You are on page 1of 4

The Laryngoscope

Lippincott Williams & Wilkins, Inc., Philadelphia


2000 The American Laryngological,
Rhinological and Otological Society, Inc.

Effectiveness of the Particle Repositioning


Maneuver in Subtypes of Benign
Paroxysmal Positional Vertigo
Robert C. OReilly, MD; Brian Elford, DO; Robert Slater, MD

Objectives: To assess the efficacy of the particle


repositioning maneuver (PRM) in patients presenting
with idiopathic benign paroxysmal positional vertigo
(BPPV) compared with those with evidence of additional peripheral vestibulopathies. Methods: Retrospective administration of the Dizziness Handicap Inventory (DHI) to 41 patients with primary BPPV and
31 patients with secondary BPPV to subjectively evaluate their symptoms before and after the PRM.
Results: Both groups indicated a marked improvement in symptoms after the PRM. Only two patients
reported an increase in their symptoms after the
PRM and both had secondary BPPV. Conclusions: The
PRM was found to be highly effective in all forms of
BPPV, but careful history and judicious testing may
identify patients requiring additional intervention to
relieve their symptoms.
Laryngoscope, 110:13851388, 2000

INTRODUCTION
Benign paroxysmal positional vertigo (BPPV) is a
disorder of the semicircular canals characterized by freefloating debris thought to be displaced otoconia. It is the
most frequently encountered disease among patients with
balance complaints.13 The diagnosis rests on the appropriate history and demonstration of compatible nystagmus with the Dix-Hallpike test.4,5 The posterior semicircular canal is most commonly involved.1,6
Many authors have noted that BPPV can be found in
isolation, termed idiopathic BPPV, or in combination with,
and possibly a consequence of, other vestibular disorders.4,710 The expression of BPPV as a consequence of the
vestibular insult has temporally varied from 1 week to 20
years after the initial injury.7,8 The most frequent association is with significant head trauma, but several progressive degenerative vestibular disorders have been found to
result in the clinical syndrome of BPPV. It has been specFrom the Mercy Hearing and Balance Center (R.C.O., R.S.), Darby,
and Mercy Hospital Department of Medicine (B.E.), Pittsburgh, Pennsylvania.
Editors Note: This Manuscript was accepted for publication April
26, 2000.
Send Correspondence to Robert C. OReilly, MD, Mercy Hearing and
Balance Center, Second Floor, 1503 Lansdowne Avenue, Darby, PA 19023,
U.S.A.

Laryngoscope 110: August 2000

ulated that otolith infarction resulting from various vestibular pathologies liberates free-floating particles into
the endolymphatic space.11 The clinical findings suggest
that the posterior semicircular canal has been spared by
the initial vestibular insult or has recovered function.8 We
prefer to term isolated, idiopathic BPPV primary BPPV
and BPPV associated with other vestibular disorders secondary BPPV.
The excellent response of patients with BPPV to various liberatory maneuvers has been well documented.8,9,1214 Cure rates of approximately 90% can be expected with a single treatment session.1,2,11 Few data
exist regarding the utility of these maneuvers in patients
with other concurrent vestibular derangements.15 Most
series have grouped patients with isolated BPPV together
with subjects displaying other abnormalities on history,
clinical examination, or vestibular testing. The profound
effect of other vestibulopathies on balance function is well
known.2
The goal of our study was to evaluate the efficacy of
the particle repositioning maneuver (PRM) on the balance
function of patients with primary and secondary BPPV
using the Dizziness Handicap Inventory to assess their
subjective response.16,17 The concurrent vestibulopathies
found among these patients as well as the specifics of
patients who did not meet with success will be reviewed.

