Monitoring of Caloric Response and Outcome in Patients With Benign Paroxysmal Positional Vertigo

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Otology & Neurotology 28:798Y800 Ó 2007, Otology & Neurotology, Inc. Monitoring of Caloric Response and Outcome in Patients With Benign Paroxysmal Positional Vertigo *Maria I. Molina, *Jose A. López-Escámez, *Cristobal Zapata, and * Laura Vergara *Otology & Neurotology Group CTS495, Department of Surgery, Hospital de Poniente de Almería, El Ejido, Almería; and ÞHospital de Guadix, Guadix, Granada, Spain Objective: To analyze the time course of caloric response in patients with Benign Paroxysmal Positional Vertigo (BPPV). Patients: Seventy-four individuals with diagnosis of BPPV during Dix-Hallpike (DH) test. Study Design: A prospective, longitudinal study. Setting: A tertiary referral center. Intervention: Patients were treated by particle repositioning maneuvers according to the affected canal, and the effectiveness was evaluated at 180 and 360 days. Bithermal caloric response was obtained by using 44 and 30-C water irrigations at diagnosis, 6 months, and 1 year after. Main Outcome Measure: Canal paresis (CP) and response to DH after treatment. Results: The effectiveness of the treatment for BPPV (absence of vertigo and positional nystagmus during DH) was 65.2% (45 of 69) after 1 year of follow-up. Twenty-five percent of (16 of 64) individuals with BPPV presented CP at diagnosis, 27% (12 of 44) at 6 months, and 16% (9 of 56) 1 year after. One year after, seven individuals with CP showed a normal caloric response, another seven demonstrated persistent CP, and one case developed a bilateral CP. The effectiveness of particle repositioning maneuvers was not significantly different between subjects with or without CP after 1 year of follow-up (odds ratio, 1.31 [95% confidence intervals, 0.35Y4.89], p = 0.88). Conclusion: Canal paresis is not associated with a lower outcome to repositioning. Key Words: BPPVVVestibular systemvvestibular testingvvideo-oculographic examination. Otol Neurotol 28:798Y800, 2007. Benign paroxysmal positional vertigo (BPPV) is the most common vestibular disorder, and vertigo is induced by movement of lithiasis material during head position changes. The diagnosis is confirmed by the Dix-Hallpike (DH) test, and repositioning maneuvers provide effective therapy (1). Although some patients experience complete resolution of symptoms, recurrences are typically observed several months or years after particle repositioning, and vestibular lithiasis can be found in any semicircular canal, sometimes affecting several canals. The caloric test is used to stimulate the horizontal semicircular canals so that the response of each labyrinth can be compared. The slow-phase velocity of the nystagmus is commonly used for assessement of the caloric response. The finding of a reduced response is called canal paresis (CP), and this is considered a vestibular hypofunction. Canal paresis in patients with BPPV has been variously reported to be present in 26 to 50% (2Y4). The side of the paresis can be ipsilateral or contralateral with the side of BPPV. However, it is not known if CP is associated with the side affected and if CP may be a prognosis factor for recurrences in BPPV. The aim of this study is to analyze the frequency of CP in BPPV and if CP is associated with the outcome of treatment in BPPV. PATIENTS AND METHODS Address correspondence and reprint requests to Dr. Jose A. López- Escámez, Otology and Neurotology Group CTS495, Department of Surgery, Hospital de Poniente de Almería, Ctra de Almerimar, s/n 04700, El Ejido, Almería, Spain; E-mail: jalopeze@cajamar.es Patients We studied a series of 74 individuals with BPPV from 2003 to 2005. Clinical diagnosis was performed by positional testing: DH test and head-hanging maneuver, for posterior (PC) and anterior canal (AC), respectively, and lateral turning of the 798

