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Subjective visual vertical before and after treatment of a BPPV episode
Auris Nasus Larynx 38 (2011) 307–311 www.elsevier.com/locate/anl
Subjective visual vertical before and after treatment of a BPPV episode Mario Faralli a,*, Leonardo Manzari b, Roberto Panichi c, Fabio Botti c, Giampietro Ricci a, Fabrizio Longari a, Vito Enrico Pettorossi c a
Department of Medical-Surgical Specialization, Otolaryngology and Cervicofacial Surgery Division, University of Perugia, Via Delle Danaidi 21, Perugia, Italy b Department of Experimental Medicine and Pathology, ‘‘La Sapienza’’ University of Rome, Italy c Department of Internal Medicine, Section of Human Physiology, University of Perugia, Italy Received 1 April 2010; accepted 13 October 2010 Available online 11 January 2011
Abstract Objective: The study analyses the behavior of subjective visual vertical (SVV) in benign paroxysmal positional vertigo (BPPV) before and after treatment, and offers a clinical-pathogenic interpretation. Methods: We studied 30 consecutive patients with BPPV of the posterior semicircular canal treated with the Epley repositioning maneuver. SVV was determined at three different stages: at the time of diagnosis (1st test), after the repositioning maneuver (2nd test), and then 7 days after the resolution of the clinical picture (3rd test). The main study parameter was represented by the mean of 6 consecutive measurements (SVV0) for each patient. SVV was also examined in 20 healthy subjects, who represented the control group. The comparison between mean values and standard deviations showed a statistical significance of p < 0.05. Results: During the first test, the degree of deviation of SVV was significantly higher in the patient group than in the control group. Tilting towards the affected side was observed in all cases. The 2nd test showed an inversion in the orientation of SVV in 16 patients, and as a result of the Epley maneuver there was a statistically significant variation in SVV0 values in 20 patients with respect to the previous test (2nd test vs. 1st test). This involved 87% (23 patients) of those who then had a negative Dix–Hallpike test, and none of the ones in whom paroxysmal positional nystagmus persisted. Lastly, no differences emerged in the behavior of the patient group vs. the control group during the third test. Conclusions: SVV is often altered during active BPPV. The degree of otolithic dysfunction is never high and, in all cases, it is brief in duration. Tilting towards the dysfunctional side is essentially a constant in untreated BPPV. This could be due to a substantial loss of otoconia, with a decrease in the density and specific weight of the macula, and thus hypofunction of the receptor. The observation of a significant variation in SVV after therapeutic maneuvers has a favorable predictive value, as it probably reflects the migration of otoliths to the utricle, where saturation mechanisms can often have irritative effects leading to the inversion of SVV. # 2010 Published by Elsevier Ireland Ltd. Keywords: Subjective visual vertical; Otoliths; Benign paroxysmal positional vertigo
1. Introduction Benign paroxysmal positional vertigo (BPPV) is a pathology of the posterior labyrinth that is characterized by objective attacks of paroxysmal vertigo caused by head movements on the vertical and/or horizontal plane, without any hearing disorders but often accompanied by an intense neurovegetative reaction. Over time, critical periods lasting * Corresponding author. Tel.: +39 075 578 3236; fax: +39 075 572 6886. E-mail address: [email protected] (M. Faralli). 0385-8146/$ – see front matter # 2010 Published by Elsevier Ireland Ltd. doi:10.1016/j.anl.2010.10.005
several days or weeks (active phase) are alternated with periods of seeming remission of the clinical picture (inactive phase). However, there is a tendency towards relapses following silent intervals whose duration is unpredictable [1]. BPPV can be defined as a canal pathology of macular origin. In this specific case, observation of paroxysmal nystagmus provides indirect information about the processes that occur in the canal during the active phase. Only recently, methods have been developed to study reflexes originating from the utricular macula, and one of them involves determining subjective visual vertical (SVV) [2]. The
308
M. Faralli et al. / Auris Nasus Larynx 38 (2011) 307–311
perception of verticality is a complex phenomenon in which the otolithic organs supply sensory input that is indispensable for regulating this function. By SVV we mean an individual’s ability to indicate what he or she perceives to be a vertical line. Normally, it will closely approximate the gravitational line even in the absence of visual landmarks [3]. When the central or peripheral vestibular function is asymmetrical, SVV can be tilted to one side, thus no longer coinciding with the gravitational vertical [4]. The mechanism through which a dysfunction of the otolithic system triggers this error in perception is not entirely clear, but the most compelling explanation – substantiated by experimental data – is that torsional eye movement occurs as an integral part of a postural synkinesia known as ocular tilt reaction [5–7]. In the case of unilateral peripheral vestibular dysfunction, a dimly lit bar