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New views on benign paroxysmal positional vertigo

Wang, Weia,d,e,f,g; Lin, Penga,d,e,f,g; Han, Xia,d,e,f,g; Mao, Xianga,d,e,f,g; Li, Shanshana,d,e,f,g; Wen, Chaoa,d,e,f,g; Liu, Qianga,d,e,f,g; Ni, Guangjianb,c,∗; Chen, Taishenga,d,e,f,g,∗

Author Information
Journal of Bio-X Research: June 2020 - Volume 3 - Issue 2 - p 78-82
doi: 10.1097/JBR.0000000000000069
  • Open

Abstract

Introduction

Benign paroxysmal positional vertigo (BPPV) is the most common vestibular peripheral disease. The proportion of vertigo patients with BPPV is 17% to 42%.[1] BPPV is characterized by brief spinning sensations, usually lasting less than 1 minute, which are generally induced by a change in head position with respect to gravity.[2] In clinical practice, some patients complain of vertigo when getting up in the morning, an improvement in vertigo symptoms after a while, but a recurrence of symptoms when they lay back down in bed, roll over in bed, or get up again. BPPV brings discomfort, such as vertigo, fear, and nausea, as well as an extremely high risk of falling.[3] Although BPPV is usually self-limiting, it still inflicts a considerable personal and socio-economic burden.[4] Therefore, it is important to study the diagnosis, etiology, and treatment of BPPV.

In 2017, the Otolaryngology Head and Neck Surgery Branch of the Chinese Medical Association revised and supplemented the BPPV diagnosis and treatment standards based on the current situation in China and with reference to foreign BPPV guidelines.[5] The Chinese BPPV guidelines have a high clinical value and have guided current research into the diagnosis and treatment of BPPV. With the continuous development of BPPV research, its etiology, risk factors, underlying pathological mechanisms, clinical features, and prognosis have attracted wide attention. We searched the PubMed online database including all articles published until February 2020. The following combinations of key words were used to initially select the articles to be evaluated: “benign paroxysmal positional vertigo”, “vertigo”, “vertigo disease”, “vestibular disease”, and “vestibular function”. In this review of the literature, we examined the current state of BPPV research.

Clinical classification

Etiology and classification of BPPV

The etiology of BPPV remains unclear. BPPV is divided into two types, primary (idiopathic) and secondary. Primary BPPV has no definite etiology and accounts for about 50% to 97% of BPPV cases[6]; secondary BPPV is often secondary to various disorders of the inner ear, such as Meniere disease, vestibular neuritis, and sudden deafness. BPPV has been associated with head trauma, a prolonged recumbent position (eg, at a dentist's office or hair salon), head injury, and otology, oral, and maxillofacial surgery, during which the vibration during surgery can cause otoliths to fall off.

The study of BPPV risk factors has considered sex, age, hypertension, hyperlipidemia, diabetes, calcium and phosphorus metabolism, and estrogen levels[4,7,8]; however, the results have been inconsistent. Current research suggests that older women are more vulnerable to the disease, and that there is female-to-male ratio of 2:1 to 3:1.[4] Further etiological research is therefore required. In the future, etiological treatment may become the main method to treat and prevent BPPV recurrence.

Classification of semicircular canals

The peripheral vestibular apparatus includes the semicircular canals and the otolith organs. Humans have three pairs of semicircular canals, namely, the horizontal semicircular canals, posterior semicircular canals, and anterior semicircular canals. The otolith comprises a utricle and sacculus. A widely accepted pathophysiological theory of BPPV is that otoconia become dislodged from the macula of the utricular otolith and enter the semicircular canals. Changes in static head position with respect to gravity can cause the otolithic debris to move to a new position within the semi-circular canals, which leads to an abnormal endolymph flow that deflects the cupula and thus modulates activity of the vestibular afferents of the affected canal, causing attacks of positional vertigo and nystagmus (canalolithiasis).[9,10] Another line of research has attributed BPPV to otoconia that are attached to the cupula of a semicircular canal that render it sensitive to gravity (cupulolithiasis).[11,12] Otoliths that fall off from the utriculus can potentially enter the anterior semicircular canal, posterior semicircular canal, or horizontal semicircular canal, which results in BPPV of different semicircular canals. Given the anatomical location of the semicircular canals, BPPV of the posterior semicircular canal is the most common and accounts for 60% to 90% of all cases.[2] BPPV of the horizontal semicircular canal is the next most common, and BPPV of the anterior semicircular canal is the least common. Multi-semicircular canal BPPV is also common.[20]