MATERIALS AND METHODS


A retrospective chart review was conducted for patients
presenting to the Mercy Hearing and Balance Center between
October 1996 and March 1999 with a final diagnosis of BPPV.
Only patients with documented BPPV on physical examination or
objective testing were included. Subjects were restricted to those
with unilateral disease displaying the characteristic delayed onset, fatigable torsional-vertical nystagmus characteristic of posterior semicircular canalithiasis.2 A minimum of 1 month
follow-up was required. All patients underwent the PRM as described by Parnes and McClure18 on the initial visit and underwent repeat PRM on subsequent follow-up visits only if they
continued to have objective evidence of BPPV on Dix-Hallpike
testing.4 No other neurotologic therapeutic interventions were
carried out before the conclusion of the study (vestibular rehabilitation, medications, surgical intervention, etc.). On the conclusion of therapy, patients were asked to complete a pretreatment

OReilly et al.: Particle Repositioning Maneuver

1385

and posttreatment Dizziness Handicap Inventory (DHI)16 to subjectively assess their response to treatment.
Patients were divided into two groups by history, physical
examination, and objective testing. Those individuals who displayed positive unilateral Dix-Hallpike test results, without other
abnormalities on complete neurotologic examination, historical
evidence of peripheral vestibulopathy, or recent (3 mo) head
trauma were categorized as having primary BPPV. Patients were
considered to have secondary BPPV if, in addition to the described positive Dix-Hallpike test results, they showed evidence
of unilateral peripheral vestibular weakness on neurotologic examination (abnormal head thrust, head-shake with Frenzel
lenses, strong rotation on Fukuda stepping test, spontaneous or
gaze-evoked nystagmus, abnormalities on neurologic examination), strong history of peripheral vestibular disturbance (prolonged or nonpositional vertigo, with or without auditory symptoms, severe, recent head trauma, symptoms of progressive
neurologic disease or cerebrovascular insufficiency), or objective
evidence of unilateral or bilateral abnormalities on cochleovestibular testing (electronystagmography, rotational chair testing,
computerized dynamic posturography, or fluctuating or unilateral sensorineural hearing loss).
The data were analyzed using the InStat software (GraphPad Software, San Diego, CA.). The Kolmogorov-Smirnov test for
normality was used on each data set to determine whether parametric or nonparametric comparisons could be employed. Box and
whisker plots were developed to display the results.

RESULTS
Of 121 patients identified, 72 met the inclusion criteria. Forty-one patients were categorized with primary
BPPV, and 31 with secondary BPPV. Table I lists associated vestibular disorders found in patients categorized as
having secondary BPPV. The majority had historic evidence of a viral vestibular insult, reporting a single distinct episode of the acute onset of vertigo, nausea, and
emesis lasting days to weeks. Those with a demonstrable
sensorineural hearing loss in the involved ear received a
diagnosis of labyrinthitis (19%) and those without a loss
received a diagnosis of vestibular neuritis (26%). Patients
without a clear history of an acute vestibular insult but
with objective evidence of a unilateral auditory deficit or

TABLE I.
Other Vestibular Disorders in Secondary Benign Paroxysmal
Positional Vertigo (BPPV).
Disorder

n (%)

Vestibular neuritis
Labyrinthitis
Head trauma/vestibular concussion
Progressive idiopathic vestibulopathy
Cerebrovascular insufficiency/cerebrovascular
accident
Endolymphatic hydrops
Vestibular migraine
Multiple sclerosis
Congenital vestibulopathy
Cervical vertigo
Total

8 (26)
6 (19)
4 (13)
4 (13)
3 (10)

Laryngoscope 110: August 2000

1386

2 (7)
1 (3)
1 (3)
1 (3)
1 (3)
31 (100)

TABLE II.
Patient Demographics and Treatment Outcome.