used as a visual landmark is tilted towards the dysfunctional side. This occurs because the patient has the impression – due to ocular cyclotorsion – that the bar, initially placed in a vertical position, is tilted towards the healthy side and thus ends up tilting it towards the dysfunctional side until he/she feels that it is straight. Because of this perceptual error, the bar will be tilted towards the affected side, sometimes by many degrees [4]. In the event of a central pathology, the behavior of SVV is affected by the location of the dysfunction. For example, when the vestibular nuclei are affected, the bar will be tilted to the dysfunctional side, as is also the case with peripheral disorders. In the case of supranuclear lesions the bar may be tilted towards the healthy side [8–10]. In this study we evaluated SVV in a group of patients with active BPPV who underwent physical therapy. The aims of this study were: to verify the possibility that a dysfunction or macular damage during BPPV is great enough to account for statistically significant alterations of SVV; to provide a pathogenic interpretation of any variations in SVV emerging during a single episode of BPPV; to establish any relationships that have a clinical and prognostic meaning between said variations and the clinical evolution of BPPV following therapy. 2. Materials and methods 2.1. Subjects We studied 30 consecutive patients (17 females and 13 males, mean age 52 years 9.4) presenting with BPPV of the posterior semicircular canal (PSC) who were referred to us between 15 March and 30 June 2008. The right PSC was involved in 18 cases and the left in 12. All patients were treated with the otolith repositioning maneuver according to Epley [11]. Inclusion criteria
Patients who came to us within 48 h of the onset of vertiginous symptoms. Patients with a typical oculomotor pattern whose morphological and temporal characteristics are compatible with the pathogenic mechanisms of canalolithiasis. Exclusion criteria Patients with severe neurological disorders and/or documented prior peripheral vestibulopathy. Patients presenting signs of functional asymmetry between the two halves of the vestibular system during a complete examination conducted a week after paroxysmal positional nystagmus disappeared. This evaluation included caloric tests, head-shaking tests, and mastoid oscillation at 100 Hz. SVV was also measured in 20 normal subjects (control group) who had no history of vertiginous episodes and/or balance problems, and whose vestibular function tests and neurological clinical exam were in normal range. 2.2. SVV evaluation SVV was determined at three different stages. First test – At the time BPPV was diagnosed, following execution of the vestibular diagnostic tests, and before any therapeutic maneuver was performed. Second test – After the therapeutic maneuver was performed and before its effectiveness was checked by repeating the positioning maneuvers. Third test – Seven days following resolution, once repetition of the Dix–Hallpike diagnostic maneuver confirmed that nystagmus was absent. Those who represented paroxysmal positional nystagmus during the Dix–Hallpike maneuver were instead excluded from the test. To determine SVV, we used a dimly lit fluorescent bar (40 cm long and 1 cm wide), which was placed in a darkened room and set 1 m away from the subject. The bar was wallmounted with a central rod allowing it to rotate in both directions. The upper end had a pointer sliding with the bar on a graduated scale, on which 08 corresponded to perfect alignment of the longitudinal line of the bar with the direction of gravity. Rotation of the pointer to the right corresponded to positive angles, whereas rotation to the left corresponded to negative angles. The inclination expressed in degrees was indicated on a display with a maximum resolution of 0.18. SVV was determined with the subject seated and holding his/her head in a 08 position (head straight). In this condition, six alternating measurements were conducted with the bar initially tilted to the right and then to the left by 458, for a total of three measurements per side. The subjects were then asked to rotate the bar, activated via remote control, until they thought it was perfectly vertical.
M. Faralli et al. / Auris Nasus Larynx 38 (2011) 307–311
2.3. Statistical analyses For the first and third tests we compared the mean values (SVVmed) of all the measurements performed on the control group and in the groups of patients presenting with BPPV of the right PSC and of the left PSC, respectively. The main study parameter was represented by the average of the six consecutive measurements (SVV0) performed for each patient. Any variations in SVV0 induced by the repositioning maneuvers (1st test vs. 2nd test) were evaluated for each one. The 2nd test (SVV0 test) was thus considered positive or negative in the presence of variations in SVV0 that were or were not statistically significant, respectively. We also analyzed the predictive value of this variation by calculating the percentage of positive tests in patients in whom the dysfunction proved to be resolved when the Dix– Hallpike test was performed. Student’s t-test was used for statistical analysis, and the comparison between mean values and standard deviations showed a statistical significance of p < 0.05.