Extension of otolith pathology

BPPV is caused by otoliths falling from the utricle into the semicircular canal. The pathology of cupulolithiasis and canalithiasis has been widely studied. Otolithiasis reduction therapy has also become the first-choice treatment for BPPV and confirms the BPPV pathological theory, but the etiology of BPPV is still not completely clear. One recent study reported that blood cell fragments that have accumulated in endolymph fluid caused by inner ear hemorrhage may cause sudden deafness of the same ear, accompanied by multiple types of BPPV.[13] That study expands the pathological theory of BPPV otoliths. The light crest cap hypothesis of the ampullary crest of the semicircular canal enriches our pathological understanding of BPPV. Recent research has suggested that the entry of otoliths or other substances into the semicircular canal changes the relative proportion of lymph to ampulla crests in the semicircular canal, which may be pathological factors of BPPV.[14,15]

Clinical diagnosis

The complete diagnosis of BPPV includes the specification of the affected semicircular canal(s) and the pathophysiology (canalolithiasis or cupulolithiasis).[9] Otolith mass that can excite or inhibit each semicircular canal is linked to a specific nystagmus, because every vestibular stimulus triggered by each ampullary cupula deflection provokes the contraction of extrinsic ocular muscles, thus generating a specific and characteristic eye movement in response to each ampullary nerve input. Unlike central positional nystagmus, positional nystagmus in BPPV always observes the law, and beats in the plane of the affected canal and in the expected direction for canal excitation or inhibition.[16]

There are many types of positional testing, and different maneuvers test the involvement of different semicircular canals. Nystagmus in patients with BPPV is typically induced using the Dix–Hallpike or roll test maneuver. The latency, direction, time course, and duration of positional nystagmus are important feature indexes. For example, BPPV involving the posterior canal is diagnosed on the basis of nystagmus beating in an upward and torsional direction, with the top poles of the eyes beating toward the lower ear, as observed when the patient is lying on their side during the Dix–Hallpike maneuver. The nystagmus usually develops after 2 to 5 seconds and reverses direction when the patient sits up. After patients lie down or sit up, the nystagmus resolves within 1 minute.[17] If the otoconia become attached to the cupula (cupulolithiasis), the evoked nystagmus is similar to that observed in canalolithiasis, but usually lasts longer than 1 minute.[18]

To test the horizontal canal, the supine roll test is used, whereby the head in the supine position is elevated by about 30° and then turned quickly to either side. Canalolithiasis of horizontal canal (hc-) is characterized by nystagmus that is either geotropic (beating toward the ground) or apogeotropic (beating toward the ceiling) when the head is turned to either side while the patient is in the supine position. The nystagmus in cupulolithiasis is opposite to that of hc-BPPV. The duration is longer than 1 minute.

According to the characteristics of nystagmus induced by different position tests,[19] it is possible to identify the semicircular canal into which the otolith has fallen off. It should be noted that the characteristic nystagmus of BPPV of the posterior and horizontal semicircular canal can be identified by the position test. Some patients may exhibit a lower intensity nystagmus after the initial positional nystagmus has ceased. The reversed direction nystagmus is often misdiagnosed as anterior semicircular canal BPPV, and can make it difficult to determine the affected side in horizontal semicircular canal BPPV.[20

The BPPV diagnosis primarily relied on subjective positional vertigo symptom and face-to-face observation of eye movement in the past, and current BPPV diagnosis mainly relies on videonystagmography, which can show more precise characteristics of nystagmu.[9] Canalith-repositioning maneuvers (eg, Epley and Semont maneuvers for the posterior canal) are the first choice of treatment for BPPV. The key to successful reduction is to identify the semicircular canal in which otoliths have fallen. The diagnosis of BPPV not only considers the patient's complaint, but also relies on the observation of characteristic nystagmus induced by the positional test. However, the otolith location diagnostic tests described by the BPPV clinical guidelines of many countries, including China, currently rely on direct observation of nystagmus induced by the positional test. Positional nystagmus is often accompanied by difficulty distinguishing between the strong and weak sides (especially for the horizontal semicircular canal) by face-to-face observation. When nystagmus is weak, it is easily suppressed by fixation or can be overlooked during visual observation. This makes it difficult to determine the affected semicircular canal and to decide upon subsequent otolith reduction treatment, and can even lead to a subjective BPPV diagnosis. Therefore, developing a more objective and accurate otolith localization method has become a primary focus in BPPV research.

