Anterior Canal Benign Paroxysmal Positional Vertigo

Santosh Kumar Swain

doi:10.25259/AONO_4_2025

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Review Article

2025

:6;

e014

doi:

10.25259/AONO_4_2025

Anterior Canal Benign Paroxysmal Positional Vertigo

Santosh Kumar Swain¹

1Department of Otorhinolaryngology and Head and Neck Surgery, All India Institute of Medical Sciences, Bhubaneswar, Odisha, India

*Corresponding author: Santosh Kumar Swain, Department of Otorhinolaryngology and Head and Neck Surgery, All India Institute of Medical Sciences, Bhubaneswar, Odisha, India. santoshvoltaire@yahoo.co.in

Received: 2025-01-03, Accepted: 2025-04-26, Published: 2025-06-23

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This is an open-access article distributed under the terms of the Creative Commons Attribution-Non Commercial-Share Alike 4.0 License, which allows others to remix, transform, and build upon the work non-commercially, as long as the author is credited and the new creations are licensed under the identical terms.

How to cite this article: Swain SK. Anterior Canal Benign Paroxysmal Positional Vertigo. Ann Otol Neurotol. 2025;6:e014. doi: 10.25259/AONO_4_2025

Abstract

Benign paroxysmal positional vertigo (BPPV) is a leading aetiology for manifesting vertigo among the adult age group. Posterior or lateral canal BPPV is well documented in clinical practice and widely approved among clinicians. However, the same does not apply to BPPV affecting the anterior semicircular canal. Downbeat vertical nystagmus with a small torsional component is a characteristic of anterior canal benign paroxysmal positional vertigo (ac-BPPV), an uncommon form of BPPV. Due to its anatomical site, the anterior semicircular canal is rarely impacted. Clinical history and the Dix-Hallpike or head-hanging tests, which detect distinctive nystagmus, are typically used to make the diagnosis. A less noticeable torsional component, which is assumed to represent the affected side, is frequently linked to the downbeat nystagmus in ac-BPPV. When bilateral, ac-BPPV can imitate downbeat positional nystagmus arising from a central cause. No matter which side is affected, the Yacovino manoeuvre is symmetrical for unilateral ac-BPPV. This review article discusses the characteristics of ac-BPPV with its diagnosis and treatment.

Keywords

Anterior canal benign paroxysmal vertigo

Down beat nystagmus

Torsional nystagmus

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INTRODUCTION

Dizziness or vertigo is a common clinical symptom for patients attending the outpatient department of otolaryngologists or physicians.¹ Benign paroxysmal positional vertigo (BPPV) is the most common cause of vertigo of labyrinthine origin in patients.² One of the most prevalent and curable causes of peripheral vertigo is BPPV, which occurs when loose otoconia that have been displaced from the otolith organs that activate one or more semicircular canals.³ The most commonly affected semicircular canal is the posterior one, which is followed by the lateral and anterior semicircular canals (least common). Anterior canal benign paroxysmal positional vertigo (ac-BPPV) was thought a myth until first documented in 1987.⁴ After videonystagmography systems, the diagnosis of ac-BPPV is presently easier. So, more number of patients with ac-BPPV are not documented in the clinical practice. Ac-BPPV is an uncommon type of semicircular canalolithiasis.⁵ A torsional vertical down beating positional nystagmus can be detected on either side in the Dix-Hallpike test or in the supine straight head hanging position test in a patient with BPPV.⁵ Both ac-BPPV and the apogeotropic form of contralateral posterior semicircular canal BPPV can account for this kind of nystagmus.

METHODS OF LITERATURE SEARCH

We conducted a search for research articles on the anterior canal benign paroxysmal positional vertigo using various methods. This began with searching online databases such as Scopus, PubMed, Medline, and Google Scholar. A search strategy was created based on the Preferred Reporting Items for Systematic Reviews and Meta-Analysis guidelines. The search approach found published article abstracts, and citations were used to manually find more research publications. The suitability of observational studies, comparative studies, case series, case reports, and randomised controlled trials for inclusion in this review were evaluated. A total of 61 articles (23 case reports, 17 case series, and 21 original articles) were found across various databases, with 44 being included in this review [Figure 1]. This article discusses the prevalence, pathophysiology, clinical presentations, diagnosis, differential diagnosis, and current treatment of anterior canal benign paroxysmal positional vertigo.

