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Figure 1.
Consolidated Standards of Reporting Trials Diagram
Consolidated Standards of Reporting Trials Diagram

Flowchart of the study protocol.

Figure 2.
Canal Paresis During the Follow-up Period
Canal Paresis During the Follow-up Period

Caloric paresis percentages in the 2 study groups at the follow-up evaluations. Percentages were calculated using the vestibular paresis formula by Jongkees et al,13 which indicates the extent of unilateral caloric paresis.

Figure 3.
Complete Vestibular Neuritis Resolution During the Follow-up Period
Complete Vestibular Neuritis Resolution During the Follow-up Period

Complete disease resolution in the 2 study groups at the follow-up evaluations. At the 6-month examination, patients in the corticosteroids group had a statistically higher resolution rate (P < .05). At the 12-month evaluation, the resolution rate was not significantly different between the treatment groups (P > .05).

Table 1.  
Vestibular Rehabilitation Program
Vestibular Rehabilitation Program
Table 2.  
Baseline Characteristics of Patients
Baseline Characteristics of Patients
Table 3.  
Clinical Status of Patients
Clinical Status of Patients
Table 4.  
Caloric Paresis and Otolith Dysfunction of Patients
Caloric Paresis and Otolith Dysfunction of Patients
1.
Sekitani  T, Imate  Y, Noguchi  T, Inokuma  T.  Vestibular neuronitis: epidemiological survey by questionnaire in Japan. Acta Otolaryngol Suppl. 1993;503:9-12.
PubMedArticle
2.
Brandt  T. Vertigo: Its Multisensory Syndromes.2nd ed. London, England: Springer; 1999.
3.
Okinaka  Y, Sekitani  T, Okazaki  H, Miura  M, Tahara  T.  Progress of caloric response of vestibular neuronitis. Acta Otolaryngol Suppl. 1993;503:18-22.
PubMedArticle
4.
Ohbayashi  S, Oda  M, Yamamoto  M,  et al.  Recovery of the vestibular function after vestibular neuronitis. Acta Otolaryngol Suppl. 1993;503:31-34.
PubMedArticle
5.
Vidal  PP, de Waele  C, Vibert  N, Mühlethaler  M.  Vestibular compensation revisited. Otolaryngol Head Neck Surg. 1998;119(1):34-42.
PubMedArticle
6.
Brusaferri  F, Candelise  L.  Steroids for multiple sclerosis and optic neuritis: a meta-analysis of randomized controlled clinical trials. J Neurol. 2000;247(6):435-442.
PubMedArticle
7.
Schweinfurth  JM, Parnes  SM, Very  M.  Current concepts in the diagnosis and treatment of sudden sensorineural hearing loss. Eur Arch Otorhinolaryngol. 1996;253(3):117-121.
PubMedArticle
8.
Goudakos  JK, Markou  KD.  Corticosteroids vs corticosteroids plus antiviral agents in the treatment of Bell palsy: a systematic review and meta-analysis. Arch Otolaryngol Head Neck Surg. 2009;135(6):558-564.
PubMedArticle
9.
Engström  M, Berg  T, Stjernquist-Desatnik  A,  et al.  Prednisolone and valaciclovir in Bell’s palsy: a randomised, double-blind, placebo-controlled, multicentre trial. Lancet Neurol. 2008;7(11):993-1000.
PubMedArticle
10.
Hillier  SL, McDonnell  M.  Vestibular rehabilitation for unilateral peripheral vestibular dysfunction. Cochrane Database Syst Rev. 2011;(2):CD005397.
PubMed
11.
Herdman  SJ. Vestibular Rehabilitation.3rd ed. Philadelphia, PA: FA Davis Co; 2007.
12.
Unterberger  S.  Neue objective registrierbare vestibular-skorper-drehreaktion, erhalten durch treten aut der stele: der “tretversuch.” Arch Ohren-usw Heilk. 1938;145:478.
PubMedArticle
13.
Jongkees  LB, Maas  JP, Philipszoon  AJ.  Clinical nystagmography: a detailed study of electro-nystagmography in 341 patients with vertigo. Pract Otorhinolaryngol (Basel). 1962;24:65-93.
PubMed
14.
Fife  TD, Tusa  RJ, Furman  JM,  et al.  Assessment: vestibular testing techniques in adults and children: report of the Therapeutics and Technology Assessment Subcommittee of the American Academy of Neurology. Neurology. 2000;55(10):1431-1441.
PubMedArticle
