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Med Sci Monit, 2007; 13(6): CR275-282 PMID: 17534234

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Received: 2006.08.10 Accepted: 2007.01.15 Published: 2007.06.01

Benign paroxysmal positional vertigo and its management


Stavros G. Korres1 ABCDE, Dimitrios G. Balatsouras2 ABCDEF, Sotiris Papouliakos1 BEF, Eleftherios Ferekidis1 ADE
1 2

Authors Contribution: A Study Design B Data Collection C Statistical Analysis D Data Interpretation E Manuscript Preparation F Literature Search G Funds Collection

Ear, Nose, and Throat Department, National University of Athens, Hippokration Hospital, Greece Ear, Nose, and Throat Department, Tzanion General Hospital, Piraeus, Greece

Source of support: Departmental sources

Summary
Background:
Benign paroxysmal positional vertigo (BPPV) is a common peripheral vestibular disorder encountered in primary care and specialist otolaryngology and neurology clinics. It is associated with a characteristic paroxysmal positional nystagmus, which can be elicited with specic diagnostic positional maneuvers. In recent years, specic therapeutic maneuvers have resulted in its effective treatment. In this paper the current knowledge of the pathogenesis, diagnosis, and treatment of BPPV as well as the authors own clinical experience in treating such patients are presented. A retrospective review of the records of 204 patients with BPPV was performed. Epidemiological data and results from the audiological and neuro-otological work-up were recorded. All patients were treated with an appropriate repositioning maneuver, depending on the type of BPPV. Of the 204 patients, 163 had posterior canal involvement, 19 had horizontal canal involvement, and 6 had the anterior canal variant. Another 11 patients had bilateral posterior canal involvement and 5 had disease of two canals. The canalith repositioning procedure was immediately successful in 165 patients and in 23 more patients proved successful after its repetition in a second session, resulting in a total success rate of 92.1%. Most of the patients with BPPV responded very well to treatment. However, differential diagnosis of the type of BPPV was necessary to apply the appropriate canalith repositioning procedure. The canalith repositioning procedure is easy and safe to perform, is noninvasive, can be repeated if needed, and can provide rapid relief of vertigo.

Material/Methods: Results:

Conclusions:

key words:

benign paroxysmal positional vertigo canalith repositioning procedure vertigo dizziness nystagmus semicircular canal

Full-text PDF: Word count: Tables: Figures: References:

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Authors address:

Dimitrios Balatsouras, MD, 23 Achaion Str. Agia Paraskevi, 15343 Athens, Greece, E-mail: balats@panafonet.gr

Current Contents/Clinical Medicine SCI Expanded ISI Alerting System Index Medicus/MEDLINE EMBASE/Excerpta Medica Chemical Abstracts Index Copernicus

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BACKGROUND
Vertigo occurs when an imbalance or disturbance in vestibular function is present anywhere in the peripheral or central vestibular system and it is associated with several different disorders. A common form of vertigo is benign paroxysmal positional vertigo (BPPV). Patients with this disorder complain of episodic vertigo provoked by abrupt head movements, especially when looking upward, lying down, turning over in bed, or bending over. In most cases the patients can accurately recollect the specic event that triggered their symptoms. The clinical presentation of acute vertigo after certain head movements is believed to be caused by free-oating degenerative debris in the endolymph, originating from the macula of the utricle, which moves during a head movement and gravitates into one of the semicircular canals, usually the posterior (p-SCC), rarely the horizontal (h-SCC) and more rarely the anterior (a-SCC). The term BPPV accurately describes the clinical entity. The word benign implies the peripheral labyrinthine origin of the disease, paroxysmal portrays the episodic character of the vertigo, and positional denotes a disorder that is most commonly induced by rapid head position changes. However, the symptoms associated with BPPV are elicited by a particular rotational movement of the head rather than by the nal position of the head [1]. BPPV is a commonly encountered disorder [2] and is reported to comprise up to 43% of the patient population in an otology clinic [3]. History Brny, in 1921, was the rst to provide a clear description of paroxysmal vertigo with nystagmus following changes in head position in relation to gravity and attributed it to otolith disease [4]. Dix and Hallpike in 1952 [5] used the descriptive term benign paroxysmal positioning vertigo and described in detail the signs and symptoms of this disorder. They also described a maneuver to provoke the vertigo attack, by moving the patient rapidly from a sitting position to a position of the head hanging with each ear alternately downward. Characteristics BPPV can be dened as brief, episodic, and transient vertigo induced by a rapid change in head position, associated with a characteristic paroxysmal positional nystagmus. The nystagmus is mixed, with a torsional and an upbeating component and is characterized by ndings such as latency (1 to 5 seconds), crescendo and decrescendo, transience (usually lasts less than 30 seconds), reversibility on returning to the upright position, and fatigability (it is diminished or abolished on repeat testing) [6]. Pathogenic theories

