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Table of Contents
Year : 2022  |  Volume : 24  |  Issue : 2  |  Page : 51-55

Benign paroxysmal positional vertigo in patients with Meniere's disease

Department of Otorhinolaryngology and Head and Neck Surgery, IMS and SUM Hospital, Siksha “O” Anusandhan University, Bhubaneswar, Odisha, India

Date of Submission05-Apr-2022
Date of Decision23-Apr-2022
Date of Acceptance24-Apr-2022
Date of Web Publication28-Jun-2022

Correspondence Address:
Dr. Santosh Kumar Swain
Department of Otorhinolaryngology and Head and Neck Surgery, IMS and SUM Hospital, Siksha “O” Anusandhan University, K8, Kalinga Nagar, Bhubaneswar - 751 003, Odisha
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/sjoh.sjoh_15_22

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Benign paroxysmal positional vertigo (BPPV) is the most common type of peripheral vertigo. BPPV often occurs after head trauma, viral neurolabyrinthitis, following surgery, and prolonged bed rest. BPPV may be associated with Meniere's disease (MD) and may be found at any stage of this disease. There is a recognized relationship between MD and BPPV. However, the frequency and clinical characteristics of BPPV in MD are not clear. Hydropically induced damage to the maculae of the utricle and saccule or partial obstruction of the membranous labyrinth may be the cause for the coexistence of MD and BPPV. MD may be considered one of the important causes of persistent vertigo in patients with BPPV, which makes it difficult in obtaining the correct diagnosis and aggravates the ability to predict the prognosis. Patients with both MD and BPPV suffer from the intractable type of BPPV despite medical or surgical control of their MD. There are a lower treatment success rate and a higher chance of recurrence rate in patients of BPPV with MD compared to BPPV patients without MD. The recurrence rate is higher in patients with multiple semicircular canal BPPV with MD. The objective of this review article is to discuss the epidemiology, etiopathology, clinical features and diagnostic evaluation, and treatment of BPPV in patients with MD. The databases searched are PubMed, Scopus, Medline, and Google Scholar.

Keywords: Benign paroxysmal positional vertigo, canalith repositioning procedure, Meniere's disease, vertigo

How to cite this article:
Swain SK. Benign paroxysmal positional vertigo in patients with Meniere's disease. Saudi J Otorhinolaryngol Head Neck Surg 2022;24:51-5

How to cite this URL:
Swain SK. Benign paroxysmal positional vertigo in patients with Meniere's disease. Saudi J Otorhinolaryngol Head Neck Surg [serial online] 2022 [cited 2023 Jan 30];24:51-5. Available from: https://www.sjohns.org/text.asp?2022/24/2/51/348719

  Introduction Top

Benign paroxysmal positional vertigo (BPPV) is the most common etiology of vertigo in routine clinical practice. It occurs due to degeneration of the utricular neuroepithelium resulting in detachment of otoconia which float freely in the semicircular canals (SSCs), or attached to the cupula, making the labyrinth sensitive to the gravitational forces.[1] In the majority of cases of BPPV, the causes are idiopathic; however, some cases are secondary. The secondary causes include inner ear diseases, vestibular neuritis, and head trauma.[2] There is an established association between MD and BPPV.[3] The spectrum of onset age for BPPV and MD has similarities which raise questions about the role of otoconia in the development and progression of MD.[4] The pathophysiology of BPPV is the dislodgment of otoconia from the utricle. The otoconia are microscopic crystals of calcium carbonate which drift into the ampulla of the posterior semicircular canal, where these stimulate the end organ and trigger an attack of vertigo.[5] BPPV less commonly affects the lateral semicircular canal or anterior semicircular canal. The early diagnosis and treatment can greatly improve the quality of life in BPPV with MD, so patients should be evaluated timely with appropriate treatment. The objective of this review article is to discuss the etiopathology, clinical characteristics, and its diagnosis and treatment of BPPV in MD patients.