15.
Strupp  M, Zingler  VC, Arbusow  V,  et al.  Methylprednisolone, valacyclovir, or the combination for vestibular neuritis. N Engl J Med. 2004;351(4):354-361.
PubMedArticle
16.
Strupp  M, Arbusow  V, Maag  KP, Gall  C, Brandt  T.  Vestibular exercises improve central vestibulospinal compensation after vestibular neuritis. Neurology. 1998;51(3):838-844.
PubMedArticle
17.
Sood  A, Ebbert  JO.  Methylprednisolone, valacyclovir, or both for vestibular neuritis. N Engl J Med. 2004;351(22):2344-2345.
PubMedArticle
18.
Vroomen  P.  Methylprednisolone, valacyclovir, or both for vestibular neuritis. N Engl J Med. 2004;351(22):2344-2345.
PubMedArticle
19.
Aw  ST, Halmagyi  GM, Curthoys  IS, Todd  MJ, Yavor  RA.  Unilateral vestibular deafferentation causes permanent impairment of the human vertical vestibulo-ocular reflex in the pitch plane. Exp Brain Res. 1994;102(1):121-130.
PubMed
20.
Shupak  A, Issa  A, Golz  A, Kaminer  M, Braverman  I.  Prednisone treatment for vestibular neuritis. Otol Neurotol. 2008;29(3):368-374.
PubMedArticle
21.
Goudakos  JK, Markou  KD, Franco-Vidal  V, Vital  V, Tsaligopoulos  M, Darrouzet  V.  Corticosteroids in the treatment of vestibular neuritis: a systematic review and meta-analysis. Otol Neurotol. 2010;31(2):183-189.
PubMedArticle
22.
Fishman  JM.  Corticosteroids effective in idiopathic facial nerve palsy (Bell’s palsy) but not necessarily in idiopathic acute vestibular dysfunction (vestibular neuritis). Laryngoscope. 2011;121(11):2494-2495.
PubMedArticle
23.
Fishman  JM, Burgess  C, Waddell  A.  Corticosteroids for the treatment of idiopathic acute vestibular dysfunction (vestibular neuritis). Cochrane Database Syst Rev. 2011;(5):CD008607.
PubMed
24.
Venosa  AR, Bittar  RS.  Vestibular rehabilitation exercises in acute vertigo. Laryngoscope. 2007;117(8):1482-1487.
PubMedArticle
25.
Herdman  SJ, Schubert  MC, Das  VE, Tusa  RJ.  Recovery of dynamic visual acuity in unilateral vestibular hypofunction. Arch Otolaryngol Head Neck Surg. 2003;129(8):819-824.
PubMedArticle
26.
Herdman  SJ, Hall  CD, Schubert  MC, Das  VE, Tusa  RJ.  Recovery of dynamic visual acuity in bilateral vestibular hypofunction. Arch Otolaryngol Head Neck Surg. 2007;133(4):383-389.
PubMedArticle
27.
Bergenius  J, Perols  O.  Vestibular neuritis: a follow-up study. Acta Otolaryngol. 1999;119(8):895-899.
PubMedArticle
28.
Schmid-Priscoveanu  A, Böhmer  A, Obzina  H, Straumann  D.  Caloric and search-coil head-impulse testing in patients after vestibular neuritis. J Assoc Res Otolaryngol. 2001;2(1):72-78.
PubMed
29.
Brandt  T, Huppert  T, Hüfner  K, Zingler  VC, Dieterich  M, Strupp  M.  Long-term course and relapses of vestibular and balance disorders. Restor Neurol Neurosci. 2010;28(1):69-82.
PubMed
30.
MacDougall  HG, Weber  KP, McGarvie  LA, Halmagyi  GM, Curthoys  IS.  The video head impulse test: diagnostic accuracy in peripheral vestibulopathy. Neurology. 2009;73(14):1134-1141.
PubMedArticle
Original Investigation
May 2014

Corticosteroids and Vestibular Exercises in Vestibular NeuritisSingle-blind Randomized Clinical Trial

Author Affiliations
  • 1First Department of Otorhinolaryngology–Head and Neck Surgery, AHEPA University Hospital, Aristotle University of Thessaloniki, Thessaloniki, Greece
JAMA Otolaryngol Head Neck Surg. 2014;140(5):434-440. doi:10.1001/jamaoto.2014.48
Abstract

Importance  The management of patients with unilateral acute vestibular neuritis (VN) has not been established to date.

Objective  To compare the use of vestibular exercises vs corticosteroid therapy in the recovery of patients with acute VN.

Design, Setting, and Participants  Prospective, single-blind, randomized clinical trial at a primary referral center. Among all patients with acute vertigo, those having VN were eligible for inclusion in the study.

