Balance in posterior and horizontal canal type benign paroxysmal positional vertigo before and after canalith repositioning maneuvers (original) (raw)
Balance in posterior and horizontal canal type benign paroxysmal positional vertigo before and after canalith repositioning maneuvers
Neşe Çelebisoy a, { }^{\text {a, }}, Ece Bayam a { }^{\text {a }}, Feray Güleç a { }^{\text {a }}, Timur Köse b { }^{\text {b }}, Önder Akyürekli a { }^{\text {a }}
a{ }^{a} Ege University, Medical School, Department of Neurology, Bornova, İzmir 35100, Turkey
b{ }^{\mathrm{b}} Biostatistics and Medical Informatics, Bornova, İzmir, Turkey
A R T I C L E I N F O
Article history:
Received 17 July 2008
Received in revised form 26 November 2008
Accepted 1 December 2008
Keywords:
Benign paroxysmal positional vertigo
Posterior semicircular canal
Horizontal semicircular canal
Canalith repositioning maneuvers
Postural control
A B STR ACT
Benign paroxysmal positional vertigo (BPPV) is characterized by acute, brief and rotatory vertigo attacks provoked by changes in head position. Most patients complain of a loss of equilibrium and unstable gait during and between the vertigo attacks. Canalith repositioning maneuvers (CRM) relieve attacks and improve postural stability. In this study balance ability of 32 patients with PC BPPV and 12 patients with HC BPPV before and after treatment with CRM was investigated. 50 healthy volunteers served as the control group. Static balance was measured as mean center of gravity sway velocity recorded in four different conditions: on a static platform and on foam with eyes open and closed. Dynamic balance was measured in tandem walk test. PC BPPV patients demonstrated greater sway velocity in stance on foam with eyes closed. After CRM the velocity decreased significantly. The results of the HC BPPV patients were not different from the healthy volunteers all through the four test conditions. Walking speed of the patients both with PC BPPV and HC BPPV was significantly low. It increased after treatment in both groups. In conclusion, patients with PC BPPV had impaired static balance ability due to a clot in the affected canal. Dynamic balance ability measured by walking speed was impaired both in PC and HC BPPV patients. Static and dynamic deficits improved significantly after CRM.
© 2008 Elsevier B.V. All rights reserved.
1. Introduction
Information coming from the three sensory systems; visual, vestibular and proprioceptive is used for the maintenance of balance [1]. Disorders of the vestibular system are characterized by impaired gaze and head stability associated with an upright posture deficit [2].
Benign paroxysmal positional vertigo (BPPV) is the most common peripheral vestibular disorder accounting for about 20−30%20-30 \% of diagnoses in specialized dizziness clinics [3,4]. BPPV is characterized by brief episodes of vertigo triggered by changes in head position. In addition, many patients complain about imbalance, standing and walking disturbances during and between the vertigo attacks. The posterior canal (PC) variant of BPPV (PC BPPV) is a well-recognized condition in which a paroxysmal torsional-upbeat nystagmus is induced by the Dix-Hallpike maneuver. However, in 1985 horizontal canal (HC) variant (HC BPPV) was described characterized by a direction-changing horizontal nystagmus induced by rolling the head of a recumbent patient from side to side [5]. The most common hypothesis for BPPV is the accumulation of calcium carbonate crystals called
[1]otoconia in the lumen or in the cupula of the semicircular canals (SCC). Vertigo and nystagmus provoked by certain head movements is accepted to be due to stimulation of the vestibular receptors through the endolymph shift in the semicircular canal or by the cupula deflection produced by the otoconia [5-7].
Canalith repositioning maneuvers (CRM), designed to move the otoconia from the SCC involved, into the utricle result in resolution of the symptoms. However, a residual postural impairment has been described by some of the patients.
A deficit of postural control in patients with BPPV has been documented by posturographic studies [8-14]. The efficacy of CRM has also been investigated in some of them [9-13].
In this study we aimed to investigate and compare not only static but also dynamic balance abilities of the patients with PC BPPV and HC BPPV before and after treatment with CRM.
2. Materials and methods
The study was conducted in the specialized neurotology clinic at Ege University Medical School Department of Neurology, İzmir, Turkey. The study protocol was approved by the local ethic committee. From January 2007 to January 2008 patients with the diagnosis of BPPV were assessed. All patients had a detailed neurotological examination which included examination of stance and gait in addition to positional tests consisting of the Dix-Hallpike and roll maneuvers. The eye movements were recorded by videonystagmography during these tests. All patients underwent pure-tone audiometry and bithermal caloric tests using air calorics as well. For videonystagmography Visual Eyes 4 channel VNG (Micromedical
- Corresponding author. TeL: +232 3880980: fax: +232 3880980.