  Methods of Literature Search Top

Multiple systematic methods were used to find the current research publications on the BPPV in patients with MD. We started by searching the Scopus, PubMed, Medline, and Google Scholar databases online. A search strategy using the Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines was developed. This search strategy recognized the abstracts of published articles, while other research articles were discovered manually from the citations. Randomized controlled studies, observational studies, comparative studies, case series, and case reports were evaluated for eligibility. There were a total of 72 articles (18 case reports, 24 cases series, and 30 original articles) [Figure 1]. This study focuses only on BPPV in patients with MD. This study examines the epidemiology, etiopathology, clinical characteristics, diagnostic evaluation, and treatment of BPPV in patients with MD. This analysis provides a better understanding for easy diagnosis of BPPV in patients with MD which will provide prompt treatment. It will also serve as a catalyst for additional study into a newer diagnostic protocol for BPPV in patients with MD.
Figure 1: Flowchart showing the method of literature search. MD: Meniere's disease

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  Epidemiology Top

Barany first described the BPPV in 1921.[6] The term BPPV was coined in 1952, and this disorder was fully defined this year.[7] BPPV is the most common clinical entity found in a neurotology clinic on an outpatient basis, with a lifetime prevalence of 2.4%.[8] The exact frequency of BPPV in MD is unclear. It ranges from 0.3% to 70% as per the different studies.[9],[10] It is still doubtful whether clinical characteristics of BPPV in MD differ from MD with idiopathic etiology. Epidemiological studies showed that both MD and BPPV are found after head injuries (19% for MD and 28% for BPPV).[11] One study showed that 45 patients were diagnosed as MD among 151 patients with BPPV.[12]

  Etiopathology Top

In the majority cases, BPPV occurs spontaneously, but it may occur secondary to different conditions such as head trauma, viral neurolabyrinthitis, MD, and vertebrobasilar ischemia, or it may be due to surgery of the ear and prolonged bed rest.[13] It is thought that any inner ear disease which detaches otoconia and yet does not destroy SCC function can result in secondary BPPV. Idiopathic and secondary BPPV differ in several aspects which implies that the pathophysiology of secondary BPPV may differ qualitatively or quantitively from idiopathic BPPV. BPPV may be associated with MD, and it may occur at any stage of this disease. The basic histopathological feature of MD is excessive endolymph in the endolymphatic sac, known as endolymphatic hydrops. The etiology of hydrops is still not known. The important theories for endolymphatic hydrops are viral infection, autoimmune involvement of the endolymphatic sac, a genetically determined abnormality for endolymph control, and variations in the position and size of the endolymphatic sac and its duct.[14] As per Schuknecht's histopathological studies, the vertigo spells in MD are due to rupture of the Reissner's membrane and potassium intoxication of the perilymph.[15] However, contemporary studies do not support this theory.[16] The drainage theory developed by Gibson and Arenberg tried to explain the vertigo attacks by a dysfunctional or blocked endolymphatic sac, which hampers the longitudinal flow of endolymph, resulting in the building up of the sinus of the endolymphatic duct.[16] Excessive refluxes of the endolymph via the utricular valve of Bast and into the ampullae of SSCs cause vertigo spells.[17] Currently, it is thought that detached saccular otoconia are the causative factor for hydrops. There is evidence from imaging for detached saccular otoconia which may result in obstruction of the reuniting duct, leading to endolymphatic hydrops.[18] The combination of drainage theory and otoconia theory can explain the pathophysiology of MD in BPPV.[4] The high prevalence of BPPV in MD patients could be explained by damage to the utricle caused by hydrops and subsequent otoconia detachment.[19] Distension of the membranous labyrinth in MD can result in loss of its resilience, otolith detachment, and its partial obstruction. Dilatation of the vestibular aqueduct may also contribute to the development of BPPV in patients with MD.[20] One study showed that there are significant differences in the incidence of cupular and free-floating deposits in the posterior and lateral SCCs between temporal bones in patients with and without MD.[17] This study revealed that the incidence of these deposits is associated with the duration of disease rather than the aging process. As many authors supported that BPPV is secondary to MD, one author proposed that MD is secondary to BPPV because loose otoconia can result in a reduction of endolymphatic absorption, leading to endolymphatic hydrops.[21]