The development of the videonystagmography has allowed for more accurate and objective observations of nystagmus direction, intensity, and duration, and has provided technical support for BPPV nystagmus analysis. In previous work, we found that horizontal nystagmus can be recorded in patients with canalolithiasis of the horizontal canal on both sides of the head during the roll test.[21] The direction of nystagmus induced by horizontal semicircular calculus is the same as that induced by head-turning. The duration of nystagmus on the diseased side is longer than that on the healthy side. The nystagmus induced by the diseased side is also stronger, with a nystagmus intensity ratio of about 2:1. The direction of nystagmus induced by cupulolithiasis of the horizontal semicircular canal is opposite to the direction of head deviation. In patients with cupulolithiasis of the horizontal canal, the duration of nystagmus is more than 1 minute and nystagmus is strong on the healthy side. The ratio of nystagmus intensity on the affected side to that on the healthy side is about 1:2. BPPV of the posterior semicircular canal has been reported to be accompanied by strong vertical upward and weak horizontal contralateral nystagmus at the hanging head position of the Dix–Hallpike test and a reversed nystagmus direction when returning to the sitting position. The intensity of nystagmus induced by a hanging the head on the affected side is greater than that induced by returning to the sitting position, and the intensity ratio is approximately 2:1, while there is no difference in the duration of nystagmus induced by the two positions.[22] The spatial position of the ampulla of the posterior semicircular canal determines that in the hanging the head position, both canalolithiasis of the posterior canal and cupulolithiasis of the posterior canal drive the endolymph to produce excitatory stimulation away from the ampulla. The duration of canalolithiasis of the posterior canal is less than 1minute, while the cupulolithiasis of the posterior canal has a duration of more than 1 minute. The Dix–Hallpike test has revealed that the direction of nystagmus induced by the anterior semicircular canal BPPV at each head position is opposite to that of induced by posterior semicircular canal BPPV.[10] The duration of nystagmus is a key parameter that can be used to distinguish between semicircular canal calculus and cupulolithiasis, while the direction and intensity of nystagmus are key indicators to identify where otoliths have fallen off. The results of our research about objective characteristics of nystagmus in horizontal semicircular canal BPPV and objective characteristics of nystagmus in patients with posterior semicircular canal BPPV[22] are in line with the current diagnostic guidelines, but our methods are more objective and comprehensive, and thus promote a more accurate diagnosis of BPPV and support the study of the mechanisms underlying nystagmus. On the basis of previous research, we conducted a detailed quantitative analysis on nystagmus data. The application of the three-dimensional videonystagmography will allow for more objective BPPV diagnoses. Atypical BPPV has also been reported, such as horizontal semicircular canal forearm or short arm canalolithiasis, variably canalolithiasis of the posterior canal, but it needs to be distinguished from nystagmus of vestibular central lesion and vestibular decompensation period.