E-mail address: nese.celebisoy@ege.edu.tr (N. Çelebisoy). ↩︎
- Corresponding author. TeL: +232 3880980: fax: +232 3880980.
technologies) was used. ICS air caloric stimulator model NCA-200 was used for caloric tests with an air flow of 8 L/min8 \mathrm{~L} / \mathrm{min} at 25 and 50∘C50^{\circ} \mathrm{C} within 60 s . Maximum slow phase velocity (SPV) was determined by using ICS velocity computer system. Vestibular asymmetry larger than 25%25 \% was considered abnormal.
The diagnosis of BPPV was relied on a typical history of brief episodes of positional vertigo, no spontaneous nystagmus, absence of a sign indicating a central nervous system disorder on neurological examination and the presence of the typical positional nystagmus. Patients with only idiopathic BPPV were enrolled. Ones with BPPV secondary to Meniere’s disease, vestibular neuritis and labyrinthitis with vestibular paresis on one or both sides on caloric testing were excluded from the study. Similarly patients with neurological pathology, proprioceptive impairment, cardiovascular diseases or orthopedic problems were excluded in order not to interfere with the posturography results. Modified Epley maneuver [15] was used for the treatment of PC BPPV and Lempert maneuver (barbeque rotation) [16] was used for the treatment of HC BPPV.
Balance ability of the patients was studied by NeuroCom System Version 8.0.3 (NeuroCom International Inc.). In order to avoid possible interference due to diagnostic maneuver posturography was performed 1 h after the examination. Static balance was measured as mean center of gravity (COG) sway velocity ( ⋅s\cdot \mathrm{s} ) recorded in four different conditions: on a static platform with eyes open (firmen) and closed (firmec), on foam with eyes open (foameo) and closed (foamec). Each test consisted of three trials, each lasting for 10 s . All patients were asked to stand upright as steadily as possible during these test conditions and the mean sway velocities recorded during three trials were taken into consideration. Dynamic balance was tested by tandem walk test. The subjects were asked to stand heel-to-toe as the starting position. They tandem walked as quickly as possible through the platform which was 150 cm long and 45 cm wide when the “Go” instruction appeared on the screen and held steady at the end of the platform again on heel-to-toe position. Walking speed (cm/s) and end sway velocity ( ⋅s\cdot \mathrm{s} ) was measured three times and the mean values recorded from these three trials were taken into consideration. One week after the treatment, patients underwent a second comprehensive clinical evaluation to determine whether the treatment was successful. Patients with no vertigo or nystagmus were asked to repeat a posturographic assessment. In patients with ongoing symptoms and signs a second repositioning maneuver was performed and they were examined a week later. Data recorded from the patients was compared with age matched healthy controls with normal neurotological examination.
Statistical analyses were done by Statistical Package for Social Sciences 15.0 for Windows (SPSS Inc, Chicago, IL, USA). Kolmogorov Smirnov test was used to determine the variables showing normal distribution. Posturographic parameters
not showing normal distribution were evaluated with non-parametric tests. Kruskal-Wallis Test was used to find out the difference among three groups and comparison of the results of the patients with PC BPPV and HC BPPV with healthy controls was performed with Mann-Whitney UU Test with Bonferroni correction. Parameters showing normal distribution were evaluated with one-way Anova. In multiple comparisons, when the variances between groups were homogeneous Bonferroni test was used, whereas Dunnet T3 was used for nonhomogenous variances as post hoc analysis. In order to compare the pretreatment and posttreatment posturographic values Wilcoxon Signed Ranks Test was used for the parameters not showing normal distribution and Paired Samples t-Test was used for the parameters showing normal distribution. All the tests were performed at α=0.05\alpha=0.05 level of significance ( p<0.05p<0.05 ).
3. Results
32 patients with the diagnosis of PC BPPV with a mean age of 55 years (range 32-77 years) and 12 patients with HC BPPV with a mean age of 55.6 years (range 39-74 years) were included in the study. 50 healthy volunteers with a mean age of 48.3 years (range 27-70 years) served as the control group. First the results of the static posturographic parameters were analyzed (Table 1). Sway velocity values recorded in patients with PC and HC BPPV, on a firm surface with eyes open and closed and on foam with eyes open were not significantly different from the values of the healthy controls. However, the sway velocity values recorded in patients with PC BPPV, on foam with eyes closed were significantly high (p=0.009)(p=0.009). The sway velocity values recorded from the HC BPPV group were not statistically different from the healthy controls. For assessing dynamic balance tandem walking speed and end sway velocity values were recorded (Table 2). Walking speed of the patients with PC BPPV ( p<0.001p<0.001 ) and HC BPPV ( p=0.007p=0.007 ) was significantly low. End sway velocity was not different from the healthy controls in either group of patients.
