Prednisone Treatment for Vestibular Neuronitis
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|ClinicalTrials.gov Identifier: NCT00271791|
Recruitment Status : Completed
First Posted : January 4, 2006
Last Update Posted : November 6, 2007
|Condition or disease||Intervention/treatment||Phase|
|Vestibular Diseases Vestibular Neuronitis||Drug: Prednisone||Phase 2|
Vestibular neuronitis is the second most common cause of peripheral vestibulopathy (the first being benign paroxysmal positional vertigo) with incidence of about 3.5/100000. Currently vestibular neuronitis is explained by a viral pathogenesis.
Vestibular neuronitis is considered to have a benign course. The static rotatory vertigo and disequilibrium, present even when the patient is completely at rest, subside in most cases within a few days, and a gradual return to daily activities is the rule. However, it has been shown that there is generally incomplete restoration of peripheral function, and clinical recovery is achieved by proprioceptive and visual substitution for the unilateral vestibular deficit, combined with central vestibular compensation of the imbalance in vestibular tone. Although vestibular neuronitis is usually restricted to one attack, several studies have reported continuous or episodic vertigo or unsteadiness in 43% -53% of patients. The main residua include impaired vision and disequilibrium during walking and especially during head movement toward the affected ear. The rate of positive finding on vestibular evaluation may reach 60%. However, vestibular impairment as reflected by positive bedside testing and vestibular laboratory evaluation is not necessarily accompanied by subjective complaints and does not always reflect the level of incapacity.
The assumed HSV-1 etiology of vestibular neuronitis and the reported benefit of the combination of steroids and acyclovir in Bell's palsy suggest similar advantage in the treatment of vestibular neuronitis. Also, glucocorticoid receptors activation was reported to enhance vestibular compensation after acute peripheral vestibular insults in various animal models. A recent study investigated the effect of prednisolone versus valacyclovir and placebo on canal paresis in vestibular neuronitis patients. It was found that steroid treatment significantly improved peripheral vestibular function to the extent reflected by the caloric testing. However, bedside findings, patients' complaints and daily handicap were not evaluated. The relevance of the EOG caloric test results to clinical improvement could be argued in light of a previous report showing no correlation between EOG findings and residual symptoms in a long-term follow-up of vestibular neuronitis patients, and the finding that corticosteroid therapy had no effect on symptoms despite significant recovery of the caloric-test results.
The purpose of the study:
Prospective controlled longitudinal 12-month evaluation of the value of steroids in the treatment of vestibular neuronitis. The potential benefits of steroid therapy would be analyzed by the clinical response, self-perceived handicap and EOG laboratory parameters.
|Study Type :||Interventional (Clinical Trial)|
|Actual Enrollment :||17 participants|
|Intervention Model:||Parallel Assignment|
|Masking:||Double (Participant, Investigator)|
|Official Title:||Prednisone Treatment for Vestibular Neuronitis|
|Study Start Date :||September 2005|
|Actual Study Completion Date :||May 2007|
PO, 1 mg/kg body weight, 5 days Short tapering regimen: daily reductions in the dose, 12 days
Placebo Comparator: 2
PO, Placebo, 17 days
- Clinical: The presence of static and dynamic nystagmus, positional and positioning nystagmus, and disequilibrium on bedside examination. [ Time Frame: 12 months ]
- Functional: Scores on the Dizziness Handicap Inventory questionnaires. [ Time Frame: 12 months ]
- Laboratory: Caloric lateralization and directional preponderance on electro-oculography (EOG). [ Time Frame: 12 months ]
To learn more about this study, you or your doctor may contact the study research staff using the contact information provided by the sponsor.
Please refer to this study by its ClinicalTrials.gov identifier (NCT number): NCT00271791
|Unit of Otolaryngology Head and Neck Surgery, Hillel Yaffe Medical Center|
|Hadera, Israel, 38100|
|Department of Otolaryngology Head and Neck Surgery, Rambam Medical Center|
|Haifa, Israel, 31096|
|Department of Otolaryngology Head and Neck Surgery, Carmel Medical Center|
|Haifa, Israel, 34362|
|Otoneurolgy Unit, Lin Medical Center, Clalit Health Services|
|Haifa, Israel, 35152|
|Principal Investigator:||Avi Shupak, MD||Carmel Medical Center and Clalit Health Services, Haifa and West Galilee|
|Principal Investigator:||Itzhak Braverman, MD||Hillel Yaffe Medical Center|
|Principal Investigator:||Avishai Golz, MD||Rambam Health Care Campus|
|Principal Investigator:||Elhanan Greenberg, ND||Carmel Medical Center|
|Study Chair:||Avi Shupak, MD||Carmel Medical Center and Clalit Health Services, Haifa and West Galilee|