Average age in years (range)


Sex ratio: male to female
Ear (right/left)
Average number of PRMs (range)
Average follow-up months (range)
Average pre-PRM DHI (range)
Average post-PRM DHI (range)
Average change DHI (range)

Primary BPPV
N 41

Secondary BPPV
N 31

61 (3087)
29:12
22:19
1.3 (13)
10.6 (124)
38.5 (088)
10.7 (080)
28 (082)

61 (1690)
24:7
17:14
1.3 (12)
9.2 (220)
49.9 (14100)
15.6 (072)
34.3 (296)

PRM particle repositioning maneuver; DHI Dizziness Handicap


Inventory.

vestibular weakness in the ear displaying BPPV were


categorized as having progressive idiopathic vestibulopathy (13%). Patients with significant recent head trauma
(skull fracture, concussion, loss of consciousness) accounted for 13% of the group.
Table II shows the demographics and response to
treatment in each group. The average age for both groups
was 61 years. A female preponderance was found in both
groups. With an average of 10.6 and 9.2 months follow-up,
both groups had an equivalent number of PRMs. All data
sets had a normal distribution except for the posttreatment scores in the primary BPPPV group. The pretreatment and posttreatment DHI was slightly higher among
patients with secondary BPPV, but both groups reported a
large improvement in their DHI, averaging 28 points in
patients with primary BPPV and 34.3 points in those with
secondary BPPV.
Statistical analysis revealed a highly significant difference in the pretreatment and posttreatment DHI in
primary BPPV (P .0001, Wilcoxon matched-pairs
signed-ranks test) and secondary BPPV (P .0001, paired
t test). The pretreatment DHI was statistically different
between the primary and secondary BPPV groups (P
.03, unpaired t test), but the posttreatment scores were
not (P .3, Mann-Whitney test). There was no significant
difference in the improvement in DHI between the groups
(P .2, unpaired t test).
There were a few patients in both groups who did not
follow this trend. One patient with primary BPPV failed to
show an improvement in the DHI. This was a 74-year-old
woman with a history of hypertension, hyperlipidemia,
coronary artery disease, and anemia who was found to be
normal on neurotologic examination except for left BPPV.
The PRM was performed successfully on the first visit
with complete resolution of the positional nystagmus on
post-PRM Dix-Hallpike testing. The patient reported no
change in her DHI. Further neurotologic evaluations were
negative for other vestibular disorders. No patients with
primary BPPV reported an increase in their DHI.
Two patients with secondary BPPV had an increase
in their DHI. One patient reported control of positional
symptoms but continued dysequilibrium. This was an 88year-old man with cardiac and cerebrovascular disease
OReilly et al.: Particle Repositioning Maneuver

TABLE III.
Summary Parameters.
DHI

Median

Upper
Extreme

Lower
Extreme

Upper
Quartile

Lower
Quartile

Primary BPPV pre-PRM


Primary BPPV post-PRM
Secondary BPPV pre-PRM
Secondary BPPV post-PRM

41
41
31
31

34
4
46
8

88
80
100
72

0
0
14
0

54
15
60
24

23
0
34
0

with several abnormalities on neurotologic work-up (falling gain and failure of fixation suppression on rotational
chair testing, surface-dependent pattern on computerized
dynamic posturography, small vessel ischemic changes on
contrast head computed tomography). A 57-year-old
woman with abnormal caloric tests on electronystagmography and panic disorder reported no improvement after
PRM despite resolution of nystagmus on follow-up DixHallpike testing.
Two patients with secondary BPPV reported no
change in their DHI. A 74- year-old woman with a history
of otosclerosis in the involved ear and abnormalities on
neurotologic testing (asymmetric sensorineural hearing
loss, abnormal phase and gain on rotational chair testing)
required PRM on two separate visits because her DixHallpike test results were positive. She failed to note
improvement on DHI despite clinical evidence of resolution of the positional nystagmus. A 73-year-old woman
reported 1 week of relief of positional symptoms after left
PRM. She had a history of whiplash injury and head
trauma from a motor vehicle accident in 1989. Prior neurotologic examination had shown a positive contralateral
right Dix-Hallpike test in 1990. Past medical history included breast cancer, insulin-dependent diabetes, and hypertension. Physical examination showed severe cervical
spine arthritic degeneration, positive Romberg and cere-

bellar abnormalities. Results of post-PRM Dix-Hallpike


tests were negative.
Summary parameters (Table III) and graphic representation of the results in box and whisker format19 are
shown in Figure 1. A significant benefit from the PRM can
be clearly seen in both groups with a sharp decline in the
median DHI in both primary and secondary BPPV. Although the pretreatment and posttreatment DHI was
higher in the secondary BPPV group, the relative gain
(improvement) in this group was larger, with a median
gain of 34 points as opposed to 26 points in the primary
BPPV group. There is less dispersion of the results in
posttreatment DHI in both groups.

