ABSTRACT
We performed steroid therapy on 34 cases with vestibular neuronitis and compared them with 77 patients not subjected to this therapy to examine the role of recovery of their vestibular function. Since no relation was noted between use of steroid and changes in subjective symptom of dizziness, the use of steroid is likely to facilitate the disappearance of spontaneous nystagmus in the early recovery stage. Canal paralysis recovered significantly by steroid and in cases of slight and moderate paralysis at the onset, recovery was more significant. Steroid therapy is argued to be effective for the recovery of vestibular function in cases of vestibular neuronitis.
Subject(s)
Neuritis/physiopathology , Vestibular Function Tests , Vestibular Nerve/physiopathology , Vestibulocochlear Nerve Diseases/physiopathology , Administration, Oral , Adolescent , Adult , Aged , Caloric Tests , Dose-Response Relationship, Drug , Drug Administration Schedule , Electronystagmography , Female , Follow-Up Studies , Humans , Hydrocortisone/administration & dosage , Infusions, Intravenous , Male , Middle Aged , Neuritis/diagnosis , Neuritis/drug therapy , Prednisolone/administration & dosage , Vestibular Nerve/drug effects , Vestibulocochlear Nerve Diseases/diagnosis , Vestibulocochlear Nerve Diseases/drug therapyABSTRACT
We observed 9 cases of BPPV developed after vestibular neuronitis. The interval between the onset of BPPV and vestibular neuronitis ranged from 2 weeks to 20 years. All cases were examined for critical head position which provoked vertigo, non-gaze nystagmus, positional and positioning nystagmus and caloric nystagmus. No characteristic signs and symptoms could be observed. The function of the posterior canal is thought to be necessary to provoke positional vertigo. Thus in BPPV after vestibular neuronitis the function of the posterior canal would presumably have been preserved to some degree. The first possibility is that the function of the posterior canal was not impaired in spite of the damage of the lateral canal. The fact that each canal differs in involvement in vestibular neuronitis may be explained by the difference in the blood supply or the innervation between lateral and posterior canals. If only the artery or nerve which is related to the lateral canal is damaged and the artery or nerve to the posterior canal is not involved, then the function of the posterior canal is preserved. So BPPV may occur soon after the disappearance of severe vertigo. The second possibility is that if the posterior canal had been damaged together with the lateral canal and the functions are recovering, BPPV may occur some time after the onset of vestibular neuronitis. The locus of vestibular neuronitis is in the peripheral vestibular system and the extent and degree of the lesion vary, which may explain why there can be time difference of the recovery between the two canals.