309
Table 1 Comparison between the 1st and 2nd tests (the significant values are in italic). BPPV of the right PSC Patient
SVV0 (1st test)
1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18
0.58 0.38 0.83 0.52 0.92 0.49 0.67 0.52 1.00 0.32 0.25 0.27 0.75 0.69 1.25 0.27 0.67 0.41 1.25 0.52 1.00 0.32 1.08 0.58 0.83 0.26 0.75 0.61 0.83 0.52 1.00 0.32 1.00 0.71 1.25 0.42
SVV0 (2nd test) 0.33 0.41 0.42 0.74 0.42 0.80 0.92 0.80 1.67 0.41 0.58 0.38 0.58 0.49 0.33 0.75 1.08 0.66 0.08 0.49 0.83 0.26 0.08 0.66 0.83 0.52 1.00 0.71 1.75 0.27 0.75 0.27 1.33 0.41 0.75 0.42
p 0.002 0.007 0.222 0.002 0.010 0.110 0.640 0.000 0.000 0.003 0.341 0.020 0.000 0.001 0.003 0.174 0.000 0.000
3.2. Second test (SVV0 test) 3. Results
[()TD$FIG]
3.1. First test The determination of SVV, performed when BPPV was diagnosed and before the repositioning maneuver, showed that all 30 patients tilted the bar to the dysfunctional side (Fig. 1). SVVmed values were 0.88 0.50 in the group of patients with BPPV of the right PSC and 0.62 0.47 in those in whom the pathology was on the left side. A comparison with the control group (0.10 0.73) thus shows that in both cases there was a statistically significant increase in the degree of tilting of the bar ( p = 0.000).
Determination of SVV following the repositioning maneuver demonstrated a trend reversal in the orientation of the bar in 16 of the 30 patients we examined. Specifically, 9 of the patients with BPPV of the right PSC (Table 1) and 7 of those with BPPV of the left PSC (Table 2) tilted the bar contralaterally, whereas the behavior of the remaining 14 (9 with BPPV of the right PSC; 5 with BPPV of the left PSC) was unchanged with respect to the first test and they continued to tilt the bar ipsilaterally. A significant variation in SVV0 values was recorded in 13 of the 18 patients (72.2%) with BPPVof the right PSC (Table 1) and in 7 of the 12 (58.3%) with BPPV of the left PSC (Table 2). Instead, in the remaining 10 patients (5 with BPPVof the right PSC and 5 with BPPV of the left PSC) there was no significant variation in SVV0 values (negative test). Table 2 Comparison between the 1st and 2nd tests (the significant values are in italic). BPPV of the left PSC Patient
Fig. 1. SVV before the Epley maneuver (1st test).
1 2 3 4 5 6 7 8 9 10 11 12
SVV0 (1st test)
SVV0 (2nd test)
0.33 0.41 0.83 0.26 1.00 0.55 0.42 0.38 0.42 0.38 0.50 0.45 0.67 0.52 1.00 0.55 0.33 0.41 0.75 0.27 0.75 0.61 0.42 0.38
0.75 0.42 0.33 0.52 0.58 0.38 0.08 0.49 1.17 0.52 0.33 0.68 0.83 0.41 0.75 0.27 0.50 0.55 0.58 0.38 0.33 0.52 0.08 0.49
p 0.001 0.000 0.000 0.076 0.017 0.031 0.000 0.000 0.563 0.401 0.231 0.217
310 [()TD$FIG]
M. Faralli et al. / Auris Nasus Larynx 38 (2011) 307–311 [()TD$FIG]
Fig. 2. Patient behavior after treatment during the SVV0 test and the Dix– Hallpike test.
Overall, the Dix–Hallpike test showed resolution of nystagmus in 23 cases (76.6%), specifically in 15 of the 18 (83.3%) and in 8 of the 12 (66.6%) in whom BPPV was respectively located on the right and left. Among patients with BPPVof the right PSC, there was a significant variation in SVV0 values (positive SVV0 test) in 13 of the 15 (86.6%) in whom BPPV had just been resolved, but there were no significant variations in the 3 patients who continued to show nystagmus with the Dix–Hallpike diagnostic maneuver. In the 8 patients with BPPV of the left PSC who presented resolution of nystagmus, the test was positive in 7 (87.5%) cases and negative only in one (12.5%). Likewise, there were no significant variations in SVV0 values in the 4 patients in whom nystagmus persisted in the Dix–Hallpike test (Fig. 2). 3.3. Third test This test was performed a week later in 21 of the 23 patients who were negative in the second test. In one case, the right Dix–Hallpike maneuver revealed the reappearance of paroxysmal positional nystagmus, whereas the other one (BPPV of the left PSC) showed asymmetrical vestibular function (dysfunction on the left) in the caloric tests and at high stimulation frequencies. This test showed SVVmed values of 0.25 0.78 (right PSC) and 0.04 0.66 (left PSC). Consequently, determination of SVV did not show statistically significant variations in the behavior of the patient group versus the control group ( p > 0.05) (Fig. 3) (Tables 1 and 2).
