AMERI CAN JOURNAL OF OTOLAR YNGOLOGY–H E AD AN D N E CK M EDI CI N E AN D S U RGE RY 3 8 ( 2 0 17 ) 38–4 3

Available online at www.sciencedirect.com

ScienceDirect
www.elsevier.com/locate/amjoto

Repeated canalith repositioning procedure in BPPV:

Effects on recurrence and dizziness prevention☆

Giancarlo Tirelli, MD a , Luca Nicastro, MD b ,

Annalisa Gatto, MD a , Margherita Tofanelli, MD a,⁎
a
Department of Otorhinolaryngology and Head and Neck Surgery, Cattinara Hospital, University of Trieste, Strada di Fiume 447, Trieste, Italy
b
Unit of Otolaryngology, Azienda Ospedaliera “S. Maria degli Angeli”, Via Montereale, 27, Pordenone, Italy

ARTI CLE I NFO A BS TRACT

Article history: Purpose: To evaluate whether a repeated canalith repositioning procedure (CRP) influences
Received 26 July 2016 the residual symptoms and the rate of recurrence of benign paroxysmal positional vertigo
(BPPV) in patients with post-CRP dizziness.
Materials and methods: In this retrospective study, we analyzed 292 patients at the referral
center for ENT diseases with a first episode of BPPV treated with a single CRP following
clinical practice guidelines. In 178 patients (67.9%) who presented dizziness after BPPV
recovery at the follow-up visit, 94 patients underwent CRP (treated group) and 84 did not
(non-treated group). A subjective evaluation of vertigo was made by way of a questionnaire.
The rates of recurrence of BPPV and residual dizziness were statistically compared between
the treated and the non-treated groups; survival analysis was carried out as well.
Results: In an observational period ranging from 1 to 6 years, BPPV recurred in 122 subjects
(46.6%) of the investigated population. Among the patients with residual dizziness, the
difference in rate of recurrence of BPPV between the treated group and the non-treated
group was not statistically significant (p = 0.84). The treated group presented a significantly
higher rate of recovery from dizziness compared to the non-treated group (p < 0.001).
Conclusions: A repeated CRP in patients with post-CRP dizziness increased the rate of
recovery from dizziness but had no influence on BBPV recurrence.
© 2016 Elsevier Inc. All rights reserved.

1. Introduction arise two times out of three in various combinations rather

Vertigo, dizziness and unsteadiness represent the most
common symptoms requiring medical attention in industri-
alized countries, with a prevalence of 48.3% for vertigo, 39.1%
for unsteadiness, and 35.6% for dizziness. These three
symptoms are often correlated to each other, in fact, they
than isolated, and 90% of episodes last less than 2 minutes [1].
The term “dizziness” implies a non-specific sensation of
disorientation, in which the patient feels as if standing in a
boat, unsteady, light-headed, foggy or drowsy. The term is
often improperly used as a synonym for vertigo, whereas the
two symptoms are expressions of two different pathogenetic

Abbreviations: BPPV, Benign paroxysmal positional vertigo; CRP, Canalith repositioning procedure; HSC, Horizontal semicircular canal;
PSC, Posterior semicircular canal.
☆
Disclosure statement: The authors declare that there is no conflict of interest.
⁎ Corresponding author at: Department of Otorhinolaryngology and Head and Neck Surgery, Cattinara Hospital, University of Trieste,
Strada di Fiume 447, Trieste, Italy. Tel.: +39 3402927827; fax: +39 0403994180.
E-mail address: margheritatofanelli@hotmail.com (M. Tofanelli).

http://dx.doi.org/10.1016/j.amjoto.2016.09.009
0196-0709/© 2016 Elsevier Inc. All rights reserved.