Interventions  Forty patients with acute VN were randomly assigned to perform vestibular exercises or to receive corticosteroid therapy. After a baseline examination, follow-up evaluations were performed at 1, 6, and 12 months.

Main Outcomes and Measures  Efficacy outcomes included clinical, canal, and otolith recovery. Scores on the European Evaluation of Vertigo Scale and the Dizziness Handicap Inventory were used for the evaluation of clinical recovery. Findings of caloric irrigation and vestibular evoked myogenic potentials indicated canal and otolith improvement, respectively.

Results  Comparing the 2 treatment groups, no statistically significant differences were found in clinical, canal, or otolith recovery. At the 6-month examination, the number of patients with complete disease resolution in the corticosteroids group was significantly higher than that in the vestibular exercises group. However, at the end of the follow-up period, 45% (9 of 20) of patients in the vestibular exercises group and 50% (10 of 20) of patients in the corticosteroids group had complete disease resolution (P > .05).

Conclusions and Relevance  Treating patients who have acute VN with vestibular exercises seems equivalently effective as treating them with corticosteroid therapy in clinical, caloric, and otolith recovery. Corticosteroid therapy seems to enhance earlier complete acute VN resolution, with no added benefit in the long-term prognosis.

Trial Registration  clinicaltrials.gov Identifier: NCT01231009

Quiz Ref IDVestibular neuritis (VN) is among the 3 most common causes of peripheral vestibulopathy (the first is benign paroxysmal positional vertigo); an incidence of 3.5 cases per 100 000 is reported.1 Data from outpatient clinics specializing in the treatment of dizziness indicate that 7% of their patients have VN.2

Despite the benign course of VN, restoration of peripheral function after unilateral vestibular deficit is incomplete. This deficit leads to impaired vision and postural imbalance during walking and especially during rapid head movement toward the affected ear.3,4 Clinical recovery is achieved via central compensation in combination with vestibular substitution.5

The treatment strategy for peripheral recovery of function after VN has not been established to date. The therapeutic choices are (1) corticosteroids, (2) antiviral therapy (acyclovir or valacyclovir hydrochloride), (3) a combination of corticosteroids and an antiviral agent, and (4) vestibular exercises. The rationale for treating patients having VN with corticosteroids is based on studies69 documenting positive effects among patients with acute peripheral neuritis such as optic neuritis, idopathic facial nerve paresis, and idiopathic hearing loss. Vestibular rehabilitation seems to be a safe and effective management of unilateral vestibular hypofunction, maximizing central nervous system compensation.10

We performed a prospective, single-blind, randomized clinical trial comparing the treatment effects of vestibular exercises vs corticosteroid therapy in patients with VN. Clinical recovery and vestibular function were assessed at baseline and at 1, 6, and 12 months.

Methods
Patients

The local ethics committee approved the study protocol, and written informed consent was obtained from all patients. This study is registered with clinicaltrials.gov (identifier NCT01231009). All patients (age range, 18-80 years) who were seen in the emergency department of AHEPA University Hospital, Thessaloniki, Greece, with symptoms and signs of VN were recruited for the study.

The initial evaluation of patients included complete neuro-otologic, neurologic, and cardiovascular examinations. Patient inclusion in the study was based on diagnostic symptoms and signs. Patients with VN had a history of an acute onset of severe prolonged rotatory vertigo, nausea, vomiting, and postural imbalance. Quiz Ref IDThe main diagnostic signs were the following: no recent hearing loss, no findings of a central lesion on neurologic examination, ipsilateral deficit of the horizontal semicircular canal on the head thrust test, horizontal spontaneous nystagmus with a rotational component toward the unaffected ear, and unilateral reduced caloric response (caloric lateralization 25%) on caloric electronystagmography (ENG).

Exclusion criteria were the following: glaucoma; recent infection; signs of central vestibular dysfunction; history of chronic vestibular dysfunction; acute hearing loss (before, during, or after the onset of vertigo); symptoms of a central lesion, such as brainstem or cerebellar disorders; abnormal findings on magnetic resonance imaging of the brainstem or cerebellum; severe hypertension (blood pressure on admission >180 mm Hg systolic or >110 mm Hg diastolic); and severe diabetes mellitus (fasting blood glucose level >180 mg/dL on admission despite treatment) (to convert glucose level to millimoles per liter, multiply by 0.0555). Also excluded were patients with contraindications to the use of corticosteroids such as peptic ulcer disease, psychiatric disorders, pregnancy, and breastfeeding women.