Figure 1. Theories of posterior semicircular canal stimulation. A, B: Cupulolithiasis. C, D: Canalolithiasis. (a. sensory epithelium; b. cupula; c. otoconia; d. ampulla).
cupula of the p-SCC. This renders the organ sensitive to gravity, because otoconia has a specic gravity greater than that of endolymph, which stimulates pathologic vestibuloocular reexes when the head is held in a dependent position. In support of his theory, Shuknecht documented basophilic deposits in the cupula of the p-SCC. The latency before the onset of nystagmus reects the time required for the otoconial mass to be displaced due to inertia, and the fatigability is caused by the dispersal of the particles in the endolymph. The main weakness of this theory is that it does not convincingly explain the fatigability on repetitive provocation, because it is unlikely that one or two positioning maneuvers are enough to disperse the otoconia into the endolymphatic space. Additionally, if cupulolithiasis was valid, then spontaneous nystagmus would be expected and the patient would be sensitive not only to the specic Dix-Hallpike maneuver, but to vertical and horizontal linear accelerations of the head as well [8]. Hall et al. in 1979 [9] proposed the more convincing theory of canalolithiasis. They proposed that free-oating particles, derived from the otoconia of the utricular membrane, moving within the p-SCC could cause BPPV and would better explain the phenomenon of fatigability, which occurs when the debris becomes dispersed or trapped within another part of the labyrinth. This canalolithiasis hypothesis can sufciently explain all the characteristics of BPPV and has been corroborated by the success of therapist-guided positioning maneuvers that aim to clear the p-SCC of trapped particles [10]. However, it is probable that in a few cases the cupulolithiasis theory is valid, especially in patients resistant to standard treatment. Gacek [11] proposed recently a neural theory for the pathogenesis of BPPV, according to which BPPV is caused by degeneration of the saccular ganglion owing to reactivation of latent neurotropic viral infections. This results in loss of its antagonistic effect on p-SCC input and manifestation of the typical rotatory upbeat nystagmus, associated with posterior canal receptor activation. According to this theory, the limited duration of the nystagmus and the fatigability of the response are consistent with the refractory state of rst-order vestibular neurons. However, the unanimously accepted success of the therapeutic maneuvers may not be sufciently explained. Types of BPPV

Two main theories have been proposed to clarify the pathophysiological mechanism (Figure 1). Shuknecht in 1969 [7] proposed that BPPV resulted from a lesion of the pSCC and introduced the term cupulolithiasis. This theory argues that otolithic debris (normally found in the utricle and saccule) becomes dislodged and attached on the

The posterior canal is the most commonly involved semicircular canal in the pathogenesis of BPPV (p-BPPV) [12]. This may be attributed to the fact that this canal is located at the most dependent position in the vestibular apparatus in an upright person. If debris dislodges, it will tend

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Korres SG et al Benign paroxysmal positional vertigo and its management

Table 1. Diagnostic test, characteristics and treatment of BPPV types. p-BPPV Diagnostic Test Latency Duration Fatigability Nystagmus type Nystagmus direction Nystagmus intensity Reversal of nystagmus Treatment Dix-hallpike 15 sec Limited, <30 sec Yes Mixed torsional/upbeating Geotropic Crescendo and decrescendo Yes, in most of the cases (on returning to the upright position) Epleys maneuver Semonts liberatory maneuver h-BPPV Turning the head from the supine to either lateral position Very short, 03 sec >30 sec No, in most of the cases Horizontal a-BPPV Dix-Hallpike 35 sec <30 sec Yes Mixed torsional/downbeating