PREVALENCE

Benign paroxysmal positional vertigo is showing more prevalent than previously appreciated. Benign paroxysmal positional vertigo is the most common cause of peripheral vertigo and accounts for 1% of all patients attending ear, nose, and throat specialists and neurologists.⁶ Approximately 9% of a randomly selected urban geriatric population showed undiagnosed BPPV on a positional test.⁷ The most common type of BPPV is posterior canal BPPV, which has a life-type prevalence of 2.4%.⁶ Ac-BPPV is considered the rarest type of semicircular canalolithiasis.⁸

ANATOMICAL ORIENTATION OF ANTERIOR SEMICIRCULAR CANAL

The anterior or superior semicircular canal’s anatomical configuration makes it less conducive to displaced otoconia floating in its free arm.⁹ Its low incidence is caused by two factors: the anterior canal is located in the superior location of the labyrinth, and its non-ampullary arm descends straight into the common crus before continuing into the vestibule.⁹ One of the two semicircular canals in the sagittal plane is the anterior one, which has an anatomical orientation of 41° to the sagittal plane and a posterior orientation of 56° to the sagittal plane.¹⁰ The crus commune, which leads to the utricle, is where these converge to meet. The anterior canal is higher than both lateral and posterior canals. This anatomical location makes it less likely for otoconial debris to enter into the canal against gravity.⁹ These anatomical positions also facilitate self-clearance of the otoconial debris due to gravity. The low incidence of ac-BPPV may be one of the common reasons for a paucity of the studies and literature. The Barany Society Consensus documents this clinical entity as an emerging and controversial entity.¹¹ Ac-BPPV accounts for approximately 3%–12% of all BPPV types.¹² According to a study, ac-BPPV can be caused by anatomical variations such as changes in the diameter of the common crus, stenosis of the anterior semicircular canal’s membranous duct, or changes in the diameter of the anterior semicircular canal itself.¹³ The presence of vertical downbeat nystagmus in certain situations can be explained by the anterior semicircular canal’s increased proximity to the sagittal plane. For this reason, isolated downbeat nystagmus without or with a little torsional component may be seen in certain ac-BPPV patients.¹⁴ The downward-beating eye movement arises due to a relatively weaker torsional vestibulo-ocular reflex when compared to the horizontal and vertical reflexes. This difference accounts for the characteristic features of ac-BPPV, which include both downbeat vertical nystagmus and a torsional element. However, isolated downbeat nystagmus may also indicate central nervous system abnormalities, especially involving the cerebellum. Therefore, it’s essential to exclude such central lesions before confirming a diagnosis of ac-BPPV.¹⁵

PATHOPHYSIOLOGY

Ac-BPPV exists in two forms: canalolithiasis and cupulolithiasis.¹⁶ In the canalolithiasis type, particles (otoliths) are freely floating within the anterior canal, typically causing symptoms that begin after a delay of around 10 seconds and can last for up to 1 minute.¹⁷ The otoliths are attached to the cupula in anterior canal cupulolithiasis, which manifests as a persistent downbeat nystagmus that lasts longer than a minute and may or may not have a torsional component.¹⁸ Ac-BPPV may be proved when the long arm of the anterior canal (part of the canal between the cupula and common crus) is sufficiently lower than the cupula. Canalithic debris drifts downward, away from the cupula, and toward the pull of gravity during orientation of the head. The falling canalithic debris provokes a vacuum that distends the cupula, which in turn provokes nystagmus in the plane of the anterior semicircular canal. These expectations align with Ewald’s first law and the principles of canalithiasis. Positioning-induced nystagmus that is downbeat and torsional, or purely downbeat, is a recognised hallmark of ac-BPPV. It can be identified through the standard Dix-Hallpike manoeuvre or by placing the patient’s head in a straight, extended position over the edge of the edge of the examination couch. The anterior semicircular canal is anatomically situated in a superior position during most activities, with the posterior arm of the anterior canal descending directly into the common crus and vestibule.¹⁹ Normally, particles in the anterior semicircular canal are expected to clear on their own, but this doesn’t happen in ac-BPPV. Due to the almost vertical alignment of the ampullary portion of the anterior canal, debris can come into close contact with the cupula, leading to cupulolithiasis. Unlike canalolithiasis, cupulolithiasis is characterised by persistent vertigo and nystagmus, without the typical adaptation or reduction in symptoms over time.¹⁹