 AMERI CA N JOURNAL OF OT OLAR YNGOLOGY–H E AD AN D N E CK M EDI CI N E AN D S U RGE RY 3 8 ( 2 0 17 ) 38–4 3
processes. The incidence of dizziness in the general popula-
tion ranges from 20% to 30% and it has been demonstrated
that with every 5 years of age increase, there is a 10% increase
in the probability of an elderly individual suffering from
dizziness [2,3]. It has been estimated that every year 7.5
million of patients suffering from dizziness in North America
are evaluated in the primary care setting, in emergency
departments and in specialized dizziness clinics [3–5]. We
can recognize the following as causes of dizziness: peripheral
vestibular dysfunction (40%), central nervous system lesion
(10%), psychiatric disorders (15%), presyncope/disequilibrium
(25%) and non-specific dizziness (10%) [3]. Benign paroxysmal
positional vertigo (BPPV) accounts for 26% of all dizziness
cases in older people [6]. Although a cross-sectional study of a
group of 100 elderly patients with multiple chronic conditions
found a 9% prevalence of undiagnosed BPPV, the lifetime
prevalence of BPPV was 2.4% and the its incidence was 0.6%
[7,8].
About two-thirds of the patients successfully treated with
the first canalith repositioning procedure (CRP) have residual
dizziness that appears 24–72 hours after CRP and disappears
within 3 months without a specific treatment in all cases;
early CRP is thought to reduce the incidence of residual
dizziness [9].
The reported rates of BPPV recurrence vary considerably,
from 3.8% at 6 months to 50% in long-term follow-up [10,11];
however, some authors report rates from 50% to 80% in the
first 6–12 months after the first CRP [11,12]. This variation in
recurrence rates depends on the different observational
periods of the studies published to date, and on the attempt
to demonstrate the existence of a correlation between BPPV
recurrence and predisposing factors such as age, sex, patient
risk factors, association with other conditions, type, number
and timing of the performed treatments.
The aim of this study was to assess the possible correlation
between BPPV recurrence and the repetition of a second CRP
in subjects with post-CRP residual dizziness, and more
specifically to investigate whether repeating CRPs prevents
BPPV recurrence.
2. Material and methods
This retrospective study involved 292 patients who experi-
enced a first episode of BPPV and were treated with a single
Table 1 – Patient selection criteria.
Sr. no Inclusion criteria Exclusion criteria
Previous labyrinthopathy
1 First episode of BPPV (Menière, vestibular neuritis,
labyrinth fistula)
2 Residual dizziness post-CRP Post-traumatic BPPV
Absence of spontaneous Presence of spontaneous
4
nystagmus nystagmus
Completed DHI
5 Neurological signs
questionnaire
6 Absence of migraine Use of sedative drugs
39
type of CRP at the Ear, Nose, Throat Department in Trieste
from January 2008 through December 2013. The patient
selection criteria are summarized in Table 1. The study
protocol was approved by local ethics committee on clinical
investigation.
Patients underwent routinely anamnestic evaluation,
vestibular clinical examination with otoscopy, balance and
posture tests (Romberg test, Unterberger test, Mingazzini
test) and coordination tests (index finger to nose and heel to
knee). According to evidence-based guidelines published in
2008 by the American Academy of Otolaryngology – Head
and Neck Surgery [13], clinical examination included the
Dix–Hallpike diagnostic maneuver to test the posterior
semicircular canal (PSC); if a patient had a history compat-
ible with BPPV and the Dix–Hallpike test is negative, the
clinician should perform a supine roll test to assess for
horizontal semicircular canal (HSC) BPPV. Further, we
looked for onset of the provoked positional nystagmus by
using Fresnel lenses.
According to the guidelines [13], we performed the Epley
maneuver or the Lempert maneuver to treat posterior or
horizontal semicircular canal BPPV, respectively as follows.
• Dix–Hallpike diagnostic test is performed by bringing the
patient from an upright seated position to a supine
position with the head turned 45 degrees to one side and
the neck extended 20 degrees. The patient may be slowly
returned to the upright position, and a reversal of the
nystagmus may be observed; the maneuver is then
repeated for the other side [14].