28 of the 32 patients with PC BPPV ( 87.5%87.5 \% ) and 10 of the 12 patients with HC BPPV ( 84%84 \% ) were symptom free at the end of the
Table 1
Mean center of gravity sway velocity of 50 healthy controls and 32 patients with posterior canal benign paroxysmal positional vertigo (PC BPPV) and 12 patients with horizontal canal benign paroxysmal positional vertigo (HC BPPV) before (1) and after (2) canalith repositioning maneuvers.
| Sway velocity (⋅/s)(\cdot / s) | Normal controls mean ±\pm S.D. | PC BPPV 1 mean ±\pm S.D. | PC BPPV2 mean ±\pm S.D. | HC BPPV1 mean ±\pm S.D. | HC BPPV2 mean ±\pm S.D. |
|---|---|---|---|---|---|
| Firm eyes open | 0.21±0.090.21 \pm 0.09 | 0.23±0.10sNS\begin{aligned} & 0.23 \pm 0.10 \\ & { }^{\mathrm{s}} \mathrm{NS} \end{aligned} | 0.28±0.14sNSsNS\begin{aligned} & 0.28 \pm 0.14 \\ & { }^{\mathrm{s}} \mathrm{NS} \\ & { }^{\mathrm{s}} \mathrm{NS} \end{aligned} | 0.25±0.12sNS\begin{aligned} & 0.25 \pm 0.12 \\ & { }^{\mathrm{s}} \mathrm{NS} \end{aligned} | 0.23±0.16sNSsNS\begin{aligned} & 0.23 \pm 0.16 \\ & { }^{\mathrm{s}} \mathrm{NS} \\ & { }^{\mathrm{s}} \mathrm{NS} \end{aligned} |
| Firm eyes closed | 0.31±0.100.31 \pm 0.10 | 0.35±0.12sNS\begin{aligned} & 0.35 \pm 0.12 \\ & { }^{\mathrm{s}} \mathrm{NS} \end{aligned} | 0.36±0.15sNSsNS\begin{aligned} & 0.36 \pm 0.15 \\ & { }^{\mathrm{s}} \mathrm{NS} \\ & { }^{\mathrm{s}} \mathrm{NS} \end{aligned} | 0.33±0.28sNS\begin{aligned} & 0.33 \pm 0.28 \\ & { }^{\mathrm{s}} \mathrm{NS} \end{aligned} | 0.33±0.20sNSsNS\begin{aligned} & 0.33 \pm 0.20 \\ & { }^{\mathrm{s}} \mathrm{NS} \\ & { }^{\mathrm{s}} \mathrm{NS} \end{aligned} |
| Foam eyes open | 0.65±0.180.65 \pm 0.18 | 0.69±0.22sNS\begin{aligned} & 0.69 \pm 0.22 \\ & { }^{\mathrm{s}} \mathrm{NS} \end{aligned} | 0.68±0.20sNSsNS\begin{aligned} & 0.68 \pm 0.20 \\ & { }^{\mathrm{s}} \mathrm{NS} \\ & { }^{\mathrm{s}} \mathrm{NS} \end{aligned} | 0.75±0.29sNS\begin{aligned} & 0.75 \pm 0.29 \\ & { }^{\mathrm{s}} \mathrm{NS} \end{aligned} | 0.71±0.29sNSsNS\begin{aligned} & 0.71 \pm 0.29 \\ & { }^{\mathrm{s}} \mathrm{NS} \\ & { }^{\mathrm{s}} \mathrm{NS} \end{aligned} |
| Foam eyes closed | 1.33±0.301.33 \pm 0.30 | 1.73±0.67sp=0.009\begin{aligned} & 1.73 \pm 0.67 \\ & { }^{\mathrm{s}} p=0.009 \end{aligned} | 1.35±0.47sp=0.002sNS\begin{aligned} & 1.35 \pm 0.47 \\ & { }^{\mathrm{s}} p=0.002 \\ & { }^{\mathrm{s}} \mathrm{NS} \end{aligned} | 1.66±0.70sNS\begin{aligned} & 1.66 \pm 0.70 \\ & { }^{\mathrm{s}} \mathrm{NS} \end{aligned} | 1.52±0.81sNSsNS\begin{aligned} & 1.52 \pm 0.81 \\ & { }^{\mathrm{s}} \mathrm{NS} \\ & { }^{\mathrm{s}} \mathrm{NS} \end{aligned} |
a{ }^{a} Comparison with normal controls.
b{ }^{\mathrm{b}} Comparison of the pre- and the post-treatment values.
c { }^{\text {c }} Comparison of the post-treatment values with normal controls.