CLINICAL PRESENTATIONS

The key feature of ac-BPPV is the distinctive downbeat vertical nystagmus with a torsional component, primarily observed during deep head hanging and Dix-Hallpike manoeuvres, without any inversion of the vertical component when returning to an upright position.⁴ A marked extension of the head can allow deposition of otoliths in the anterior semicircular canal and result in vertigo and nystagmus. One study showed an isolated ac-BPPV was seen in a plumber following a long period of work underneath a hand basin with his head in forced hyperextension and turned towards the affected side.²⁰ The low incidence of ac-BPPV contrasts with the clinical importance of its most prominent feature, positional down-beating nystagmus, which is also seen as central positional nystagmus associated with different brainstem and cerebellar lesions, and may indicate a sinister pathology.²¹ There are certain factors that increase the chance of bilateral ac-BPPV include a history of bilateral multi-canal BPPV, transient down-beating and torsional nystagmus that follows the plane of the provoked semicircular canal, and lack of co-occurring neurological symptoms and signs of central nervous system dysfunction. During clinical examination, a nystagmus beating predominantly downward but with a small torsional component in which the upper pole of the eye beats towards the affected ear is called torsional-vertical down-beating positional nystagmus.⁴ When transitioning the patient from a sitting to a lying position with the head straight and tilted backward as far as possible, a clockwise torsional nystagmus suggests right-sided ac-BPPV. This nystagmus can be triggered during the supine straight head-hanging position test or the Dix-Hallpike test on either side. In ac-BPPV, there is typically no latency, and the nystagmus is fatigable.⁴ However, a short latency and long-duration nystagmus have also been reported.²² When returning to the sitting position, some described the absence of down-beating vertical nystagmus, while others documented an inversion in 42% of cases.²³ The torsional component is often challenging to detect through visual inspection alone. Advanced techniques, such as three-dimensional scleral-coil or video-oculographic recordings, are required to accurately determine the direction of the nystagmic fast phases.²⁴ Unlike the posterior and horizontal canal variants, there is limited data on the frequency, diagnostic methods, and therapeutic manoeuvres for ac-BPPV, with many studies focusing on only a small number of patients. This study performed a systematic review of research examining the incidence, diagnostic approaches, and treatment options for this rare form of canalolithiasis.

DIAGNOSIS

The positional tests, such as the Dix-Hallpike and supine head-hanging tests, are commonly used for the diagnosis of ac-BPPV.⁴ In ac-BPPV, patients present with a vertical down-beating nystagmus with a torsional component toward the affected side evoked by the Dix-Hallpike test and supine head-hanging test.²⁵ In head-hanging position, free otoconia in the anterior semicircular canal drift away from the cupula, producing an excitatory response, and consequently, the clinical examination will show a torsional vertical down-beating nystagmus. The torsional component is often less intense than the vertical, due to the proximity of the anterior canal to the sagittal plane (41°) when compared to the posterior canal (56°), and its presence gives a localising clue.²⁶ In ac-BPPV, latency is typically absent and nystagmus is fatigable. However, a short latency and a long-duration nystagmus have also been described in ac-BPPV. When returning to the sitting position, some authors document the absence of inversion of the down-beating vertical nystagmus, while others describe an inversion in approximately 42% of cases.²⁷ However, the torsional component of nystagmus is not often clear and with less intense than the vertical one, and so it require differentiation from the posterior canal down-beating BPPV.²⁸ So, the determination of the affected side in ac-BPPV is often difficult in Dix-Hallpike test. The supine head-hanging test is more sensitive test for the diagnosis of ac-BPPV, as it acts in the sagittal plane and stimulates bilateral anterior semicircular canals at the same time.²⁹ However, there are not accepted diagnostic positional tests for ac-BPPV so far. Down-beating nystagmus can be associated with central lesions and should be ruled out from the peripheral down-beating nystagmus. Patients with ac-BPPV are frequently assessed using gadolinium-enhanced brain MRI to exclude posterior fossa lesions since cerebellar abnormalities can also cause positional vertigo accompanied by vertical down-beating nystagmus.³⁰ MRI of the brain must be done in all cases of BPPV of posterior semicircular canal (SCC) and ac-BPPV that do not respond to a particle repositioning manoeuvre to rule out posterior fossa tumor.³⁰

Diagnostic Criteria of Ac-BPPV

The diagnostic criteria for ac-BPPV are not well established. Vertical down-beating nystagmus, often with a slight torsional component, occurs regardless of head turn direction, which complicates identification of the affected side.³¹ The present diagnostic criteria of ac-BPPV include³²: (a) Recurrent episodes of positional vertigo or positional vertigo induced by lying down or turning over in the supine position; (b) the duration of vertigo is less than 1 minute; (c) existence of a positional vertical downbeat nystagmus with a slight torsional component that is triggered by the Dix-Hallpike positioning test and the straight head hanging test [Figures 2 and 3], without the downbeat vertical nystagmus inverting when the person returns to a sitting posture; and (d) not caused by any other illnesses.

Right ac-BPPV (nystagmus is down beating and counter clockwise) elicited in Dix-Hallpike manoeuvre or deep head-hanging manoeuvre. ac-BPPV: Anterior canal - Benign paroxysmal positional vertigo.

