Evaluation and Treatment of Bilateral Benign Paroxysmal Positional Vertigo (BPPV)

1. Evaluation and Treatment of Bilateral Benign Paroxysmal Positional Vertigo: A Case
Report
Thomas G. Lavosky, DPT, Cert. MDT
Widener University
Chester, PA

2. Introduction:
Symptoms of peripheral vestibular disorders include vertigo, disequilibrium, and frequently
nausea, and emesis. The most common cause of vertigo due to peripheral vestibular
disorders is benign paroxysmal positional vertigo (BPPV). 1 BPPV is characterized by
complaints of brief periodic vertigo when the head is moved into certain positions. The
most prevalent etiology of this disorder is idiopathic (>50%) followed by post-traumatic
(14-27%).2 Other causes include labyrinthitis, vertebral-basilar ischemia, Meniere’s
disease, chronic otitis, and ototoxicity. 2 Patients with post-traumatic BPPV have a
significantly higher incidence of bilateral involvement than do those with idiopathic BPPV.
In addition, BPPV may present bilaterally in 7.5 to 15% of all cases.3 There are two
commonly accepted theories as to the cause of BBPV.
The first theory, cupulolithiasis, proposes that otoconia from the maccule of the utricle
becomes adhered to the cupula in one of the semi-circular canals,4 usually the posterior
canal. The increased density of the attached otoconia to the cupula produces excessive
deflection when the patient’s head is moved into certain positions, hence bringing on
symptoms. Resulting nystagmus and vertigo is sustained as long as the patient’s head
remains in the provoking position. This form of BPPV is rare. The second theory,
canalithiasis, proposes that dislodged otoconia from the utricle is free floating in the
endolymphatic fluid in one of the semi-circular canals,5,6 usually the posterior canal. When
the head is moved into a provoking position, the otoconia moves into the most dependent
position in the canal. This results in a movement of endolymph and thus a deflection of the
cupula. The vertigo and nystagmus occur with a1 to 40 seconds latency after the patient is
2

3. placed in a provoking position. The symptoms initially increase and then resolve within 60
seconds. The symptoms usually fatigue if the patient is repeatedly placed into the
provoking position. BPPV resulting from canalithiasis is the most common form.
Involvement of the posterior, anterior, or horizontal canal can occur with BPPV. The
posterior canal is involved the most frequently followed by the anterior and horizontal
canals.7 The direction of the nystagmus when the patient is moved into the provoking
position indicates which canal is involved. The most commonly used test to confirm the
diagnosis of BPPV with posterior or anterior canal involvement is the Hallpike-Dix test.8
According to Lopez-Escamez et al, 9 the Hallpike-Dix test has a sensitivity of 82% and a
specificity of 71%, thus it is effective in ruling out and in BPPV involving the anterior or
posterior canal. The positive and negative likelihood ratios are 2.8 and .25, respectively.9
The gold standard in this study was defined as independent selection of the same
diagnostic category by all three investigators after examining a questionnaire regarding
each patient’s history. The roll test is used to detect BPPV with horizontal canal
involvement.
The treatment of choice for posterior or anterior canalithiasis is the canalith repositioning
technique (CRT). During this technique it is theorized that canalith moves out of semi-
circular canal into the common crus and finally into the vestibule. For cupulolithiasis
involving the posterior or anterior canal the treatment of choice is the liberatory maneuver.
Finally, the treatment of choice for horizontal canalisthiasis and cupulolithiasis are the
CRT horizontal canal and the Brandt-Daroff exercises, respectively.10 Studies focused on
3

4. the outcome of CRT, including several randomized control trials, have shown success rates
of > 60% after a single treatment and of > 95% after 3 treatments.11 Ostensibly, because of
multiple canal involvement with bilateral BPPV, usually more than one CRT is necessary
for complete or substantial resolution of symptoms. The presence of bilateral disease has a
statistically significant influence on the number of treatments necessary for the relief of
symptoms (P< .05).12 There are infrequent cases, however, where resolution occurs after
performing the CRT on the more symptomatic side only. Kaplan et al13 reported successful
management of patients with bilateral BPPV by performing the CRT on the more
symptomatic side first; i.e., the side that has nystagmus of faster and higher amplitude.
After the Hallpike-Dix test is negative on this side, the CRT is performed on the
contralateral side.
The purpose of this case study is to discuss the management and outcome of a patient with
bilateral BPPV using the CRT, gaze stabilization exercises, and static and dynamic balance
exercises. A CAT scan ruled out disequilibrium resulting from a cerebellum or a brain stem
lesion.
Description of Subject:
The patient is a 51-year old male with chief complaints of 4-month history of vertigo,
disequilibrium, tinnitus, inability to smell, and headaches resulting from hitting the back of
his head after falling from a ladder. He reported that he fractured his skull and had bleeding
from the nose and ears after the injury. Precipitating factors for vertigo and disequilibrium
included transferring from sitting to standing, looking up, and laughing. In addition, he
4

