Evaluation and Treatment of Bilateral Benign Paroxysmal Positional Vertigo: A Case

                                     R...
Introduction:

Symptoms of peripheral vestibular disorders include vertigo, disequilibrium, and frequently

nausea, and em...
placed in a provoking position. The symptoms initially increase and then resolve within 60

seconds. The symptoms usually ...
the outcome of CRT, including several randomized control trials, have shown success rates

of > 60% after a single treatme...
stated that the duration of the dizziness was less than one minute. A CAT scan did not

reveal a brain stem, cerebral, or ...
posterior or anterior semi-circular canal.



Description of Intervention:

On 6/8, two days after the initial evaluation ...
head right-upward and left-downward every 3 steps and vise versa).



Outcomes:



Upon discharge on 7/13, objective findi...
caused by the co-morbidity of vestibular hypofunction notwithstanding a negative post

head shaking nystagmus and head thr...
References

1. Froehling DA, et al: Benign positional vertigo: Incidence and prognosis in a

   population-based study in ...
positional vertigo. Otolaryngol Head neck surg. 1992;107:399-404.

12. Marcias JD. Variables affecting treatment in benign...
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Bi BPPV

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

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Bi BPPV

  1. 1. Evaluation and Treatment of Bilateral Benign Paroxysmal Positional Vertigo: A Case Report Thomas G. Lavosky, DPT, Cert. MDT Widener University Chester, PA
  2. 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. 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. 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. 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. 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. 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. 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. 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. 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

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