely heavily on the clinician’s expertise in evaluating and managing patients, this paper aims to provide the most practical and up-to-date information.
Epidemiology and Etiology
BPPV is known to be the most frequent vestibular disorder with cumulative lifetime incidence in the general population between 2.4% and 10% [3,7]. The 1-year incidence was known to be 0.6% [3,7]. Higher prevalence is reported in female population (3.2%) than in male population (1.6%) in lifetime prevalence with significantly increased risk in meta-analysis (odds ratio=1.18, p=0.004) [2,3,5]. It occurs more frequently in the elderly [4,5,7]. It follows a recurrent course in about 50% of cases, with gradual spontaneous remission occurring over days to weeks [8]. PC-BPPV reportedly accounts for 60%–90% of cases, whereas HC-BPPV including both canalolithiasis and cupulolithiasis occurs in 10%–17% of patients [3,4,9,10]. However, several recent investigations suggest a higher prevalence of HC-BPPV and indicate that the frequency of PC-BPPV may have been overestimated [6]. In a Korean multicenter study, horizontal canal variants accounted for up to 31.9% of cases, while PC-BPPV represented 60.9% [6].
Although BPPV is considered idiopathic in the majority of cases, accumulating evidence indicates that several clinical and biological factors may predispose individuals to its development. Degenerative, mechanical, and ischemic alterations of the utricular macula have been widely proposed as key mechanisms underlying otoconial detachment, and head trauma or concomitant inner ear disorders are well-established secondary causes [11]. Increasing attention has also been directed toward systemic factors that influence otoconial integrity. In particular, abnormalities in bone metabolism including reduced bone mineral density, osteoporosis, and low serum vitamin D levels have been consistently reported in association with BPPV [5]. These findings are supported by observations that postmenopausal hormonal changes may accelerate both skeletal demineralization and impaired otoconial turnover, thereby heightening susceptibility to otoconial instability [5,12]. Additional metabolic and endocrine factors, such as altered thyroid function, corticosteroid exposure, aberrant growth hormone levels, and hyperuricemia, have been suggested as potential contributors; however, the evidence supporting these associations remains limited and controversial [5,12–14].
Pathophysiology
The cupulolithiasis hypothesis posits that otoconia detached from the utricular macula may adhere to the cupula, increasing its specific gravity relative to the surrounding endolymph. When the affected semicircular canal is positioned inferiorly, the weight-altered cupula is displaced either toward or away from the utricle, resulting in excitation or inhibition of the corresponding canal [15]. In theory, the symptoms and nystagmus induced by cupulolithiasis should begin immediately and persist as long as the cupula remains deflected. In clinical practice, however, the elicited response usually lasts only several minutes. This discrepancy is thought to reflect a combination of central vestibular adaptation, peripheral receptor fatigue, and mechanical factors that progressively diminish the stimulus over time [15–17].
The canalolithiasis hypothesis proposes that otoconial debris dislodged from the utricular macula freely migrates within the membranous labyrinth of the semicircular canal, generating transient rotatory vertigo during head motion. In contrast to cupulolithiasis, the symptoms and nystagmus typically exhibit a brief latency before onset and diminish once the head movement ceases. The response progressively fatigues with repeated provocative maneuvers, a phenomenon attributed to the redistribution of otoconia within the canal, the effects of viscous drag on endolymph flow, and central adaptation to recurrent vestibular stimulation [17].
According to Ewald’s first law, each semicircular canal responds more strongly to excitatory than to inhibitory stimuli. The horizontal and vertical semicircular canals produce different directions of nystagmus in response to otolith movement. According to Ewald’s second law, endolymph flow toward the utricle (utriculopetal) produces a stronger response than flow away from the utricle (utriculofugal) in the horizontal canal. In contrast, the third law states that endolymph flow away from the utricle (utriculofugal) produces a stronger response than flow toward it (utriculopetal) in the vertical canals [18–20].