• Supine roll test is performed by initially positioning the
patient supine with the head in neutral position follow-
ed by quickly rotating the head 90 degrees to one side to
examine for characteristic nystagmus. Then the head is
returned to the face-up position, allowing all nystagmus
to subside. The head is then turned rapidly to the other
side to examine for nystagmus once again [13].
At the routinely scheduled two-week recall, the patients
were subjected to clinical examination and administered the
Italian translation of the Dizziness Handicap Inventory (DHI)
[15], a 25-item questionnaire which investigates objectively
the psychological, physical, and practical aspects of dizziness.
The score ranges from 0 (absence of symptoms) to 100
(maximum intensity of symptoms).
Patients were classified according to the following criteria
based on the results of the clinical assessment:
1. Complete resolution: asymptomatic patient, no nystag-
mus nor vertigo and nausea during positional tests, DHI
score <30;
2. Partial resolution: patients without nystagmus, vertigo
and nausea during positional tests, but with DHI score
>30 (dizzy patients);
3. Persistent BPPV: according to the guidelines [13], we
considered BPPV as persistent when symptoms with
nystagmus and/or vertigo and/or nausea continued for
more than 2 weeks and whether BPPV relapsed 2 weeks
after a complete resolution
40 AMERI CAN JOURNAL OF OTOLAR YNGOLOGY–H E AD AN D N E CK M EDI CI N E AN D S U RGE RY 3 8 ( 2 0 17 ) 38–4 3
4. Changing BPPV (canal switch): presence of nystagmus
and/or vertigo and/or nausea evoked by positional tests
but involving a different canal in the same labyrinth.
We decided to focus on groups 1 and 2 and in the latter we
identified two subgroups depending on whether the patients
underwent a second CRP or not: 94 had undergone a second
CRP (treated group), while 84 patients had not (non-treated
group). This distinction was made because there has been a
progressive shift in our approach consequent to the publica-
tion of the clinical practice guidelines in 2008 [13], as we
introduced the option to repeat a second CRP to treat patients
with residual dizziness, instead of adopting an observational
monitoring as in the past.
Three to four weeks after follow-up vestibular assessment,
the patients underwent a clinical examination and they filled
in the DHI questionnaire once again.
In order to analyze the recurrence rate of BPPV in dizzy
patients, in January 2015, patients belonging to the groups 1
and 2 (complete and partial resolution) were individually
contacted by the department staff to question them about
possible BPPV relapses during the period passed from their
first episode until 31 December 2013. Patients with persistent
BPPV (group 3) or canal-switch BPPV (group 4) were not
contacted because they had undergone more than one CRP
with curative intent and they were not the focus of this study.
Statistical analysis was performed using dedicated software
(Statistical Package for Social Sciences v.15, SPSS Inc., Chicago,
IL). The rate of recurrence of BPPV was compared between the
treated group and the non-treated group with a Pearson χ2 test.
The survival analysis was carried out by Kaplan–Meier curves;
a log-rank test was used to assess the difference in survival
distribution between the groups. In consideration of the fact
that the observational periods of this study started at different
times, we applied the Kaplan–Meier product-limit method to
estimate the survival function in order to determine whether
the time to recurrence differed between the complete and the
partial resolution groups and between the treated and non-
treated groups. Survival time was defined as the number of
days passed from the first treatment to the day in which the
symptoms of BPPV recurred. For patients without BPPV
recurrence, the timeline was censored at the last day of the
observational period. The estimated survival functions were
plotted for the groups with complete resolution and partial
resolution, and for the treated group and non-treated group.
Furthermore, we estimated the degree of dizziness resolu-
tion, by comparing the DHI results obtained from the partial
resolution group, and in relation to which semicircular canal
was involved. In particular we considered dizziness recovery to
be significant when patients passed from a DHI score >32 to a
DHI score <30 after 4 weeks. The level of significance for all
tests was p < 0.05.