5. stated that the duration of the dizziness was less than one minute. A CAT scan did not
reveal a brain stem, cerebral, or cerebellar lesion. Plain film radiographs revealed a
fractured occiput. An audiography did not reveal a loss of hearing.
Examination:
On initial evaluation, objective findings were as follows: no spontaneous or gaze-evoked
nystagmus, normal smooth pursuits in the horizontal plane with production of dizziness
after 7 second, normal smooth pursuits in the vertical plane with production of dizziness
after 10 second, normal saccadic tracking in horizontal plane with production of dizziness
after 5 seconds, production of oscillopsia after 7 seconds with vestibular ocular reflex
(VOR) in horizontal plane, normal VOR in the vertical plane, negative right and left head
thrust, no nystagmus post head-shaking in horizontal and vertical planes (Frenzel lenses
were not used), valsalva maneuver produced head pain but no dizziness, performed
Romberg stance for > 30 seconds with eyes open and with eyes closed with minimal sway,
performed sharpened Romberg stance with eyes open for > 30 seconds with minimal sway,
performed sharpened Romberg stance with eyes closed for 20 seconds with severe sway,
performed 4 consecutive tandem steps with eyes open, periodic staggering with walking
with head rotation every 5th step, positive right and left Hallpike-Dix maneuver producing
right and left torsional nystagmus, respectively. The right side was more symptomatic. Up
beating and down beating nystagmus were not detected because of fixation suppression of
vertical nystagmus as the result of performing the Hallpike-Dix without Frenzel lenses.10
The latency and duration of the nystagmus (5 seconds and 15 seconds, respectively), and
concurrent vertigo, was consistent with BPPV (canalithiasis) with involvement of the
5

6. posterior or anterior semi-circular canal.
Description of Intervention:
On 6/8, two days after the initial evaluation a CRT was performed on the right side. (This
technique was not performed during the initial evaluation because I had not treated a
patient with bilateral BPPV before and wished to consult with a physical therapist at NYU
vestibular department before I proceeded). The patient was instructed to wear a cervical
spine collar, to avoid tilting his head up or down, and to sleep supine on extra pillows to
keep his head elevated at night for a period of 48 hours. In addition, he was advised not to
sleep on his right side for 5-days. During his follow-up visit on 6/13, the right Hallpike-
Dix did not produce nystagmus or vertigo. The left Hallpike-Dix, however, produced (L)
torsional nystagmus with concurrent vertigo. On 6/22, a CRT on the left side was
performed and the patient was given post CRT instructions as above. Upon re-evaluation
6/26, the right and left Hallpike-Dix were negative for production of nystagmus and
vertigo. During the four visits from 6/29 to 7/13, visual-vestibular exercises were initiated
and progressed (smooth pursuits⇒active eye movements between two targets⇒VOR I and
II exercises in sitting⇒VOR I and II exercises in standing⇒VOR I exercise in standing
with word on checker board background⇒VOR I while standing on foam with word
checker board background⇒VOR I while walking with word on checker board
background). During this period, static and dynamic balance exercises were also initiated
and progressed (sharpened Romberg stance with eye close⇒marching on foam with eyes
open⇒upper extremity side to side ball toss with visual tracking while standing on
foam⇒forward and backward tandem walking with eyes open⇒walking while moving
6

7. head right-upward and left-downward every 3 steps and vise versa).
Outcomes:
Upon discharge on 7/13, objective findings were as follows: no production of dizziness
with smooth pursuits in vertical or horizontal plane, no production of oscillopsia with VOR
in horizontal plane while focusing on a V with a checker board background for > 45
seconds, performed sharpened Romberg with eyes closed for > 30 seconds with minimal
sway, normal reach test, negative Singleton’s test, performed 10 consecutive tandem steps
with eyes open, unable to perform tandem walking with eyes closed, and no intermittent
staggering while walking with rotating head every 5th step. He reported that he no longer
had vertigo or disequilibrium, but continued to complain of an inability to smell and
tinnitus. (Although I did not formally re-test and record static and dynamic balance and
gaze stabilization after performing the CRT, they had improved—but were still impaired.
Therefore, I would conclude that BPPV was partially responsible for balance and visual
deficits.)
Discussion:
Although it cannot be directly shown that the CRT actually moves canalith out of the semi-
circular canal into the common crus and finally into the vestibule, this is a plausible
explanation in this patient since his symptoms of vertigo resolved shortly after performing
the maneuver. The CAT scan ruled out disequilibrium resulting from a cerebellum or a
brain stem lesion. The patient’s gaze instability and disequilibrium might have been
7