A frequently overlooked aspect in understanding canalith repositioning procedures is the pathway through which otoliths are directed to the utricle. Notably, otoliths cannot traverse the ampulla. Therefore, the posterior and anterior semicircular canals must guide the otoliths to the utricle via the common crus, while the lateral semicircular canal directs them through the posterior arm, which lacks an ampulla [21,22].
Otoconial calcium carbonate crystals are not inert, non-resorbable structures; rather, they undergo continuous cycles of dissolution and re-precipitation within the endolymph [23]. As a result, vertigo symptoms are often more pronounced in the morning, as calcium carbonate tends to precipitate and aggregate into otoconial particles during periods of relative head immobility at night. These symptoms typically diminish by the afternoon, when ongoing head movements promote the partial dissolution and dispersion of otoconial material into the endolymph.
Posterior Canal BPPV
Clinical feature
PC-BPPV is the most common form of BPPV and is primarily caused by canalolithiasis. Free-floating otoconia dislodged from the utricle are more likely to enter and stay in the non-ampullary arm of the posterior semicircular canal as this canal forms the most gravity-dependent segment of the labyrinth in both upright and supine positions [24–26]. Patients may experience sensations of impending collapse, floating, or nausea. Typically, the vertigo lasts about 1–2 minutes.
Diagnosis
The diagnosis of posterior semicircular canal BPPV can be made when a patient exhibits characteristic nystagmus during the Dix-Hallpike test. Before performing the Dix-Hallpike test, the patient should be informed that severe vertigo may occur. During the procedure, the patient should be instructed to keep their eyes open and maintain central gaze as much as possible. When the head position is changed during the Dix-Hallpike test, otoconial particles move away from the ampulla of posterior canal causing ampullofugal flow (Fig. 1). This endolymphatic flow in turn makes the cupula deflect away from the utricle inducing the excitation of the posterior ampullary nerve according to Ewald’s third law [18]. Excitation of the posterior canal contracts the ipsilateral superior oblique and the contralateral inferior rectus muscles, causing both eyes to slowly deviate downward and rotate toward the contralateral side. This results in characteristic fast torsional and up-beating nystagmus directed toward the affected ear. The Dix-Hallpike test is performed by seating the patient, turning the head 45° toward the affected side. Then the examiners quickly bring the patient to a supine position with the patient’s head hanging off the edge of the examination table with keeping the head typically 20°–30° below horizontal [2,3,10]. This head-hanging position is held for at least 30 seconds to observe for nystagmus (Fig. 1). In patients with PC-BPPV, the latency of nystagmus usually ranges from 5 to 20 seconds, which corresponds to the time required for the otoconia to go down to the most gravity-dependent portion of the canal. In rare cases, it may take up to one minute, so it is advisable to maintain the position and continue observation until nystagmus appears [2,27]. Upon returning to the sitting position, reversal of the nystagmus can be observed [10]. Repeated positional tests result in fatigability, where the intensity of the nystagmus diminishes and eventually is no longer observed. Although the Dix-Hallpike test is the preferred diagnostic maneuver for PC-BPPV, it should be used with caution—or avoided altogether—in patients with cervical spine instability. For these patients, the side-lying test serves as a safe alternative. In this maneuver, the patient, seated on the examination table, rotates the head 45° away from the affected side and then rapidly lies down onto the affected side, thereby positioning the posterior canal in the frontal plane to elicit stimulation [2,3,10,27]. A similar torsional, up-beating nystagmus directed toward the affected ear can be observed (Fig. 2).
