Journal List > J Korean Med Assoc > v.51(11) > 1042093

Choi and Goh: Vestibular Neuritis and Bilateral Vestibulopathy

Abstract

Vestibular neuritis is the second most common cause of peripheral vestibular vertigo. The key signs and symptoms are the acute onset of sustained rotatory vertigo without hearing loss, postural imbalance with Romberg's sign, and peripheral type nystagmus. Head thrust and caloric tests show ipsilateral hyporesponsiveness, but hearing test shows normal. Either an inflammation of the vestibular nerve or labyrinthine ischemia was proposed as a cause of vestibular neuritis. Recovery after vestibular neuritis is usually incomplete. Despite the assumed viral cause, the effects of corticosteroids, antiviral agents, or the two in combination are uncertain. Bilateral vestibulopathy is a rare disorder of the peripheral labyrinth or the eighth nerve. The most frequent etiologies include ototoxicity, autoimmune disorders, meningitis, neuropathies, sequential vestibular neuritis, cerebellar degeneration, tumors, and miscellaneous otological diseases. The two key symptoms are unsteadiness of gait and oscillopsia associated with head movements or when walking. The diagnosis is made with the simple bedside tests for defective vestibulo-ocular reflex (head thrust and dynamic visual acuity tests). Bilateral vestibulopathy is confirmed by the absence of nystagmus reaction to both caloric and rotatory chair tests. The spontaneous recovery is relatively rare and incomplete. Vestibular rehabilitation is supportive of the improvement, but the efficacy of physical therapy is limited.

Figures and Tables

Figure 1
Spontaneous nystagmus in a patient with right vestibular neuritis. The fast phases of mixed torsional-horizontal nystagmus directs toward the intact ear. The nystagmus increases with gaze in the direction of nystagmus, and decreases with gaze in the opposite direction. Visual fixation markedly suppress the nystagmus.
*Recording of horizontal eye movement of the left eye
Recording of vertical eye movement of the left
Recording of torsional eye movement of the left eye
jkma-51-992-g001
Figure 2
Bithermal caloric tests show a complete canal paresis in the left ear in a patient with left vestibular neuritis.
jkma-51-992-g002
Figure 3
Rotatory chair test shows increased phase lead and the asymmetry with normal gain of the vestibulo-ocular reflex in a patient with left vestibular neuritis.
jkma-51-992-g003
Figure 4
Ocular torsion to the left side in a patient with left vestibular neuritis.
jkma-51-992-g004
Figure 5
Normal vestibular- evoked myogenic potentials in a patient with right vestibular neuritis.
jkma-51-992-g005
Figure 6
Posturographic data in a patient with vestibular neuritis. The scores of condition 4, 5, 6 are decreased.
jkma-51-992-g006
Figure 7
Bithermal caloric tests show markedly decreased respones to warm and cold stimulation bilaterally in a patient with bilateral vestibulopathy.
jkma-51-992-g007
Figure 8
Rotatory chair test shows increased phase lead and decreased gain of the vestibulo-ocular reflex in a patient with bilateral vestibulopathy.
jkma-51-992-g008
Table 1
Commonly used antivertiginous and antiemetic drugs
jkma-51-992-i001
Table 2
Causes of bilateral vestibulopathy
jkma-51-992-i002