3. Results
The study consisted of 292 patients, 103 males and 189 females,
who were 53.4 ± 15.2 years old. The PSC was involved in
patients 176 (60.3%) and the HSC in 116 patients (39.7%).
CRP failed in 30 subjects; of these, 21 patients had
persistent BPPV (13 with PSC BPPV and 8 with HSC BPPV)
and 9 had canal-switch BPPV, with transition from the PSC to
the HSC; these patients were excluded from the analysis. Our
study therefore focused on 262 patients (89.7%) who were
successfully treated after the first CRP; of these, 84 patients
belonged to the group 1 (complete resolution) and 178
patients (67.9%) presenting dizziness post-CRP, belonged to
the group 2 (partial resolution), who in turn have been divided
into a treated group composed of 94 patients and a non-
treated group with 84 patients.
Considering the 31st December 2013 as the final time point
of our observation period, 122 patients (42%) presented a
recurrence of BPPV: 40 subjects (32.8%) in the group 1
(complete resolution), 44 patients (36,1%) in the treated
group and 38 patients (31.1%) in the non-treated group. The
difference in terms of BPPV recurrence rates between the
treated and non-treated groups was not statistically signifi-
cant (p = 0.84).
Figs. 1 and 2 show that patients without dizziness after
CRP had a longer interval until BPPV relapsed compared to
dizzy patients. Moreover, patients with residual dizziness
after CRP who did not undergo a second CRP had a shorter
BPPV-free period compared to those who repeated CRP.
However, the log-rank test revealed that the difference was
not statistically significant (p = 0.45 and p = 0.54,
respectively).
The treated group exhibited a greater difference in DHI
score compared to the non-treated group (Fig. 3, p < 0.001). In
relation to which semicircular canal was involved, there was
no significant difference in dizziness recovery between HSC
and PSC in the treated group (p > 0.05) (Fig. 4A); by contrast,
patients suffering for HSC BPPV in the non-treated group had
greater rate of spontaneous resolution compared to those
with PSC form of BPPV (p > 0.05) (Fig. 4B).
Fig. 1 – Kaplan–Meier curves of recurrence in the complete
recovery group and the partial recovery group (p > 0.05).
 AMERI CA N JOURNAL OF OT OLAR YNGOLOGY–H E AD AN D N E CK M EDI CI N E AN D S U RGE RY 3 8 ( 2 0 17 ) 38–4 3
Fig. 2 – Kaplan–Meier curves of recurrence in the treated
group and the non-treated group (p > 0.05).
4. Discussion
Despite the fact that the etiology of BPPV has yet to be
clarified, several hypotheses as to its pathophysiology were
put forward more than a century ago. Bàràny and Adler are
considered the pioneers in studying BPPV and they first
described the clinical aspects of BPPV [16,17] and many
authors have already described several processes that may
explain the recovery. Dix and Hallpike supported the hypo-
thesis of utricular dysfunction, Shuknecht proposed the
theory of otoconial migration and gave the first definition of
cupulolithiasis, Hall later described canalolithiasis. Epley and
Semont demonstrated the efficacy of CRP in the treatment of
BPPV [13,16,18–22].
Fig. 3 – Box and whiskers plot of dizziness scores in the
partial recovery group. The treated group had significantly
lower dizziness scores compared to the non-treated group
(p < 0.05).
41
Fig. 4 – A: Dizziness recovery in the treated group correlated
to the semicircular canal reported as distribution of
dizziness scores. There was no significant difference in
dizziness recovery between the HSC and PSC (p > 0.05).B:
Dizziness recovery in the non-treated group correlated to the
semicircular canal reported as distribution of dizziness
scores. PSC cupulo-canalolithiasis had worse spontaneous
dizziness recovery compared to HSC cupulo-canalolithiasis
(p < 0.05).