4. Discussion Previous studies on the determination of SVV in patients with BPPV diverge widely. Bohmer and Rikenmann found no alterations [3], whereas Gall et al. observed an altered SVV in 10 out of their 16 patients [12]. According to Vannucchi, SVV is not altered overall in recently resolved BPPV, but if the patients who still complain of marked
Fig. 3. SVV one week after resolution of BPPV (3rd test).
instability despite resolution are taken into consideration, it is possible that certain subjects have values of over 28, probably expressing macular damage [13]. Our investigation shows that the degree of inclination of the bar during BPPV never rises to significant values comparable to those usually observed in the acute phase of sudden unilateral vestibular dysfunction [14]. While the values recorded in all cases were at most 28, considered the limit of normality [3], it is nevertheless legitimate to consider the possibility of subclinical otolithic damage, which was also revealed by the patients’ behavior when the tests were performed. In addition to a significant increase in recorded values compared to control values, there was also a uniform distribution of the results, nearly all of which – and there were only a few exceptions – presented the same sign ( /+) in the patients considered individually. This behavior emerged during the first test performed in the presence of the pathogenic mechanisms that characterize active BPPV. Instead, the third test showed that resolution of the pathology was accompanied not only by the normalization of SVV, but also by the disappearance of the manifestly lateral response of each patient, which in this phase showed an uneven distribution of the 6 recorded measurements that was quite similar to the behavior of the control group (Fig. 4). The orientation of the bar and the variation of SVV0 values in the same patient during a BPPV episode seem to be affected by the functional status of the otolithic organs and the contingent spatial relationship between the otoconial mass and the utricular structure. Ipsilateral deviation of SVV seems to be a constant of BPPV in the untreated active phase. The otolithic dysfunction responsible for this could also be due to the substantial detachment of macular otoconia, forming a ‘‘minus’’ zone that would thus lead to a decrease in the density and specific weight of the otolithic membrane. This hypothesis seems to be reinforced by the inclusion criterion adopted for the study, which called for clinical
[()TD$FIG]
M. Faralli et al. / Auris Nasus Larynx 38 (2011) 307–311
Fig. 4. Distribution range of the 6 measurements in the groups of patients examined for the first and third tests.
observation of the patient within 48 h of the onset of symptoms. This time limit would theoretically decrease the possibility of repair of the macular damage during the active phase of BPPV with respect to the persistence of floating intracanal material responsible for the vertiginous symptoms. In any event, the diversity between the utricular afferent inputs leads to an asymmetrical discharge that ultimately alters SVV. This behavior should thus be attributed exclusively to the state of the receptor, which – being hypofunctional – can only be expressed as an ipsilesional deviation of SVV. At the same time, from a conceptual standpoint it is legitimate to admit that the otoconial mass responsible for BPPV in terms of symptoms cannot have any influence on SVV, given that it is located in the canal in this phase. The data emerging from the second test cannot be due solely to a macular lesion remaining after rehabilitation, as this would not explain the behavior of patients who presented a significant variation in SVV0 with respect to the initial test. It seems reasonable to suspect the appearance of a new functional state of the utricular receptor during this phase, induced by performing the specific liberatory maneuver for that canal. Therefore, otolithic dysfunction would be due chiefly to the otoconial mass and its mobilization through the common crus, subsequently transiting to the utricle, where the debris could exert unusual pressure on the macula – with ensuing disturbance – that would continue until it is fully reabsorbed. It seems that sudden filling of the utricle by excess free otoliths and the ensuing alteration of the endolymphatic material at this level can generate a new state of functional asymmetry due to its irritative effect, likely induced by the stimulation mechanism described here. This seems to be confirmed by the behavior of patients during the test performed after the liberatory maneuver, who often tilted the bar away from the dysfunctional side, thus reversing the response recorded
311
previously. The evidence of resolution of BPPV after the liberatory maneuver in all patients who presented a significant variation of SVV0 values at the second test points to otolithic migration to the utricle and confirms the favorable prognostic value of these statistic data. Furthermore, a quantitative variability of these pathogenic mechanisms can sometimes induce opposite functional effects, thus explaining the behavior of patients in whom a positive SVV0 test was accompanied by increased ipsilesional tilting of the bar. Consequently, this expresses a functional asymmetry caused by a further reduction in utricular function, probably produced by the over-accumulation of otoconial material. In all cases, otolithic dysfunction is brief, as demonstrated by the normalization of SVV a week after the resolution of BPPV. This shows the efficacy of the mechanisms responsible for repairing the macular membranes, and for eliminating excess free otoliths and any secondary effects in the utricle.