DISCUSSION
The effectiveness of PRM in relieving the vertigo
associated with BPPV has been repeatedly demonstrated.
It is a simple therapeutic maneuver and is contraindicated
only in patients with high-grade carotid stenosis, unstable
heart disease, or severe neck disease.2 A 15% per year
recurrence rate has been noted by Furman and Cass.2 The
end-point for success in most studies has been the elimination of nystagmus during repeat Dix-Hallpike testing
and the subjective relief of positional vertigo.1,7,12,20 Our
study demonstrates the impact of the PRM on the patients subjective sense of improvement in the context of

Fig. 1. Multiple box and whisker plots of Dizziness Handicap Inventory (DHI) before and
after treatment with the particle repositioning maneuver
(PRM). Left to right: DHI before treatment for primary benign paroxysmal positional
vertigo (BPPV); DHI after treatment for primary BPPV; DHI
before treatment for secondary BPPV; DHI after treatment
for secondary BPPV; change
in DHI (gain) in patients with
primary BPPV; change in DHI
(gain) in patients with secondary BPPV. Open dots represent median value and closed
dots represent outliers.

Laryngoscope 110: August 2000

OReilly et al.: Particle Repositioning Maneuver

1387

their overall balance disorder utilizing the DHI and evaluates its comparative utility in subjects with concurrent
vestibular disorders.
The results of this study substantiate the excellent
control of positional vertigo obtained with the PRM and
also demonstrate a more global improvement in perceived
balance function. This is demonstrated by the predictable
improvement in the DHI in both forms of BPPV and suggests that patients not only suffer from acute episodes of
vertigo but also have more persistent disruption of their
sense of balance. The motion sensitivity of patients with
active BPPV has been documented and thought to be
secondary to either cupulolithiasis or the free movement
of otoliths in the endolymphatic space with head movement.2 In patients with secondary BPPV, uncompensated
vestibular imbalance, fluctuations in vestibular function,
and central disorders augment the sense of imbalance.
Unlike other investigators, we found the most common associated vestibular disorder in patients with secondary BPPV to be viral inner ear infection as opposed to
head trauma.2,7,21 However, this may reflect the fact that
we restricted the diagnosis of secondary BPPV to patients
with proximate and severe head trauma to reflect the
impact of vestibular concussion on their syndrome. It
should be noted that Katsarkas and Kirkham22 found no
association between the severity of head injury and the
development of BPPV.
The average age in our study (61 years) is comparable
to other studies7,23 and may reflect the degenerative nature of this disorder, particularly in primary BPPV. A
female preponderance was also found, although the significance of this is not clear.
The higher pretreatment DHI scores in patients with
secondary BPPV reflect the additive impact of concurrent
vestibular disorders on this population and quantitate
this effect relative to the subgroup with primary BPPV.
The slightly higher posttreatment scores in patients with
secondary BPPV illustrate the residual impact of these
vestibular disorders, because no treatments beyond the
PRM had been instituted at the time of data collection. It
is likely, however, that the few cases reporting an elevation in posttreatment DHI reflect fluctuations in their
underlying vestibular disorders, rather than representing
a negative effect of the PRM on their status. Atypical
forms of BPPV have been found to have a more prolonged
clinical course and less favorable prognosis.15 The findings suggest that an excellent response to the PRM can be
anticipated in all forms of BPPV.

CONCLUSION
The PRM is effective in improving the subjective
assessment of balance function in patients with both primary and secondary BPPV. Patients with secondary
BPPV may require additional testing and treatment for
optimal outcome.