Table 2
Tandem walk test results of the 50 healthy controls and 32 patients with posterior canal benign paroxysmal positional vertigo (PC BPPV) and 12 patients with horizontal canal benign paroxysmal positional vertigo (HC BPPV) before (1) and after (2) canalith repositioning maneuvers.
| Tandem walk | Normal controls mean ±\pm S.D. | PC BPPV1 mean ±\pm S.D. | PC BPPV2 mean ±\pm S.D. | HC BPPV1 mean ±\pm S.D. | HC BPPV2 mean ±\pm S.D. |
|---|---|---|---|---|---|
| Speed (cm/s)(\mathrm{cm} / \mathrm{s}) | 22.23±5.7022.23 \pm 5.70 | 17.24±4.90sp<0.001\begin{aligned} & 17.24 \pm 4.90 \\ & { }^{\mathrm{s}} p<0.001 \end{aligned} | 20.10±6.03sp=0.001sNS\begin{aligned} & 20.10 \pm 6.03 \\ & { }^{\mathrm{s}} p=0.001 \\ & { }^{\mathrm{s}} \mathrm{NS} \end{aligned} | 16.97±3.37sp=0.007\begin{aligned} & 16.97 \pm 3.37 \\ & { }^{\mathrm{s}} p=0.007 \end{aligned} | 19.02±3.50sp=0.004sNS\begin{aligned} & 19.02 \pm 3.50 \\ & { }^{\mathrm{s}} p=0.004 \\ & { }^{\mathrm{s}} \mathrm{NS} \end{aligned} |
| End sway (⋅/s)(\cdot / s) | 4.46±1.714.46 \pm 1.71 | 4.77±1.58sNS\begin{aligned} & 4.77 \pm 1.58 \\ & { }^{\mathrm{s}} \mathrm{NS} \end{aligned} | 4.41±1.30sNSsNS\begin{aligned} & 4.41 \pm 1.30 \\ & { }^{\mathrm{s}} \mathrm{NS} \\ & { }^{\mathrm{s}} \mathrm{NS} \end{aligned} | 4.70±1.34sNS\begin{aligned} & 4.70 \pm 1.34 \\ & { }^{\mathrm{s}} \mathrm{NS} \end{aligned} | 5.35±1.57sNSsNS\begin{aligned} & 5.35 \pm 1.57 \\ & { }^{\mathrm{s}} \mathrm{NS} \\ & { }^{\mathrm{s}} \mathrm{NS} \end{aligned} |
- a{ }^{a} Comparison with normal controls.
b{ }^{\mathrm{b}} Comparison of the pre- and the post-treatment values.
c { }^{\text {c }} Comparison of the post-treatment values with normal controls. ↩︎
Fig. 1. Mean center of gravity sway velocity recorded on foam with eyes closed (foamec) in healthy controls ( 50 subjects) and in patients with posterior canal benign paroxysmal positional vertigo (PC BPPV) (32 subjects) and horizontal canal benign paroxysmal positional vertigo (HC BPPV) (12 subjects) before (1) and after (2) canalith repositioning maneuvers, showing increased sway velocity in patients with PC BPPV. Post-treatment values are not different from the normal controls.
Fig. 2. Tandem walk speed of the healthy controls ( 50 subjects) and the patients with posterior canal benign paroxysmal positional vertigo (PC BPPV) (32 subjects) and horizontal canal benign paroxysmal positional vertigo (HC BPPV) (12 subjects) before (1) and after (2) canalith repositioning maneuvers (CRM). The values are lower than the normal controls in patients with both PC and HC BPPV and increased values are recorded after CRM.
first week. In the remainder a second maneuver was performed and the repeat posturographic tests were performed a week later.
