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030313 vestibular neuritis

The new england journal of medicine This Journal feature begins with a case vignette highlighting a common clinical problem. Evidence supporting various strategies is then presented, followed by a review of formal guidelines, when they exist. The article ends with the author’s clinical recommendations. A 53-year-old man awoke in the morning with acute dizziness. He staggered to the
bathroom, where he vomited repeatedly. When he was seen at a local emergency room
12 hours later, he had left-beating nystagmus in all positions of gaze but otherwise no
focal neurologic findings. How should he be evaluated and treated?

Acute spontaneous vertigo results from an imbalance in tonic vestibular activity. The From the Departments of Neurology and patient has an intense sensation of rotation that is aggravated by head motion and of Medicine, Los Angeles. Address reprint change of position. It is difficult to stand and to walk, and there is a tendency to veer to- requests to Dr. Baloh at the UCLA Dept. ofward the affected side. Autonomic symptoms including malaise, pallor, sweating, nau- Neurology, Box 951769, Los Angeles, CA sea, and vomiting are nearly always present.
The first task of the examining physician is to determine whether the vertigo is of N Engl J Med 2003;348:1027-32.
central or peripheral origin, since some central causes of acute vertigo, such as cerebel- Copyright 2003 Massachusetts Medical Society.
lar hemorrhage or infarction, can be life-threatening and may require immediate inter-vention.1 This differentiation can usually be made at the bedside on the basis of the typeof the spontaneous nystagmus, the results of the head-thrust test (described below),the severity of the imbalance, and the presence or absence of associated neurologicsigns. Spontaneous nystagmus of peripheral origin is typically horizontal with a tor-sional (rotational) component; it does not change direction with a change in gaze. Bycontrast, spontaneous nystagmus of central origin is often purely horizontal, vertical,or torsional and usually changes direction with changes in the position of the gaze.
The head-thrust test is a simple bedside test of the horizontal vestibulo-ocular re- flex.2 It is performed by grasping the patient’s head and applying a brief, small-ampli-tude, high-acceleration head turn, first to one side and then to the other. To start, theeyes should be about 10 degrees away from the primary position in the orbit so that af-ter a 10-degree head turn, the eyes will be near the primary position. The patient fixateson the examiner’s nose and the examiner watches for corrective rapid eye movements(saccades), which are a sign of decreased vestibular response (i.e., the eyes move withthe head rather than staying fixed on the nose). If “catch-up” saccades occur after headthrusts in one direction but not after those in the other direction, this indicates thepresence of a peripheral vestibular lesion on that side (in the labyrinth or the 8th nerveincluding the root’s entry zone in the brain stem).
Patients with an acute peripheral vestibular lesion typically can stand, although they will veer toward the side of the lesion. By contrast, patients with vertigo of central originare often unable to stand without support. Associated neurologic signs such as dysar-thria, incoordination, numbness, or weakness suggest a central origin.
The syndrome of acute, prolonged vertigo of peripheral origin is commonly called vestibular neuritis, although other terms such as “vestibular neuronitis,” “labyrinthitis,”“neurolabyrinthitis,” and “unilateral vestibulopathy of unknown cause” have also been Downloaded from www.nejm.org at ST MATTHEWS UNIV SCH MED on August 12, 2005 . Copyright 2003 Massachusetts Medical Society. All rights reserved. The new england journal of medicine used.3 The vertigo typically develops over a period labyrinth (horizontal and anterior semicircular ca-of hours, is severe for a few days, and then subsides nals and utricle) supplied by the superior divisionover the course of a few weeks. Some patients can of the vestibular nerve, with sparing of the inferiorhave residual nonspecific dizziness and imbalance part (posterior semicircular canal and saccule) sup-that lasts for months. The condition is thought to plied by the inferior division.8 Benign paroxysmalresult from a selective inflammation of the vestibu- positional vertigo (originating from the posteriorlar nerve, presumably of viral origin. The facts that semicircular canal) often develops as a sequela eventhe disorder often has a viral prodrome, that it oc- if the patient has no remaining function in the hor-curs in epidemics, that it may affect several mem- izontal or anterior semicircular canal.3,9 Selectivebers of the same family, and that it occurs more inflammation of the superior division of the ves-commonly in spring and early summer all support tibular nerve10 or anatomical differences in thea viral cause.3 Postmortem studies have found atro- bony canals of the two divisions11 might explainphy of the vestibular nerve and the vestibular sen- this relative vulnerability.