Laryngoscope 110: August 2000

1388

BIBLIOGRAPHY
1. Honrubia V, Baloh RW, Harris RM, Jacobson KM. Paroxysmal positional vertigo syndrome. AM J Otol 1999;20:
465 470.
2. Furman JM, Cass SP. Benign paroxysmal positional vertigo.
N Engl J Med 1999;341(21):1590 1596.
3. Sauron B, Dobler S. Benign positional vertigo. Diagnosis,
course, physiopathological treatment [in French]. Rev Prat
1994;44(3):313318.
4. Dix MR, Hallpike CS. The pathology, symptomology and diagnosis of certain common disorders of the vestibular system. Proc R Soc Med 1952;45:341354.
5. Norre ME. Diagnostic problems in patients with benign paroxysmal positional vertigo. Laryngoscope 1994;104(11):
13851388.
6. Baloh RW. Benign positional vertigo. In: Baloh RW, Halmagyi GM, eds. Disorders of the Vestibular System. New
York: Oxford University Press, 1996:328 339.
7. Baloh RW, Honrubia V, Jacobson K. Benign positional vertigo: clinical and oculographic features in 240 cases.
Neurology 1987;37:371378.
8. Harada K, Oda M, Yamamoto M, Nomura T, Ohbayashi S,
Kitsuda C. A Clinical observation of benign paroxysmal
positional vertigo (BPPV) after vestibular neuronitis (VN).
Acta Otolaryngol (Stockh) 1993;Suppl:503:61 63.
9. Von Brevern M, Lempert T, Bronstein AM, Kocen R. Selective
vestibular damage in neurosarcoidosis. Ann Neurol 1997;
42:117120.
10. Andaz C, Whittet HB, Ludman H. An unusual cause of benign paroxysmal positional vertigo. J Laryngol Otol 1993;
107:11531154.
11. Parnes LS, Robichaud J. Further observations during the
particle repositioning maneuver for benign paroxysmal positional vertigo. Otolaryngol Head Neck Surg 1997;116:
238 243.
12. Cohen HS, Jerabek J. Efficacy of treatments for posterior
canal benign paroxysmal positional vertigo. Laryngoscope
1999;109:584 588.
13. Collision PJ, Kohlberg A. Canalith repositioning procedure
for relief of post-stapedectomy benign paroxysmal positional vertigo. S D J Med 1998;51(3):85 87.
14. Epley J. The canalith repositioning procedure for treatment
of benign paroxysmal positional vertigo. Otolaryngol Head
Neck Surg 1992;107:399 404.
15. Smouha EE, Roussos C. Atypical forms of paroxysmal positional nystagmus. Ear Nose Throat J 1995;74(9)649 656.
16. Jacobson GP, Newman CW. The development of the Dizziness Handicap Inventory. Arch Otolaryngol Head Neck
Surg 1990;116(4):424 427.
17. Jacobson GP, Newman CW, Hunter L, Balzer GK. Balance
Function test correlates of the Dizziness Handicap Inventory. J Am Acad Audiol 1991;2(4):253260.
18. Parnes LS, McClure JA. Free-floating endolymph particles: a
new operative finding during posterior semicircular canal
occlusion. Laryngoscope 1992;102:988 992.
19. Govaerts PJ, Somers T, Offeciers FE. Box and whisker plots
for graphic representation of audiometric results of conductive hearing loss treatment. Otolaryngol Head Neck Surg
1998;118(6):892 895.
20. Fung K, Hall SF. Particle repositioning maneuver: effective
treatment for benign paroxysmal positional vertigo. J Otolaryngol 1996;25(4):243248.
21. Harrison MS, Ozsahinoglu C. Positional vertigo. Arch Otol
1975;101:675 678.
22. Katsarkas A, Kirkham TH. Paroxysmal positional vertigoa
study of 255 cases. J Otolaryngol 1978;7(4):320 330.
23. Mizukoshi K, Watanabe Y, Shojaku H, Okubo J, Watanabe I.
Epidemiological studies on benign paroxysmal positional
vertigo in Japan. Acta Otolaryngol Suppl (Stockh) 1988;
447:6772.

OReilly et al.: Particle Repositioning Maneuver