Treatment
Most widely performed maneuver for treatment of PC-BPPV is modified Epley’s repositioning maneuver [25]. Epley proposed that PC-BPPV stems from free-floating debris in the posterior canal and designed a series of positional changes to guide canaloliths through the common crus back into the utricle [22,25]. The original Epley maneuver incorporated the use of a mechanical vibrator to help dislodge otoconia and involved administering a sedative prior to the procedure [25]. Subsequently, Parnes, et al. [26] introduced a modified version of the Epley maneuver that eliminates both the vibrator and sedatives, relying instead on three sequential positional steps performed once [26]. This modified method is now widely used in clinical practice. In the modified Epley maneuver, the patient begins in a seated position and is then placed into the Dix-Hallpike position on the affected side while the clinician observes for nystagmus. The head is subsequently rotated 90° toward the opposite side while maintaining full neck extension. Next, the patient’s head and body are rotated an additional 90° toward the unaffected side, with nystagmus again assessed. If the elicited nystagmus resembles that observed during the initial Dix-Hallpike test, it suggests that the otoconia are migrating through the common crus toward the utricle, indicating an effective treatment response. In contrast, if the nystagmus reverses at this stage, it may imply movement of the otoconia toward the ampulla or the presence of cupulolithiasis, both of which are associated with poorer treatment outcomes [21,22,24,26,27]. The patient is then returned to the seated position (Fig. 3). In such cases, the Brandt-Daroff exercises can be recommended [28]. It is generally recommended that each positional step be maintained for approximately 1 to 2 minutes or until the nystagmus resolves. Earlier guidelines advised patients to avoid lying down for 24 to 48 hours after treatment. However, more recent studies indicate that strict postural restrictions do not substantially influence treatment outcomes, and post-treatment instructions may therefore be individualized according to the patient’s condition [2,11,27,29]. Although opinions vary for the repetition of the maneuver, the majority recommend a single session, especially if secondary or reversed nystagmus was not observed when the patient returns to a sitting position. In such cases, further treatments may not be necessary [2,8,10,21,27]. The treatment is considered complete when both nystagmus and vertigo have fully resolved. Epley initially reported an 80% success rate after a single treatment, and the rate increased with repeated sessions [2,5,8,10,21,27]. Recent reports have also shown a better cure rate of modified Epley maneuver around 84%–90% with the first round and around 90%–100% with the second round, especially compared to that of observation-only group (27.3%) [2,5,8,10,21,27,29–31]. A recent meta-analysis demonstrated that patients had a fourfold higher chance of symptomatic improvement and more than a fivefold higher rate of nystagmus resolution at the first follow-up compared to placebo [5].
The Semont liberatory maneuver aims to detach debris adhering to the cupula via inertial and gravitational forces [32]. From a seated position, the patient quickly turns the face 45° toward the unaffected side and lies down rapidly onto the affected side. After maintaining this position for up to 5 minutes, the patient is then quickly moved to lie on the opposite side, so that the face is turned downward with the affected ear facing upward. This position is maintained for up to 10 minutes, after which the patient is slowly brought back to a seated position (Fig. 4). While laboratory simulations indicate that approximately 30 seconds are needed for a dislodged otolith to reach the lowest point of the semicircular canal, most clinical guidelines and reports recommend maintaining each position for a longer duration, typically up to 5–10 minutes [2,27,32]. Although the Semont maneuver is supported by less clinical evidence compared to the Epley maneuver, its reported success rate ranges from 74% to 90% [33,34]. It is particularly useful for patients who are unable to tolerate the Dix-Hallpike maneuver or neck extension due to cervical spine instability [32–34].
Brandt-Daroff habituation exercise is a habituation maneuver often reserved for patients with residual or recurrent symptoms even after repositioning maneuvers or those who cannot tolerate conventional canalith repositioning maneuvers [28]. It can also be applied in the case with limited improvement due to cupulolithiasis. From a seated position, the patient quickly lies down toward the side that provokes dizziness, with the head turned upward approximately 45°. Once the dizziness subsides, the patient remains in this position for about 30 seconds before returning to the seated position. After an additional 30 seconds in the seated position, the same maneuver is repeated toward the opposite side (Fig. 5). This exercise is generally recommended to be performed several times daily and continued until the provoked symptoms gradually decrease, with many guidelines suggesting continuation until the symptoms are absent for two consecutive days [28,35,36]. Brandt-Daroff exercise aims to induce habituation by repeatedly exposing the brain to dizziness-provoking movements, thereby training the central nervous system to reduce its sensitivity and perceive these motions as non-threatening stimuli [28,35,36]. Another suggested mechanism involves fragmentation of the otoconia within the posterior semicircular canal by rapid movements [28,35,36]. However, the precise mechanism has yet to be clearly elucidated. The Brandt-Daroff habituation exercise is not primarily a curative treatment that addresses the underlying cause, but rather a supportive method aimed at alleviating residual dizziness following a canalith repositioning maneuver. In randomized controlled trials, its effectiveness has been reported to be approximately 24% [35,36].