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Mainly geotropic and occasionally Either geotropic or apogeotropic apogeotropic Intense persistent nystagmus Yes, mainly on changing head position Vannucchis forced prolonged position Crescendo and decrescendo Occasionally yes (on returning to upright position) Epleys maneuver

to fall to the back and bottom of the system where the pSCC is located [3]. Horizontal canal BPPV (h-BPPV) was identied by McClure from the United States [13] and Cipparone et al. from Italy in 1985 [14], assuming a similar pathogenic mechanism. Although p-SCC involvement is the most common, the hSCC is involved in a signicant number of cases, exceeding 20% of all cases according to some authors [15], although from other series, including ours, the percentage appears to be quite lower (ca. 8%) [12]. The occurrence of anterior semicircular canal involvement (a-BPPV) is not exactly known at present because it is not a well-studied entity. In the series of Herdman and co-workers [16], its rate was reported as high as 12%, although in other series [17] and according to our data [12] its occurrence appears to be much smaller (12%). Involvement of two semicircular canals and bilateral involvement has also been reported [15,18]. Etiology The etiology of BPPV in most cases is considered to be idiopathic. However, numerous conditions have been associated with BPPV (secondary BPPV), including head and neck trauma, post-surgery, vertebrobasilar insufciency, viral labyrinthitis, vestibular degeneration, and prolonged bed-rest [19]. Diagnosis Involvement of the posterior canal comprises the majority of the cases which a general practitioner comes into contact with and thus we are going to discuss this in more detail. The diagnosis of h-BPPV and a-BPPV are presented briey in Table 1. The diagnostic work-up in patients suffering from vertigo starts with a thorough evaluation of their medical history

(associated symptoms and their duration, previous surgical interventions, history of infections or trauma, medications, etc) followed by a general physical and neurological examination. Otoscopy should be performed in order to exclude obvious pathology in the external or middle ear. The examiner should be able at this point to identify the possible cause of the disease or, at least, to distinguish between peripheral and central vertigo. The diagnosis of BPPV from patients history is straightforward. The patients may describe spinning of their surroundings either when they rst lie down to sleep, upon rolling to one side or the other, sitting up from a supine position, extending the neck to look up, or getting something from above (bookshelf syndrome). The duration of the vertigo is brief, usually a few seconds, but a feeling of postural imbalance may remain longer. The Dix-Hallpike test conrms the diagnosis. The test is performed by moving the patient rapidly from a sitting position to a position with the head hanging 45 below the horizontal (Figure 2), with each ear alternately undermost [20]. A positive response is considered a burst of vertigo accompanied by a characteristic nystagmus, which is typical of stimulation of the p-SCC. The nystagmus starts after a short latent period and typically beats towards the undermost and affected ear, with a torsional component clockwise when following a leftward movement or counterclockwise when following a rightward movement, as seen by the physician. Typically, an upbeating component is superimposed, resulting in a mixed torsional-vertical eye movement. Intense vertigo in coexistence with this pattern of nystagmus and its additional characteristics previously described may easily establish the diagnosis [6]. Electronystagmography is not useful in diagnosis because recording of the torsional component of the nystagmus is not possible by standard techniques. Nevertheless, electronystagmographic abnormalities are quite common in patients with BPPV, but not specic to the disease [21,22]. The role of imaging techniques is controversial. In most cases, history and physical examination are sufcient for a work-

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Figure 2. The Dix-Hallpike test.


