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Journal of Vestibular Research 25 (2015) 105117 105

DOI 10.3233/VES-150553
IOS Press

Benign paroxysmal positional vertigo:


Diagnostic criteria
Consensus document of the Committee for the Classification of Vestibular Disorders of the Brny
Society

Michael von Breverna,, Pierre Bertholonb , Thomas Brandtc , Terry Fifed , Takao Imaie ,
Daniele Nutif and David Newman-Tokerg
a
Department of Neurology, Park-Klinik Weissensee, Berlin, Germany
b
Department of Otolaryngology Head and Neck Surgery, Bellvue Hospital, Saint-Etienne, France
c
Institute of Clinical Neuroscience, Ludwig-Maximilian University, Munich, Germany
d
Barrow Neurological Institute, University of Arizona College of Medicine, Phoenix, AZ, USA
e
Department of Otolaryngology Head and Neck Surgery, Osaka University Graduate School of Medicine, Japan
f
Department of Otolaryngology Head and Neck Surgery, University of Siena, Italy
g
Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MA, USA

Received 2 May 2014


Accepted 3 June 2015

Abstract. This article presents operational diagnostic criteria for benign paroxysmal positional vertigo (BPPV), formulated by
the Committee for Classification of Vestibular Disorders of the Brny Society. The classification reflects current knowledge of
clinical aspects and pathomechanisms of BPPV and includes both established and emerging syndromes of BPPV. It is anticipated
that growing understanding of the disease will lead to further development of this classification.

Keywords: Vertigo, positional, nystagmus, diagnosis, criteria

1. Introduction lar symptoms [13]. Individual subcommittees includ-


ing otolaryngologists and neurologists from at least
The following diagnostic criteria for benign parox- three continents have been tasked with defining con-
ysmal positional vertigo (BPPV) are part of the Inter- sensus diagnostic criteria for specific vestibular disor-
national Classification of Vestibular Disorders (ICVD) ders.
an endeavour for classification of vestibular disorders We have taken additional steps to ensure the broad-
steered by the Committee for Classification of Vestibu- est possible consensus for the criteria. The classifica-
tion has been presented and discussed at two meet-
lar Disorders of the Brny Society. As a first step and
ings of the Brny Society in 2010 and 2012. Fur-
prerequisite for the classification of vestibular disor-
thermore, a draft of the classification was presented
ders, the Classification Committee of the Brny Soci-
to five other medical societies engaged in neurotology
ety published a consensus on the definition of vestibu- (American Academy of Otolaryngology Head and
Neck Surgery, American Neurotology Society, Amer-
Corresponding author: Michael von Brevern, Department of
ican Otological Society, European Academy of Otol-
Neurology, Park-Klinik Weissensee, Schnstrasse 80, 13086 Berlin,
ogy and Neuro-Otology, and Japan Society of Equilib-
Germany. Tel.: +49 30 96283700; Fax.: +49 30 96283705; E-mail: rium Research). The members of the Brny-Society
von.brevern@park-klinik.com. were invited to comment on the last draft of this clas-

ISSN 0957-4271/15/$35.00 
c 2015 IOS Press and the authors. All rights reserved
106 M. von Brevern et al. / Benign paroxysmal positional vertigo: Diagnostic criteria