Treatment Groups

All study patients were admitted to our department for 10 days. During the acute phase of the disease, all patients regardless of their treatment group allocation received an antiemetic agent (dimehydrinate [150 mg/d]) for a maximum of 3 days and a proton pump inhibitor. Based on computer-generated block randomization, the included patients were randomly assigned to 2 treatment groups.

Patients in the vestibular exercises group performed a vestibular rehabilitation program for 3 weeks. This program consisted of adaptation and substitution exercises (Table 1).11 They also performed exercises for balance and gait enhancement. During the first week of the program, patients performed the exercises under the supervision of a member of our scientific team (J.K.G.). On discharge from the hospital, they received written instructions and drawings describing the home exercises.

During their hospitalization, patients in the corticosteroids group received intravenous dexamethasone sodium phosphate (24 mg/d), tapering down during 7 days. On discharge from the hospital, all patients received a 14-day supply of the study drug in standardized packages of the daily regimen (dexamethasone sodium phosphate [2 mg/d by mouth], tapering down), with written instructions for taking the drug.

Adverse Effects

During the hospitalization, measurements of arterial pressure (3 times a day) and blood glucose level (once a day) were obtained. Patients were informed of the potential adverse effects of the medications and were asked to report them as soon as possible. At the 1-month follow-up evaluation, patients were asked about compliance to the treatment plan, whether adverse effects had developed during the treatment, if any vertigo episodes had occurred, and about any new symptoms or signs that had developed during the course of the disease such as tinnitus, hearing loss, or aural fullness.

Follow-up Outcome Measures

The clinical status and improvement of our patients were assessed after an otoneurologic examination and laboratory tests at specific time points. The investigator who performed the follow-up evaluations of outcomes was masked to the patients’ allocation to the treatment groups. The baseline assessment was on the fourth day after admission, and follow-up appointments occurred at 1, 6, and 12 months after the disease onset.

The otoneurologic examination consisted of a general head and neck examination, as well as micro-otoscopy, head-shaking test and head-impulse test, and tests for pathologic nystagmus (spontaneous, gaze-evoked, positional, and Dix-Hallpike maneuver). Babinski-Weil test, Romberg sign, and Unterberger test12 were used for the evaluation of postural balance and gait. To quantitatively evaluate a patient’s vertigo relative to the accompanying symptoms, we used the European Evaluation of Vertigo Scale (EEV), a physician-administered questionnaire. Patients’ functional, emotional, and physical handicaps were measured with the Dizziness Handicap Inventory (DHI), a self-administered questionnaire.

Caloric irrigation and vestibular evoked myogenic potentials (VEMPs) were used as measures of unilateral vestibular loss. The extent of canal paresis was measured using caloric irrigation with water at 30°C and 44°C. Because the nystagmus induced by caloric irrigation may vary considerably among individuals with vertigo but only to a small extent in a healthy person,13,14 the vestibular paresis formula by Jongkees et al13 was used to calculate caloric lateralization as follows:{[(R30° + R44°) − (L30° + L44°)] ÷ (R30° + R44° + L30° + L44°)} × 100,where R indicates right and L left, and ° is °C. Based on our vestibular laboratory norms, abnormal caloric findings were recorded if caloric lateralization was 25% or higher.

The VEMPs were recorded in the supine position from one side each time using surface electrodes over the unilateral sternocleidomastoid muscle, with a reference electrode on the unilateral clavicle and a ground electrode on the forehead. During the test, the patient was instructed to rotate and raise the head from the pillow to activate the sternocleidomastoid muscle. The VEMPs were considered abnormal if they were absent or if the amplitude asymmetry ratio of the affected side to the unaffected side was 25% or higher. Complete disease resolution was recorded if the EEV score was 0, the DHI score was less than 6, caloric lateralization was less than 25%, and the VEMPs were normal.

Statistical Analysis

Differences in the proportions of patients with abnormal VEMPs and with complete disease resolution were analyzed by Fisher exact test. The means of EEV scores, DHI scores, and caloric lateralization were compared using independent-samples 2-tailed t test.

Results

During the 3 years of the study protocol, 52 patients with symptoms of acute VN were seen in the emergency department of AHEPA University Hospital (Figure 1). Forty patients fulfilled the inclusion criteria and consented to participate in the study. These patients were randomly assigned to the vestibular exercises group (20 patients) or to the corticosteroids group (20 patients). Table 2 summarizes the baseline characteristics of the included patients. No statistically significant differences between the groups were found in the mean age, sex ratio, lesion side, and mean time from the disease onset to admission to our department. The baseline vestibular deficit, as measured with the mean EEV score, the mean caloric lateralization, and abnormal VEMPs also did not differ significantly between the 2 groups.

