Vestibular Neuritis

Introduction

Vestibular neuritis is characterized by the acute onset of vertigo with associated nausea, vomiting, and generalized imbalance. The acute phase is often severe and can last from a few hours to several days. A sense of imbalance and unsteadiness, exacerbated by motion, may linger for weeks to months. Auditory symptoms are uncommon, although patients may occasionally report ear fullness and tinnitus. Patients with accompanying hearing loss are believed to have a slightly different pathophysiologic entity termed acute labyrinthitis.

The precise etiology of vestibular neuritis remains elusive. Several theories have been postulated and supported, at least partially, within the literature. Dix and Hallpike in the 1950s suggested that an infectious process affecting Scarpa’s ganglion or the vestibular nerve might be responsible. Lindsay and Hemenway felt that an ischemic process might be responsible, although they found no direct evidence of vascular occlusion. More recent efforts have suggested that a viral agent may be the underlying cause. While individual studies have demonstrated the presence of herpes simplex virus DNA within vestibular nerve fibers and Scarpa’s ganglion, others have demonstrated histologic changes within the vestibular nerve suggestive of viral-induced atrophy and inflammation. Anatomic studies have also demonstrated that the superior vestibular nerve, which supplies the utricle, superior, and horizontal semicircular canals, is more likely to be involved in cases of vestibular neuritis. Goebel and colleagues have shown an anatomic basis for this observation related to the increased length, reduced diameter, and increased bony trabeculae of the bony canal housing the superior vestibular nerve (and its divisions) as compared with the inferior vestibular nerve.

In clinics specializing in vestibular disorders, vestibular neuritis accounts for between 3% and 10% of diagnoses. An annual incidence of vestibular neuritis approximating 3.5 cases per 100,000 persons was reported by Sekitani and colleagues, but further literature on the subject is lacking. In this same report, which was based on a large Japanese population, the peak age distribution for vestibular neuritis was between 30 and 50 years, with a range of 3–88 years. Furthermore, approximately 12% of patients in this study were more than 65 years. Dix and Hallpike, in their review of 100 cases of vestibular neuritis, found that 94% of cases occurred among patients between the ages of 20 and 59 years. While middle-aged individuals do seem to be more commonly affected, the authors’ experience would suggest that vestibular neuritis likely accounts for a larger percentage of vestibular diagnoses than outlined in these reports. This may be a consequence of differences in geographic referral patterns, variations in health care access, and a general lack of follow-up in patients achieving rapid resolution of symptoms.

Clinical Characteristics

Despite an inability to clearly identify the cause of vestibular neuritis, a thorough understanding of its clinical course and management has been established. The typical onset is one of intense vertigo, often noted on awakening. Patients may have a tendency to fall toward the involved side and will frequently demonstrate spontaneous nystagmus with direction being constant despite changes in gaze. Head or body movements exacerbate the symptoms, and patients will often try to minimize any such movements by lying completely still. Although the initial vertigo symptoms often subside over a period of days, patients may have a longer period of continued imbalance. This imbalance may manifest as difficulty making quick movements or turns, slight swaying during walking, or a generalized feeling of unsteadiness. Patients also often complain of a heavy feeling in their head or simply feeling “off” for days to weeks after the initial episode. Benign paroxysmal positional vertigo (BPPV) is common in patients who have had vestibular neuritis and can occur at varying intervals after the acute attack. The cause of frequent occurrence of BPPV in these patients is not known, although Schuknecht suggested that utricular otoconia might be loosened with the initial neuritis. Repeated bouts of vestibular neuritis have also been described, which many contend lends evidence toward a possible viral reactivation process as seen in herpes zoster oticus. Another theory to account for recurrent vertigo seen following acute vestibular neuritis is that stepwise compensation or periodic decompensation of unilateral vestibular loss causes reemergence of dizziness that eventually fully compensates. Some patients will be left with unilateral vestibular loss.