When the pretreatment and post-treatment values were compared it was found that sway velocities recorded on foam with eyes closed showed significant reduction ( p=0.002p=0.002 ) in the PC BPPV group. Comparison of the post-treatment values with the results of the healthy controls showed no significant difference ( p>0.05p>0.05 ) (Fig. 1). Walking speed of patients both with PC BPPV ( p=0.001p=0.001 ) and with HC BPPV ( p=0.004p=0.004 ) increased significantly after treatment and the post-treatment values were not different from the values recorded in healthy controls ( p>0.05p>0.05 ) (Fig. 2).
4. Discussion
Our patients with PC BPPV had impairment in balance as indicated by a greater sway velocity recorded on a foam surface without visual inputs. This means they are unable to maintain
postural balance in conditions where the visual information is unavailable, proprioceptive information is inaccurate and the postural control relies mostly on vestibular cues. Blatt et al. [11] and Chang et al. [14] have reported similar results whereas Di Girolamo et al. [10] have shown impairments of postural control in conditions with altering either proprioceptive, visual or both inputs during the sensory organization test. All three studies mentioned above [10,11,14] were about patients with PC BPPV. The single study on patients with HC BPPV was conducted by Di Girolamo et al. [17]. These authors reported normal sway velocities in patients with HC BPPV. Similar results have been gathered from our patients with HC BPPV. It has been proposed that disorders of the horizontal semicircular canal do not affect postural control and vertical semicircular canals contribute to the control of postural sway [17]. However, further studies are necessary to confirm these results.
Another parameter taken into consideration in our study was dynamic balance studied during tandem walk test. In the other single study performed just on patients with PC BPPV, slower walking speed and greater end sway velocity was recorded [14]. Our study was the first to include HC BPPV patients. Walking speed of our patients both with PC BPPV and HC BPPV was significantly low. When the base of support was narrowed patients needed to slow down for dynamic balance. Balance during locomotion requires that the input of the vestibular system in the head be integrated with the somatosensory input from the feet. Though simply slowing down can be accepted to be due to anxiety we know well that walking is particularly affected in acute peripheral vestibular lesions and patients are better off running than walking as an automatic spinal locomotor programme suppresses destabilizing vestibular inputs while running [18]. Abnormal vestibular signals caused by the debris in PC and HC seem to interfere with the fluency and speed of the tandem walk in patients with PC and HC BPPV. Here, the accuracy of tandem gait could also give us valuable results. However, as it was not possible to interpret accuracy as numeric values in our posturography device only the speed was taken into consideration. On the other hand, end sway velocity recorded at the end of the platform on heel-to-toe position with eyes open was not different from the healthy controls in either group of our patients. This test again a measure of static balance showed that even on a narrow base when the visual inputs were present the patients did not show increased sway. After treatment a significant increase in walking speed was noted in our patients with both PC and HC BPPV.
After CRM sway velocities recorded on foam with eyes closed showed significant reduction in the PC BPPV group reaching values recorded from the healthy controls. These results are concordant with those obtained by Bonvier [9] who showed a complete recovery in postural balance in BPPV patients after CRM. The pretreatment values recorded from the HC BPPV group were not statistically different from the healthy controls and no significant change was detected after treatment like the other single study performed on patients with HC BPPV [17]. Different degrees of postural impairment have been reported in patients with PC BPPV after treatment [10-13]. The otolithic dysfunction induced by the unequal loads of the macula beds has been considered as the underlying mechanism [10]. However, after finding normal postural control in patients with HC BPPV before and after treatment Di Girolamo et al. [17] have proposed that such a mechanism has to be ignored. The residual deficit observed after CRM has been assigned to the persistence of small amounts of residual debris in the canal, to paresis of ampullar receptors or to the time needed for vestibular re-adaptation after a peripheral vestibular disorder [13,17]. An alternative explanation can be the repetitive bouts of vertigo causing an unstable vestibular function could blur the body scheme in space and lead to less precise postural control [19].
In conclusion, our study showed that patients with PC BPPV had impaired static balance ability when the visual and proprioceptive inputs were eliminated. On the other hand, patients with HC BPPV did not show static balance impairment. After CRM patients with PC BPPV showed significant improvement. This improvement in postural stability may be related to successful movement of the debris from the affected PC, which would eliminate the abnormal signal from that canal. Dynamic balance deficits characterized by decreased velocity in tandem walk was recorded both in patients with PC and HC BPPV. A prominent increase in speed was noted after treatment. Further studies about patients with HC BPPV interpreting not only static but also dynamic balance are necessary to say more about the effect of this canal on balance.
Conflict of interest
None of the authors of this manuscript has any financial or personal relationshipwith other people or organization that could inappropriately influence their work.
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