sification before publication by means of an online otolith macula beds and are trapped in a semicircular
internal review system. Comments from Brny So- canal. Gravity causes them to move after changes of
ciety members and from the consulted medical so- the head position in the plane of the affected canal. The
cieties were discussed and, where appropriate, incor- resulting inappropriate endolymph flow deflects the
porated by the subcommittee before the final version cupula and thus modulates the activity of the vestibu-
of this classification was approved. Finally, we have lar afferents of the affected canal, causing attacks of
taken steps to ensure that our document is harmonious positional vertigo and nystagmus (canalolithiasis) [15].
with current published therapeutic guidelines from the Less common, BPPV can be attributed to otoconia that
American Academy of Neurology [31] and the Amer- are attached to the cupula of a semicircular canal and
ican Academy of Otolaryngology Head and Neck render it sensitive to gravity (cupulolithiasis) [5,51,73].
Surgery [11]. The development of pathophysiological concepts of
The format of this classification is modelled on the BPPV that aimed to understand the clinical features
International Classification of Headache Disorders. It of the disease as a mechanical irritation of a semicir-
includes both established syndromes (Sections 2.1 to cular canal has been an intellectual challenge [15,50].
2.4) and emerging and controversial syndromes (Sec- Schuknecht coined the term cupulolithiasis on the ba-
tions 3.1 to 3.4). The operational criteria are supported sis of histological studies of the temporal bones from
by notes and comments. patients with BPPV [67]. Incidentally, he also has pro-
vided a documentation of canalolithiasis, although he
1.1. Terminology did not recognize the pathophysiological meaning of
this finding [67].
Because symptoms are triggered by the act of mov- The critical role of the receptors of the semicir-
ing the head to a new position, rather than by maintain- cular canals is supported by the direction of posi-
ing the head in a particular posture or position, some tional nystagmus in BPPV reflecting the known exci-
authors have advocated for the use of the term po- tatory and inhibitory connections of the canal recep-
sitioning vertigo rather than positional vertigo for tors with specific extraocular eye muscles [2]. The hy-
BPPV. A similar issue arises in distinguishing posi- pothesis of canalolithiasis and cupulolithiasis is sup-
tioning nystagmus from positional nystagmus on ported by in-vitro and in-vivo animal models [63,71],
the basis of whether the finding is transient after head by mathematical models [33,40,65] and by the effi-
positioning. While these distinctions make mechanis- cacy of specific canal clearing procedures [31,32,54]
tic sense and may be of diagnostic value, it was the and plugging of the affected semicircular canal [10].
groups judgment that current usage of the term po- Furthermore, particulate matter within the posterior
sitional in BPPV or to describe its associated nystag- canal has been observed intraoperatively in patients
mus is too ubiquitous to change clinical practice. Thus, with BPPV [64,80]. This debris has been examined by
the term positional is preserved in the definitions be- scanning electron microscopy and appeared morpho-
low and positioning is not used. logically consistent with degenerated otoconia [80]. Of
note, particulate matter has also been found in the pos-
1.2. Epidemiology terior semicircular canal of subjects without a history
of BPPV [49,59]. This finding is not contradictory to
BPPV is the most frequent vestibular disorder: the pathophysiology of BPPV as discussed above as
its cumulative incidence in the general population physio-mathematical models have shown that the pre-
amounts during lifetime to 10% [79]. The time course requisite for BPPV is a certain amount of otoconia
of BPPV is characterised by spontaneous remissions within the affected semicircular canal reaching a crit-
that occur typically after days to weeks [41] and re- ical mass and that an agglomeration of these particles
currences that occur in about 50% of patients [61]. Al- promotes the hydrodynamic effect of otoconia moving
though BPPV is usually self-limiting, it inflicts a con- in the canal [33,40].
siderable personal and socio-economic burden [55,79]. There are open questions that need to be addressed
in the future. It has been postulated that loose otoco-
1.3. Pathophysiology nia within the short arm of the semicircular canals (on
the utricular side of the cupula) may also cause posi-
According to a widely accepted theory BPPV is tional vertigo [17,18]. Furthermore, canalolithiasis and
usually caused by otoconia that are dislodged from the cupulolithiasis are not mutually exclusive and may co-
M. von Brevern et al. / Benign paroxysmal positional vertigo: Diagnostic criteria 107

exist simultaneously in the same semicircular canal but a pre-existing disorder of the inner ear (e.g. vestibu-
such a combination has not been documented with eye lar neuritis, Menires disease) is suspected. Similarly,
movement recording so far. brain or ear imaging is not required in typical cases of
There are clinical findings that are possibly associ- BPPV [11].
ated with BPPV but not yet sufficiently understood. Positional testing involves the provocation of ver-
Spontaneous nystagmus not provoked by positioning is tigo and nystagmus, and different maneuvers test dif-
not a core feature of BPPV, although pseudosponta- ferent semicircular canals. A canal-specific response
neous nystagmus is typical of horizontal canal BPPV is diagnosed when a rotation of the head in the plane
(see comment to 1.3 further below). Rarely, however, of a semicircular canal evokes positional nystagmus of
spontaneous nystagmus beating in a direction that cor- maximal intensity (in terms of slow phase velocity).
responds to the stimulation of a single semicircular As a rule (and in contrast to central positional nystag-
canal irrespective of head position has been observed mus), positional nystagmus in BPPV always beats in
in patients that otherwise fulfilled diagnostic criteria the plane of the affected canal and in the expected di-
for canalolithiasis or cupulolithiasis. This finding is rection for canal excitation or inhibition [19].
usually brief, rarely lasting longer than a few minutes Basically, the head is brought first into such a po-
and has been described as a complication of positional sition that the affected semicircular canal is spatially
therapy and after shaking the head in the plane of the vertical and thus aligned with gravity. In a second step,
canal affected by canalolithiasis [28,76] and may pos- the head is then rotated in the plane of the affected
sibly also occur spontaneously [58]. The pathophys- canal. In the Dix-Hallpike maneuver, the head of the
iology is unclear. A canalith jam implying a lock- sitting patient is turned 45 toward the side to be tested
ing of the cupula in a fixed position by canalith de- and then laid back quickly into a head-hanging posi-
bris, either directly jamming the cupula or indirectly tion [27]. In the side-lying maneuver (Semont diagnos-
blocking endolymph flow in the canal has been postu- tic maneuver) the sitting patient is tilted quickly to the
lated [28,58,76]. side to be tested with the head turned 45 to the oppo-
Finally, patients with persistent geotropic direction- site side [24]. It is noted that both maneuvers not only
changing positional nystagmus in the supine lateral test for lithiasis of the posterior canal of one side but
head positions in the absence of central neurologic also for the anterior canal of both sides [2,6,16]. For
signs and with normal results in cerebral imaging have testing of the horizontal canal, the supine roll test is
been described [37,44]. This type of nystagmus is nei- used: the head of the patient in the supine position is el-
ther compatible with mobile otoconia in a semicircu- evated about 30 and then turned quickly to either side.
lar canal nor with dense otoconia attached to a cupula. It is essential to perform positional maneuvers for both
However, there seems to be an association between the vertical and the horizontal semicircular canals in
persistent geotropic direction-changing positional nys- every patient with positional vertigo as multiple canals
tagmus and canalolithiasis and cupulolithiasis, as some may be affected [8,60].
of these patients have developed classical variants of For observation of positional nystagmus, Frenzel
BPPV at follow-up [37,44]. It has been suggested that goggles or video-oculography can be helpful, partic-
this phenomenon may be due to changes of the den- ularly when the nystagmus is weak or momentary.
sity of the cupula or the endolymph [37,44], but this Recording of eye movements may enhance ones abil-
remains speculative. ity to observe and to classify nystagmus in canalolithi-
asis of the anterior canal (3.1), in cupulolithiasis of
1.4. Diagnosis the posterior canal (3.2), in lithiasis of multiple canals
(3.3.) and in possible BPPV (3.4). In most cases, how-
The complete diagnosis includes the specification of ever, nystagmus can be seen clinically without spe-
the affected semicircular canal(s) and the pathophysi- cial equipment. The direction of nystagmus is essen-
ology (canalolithiasis or cupulolithiasis). The definite tial to specify the affected canal. Indeed, the posterior
diagnosis of BPPV requires diagnostic positional ma- canal is by far the most frequently affected canal (80
neuvers that lead to the observation of a canal-specific 90%); next is the horizontal canal (530%) [25,38,73].
positional nystagmus. Clinical features essential for Involvement of the anterior canal is rare, account-
the diagnosis are the latency, direction, time course, ing for only 1% to 2% of patients in large case se-
and duration of positional nystagmus. Usually, further ries [38,60,81] although some recent reports have sug-
vestibular and auditory testing is indicated only when gested a considerably higher incidence [20,45]. Theo-
108 M. von Brevern et al. / Benign paroxysmal positional vertigo: Diagnostic criteria