Clinical recovery, as measured with the EEV and DHI, demonstrated similar improvement among the patients of both study groups. After 1 month of the received treatment, the mean (SD) EEV scores were 3.75 (1.61) in the vestibular exercises group and 4.17 (3.82) in the corticosteroids group (Table 3). The difference in EEV score improvement between the study groups at the 1-month follow-up visit did not reach statistical significance (P > .05). Patient handicaps, as measured with the DHI score, were not significantly different between the study groups at the follow-up evaluations. During 12 follow-up months, patients performing vestibular exercises showed greater improvement in the DHI score compared with patients receiving corticosteroids, although the difference was not statistically significant.

Quiz Ref IDThe extent of vestibular paresis, as calculated with the formula by Jongkees et al,13 did not differ significantly between the 2 study groups at the baseline evaluation. At the 1-month follow-up visit, the corticosteroids group showed better canal improvement, although the difference was not statistically significant between the study groups. The mean (SD) caloric lateralizations at the 1-month follow-up visit were 53.25 (14.23) in the vestibular exercises group and 44.88 (18.21) in the corticosteroids group. In both study groups, the canal response was statistically better at the 6-month follow-up visit compared with the 1-month follow-up visit (P < .05 by paired t test) (Table 4). These results were stable when comparing the caloric response between the 6-month and 12-month follow-up visits in each study group (P < .05 by paired t test). However, at both the 6-month and 12-month follow-up visits, the extent of canal paresis improvement was not statistically significantly different between the vestibular exercises group and the corticosteroids group (Figure 2). At 12 months after the disease onset, 12 of 20 patients performing vestibular exercises and 9 of 20 patients receiving corticosteroids had caloric lateralization less than 25%.

At the baseline evaluation, otolith dysfunction (measured by the VEMPs) was observed in 7 patients of the vestibular exercises group and in 4 patients of the corticosteroids group. At the 1-month follow-up visit, 2 patients in the vestibular exercises group had recovered from otolith dysfunction, while 4 patients in the corticosteroids group maintained abnormal VEMPS. At the 6-month assessment, all patients with otolith dysfunction regardless of the received treatment had recovered completely, manifesting normal VEMPs.

At the 12-month follow-up visit, 9 of 20 patients (45%) in the vestibular exercises group and 10 of 20 patients (50%) in the corticosteroids group had complete disease resolution (P > .05). No significant differences were found between the 2 treatment groups in the number of patients who had achieved complete resolution of acute vestibular loss at 12 months. However, at the 6-month evaluation, more patients in the corticosteroids group had complete resolution (Figure 3).

Only 2 of 40 patients (5%) experienced benign paroxysmal positional vertigo (BPPV) during the interval between the 1-month and 6-month follow-up evaluations. The diagnosis of BPPV was based on the Dix-Hallpike maneuver, which was included in the diagnostic protocol of our follow-up visits. In the 2 patients with secondary BPPV, the VEMPs were preserved, indicating VN of the superior branch. In the corticosteroids group, 1 patient with controlled diabetes mellitus using antidiabetic agents had destabilization of the disease and developed hyperglycemia. Modification of the hypoglycemic dosage normalized the blood glucose level. Patients in the vestibular exercises group reported no adverse effects or complications due to the performed vestibular rehabilitation program.

Discussion

Based on the results herein, a 3-week program of vestibular exercises in patients with acute VN seems to be equivalent to dexamethasone therapy (cumulative dose of 96 mg during 21 days) in terms of clinical, canal, and otolith recovery. The role of corticosteroids in the treatment of VN remains uncertain because their beneficial effects have been based on investigations of patients experiencing acute cranial nerve neuropathies such as optic neuritis, Bell palsy, and idiopathic hearing loss.8 In a prospective randomized clinical trial reported in 2004, Strupp et al15 investigated the role of corticosteroids and antiviral agents in patients with acute VN, with the primary outcome being improvement in the mean caloric lateralization on ENG at 12 months after the disease onset. The authors reported that methylprednisolone significantly improved the peripheral vestibular function recovery. Previous authors chose the vestibular paresis formula by Jongkees et al13 as a validated efficacy outcome measure to compare the function of the 2 labyrinths.16 Despite criticism that the authors did not use a symptom-based outcome measure,17 their choice was justifiable because other studies18,19 have demonstrated that better peripheral vestibular function recovery is associated with a smaller persistent dynamic deficit in the vestibulo-ocular reflex and with less oscillopsia and imbalance during head and body movement.

