Beruflich Dokumente
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clinical practice
Vestibular Neuritis
Robert W. Baloh, M.D.
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 authors 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 Surgery (Head and Neck), UCLA School
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. of
ward the affected side. Autonomic symptoms including malaise, pallor, sweating, nau- Neurology, Box 951769, Los Angeles, CA
sea, and vomiting are nearly always present. 90095-1769, or at rwbaloh@ucla.edu.
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 type
of the spontaneous nystagmus, the results of the head-thrust test (described below),
the severity of the imbalance, and the presence or absence of associated neurologic
signs. Spontaneous nystagmus of peripheral origin is typically horizontal with a tor-
sional (rotational) component; it does not change direction with a change in gaze. By
contrast, 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 patients head and applying a brief, small-ampli-
tude, high-acceleration head turn, first to one side and then to the other. To start, the
eyes 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 fixates
on the examiners nose and the examiner watches for corrective rapid eye movements
(saccades), which are a sign of decreased vestibular response (i.e., the eyes move with
the head rather than staying fixed on the nose). If catch-up saccades occur after head
thrusts in one direction but not after those in the other direction, this indicates the
presence of a peripheral vestibular lesion on that side (in the labyrinth or the 8th nerve
including the roots 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 origin
are 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
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 division
over the course of a few weeks. Some patients can of the vestibular nerve, with sparing of the inferior
have 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 paroxysmal
result from a selective inflammation of the vestibu- positional vertigo (originating from the posterior
lar nerve, presumably of viral origin. The facts that semicircular canal) often develops as a sequela even
the 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 Selective
bers 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 the
a viral cause.3 Postmortem studies have found atro- bony canals of the two divisions11 might explain
phy of the vestibular nerve and the vestibular sen- this relative vulnerability.
sory epithelium that is similar to the pathological
findings with known viral disorders of the inner ear, strategies and evidence
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-
Vestibular Develops over a period of hours; Spontaneous peripheral nys- Electronystagmography: unilateral caloric hypo-
neuritis resolves over a period of days; tagmus; positive head-thrust excitability
may follow an influenza-like test; imbalance Audiography: normal
illness Brain imaging: normal
Labyrinthitis Develops over a period of minutes Same as for vestibular neuritis, Electronystagmography: unilateral caloric hypoex-
to hours; may be associated but also unilateral hearing citability
with systemic, ear, or menin- loss Audiography: moderate-to-severe ipsilateral
geal infection sensorineural hearing loss
Brain imaging: normal
Labyrinthine Abrupt onset; previous vascular Same as for vestibular neuritis, Electronystagmography: absence of a unilateral ca-
infarction disease; may be associated but also unilateral hearing loric response
with neurologic symptoms loss; may be associated with Audiography: severe ipsilateral sensorineural hear-
neurologic signs ing loss
Brain imaging: MRI may show silent brain infarcts
Perilymph Abrupt onset associated with Same as for vestibular neuritis, Electronystagmography: unilateral caloric hypo-
fistula head trauma, barotrauma, or but usually associated with excitability
sudden strain during heavy unilateral hearing loss; pos- Audiography: mild-to-moderate ipsilateral sensori-
lifting, coughing, or sneezing; sible perforation of the tym- neural hearing loss
may be associated with chron- panic membrane; positive Brain imaging: CT of temporal bone may show ero-
ic otitis with cholesteatoma fistula test (vertigo and nys- sion from cholesteatoma
tagmus induced by pressure
in external ear canal)
Brain-stem and Abrupt onset, history of transient Spontaneous central nystag- Electronystagmography: unilateral caloric hypoex-
cerebellar ischemic attacks and vascular mus; positive head-thrust citability if entry zone of root is involved
infarction disease; usually associated test if entry zone of root of Audiography: ipsilateral hearing loss if anterior infe-
with neurologic symptoms 8th nerve is involved; usually rior cerebellar artery is involved
focal neurologic signs Brain imaging: MRI shows infarction in medulla,
pons, or cerebellum
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 initial
ally be confident in the diagnosis of a unilateral pe- dose (Table 2) is not effective, higher doses should
ripheral 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 neurons
they 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 gastrointestinal
considered. Menieres syndrome can initially present tract. All the medications can be sedating, so they
with vertigo alone, but attacks rarely last longer than should not be used when patients are engaged in
four to five hours. The diagnosis requires recurrent activities that require a high level of alertness, such
attacks with associated hearing loss. A positive head- as driving, operating machinery, or participating in
thrust test can occur with brain-stem infarction in- athletic activities. Less sedating drugs such as oral
volving the entry zone of the root of the 8th nerve, meclizine and transdermal scopolamine are useful
but invariably, there will be other associated signs for milder vertigo and prevention of motion sick-
of the lateral brain stem (e.g., Horners syndrome, ness. Because of the multiple effects of each of these
facial numbness and weakness, hemiataxia, and dys- drugs, possible drug interactions should always be
arthria). 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 and
central vestibular compensation for the imbalance
therapy 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 permanent
underlying disease, but because the pathophysiol- unilateral loss of vestibular function. Recovery from
ogy 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 complete
agents, antidopaminergic agents, and g-aminobu- if the patient begins exercising as soon as possible
tyric acidenhancing (GABAergic) agents (Table after the occurrence of a vestibular lesion.16 The
2).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 animals17
there 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 to
hydrinate (50 mg) with lorazepam (2 mg)13 and the the final level of recovery. In animals, compensation
other 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 leads
emergency 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 and
During the acute phase, because of severe nausea balance.21 While nystagmus is present, the patient
and decreased gastric motility, the intramuscular should try to suppress it with fixation in all posi-
Range of Doses
Usual and Frequency of Antiemetic
Drug Starting Dose Administration Action Common Precautions Common Side Effects Common Drug Interactions
Dimenhydrinate 50 mg IM, IV, 25100 mg every Moderate Asthma, glaucoma, pros- Dryness, drowsiness Alcohol, hypnotics, antidepressants, sed-
(Dramamine) or orally 48 hr tate enlargement atives, tranquilizers
Promethazine 25 mg IM, IV, 12.550 mg every Moderate Same as for dimenhydrinate Same as for dimenhydrinate Same as for dimenhydrinate
(Phenergan) orally, or by 48 hr
The
suppository
Meclizine (Antivert, 25 mg orally 12.550 mg every Mild Same as for dimenhydrinate Same as for dimenhydrinate Same as for dimenhydrinate
Bonine) 48 hr
Scopolamine 0.2 mg IM or 0.10.4 mg every Moderate Same as for dimenhydrinate Dryness, visual blurring, memory Alcohol, antidepressants, antihistamines,
www.nejm.org
Prochlorperazine 10 mg IM, IV, 520 mg every Prominent Same as for droperidol Same as for droperidol Alcohol, anesthetics, propranolol, pheny-
of
Lorazepam (Ativan) 1 mg IM, IV, or 0.52 mg every Mild Same as for diazepam Same as for diazepam Same as for diazepam
march 13 , 2003
Downloaded from nejm.org at UAB LISTER HILL LIBRARY on December 22, 2012. For personal use only. No other uses without permission.
