Abstract
Vestibular neuritis is a common condition characterized by the acute onset of vertigo that can last for several days. This chapter examines the epidemiology, diagnostic features, differential diagnosis, and treatment of vestibular neuritis. Considerations regarding physical examination, imaging, and management in both the acute and chronic phases of this disease are discussed. Differentiation of vestibular neuritis from stroke or other central insult is discussed and emphasized.
Keywords
Dizziness, Labyrinthitis, Vertigo, Vestibular neuritis, Vestibular neuronitis
Case study: L.R. is a 40-year-old female referred by her primary care physician with a chief complaint of acute, severe, room-spinning vertigo. She stated that she awoke at 4 a.m. when the sensation of vertigo came on very suddenly, was quite violent, and was accompanied by nausea and vomiting. She recalled having to crawl on the floor to make it to the bathroom and felt that the room continued to spin any time she opened her eyes. She eventually made it back to her bed and had to lie still, without moving her head, to minimize the waves of nausea and episodes of vomiting. She felt a “heavy” sensation in her head for several days afterward. Although it was difficult to remember the details, she did not recall a loss of hearing or any associated ringing in her ears with the episode. The patient felt a bit nauseated the day before the vertigo began but otherwise had been in good health. The patient was ultimately taken to the emergency room by her spouse, where she was hydrated intravenously and given vestibular suppressants and antiemetics. Several days after the onset of the vertigo, the patient described feeling quite unsteady, especially with any rapid movement of her head or body.
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.
Diagnosis and Differentiation From Central Insult/Stroke
As with most vestibular disorders of peripheral origin, a diagnosis of vestibular neuritis is primarily reached through a complete and thorough history and physical examination. A history of chronic ear disease should be elicited, as complications of chronic otitis media are quite common and may present with vertigo (e.g., labyrinthine fistula or cerebellar abscess). The duration of the vertigo attack is a critical component in the history of any patient with a complaint of dizziness and is particularly helpful in diagnosing vestibular neuritis. However, variability in the duration of the initial attack of vertigo is possible (i.e., from several hours to several days), while recurrent episodes of intense vertigo may occur with years of time between individual events. The presence of any other neurologic symptoms is as important as the duration of the vertigo attack. As there are several potentially dangerous causes of dizziness, a high degree of suspicion for a central cause must always be maintained ( Box 10.1 ). Directed questioning regarding associated symptoms is of paramount importance in ruling out vertigo resulting from a stroke syndrome (see Chapter 16 ). In particular, clinicians should ask about any weakness or change in sensation (pain, temperature, or numbness) of the limbs or face, slurred speech, vision changes including diplopia, dysphagia, change in voice, memory loss, or ataxia. These symptoms are indicative of a central insult and require a distinctly different management paradigm than that used in patients with vestibular neuritis. Brainstem/cerebellar infarct (e.g., Wallenberg syndrome) or hemorrhage may present with some form of dizziness but will invariably be accompanied by other neurologic signs and symptoms (see Chapter 2 ). These patients often will be unable to stand or walk. Physical examination findings highly suggestive of central neurologic insult include direction changing or vertical nystagmus, skew deviation, Horner’s syndrome (ptosis, miosis [constricted pupil], anhidrosis [decreased sweating], possible enophthalmos), and loss of pain and temperature sensation on the contralateral side of the body. The head impulse test will be normal with vertebrobasilar stroke. In fact, Newman-Toker et al. reported that the presence of normal horizontal head impulse test, direction-changing nystagmus in eccentric gaze, or skew deviation (vertical ocular misalignment) was 100% sensitive and 96% specific for stroke in the first 48 h of symptom onset. In patients in whom a central neurologic deficit is identified or suspected, imaging is diagnostic, with magnetic resonance imaging (MRI) being the preferred modality. Although rare, compromise of the posterior cerebral circulation may manifest with neck pain (from trauma or vertebral artery dissection) and associated dizziness and requires prompt neurosurgical consultation.