  Clinical Characteristics Top

MD is a chronic inner disease with clinical manifestations of recurrent vertigo attacks, fluctuating sensorineural hearing loss (SNHL), tinnitus, and aural fullness. BPPV is defined as transient vertigo induced by rapid changes in head position and associated with characteristic paroxysmal positional nystagmus. The nystagmus may be torsional, vertical, or horizontal and characterized by features of latency, transience, reversibility, and fatigability.[22] BPPV patients often experience severe rotatory vertigo lasting for a few seconds that is brought on by a change in head position such as lying back quickly turning in the bed, reaching for the top shelf, or bending the head. Dix–Hallpike positional maneuver is considered a diagnostic test for BPPV. In this maneuver, the patient usually experiences vertigo along with geotropic torsional nystagmus when brought rapidly from a sitting position to a lying position with the head hanging and turned with the affected ear down. These three forms of BPPV are self-limited, recurrent, and permanent.[23] The self-limiting type is the most common form and is not associated with recurrence. Recurrent BPPV shows recurrent episodes of vertigo with periods of remission lasting for weeks to years. Permanent BPPV is often recalcitrant to treatment with otolith repositioning maneuvers and is considered intractable. BPPV is commonly developed in females with MD. It could be associated with impaired calcium metabolism, which is usually found in perimenopausal females.[24] Female preponderance in MD may be due to misdiagnosis of MD with vestibular migraine, as both diseases are very similar at early stages.[25] Patients with BPPV associated with MD differ from patients with idiopathic BPPV. Patients of BPPV with MD have a higher percentage of female patients, longer duration of symptoms, frequent involvement of horizontal SCC, greater incidence of canal paresis and poorer treatment results, and a higher rate of recurrence. These features may imply that BPPV with MD differs from idiopathic BPPV in terms of several demographic and clinical features that may follow a different course and responds less effectively to the treatment. Patients with one-side hearing loss due to MD usually prefer to sleep on the side of the affected ear and making the unaffected ear prone to developing BPPV. BPPV in MD often affects the horizontal SCC, and the predilection of horizontal SCC is because of development of otolithiasis in MD. One study shows that anatomical factors are responsible for this involvement where horizontal SCC is the predominant canal affected in MD.[26] Several authors have proposed that secondary BPPV has specific clinical characteristics which differ from those of idiopathic BPPV. The first difference is the longer duration of clinical manifestations. This may be due to either different pathogenetic mechanisms or treatment difficulties.

  Diagnostic Evaluation Top

BPPV may be found in the patient with MD, or it can occur at any stage of this disease. MD may be considered one of the causes of persistent vertigo among patients with BPPV, which poses difficulties for getting the correct diagnosis and aggravates the ability to predict the prognosis.[27] Timely and accurate diagnosis of BPPV in patients of MD is challenging for clinicians and patients. The diagnosis of MD is based on clinical presentations such as episodic vertigo, SNHL (usually unilateral) involving low and medium frequencies, tinnitus, and aural fullness in the affected ear.[28] In the case of BPPV, the patient experiences severe rotatory vertigo lasting for a few seconds by changing the head position, such as lying back quickly or turning on the bed.[29] The Dix–Hallpike test is considered positive for posterior (or anterior) semicircular canal BPPV when vertigo is provoked, associated with a burst of torsional-vertical two-component nystagmus with typical characteristics. The supine roll test is positive for horizontal semicircular canal BPPV when intense vertigo is provoked, associated with horizontal geotropic (sialolithiasis) or apogeotropic (cupulolithiasis or canalolithiasis of the short arm of horizontal semicircular canal) paroxysmal nystagmus of latency, crescendo, and transience.[30]