In a randomized clinical trial reported in 2008 using clinical and ENG outcome measures, Shupak et al20 showed that corticosteroids might enhance earlier recovery but do not benefit the long-term prognosis of patients with VN. A systematic review and meta-analysis21 of all studies exploring the therapeutic effect of corticosteroids in patients with VN supported their use in benefitting the caloric extent and canal paresis recovery but not in improving clinical symptoms. Quiz Ref IDWork by Fishman22 and a recent Cochrane review23 found insufficient evidence to support the use of corticosteroids in the management of patients with VN, stating that well-designed randomized clinical trials with symptom-based outcome measures, in addition to objective measures of vestibular improvement, are needed to clarify the effectiveness of such therapy.22,23

The present study comparing drug administration (corticosteroids) with a physical treatment (vestibular exercises) in patients with acute VN supports that patients treated with corticosteroids have no advantage in the long-term prognosis of their disease. However, the use of corticosteroids seems to accelerate patient recovery both clinically and on caloric ENG.

The role of vestibular exercises is mainly to accelerate and improve central compensation via the mechanisms of habituation training, as well as to increase substitution. Based on the results of clinical studies,10,24 vestibular exercises seem to be effective in reducing the duration of symptoms and the need for medication in patients with acute vertigo. Herdman et al25,26 in 2 randomized clinical trials showed that vestibular exercises facilitate the recovery of gaze stability during head movement, enhancing the development of programmed eye movement, in patients with unilateral or bilateral vestibular hypofunction. In a 1998 study, Strupp et al16 reported the efficacy of vestibular exercises in patients with VN and found that vestibulospinal compensation improved more in a group of patients with VN who performed vestibular rehabilitation (home-based physical therapy) compared with a group of patients who received no specific intervention (other than encouragement to move).16 Our results suggest that vestibular rehabilitation seems equivalently effective, in terms of clinical, canal, and otolith recovery, as corticosteroid therapy in the recovery of patients with VN.

Considering the natural course of VN, the findings herein confirm a previously reported lack of correlation between clinical disease resolution and caloric lateralization regardless of the performed treatment.4,20,21,27 However, in contrast to the findings by Shupak et al,20 the clinical recovery efficacy measures (the EEV and DHI scores) in the present study had greater improvement than the caloric irrigation findings. At 1 month after the disease onset, the mean EEV score improvements were 78.49% for patients in the vestibular exercises group and 71.05% for patients in the corticosteroids group (Table 3), but the caloric lateralization improvements were only 31.71% and 33.42% for the 2 study groups, respectively (Table 4). The DHI score improvements were 97.70% for patients in the vestibular exercises group and 96.58% for patients in the corticosteroids group at the end of the follow-up period (12 months) (Table 3), but only 60% (12 of 20) of patients in the vestibular exercises group and 45% (9 of 20) of patients in the corticosteroids group had caloric lateralization less than 25% (Table 4). However, only 45% (9 of 20) of patients in the vestibular exercises group and 50% (10 of 20) of patients in the corticosteroids group had complete disease resolution at the end of the follow-up period (Figure 3), with the remaining symptoms being slight oscillopsia and impaired balance after rapid head movement.

Quiz Ref IDThe caloric test, the most important assessment in the ENG battery, is invaluable in diagnosing peripheral vestibular disorders such as VN and is the only test that allows the stimulation of each horizontal semicircular canal separately. Despite the usefulness of the caloric test in diagnosing VN, its value is limited to follow-up evaluation in patients with VN due to some inherent characteristics. The caloric test provides a nonphysiological stimulation, producing endolymph accelerations in the range of low frequencies of 0.002 to 0.004 Hz. Previous authors have stated that, in chronic VN, the low-frequency function of the peripheral vestibular system recovers or becomes symmetrical but that deficits in the high-frequency horizontal vestibulo-ocular reflex to the lesioned side are permanent.28 Brandt et al29 reported that the average recovery, based on 10 studies of low-frequency vestibular function, occurs over time, with most of the function being regained within the first month after the disease onset. In the present study, vestibular function after VN (as measured by the nystagmus response to the caloric irrigation) improved over time, with the highest rate of improvement occurring within the first month after the disease onset regardless of the treatment strategy. In chronic VN, the search coil head-impulse test and the video head-impulse test are the most reliable in measuring vestibular function because they provide high-frequency accelerations.28,30

Our study has several limitations. Despite our power analysis based on clinical improvement, a study group with combined treatment would strengthen our conclusions, presuming a larger sample size. Furthermore, our aim was to assess the clinical improvement of patients in the 2 study groups, and our data allow no conclusions about the background improvement, central compensation procedure, or peripheral vestibular function enhancement. Our diagnostic protocol did not include the full range of available examinations to assess the natural course of VN such as subjective visual vertical, ocular torsion, and video head-impulse tests. These tests could add valuable data concerning the improvement of both static and dynamic imbalance in patients after acute VN.