8. caused by the co-morbidity of vestibular hypofunction notwithstanding a negative post
head shaking nystagmus and head thrust test. The sensitivity of the head-shaking test in
patient’s with unilateral or asymmetrical vestibular hypofunction is decreased when frenzel
lenses are not used because of fixation suppression of horizontal nystagmus.14 In addition,
the head thrust is less sensitive in detecting hypofunction in patients with incomplete loss
of peripheral vestibular function. The sensitivity of the head thrust test with incomplete and
complete unilateral vestibular hypofunction is 58% and 88%, respectively.15 The specificity
of the head thrust test with incomplete and complete bilateral vestibular hypofunction is
76% and 100%, respectively.15 The gold standard was an abnormal caloric or rotary chair
test.15 Perhaps the Fukuda’s stepping test should have been included in the examination, for
patients with unilateral vestibular hypofunction often turn excessively toward the involved
side when their eyes are closed, whereas patients with bilateral vestibular hypofunction
typically fall or translate forward during this test.10 If vestibular hypofunction was a co-
morbidity in this patient, the VOR and VSR exercises may have facilitated adaptation
within the CNS and resolved the disequilibrium and restored gaze stability.
Disequilibrium, however, is more severe in bilateral as compared to unilateral BPPV even
in the absence of a co-morbidity, possibly causing a continuous, generalized imbalance
between classic bouts.13 To obtain a better quantitative measure of the patient’s pre and
post intervention function, the dizziness handicap inventory should have been
administered. This questionnaire provides a reliable, valid, and sensitive measurement of a
patient’s perception of the effects of dizziness and unsteadiness.16 Since BPPV is
considered the most common cause of vertigo, it is incumbent of physical therapists to be
proficient in the assessment and treatment of this peripheral vestibular disorder.
8

9. References
1. Froehling DA, et al: Benign positional vertigo: Incidence and prognosis in a
population-based study in Olmsted county, Minnesota. Mayo Clin Proc. 1991;66:596.
2. Baloh, RW, et al: Benign positional vertigo: Clinical and oculographic features in 240
cases. Neurology. 1987;37:371.
3. Katsaakas A. Benign paroxymal positional vertigo (BPPV): idiopathic versus post-
traumatic. Acta Otolaryngol.1999;119:745-749.
4. Schuknecht HF. Cupulolithiasis. Arch otolaryngol. 1969;90:765-778.
5. Epley JM. The canalith repositioning procedure for treatment of benign paroxysmal
positional vertigo. Otolaryngol Head Neck Surg. 1992;107:399-404.
6. Hall SF, Ruby RR, McClure J. The mechanisms of benign paroxysmal vertigo. J
Otolaryngol. 1979;8:151-158.
7. Herdman SJ, et al. Eye movement sings in vertical canal benign paroxysmal positional
vertigo. In Fuchs, AF, et al (eds): Contemporary ocular motor and vestibular research:
A tribute to David S. Robinson. Stuttgart, Thieme, 1994, pp 385-387.
8. Dix MR, Hallpike CS. Pathology, symptomatology and diagnosis of certain disorders
of the vestibular system. Proc Roy Soc Med. 1952; 45:341.
9. Lopez-Escamez JA, et al. Diagnosis of common causes of vertigo using a structured
clinical history. Acta Otorrinolaringol Esp. 2000;51(1):25-30.
10. Herdman SJ. Vestibular Rehabilitation. 2nd ed. Philadelphia, PA: FA Davis Company,
2000.
11. Epley JM. The canalith repositioning procedure for treatment of benign paroxysmal
9

10. positional vertigo. Otolaryngol Head neck surg. 1992;107:399-404.
12. Marcias JD. Variables affecting treatment in benign paroxysmal positional vertigo.
Laryngoscope. 2000;110(11):1921-1924
13. Kaplan DM et al. Management of bilateral benign paroxymal positional vertigo.
Otolaryngology-Head and Neck Surgery. 2005;133:769-773.
14. Watabe V, Hashiba M, Baba S. Voluntary suppression of caloric nystagmus under
fixation of imaginary of after-image target. Acta Otolaryngol Suppl. 1996;525:155-157.
15. Schubert MC, Tusa RJ, Grine LE, Herdman SJ. Optimizing the sensitivity of the head
thrust test for identifying vestibular hypofunction. Physical Therapy.
2004;84(2):1069-1080.
16. Jacobson GP, Newman CW. The development of the Dizziness Handicap Inventory.
Arch Otolaryngol Head Neck Surg. 1990;116:424-427.
10