References [1] Vicini C, De Vito A, Campanini A. La vertigine otolitica: analisi nel domino dei tempi. Acta Otorhinolaryngol Ital 2003;5(Suppl 75):39– 44. [2] Halmagyi GM, Colebatch JG, Curthoys IS. New test of vestibular function. Baillie`re’s Neurol 1994;3:485–500. [3] Bohmer A, Rikenmann J. The subjective visual vertical as a clinical parameter of vestibular diseases. J Vest Res 1995;5:35–45. [4] Halmagy GM, Curthoys IS. Clinical testing of otolith function. Ann N Y Sci 1999;871:195–204. [5] Rabinovitch HE, Sharpe JA, Sylvester TO. The ocular tilt reaction. A paroxysmal dyskinesia associated with elliptical nystagmus. Arch Ophthalmol 1977;95:1395–13998. [6] Halmagyi GM, Gresty MA, Gibson WPR. Ocular tilt reaction with peripheral vestibular lesion. Ann Neurol 1979;6:80–3. [7] Diamond SG, Markham CH. Ocular counter-rolling as an indicator of vestibular otolith function. Neurology 1983;33:1460–9. [8] Halmagyi GM, Brandt TH, Dieterich M, Curthoys IS, Stark RJ, Hoyt WF. Tonic controversive ocular tilt reaction due to unilateral mesodiencephalic lesion. Neurology 1990;40:1503–9. [9] Dieterich M, Brandt T. Ocular torsion and tilt of subjective visual vertical are sensitive brainstem signs. Ann Neurol 1993;33:292–9. [10] Dieterich M, Brandt T. Thalamic infarction: differential on vestibular function in the roll plane (35 patients). Neurology 1993;43:1732–40. [11] Epley JM. The canalith repositioning procedure for treatment of benign paroxysmal positional vertigo. Otolaryngol Head Neck Surg 1992;107:399–404. [12] Gall RM, Ireland DJ, Robertson DD. Subjective visual vertical in patients with benign paroxysmal positional vertigo. J Otolaryngol 1999;28:162–5. [13] Vannucchi P. La verticale e/o orizzontale visiva soggettiva. Acta Otorhinolaryngol Ital Suppl 2003;75:74–9. [14] Halmagyi GM, Curthoys IS. A clinical sign of canal paresis. Arch Neurol 1988;45:737–9.
Subjective visual vertical before and after treatment of a BPPV episode Mario Faralli a,*, Leonardo Manzari b, Roberto Panichi c, Fabio Botti c, Giampietro Ricci a, Fabrizio Longari a, Vito Enrico Pettorossi c a
Department of Medical-Surgical Specialization, Otolaryngology and Cervicofacial Surgery Division, University of Perugia, Via Delle Danaidi 21, Perugia, Italy b Department of Experimental Medicine and Pathology, ‘‘La Sapienza’’ University of Rome, Italy c Department of Internal Medicine, Section of Human Physiology, University of Perugia, Italy Received 1 April 2010; accepted 13 October 2010 Available online 11 January 2011
Abstract Objective: The study analyses the behavior of subjective visual vertical (SVV) in benign paroxysmal positional vertigo (BPPV) before and after treatment, and offers a clinical-pathogenic interpretation. Methods: We studied 30 consecutive patients with BPPV of the posterior semicircular canal treated with the Epley repositioning maneuver. SVV was determined at three different stages: at the time of diagnosis (1st test), after the repositioning maneuver (2nd test), and then 7 days after the resolution of the clinical picture (3rd test). The main study parameter was represented by the mean of 6 consecutive measurements (SVV0) for each patient. SVV was also examined in 20 healthy subjects, who represented the control group. The comparison between mean values and standard deviations showed a statistical significance of p < 0.05. Results: During the first test, the degree of deviation of SVV was significantly higher in the patient group than in the control group. Tilting towards the affected side was observed in all cases. The 2nd test showed an inversion in the orientation of SVV in 16 patients, and as a result of the Epley maneuver there was a statistically significant variation in SVV0 values in 20 patients with respect to the previous test (2nd test vs. 1st test). This involved 87% (23 patients) of those who then had a negative Dix–Hallpike test, and none of the ones in whom paroxysmal positional nystagmus persisted. Lastly, no differences emerged in the behavior of the patient group vs. the control group during the third test. Conclusions: SVV is often altered during active BPPV. The degree of otolithic dysfunction is never high and, in all cases, it is brief in duration. Tilting towards the dysfunctional side is essentially a constant in untreated BPPV. This could be due to a substantial loss of otoconia, with a decrease in the density and specific weight of the macula, and thus hypofunction of the receptor. The observation of a significant variation in SVV after therapeutic maneuvers has a favorable predictive value, as it probably reflects the migration of otoliths to the utricle, where saturation mechanisms can often have irritative effects leading to the inversion of SVV. # 2010 Published by Elsevier Ireland Ltd. Keywords: Subjective visual vertical; Otoliths; Benign paroxysmal positional vertigo
1. Introduction Benign paroxysmal positional vertigo (BPPV) is a pathology of the posterior labyrinth that is characterized by objective attacks of paroxysmal vertigo caused by head movements on the vertical and/or horizontal plane, without any hearing disorders but often accompanied by an intense neurovegetative reaction. Over time, critical periods lasting * Corresponding author. Tel.: +39 075 578 3236; fax: +39 075 572 6886. E-mail address: [email protected] (M. Faralli). 0385-8146/$ – see front matter # 2010 Published by Elsevier Ireland Ltd. doi:10.1016/j.anl.2010.10.005
several days or weeks (active phase) are alternated with periods of seeming remission of the clinical picture (inactive phase). However, there is a tendency towards relapses following silent intervals whose duration is unpredictable [1]. BPPV can be defined as a canal pathology of macular origin. In this specific case, observation of paroxysmal nystagmus provides indirect information about the processes that occur in the canal during the active phase. Only recently, methods have been developed to study reflexes originating from the utricular macula, and one of them involves determining subjective visual vertical (SVV) [2]. The
308
M. Faralli et al. / Auris Nasus Larynx 38 (2011) 307–311