Horizontal Canal BPPV
Clinical features
Vertigo from HC-BPPV may be evoked simply by turning the head while standing up and lying down. Consequently, it is common for patients to enter the consultation room with a constrained and awkward gait, endeavoring to minimize head movement. The nystagmus is primarily horizontal and changes direction with head turning. It rarely shows fatigability upon repeated provocation [37–39]. A careful investigation on directional changes of nystagmus relative to gravity established the pathophysiology of HC-BPPV including that of the cupulolithiasis [37–39].
Diagnosis
The supine head-roll test (Pagnini–McClure maneuver), which involves turning the head to either side while lying down, can aid in diagnosis [37–40]. During this test, the examiner rapidly turns the patient’s head 90° to the left or right in the supine position and observes the resulting nystagmus. In canalolithiasis, horizontal nystagmus beating toward the ground (geotropic) is typically seen (e.g., right-beating nystagmus with right head turn). In contrast, horizontal nystagmus directed toward the ceiling (apogeotropic) is characteristic of cupulolithiasis (e.g., left-beating nystagmus with right head turn). Compared to PC-BPPV, this nystagmus usually exhibits shorter latency, longer duration (approximately 1 minute), and less fatigability upon repeated provocation (Fig. 6) [37–40].
The affected side can be inferred based on Ewald’s second law, which states that excitatory stimuli elicit a stronger response than inhibitory stimuli of equal intensity [18]. Accordingly, in geotropic nystagmus (canalolithiasis), turning the head toward the affected side produces stronger nystagmus, whereas in apogeotropic nystagmus (cupulolithiasis), stronger nystagmus occurs when the head is turned toward the opposite side [40–43]. In clinical practice, however, the intensity of nystagmus on either side is often similar, making lateralization challenging. In such cases, assessment of lying-down nystagmus and head-bending nystagmus can provide valuable additional information for determining the affected side [40–43]. In geotropic nystagmus (canalolithiasis), head-bending nystagmus typically beats toward the affected side, whereas in apogeotropic nystagmus (cupulolithiasis), it usually beats toward the unaffected side. However, for apogeotropic nystagmus, lying-down nystagmus is generally considered more reliable than head-bending nystagmus, which may beat toward the affected side [42]. In cupulolithiasis, a null point can often be observed during slow rotation of the head toward the affected side while the patient is supine. At this point, the orientation of the cupula aligns with gravity, preventing deflection and resulting in disappearance of the nystagmus. This finding can be useful for lateralizing the lesion in cupulolithiasis [41,44].
Treatment
In geotropic HC-BPPV, the barbecue roll (Lempert) maneuver is generally the first-line treatment [45]. The maneuver begins with the head turned 90° toward the affected side, following confirmation of canalolithiasis on the head-roll test. The head is then rapidly rotated 90° toward the unaffected side, with each position maintained for approximately 30 seconds. Subsequent 90° rotations are performed in sequence, totaling 270°–360° toward the unaffected side, thereby directing the otoliths away from the ampulla and out of the horizontal canal (Fig. 7) [10,27,45].