ing diagnosis. Computed tomographic scans and magnetic resonance imaging are performed to rule out a central pathology of the disease [23]. Treatment During the past 15 years, several maneuvers have been proposed for the treatment of BPPV. They aim at returning the displaced otoconia to the utricle so that there is no abnormal manifestation of the vestibulo-ocular reexes on changing the position of the head. p-BPPV In 1980, Brandt and Daroff [24], based on the theory of cupulolithiasis, proposed the rst effective therapy for BPPV that consisted of a set of physiotherapeutic exercises repeated many times a day for two to three weeks. As an alternative, Semont et al. [25] in 1988 introduced a single liberatory maneuver based on the same theory, but the major breakthrough was the canalith repositioning procedure (CRP) induced by Epley in 1992, based on the theory of canalolithiasis [26]. CRP begins with the patient sitting on the examination table with the head turned 45 to the affected ear. Then the patients body is quickly brought backwards, into a slight head-hanging position, keeping the head turned to the same side. The next stage includes rotating the head slowly towards the unaffected ear, which is now undermost. Then the patient is rolled to a side-lying position with the head turned 45 more towards the same (unaffected) ear and downward to the oor. Finally, the patient is brought slowly back to the sitting position (Figure 3). The result of this procedure is that otoconia moves through the common crus of the posterior and anterior semicircular canal and nally enters the utricular cavity, where it becomes harmless. After the procedure, the patient is advised not to bend over, lie back, or tilt the head during the next 48 hours. The patient is also asked to sleep in a slightly elevated position and to avoid turning during sleep toward the affected ear. In case of failure, the maneuver must be repeated once or twice, but if the symptoms persist, Semonts liberatory maneuver [25], which is thought to be useful in cases of both cupulolithiasis and canalolithiasis, should be used (Figure 4). The liberatory maneuver aims at dislodging the otoconia from the cupula and moving it out of the posterior semicircular canal into the vestibule, where it becomes harmless. In the sitting position, the head of the patient is turned horizontally 45 towards the unaffected ear. The pa-

Figure 3. The Epley CRP when the posterior semicircular canal of the left ear is affected. (A) The patient is sitting with the head turned horizontally 45 to the affected (left) ear. (B) Left head-hanging position. (C), (D) Rightward roll, right headhanging position. (E) Further rightward roll. (F) Sitting up. The head is held still in positions (B) and (E) for 1 to 3 minutes.
tient is moved quickly to the side-lying position on the affected side, with the head hanging down towards the lowermost shoulder. After one to three minutes, the patient is brought quickly through the initial sitting position to the contralateral side-lying position, with the head still turned 45 toward the unaffected side and with the nose down. After one to three minutes the patient is returned slowly to the sitting position. The same instructions are given as described for the Epley maneuver. h-BPPV Although several methods of treatment have been proposed [2729], we consider the forced prolonged position introduced by Vannucchi et al. [29] as more effective and simpler to perform. The patients are told to lie on their beds and turn their heads or whole body from the supine position toward the healthy ear and to stay there for approximately 12 hours. In this way, the affected ear is uppermost and the horizontal semicircular canal is in a vertical position. The result is that the owing otoconia lying on the nonampullary arch of the canal can gradually pass through the canal into the vestibule by the force of gravity.

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Figure 4. The Semont maneuver when the posterior semicircular canal of the left ear is affected. (A) The patient is sitting with the head turned horizontally 45 to the healthy (right) ear. (B) Moving to left side-lying position. (C) Moving to the right side-lying position. Then the patient returns to initial position (D).
a-BPPV Baloh in 1996 [30] and Herdman in 1997 [31] reported treatment of a-BPPV by the same CRP that is usually used for the much more common p-BPPV. The Dix-Hallpike maneuver was performed on all patients to diagnose posterior or anterior canal BPPV. Intense vertigo in conjunction with a burst of nystagmus with the typical characteristics of latency, crescendo, fatigability, and transience was considered necessary to establish the diagnosis. A diagnosis of posterior canal involvement was based on the type of paroxysmal positioning nystagmus produced during the Dix-Hallpike maneuver. The direction of the vertical component of the fast phase of the nystagmus response was upward and the torsional component of the nystagmus beat towards the down-side affected ear: counterclockwise during the right Dix-Hallpike maneuver when the right ear was involved and clockwise during the left Dix-Hallpike maneuver when the left ear was involved [12]. Anterior canal involvement was characterized mainly by positioning nystagmus with the same torsional component as observed in the posterior canal BPPV, but with the vertical component beating downward during the fast phase of the nystagmus. Differential diagnosis between posterior and anterior canal BPPV was based on the direction of the vertical component of the nystagmus [32]. Finally, the horizontal canal type of vertigo was diagnosed by the presence of horizontal geotropic and apogeotropic paroxysmal nystagmus provoked by turning the head from the supine to either lateral position [32]. The patients with posterior or anterior canal BPPV were treated by the modied Epley CRP and the patients with