CALORIC RESPONSE IN BPPV 799 head in decubito for the lateral canal. Physical examination included examination of the ears, Rinne and Weber test, pure-tone audiometry, and a basic neurotologic examination. Only those patients demonstrating a positional nystagmus associated with vertigo were included. Patients with perforation of the tympanic membrane or those with a cognitive or psychiatric disorder were excluded. Written information was facilitated, and an informed consent was obtained for all the individuals after explaining the purpose of the study. The ethical and research committee of the hospital approved this research study. Vestibular Examination Eye movements were recorded by a video-oculographic (VOG) system (SMI, Berlin, Germany) as previously described (5). The recording included spontaneous nystagmus, positional, and caloric testing. The DH test was considered positive for PC BPPV if nystagmus was recorded with appropriate positioning, latency, duration, and fatigue, and reversed when the patient was sited up. Differential diagnosis between PC and AC involvement was based on the direction of the vertical component of the fast phase of the nystagmus response during DH, being upward in cases of PC involvement and downward with a torsional component in cases of AC disease. Horizontal canal (HC) BPPV was identified by horizontal direction-changing positional nystagmus (6). A standard caloric test by using a Variotherm Plus model irrigator (Atmos, Berlin, Germany) was performed on each subject, with a water flow of 250 ml/20 s at 30 and 44-C with an interval of 10 min between irrigations. Caloric test was performed at diagnosis 180 and 360 days posttreatment. The percentage of CP and directional preponderance (DP) was calculated using the Jongkees Index formula on the difference of maximal slow-phase velocity and compared with reference values in our laboratory (G28%). FIG. 1. Percentage of individuals with BPPV, CP and DP. Treatment of BPPV Patients were treated according to the canal affected and evaluated at 30, 180, and 360 days posttreatment, and if they presented a positional nystagmus, repositioning was repeated up to four times. Statistical Analysis Response to DH, CP, and DP were evaluated, and odds ratio with 95% confidence intervals were calculated. Significant differences were analyzed by W 2 method and Fisher s exact test. Analysis of variance was used to compare clinical variables between patients with and without CP. Spearman s rank correlation coefficient was calculated to analyze the association between DH response and CP. p G 0.05 was considered significant. RESULTS TABLE 1. Clinical features of BPPV patients BPPV patients (n = 74) Age, mean T SD (median) 56.76 T 14.50 (59) Sex, n (%) Women 43 (58.1) Men 31 (41.9) Time course (d), mean T SD (median) 45.25 T 68.98 (24) Previous history of vertigo (%) Total (31.1) neuritis (6.8), Méniére (5.4) Minor head trauma, n (%) 17 (23) Sensorineural hearing loss 940 db, n (%) Left 8 (10.8) Right 9 (12.2) Bilateral 12 (16.2) Headache, n (%) Tensional 13 (17) Migraine 15 (20) Canal variant, n (%) Posterior right 24 (32) Posterior left 14 (19) Posterior bilateral 7 (9) Lateral right 9 (12) Lateral left 6 (8) Anterior 10 (13) Multiple canal 4 (5) The clinical features of our series is shown in Table 1. Of 74 subjects, 23 (31%) presented a previous history of vertigo, 5 (6.8%) were vestibular neuritis, and 4 (5.4%) Méniére s disease. Minor head trauma was also associated with BPPV in 17 cases (23%). In our series, 38 cases (51%) presented a PC BPPV, 15 patients (20%) showed an HC BPPV, and 10 individuals (13%) presented a unilateral down-beating nystagmus, suggesting an AC BPPV. Eleven patients (15%) showed multiple positional nystagmus (7 were bilateral PC BPPV); however, four individuals showed positional horizontal and vertical side-changing nystagmus that could not be explained by a single canal stimulation. These cases did not show a spontaneous nystagmus except for one patient with a spontaneous up beating nystagmus. Caloric Response in Patients With BPPV Bithermal caloric test was performed in 64 of the 74 individuals with BPPV. Ten patients did not accept the test or were unable to finish it because of nausea and vomiting. Of 64 individuals with BPPV, 16 showed CP at diagnosis (9 PC, 3 HC, 2 AC, 1 patient with bilateral PC disease, and 1 patient with multiple

800 M. I. MOLINA ET AL. positional nystagmus). To analyze if the CP side was associated with the side affected by BPPV, we excluded the two patients with bilateral disease. The CP was observed in the same side of BPPV in 11 of 14 cases, but our sample is too small to demonstrate a significant association (odds ratio, 9.0 [95% confidence interval, 0.33Y500], p = 0.17). Age, time course, or hearing loss (pure-tone average 940) did not differ between individuals with or without CP (Table 2; supplementary material available online). Moreover, sex, history of head trauma, migraine comorbidity, or risk factors for vascular disease were not associated with CP (Table 3; supplementary material available online). The general caloric response observed did not change during the first year (Fig. 1). The percentages of patients with BPPV and CP were 25, 26, and 19% at