When symptoms are severe or when the barbecue roll maneuver cannot be performed due to patient limitations, the forced prolonged position (FPP, Vannucchi maneuver) may be used as an alternative. In this technique, the patient lies on the healthy side with the unaffected ear down for approximately 12 hours, allowing gravity to facilitate migration of otoliths from the non-ampullary arm of the lateral canal into the vestibule [44,46]. Clinical reports indicate symptom resolution in over 90% of patients within 3 days [47–49]. In some cases, HC-BPPV subsequently converts to PC-BPPV, which can then be effectively treated with the Epley maneuver [50,51].
Treatment of apogeotropic HC-BPPV is more complex. The initial step is to detach the otolithic debris adhered to the cupula. Vigorous head shaking or mastoid vibration can be used for this purpose. When the debris are attached to the utricular side of the cupula, symptoms often resolve immediately once they are detached. However, if they are located on the canal side, detachment may convert the presentation into a canalolithiasis pattern with geotropic nystagmus. Accordingly, after efforts to detach the debris, the supine roll test should be repeated to verify whether a conversion to canalolithiasis has taken place. If conversion is confirmed, treatment can proceed as for geotropic HC-BPPV, typically using the barbecue roll maneuver or FPP. Kim, et al. [52] proposed an effective maneuver for HC-BPPV that integrates the principles of the barbecue roll with optimized head rotation angles to enhance detachment of cupula-adherent otoconia using vibration stimulation.
A series of repositioning maneuvers have been reported and refined by Gufoni, Appiani, and Casani, all aimed at treating HC-BPPV. These maneuvers are applied according to the subtype of HC-BPPV, whether geotropic or apogeotropic. In practice, the maneuvers are often very similar in terms of patient positioning and head rotation, differing only in subtle aspects such as the starting side, the direction or degree of head rotation [53–57]. These minor variations can make it challenging to distinguish among the maneuvers clinically. The Casani maneuver, originally described in 1996, involves rapidly moving the patient from a sitting position onto the affected side, followed by a 45° upward (toward the ceiling) head turn (Fig. 8) [53,54]. The Gufoni maneuver, subsequently introduced as a modification for HC-BPPV, requires positioning the patient on the unaffected side, with the head turned downward (toward the ground) primarily for HC canalolithiasis (geotropic nystagmus on head roll test) (Fig. 9) [54,55]. Another variant of the Gufoni maneuver involves positioning the patient on the unaffected side, with the head turned upward (toward the ceiling) primarily for HC cupulolithiasis (apogeotropic nystagmus on head roll test) to facilitate detachment of cupula-adherent otoliths. However, based on the anatomical configuration and spatial orientation of the horizontal semicircular canal, positioning the patient on the affected side, as in the Casani maneuver, may achieve more effective repositioning, as illustrated in Fig. 8 [53–55]. The Appiani maneuver consists of positioning the patient on the affected side followed by a 45° upward head turn like the Gufoni maneuver in HC cupulolithiasis (apogeotropic nystagmus on head roll test) [56,57]. To summarize the indications more clearly, the Gufoni maneuver is primarily indicated for geotropic nystagmus, typically associated with canalolithiasis or cupulolithiasis on the utricular side. Conversely, the Casani maneuver is considered more effective for apogeotropic nystagmus, which is generally attributed to cupulolithiasis on the canal side. These maneuvers have shown good results in treating both geotropic and apogeotropic HC-BPPV [54,58–60]. However, because large-scale randomized controlled trials have not yet been conducted on these treatments, further studies are necessary to assess their efficacy and compare treatment outcomes among the various methods.
Anterior Canal BPPV
Clinical features
Anterior canal BPPV (AC-BPPV) is considerably less common than PC-BPPV and HC-BPPV [4,6,7]. AC-BPPV was first described by Baloh, et al. [11] in 1987 and was thought to result from free-floating otoconia entering the anterior canal via the common crus during treatment of PC-BPPV. Clinically, AC-BPPV presents with symptoms similar to those of PC-BPPV, but provocative maneuver typically reveals characteristic down-beating torsional nystagmus. In AC-BPPV, the torsional component of the nystagmus is relatively small, with predominantly down-beating movement [61,62]. This is largely attributable to the excitation of the superior rectus muscle by the anterior semicircular canal, which produces a smaller torsional component compared with the superior oblique muscle in the posterior canal. Additionally, the anterior canal has a shallower angle relative to the sagittal plane (approximately 35°–41°) compared with the posterior canal (approximately 49°–56°), further contributing to the predominance of down-beating nystagmus [61,62].