MATERIAL AND METHODS


One hundred and fty-ve consecutive patients suffering from BPPV who were examined and treated at the neurology units of our departments were included in the study. Patients with a clinical examination, laboratory ndings, or imaging studies suggesting abnormal conditions of the central nervous system were excluded from the study. From all the patients a comprehensive interview was obtained regarding medical history, history of falls or imbalance relative to the vertigo, anxiety, onset of symptoms, and provoking factors. All patients underwent a complete otolaryngological, audiological, and neurological evaluation, including pure tone audiometry, measurements of acoustic immittance and, occasionally, auditory brainstem response. Eye movements were recorded by electronystagmography (ENG) using a standard test protocol of visual and vestibular stimulation, described elsewhere [21].

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horizontal canal BPPV were treated by the Vannucchi maneuver. The appropriate maneuver was applied once, and after 15 days all the patients were reexamined. In case of failure or incomplete remission of the symptoms, the same maneuver was repeated. Assessment of the success of the treatment included both the patients report of relief from vertigo and a negative Dix-Hallpike test result. In the case of a new failure, the liberatory maneuver of Semont et al. was nally used [14]. Follow-up care included communication by phone and, in case of recurrence of symptoms, re-examination and repetition of the repositioning procedures, according to the same plan. In case of recurrence, the repositioning procedures were repeated according to the same plan. After three years of absence of symptoms it was considered that a denite cure had been achieved.

Table 2. Clinical features of patients treated for benign paroxysmal positional vertigo. Number Total Male Female Mean age (years) Total Men Women Age range (years) Total Male Female Localization of the lesion Right Left Bilateral Vertigo related to sleep Hearing impairment Bilateral Unilateral Ipsilateral Contralateral Tinnitus Bilateral Unilateral Ipsilateral Contralateral Canal involvement Posterior Horizontal Anterior Bilateral Two canals Aetiology Idiopathic Metatraumatic Cochleovestibular disease Other causes 204 86 118 59.2 (13.5) 58.4 (12.8) 60.3 (14.7) 986 2786 986 118 75 11 155 60 26 34 21 13 72 57 15 11 4 163 19 6 11 5 158 13 26 7

RESULTS
Eighty-six patients were male and 118 were female, with mean ages of 58.4 and 60.3 years, respectively. The clinical features of our patients are shown in Table 2. The list of diagnoses included metatraumatic BPPV in 13 subjects, cochleovestibular disease in 26 (including Menieres disease), and other causes of BPPV (including viral disease) in 7 subjects. In most of the cases (75.9%), vertigo was related to sleeping, and vertiginous episodes were provoked either when the patient rst lay back or rolled on to one side or the other or when rising from bed. Electronystagmographic abnormalities were frequently observed in our patients (canal paresis in 36.7% and directional preponderance in 25.4%). A total of 163 patients had p-BPPV, 19 patients presented with hBPPV, and 6 patients had ndings compatible with anterior canal involvement. Another 11 patients were found with bilateral posterior canal involvement and 5 patients had disease of two canals on the same side. In the group of patients with p-SCC, treatment was successful in 143 cases (Table 3), resulting in an initial success rate of 87.7%. In the remaining patients, the vertigo either did not recede completely or remained unchanged. In those cases, repetition of the maneuver proved successful in another 8 patients, resulting in a total success rate of 92.6%. In all patients suffering from h-BPPV or a-BPPV, treatment was successful and symptoms disappeared, with the exception of 2 cases with h-BPPV and 1 case with a-BPPV. Repetition of the maneuver proved successful in the patient with aBPPV, but did not succeed in the 2 patients with h-BPPV. In the cases with bilateral or two-canal involvement, although none were successfully treated with the initial maneuver, most cases were cured on repeat treatment, with the exception of 1 patient with bilateral and 1 with two-canal involvement. Considering the entire group of patients, the total success rate of the treatment was 92.1%. There were no complications observed following the therapeutic maneuvers. In some of our patients we found auditory symptoms, such as hearing loss (29.4%) and tinnitus (35.2%), but they did not help to localize the involved side because they were quite often bilateral. When unilateral, they were also found quite often on the normal side.

