eMedicine Specialties > Otolaryngology and Facial Plastic Surgery > Inner Ear

Labyrinthitis Ossificans

Author: Hilary A Brodie, MD, PhD, Professor and Chairman, Department of Otolaryngology-Head and Neck Surgery, University of California at Davis Medical Center
Coauthor(s): Andrea H Yeung, MD, BS, Clinical Instructor, Department of Otolaryngology-Head and Neck Surgery, University of California San Francisco
Contributor Information and Disclosures

Updated: Sep 9, 2008

Introduction

Background

The human osseous labyrinth is composed of endosteal, enchondral, and periosteal layers. The endosteal layer consists of bone lined with a single thin layer of cells that have numerous gaps that separate them. The enchondral layer is unique in that it reaches adult size by 23 weeks' gestation and undergoes minimal remodeling after age 2 years. The periosteal layer consists of lamellar bone and is capable of remodeling and repair.

In the absence of a pathologic condition, the lumen within the otic capsule remains stable in size and patency throughout life; however, in various diseases (eg, Paget disease of bone, osteopetrosis, otosclerosis, trauma, inflammatory and infectious conditions), new disorganized bone replaces healthy bone or obliterates spaces within the otic capsule. Labyrinthitis ossificans (LO) is the pathologic formation of new bone within the lumen of the otic capsule and is associated with profound deafness and loss of vestibular function. Cochlear ossification in this disease generally does not cross the endosteal layer or alter the architecture of the enchondral bone.

Labyrinthitis ossificans (LO) most commonly occurs as a sequela of inflammation of the inner ear that results from bacterial meningitis and subsequent purulent labyrinthitis. Other etiopathologic causes of labyrinthitis ossificans (LO) include vascular obstruction of the labyrinthine artery, temporal bone trauma, autoimmune inner ear disease, otosclerosis, leukemia, and tumors of the temporal bone. In addition, suppurative labyrinthitis associated with otitis media can cause labyrinthitis ossificans (LO).

Pathophysiology

Labyrinthitis ossificans (LO) is the pathologic ossification of spaces within the lumen of the bony labyrinth and cochlea that occurs in response to a destructive or inflammatory process (see Image 1). Regardless of the etiology, the most common region of cochlear ossification is the scala tympani of the basal turn, with the most extensive disease noted in postmeningitic cases.

Studies of the pathophysiology of deafness after meningitis suggest that an inflammatory labyrinthitis develops from the spread of infection into the inner ear via the cochlear aqueduct or internal auditory canal. In 1991, Bhatt et al proposed an animal model of pneumococcal meningitis that strengthened the hypothesis that the most likely conduit of meningogenic labyrinthitis is extension of the disease through the cochlear aqueduct.1 Because the cochlear aqueduct drains into the scala tympani adjacent to the round window, the initial concentration of inflammatory mediators occurs in this region, perhaps explaining the predominant degree of injury in this area. Another possibility for the disproportionate degree of ossification in the scala tympani of the basal turn is the relative decreased blood flow in this area. This decreased perfusion explains the propensity to develop ossification in this area, regardless of the underlying etiology.

Paparella and Sugiura outlined the pathologic stages associated with purulent labyrinthitis and the process leading to ossification of the labyrinth in laboratory animals and human beings.2 They divided the evolution of labyrinthitis ossificans (LO) into 3 characteristic stages: acute, fibrous, and ossification (see Image 2). The acute stage is characterized by purulence that fills the perilymphatic spaces but spares the endolymphatic space, followed by serofibrinous exudate. The second stage, or fibrous stage, consists of fibroblastic proliferation within the perilymphatic spaces, which begins approximately 2 weeks after the onset of infection. Angiogenesis is also present. The third, or ossification, stage is characterized by bone formation first observed in the basal turn of the cochlea as early as 2 months after the onset of infection (see Image 3).

Formation of osteoid with subsequent mineralization and remodeling obliterates the perilymphatic and endolymphatic spaces. Ossification in humans has been noted to occur within a year after meningitis, although the hearing loss may occur as early as 48 hours after infection.