retically, each of the three semicircular canals of the C. Positional nystagmus7 elicited after a latency of
labyrinth can be affected by canalolithiasis or cupu- one or few seconds8 by the Dix-Hallpike maneu-
lolithiasis, resulting in six combinations (not counting ver or side-lying maneuver (Semont diagnostic
multiple canal involvement) for each ear. Except for maneuver). The nystagmus is a combination of
cupulolithiasis of the anterior canal, all these combina- torsional nystagmus with the upper pole of the
tions have been documented by eye movement record- eyes beating toward the lower ear combined with
ings and are included in this classification. vertical nystagmus9 beating upward (toward the
Therapeutic positional maneuvers are highly effec- forehead) typically lasting < 1 minute10,11,12,13 .
tive for treatment of BPPV, particularly when canaloli- D. Not attributable to another disorder14.
thiasis is present [11,31]. Thus, if positional nystag-
mus disappears immediately after positional therapy,
this strongly supports the diagnosis of BPPV. Such a Notes
favourable response to treatment is not mandatory for
the diagnosis, and patients refractory to treatment do 1. In addition to attacks of positional vertigo, pati-
occur. However, repeated lack of response to therapy ents may have prolonged mild unsteadiness [26],
even after successful treatment of benign parox-
should generally prompt consideration of alternative
ysmal positional vertigo [66].
diagnoses that may mimic BPPV closely [11].
2. BPPV typically leads to positional vertigo but oc-
The differential diagnosis of BPPV includes cen-
casionally patients may complain of positional
tral positional vertigo due to vestibular migraine [77]
dizziness.
and structural brainstem and cerebellar lesions, typi-
3. Other complaints during the attacks include ex-
cally in the vicinity of the fourth ventricle [14]. CNS
ternal vertigo (the visual sense of environmen-
disease can usually be excluded by a thorough neuro- tal motion that often accompanies the internal
logical examination, but some cases may be challeng- vestibular sense) [13], unsteadiness, and vege-
ing to diagnose [48]. Greater care should be taken in tative symptoms such as nausea, sweating, and
patients with dominantly horizontal or downbeat po- tachycardia.
sitional nystagmus forms, since these are most fre- 4. Positional vertigo or dizziness must be distin-
quently reported in central mimics [9,46,48]. Cere- guished from orthostatic symptoms present only
bral imaging with MRI is usually only indicated when on arising but not with other positional trig-
symptoms or signs of concurrent brainstem or cerebel- gers [13].
lar dysfunction are present, or when positional vertigo 5. Attacks may not only be provoked in bed but also
and nystagmus present with atypical features or fail by other head movements (e.g., tilting the head
to resolve with repeated therapeutic positional maneu- backward [i.e., chin upward] or forward).
vers [11]. 6. Patients may overestimate the duration of single
attacks and mild, residual symptoms after an at-
tack occasionally last minutes or hours. Further-
2. Diagnostic criteria for benign paroxysmal more, attacks may be triggered repetitively, caus-
positional vertigo ing more extended symptoms. The duration of
vertigo should not, however, generally exceed 1
minute; single attacks lasting consistently longer
Previously used terms: benign paroxysmal position- should be considered atypical and spark consid-
ing vertigo, benign positional vertigo, paroxysmal po- eration of alternate or additional diagnoses.
sitional vertigo, vestibular lithiasis. 7. If positional nystagmus disappears immediately
after positional therapy, this further supports the
diagnosis.
2.1. Canalolithiasis of the posterior canal (pc-BPPV)
8. The latency between the completion of the diag-
nostic positional maneuver and the onset of po-
A. Recurrent attacks1 of positional vertigo or posi- sitional nystagmus may be as long as 40 seconds
tional dizziness2,3,4 provoked by lying down or in rare cases [3].
turning over in the supine position5 . 9. The torsional component of positional nystag-
B. Duration of attacks < 1 min6 . mus is slightly more prominent in the lower eye,
M. von Brevern et al. / Benign paroxysmal positional vertigo: Diagnostic criteria 109