causes of vertigo is BPPV, which is characterized by brief, episodic, and intermittent attacks of vertigo and a typical nystagmus produced by certain provocative head movements. Although in most cases the diagnosis is straightforward, differential diagnosis from other common causes of benign recurrent vertigo is occasionally required [33]. BPPV has a signicant impact on the quality of life and patients do not perceive it as a benign disease, although the particle repositioning maneuver succeeds in restoring the patients morale [34]. The psychosocial impact of the disease has been explored in a study in which high scores for depression and loneliness were found in patients with BPPV [35]. The importance of an accurate diagnosis should be emphasized because expensive examinations may be avoided, selfcondence is obtained, and successful therapy is available.

DISCUSSION
Dizziness and vertigo are among the most frequently encountered symptoms in primary care. One of the most common

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Table 3. Semicircular canal involvement and treatment results. N Posterior canal Horizontal canal Anterior canal Bilateral Two canals Total 163 19 6 11 5 204 Success of 1st treatment Success of 2nd treatment 143 17 5 0 0 165 8 0 1 10 4 23 Failures 12 2 0 1 1 16

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The introduction of therapeutic positioning maneuvers has made BPPV the most successfully treatable cause of vertigo. CRP, with several modications since Epleys original description, has become an essential and efcient therapeutic tool because of its simplicity, noninvasive nature, and apparent effectiveness in relieving vertigo. According to our series, complete recovery was achieved in more than 80% of the patients after a single CRP. Repetition of the maneuver on a second session increased the success rate to approximately 92%, and similar results were reported by other authors [3640]. Attention should be drawn to patients with BPPV and other concomitant vestibular pathology, because they have more frequently persistent symptoms after a CRP maneuver than patients with pure BPPV [41]. Diagnosis for the various types of BPPV is easily reached based on the patients history and the position-induced nystagmus during the Dix-Hallpike test, and treatment of the disease is safe to perform. However, most of these patients tend to visit several medical specialties, especially during the symptom-free period. It is important for physicians who examine such patients to be acquainted with the symptoms and signs as well as with the treatment of this common and benign cause of vertigo. In a recent study, Von Brevern et al. [42] reported that in Germany, three different medical specialties were consulted on average: internal/general medicine (86%), otolaryngology (72%), and neurology (51%). Brain imaging (42%), caloric testing (46%), audiometry (49%), and carotid Doppler ultrasonography (34%) were performed more often than diagnostic positioning (28%). Only 31% of the consulted neurologists, 16% of otolaryngologists, and 2% of specialists for internal medicine and general practitioners performed positioning tests; overall 30% of patients were not properly diagnosed. BPPV was suspected in 45% of patients. Most patients received ineffective therapy such as antivertiginous medication (39%), physical therapy (14%), chiropractic treatment (13%), betahistine (10%), or acupuncture (7%) or did not receive any therapy at all (39%). Furthermore, in a retrospective study, Fife et al. [43] analyzed how these patients were managed across the board from primary care to treatment in tertiary centers. At least 85% of cases had typical symptoms of BPPV and could have been easily identied by primary care physicians on rst referral. It was concluded that patients could be treated more efciently and at less cost if the condition was identied on the rst referral in primary care and treated in either primary care or dedicated vestibular clinics receiving referrals from primary care.

CONCLUSIONS
Most of the patients with BPPV responded very well to treatment. However, differential diagnosis of the type of BPPV was necessary to apply the appropriate canalith repositioning procedure. We believe that physicians who come into contact with patients suffering from vertigo should be able to recognize this common clinical entity and be able to diagnose it by performing the Dix-Hallpike test to avoid costly investigations and reduce waiting time for treatment. CRP, after some practice, is easy and safe to perform, is noninvasive, can be repeated if needed, and can provide rapid relief of vertigo. Thus it should be familiar to every general practitioner, internist, neurologist, and otolaryngologist. However, care should be taken whenever the previously described criteria of BPPV are not met, especially when nystagmus persists as long as the provoking position is maintained or direction-changing nystagmus is observed. In this case the patient should be referred for neurological investigation because the presence of central positional nystagmus should be suspected.

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