In 1998, Brodie et al developed a gerbil model of labyrinthitis ossificans (LO) subsequent to Streptococcus pneumoniae –induced meningitis.3 This model demonstrates 3 main histological features: fibrosis, osteoid deposition, and osteoneogenesis. Osteoid deposition appears as homogenous, eosinophilic, and moderately cellular deposits and occurs more prominently in areas of denser fibrosis. Osteoneogenesis that involves calcification of the bone matrix and subsequent remodeling develops adjacent to the endosteal layer within the cochlea, with preservation of the normal contour of the otic capsule.

Using the same model, Nabili and Brodie documented the occurrence of osteoneogenesis and mineralization as early as 21 days postinfection, and new bone growth was shown to be active for at least 12 months.4 This study was extended by Tinling et al in 2004 to show osteoid deposition and mineralization occurring as early as 3 days postinfection and continuing at least through the first 28 days postinfection.5 Resorption of new bone and remodeling by 84 days postinfection was not apparent.

In another study, Nadol et al documented that severe inflammation occurs in the scala tympani of the basal turn where the aqueduct enters the cochlea.6 They found that reduction in the inflammatory response in the internal auditory canal occurs as it proceeds from medial to lateral. This study also documented the preservation of auditory nerve fibers despite the intense labyrinthitis and ossification with accompanying degenerative changes in the stria vascularis and organ of Corti. The number of remaining spiral ganglion cells was shown to be inversely proportional to the severity of new bone formation.

The phenomenon of labyrinthitis ossificans (LO) was recognized as early as the 19th century; however, the pathogenic mechanisms remain poorly understood. Early theories divided new bone formation into 2 types: metaplastic and osteoplastic. Metaplastic bone originates from scar or granulation tissue that has filled the bony labyrinth. Osteoplastic bone forms as an extension from the endosteum that lines the lumen of the otic capsule.

Frequency

United States

Bacterial meningitis, which affects an estimated 15,000 infants and children in the United States each year, is the most common cause of both acquired sensorineural hearing loss in childhood and labyrinthitis ossificans (LO). The reported incidence of hearing loss following meningitis ranges from 6-37%, with an estimated 5% suffering from profound deafness. Deafness results from spread of the infection to the labyrinth and consequent end organ damage. Ossification within the labyrinth compounds destruction of neural elements.

Dodge et al reviewed the outcome of 185 infants and children with meningitis and found a 10% overall incidence of hearing loss.7 The incidence of hearing loss was greatest with S pneumoniae (31%) infection and lowest with Haemophilus influenzae (6%) infection. The mortality rate of S pneumoniae –induced meningitis (19% in children, 20-30% in adults) also is the highest of the 3 infecting organisms (see the Causes section). As many as 80% of patients with profound postmeningitic deafness have some degree of labyrinthine ossification. Complete ossification is associated with a very poor prognosis for residual hearing.

Clinical

Causes

  • The most common cause of labyrinthitis ossificans (LO) is bacterial infection of the inner ear that results in suppurative labyrinthitis. Bacterial invasion of the labyrinth can occur via 3 routes: hematogenic spread through the cochlear vasculature, a sequela to otitis media that passes through the round window membrane, or meningogenic spread from the subarachnoid space in meningitis (see Image 6).
  • Based on data from 1995, the 3 most common organisms responsible for bacterial meningitis in the United States are H influenzae (0.2 cases per 100,000 population), S pneumoniae (1.1 cases per 100,000 population), and Neisseria meningitidis (0.6 cases per 100,000 population). With the success of conjugate vaccines in preventing invasive H influenzae type b (Hib) disease, S pneumoniae has become the leading cause of bacterial meningitis in the United States. Children younger than 1 year have the highest incidence of pneumococcal meningitis (approximately 10 cases per 100,000 population).
  • Woolley et al performed a retrospective study of 432 patients with meningitis and determined that 59 (13.7%) developed hearing loss.8 Forty-six (78%) of these children with hearing loss had stable auditory thresholds over time, and 13 (22%) exhibited deterioration or fluctuation of acuity over time. The authors determined that significant predictors of future hearing loss included increased intracranial pressure (revealed with CT scan), male sex, low cerebrospinal fluid glucose levels, S pneumoniae as a causative organism, and the presence of nuchal rigidity.
  • The cells and mechanisms responsible for ossification in labyrinthitis ossificans (LO) are unknown; however, several hypotheses have been proposed.
    • In 1967, Paparella and Sugiura hypothesized that bone-lining cells of the cochlea are pluripotent mesenchymal stem cells that remain uncommitted until stimulated to differentiate into osteoblasts.2
    • In 1985, Kotzias and Linthicum hypothesized that this type of bone originates from osteoblasts within the otic capsule.9 They suggested that ectopic bone forms on the endosteal layer after inflammatory insult, but the bone is not incorporated beyond the surface.
    • Additionally, pericytes associated with blood vessels that supply the modiolus and spiral ligament fibroblasts have been hypothesized as cells of origin.
    • In an antemortem analysis of labyrinthitis ossificans (LO) in a human case report, metaplastic bone was reported to have formed within serofibrinous exudate; however, the cell of origin for the osteoneogenesis has not been identified. Because the new bone deposition occurs in continuity with endosteal bone, postmortem studies are not able to differentiate metaplastic bone from osteoplastic bone within the cochlea. The cells and mechanisms responsible for ossification in labyrinthitis ossificans (LO) remain undefined.

