Disclaimer: The information contained within the Grand Rounds Archive is intended for use by doctors and other health care professionals. These documents were prepared by resident physicians for presentation and discussion at a conference held at Baylor College of Medicine in Houston, Texas. No guarantees are made with respect to accuracy or timeliness of this material. This material should not be used as a basis for treatment decisions, and is not a substitute for professional consultation and/or peer-reviewed medical literature. Vestibular Neuritis Vestibular neuritis refers to a disorder of the vestibular system without an associated auditory deficit or other disease of the central nervous system. It is a unilateral peripheral disorder, primarily affecting patients in their third and fourth decades, which is associated with ipsilateral caloric weakness. Except for persistent unsteadiness, symptoms usually resolve by 3-6 months. The episode of vertigo usually consists of a series of attacks within a 10 day period. Of the patients in Coats' series, 38.2% had an antecedent infection, 20% with sinusitis, and 61% had spontaneous nystagmus. Besides the unilateral caloric weakness, electronystagmography reveals a directional preponderance and beating nystagmus away from the affected side. Vestibular neuritis has also been referred to in the literature as vestibular neuronitis, epidemic vertigo, acute labyrinthitis, vestibular paralysis, and vestibular neuropathy. A multiple attack variant of vestibular neuritis occurs in a younger age group and consists of recurrent attacks over months to years. Symptoms of unsteadiness and disequilibrium have shorter duration, and patients have less severe caloric weakness. Preceding upper respiratory illness is more commonly reported in this subset of patients. The differential diagnosis of vestibular neuritis includes Meniere's disease, vestibular schwannoma, perilymphatic fistula, cerebellar infarction, multiple sclerosis, disequilibrium of aging, basilar artery insufficiency, vestibular atelectasis, and metastatic carcinoma. Meniere's disease (endolymphatic hydrops) patients describe tinnitus, fluctuating hearing loss, and frequent episodes of vertigo of duration limited to hours. Caloric responses are normal early in the course of endolymphatic hydrops. Tinnitus and hearing losses are much more common in the presentation of vestibular schwannoma than is vertigo. Patients can have signs of brainstem compression and often have other deficits in cranial nerves, primarily V and VII. The majority of perilymphatic fistula patients describe "popping" while straining as a precipitating event to their symptoms. Vertigo is often positional with fluctuating hearing loss and normal caloric testing. Cerebellar infarction can be caused by hemorrhagic or ischemic events in the distribution of the anterior inferior or posterior inferior cerebellar arteries. These patients report symptoms consistent with the single attack variant of vestibular neuritis. Multiple sclerosis is a demyelinating disease of mainly white matter. Early symptoms include blurred vision, vertigo, cranial nerve palsies, and awkward extremity use. Nystagmus, scanning speech, and intention tremors occur later. There is no sex predilection and patients are typically in their third to fourth decades of life when diagnosed. This disease has an average duration of 20 years from discovery until eventual death. Findings of oligoclonal banding in CSF and white matter plaques on MRI scanning help establish the diagnosis. Disequilibrium of aging is due to degenerative changes seen in the vestibular labyrinth and to interference with fluid motion within labyrinthine sense organs. Sudden head movements exacerbate the vertigo. Basilar artery insufficiency is caused by occlusion of the vestibular branch of the internal auditory artery. This most often occurs in an older age group of people who also have high frequency hearing loss. Additional neurotologic findings are not uncommon. Collapse of vestibular membranous structures either primarily or as a component of another process such as endolymphatic hydrops is described as vestibular atelectasis. The most likely etiologies include viral and degenerative changes seen in aging patients. The principle symptom is unsteadiness with head movement that is not amenable to medical management but is not severe enough to warrant surgical therapy. The symptoms associated with metastatic carcinoma to the temporal bone depend on where the metastasis occurs and can include vertigo or unsteadiness. Work-up of patients with vestibular neuritis begins with thorough history and physical examination. Audiometry and vestibular testing are the cornerstones to diagnosis with imaging and laboratory studies being guided by findings on examination. Bedside examination includes Doll's eye test, head shaking nystagmus, dynamic visual acuity, caloric testing, rotational testing, past pointing, Romberg and Fukuda tests, and tandem walking. Treatment is primarily supportive with reassurance that symptoms will resolve in most cases. Vestibular suppressants are reserved for patients with severe symptomatology. Medical labyrinthine ablation or surgical therapy are rarely indicated. In conclusion, the characteristic symptom complex of unilateral vestibular weakness without auditory or other central nervous system pathology comprises vestibular neuritis. Vestibular nerve atrophy or degeneration may occur but vascular etiologies are unlikely. Treatment is primarily conservative and the majority of patients will recover in 3-6 months. Refractory cases should be investigated for other etiologies.