perception of verticality is a complex phenomenon in which the otolithic organs supply sensory input that is indispensable for regulating this function. By SVV we mean an individual’s ability to indicate what he or she perceives to be a vertical line. Normally, it will closely approximate the gravitational line even in the absence of visual landmarks [3]. When the central or peripheral vestibular function is asymmetrical, SVV can be tilted to one side, thus no longer coinciding with the gravitational vertical [4]. The mechanism through which a dysfunction of the otolithic system triggers this error in perception is not entirely clear, but the most compelling explanation – substantiated by experimental data – is that torsional eye movement occurs as an integral part of a postural synkinesia known as ocular tilt reaction [5–7]. In the case of unilateral peripheral vestibular dysfunction, a dimly lit bar used as a visual landmark is tilted towards the dysfunctional side. This occurs because the patient has the impression – due to ocular cyclotorsion – that the bar, initially placed in a vertical position, is tilted towards the healthy side and thus ends up tilting it towards the dysfunctional side until he/she feels that it is straight. Because of this perceptual error, the bar will be tilted towards the affected side, sometimes by many degrees [4]. In the event of a central pathology, the behavior of SVV is affected by the location of the dysfunction. For example, when the vestibular nuclei are affected, the bar will be tilted to the dysfunctional side, as is also the case with peripheral disorders. In the case of supranuclear lesions the bar may be tilted towards the healthy side [8–10]. In this study we evaluated SVV in a group of patients with active BPPV who underwent physical therapy. The aims of this study were: to verify the possibility that a dysfunction or macular damage during BPPV is great enough to account for statistically significant alterations of SVV; to provide a pathogenic interpretation of any variations in SVV emerging during a single episode of BPPV; to establish any relationships that have a clinical and prognostic meaning between said variations and the clinical evolution of BPPV following therapy. 2. Materials and methods 2.1. Subjects We studied 30 consecutive patients (17 females and 13 males, mean age 52 years 9.4) presenting with BPPV of the posterior semicircular canal (PSC) who were referred to us between 15 March and 30 June 2008. The right PSC was involved in 18 cases and the left in 12. All patients were treated with the otolith repositioning maneuver according to Epley [11]. Inclusion criteria
Patients who came to us within 48 h of the onset of vertiginous symptoms. Patients with a typical oculomotor pattern whose morphological and temporal characteristics are compatible with the pathogenic mechanisms of canalolithiasis. Exclusion criteria Patients with severe neurological disorders and/or documented prior peripheral vestibulopathy. Patients presenting signs of functional asymmetry between the two halves of the vestibular system during a complete examination conducted a week after paroxysmal positional nystagmus disappeared. This evaluation included caloric tests, head-shaking tests, and mastoid oscillation at 100 Hz. SVV was also measured in 20 normal subjects (control group) who had no history of vertiginous episodes and/or balance problems, and whose vestibular function tests and neurological clinical exam were in normal range. 2.2. SVV evaluation SVV was determined at three different stages. First test – At the time BPPV was diagnosed, following execution of the vestibular diagnostic tests, and before any therapeutic maneuver was performed. Second test – After the therapeutic maneuver was performed and before its effectiveness was checked by repeating the positioning maneuvers. Third test – Seven days following resolution, once repetition of the Dix–Hallpike diagnostic maneuver confirmed that nystagmus was absent. Those who represented paroxysmal positional nystagmus during the Dix–Hallpike maneuver were instead excluded from the test. To determine SVV, we used a dimly lit fluorescent bar (40 cm long and 1 cm wide), which was placed in a darkened room and set 1 m away from the subject. The bar was wallmounted with a central rod allowing it to rotate in both directions. The upper end had a pointer sliding with the bar on a graduated scale, on which 08 corresponded to perfect alignment of the longitudinal line of the bar with the direction of gravity. Rotation of the pointer to the right corresponded to positive angles, whereas rotation to the left corresponded to negative angles. The inclination expressed in degrees was indicated on a display with a maximum resolution of 0.18. SVV was determined with the subject seated and holding his/her head in a 08 position (head straight). In this condition, six alternating measurements were conducted with the bar initially tilted to the right and then to the left by 458, for a total of three measurements per side. The subjects were then asked to rotate the bar, activated via remote control, until they thought it was perfectly vertical.
M. Faralli et al. / Auris Nasus Larynx 38 (2011) 307–311
2.3. Statistical analyses For the first and third tests we compared the mean values (SVVmed) of all the measurements performed on the control group and in the groups of patients presenting with BPPV of the right PSC and of the left PSC, respectively. The main study parameter was represented by the average of the six consecutive measurements (SVV0) performed for each patient. Any variations in SVV0 induced by the repositioning maneuvers (1st test vs. 2nd test) were evaluated for each one. The 2nd test (SVV0 test) was thus considered positive or negative in the presence of variations in SVV0 that were or were not statistically significant, respectively. We also analyzed the predictive value of this variation by calculating the percentage of positive tests in patients in whom the dysfunction proved to be resolved when the Dix– Hallpike test was performed. Student’s t-test was used for statistical analysis, and the comparison between mean values and standard deviations showed a statistical significance of p < 0.05.