More on Labyrinthitis Ossificans

Overview: Labyrinthitis Ossificans
Differential Diagnoses & Workup: Labyrinthitis Ossificans
Treatment & Medication: Labyrinthitis Ossificans
Follow-up: Labyrinthitis Ossificans
Multimedia: Labyrinthitis Ossificans
References
[ CLOSE WINDOW ]

References

  1. Bhatt S, Halpin C, Hsu W, et al. Hearing loss and pneumococcal meningitis: an animal model. Laryngoscope. Dec 1991;101(12 Pt 1):1285-92. [Medline].

  2. Paparella MM, Sugiura S. The pathology of suppurative labyrinthitis. Ann Otol Rhinol Laryngol. Aug 1967;76(3):554-86. [Medline].

  3. Brodie HA, Thompson TC, Vassilian L, et al. Induction of labyrinthitis ossificans after pneumococcal meningitis: an animal model. Otolaryngol Head Neck Surg. Jan 1998;118(1):15-21. [Medline].

  4. Nabili V, Brodie HA, Neverov NI, et al. Chronology of labyrinthitis ossificans induced by Streptococcus pneumoniae meningitis. Laryngoscope. Jun 1999;109(6):931-5. [Medline].

  5. Tinling SP, Colton J, Brodie HA. Location and timing of initial osteoid deposition in postmeningitic labyrinthitis ossificans determined by multiple fluorescent labels. Laryngoscope. Apr 2004;114(4):675-80. [Medline].

  6. Nadol JB Jr, Hsu WC. Histopathologic correlation of spiral ganglion cell count and new bone formation in the cochlea following meningogenic labyrinthitis and deafness. Ann Otol Rhinol Laryngol. Sep 1991;100(9 Pt 1):712-6. [Medline].

  7. Dodge PR, Davis H, Feigin RD, et al. Prospective evaluation of hearing impairment as a sequela of acute bacterial meningitis. N Engl J Med. Oct 4 1984;311(14):869-74. [Medline].

  8. Woolley AL, Kirk KA, Neumann AM, et al. Risk factors for hearing loss from meningitis in children: the Children's Hospital experience. Arch Otolaryngol Head Neck Surg. May 1999;125(5):509-14. [Medline].

  9. Kotzias SA, Linthicum FH Jr. Labyrinthine ossification: differences between two types of ectopic bone. Am J Otol. Nov 1985;6(6):490-4. [Medline].

  10. Novak MA, Fifer RC, Barkmeier JC, et al. Labyrinthine ossification after meningitis: its implications for cochlear implantation. Otolaryngol Head Neck Surg. Sep 1990;103(3):351-6. [Medline].

  11. Arriaga MA, Carrier D. MRI and clinical decisions in cochlear implantation. Am J Otol. Jul 1996;17(4):547-53. [Medline].

  12. Lebel MH, Freij BJ, Syrogiannopoulos GA, et al. Dexamethasone therapy for bacterial meningitis. Results of two double- blind, placebo-controlled trials. N Engl J Med. Oct 13 1988;319(15):964-71. [Medline].

  13. Kadurugamuwa JL, Hengstler B, Zak O. Effects of antiinflammatory drugs of arachidonic acid metabolites and cerebrospinal fluid proteins during infectious pneumococcal meningitis in rabbits. Pediatr Infect Dis J. 1987;6:1153-4.