At the start of this century, some authors focused on
understanding the mechanism of post-CRP dizziness onset:
Seok and colleagues noticed the presence of residual dizzi-
ness arising 48–72 hours after CRP in 65%–75% of patients and
this symptom disappeared after 3 months [9]. Different
hypotheses to explain this phenomenon were proposed by
Di Girolamo, Von Breven, Gall, Pollak and colleagues [23–26].
Inagaki et al. prepared an experimental model of BPPV to
investigate the effect of returned otoconia on the utricular
macula. In their experiment, when the otoconial mass was
positioned on the macula, the utricular potentials transiently
increased; they concluded that dizziness occurring after CRP
is possible due to the bio-electrical re-arrangement of
otoconia when they return to the utricula, pressing on a
different portion of the macula [27].
Nowadays, we need to distinguish the concept of post-CRP
dizziness and subjective vertigo, also called vertigo without
nystagmus. Haynes, Tirelli, Weider and colleagues [28–30]
42 AMERI CAN JOURNAL OF OTOLAR YNGOLOGY–H E AD AN D N E CK M EDI CI N E AN D S U RGE RY 3 8 ( 2 0 17 ) 38–4 3
agree that there are situations in which the mass of otoconial
debris is so poor that the transduction of the neural signal is
adequate to elicit vertigo but not intense enough to stimulate
the vestibulo-ocular pathway, so that during positional tests
patients may experience vertigo, dizziness or nausea but with
no association with nystagmus [29].
In literature the recurrence rates of BPPV ranges from 3.8%
to 80%. Three prospective long-term follow-up studies found
low BPPV recurrence rates equal to 12%, 22%, and 26%,
respectively [11,31,32]; in one of them, 50% of BPPV relapses
occurred in the first 6 months [11]. In a cohort of 100 patients,
26 presented a BPPV relapse in the first year [33]. Two
retrospective studies revealed a statistically significant pre-
disposition for BPPV recurrence in the post-traumatic type
[34] and when associated with Menière syndrome [35].
Performing a CRP early in relation to the beginning of
symptoms, should prevent BPPV relapse and decrease the
incidence of residual dizziness [12,36]. There are several
factors that seem to be independent from the risk of BPPV
recurrences: the number of CRP performed, exercises at
home, postural restriction, sex, age and the specific canal
involved [37–40].
The aim of our study was to assess whether a relationship
exists between residual dizziness after the first CRP and the
BPPV relapse. In this study we deliberately selected patients
with a first episode of idiopathic BPPV without factors that
could modify the natural course of the pathology towards
recovery (Fig. 1).
Our overall results agree with those reported in the
literature [36] with regard to the incidence of post-CRP
dizziness (67.9%) and success rate after first CRP (89.7%). The
global recurrence rate of BPPV was approximately 42%. The
main significant outcome of this study is that the dizzy
patients who underwent a second CRP improved the dizzi-
ness score in comparison to the non-treated group. In
particular, patients suffering from PSC BPPV who did not
repeat the CRP had longer spontaneous recovery time from
dizziness compared to those with HSC BPPV, while in the
treated group HSC and PSC presented the same outcome in
dizziness recovery.
Therefore, dizzy patients could be treated with a second
CRP that clinicians choose according to the international
guidelines [13]. In the light of the results obtained, this
approach demonstrated the potential to improve the residual
dizziness after CRP and enhance the recovery time regardless
of the canal involved. Nevertheless, it is not possible to state
that repeated CRP in patients with clinical recovery from BPPV
and residual dizziness post-CRP lowers the risk of BPPV
relapse.
The main limits of this study are the retrospective design,
the relatively small size of the study population and the short
observational period. Further studies are required with
prospective and randomized design to avoid selection bias.
5. Conclusion
This study did not show any significant difference in terms of
recurrence of BPPV between patients with post-CRP dizziness
who did not underwent a second CRP and patients who
repeated the CRP. However, the latter group had improved
dizziness symptoms. Therefore, repeating CRPs may improve
post-CRP dizziness but it does not reduce the risk of BBPV
recurrence.
