Copyright @ 200 Otology & Neurotology, Inc. Unauthorized reproduction of this article is prohibited. 8 Prednisone Treatment for Vestibular Neuritis *Avi Shupak, *Anthony Issa, †‡Avishay Golz, *Margalit Kaminer, and ‡§Itzhak Braverman *Unit of Otoneurology, Carmel and Lin Medical Centers; ÞThe Department of OtolaryngologyVHead and Neck Surgery, Rambam Medical Center; þThe Bruce Rappaport Faculty of MedicineVTechnion, Haifa; and §The Unit of OtolaryngologyYHead and Neck Surgery, Hillel Yaffe Medical Center, Hadera, Israel Objective: To evaluate the value of corticosteroids in the treat- ment of vestibular neuritis (VN). Design: Prospective controlled randomized. Methods: Thirty VN patients, 15 in the study and 15 in the control group, were the subjects of the study. The study group was treated by 1 mg/kg prednisone for 5 days, followed by gradually reduced doses of prednisone for an additional 15 days, and ves- tibular sedatives for symptomatic relief during the first 5 days after presentation. The control group received a placebo and similar vestibular sedatives. The patients had a baseline evaluation and follow-up examinations after 1, 3, 6, and 12 months. The groups were compared for the presence of symptoms and signs, caloric lateralization on the electronystagmography (ENG), the presence of other pathologic findings in the ENG, and Dizziness Handicap Inventory scores. Results: No differences were found between the groups in the occurrence of symptoms and signs, degree of caloric lateraliza- tion, presence of other ENG pathologic findings, and Dizziness Handicap Inventory scores at the end of the study. Complete resolution was observed in 64% of the study and in 80% of the control group. The study group showed earlier recovery of ENG lateralization at the 1- and 3-month follow-up evaluations and higher rates of complete resolution at the 3- and 6-month follow-up points. Conclusion: Prednisone therapy might enhance earlier reco- very but does not improve the long-term prognosis of VN. The clinical and laboratory parameters in VN are not correlated, and both are required for complete patient evaluation. Key Words: Corticosteroids VElectronystagmographyVPrednisone V QuestionnairesVVertigoVVestibular function testsVVestibular neuronitis. Otol Neurotol 29:368Y374, 2008. Vestibular neuritis (VN) is the second most common cause of peripheral vestibulopathy (the first being benign paroxysmal positional vertigo), with incidence of appro- ximately 3.5 per 100,000 (1). Currently, VN is explained by a viral pathogenesis. Postmortem studies have shown atrophy of the vestibular nerve and sensory epithelium that are similar to the histopathologic findings in herpes zoster oticus (2). Herpes simplex virus 1 (HSV-1) DNA has been detected in human vestibular ganglia (3,4), indicating a latent infection by HSV-1 (5). Vestibular neuritis 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 patients 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 func- tion, and clinical recovery is achieved via proprioceptive and visual substitution for the unilateral vestibular deficit combined with central vestibular compensation of the imbalance in vestibular tone (6,7). Although VN is usually restricted to 1 attack, several studies have reported contin- uous or episodic vertigo or unsteadiness in 43 to 53% of patients (8,9). The main residues include impaired vision and disequilibrium during walking and especially during head movement toward the affected ear (10). The rate of positive finding on vestibular evaluation may reach 60% (11Y14). 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 (15). The assumed HSV-1 cause of VN and Bell’s palsy (16) and the reported benefit of corticosteroids in Bell’s palsy (17) suggest similar advantage in the treatment of VN. In addition, glucocorticoid receptor activation was reported to enhance vestibular compensation after acute peripheral ves- tibular insults in various animal models (18,19). The goal of our study was to examine the value of pred- nisone in the treatment of VN by the evaluation of the clinical response, patients’ self-perceived handicap, and Address correspondence and reprint requests to Avi Shupak, M.D., Department of OtolaryngologyYHead and Neck Surgery, Carmel Med- ical Center, 7 Michal Street, Haifa 34362, Israel; E-mail: shupak@ internet-zahav.net Otology & Neurotology 29:368Y374 Ó 2008, Otology & Neurotology, Inc. 368