  14. Hartnick CJ, Kim HH, Chute PM, et al. Preventing labyrinthitis ossificans: the role of steroids. Arch Otolaryngol Head Neck Surg. Feb 2001;127(2):180-3. [Medline].

  15. Tuomanen E, Hengstler B, Rich R, et al. Nonsteroidal anti-inflammatory agents in the therapy for experimental pneumococcal meningitis. J Infect Dis. May 1987;155(5):985-90. [Medline].

  16. DeSautel MG, Brodie HA. Effects of depletion of complement in the development of labyrinthitis ossificans. Laryngoscope. Oct 1999;109(10):1674-8. [Medline].

  17. Yeung AH, Tinling SP, Brodie HA. Inhibition of post-meningitic cochlear injury with cerebrospinal fluid irrigation. Otolaryngol Head Neck Surg. Feb 2006;134(2):214-24. [Medline].

  18. Ge NN, Brodie SA, Tinling SP, et al. The effects of superoxide dismutase in gerbils with bacterial meningitis. Otolaryngol Head Neck Surg. Nov 2004;131(5):563-72. [Medline].

  19. Aminpour S, Tinling SP, Brodie HA. Role of tumor necrosis factor-alpha in sensorineural hearing loss after bacterial meningitis. Otol Neurotol. Jul 2005;26(4):602-9. [Medline].

  20. Balkany T, Gantz B, Nadol JB Jr. Multichannel cochlear implants in partially ossified cochleas. Ann Otol Rhinol Laryngol Suppl. Sep-Oct 1988;135:3-7. [Medline].

  21. Gantz BJ, McCabe BF, Tyler RS. Use of multichannel cochlear implants in obstructed and obliterated cochleas. Otolaryngol Head Neck Surg. Jan 1988;98(1):72-81. [Medline].

  22. Lambert PR, Ruth RA, Hodges AV. Multichannel cochlear implant and electrically evoked auditory brainstem responses in a child with labyrinthitis ossificans. Laryngoscope. Jan 1991;101(1 Pt 1):14-9. [Medline].

  23. Steenerson RL, Gary LB. Multichannel cochlear implantation in obliterated cochleas using the Gantz procedure. Laryngoscope. Sep 1994;104(9):1071-3. [Medline].

  24. Rauch SD, Herrmann BS, Davis LA, et al. Nucleus 22 cochlear implantation results in postmeningitic deafness. Laryngoscope. Dec 1997;107(12 Pt 1):1606-9. [Medline].

  25. Brookhouser PE, Auslander MC, Meskan ME. The pattern and stability of postmeningitic hearing loss in children. Laryngoscope. Sep 1988;98(9):940-8. [Medline].

  26. Benitez JT, Bouchard KR, Lane-Szopo D. Pathology of deafness and disequilibrium in head injury:a human temporal bone study. Am J Otol. Jan 1980;1(3):163-7. [Medline].

  27. Berlow SJ, Caldarelli DD, Matz GJ, et al. Bacterial meningitis and sensorineural hearing loss: a prospective investigation. Laryngoscope. Sep 1980;90(9):1445-52. [Medline].

  28. Blamey P, Arndt P, Bergeron F, et al. Factors affecting auditory performance of postlinguistically deaf adults using cochlear implants. Audiol Neurootol. Sep-Oct 1996;1(5):293-306. [Medline].

  29. Brookhouser PE, Auslander MC. Aided auditory thresholds in children with postmeningitic deafness. Laryngoscope. Aug 1989;99(8 Pt 1):800-8. [Medline].

  30. Chen MC, Harris JP, Keithley EM. Immunohistochemical analysis of proliferating cells in a sterile labyrinthitis animal model. Laryngoscope. May 1998;108(5):651-6. [Medline].

  31. Chole RA, Tinling SP. Incomplete coverage of mammalian bone matrix by lining cells. Ann Otol Rhinol Laryngol. Jul 1993;102(7):543-50. [Medline].

  32. Clopton BM, Spelman FA, Miller JM. Estimates of essential neural elements for stimulation through a cochlear prosthesis. Ann Otol Rhinol Laryngol Suppl. Mar-Apr 1980;89(2 Pt 2):5-7. [Medline].