whereas the vertical component is slightly more ver is executed without appropriate alignment of the
prominent in the upper eye [39]. If fixation is head [68].
not suppressed, the nystagmus may appear dom- The occurrence of canalolithiasis of the posterior
inantly torsional, since fixations ability to sup- canal without positional nystagmus is controversial but
press torsional eye movements is limited relative improvement of positional vertigo after a therapeutic
to suppression for vertical movements. The di- positional maneuver in such patients with a typical his-
rection of the patients gaze may influence the tory of benign paroxysmal positional vertigo has been
appearance of positional nystagmus. If gaze is reported [34,72]. These patients should be coded as
directed to the lower ear, nystagmus may ap- 3.4. Possible benign paroxysmal positional vertigo. It
pear predominately torsional; if directed to the is conceivable that the number of otoconia in the pos-
upper ear, it may appear predominantly verti- terior canal is sufficient to evoke subjective symptoms
cal [14]. Independent of orbital eye position, the but insufficient to stimulate the vestibulo-ocular re-
eye movement in a head-referenced coordinate flex [40].
system remains fixed in the plane of the posterior
semicircular canal. 2.2. Canalolithiasis of the horizontal canal
10. Usually, the duration of positional nystagmus (hc-BPPV)
does not exceed 40 seconds before it damps spon-
taneously [3]. A. Recurrent attacks1 of positional vertigo or posi-
11. Typically, positional nystagmus increases rapidly tional dizziness2,3,4 provoked by lying down or
in intensity and then declines more slowly (cre- turning over in the supine position5 .
scendo-decrescendo) [3]. B. Duration of attacks < 1 min6 .
12. Nystagmus of lower intensity with reversed di- C. Positional nystagmus7 elicited after a brief la-
rection may appear after the initial positional tency or no latency8 by the supine roll test, beat-
nystagmus has ceased [3]. ing horizontally9 toward the undermost ear10,11
13. After the patient returns to the upright position, with the head turned to either side (geotropic
positional nystagmus with reversed direction of direction changing nystagmus) and lasting <
lesser intensity and shorter duration often occurs. 1 min12,13 .
Furthermore, fatigability of nystagmus and ver- D. Not attributable to another disorder14.
tigo with repetitive positional testing is a com-
mon finding.
14. History and physical and neurological examina- Notes
tions do not suggest another vestibular disorder
or such a disorder is considered but ruled out 1. Besides attacks of positional vertigo, patients
by appropriate investigations or such disorder may have prolonged mild unsteadiness.
is present as a comorbid condition that can be 2. BPPV typically leads to positional vertigo but oc-
clearly differentiated. casionally patients may complain of positional
dizziness.
3. Other complaints during the attacks include ex-
Comments ternal vertigo (the visual sense of environmen-
tal motion that often accompanies the internal
Canalolithiasis of the posterior canal is by far the vestibular sense) [13], unsteadiness, and vege-
most common variant of benign paroxysmal positional tative symptoms such as nausea, sweating, and
vertigo, accounting for 8090% of cases [60]. The tachycardia.
right labyrinth is affected slightly more often than the 4. Positional vertigo or dizziness must be distin-
left [78]. guished from orthostatic symptoms present only
The occurrence of a bilateral canalolithiasis of the on arising but not with other positional trig-
posterior canal is not rare, but is more prevalent in post- gers [13].
traumatic cases than in idiopathic canalolithiasis [47]. 5. Attacks may not only be provoked in bed but also
Note that unilateral benign paroxysmal positional ver- by other head movements (e.g., during rapid lat-
tigo may mimic bilateral benign paroxysmal positional eral head rotations while erect [4], tilting the head
vertigo of the posterior canal if the positional maneu- backward [i.e., chin upward] or forward).
110 M. von Brevern et al. / Benign paroxysmal positional vertigo: Diagnostic criteria