Evaluation of vestibular function

Until now, the examination recommended by the BPPV diagnosis and treatment guidelines of various countries is still limited to the bedside positional test for otolith localization. Analysis of the causes of otolith detachment, lesions of the affected semicircular canal, and the corresponding clinical vertigo symptoms has not attracted much attention. Almost all the international diagnosis and treatment guidelines for vestibular function tests of patients with BPPV hold a different view, which may be based on the perspective of health economics and the popularization of vestibular examination technology; indeed, vestibular function tests consume a lot of time and money. The consequence of saving vestibular function examination costs is that the functional status of semicircular canals and otoliths in patients with BPPV cannot be further explored, which limits the further study of BPPV. Indeed, when a patient still has slight vertigo imbalance after otolith reduction, most of the current research has considered this as a residual symptom of otolith reduction and has not further analyzed the influence of the utriculus and corresponding semicircular canal lesions on vestibular function. Previous studies have shown that 56.7% of patients with BPPV have ocular vestibular-evoked myogenic potential abnormalities,[23] the presence of semicircular canal paresis that affects the prognosis of BPPV treatment,[24] that around 2/3 patients with BPPV have vestibular semicircular canal dysfunction, and the abnormal proportion of vestibular semicircular canal of BPPV shows an upward trend with a longer disease course.[25] Therefore, BPPV is especially attributed to the semicircular canals and otolith lesions that can be caused by various pathological factors. Vestibular function evaluation is beneficial to an understanding of BPPV pathophysiology, the mechanisms underlying nystagmus, clinical symptoms, prognosis analysis, and the evaluation of residual symptoms after otolith reduction. Based on national clinical practice requirements, the Otolaryngology Head and Neck Surgery Branch of the Chinese Medical Association has recommended vestibular function examinations for patients with BPPV in the 2017 edition of BPPV diagnosis and treatment guidelines, and has listed this examination as the first item in the optional examination series (the other examination items are audiology, radiographic evaluation, balance function, and etiological examination).[9]

The three elements of BPPV

BPPV can be caused by otolith pathology involving lesions or damage to the utriculus, whereas nystagmus is caused by stimulation of the semicircular canal. First element, when enough otoliths have fallen off, the movement of these fallen otoliths to the semicircular canal causes BPPV[26]; otoliths are similar to the endogenous rotation stimulating factors in the semicircular canal. Second element, head position change relative to the direction of gravity causes movement of otoliths and drives endolymphatic flow to cause ampullary crest deflection, or directly causes ampullary crest deflection to induce nystagmus in the corresponding semicircular canal plane, such that head position change is the cause of endogenous rotation of the semicircular canal. Third element, the semicircular canal is functional, in that hair cells of ampulla crista respond to appropriate suprathreshold stimulation. Therefore, if otoliths that fall off the oval capsule are not ectopic to the semicircular canal, and if the otoliths are ectopic to the semicircular canal, there is no head position change, even if the first and second elements are available, or if any of these three elements is paralyzed, BPPV does not occur.

The three elements of BPPV bring us some enlightenment. First, BPPV research should shift its interest from the current shallow otolith localization and reduction to BPPV etiology, pathology, and relapse prevention, as well as the otolith source. Researchers have started to take interest in otolith metabolism and oval capsule function. Second, BPPV caused by otolith movement from the oval capsule to the semicircular canal is accompanied by vertigo. This scenario also provides a physiological model of the response effect of a single semicircular canal to a single stimulus factor, which could help to further verify and develop vestibular physiological theory. This will be beneficial to a deeper understanding, verification, and development of vestibular physiological theories previously derived from animal experiments (eg, Flours Ens and Ewald Law).[27]

According to the above three elements, the clinical symptoms of BPPV are caused by the physiological responses of the corresponding semicircular canals, which has allowed us to more precisely define BPPV as benign, paroxysmal, or positional BPPV. Benign BPPV describes the physiological response of a semicircular canal. Paroxysmal BPPV is related to semicircular canal function, whereby otolith stimulation causes a reaction that disappears when the stimulation stops. Repeated stimulation will lead to fatigue, showing paroxysmal, which conforms to a physiological reaction. Positional BPPV describes the physiological response of the semicircular canal to head position change relative to gravity, which disappears when the head position change stops. Therefore, rather than a disease, BPPV is a physiological reaction of the vestibule. Clinicians should understand this feature of BPPV and explain it to patients, which would help to relieve their psychological pressure, as well as follow-up diagnosis and rehabilitation.

BPPV can be used as a model to study the physiological effects of a single semicircular canal, especially the semicircular canal-nystagmus effect. This would help us to understand the clinical symptoms and signs of BPPV and more fully understand its physiological properties. Flourens and Ewald studied the semicircular canal physiology using animal models.[27] The use of animal models means that it is unclear whether their results are consistent with semicircular canal physiology in humans. Although the labyrinthine fistula test is similar, it cannot reflect the situation of each semicircular canal. BPPV is a human model helping to better understand human semicircular canal physiology in which a single factor stimulates the semicircular canals to produce excitatory or inhibitory reactions.