309
Table 1 Comparison between the 1st and 2nd tests (the significant values are in italic). BPPV of the right PSC Patient
SVV0 (1st test)
1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18
0.58 0.38 0.83 0.52 0.92 0.49 0.67 0.52 1.00 0.32 0.25 0.27 0.75 0.69 1.25 0.27 0.67 0.41 1.25 0.52 1.00 0.32 1.08 0.58 0.83 0.26 0.75 0.61 0.83 0.52 1.00 0.32 1.00 0.71 1.25 0.42
SVV0 (2nd test) 0.33 0.41 0.42 0.74 0.42 0.80 0.92 0.80 1.67 0.41 0.58 0.38 0.58 0.49 0.33 0.75 1.08 0.66 0.08 0.49 0.83 0.26 0.08 0.66 0.83 0.52 1.00 0.71 1.75 0.27 0.75 0.27 1.33 0.41 0.75 0.42
p 0.002 0.007 0.222 0.002 0.010 0.110 0.640 0.000 0.000 0.003 0.341 0.020 0.000 0.001 0.003 0.174 0.000 0.000
3.2. Second test (SVV0 test) 3. Results
[()TD$FIG]
3.1. First test The determination of SVV, performed when BPPV was diagnosed and before the repositioning maneuver, showed that all 30 patients tilted the bar to the dysfunctional side (Fig. 1). SVVmed values were 0.88 0.50 in the group of patients with BPPV of the right PSC and 0.62 0.47 in those in whom the pathology was on the left side. A comparison with the control group (0.10 0.73) thus shows that in both cases there was a statistically significant increase in the degree of tilting of the bar ( p = 0.000).
Determination of SVV following the repositioning maneuver demonstrated a trend reversal in the orientation of the bar in 16 of the 30 patients we examined. Specifically, 9 of the patients with BPPV of the right PSC (Table 1) and 7 of those with BPPV of the left PSC (Table 2) tilted the bar contralaterally, whereas the behavior of the remaining 14 (9 with BPPV of the right PSC; 5 with BPPV of the left PSC) was unchanged with respect to the first test and they continued to tilt the bar ipsilaterally. A significant variation in SVV0 values was recorded in 13 of the 18 patients (72.2%) with BPPVof the right PSC (Table 1) and in 7 of the 12 (58.3%) with BPPV of the left PSC (Table 2). Instead, in the remaining 10 patients (5 with BPPVof the right PSC and 5 with BPPV of the left PSC) there was no significant variation in SVV0 values (negative test). Table 2 Comparison between the 1st and 2nd tests (the significant values are in italic). BPPV of the left PSC Patient
Fig. 1. SVV before the Epley maneuver (1st test).
1 2 3 4 5 6 7 8 9 10 11 12
SVV0 (1st test)
SVV0 (2nd test)
0.33 0.41 0.83 0.26 1.00 0.55 0.42 0.38 0.42 0.38 0.50 0.45 0.67 0.52 1.00 0.55 0.33 0.41 0.75 0.27 0.75 0.61 0.42 0.38
0.75 0.42 0.33 0.52 0.58 0.38 0.08 0.49 1.17 0.52 0.33 0.68 0.83 0.41 0.75 0.27 0.50 0.55 0.58 0.38 0.33 0.52 0.08 0.49
p 0.001 0.000 0.000 0.076 0.017 0.031 0.000 0.000 0.563 0.401 0.231 0.217
310 [()TD$FIG]
M. Faralli et al. / Auris Nasus Larynx 38 (2011) 307–311 [()TD$FIG]
Fig. 2. Patient behavior after treatment during the SVV0 test and the Dix– Hallpike test.
Overall, the Dix–Hallpike test showed resolution of nystagmus in 23 cases (76.6%), specifically in 15 of the 18 (83.3%) and in 8 of the 12 (66.6%) in whom BPPV was respectively located on the right and left. Among patients with BPPVof the right PSC, there was a significant variation in SVV0 values (positive SVV0 test) in 13 of the 15 (86.6%) in whom BPPV had just been resolved, but there were no significant variations in the 3 patients who continued to show nystagmus with the Dix–Hallpike diagnostic maneuver. In the 8 patients with BPPV of the left PSC who presented resolution of nystagmus, the test was positive in 7 (87.5%) cases and negative only in one (12.5%). Likewise, there were no significant variations in SVV0 values in the 4 patients in whom nystagmus persisted in the Dix–Hallpike test (Fig. 2). 3.3. Third test This test was performed a week later in 21 of the 23 patients who were negative in the second test. In one case, the right Dix–Hallpike maneuver revealed the reappearance of paroxysmal positional nystagmus, whereas the other one (BPPV of the left PSC) showed asymmetrical vestibular function (dysfunction on the left) in the caloric tests and at high stimulation frequencies. This test showed SVVmed values of 0.25 0.78 (right PSC) and 0.04 0.66 (left PSC). Consequently, determination of SVV did not show statistically significant variations in the behavior of the patient group versus the control group ( p > 0.05) (Fig. 3) (Tables 1 and 2).