sory epithelium that is similar to the pathologicalfindings with known viral disorders of the inner ear, s t r a t e g i e s a n d e v i d e n c e such as measles and mumps.4,5 Several viruses se-
lectively infect the labyrinth, the 8th nerve, or both diagnosis
in animal models.6,7
As indicated above, the key differentiation is be- A common feature of vestibular neuritis is se- tween peripheral and central causes of acute, pro- lective damage to the superior part of the vestibular longed vertigo (Table 1). On the basis of the appear- Table 1. Differential Diagnosis of Common Causes of Acute, Prolonged Vertigo.*
Physical Examination
Laboratory Testing†
Electronystagmography: unilateral caloric hypo- Develops over a period of minutes Same as for vestibular neuritis, Electronystagmography: unilateral caloric hypoex- Audiography: moderate-to-severe ipsilateral Electronystagmography: absence of a unilateral ca- loss; may be associated with Audiography: severe ipsilateral sensorineural hear-neurologic signs Brain imaging: MRI may show silent brain infarcts Electronystagmography: unilateral caloric hypo- Audiography: mild-to-moderate ipsilateral sensori- Brain imaging: CT of temporal bone may show ero- tagmus induced by pressure in external ear canal) Brain-stem and Abrupt onset, history of transient Electronystagmography: unilateral caloric hypoex- citability if entry zone of root is involved Audiography: ipsilateral hearing loss if anterior infe- Brain imaging: MRI shows infarction in medulla, * Prolonged vertigo is defined as vertigo lasting more than a few hours.
† Expected results of these tests are given. However, it should be noted that these tests are not routinely recommended, except for magnetic resonance imaging (MRI) of the brain, if a central cause is suspected. CT denotes computed tomography.
Downloaded from www.nejm.org at ST MATTHEWS UNIV SCH MED on August 12, 2005 . Copyright 2003 Massachusetts Medical Society. All rights reserved. ance of the nystagmus, a positive head-thrust test, or intravenous route is usually preferable. The re-and a negative neurologic examination, one can usu- sponse is clearly dose-dependent, so if the initialally be confident in the diagnosis of a unilateral pe- dose (Table 2) is not effective, higher doses shouldripheral vestibulopathy. Electronystagmography, be tried.
if available, can document the unilateral vestibular Although the exact mechanism of action of these loss (i.e., unilateral caloric hypoexcitability) but is drugs is unclear, they act at the level of the neuro-rarely necessary. Currently, viral studies (serologic transmitters involved in the propagation of impuls-analysis or cultures) are not recommended, since es from primary to secondary vestibular neuronsthey cannot prove a causal relation between a viral and in the maintenance of tone in the vestibular nu-infection and the vestibular syndrome.
clei. They also act on the areas of the nervous sys- When there is associated unilateral hearing loss, tem that control vomiting, including central com- inner-ear disorders such as labyrinthitis, labyrin- ponents loosely described as the “emetic center”thine infarction, and perilymph fistula should be and peripheral components in the gastrointestinalconsidered. Meniere’s syndrome can initially present tract. All the medications can be sedating, so theywith vertigo alone, but attacks rarely last longer than should not be used when patients are engaged infour to five hours. The diagnosis requires recurrent activities that require a high level of alertness, suchattacks with associated hearing loss. A positive head- as driving, operating machinery, or participating inthrust test can occur with brain-stem infarction in- athletic activities. Less sedating drugs such as oralvolving the entry zone of the root of the 8th nerve, meclizine and transdermal scopolamine are usefulbut invariably, there will be other associated signs for milder vertigo and prevention of motion sick-of the lateral brain stem (e.g., Horner’s syndrome, ness. Because of the multiple effects of each of thesefacial numbness and weakness, hemiataxia, and dys- drugs, possible drug interactions should always bearthria). Magnetic resonance imaging of the brain is considered before use (Table 2).