  33. Cohen NL, Hoffman R, Waltzman S. Electrode insertion in the totally obstructed cochlea. Presented at: Third Annual Cochlear Implant Conference. Innsbruk, Austria: 1993.

  34. Crowe SJ. Pathologic changes in meningitis of the internal ear. Arch Otolaryngol. 1930;11(5):537-568.

  35. deSouza C, Paparella MM, Schachern P, et al. Pathology of labyrinthine ossification. J Laryngol Otol. Aug 1991;105(8):621-4. [Medline].

  36. Dorman MF, Loizou PC, Rainey D. Speech intelligibility as a function of the number of channels of stimulation for signal processors using sine-wave and noise-band outputs. J Acoust Soc Am. Oct 1997;102(4):2403-11. [Medline].

  37. Druss JG. Labyrinthitis secondary to meningococcic meningitis: a clinical and histopathologic study. Arch Otolaryngol. 1936;24:19-28.

  38. Eisenberg LS, Luxford WM, Becker TS, et al. Electrical stimulation of the auditory system in children deafened by meningitis. Otolaryngol Head Neck Surg. Dec 1984;92(6):700-5. [Medline].

  39. Finitzo-Hieber T, Simhadri R, Hieber JP. Abnormalities of the auditory brainstem response in post-meningitic infants and children. Int J Pediatr Otorhinolaryngol. Dec 1981;3(4):275-86. [Medline].

  40. Fredrickson JM, Griffith AW, Lindsay JR. Transverse fracture of the temporal bone: a clinical and histopathologic study. Arch Otolaryngol. 1963;78:770-784.

  41. Friedmann I, Arnold W. Pathology of the Ear. New York, NY: Churchill Livingstone; 1993:752.

  42. Green JD Jr, Marion MS, Hinojosa R. Labyrinthitis ossificans: histopathologic consideration for cochlear implantation. Otolaryngol Head Neck Surg. Mar 1991;104(3):320-6. [Medline].

  43. Hagens EW. Pathology of the inner ear in a case of deafness from epidemic cerebrospinal meningitis. Ann Otol Rhinol Laryngol. 1940;49:168-176.

  44. Igarashi M, Saito R, Alford BR, et al. Temporal bone findings in pneumococcal meningitis. Arch Otolaryngol. Feb 1974;99(2):79-83. [Medline].

  45. Jackler RK, Luxford WM, Schindler RA, et al. Cochlear patency problems in cochlear implantation. Laryngoscope. Jul 1987;97(7 Pt 1):801-5. [Medline].

  46. Johnson MH, Hasenstab MS, Seicshnaydre MA, et al. CT of postmeningitic deafness: observations and predictive value for cochlear implants in children. AJNR Am J Neuroradiol. Jan 1995;16(1):103-9. [Medline].

  47. Kawano A, Seldon HL, Pyman B, et al. Intracochlear factors contributing to psychophysical percepts following cochlear implantation: a case study. Ann Otol Rhinol Laryngol Suppl. Sep 1995;166:54-7. [Medline].

  48. Keane WM, Potsic WP, Rowe LD, et al. Meningitis and hearing loss in children. Arch Otolaryngol. Jan 1979;105(1):39-44. [Medline].

  49. Kimura R, Perlman HB. Arterial obstruction of the labyrinth. Part I. Cochlear changes. Part II. Vestibular changes. Ann Otol Rhinol Laryngol. 1958;67(1):5-24; 25-40.

  50. Logan TA, Fraser JS. Labyrinthitis: a complication of middle ear suppuration: a clinical and pathologic study. J Laryngol Otol. 1928;43(609).

  51. Morgan BP, Gasque P. Expression of complement in the brain: role in health and disease. Immunol Today. Oct 1996;17(10):461-6. [Medline].

  52. Morgan WE, Coker NJ, Jenkins HA. Histopathology of temporal bone fractures: implications for cochlear implantation. Laryngoscope. Apr 1994;104(4):426-32. [Medline].

  53. Nadol JB Jr. Hearing loss as a sequela of meningitis. Laryngoscope. May 1978;88(5):739-55. [Medline].

  54. Nager FR, Fraser JS. Bone formation in the scala tympani of otosclerotics. J Laryngol Otol. 1938;52:173-180.

  55. Otte J, Schunknecht HF, Kerr AG. Ganglion cell populations in normal and pathological human cochleae. Implications for cochlear implantation. Laryngoscope. Aug 1978;88(8 Pt 1):1231-46. [Medline].