6. Patients may overestimate the duration of sin- before it damps spontaneously, however, it does
gle attacks and mild, residual symptoms after an not exceed 2 minutes [2,25].
attack occasionally last minutes or hours. Fur- 13. Typically, positional nystagmus increases rapidly
thermore, attacks may be triggered repetitively, in intensity and then declines more slowly (cres-
causing more extended symptoms. The dura- cendo-decrescendo) [4].
tion of vertigo should not, however, generally 14. History and physical and neurological examina-
exceed 1 minute; single attacks lasting consis- tions do not suggest another vestibular disorder
tently longer should be considered atypical and or such a disorder is considered but ruled out
spark consideration of alternate or additional di- by appropriate investigations or such disorder
agnoses. is present as a comorbid condition that can be
7. If positional nystagmus disappears immediately clearly differentiated.
after positional therapy, this further supports the
diagnosis.
8. The latency between the completion of the diag- Comments
nostic positional maneuver and the onset of posi-
tional nystagmus depends on the acceleration of
the positional change: the higher the acceleration Several clinical signs may indicate the side of the
of the head turn, the shorter the latency and the affected ear and are confirmatory for the diagnosis.
higher the intensity of nystagmus [4]. With brisk The intensity of nystagmus is usually stronger with the
positional maneuvers the latency is typically 1 or head turned to the affected ear in the supine roll test [4].
2 seconds. Likewise, the intensity of nystagmus Note that the net angle and acceleration of the head ro-
depends on the angle of head rotation: the inten- tation should be similar for head turns to the right and
sity of nystagmus tends to be higher with larger left to allow for comparison of nystagmus intensity.
head rotations in the head roll test [69]. Flexing the head forward in the upright position (with
9. The direction of positional nystagmus is predom- the face downward) may elicit a transient nystagmus
inantly horizontal with a smaller torsional com- beating toward the affected ear. Lying backward from
ponent beating with the upper pole of the eye to the sitting position may provoke transient nystagmus
the lower ear [2]. beating toward the healthy ear [23].
10. Nystagmus of lower intensity with reversed di- Besides positional nystagmus, pseudospontaneous
rection may appear after the initial positional nystagmus (see also comment to 2.3) may also be ob-
nystagmus has ceased [4]. served in the upright head position beating either ip-
11. Probably, canalolithiasis of the horizontal canal silesional or contralesional [1,52].
may also cause apogeotropic horizontal posi- Caloric irrigation of the affected ear [70] and the
tional nystagmus. This would be the case when head thrust test [35] may reveal horizontal canal pare-
otoconia are located in the anterior part of the sis (possibly due to partial plugging of the canal) that
horizontal canal (close to the cupula). During is reversible after successful positional therapy [70].
the supine roll test to the healthy ear, otoconia Transition from geotropic to apogeotropic nystag-
would then fall toward or onto the cupula, re- mus may occur during diagnostic and therapeutic ma-
sulting in transient or long-lasting apogeotropic neuvers, e.g. when the patient bends over from the sit-
horizontal positional nystagmus. The supine roll ting to the head-on-knees position [69]. Transition of
test to the affected ear would provoke tran- canalolithiasis from the posterior canal to the horizon-
sient apogeotropic horizontal positional nystag- tal canal may occur as a result of therapeutic positional
mus [30,42,62]. In these patients, transformation maneuvers [36].
from apogeotropic to geotropic positional nys-
tagmus can be observed during diagnostic posi-
tional maneuvers [21,42,73]. In contrast, persis- 2.3. Cupulolithiasis of the horizontal canal
tence of apogeotropic horizontal positional nys- (hc-BPPV-cu)
tagmus following several cycles of the supine roll
test is expected with cupulolithiasis. A. Recurrent attacks1,2 of positional vertigo or po-
12. The duration of nystagmus as documented with sitional dizziness3,4,5 provoked by lying down or
eye movement recording may exceed 1 minute turning over in the supine position.
M. von Brevern et al. / Benign paroxysmal positional vertigo: Diagnostic criteria 111

B. Positional nystagmus6 elicited after a brief la- apogeotropic positional nystagmus also occurs
tency or no latency by the supine roll test, beating as a sign of central-vestibular dysfunction, it is
horizontally7 toward the uppermost ear with the mandatory to exclude CNS disease.
head turned to either side (apogeotropic direction
changing nystagmus), and lasting > 1 minute8 .
C. Not attributable to another disorder9 . Comments