Case Presentation A 65-year-old white man presented to the Otolaryngology clinic with a three-day history of severe vertigo. He reported nausea and vomiting for the first two days of his illness but successfully ate breakfast on the day he was seen in clinic. He denied hearing loss and tinnitus. His past medical and surgical histories were unremarkable. He had no previous exposure to ototoxic drugs and denied further neurologic symptoms. Physical examination revealed an obviously uncomfortable white male in a wheelchair. Otologic examination was without abnormality. Weber testing with a 512 hz tuning fork was to midline. Romberg and Fukuda testing indicated right-sided pathology. Other than a crisp left beating nystagmus, cranial nerve examination was normal. In light of the nystagmus and severe vertigo, the Dix-Hallpike maneuver was not done. Audiometry revealed a symmetrical mild-to-moderate high frequency hearing loss. Acoustic reflexes were mildly elevated bilaterally with adequate speech understanding. Type A tympanograms were present bilaterally. The patient was treated with valium, m q 8 hours. He returned to the clinic 7 days later, able to walk and with persistent unsteadiness. Electronystagmography performed one week later revealed 30% unilateral weakness on the right with a 55% directional preponderance to the right. Rotatory testing revealed a right peripheral disorder. On return clinic follow-up he had a residual feeling of unsteadiness but no vertigo. Bibliography Adour KK, Sprague MA, Hilsinger RL Jr. Vestibular vertigo: a form of polyneuritis? JAMA 1981;246:1564-1567. Baloh FW, Honrubia V. Clinical Neurophysiology of the Vestibular System, ed. 2. Philadelphia: F.A. Davis, 1990. Baloh RW, Jacobson K, Honrubia V. Idiopathic bilateral vestibulopathy. Neurology 1989;39:272-275. Brandt T, Dieterich M. Vestibular falls. J Vestibular Res 1993;3:3-14. Brantberg K, Magnusson M. The dynamics of the vestibulo-ocular reflex in patients with vestibular neuritis. Am J Otolaryngol 1990;11:345-351. Coats AC. Vestibular neuronitis. Tran Am Acad Ophthalmol Otolaryngol 1969;73:395-408. Davis LE. Infections of the labyrinth. In: Cummings CW, Harker LA, eds. Otolaryngology - Head and Neck Surgery, Vol. 4. St. Louis: Mosby, 1993:2795-2807. Davis LE, Shurin S, Johnson RT. Experimental viral labyrinthitis. Nature 1975;254:329-331. Davis LE. Comparative experimental viral labyrinthitis. Am J Otolaryngol 1990;11:382-388. Disher MJ, Telian SA, Kemink JL. Evaluation of acute vertigo: unusual lesions imitating vestibular neuritis. Am J Otol 1991;12:227-231. Fluur E. Interaction between the utricles and the horizontal semicircular canals. IV. Tilting of human patients with acute unilateral vestibular neuritis. Acta Otolaryngol 1973;76:349-352. Gagey PM, Toupet M. Orthostatic postural control in vestibular neuritis: a stabilometric analysis. Ann Otol Rhinol Laryngol 1991;100:971-975. Karmody CS. Viral labyrinthitis: early pathology in the human. Laryngoscope 1983;93:1527-1533. Kemink JL, Telian SA, El-Kashlan H, Langman AW. Retrolabyrinthine vestibular nerve section: efficacy in disorders other than Meniere's disease. Laryngoscope 1991;101:523-528. Lachman J, Stahle J. Vestibular neuritis: a clinical and electronystagmographic study. Neurology 1967;17:376-380. Lindsay JR, Vital labyrinthitis - histopathologic characteristics. Acta Otolaryngol 1967;63:138-143. Magnusson M, Brantberg K, Pyykkö, Schalén L. Reduction of the time constant in the VOR as a protective mechanism in acute vestibular lesions. Acta Otolaryngol Suppl 1989;468:329-332. Montandon PB, Häusler R. Relevance of otopathological findings in the treatment of dizzy patients. Ann Otol Rhinol Laryngol Suppl 1984;112:12-16. Pfaltz CR. Vestibular compensation: physiological and clinical aspects. Acta Otolaryngol 1983;95:402-406. Rahko T, Karma P. New clinical finding in vestibular neuritis: high-frequency audiometry hearing loss in the affected ear. Laryngoscope 1986;96:198-199. Schuknecht HF, Kitamura K., Vestibular neuritis. Ann Otol Rhinol Laryngol Suppl 1981;78:1-19. Schuknecht HF, Witt RL. Acute bilateral sequential vestibular neuritis. Am J Otolaryngol 1985;6:255-257. Yoneda S, Tokumasu K. Frequency analysis of body sway in the upright posture: statistical study in cases of peripheral vestibular disease. Acta Otolaryngol 1986;102:87-92. Grand Rounds Archive | Department Home page BCM Public | BCM Intranet | Privacy Notices | Contact BCM | BCM Site Map | ©2001-2006 Baylor College of Medicine
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