diagnosis 6 and 12 months later (W 2 = 1.03, p = 0.60). In addition, the percentages of subjects with DP were 19, 21, and 15% at diagnosis 6 and 12 months later (W 2 = 0.80, p = 0.66). However, some individuals showed a change in the caloric response during the follow-up (Fig. 2; supplementary material available online). One year after, seven individuals with CP showed a normal caloric response, another seven demonstrated persistent CP, and one patient developed a bilateral CP. Effectiveness of Positional Treatment Sixty-nine patients completed the follow-up, and 5 were missed 1 year after diagnosis. The effectiveness of the treatment for BPPV was 65.2% (45 of 69) after 12 months of follow-up (22 patients showed recurrence). The effectiveness of particle repositioning maneuvers did not differ between subjects with or without CP at diagnosis; CP was not significantly associated with a worse response to DH at 6 (r = 0.044, p = 0.74) or 12 months (r = j0,067, p = 0.61). DISCUSSION This study shows that 25% cases of BPPV present a reduced response to a standard caloric test and confirms the clinical value of performing a caloric test in patients with BPPV. The purpose of the current investigation was to analyze if CP was associated with any clinical variable at diagnosis and if the caloric response can be used as a predictor for outcome to particle repositioning. Although the previous history of otologic disease has been considered a risk factor for vestibulopathy (7), our study failed to demonstrate that history of head trauma, risk factors for vascular disease, or hearing loss were associated with CP. Women and patients older than 50 years are more prone to develop BPPV, but age or sex was not associated with a reduced response to caloric testing in our study. There is a significant variability in the prevalence of vestibulopathy among previous studies (13Y50%) (6, 8Y10). This can be explained by the criteria used to define CP and a previous history of vestibular neuritis that reached up to 76% in some studies (7). The finding of a reduced caloric response of the HC should be considered as an impairment of superior vestibular nerve function. None of these conditions have been functionally related with vestibular lithiasis. Therefore, there is no clinical basis to avoid performing a caloric test in patients with BPPV, and the result may reveal an impairment of the horizontal vestibulo-ocular reflex. Inourseries,CPwasobservedin16of64cases with BPPV. Therefore, in clinical practice, the caloric response in patients with BPPV can vary from normal to CP, and different signs of incomplete compensation can be observed. Our study shows that seven patients with CP compensated the caloric response during the followup and, in contrast, two patients developed a mild CP. These observations demonstrate that temporal changes in caloric response in BPPV may occur, and the diagnostic value of monitoring this response if imbalance, oscillopsia, or head motion intolerance persist after repositioning (additional discussion online). CONCLUSION Although caloric response reveals individual temporal changes in patients with BPPV, CP is not associated with a lower outcome to repositioning. REFERENCES 1. Epley J. The canalith repositioning procedure for treatment of benign paroxysmal positional vertigo. Otolaryngol Head Neck Surg 1992;107:399Y404. 2. Stahle J, Terins J. Paroxysmal positional nystagmus: an electronystagmographic and clinical study. Ann Otolaryngol 1965;74: 69Y83. 3. Baloh RW, Honrubia V, Jacobson K. Benign positional vertigo: clinical and oculographic features in 240 cases. Neurology 1987;37:371Y8. 4. 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;23:79Y83. 5. Lopez-Escamez JA, Molina MI, Gamiz MJ, et al. Multiple positional nystagmus suggests multiple canal involvement in benign paroxysmal positional vertigo. Acta Otolaryngol 2005;125: 954Y61. 6. Baloh RW, Jacobson K, Honrubia V. Horizontal semicircular canal variant of benign positional vertigo. Neurology 1993;43: 2542Y9. 7. Roberts RA, Gans RE, Kastner AH, Lister JJ. Prevalence of vestibulopathy in benign paroxysmal positional vertigo patients with and without prior otologic history. Int J Audiol 2005;44:191Y6. 8. Blessing R, Strutz J, Beck C. Epidemiology of benign paroxysmal positional vertigo. J Laryngol Otol 1986;65:455Y8. 9. Hughes C, Proctor L. Benign paroxysmal positional vertigo. Laryngoscope 1997;107:607Y13. 10. Karlberg M, Hall K, Quickert N, Hinson J, Halmagyi M. What inner ear diseases cause benign paroxysmal positional vertigo? Acta Otolaryngol 2000;120:380Y5.