Several clinical signs can indicate the side of the af-


Notes fected ear and are confirmatory for the diagnosis. The
intensity of positional nystagmus is usually stronger
1. The duration of an attack of positional vertigo is with the head turned away from the affected ear in the
usually less than 1 minute as patients tend to re- supine roll test. Note that the net angle and acceleration
turn the head into a position where vertigo and of the head rotation should be similar for head turns to
nystagmus cease. However, the duration can be the right and left to allow for comparison of nystagmus
longer if the head is kept in the provoking posi- intensity.
tion. Furthermore, due to the spatial orientation Besides positional nystagmus, pseudospontaneous
of the affected cupula, patients may have persist- nystagmus may also be observed in the upright head
ing vertigo or dizziness of lower intensity in the position beating typically to the affected ear [1,12,52].
upright position. Pseudospontaneous nystagmus is a form of positional
2. Besides attacks of positional vertigo, patients nystagmus that happens to occur with the head in the
may have prolonged mild unsteadiness. upright position, making it appear superficially similar
3. BPPV typically leads to positional vertigo but oc- to spontaneous nystagmus. In contrast to spontaneous
casionally patients may complain of positional nystagmus, pseudospontaneous nystagmus is strongly
dizziness. influenced by head position and ceases with the head
4. Other complaints during the attacks include ex- tilted about 30 forward [12]. Pseudospontaneous nys-
ternal vertigo (the visual sense of environmen- tagmus is attributed to the 30 angle between the plane
tal motion that often accompanies the internal of the horizontal canal and the horizontal plane of the
vestibular sense) [13], unsteadiness, and vege- head in the upright position that places the ampulla in
tative symptoms such as nausea, sweating, and a higher position than the rest of the canal [12]. Grav-
tachycardia. ity causes deflection of the cupula and produces hor-
5. Positional vertigo or dizziness must be distin- izontal nystagmus beating to the side of the horizon-
guished from orthostatic symptoms present only tal canal affected by cupulolithiasis. Flexing the head
on arising but not with other positional trig- 90 forward in the upright position may elicit pseu-
gers [13]. dospontaneous nystagmus beating toward the healthy
6. If positional nystagmus disappears immediately ear [12,23]. In the supine position a weak persistent
after positional therapy, this further supports the nystagmus beating toward the affected ear may be ob-
diagnosis. served that subsides when the head is turned slightly to
7. The direction of positional nystagmus is predom- that side [12].
inantly horizontal with a smaller torsional com- Apogeotropic direction changing positional nys-
ponent beating with the upper pole of the eye to tagmus is not synonymous with cupulolithiasis but
the upper ear [2]. may also occur with canalolithiasis of the horizon-
8. Typically, intensity of positional nystagmus buil- tal canal [30,42,62,74]. Rapid transition from apo-
ds up slowly over approximately 30 seconds and geotropic to geotropic direction changing positional
then gradually decays over a longer period of sev- nystagmus during the supine roll test may be due
eral minutes [2,5]. to a variant of canalolithiasis where otoconia are lo-
9. History and physical and neurological exami- cated in the anterior part of the horizontal canal (see
nations do not suggest another vestibular disor- canalolithiasis of the horizontal canal). In contrast, per-
der or such a disorder is considered but ruled sistence of an apogeotropic direction of positional nys-
out by appropriate investigations or such disor- tagmus with repetitive performance of the supine roll
der is present as a comorbid condition that can test is supportive of the diagnosis of cupulolithiasis of
be clearly differentiated. As direction-changing the horizontal canal.
112 M. von Brevern et al. / Benign paroxysmal positional vertigo: Diagnostic criteria

2.4. Probable benign paroxysmal positional vertigo, during the symptom-free interval. As a consequence,
spontaneously resolved the formerly affected semicircular canal cannot be
identified. A history of temporary, isolated episodic po-
A. Recurrent attacks1 of positional vertigo or posi- sitional vertigo with appropriate episode duration and
tional dizziness2,3,4 provoked by lying down or characteristic triggers strongly supports the diagnosis
turning over in the supine position5 . of probable benign paroxysmal positional vertigo that
B. Duration of attacks < 1 min6 . has resolved spontaneously.
C. No observable nystagmus and no vertigo with The differential diagnosis should include vestibu-
any positional maneuver. lar migraine, which likewise can present with episodic
D. Not attributable to another disorder7 .
positional vertigo. In contrast to BPPV, episodes of
positional vertigo in vestibular migraine tend to be
Notes of shorter duration with frequent recurrences, tend to
present at an earlier age, and are often accompanied by
1. Besides attacks of positional vertigo, patients migraine symptoms (headache, photophobia, phono-
may have prolonged mild unsteadiness. phobia, migraine aura) [77].
2. BPPV typically leads to positional vertigo but oc-
casionally patients may complain of positional
dizziness. 3. Emerging and controversial syndromes
3. Other complaints during the attacks include ex-
ternal vertigo (the visual sense of environmen- The following syndromes are rare variants of BPPV
tal motion that often accompanies the internal and may be difficult to differentiate from central posi-
vestibular sense) [13], unsteadiness, and vege- tional vertigo.
tative symptoms such as nausea, sweating, and
tachycardia.
3.1. Canalolithiasis of the anterior canal1 (ac-BPPV)
4. Positional vertigo or dizziness must be distin-
guished from orthostatic symptoms present only
on arising but not with other positional trig- A. Recurrent attacks2 of positional vertigo or posi-
gers [13]. tional dizziness3,4,5 provoked by lying down or
5. Attacks may not only be provoked in bed but also turning over in the supine position6 .
by other head movements (e.g., tilting the head B. Duration of attacks < 1 min7 .
upward [i.e., chin upward] or forward). C. Positional nystagmus8 elicited immediately or
6. Patients may overestimate the duration of single after a latency of one or few seconds9 by the Dix-
attacks and mild, residual symptoms after an at- Hallpike maneuver (on one or both sides) or in
tack occasionally last minutes or hours. Further- the supine straight head-hanging position, beat-
more, attacks may be triggered repetitively, caus- ing predominantly vertically downward10 and
ing more extended symptoms. The duration of lasting < 1 min.
vertigo should not, however, generally exceed 1 D. Not attributable to another disorder11.
minute; single attacks lasting consistently longer
should be considered atypical and spark consid-
eration of alternate or additional diagnoses. Notes:
7. History and physical and neurological examina-
tions do not suggest another vestibular disorder
1. The diagnosis of definite canalolithiasis of the
or such a disorder is considered but ruled out
anterior canal (3.1.1) can be made on the basis of
by appropriate investigations or such disorder
immediate resolution of positional nystagmus af-
is present as a comorbid condition that can be
ter therapeutic maneuvers. In contrast, probable
clearly differentiated.
canalolithiasis of the anterior canal (3.1.2) can
be diagnosed only after exclusion of CNS disease
Comments when positional nystagmus is refractory to thera-
peutic maneuvers.
The diagnosis of probable benign paroxysmal posi- 2. Besides attacks of positional vertigo, patients
tional vertigo that has resolved spontaneously is made may have prolonged mild unsteadiness.
M. von Brevern et al. / Benign paroxysmal positional vertigo: Diagnostic criteria 113