  Treatment Top

The treatment of patients with BPPV associated with MD appears to be less effective and more time-consuming than patients with idiopathic BPPV. There is a high chance of recurrence of BPPV in patients with MD. One study reported that even successful treatment can cause recurrence as high as approximately 50% of cases.[31] There are several explanations for recurrence such as repeated hydropic distension of the endolymphatic sac that may reduce the elasticity of the membranous labyrinth and lead to partial collapse or adhesions of the SCC which may result in partial obstruction. Multiple canalith repositioning procedures are needed for effective treatment.[32] Partial obstruction of the endolymphatic duct may be due to a dilated saccule or adhesion of otoliths to the membranous labyrinth. Periodic hydropic distension is found in the natural course of MD and may lead to the repeated release of otoconia and manifest attack of BPPV. BPPV in MD is more prone to recurrence and needs more canal repositioning maneuver. One study shows that patients with BPPV and MD require more canal repositioning maneuvers than those with pure BPPV.[3] Another study showed no difference between such two groups.[33] Epley's maneuver is an important canal repositioning maneuver used for the treatment of BPPV. Epley described a canalith repositioning maneuver where a series of head movements replace canalith fragments back into the utricle, where these would be absorbed or eliminated by the endolymphatic sac. This maneuver is highly helpful for improvement or cure rates and commonly used for the treatment of BPPV that affects the posterior or anterior semicircular canals.[34] If positional nystagmus persists, the maneuver should be repeated on a weekly basis until the eye movement is abolished. This maneuver has undergone different modifications, all with similar success rates. Recurrence is common and needs repetition of the maneuver.[35] BPPV associated with MD may lead to recurring vertigo and positional nystagmus after repositioning maneuvers with persistent symptoms in some patients.

  Response of Benign Paroxysmal Positional Vertigo in Meniere's Disease to Repositioning Maneuvers Top

Partial blockage of the posterior semicircular canal occurs by a dilated saccule which can cause adherence of otoliths to the membranous labyrinth in MD.[36] Partial blockage allows otoliths to float within semicircular canals and prevents them from returning to the vestibule. Hence, there are a poor response to repositioning maneuvers and a high level of relapse of BPPV in MD. Anatomical alterations of the labyrinth by hydrops probably are the important cause of the intractability of BPPV in MD. One-year follow-up of patients with BPPV in MD patients showed recurrence of vertigo and positional nystagmus in 19.4% of cases but abolished nystagmus after 12 months.[37] Another study showed a 50% recurrence of symptoms in a patient of BPPV associated with MD.[38]

  Further Research Top

Currently, there is a high degree of heterogenicity among different studies of BPPV in MD patients. The majority of the studies are cross-sectional, while few longitudinal studies were found within a short period of time which may underestimate the frequency of BPPV in MD patients. There should be more research required for the evaluation of BPPV in MD. Further studies will be helpful to elucidate the nature of the association between BPPV and MD; whether the former is an etiological factor or complication in relation to the latter one. Longitudinal studies of the patients with BPPV and the involvement of high-resolution imaging techniques of the labyrinth will be more helpful for the proper assessment of BPPV in MD patients.

  Conclusion Top

BPPV patients associated with MD differ from patients with idiopathic BPPV in terms of a longer duration of symptoms, more frequent involvement of posterior semicircular canal, a higher incidence of canal paresis, poorer treatment outcomes, and a higher chance of recurrence. This is commonly found among females. BPPV often develops in an advanced stage of MD but can be found at any stage of the disease. BPPV patients with MD may have involvement in horizontal semicircular canals. The treatment of patients with MD and BPPV may need more repositioning maneuvers. MD patients with multiple semicircular canal BPPV need repeated canalith repositioning procedures and a high chance of recurrence rate.

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