Conclusions

Vestibular exercises in patients with VN seem equivalently effective as corticosteroid therapy based on clinical and laboratory criteria. Corticosteroids seem to enhance earlier complete disease resolution, with no added benefit in the long-term prognosis of patients with VN. Improvement in canal or otolith dysfunction cannot be directly translated into clinical terms, a fact that is confirmed by our study. Multicenter prospective studies with large sample sizes and multiple study outcomes (clinical and laboratory) are needed to clarify the role of vestibular exercises, corticosteroid therapy, or a combination of them in the recovery of patients with acute VN.

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Article Information

Submitted for Publication: August 31, 2013; final revision received December 11, 2013; accepted January 10, 2014.

Corresponding Author: John K. Goudakos, MD, MSc, First Department of Otorhinolaryngology–Head and Neck Surgery, AHEPA University Hospital, Aristotle University of Thessaloniki, 54636 Thessaloniki, Greece (jgoudakos@gmail.com).

Published Online: March 6, 2014. doi:10.1001/jamaoto.2014.48.

Author Contributions: Drs Goudakos and Markou had full access to all the data in the study and take responsibility for the integrity of the data and the accuracy of the data analysis.

Study concept and design: Goudakos, Markou, Tsaligopoulos.

Acquisition, analysis, or interpretation of data: Goudakos, Markou, Psillas, Vital.

Drafting of the manuscript: Goudakos, Markou, Psillas, Vital.

Critical revision of the manuscript for important intellectual content: Goudakos, Tsaligopoulos.

Statistical analysis: Goudakos, Markou, Psillas, Vital.

Obtained funding: Goudakos.

Administrative, technical, or material support: Goudakos, Markou.

Study supervision: Goudakos, Markou, Tsaligopoulos.

Conflict of Interest Disclosures: None reported.