3. BPPV typically leads to positional vertigo but oc- Comments


casionally patients may complain of positional
dizziness. Canalolithiasis of the anterior canal is rare compared
4. Other complaints during the attacks include ex- to posterior and horizontal canal variants [38,60,81].
ternal vertigo (the visual sense of environmen- This is probably related to the anatomical orientation
tal motion that often accompanies the internal of the anterior canal, which allows particles to leave
vestibular sense) [13], unsteadiness, and vege- the canal simply after lying down and sitting up again.
tative symptoms such as nausea, sweating, and Positional nystagmus can be provoked in the supine
tachycardia. position with the head hanging straight below the
5. Positional vertigo or dizziness must be distin- earth-horizontal and by Dix-Hallpike positioning, that,
guished from orthostatic symptoms present only no matter to which side the head is turned, stimu-
on arising but not with other positional trig- lates particle migration within the affected anterior
gers [13]. canal [2,6,16]. In the Dix-Hallpike position, nystag-
6. Attacks may not only be provoked in bed but also mus may be stronger or exclusively present with the
by other head movements (e.g., tilting the head affected ear up or down. The most sensitive diagnos-
upward [i.e., chin upward] or forward). tic test for BPPV of the anterior canal seems to be
7. Patients may overestimate the duration of single the straight head-hanging position [20,22]. Thus, in
attacks and mild, residual symptoms after an at- canalolithiasis of the anterior canal, the direction of
tack occasionally last minutes or hours. Further- the torsional component, rather than the side of the
more, attacks may be triggered repetitively, caus- Dix-Hallpike maneuver, indicates the affected side.
ing more extended symptoms. The duration of However, the small torsional component of the posi-
vertigo should not, however, generally exceed 1 tional nystagmus can be easily missed in clinical prac-
minute; single attacks lasting consistently longer tice, rendering identification of the affected side unreli-
should be considered atypical and spark consid- able [2,6]. Identification of the torsional component of
eration of alternate or additional diagnoses. nystagmus may be facilitated by eye movement record-
8. Therapeutic positional maneuvers in canalolithi- ing with video-oculography [16,22] or search-coils [2].
asis of the anterior canal have been reported as Attenuation of positional nystagmus with repeated
effective [22,81]. Thus, if positional nystagmus positional maneuvers (fatigability) may be supportive
disappears immediately after positional therapy, of the diagnosis of canalolithiasis of the anterior canal,
this strongly supports the diagnosis (see note 1). but it is not present in all patients [20,57].
Transition to canalolithiasis of the posterior canal Transient downbeating positional nystagmus can
(2.1), canalolithiasis of the horizontal canal (2.2) also occasionally be observed after treatment of BPPV
or cupulolithiasis of the horizontal canal (2.3), ei- of the posterior canal, when the Dix-Hallpike maneu-
ther spontaneously or during positional maneu- ver is performed. This finding may be due to translo-
vers, also strongly supports the diagnosis. cation of otoconia into the anterior canal or to otoconia
9. The latency between the completion of the diag- that have not left the posterior canal completely dur-
nostic positional maneuver and the onset of po- ing therapeutic positional maneuvers, dropping back
into the canal during the Dix-Hallpike maneuver, and
sitional nystagmus may be as long as 30 seconds
thus inducing an inhibitory nystagmus that is down-
in rare cases [20,57].
beating [75].
10. The positional nystagmus may have a small tor-
sional component, beating with the upper pole of 3.2. Cupulolithiasis of the posterior canal
the eye toward the affected ear [2]. (pc-BPPV-cu)
11. History and physical and neurological exami-
nations do not suggest another vestibular disor- A. Recurrent attacks1,2 of positional vertigo or po-
der or such a disorder is considered but ruled sitional dizziness3,4,5 provoked by lying down or
out by appropriate investigations or such disor- turning over in the supine position6 .
der is present as a comorbid condition that can B. Positional nystagmus7 elicited after a brief or
be clearly differentiated. As positional downbeat- no latency by a half Dix-Hallpike maneuver8,
ing nystagmus also occurs as a sign of central beating torsionally with the upper pole of the eye
vestibular dysfunction, it is mandatory to exclude to the lower ear and vertically upward (to the
CNS disease if positional nystagmus does not forehead) and lasting > 1 min.
cease promptly after therapeutic maneuvers. C. Not attributable to another disorder9.
114 M. von Brevern et al. / Benign paroxysmal positional vertigo: Diagnostic criteria