  56. Rarey KE, Bicknell JM, Davis LE. Intralabyrinthine osteogenesis in Cogan's syndrome. Am J Otolaryngol. Nov-Dec 1986;7(6):387-90. [Medline].

  57. Richardson MP, Reid A, Williamson TJ, et al. Acute otitis media and otitis media with effusion in children with bacterial meningitis. J Laryngol Otol. Oct 1997;111(10):913-6. [Medline].

  58. Rodriguez AF, Kaplan SL, Hawkins EP, et al. Hematogenous pneumococcal meningitis in the infant rat: description of a model. J Infect Dis. Dec 1991;164(6):1207-9. [Medline].

  59. Rosenberg RA, Cohen NL, Reede DL. Radiographic imaging for the cochlear implant. Ann Otol Rhinol Laryngol. May-Jun 1987;96(3 Pt 1):300-4. [Medline].

  60. Rosenhall U, Nylen O, Lindberg J, et al. Auditory function after Haemophilus influenzae meningitis. Acta Otolaryngol. Mar-Apr 1978;85(3-4):243-7. [Medline].

  61. Schachern PA, Paparella MM, Hybertson R, et al. Bacterial tympanogenic labyrinthitis, meningitis, and sensorineural damage. Arch Otolaryngol Head Neck Surg. Jan 1992;118(1):53-7. [Medline].

  62. Schlech WF 3rd, Ward JI, Band JD, et al. Bacterial meningitis in the United States, 1978 through 1981. The National Bacterial Meningitis Surveillance Study. JAMA. Mar 22-29 1985;253(12):1749-54. [Medline].

  63. Schuchat A, Robinson K, Wenger JD, et al. Bacterial meningitis in the United States in 1995. Active Surveillance Team. N Engl J Med. Oct 2 1997;337(14):970-6. [Medline].

  64. Schuknecht H. Pathology of the Ear. Philadelphia, Pa: Lea & Febiger; 1993:672.

  65. Schwaber MK, Tarasidis NG. Labyrinthitis ossificans following post-traumatic hearing loss and vertigo: a case report with antemortem histopathology. Otolaryngol Head Neck Surg. Jan 1990;102(1):89-91. [Medline].

  66. Seicshnaydre MA, Johnson MH, Hasenstab MS, et al. Cochlear implants in children: reliability of computed tomography. Otolaryngol Head Neck Surg. Sep 1992;107(3):410-7. [Medline].

  67. Stutman HR, Marks MI. Bacterial meningitis in children: diagnosis and therapy. A review of recent developments. Clin Pediatr (Phila). Sep 1987;26(9):431-8. [Medline].

  68. Suga F, Lindsay JR. Labyrinthitis ossificans due to chronic otitis media. Ann Otol Rhinol Laryngol. Jan-Feb 1975;84(1 Pt 1):37-44. [Medline].

  69. Sugiura S, Paparella MM. The pathology of labyrinthine ossification. Laryngoscope. Nov 1967;77(11):1974-89. [Medline].

  70. Telian SA, Zimmerman-Phillips S, Kileny PR. Successful revision of failed cochlear implants in severe labyrinthitis ossificans. Am J Otol. Jan 1996;17(1):53-60. [Medline].

  71. Vernon M. Meningitis and deafness: the problem, its physical, audiological, psychological, and educational manifestations in deaf children. Laryngoscope. Oct 1967;77(10):1856-74. [Medline].

  72. Ward PH. The histopathology of auditory and vestibular disorders in head trauma. Ann Otol Rhinol Laryngol. Apr 1969;78(2):227-38. [Medline].

  73. Wenger JD, Hightower AW, Facklam RR, et al. Bacterial meningitis in the United States, 1986: report of a multistate surveillance study. The Bacterial Meningitis Study Group. J Infect Dis. Dec 1990;162(6):1316-23. [Medline].

  74. Zimmermann CE, Burgess BJ, Nadol JB Jr. Patterns of degeneration in the human cochlear nerve. Hear Res. Oct 1995;90(1-2):192-201. [Medline].