REFERENCES
[1] Bisdorff A, Bosser G, Gueguen R, et al. The epidemiology of
vertigo, dizziness, and unsteadiness and its links to co-
morbidities. Front Neurol 2013;22:29. http://dx.doi.org/10.
3389/fneur.2013.00029.
[2] Colledge NR, Wilson JA, Macintyre CA, et al. The prevalence
and characteristics of dizziness in an elderly community. Age
Ageing 1994;23:117–20.
[3] Karatas M. Central vertigo and dizziness epidemiology,
differential diagnosis, and common causes. Neurologist 2008;
14:355–64.
[4] Kerber KA, Brown DL, Lisabeth LD, et al. Stroke among
patients with dizziness, vertigo, and imbalance in the
emergency department: a population-based study. Stroke
2006;37:2484–7.
[5] Chan Y. Differential diagnosis of dizziness. Curr Opin
Otolaryngol Head Neck Surg 2009;17:200–3.
[6] Baloh RW, Sloane PD, Honrubia V. Quantitative vestibular
function testing in elderly patients with dizziness. Ear Nose
Throat J 1989;68:935–9.
[7] Von Brevern M, Radtke A, Lezius F, et al. Epidemiology of
benign paroxysmal positional vertigo: a population based
study. J Neurol Neurosurg Psychiatry 2007;78:710–5.
[8] Oghalai JS, Manolidis S, Barth JL, et al. Unrecognized benign
paroxysmal positional vertigo in elderly patients. Otolaryngol
Head Neck Surg 2000;122:630–4.
[9] Seok JI, Lee HM, Yoo JL, et al. Residual dizziness after
successful repositioning treatment in patients with benign
paroxysmal positional vertigo. J Clin Neurol 2008;4:107–10.
[10] Salvinelli F, Trivelli M, Casale M, et al. Treatment of benign
positional vertigo in the elderly: a randomized trial. Laryn-
goscope 2004;114:827–31.
[11] Brandt T, Huppert D, Hecht J, et al. Benign paroxysmal
positioning vertigo: a long-term follow-up (6-17 years) of 125
patients. Acta Otolaryngol 2006;126:160–3.
[12] Perez P, Franco V, Cuesta P, et al. Recurrence of benign
paroxysmal positional vertigo. Otol Neurotol 2012;33:437–43.
[13] Bhattacharyya N, Baugh RF, Orvidas L, et al. Clinical practice
guideline: benign paroxysmal positional vertigo. Otolaryngol
Head Neck Surg 2008;139:47–81.
[14] Furman JM, Cass SP. Benign paroxysmal positional vertigo. N
Engl J Med 1999;341:1590–6.
[15] Jacobson GP, Newman CW. The development of the dizziness
handicap inventory. Arch Otolaryngol Head Neck Surg 1990;
116:424–7.
[16] Marom T, Oron Y, Watad W, et al. Revisiting benign
paroxysmal positional vertigo pathophysiology. Am J
Otolaryngol 2009;30:250–5.
[17] Lanska DJ, Remler B. Benign paroxysmal positioning vertigo:
classic descriptions, origins of the provocative positioning
technique, and conceptual developments. Neurology 1997;48:
1167–77.
[18] Schuknecht HF. Cupulolithiasis. Arch Otolaryngol 1969;90:765–78.
[19] Schuknecht HF, Ruby RR. Cupulolithiasis. Adv
Otorhinolaryngol 1973;20:434–43.
[20] Tirelli G, Boscolo Nata F, Gardenal N, et al. Liberatory vertigo:
a new prognostic factor for repositioning maneuvers. Am J
Emerg Med 2016;34:1548–51.
 AMERI CA N JOURNAL OF OT OLAR YNGOLOGY–H E AD AN D N E CK M EDI CI N E AN D S U RGE RY 3 8 ( 2 0 17 ) 38–4 3
[21] Tirelli G, D'Orlando E, Zarcone O, et al. Modified particle
repositioning procedure. Laryngoscope 2000;110:462–8.