Regardless of the type of BPPV, which is diagnosed according to the excitatory or inhibitory effects (including horizontal, vertical, or torsional nystagmus) of otoliths as a single stimulus in the corresponding location test, the ratio of the intensity of the excited and inhibited nystagmus is approximately 2:1.[21] Using a series of position tests in patients with BPPV, including the Roll Test and Dix-Hallpike Roll test, Flourens and Ewald results obtained from animal models have been verified in humans. Therefore, BPPV is also the best way to understand human semicircular canal physiology and the nystagmus effect, which would improve our understanding of human semicircular canal function and vertigo symptoms.

Clinical treatment

The preferred treatment for BPPV is otolith reduction, which is convenient and effective. Currently, there are two different treatment options, which are as follows: (1) the rapid reduction method: This otolith reduction process is rapid, and involves strong stimulation that results in vertigo symptoms, which allows nystagmus to be conveniently observed during reduction. Patients who undergo this process report that the symptoms disappear quickly after the sudden vertigo; they also report a remarkable treatment effect; (2) the soft reduction method: This otolith reduction process is gentle and slow. The aim is to minimize the discomfort of patients. It involves slowly changing the body position under the semicircular canal reaction threshold. During otolith reduction, vertigo symptoms are not induced, which gives patients a less distressing experience. Of course, patients may misunderstand that the rapid reduction method (the otolith reduction process is rapid, and the symptom could disappear rapidly) is so simple. Even so, this mild treatment is recommended. Additionally, according to the individual characteristics and needs of patients, an otolith reduction chair or surgical treatment can also be applied.

Based on previous research,[28,29] we concluded that the origin of BPPV is utricle lesions, the clinical manifestations of which are nystagmus and vertigo symptoms on the semicircular canal plane. Diagnosis and otolith reduction therapy are only one part of BPPV research. Further research directions of BPPV include systematic etiological analysis, objective and accurate diagnosis, comprehensive evaluation of vestibular function, corresponding etiological treatment, and relapse prevention, which should receive extensive attention in future work.

Efficacy evaluation

The 2017 edition of the BPPV Diagnostic and Therapeutic Guidelines of Otolaryngology Head and Neck Surgery Branch of the Chinese Medical Association puts forward several new ideas on evaluation of the therapeutic effect, especially those that concern the timing of therapeutic effect evaluation.[9] These include immediate, short-term, and long-term evaluations. Immediate evaluations assess the curative effect of otolith reduction. Short-term evaluations assess the effect of a comprehensive treatment, such as otolith reduction, vestibular rehabilitation training, and drug therapy. Long-term evaluations not only assess the curative effect of the comprehensive treatment, but also verify the correctness of the preliminary diagnosis and allow any necessary revisions of the diagnosis to be made. Future work should focus on the causes of BPPV and its diagnosis and treatment, such that comprehensive treatment can be applied.

Conclusion

While BPPV is a popular research topic, basic research into its pathological mechanism and etiology, for example, has not led to clear answers. Furthermore, the vestibular function examinations in clinical work have not been fully explored. We suggest that, besides paying more attention to BPPV diagnosis and curative effects, future work should more fully investigate other research fields related to BPPV, such as BPPV etiology, pathology, and pathophysiology.

Acknowledgments

The authors would like to thank all of the study participants and members of staff at the Department of Otorhinolaryngology Head and Neck Surgery, Tianjin First Central Hospital, China.

Author contributions

Conceived and designed the review: WW, PL, GN, TC. Examined the literature: SL, CW. Wrote the paper: WW, XH, TC. Revised the language: XH, QL. Revised the article: PL, GN, XM. All authors read and approved the final manuscript.

Financial support

This study was supported by the National Natural Science Foundation of China (No. 81971698), Tianjin Natural Science Foundation of China (No. 19JCYBJC27200), Beijing-Tianjin-Hebei Basic Research Cooperation Project, China (No. 18JCZDJC45300), and Key Clinical Discipline of Tianjin, China.

Conflicts of interest

The authors declare that they have no conflicts of interest.

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Keywords:

benign paroxysmal positional vertigo; vertigo; vertigo disease; vestibular disease; vestibular function

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