  75. Zwahlen A, Nydegger UE, Vaudaux P, et al. Complement-mediated opsonic activity in normal and infected human cerebrospinal fluid: early response during bacterial meningitis. J Infect Dis. May 1982;145(5):635-46. [Medline].

[ CLOSE WINDOW ]

Further Reading

[ CLOSE WINDOW ]

Keywords

labyrinthitis, labyrinthitis ossificans, inner ear, ear, osseous labyrinth, LO, human osseous labyrinth, otic capsule, lumen, vascular obstruction of the labyrinthine artery, temporal bone trauma, otosclerosis, leukemia, tumors of the temporal bone, suppurative labyrinthitis, otitis media, pathologic ossification

[ CLOSE WINDOW ]

Contributor Information and Disclosures

Author

Hilary A Brodie, MD, PhD, Professor and Chairman, Department of Otolaryngology-Head and Neck Surgery, University of California at Davis Medical Center
Hilary A Brodie, MD, PhD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Otolaryngology-Head and Neck Surgery, American Medical Association, American Neurotology Society, American Otological Society, Association for Research in Otolaryngology, and Society of University Otolaryngologists-Head and Neck Surgeons
Disclosure: Nothing to disclose.

Coauthor(s)

Andrea H Yeung, MD, BS, Clinical Instructor, Department of Otolaryngology-Head and Neck Surgery, University of California San Francisco
Andrea H Yeung, MD, BS is a member of the following medical societies: Alpha Omega Alpha and Phi Beta Kappa
Disclosure: Nothing to disclose.

Medical Editor

Jack A Shohet, MD, Chairman of Otolaryngology, Hoag Hospital
Jack A Shohet, MD is a member of the following medical societies: American Academy of Otolaryngology-Head and Neck Surgery, American Medical Association, American Neurotology Society, American Tinnitus Association, and California Medical Association
Disclosure: Envoy Medical Consulting fee Consulting

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Peter S Roland, MD, Professor, Department of Neurological Surgery, Professor and Chairman, Department of Otolaryngology-Head and Neck Surgery, Director of Clinical Center for Auditory, Vestibular and Facial Nerve Disorders, Chief of Pediatric Otology, University of Texas Southwestern Medical Center; Adjunct Professor of Communicative Disorders, School of Human Development.
Peter S Roland, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Otolaryngic Allergy, American Academy of Otolaryngology-Head and Neck Surgery, American Auditory Society, American Laryngological Rhinological and Otological Society, American Neurotology Society, American Otological Society, North American Skull Base Society, and Society of University Otolaryngologists-Head and Neck Surgeons
Disclosure: Alcon labs Honoraria Speaking and teaching; GSK Honoraria Speaking and teaching; Advanced Bionics Honoraria Board membership; Cochlear corp Honoraria Board membership; Med El corp travel grants Speaking and teaching; Insight vision Consulting fee Consulting

CME Editor

Christopher L Slack, MD, Otolaryngology-Facial Plastic Surgery, Private Practice, Associated Coastal ENT; Medical Director, Treasure Coast Sleep Disorders
Christopher L Slack, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Facial Plastic and Reconstructive Surgery, American Academy of Otolaryngology-Head and Neck Surgery, and American Medical Association
Disclosure: Nothing to disclose.

Chief Editor

Arlen D Meyers, MD, MBA, Professor, Department of Otolaryngology-Head and Neck Surgery, University of Colorado School of Medicine
Arlen D Meyers, MD, MBA is a member of the following medical societies: American Academy of Facial Plastic and Reconstructive Surgery, American Academy of Otolaryngology-Head and Neck Surgery, and American Head and Neck Society
Disclosure: Covidien Corp Consulting fee Consulting; US Tobacco Corporation unstricted gift unknown

 
 
HONcode

We subscribe to the
HONcode principles of the
Health On the Net Foundation

All material on this website is protected by copyright, Copyright© 1994- by Medscape.
This website also contains material copyrighted by 3rd parties.

DISCLAIMER: The content of this Website is not influenced by sponsors. The site is designed primarily for use by qualified physicians and other medical professionals. The information contained herein should NOT be used as a substitute for the advice of an appropriately qualified and licensed physician or other health care provider. The information provided here is for educational and informational purposes only. In no way should it be considered as offering medical advice. Please check with a physician if you suspect you are ill.