[22] Tirelli G, Russolo M. 360-Degree canalith repositioning
procedure for the horizontal canal. Otolaryngol Head Neck
Surg 2004;131:740–6.
[23] Di Girolamo S, Ottaviani F, Scarano E, et al. Postural control in
horizontal benign paroxysmal positional vertigo. Eur Arch
Otorhinolaryngol 2000;257:372–5.
[24] Von Brevern M, Schmidt T, Schönfeld U, et al. Utricular
dysfuction in patients with benign paroxysmal positional
vertigo. Otol Neurotol 2006;27:92–6.
[25] Gall RM, Ireland DJ, Robertson DD. Subjective visual vertical
in patients with benign paroxysmal positional vertigo. J
Otolaryngol 1999;28:162–5.
[26] Pollak L, Davies RA, Luxon LL. Effectiveness of the particle
repositioning maneuver in benign paroxysmal positional
vertigo with and without additional vestibular pathology.
Otol Neurotol 2002;23:79–83.
[27] Inagaki T, Suzuki M, Otsuka K, et al. Model experiments of
BPPV using isolated utricle and posterior semicircular canal.
Auris Nasus Larynx 2006;33:129–34.
[28] Haynes DS, Resser JR, Labadie RF, et al. Treatment of benign
positional vertigo using the Semont maneuver: efficacy in
patients presenting without nystagmus. Laryngoscope 2002;
112:796–801.
[29] Tirelli G, D'Orlando E, Giacomarra V, et al. Benign positional
vertigo without detectable nystagmus. Laryngoscope 2001;
111:1053–6.
[30] Weider DJ, Ryder CJ, Stram JR. Benign paroxysmal positional
vertigo: analysis of 44 cases treated by the canalith
repositioning procedure of Epley. Am J Otol 1994;15:321–6.
43
[31] Prokopakis EP, Chimona T, Tsagournisakis M, et al. Benign
paroxysmal positional vertigo: 10- year experience in treating
592 patients with canalith repositioning procedure.
Laryngoscope 2005;115:1667–71.
[32] Sakaida M, Takeuchi K, Ishinaga H, et al. Long-term outcome of
benign paroxysmal positional vertigo. Neurology 2003;60:1532–3.
[33] Dorigueto RS, Mazzetti KR, Gabilan YP, et al. Benign parox-
ysmal positional vertigo recurrence and persistence. Braz J
Otorhinolaryngol 2009;75:565–72.
[34] Choi SJ, Lee JB, Lim HJ, et al. Clinical features of recurrent or
persistent benign paroxysmal positional vertigo. Otolaryngol
Head Neck Surg 2012;147:919–24.
[35] Kansu L, Avci S, Yilmaz I, et al. Long-term follow-up of
patients with posterior canal benign paroxysmal positional
vertigo. Acta Otolaryngol 2010;130:1009–12.
[36] Do YK, Kim J, Park CY, et al. The effect of early canalith
repositioning on benign paroxysmal positional vertigo on
recurrence. Clin Exp Otorhinolaryngol 2011;4:113–7.
[37] Parnes LS, Agrawal SK, Atlas J. Diagnosis and management of
benign paroxysmal positional vertigo (BPPV). CMAJ 2003;169:681–93.
[38] Helminsky JO, Janssen I, Kotaspouikis D, et al. Strategies to
prevent recurrence of benign paroxysmal positional vertigo.
Arch Otolaryngol Head Neck Surg 2005;131:344–8.
[39] Toupet M, Ferrary E, Bozorg GA. Effect of repositioning
maneuver type and postmaneuver restrictions on vertigo
and dizziness in benign positional paroxysmal vertigo.
ScientificWorldJournal 2012;2012:162123.
[40] Papacharalampous GX, Vlastarakos PV, Kotsis GP, et al. The
role of postural restrictions after BPPV treatment: real effect
on successful treatment and BPPV's recurrence rates. Int J
Otolaryngol 2012;2012:932847.