Notes: tion after being turned 45 to the affected side may re-
veal nystagmus beating in the opposite direction com-
1. The duration of an attack of positional vertigo is pared to the half Dix-Hallpike maneuver [29].
usually less than 1 minute as patients tend to re-
turn the head into a position where vertigo and 3.3. Lithiasis of multiple canals (mc-BPPV)
nystagmus cease. However, the duration can be
longer when the head is kept in the provoking po- A. Recurrent attacks1 of positional vertigo or posi-
sition. tional dizziness2,3,4 provoked by lying down or
2. Besides attacks of positional vertigo, patients turning over in the supine position5 .
may have prolonged mild unsteadiness. B. Duration of attacks < 1 min6,7 .
3. BPPV typically leads to positional vertigo but oc- C. Positional nystagmus8,9 compatible with canalo-
casionally patients may complain of positional lithiasis of more than one canal during the Dix-
dizziness. Hallpike maneuver and the supine roll test.
4. Other complaints during the attacks include ex- D. Not attributable to another disorder10.
ternal vertigo (the visual sense of environmen-
tal motion that often accompanies the internal
vestibular sense) [13], unsteadiness, and vege- Notes:
tative symptoms such as nausea, sweating, and
tachycardia. 1. Besides attacks of positional vertigo, patients
5. Positional vertigo or dizziness must be distin- may have prolonged mild unsteadiness.
guished from orthostatic symptoms present only 2. BPPV typically leads to positional vertigo but oc-
on arising but not with other positional trig- casionally patients may complain of positional
gers [13]. dizziness.
6. Attacks may not only be provoked in bed but also 3. Other complaints during the attacks include ex-
by other head movements (e.g., tilting the head ternal vertigo (the visual sense of environmen-
upward [i.e., chin upward] or forward). tal motion that often accompanies the internal
7. If positional nystagmus disappears immediately vestibular sense) [13], unsteadiness, and vege-
after positional therapy, this further supports the tative symptoms such as nausea, sweating, and
diagnosis. tachycardia.
8. A half Dix-Hallpike maneuver is performed 4. Positional vertigo or dizziness must be distin-
with the head turned 45 toward the side to be guished from orthostatic symptoms present only
tested and resting slightly raised from supine on arising but not with other positional trig-
(about 30 in flexion). This position is best suited gers [13].
to bring the affected cupula to an earth-horizontal 5. Attacks may not only be provoked in bed but also
position to be maximally deflected by the gravi- by other head movements (e.g., tilting the head
tational force [29]. upward [i.e., chin upward] or forward).
9. History and physical and neurological examina- 6. This criterion is not required when the labyrinth
tions do not suggest another vestibular disorder is affected by cupulolithiasis.
or such a disorder is considered but ruled out 7. Patients may overestimate the duration of sin-
by appropriate investigations or such disorder gle attacks and mild, residual symptoms after an
is present as a comorbid condition that can be attack occasionally last minutes or hours. Fur-
clearly differentiated. thermore, attacks may be triggered repetitively,
causing more extended symptoms. The dura-
tion of vertigo should not, however, generally
Comments exceed 1 minute; single attacks lasting consis-
tently longer should be considered atypical and
Cupulolithiasis of the posterior canal has rarely been spark consideration of alternate or additional di-
described [43]. Positional nystagmus may disappear agnoses.
when the head is further reclined in the Dix-Hallpike 8. If positional nystagmus disappears immediately
position [43]. A reversed Dix-Hallpike maneuver after positional therapy, this further supports the
with the head bent forward 90 from the upright posi- diagnosis.
M. von Brevern et al. / Benign paroxysmal positional vertigo: Diagnostic criteria 115

9. The most frequent combination is a canalolithi- sitional nystagmus that nonetheless ceases after thera-
asis of the posterior and horizontal canal of peutic positioning, (ii) patients with presumed involve-
one labyrinth. This may result in a transient ment of multiple semicircular canals that cannot be
positional nystagmus with horizontal and tor- specified, (iii) patients with simultaneous occurrence
sional components of equal intensity in the Dix- of peripheral and central positional nystagmus [7].
Hallpike maneuver [2]. Alternatively, a mixed Do not code as 3.4. possible benign paroxysmal po-
torsional-vertical positional nystagmus compati- sitional vertigo if the patient fulfills the criteria for 1.4.
ble with excitation of the posterior canal in the probable benign paroxysmal positional vertigo, spon-
Dix-Hallpike maneuver on one side and a pre- taneously resolved.
dominantly horizontal positional nystagmus in
the supine roll test to both sides may be observed
in the same session [8]. Other combinations of Acknowledgements
lithiasis of multiple canals may also occur but are
rarer. This work was supported by travelling grants from
10. History and physical and neurological examina- the Brny Society and from Neuro+ Berlin, a non-
tions do not suggest another vestibular disorder profit association for neurological research. We thank
or such a disorder is considered but ruled out the Japan Society of Equilibrium Research, the Amer-
by appropriate investigations or such disorder ican Neurotology Society and the members of the
is present as a comorbid condition that can be Brny Society for valuable suggestions. Michael von
clearly differentiated. Brevern wishes to thank Alexandre Bisdorff and
Thomas Lempert for many fruitful discussions on the
classification of BPPV.
Comments

Lithiasis of multiple canals is probably common, af-


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