indicated if there are associated neurologic symp- Recovery from a peripheral vestibular lesion re- toms and signs, if the onset is sudden in a patient sults from a combination of the restoration of pe-with risk factors for stroke, or if there is a new, se- ripheral labyrinthine function (which is usually in-vere headache accompanying the vertigo.1 complete in the case of vestibular neuritis)15 andcentral vestibular compensation for the imbalance in vestibular tone. In other words, patients will Of course, the best approach would be to treat the typically get better even if they have a permanentunderlying disease, but because the pathophysiol- unilateral loss of vestibular function. Recovery fromogy is uncertain and there is no established treat- vestibular neuritis typically takes several weeks,ment, symptomatic therapy is typically used. The although longer periods of recovery are not uncom-main classes of drugs used for symptoms of acute mon. Clinicians have long felt that vestibular com-vertigo include antihistamines, anticholinergic pensation occurs more rapidly and is more completeagents, antidopaminergic agents, and g-aminobu- if the patient begins exercising as soon as possibletyric acid–enhancing (GABAergic) agents (Table after the occurrence of a vestibular lesion.16 The2).3 These drugs do not eliminate but rather reduce goal of vestibular exercises is to accelerate the proc-the severity of vertiginous symptoms. They are ef- ess of vestibular compensation and improve the fi-fective in most patients with vestibular neuritis, but nal level of recovery. Controlled studies in animals17there have been few controlled studies comparing and humans18,19 indicate that exercising can accel-them in terms of efficacy.12 Two recent randomized, erate the recovery of balance after a peripheral ves-clinical trials, one comparing intravenous dimen- tibular lesion, but data are lacking with regard tohydrinate (50 mg) with lorazepam (2 mg)13 and the the final level of recovery. In animals, compensationother comparing intramuscular dimenhydrinate seems to be accelerated by stimulant drugs (e.g.,(50 mg) with droperidol (2.5 mg)14 for the treat- amphetamine) and slowed by sedating drugs (e.g.,ment of acute peripheral vertigo in patients in the diazepam).20 Whether more frequent exercise leadsemergency department, found that dimenhydrinate to faster improvement is unknown.
was more effective than lorazepam and that dimen- A vestibular exercise program typically includes hydrinate and droperidol were equally effective. exercises designed to improve ocular stability andDuring the acute phase, because of severe nausea balance.21 While nystagmus is present, the patientand decreased gastric motility, the intramuscular should try to suppress it with fixation in all posi- Downloaded from www.nejm.org at ST MATTHEWS UNIV SCH MED on August 12, 2005 . Copyright 2003 Massachusetts Medical Society. All rights reserved. The new england journal of medicine ommon Drug Interactions
C

Alcohol, hypnotics, antidepressants, sed- Alcohol, antidepressants, antihistamines, Alcohol, anesthetics, propranolol, pheny- of promethazine, 150 mg of meclizine, 1.2 mg of sco- used in children and elderly persons.
ommon Side Effects
C

ommon Precautions
C

ertigo.*
Antiemetic
reatment of Acute V
requency of
Range of Doses
Administration†
Starting Dose
ommonly Used for Symptomatic T
It is recommended that the following doses not be exceeded in adults during a 24-hour period: 200 mg of dimenhydrinate, 75 mg polamine (orally), 30 mg of droperidol, 60 mg of prochlorperazine, 60 mg of diazepam, and 6 mg of lorazepam. Smaller doses are With intravenous use, equipment to maintain patent airway should be available.
Downloaded from www.nejm.org at ST MATTHEWS UNIV SCH MED on August 12, 2005 . Copyright 2003 Massachusetts Medical Society. All rights reserved. tions of gaze. As the nystagmus diminishes, eye- and-head–coordination exercises can be started(e.g., staring at a visual target while oscillating the No major medical organization has proposed spe-head from side to side and up and down). Combined cific guidelines for the diagnosis and treatment ofmovements of the eyes and head involving jumping vestibular neuritis.
quickly back and forth between two widely separat-ed targets are also useful. The patient should try to stand and walk in contact with a wall or with assist- ance in the early stages. As improvement occurs,head movements should be added while the patient The diagnosis of vestibular neuritis rests on the his-is standing and walking; these head movements tory of spontaneous, prolonged vertigo, findings onshould be slow at first and later rapid and in all di- physical examination that are consistent with a uni-rections. Balance exercises such as walking with lateral peripheral vestibulopathy, and the absenceone foot placed directly in front of the other or walk- of other neurologic symptoms and signs. The firsting on a narrow beam can then be added.
line of treatment is to suppress vertigo and nausea(Table 2). For the patient in the vignette, I wouldbegin with 25 mg of promethazine intramuscular- ly, which is usually effective for suppressing verti- The best treatment for a patient who presents with go and vomiting. If the vomiting persists, I wouldan acute episode of peripheral vestibular loss is con- add 10 mg of prochlorperazine intramuscularly.
troversial, because the pathophysiology is often un- Once the vomiting subsides, less sedating oral an-certain. Assuming that vestibular neuritis is the tivertiginous drugs such as 25 mg of meclizine orresult of a viral or postviral inflammation of the ves- 50 mg of dimenhydrinate can be used, but only fortibular nerve, treatment aimed at stopping the in- a few days, until the acute vertigo subsides. Theflammation has been proposed. The combination commonly used oral vestibular suppressants re-of corticosteroids and an antiviral agent such as acy- quire 20 to 30 minutes for action to be initiated,clovir has been reported to be effective in treating reach a peak plasma level in 1 to 2 hours, and haveBell’s palsy22 and herpes zoster infection involving a half-life of about 8 hours.