Left ac-BPPV (nystagmus is down beating and clockwise) elicited in Dix-Hallpike manoeuvre or deep head-hanging manoeuvre. ac-BPPV: Anterior canal - Benign paroxysmal positional vertigo.

DIFFERENTIAL DIAGNOSIS

Differential diagnosis of ac-BPPV is apogeotrophic posterior canal BPPV.³³ Down-beating positional nystagmus is typically related to central nervous system disease, typically in the lower posterior fossa or cervical medullary junction.³³ The anterior canal, particularly when bilateral, benign paroxysmal positional vertigo can resemble downbeat positional nystagmus of central origin. While hyperventilation has little effect on ac-BPPV, it may cause central downbeat nystagmus. Cerebellar degeneration, Arnold-Chiari malformation, and other lesions of the cerebellar flocculus, as well as lesions of the medial longitudinal fasciculus on the fourth ventricle’s floor, can all cause downbeat nystagmus.³⁴ A negative neurological finding, a positive history of BPPV (usually multi-canal), down-beating/torsional eye movements that correlate with the offending anterior canal, and a nystagmus time course compatible with canalithiasis are the criteria used to distinguish between unilateral ac-BPPV and central positioning nystagmus.

TREATMENT

A number of therapeutic approaches have been proposed to treat ac-BPPV. When the affected side is diagnosed, a technique like the Rahko manoeuvre, reverse Epley, or the one outlined by Kim et al. is suggested for the treatment of ac-BPPV.^35,36 Yacovino and Hain suggested a technique that benefits both anterior canals symmetrically, irrespective of the side that is impacted.³⁷ The anterior semicircular canal follows a different trajectory from the posterior semicircular canal, so manoeuvres for treating ac-BPPV must need different geometrically from those described for the posterior semicircular canal. In the Dix-Hallpike test, the posterior canal is the most stimulated and evaluated; therefore, it is reasonable to believe that the anterior canal is better excited and evaluated when leaning forward.³⁸ Since the anterior and posterior canals are co-planar, it may be advised to treat ac-BPPV by reversing the techniques used to treat posterior canal BPPV, such as Epley’s and Semont’s manipulations.³⁹ The important treatment options for ac-BPPV include the Yacovino manoeuvre and the reverse Epley manoeuvre. In order to cure ac-BPPV, the head is turned upside down to allow debris to reach the top of the canal. Subsequent actions cause debris to go into the common crus and eventually into the vestibule. The advantage of the Yacovino technique over the others is that it does not need knowing which side is impacted.

Yacovino Manoeuvre

It entails bringing the patient up to the sitting posture, bending the neck, flexing the neck to the chin to the chest, and then bringing the patient to the supine head-hanging position. In this manoeuvre, the chin to chest position may result in the entering of debris into the posterior canal, leading to canal switch instead of positioning to utricle. If the chin to chest position of the patient is kept for a longer time, the chance of a canal switch can happen. This is iatrogenic posterior canal BPPV following treatment of ac-BPPV by Yacovino manoeuvre.⁴⁰ The Yacovino manoeuvre is suggested as a therapeutic approach with the unique benefit that it eliminates the need to identify the side of participation for therapy. Modified Yacovino’s move has the advantage of not requiring side identification. Contralateral ac-BPPV can be treated with modified Epley. Accordingly, a left Epley’s should be performed if the patient has right ac-BPPV.⁹

Bangalore Manoeuvre

The patient is instructed to kneel on the bed and then sit up on their knees. Next, the patient quickly bends forward until the top of their head touches the bed and remains in this position for 1 minute. After 1 minute, the patient swiftly returns to the kneeling position.¹⁹

CONCLUSION

Ac-BPPV is an uncommon form of BPPV but an existent entity. Ac-BPPV is characterised by typical torsional and downbeat nystagmus, which is triggered by the Dix-Hallpike and deep head hanging tests. The nystagmus does not reverse when the patient resumes an upright posture. Downbeat nystagmus, sometimes accompanied by a torsional element observed during positional testing, is the only known characteristic of ac-BPPV. There is no reversal of nystagmus when getting up. Ac-BPPV can typically be resolved with the modified Yacovino’s manoeuvre in most cases. The majority of patients with ac-BPPV can be effectively treated with the Yacovino’s manoeuvre.

Ethical approval

The Institutional Review Board has waived the ethical approval for this study.

Declaration of patient consent

Patient’s consent not required as there are no patients in this study.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

Use of artificial intelligence (AI)-assisted technology for manuscript preparation

The authors confirm that there was no use of artificial intelligence (AI)-assisted technology for assisting in the writing or editing of the manuscript and no images were manipulated using AI.

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