4. Discussion Previous studies on the determination of SVV in patients with BPPV diverge widely. Bohmer and Rikenmann found no alterations [3], whereas Gall et al. observed an altered SVV in 10 out of their 16 patients [12]. According to Vannucchi, SVV is not altered overall in recently resolved BPPV, but if the patients who still complain of marked
Fig. 3. SVV one week after resolution of BPPV (3rd test).
instability despite resolution are taken into consideration, it is possible that certain subjects have values of over 28, probably expressing macular damage [13]. Our investigation shows that the degree of inclination of the bar during BPPV never rises to significant values comparable to those usually observed in the acute phase of sudden unilateral vestibular dysfunction [14]. While the values recorded in all cases were at most 28, considered the limit of normality [3], it is nevertheless legitimate to consider the possibility of subclinical otolithic damage, which was also revealed by the patients’ behavior when the tests were performed. In addition to a significant increase in recorded values compared to control values, there was also a uniform distribution of the results, nearly all of which – and there were only a few exceptions – presented the same sign ( /+) in the patients considered individually. This behavior emerged during the first test performed in the presence of the pathogenic mechanisms that characterize active BPPV. Instead, the third test showed that resolution of the pathology was accompanied not only by the normalization of SVV, but also by the disappearance of the manifestly lateral response of each patient, which in this phase showed an uneven distribution of the 6 recorded measurements that was quite similar to the behavior of the control group (Fig. 4). The orientation of the bar and the variation of SVV0 values in the same patient during a BPPV episode seem to be affected by the functional status of the otolithic organs and the contingent spatial relationship between the otoconial mass and the utricular structure. Ipsilateral deviation of SVV seems to be a constant of BPPV in the untreated active phase. The otolithic dysfunction responsible for this could also be due to the substantial detachment of macular otoconia, forming a ‘‘minus’’ zone that would thus lead to a decrease in the density and specific weight of the otolithic membrane. This hypothesis seems to be reinforced by the inclusion criterion adopted for the study, which called for clinical
[()TD$FIG]
M. Faralli et al. / Auris Nasus Larynx 38 (2011) 307–311
Fig. 4. Distribution range of the 6 measurements in the groups of patients examined for the first and third tests.
observation of the patient within 48 h of the onset of symptoms. This time limit would theoretically decrease the possibility of repair of the macular damage during the active phase of BPPV with respect to the persistence of floating intracanal material responsible for the vertiginous symptoms. In any event, the diversity between the utricular afferent inputs leads to an asymmetrical discharge that ultimately alters SVV. This behavior should thus be attributed exclusively to the state of the receptor, which – being hypofunctional – can only be expressed as an ipsilesional deviation of SVV. At the same time, from a conceptual standpoint it is legitimate to admit that the otoconial mass responsible for BPPV in terms of symptoms cannot have any influence on SVV, given that it is located in the canal in this phase. The data emerging from the second test cannot be due solely to a macular lesion remaining after rehabilitation, as this would not explain the behavior of patients who presented a significant variation in SVV0 with respect to the initial test. It seems reasonable to suspect the appearance of a new functional state of the utricular receptor during this phase, induced by performing the specific liberatory maneuver for that canal. Therefore, otolithic dysfunction would be due chiefly to the otoconial mass and its mobilization through the common crus, subsequently transiting to the utricle, where the debris could exert unusual pressure on the macula – with ensuing disturbance – that would continue until it is fully reabsorbed. It seems that sudden filling of the utricle by excess free otoliths and the ensuing alteration of the endolymphatic material at this level can generate a new state of functional asymmetry due to its irritative effect, likely induced by the stimulation mechanism described here. This seems to be confirmed by the behavior of patients during the test performed after the liberatory maneuver, who often tilted the bar away from the dysfunctional side, thus reversing the response recorded
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previously. The evidence of resolution of BPPV after the liberatory maneuver in all patients who presented a significant variation of SVV0 values at the second test points to otolithic migration to the utricle and confirms the favorable prognostic value of these statistic data. Furthermore, a quantitative variability of these pathogenic mechanisms can sometimes induce opposite functional effects, thus explaining the behavior of patients in whom a positive SVV0 test was accompanied by increased ipsilesional tilting of the bar. Consequently, this expresses a functional asymmetry caused by a further reduction in utricular function, probably produced by the over-accumulation of otoconial material. In all cases, otolithic dysfunction is brief, as demonstrated by the normalization of SVV a week after the resolution of BPPV. This shows the efficacy of the mechanisms responsible for repairing the macular membranes, and for eliminating excess free otoliths and any secondary effects in the utricle.
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