the 7th and 8th cranial nerves.23 There are limited Vestibular exercises should be started when the data to support such strategies for the treatment of acute stage of nausea and vomiting has ended.24vestibular neuritis. In one small controlled study,24 Many of the exercises will result in dizziness. Thiscorticosteroids were more effective than placebo sensation is a necessary stimulus for compensation;in treating the acute symptoms of vestibular neu- antivertiginous medications should be avoided asritis. In addition, a randomized, double-blind trial25 much as possible in order to maximize the benefi-comparing corticosteroids plus placebo with cor- cial effect. Exercises should be done for several min-ticosteroids plus acyclovir for the treatment of utes at least twice daily but may be done as often asidiopathic, sudden sensorineural hearing loss (a the patient can tolerate.
disorder thought to represent the auditory-nerve Although corticosteroids and antiviral agents equivalent of vestibular neuritis) revealed no sig- have been suggested for treatment of vestibularnificant difference in hearing in the two groups at neuritis, so far there have been no definitive studiesone-year follow-up.
demonstrating the efficacy of these medications.
A clear problem with studies that have attempt- Since the majority of patients will have spontane- ed to evaluate treatments for vestibular neuritis is ous improvement and will be able to return to nor-that there are no well-accepted diagnostic criteria mal activities, at present, I would only recommendfor the disorder. By including anyone with isolat- symptomatic treatment of vertigo followed by a pro-ed attacks of vertigo, these studies may include a gram of vestibular exercise while we await the re-range of different conditions. As Furstenberg and sults of more definitive clinical trials.
colleagues noted in 1934,26 “The tendency to cre- Supported by grants (AG09693 and DC05224) from the National ate a disease entity by grouping a number of cases Institutes of Health.
having one symptom in common is one of the temp-tations of medical practice. Vertigo lends itself ad-mirably to this evil.” Downloaded from www.nejm.org at ST MATTHEWS UNIV SCH MED on August 12, 2005 . Copyright 2003 Massachusetts Medical Society. All rights reserved.
r e f e r e n c e s
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sign of canal paresis. Arch Neurol 1988;45: Clanet M, Montastruc JL. Antivertigo medi- compensation from vestibular injury. Laryn- cations and drug-induced vertigo: a pharma- cological review. Drugs 1995;50:777-91.
21. Herdman SJ. Vestibular rehabilitation.
physiology of the vestibular system. 3rd ed.
13. Marill KA, Walsh MJ, Nelson BK. Intra-
In: Baloh RW, Halmagyi GM, eds. Disorders New York: Oxford University Press, 2001.
venous lorazepam versus dimenhydrinate for of the vestibular system. New York: Oxford treatment of vertigo in the emergency depart- Louis H. Clerf Lecture: vestibular neuritis.
ment: a randomized clinical trial. Ann Emerg 22. Adour KK, Ruboyianes JM, Von Doer-
sten PG, et al. Bell’s palsy treatment with acy- 14. Irving C, Richman P, Kaiafas C, Eskin B,
clovir and prednisolone compared with pred- Allegra J. Intramuscular droperidol versus nisolone alone: a double-blind, randomized, Honrubia V. Vestibular neuritis: clinical- intramuscular dimenhydrinate for the treat- controlled trial. Ann Otol Rhinol Laryngol pathological correlation. Otolaryngol Head ment of acute peripheral vertigo in the emer- gency department: a randomized clinical trial.
23. Wood MJ, Johnson RW, McKendrick MW,
Taylor J, Mandal BK, Crooks J. A randomized viral neurolabyrinthitis. Am J Otolaryngol 15. Schmid-Priscoveanu A, Bohmer A, Ob-
trial of acyclovir for 7 days or 21 days with zina H, Straumann D. Caloric and search-coil and without prednisolone for treatment of Hirata Y, Sugita T, Gyo K, Yanagihara N.
head-impulse testing in patients after vestib- acute herpes zoster. N Engl J Med 1994;330: Experimental vestibular neuritis induced by ular neuritis. J Assoc Res Otolaryngol 2001; herpes simplex virus. Acta Otolaryngol Suppl 24. Ariyasu L, Byl FM, Sprague MS, Adour
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Holliday MJ, Niparko JK. Vestibular adapta- Distribution of herpes simplex virus type 1 tion exercises and recovery: acute stage after 26. Furstenberg AC, Lashmet FH, Lathrop
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11. Goebel JA, O’Mara W, Gianoli G. Ana-
Brandt T. Vestibular exercises improve cen- Copyright 2003 Massachusetts Medical Society. full text of all journal articles on the world wide web
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