clinical practice
refer enc es
1. Hotson JR, Baloh RW. Acute vestibular tomic considerations in vestibular neuritis. tral vestibulospinal compensation after ves-
syndrome. N Engl J Med 1998;339:680-5. Otol Neurotol 2001;22:512-8. tibular neuritis. Neurology 1998;51:838-44.
2. Halmagyi GM, Curthoys IS. A clinical 12. Rascol O, Hain TC, Brefel C, Benazet M, 20. Peppard SB. Effect of drug therapy on
sign of canal paresis. Arch Neurol 1988;45: Clanet M, Montastruc JL. Antivertigo medi- compensation from vestibular injury. Laryn-
737-9. cations and drug-induced vertigo: a pharma- goscope 1986;96:878-98.
3. Baloh RW, Honrubia V. Clinical neuro- 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
4. Schuknecht HF, Kitamura K. Second treatment of vertigo in the emergency depart- University Press, 1996:583-97.
Louis H. Clerf Lecture: vestibular neuritis. ment: a randomized clinical trial. Ann Emerg 22. Adour KK, Ruboyianes JM, Von Doer-
Ann Otol Rhinol Laryngol Suppl 1981;90: Med 2000;36:310-9. sten PG, et al. Bells palsy treatment with acy-
1-19. 14. Irving C, Richman P, Kaiafas C, Eskin B, clovir and prednisolone compared with pred-
5. Baloh RW, Ishiyama A, Wackym PA, 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- 1996;105:371-8.
Neck Surg 1996;114:586-92. gency department: a randomized clinical trial. 23. Wood MJ, Johnson RW, McKendrick MW,
6. Davis LE. Comparative experimental Acad Emerg Med 2002;9:650-3. 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
1990;11:382-8. zina H, Straumann D. Caloric and search-coil and without prednisolone for treatment of
7. 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; 896-900.
herpes simplex virus. Acta Otolaryngol Suppl 2:72-8. 24. Ariyasu L, Byl FM, Sprague MS, Adour
1993;503:79-81. 16. Cooksey FS. Rehabilitation in vestibular KK. The beneficial effect of methylpredniso-
8. Fetter M, Dichgans J. Vestibular neuritis injuries. Proc R Soc Med 1946;39:273-8. lone in acute vestibular vertigo. Arch Oto-
spares the inferior division of the vestibular 17. Igarashi M, Ishikawa K, Ishii M, Yamane laryngol Head Neck Surg 1990;116:700-3.
nerve. Brain 1996;119:755-63. H. Physical exercise and balance compensa- 25. Stokroos RJ, Albers FWJ, Tenvergert EM.
9. Schuknecht HF. Positional vertigo: clin- tion after total ablation of vestibular organs. Antiviral treatment of idiopathic sudden sen-
ical and experimental observations. Trans Prog Brain Res 1988;76:395-401. sorineural hearing loss: a prospective, ran-
Am Acad Ophthalmol Otol 1962;66:319-31. 18. Herdman SJ, Clendaniel RA, Mattox DE, domized, double-blind clinical trial. Acta
10. Arbusow V, Schulz P, Strupp M, et al. Holliday MJ, Niparko JK. Vestibular adapta- Otolaryngol 1998;118:488-95.
Distribution of herpes simplex virus type 1 tion exercises and recovery: acute stage after 26. Furstenberg AC, Lashmet FH, Lathrop
in human geniculate and vestibular ganglia: acoustic neuroma resection. Otolaryngol F. Mnires symptom complex: medical treat-
implications for vestibular neuritis. Ann Neu- Head Neck Surg 1995;113:77-87. ment. Ann Otol Rhinol Laryngol 1934;43:
rol 1999;46:416-9. 19. Strupp M, Arbusow V, Maag KP, Gall C, 1035-46.
11. Goebel JA, OMara W, Gianoli G. Ana- Brandt T. Vestibular exercises improve cen- Copyright 2003 Massachusetts Medical Society.