References
1.
Sekitani  T, Imate  Y, Noguchi  T, Inokuma  T.  Vestibular neuronitis: epidemiological survey by questionnaire in Japan. Acta Otolaryngol Suppl. 1993;503:9-12.
PubMedArticle
2.
Brandt  T. Vertigo: Its Multisensory Syndromes.2nd ed. London, England: Springer; 1999.
3.
Okinaka  Y, Sekitani  T, Okazaki  H, Miura  M, Tahara  T.  Progress of caloric response of vestibular neuronitis. Acta Otolaryngol Suppl. 1993;503:18-22.
PubMedArticle
4.
Ohbayashi  S, Oda  M, Yamamoto  M,  et al.  Recovery of the vestibular function after vestibular neuronitis. Acta Otolaryngol Suppl. 1993;503:31-34.
PubMedArticle
5.
Vidal  PP, de Waele  C, Vibert  N, Mühlethaler  M.  Vestibular compensation revisited. Otolaryngol Head Neck Surg. 1998;119(1):34-42.
PubMedArticle
6.
Brusaferri  F, Candelise  L.  Steroids for multiple sclerosis and optic neuritis: a meta-analysis of randomized controlled clinical trials. J Neurol. 2000;247(6):435-442.
PubMedArticle
7.
Schweinfurth  JM, Parnes  SM, Very  M.  Current concepts in the diagnosis and treatment of sudden sensorineural hearing loss. Eur Arch Otorhinolaryngol. 1996;253(3):117-121.
PubMedArticle
8.
Goudakos  JK, Markou  KD.  Corticosteroids vs corticosteroids plus antiviral agents in the treatment of Bell palsy: a systematic review and meta-analysis. Arch Otolaryngol Head Neck Surg. 2009;135(6):558-564.
PubMedArticle
9.
Engström  M, Berg  T, Stjernquist-Desatnik  A,  et al.  Prednisolone and valaciclovir in Bell’s palsy: a randomised, double-blind, placebo-controlled, multicentre trial. Lancet Neurol. 2008;7(11):993-1000.
PubMedArticle
10.
Hillier  SL, McDonnell  M.  Vestibular rehabilitation for unilateral peripheral vestibular dysfunction. Cochrane Database Syst Rev. 2011;(2):CD005397.
PubMed
11.
Herdman  SJ. Vestibular Rehabilitation.3rd ed. Philadelphia, PA: FA Davis Co; 2007.
12.
Unterberger  S.  Neue objective registrierbare vestibular-skorper-drehreaktion, erhalten durch treten aut der stele: der “tretversuch.” Arch Ohren-usw Heilk. 1938;145:478.
PubMedArticle
13.
Jongkees  LB, Maas  JP, Philipszoon  AJ.  Clinical nystagmography: a detailed study of electro-nystagmography in 341 patients with vertigo. Pract Otorhinolaryngol (Basel). 1962;24:65-93.
PubMed
14.
Fife  TD, Tusa  RJ, Furman  JM,  et al.  Assessment: vestibular testing techniques in adults and children: report of the Therapeutics and Technology Assessment Subcommittee of the American Academy of Neurology. Neurology. 2000;55(10):1431-1441.
PubMedArticle
15.
Strupp  M, Zingler  VC, Arbusow  V,  et al.  Methylprednisolone, valacyclovir, or the combination for vestibular neuritis. N Engl J Med. 2004;351(4):354-361.
PubMedArticle
16.
Strupp  M, Arbusow  V, Maag  KP, Gall  C, Brandt  T.  Vestibular exercises improve central vestibulospinal compensation after vestibular neuritis. Neurology. 1998;51(3):838-844.
PubMedArticle
17.
Sood  A, Ebbert  JO.  Methylprednisolone, valacyclovir, or both for vestibular neuritis. N Engl J Med. 2004;351(22):2344-2345.
PubMedArticle
18.
Vroomen  P.  Methylprednisolone, valacyclovir, or both for vestibular neuritis. N Engl J Med. 2004;351(22):2344-2345.
PubMedArticle
19.
Aw  ST, Halmagyi  GM, Curthoys  IS, Todd  MJ, Yavor  RA.  Unilateral vestibular deafferentation causes permanent impairment of the human vertical vestibulo-ocular reflex in the pitch plane. Exp Brain Res. 1994;102(1):121-130.
PubMed
20.
Shupak  A, Issa  A, Golz  A, Kaminer  M, Braverman  I.  Prednisone treatment for vestibular neuritis. Otol Neurotol. 2008;29(3):368-374.
PubMedArticle
21.
Goudakos  JK, Markou  KD, Franco-Vidal  V, Vital  V, Tsaligopoulos  M, Darrouzet  V.  Corticosteroids in the treatment of vestibular neuritis: a systematic review and meta-analysis. Otol Neurotol. 2010;31(2):183-189.
PubMedArticle
22.
Fishman  JM.  Corticosteroids effective in idiopathic facial nerve palsy (Bell’s palsy) but not necessarily in idiopathic acute vestibular dysfunction (vestibular neuritis). Laryngoscope. 2011;121(11):2494-2495.
PubMedArticle
23.
Fishman  JM, Burgess  C, Waddell  A.  Corticosteroids for the treatment of idiopathic acute vestibular dysfunction (vestibular neuritis). Cochrane Database Syst Rev. 2011;(5):CD008607.
PubMed
24.
Venosa  AR, Bittar  RS.  Vestibular rehabilitation exercises in acute vertigo. Laryngoscope. 2007;117(8):1482-1487.
PubMedArticle
25.
Herdman  SJ, Schubert  MC, Das  VE, Tusa  RJ.  Recovery of dynamic visual acuity in unilateral vestibular hypofunction. Arch Otolaryngol Head Neck Surg. 2003;129(8):819-824.
PubMedArticle
26.
Herdman  SJ, Hall  CD, Schubert  MC, Das  VE, Tusa  RJ.  Recovery of dynamic visual acuity in bilateral vestibular hypofunction. Arch Otolaryngol Head Neck Surg. 2007;133(4):383-389.
PubMedArticle
27.
Bergenius  J, Perols  O.  Vestibular neuritis: a follow-up study. Acta Otolaryngol. 1999;119(8):895-899.
PubMedArticle
28.
Schmid-Priscoveanu  A, Böhmer  A, Obzina  H, Straumann  D.  Caloric and search-coil head-impulse testing in patients after vestibular neuritis. J Assoc Res Otolaryngol. 2001;2(1):72-78.
PubMed
29.
Brandt  T, Huppert  T, Hüfner  K, Zingler  VC, Dieterich  M, Strupp  M.  Long-term course and relapses of vestibular and balance disorders. Restor Neurol Neurosci. 2010;28(1):69-82.
PubMed
30.
MacDougall  HG, Weber  KP, McGarvie  LA, Halmagyi  GM, Curthoys  IS.  The video head impulse test: diagnostic accuracy in peripheral vestibulopathy. Neurology. 2009;73(14):1134-1141.
PubMedArticle
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