Differentiation from a central origin of positional down-beating nystagmus, such as lesions of the cerebellar flocculo-nodular lobe, is essential, with central nystagmus typically exhibiting minimal latency and persisting without fatigability, which can serve as a subtle clue for differential diagnosis [63,64].
Diagnosis
In clinical practice, AC-BPPV is often suspected when down-beating nystagmus is incidentally observed during the Dix-Hallpike test, which is primarily performed to diagnose more prevalent PC-BPPV [62,65]. Although, in theory, determining the affected side requires careful assessment of the torsional component, this torsional element is frequently subtle or difficult to discern, thereby complicating lateralization. In this context, the straight head-hanging maneuver has been shown to elicit characteristic down-beating nystagmus more reliably than the Dix-Hallpike test in patients with AC-BPPV [62,65].
Treatment
As positional down-beating nystagmus typically predominates with minimal torsional component, determining the affected side based on the torsional direction is often challenging. However, because the anterior semicircular canal is oriented at a relatively small angle to the sagittal plane, as noted earlier, otolithic debris within the anterior limb can migrate toward the common crus when the patient is placed in a deep head-hanging position [61,66]. On the basis of this anatomical principle, Yacovino, et al. [67] proposed a canalith repositioning maneuver for AC-BPPV, which consists of moving the patient from a seated to a supine position, maintaining a deep head-hanging posture for several minutes, then flexing the head forward into a head-bending position for a few minutes while remaining supine, before slowly returning the patient to the sitting position (Fig. 10). Although previous studies have reported relatively high success rates of approximately 80.0% to 85.6% for this maneuver, the low incidence of AC-BPPV limits the number of analyzable cases, representing a notable limitation in the existing evidence [65,68].
Refractory BPPV
In the past, the concept of refractory BPPV prompted reports of surgical interventions, such as posterior semicircular canal occlusion, with case series demonstrating high rates of symptom resolution [69,70]. However, the refinement of various canalith repositioning maneuvers and their consistently high success rates have shifted the treatment paradigm away from surgery [69,70]. Current recommendations emphasize repeated repositioning maneuvers and habituation exercises as the primary management strategies for persistent cases. Because surgical canal occlusion carries a significant risk of hearing loss and vestibular dysfunction, it should be reserved only for patients with truly intractable BPPV and undertaken with great caution.
Although terms such as “canalith impaction” or “immobilized otoconia” are occasionally used in clinical practice to describe cases that are unresponsive to repeated canalith repositioning maneuvers, this concept should be considered a plausible mechanistic hypothesis rather than a phenomenon that has been directly demonstrated. The notion is supported indirectly by biomechanical and anatomical models suggesting that agglutinated otoconial clusters may transiently impede endolymphatic flow or become immobilized within narrow segments of the semicircular canal, thereby reducing cupular deflection and attenuating the expected nystagmus response [71–74]. Alternative or modified repositioning maneuvers are often employed to manage these cases such as more vigorous accelerative maneuvers, head-shaking techniques, or prolonged positional strategies.
Conclusion
BPPV is diagnosed and treated indirectly by inferring the location of displaced otoconia within the semicircular canals based on the characteristic nystagmus elicited during specific provoking tests and canalith repositioning maneuvers. Recent advances and refinements in these maneuvers have yielded high success rates, making BPPV one of the few disorders that can be effectively cured through clinical expertise alone. However, optimal management requires the ability to conceptualize and interpret the underlying microanatomical and physiological dynamics, rather than relying solely on familiarity with standardized maneuvers.
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