References

1. Leigh RJ, Zee DS, editors. The neurology of eye movements. 2006. 4th ed. New York: Oxford University;20–81.
2. Goldberg JM, Fernandez C. Physiology of peripheral neurons innervating semicircular canals of the squirrel monkey. I. Resting discharge and response to constant angular acceleration. J Neurophysiol. 1971. 34:635–660.
crossref
3. Miles FA, Braitman DJ. Long-term adaptive changes in primate vestibuloocular reflex. II. Electrophysiological observations on semicircular canal primary afferents. J Neurophysiol. 1980. 43:1426–1436.
crossref
4. Baloh RW. Clinical practice. Vestibular neuritis. N Engl J Med. 2003. 348:1027–1032.
5. Rinne T, Bronstein AM, Rudge P, Gresty MA, Luxon LM. Bilateral loss of vestibular function. Acta Otolaryngol. 1995. 520:247–250.
crossref
6. Kroenke K, Hoffman RM, Einstadter D. How common are various causes of dizziness?: A critical review. S Med J. 2000. 93:160–167.
crossref
7. Nedzelski JM, Barber HO, McIlmoyl L. Diagnosis in a dizziness unit. J Otolaryngol. 1986. 15:101–104.
8. Baloh RW, Halmagyi GM, editors. Disorders of the vestibular system. 1996. New York: Oxford University;318–327.
9. Choi KD, Oh SY, Kim HJ, Koo JW, Cho BM, Kim JS. Recovery of vestibular imbalances after vestibular neuritis. Laryngoscope. 2007. 117:1307–1312.
crossref
10. Safran AB, Vibert D, Issoua D, Hausler R. Skew deviation after vestibular neuritis. Am J Ophthalmol. 1994. 118:238–245.
crossref
11. Furman JM, Cass SP, editors. Vestibular disorders: a case-study approach. 2003. 3rd ed. New York: FA Davis;21–29.
12. Halmagyi GM, Curthoys IS. A clinical sign of canal paresis. Arch Neurol. 1988. 45:737–739.
crossref
13. Schubert MC, Tusa RJ, Grine LE, Herdman SJ. Optimizing the sensitivity of the head thrust test for identifying vestibular hypofunction. Phys Ther. 2004. 84:151–158.
crossref
14. Cremer PD, Halmagyi GM, Aw ST, Curthoys IS, McGarvie LA, Todd MJ, Black RA, Hannigan IP. Semicircular canal plane head impulses detect absent function of individual semicircular canals. Brain. 1998. 121:699–716.
crossref
15. Colebatch JG, Halmagyi GM, Skuse NF. Myogenic potentials generated by a click-evoked vestibulocollic reflex. J Neurol Neurosurg Psychiatry. 1994. 57:190–197.
crossref
16. Murofushi T, Halmagyi GM, Yavor RA, Colebatch JG. Absent vestibular evoked myogenic potentials in vestibular neurolabyrinthitis. An indicator of inferior vestibular nerve involvement? Arch Otolaryngol Head Neck Surg. 1996. 122:845–848.
crossref
17. Hilding DA, Kanda T, House WF. Vestibular neuronitis and small acoustic neuroma: electron microscopic observations. Otol Clin N Am. 1968. 1:305–318.
crossref
18. Schuknecht HF, Kitamura K, Louis H Second. Clerf lecture, Vestibular neuritis. Ann Otol Rhinol Laryngol Suppl. 1981. 90:1–19.
19. Hirata T, Sekitani T, Okinaka Y, Matsuda Y. Serovirological study of vestibular neuronitis. Acta Otolaryngol Suppl. 1989. 468:371–373.
crossref
20. Kim JS, Lopez I, DiPatre PL, Liu F, Ishiyama A, Baloh RW. Internal auditory artery infarction: clinicopathologic correlation. Neurology. 1999. 52:40–44.
crossref
21. Fetter M, Dichgans J. Vestibular neuritis spares the inferior division of the vestibular nerve. Brain. 1996. 119:755–763.
crossref
22. Hotson JR, Baloh RW. Acute vestibular syndrome. N Engl J Med. 1998. 339:680–685.
crossref
23. Newman-Toker DE, Kattah JC, Alvernia JE, Wang DZ. Normal head impulse test differentiates acute cerebellar strokes from vestibular neuritis. Neurology. 2008. 70:2378–2385.
crossref
24. Selesnick SH, Jackler RK, Pitts LW. The changing clinical presentation of acoustic tumors in the MRI era. Laryngoscope. 1993. 103:431–436.
crossref
25. Ishikawa K, Edo M, Togawa K. Clinical observation of 32 cases of vestibular neuronitis. Acta Otolaryngol Suppl. 1993. 503:13–15.
crossref
26. Okinaka Y, Sekitani T, Okazaki H, Miura M, Tahara T. Progress of caloric response of vestibular neuronitis. Acta Otolaryngol Suppl. 1993. 503:18–22.
crossref
27. Bergenius J, Perols O. Vestibular neuritis: a follow-up study. Acta Otolaryngol. 1999. 119:895–899.
crossref
28. Meran A, Pfaltz CR. The acute vestibular paralysis. Arch Otorhinolaryngol. 1975. 209:229–244.
29. Cameron SA, Dutia MB. Lesion-induced plasticity in rat vestibular nucleus neurones dependent on glucocorticoid receptor activation. J Physiol. 1999. 518:151–158.
crossref
30. Kitahara T, Kondoh K, Morihana T, Okumura S, Horii A, Takeda N, Kubo T. Steroid effects on vestibular compensation in human. Neurol Res. 2003. 25:287–291.
crossref
31. Strupp M, Zingler VC, Arbusow V, Niklas D, Maag KP, Dieterich M, Bense S, Theil D, Jahn K, Brandt T. Methylprednisolone, valacyclovir, or the combination for vestibular neuritis. N Engl J Med. 2004. 351:354–361.
crossref
32. Cooksey FS. Rehabilitation in vestibular injury. Proc R Soc Med. 1946. 39:273–278.
33. Viber D, liard P, Hausler R. Bilateral idiopathic loss of peripheral vestibular function with normal hearing. Acta Otolaryngol. 1995. 115:611–615.
crossref
34. Dandy WE. The surgical treatment of Meniere's disease. Surg Gynecol Obstet. 1941. 72:421–425.
35. Bhansali SA, Stockwell CW, Bojrab DI. Oscillopsia in patients with loss of vestibular function. Otolaryngol Head Neck Surg. 1993. 109:120–126.
crossref
36. Chamber BR, Mai M, Barber HO. Bialteral vestibular loss, oscillopsia, and the cervico-ocular reflex. Otolaryngol Head Neck Surg. 1985. 93:403–407.
37. Mayer E, Bernstein J, Fostiropolous G. Salicylate ototoxicity. A clinical study. N Engl J Med. 1965. 273:587.
38. Rinne T, Bronstein AM, Rudge P, Gresty MA, Luxon LM. Bilateral loss of vestibular function: clinical findings in 53 patients. J Neurol. 1998. 245:314–321.
crossref
39. McGath JH, Barber HO, Stoyanoff S. Bilateral vestibular loss and oscillopsia. J Otolaryngol. 1989. 18:218–221.
40. Furman JM, Kamerer DB. Rotational responses in patients with bilateral caloric reduction. Acta Otolaryngol. 1989. 108:355–361.
crossref
41. Rinne T, Bronstein AM, Rudge P, Gresty MA, Luxon LM. Bilateral loss of vestibular function. Acta Otolaryngol. 1995. 520:247–250.
crossref
42. Gillespie MB, Minor LB. Prognosis in bilateral vestibular hypofunction. Laryngoscope. 1999. 109:35–41.
crossref
TOOLS
Similar articles