CALORIC RESPONSE IN BPPV 801 SUPPLEMENTARY MATERIALS SUPPLEMENTARY TABLE 2. Quantitative clinical variables in patients with (BPPV + CP) or without CP at diagnosis (BPPV without CP; mean T SD) Age Time course Hearing loss (patients) BPPV + CP 55.56 T 26.54 T 67.22 T 22.92 12,00 33.61 BPPV without 57.06 T 52.81 T 58.12 T 15.15 CP 15.86 80.26 F test 0.119 1.299 1.433 p value 0.731 0.260 0.243 SUPPLEMENTARY TABLE 3. Qualitative clinical variables in patients with BPPV + CP and BPPV without CP Sex Head trauma Migraine Vascular disease BPPV + CP 11 women, 5 of 16 3 of 15 10 of 16 5 men BPPV 27 women, 9of43 11of47 20of44 without CP 21 men Odds ratio 0.795 0.686 0.820 2.000 Fisher test (p) 0.558 0.307 0.545 0.381 Sex, head trauma, migraine, or history of vascular disease were not associated with CP in BPPV patients. SUPPLEMENTARY FIG. 2. Time course of caloric response in patients with BPPV. A, Summary of the caloric response observed after 1 year of follow-up. B, Individuals with CP at diagnosis. h indicates persistent CP; ), initial CP changing to normal response. Three of the seven patients with persistent CP had a history of minor head trauma, another two patients had high blood pressure, and one patient was a unilateral Méniére s disease. Among the patients with normal response, three developed a mild unilateral CP (31Y32%) 1 year after at diagnosis, and another two presented a bilateral CP 1 year after.

802 M. I. MOLINA ET AL. DISCUSSION Previous studies have found that atypical positional nystagmus is not a rare observation, and it can be found in more than 40% cases of BPPV patients (11). Positional nystagmus corresponding to AC or HC lithiasis was observed in 17 and 21%, respectively (10), suggesting that these findings are underdiagnosed in clinical practice because VOG examination is not used during positional tests (12). Recently, Jackson et al. (13) have reported a 21% occurrence of AC involvement in a series of 260 patients who were evaluated by electrooculography or VOG, and they had concluded that electrooculography/vog is critical to assess the vertical component of the positional nystagmus to diagnosis AC versus PC origin. We systematically use VOG for diagnosis of BPPV since 2002, and this practice supports the findings of a higher rate of atypical positional nystagmus in our series. REFERENCES 11. Aw ST, Todd MJ, Aw GE, McGarvie LA, Halmagyi GM. Benign positional nystagmus. A study of its three-dimensional spatiotemporal characteristics. Neurology 2005;64:1897Y905. 12 Parnes LS, Agrawal SK, Atlas J. Diagnosis and management of benign paroxysmal positional vertigo (BPPV). Can Med Assoc J 2003;169:681Y93. 13. Jackson LE, Morgan B, Fletcher JC Jr, Krueger WWO. Anterior canal benign paroxysmal positional vertigo: an underappreciated entity. Otol Neurotol 2007;28:218Y22.