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A case of
tympanogenic labyrinthitis complicated by acute otitis media.Yonsei
Med J. 2005 Feb 28;46(1):161-5.
Widespread
use of antimicrobial drugs in the management of otitis media has
significantly reduced the incidence of labyrinthitis nowadays. Cases
of tympanogenic labyrinthitis following acute otitis media have
rarely been reported in recent literature on otolaryngology. We
report an unusual case of tympanogenic labyrinthitis that presented
with sudden sensorineural hearing loss (SNHL) following acute otitis
media in an adult who had no previous otological complaints. An
audiogram revealed SNHL with pure tone threshold of 43.7 dB in the
left ear. MRI was helpful to identify the inflammatory change of the
membranous labyrinth. The patient's hearing returned to normal after
treatment. The definite diagnosis of serous labyrinthitis was
established retrospectively.
Temporal bone
histopathology in a patient suspected of inner ear extension of
otitis media. Nippon Jibiinkoka Gakkai Kaiho. 2005 May;108(5):533-6.
We report
the histopathological findings in the temporal bone of a 30-year-old
female who died of cervical esophageal carcinoma. The temporal bone
sections revealed severe bilateral suppurative labyrinthitis and
otitis media that presumably occurred immediately before her death.
Many inflammatory cells were present in the middle ear, particularly
around the stapes and the round window niche. They had also
infiltrated the inner ear via the annular ligament of the stapes and
the round window membrane. Inflammatory cell accumulation was also
observed in the peri- and endolymphatic spaces, and it was most
severe in the basal turn. Most of the inner and outer hair cells
were preserved, but some had degenerated or were missing. Numerous
round cells were observed in the modiolus, and some of the spiral
ganglion cells had degenerated. On the basis of these findings, we
concluded that bacterial otitis media had extended in to the inner
ear via the oval window and round window membrane and had resulted
in suppurative labyrinthitis. These findings are consistent with
those of stage II suppurative labyrinthitis according to the
classification of Schuknecht.
Histopathology of
labyrinthine fistulae in chronic otitis media with clinical
implications. Am J Otol.1997 Jan;18(1):15-25.
The
objective of this study was to describe the light microscopic
pathology of labyrinthine fistulae in chronic otitis media (COM) in
seven temporal bones and to discuss clinical and surgical
implications. In COM, labyrinthine fistulae are usually caused by
cholesteatoma, with the lateral semicircular canal being the most
commonly affected site. Some fistulae are asymptomatic, whereas,
others affect the auditory and vestibular systems to varying
degrees. Surgical removal of cholesteatoma matrix over a fistula
carries a risk of sensorineural hearing loss. Knowledge of the
pathology of fistulae may provide a better understanding of their
clinical manifestations and may allow a more rational approach to
surgical management. The Massachusetts Eye and Ear Infirmary
temporal bone collection contains 115 specimens with COM, of which
seven specimens show pathologic fistulization of the bony labyrinth.
Histologic sections from these seven bones were evaluated with
respect to type of COM, location and size of fistula, changes in the
inner ear adjacent to the fistula, middle ear and mastoid disease,
and pathology in the vestibular and cochlear sense organs. The
following conclusions are presented (a) Labyrinthine fistulae can be
caused not only by cholesteatoma, but also by granulomatous COM
without cholesteatoma and even by localized infection within a
canal-down mastoid cavity. (b) Cholesteatoma matrix or inflammatory
tissue usually becomes apposed to the endosteum or membranous
labyrinth within the fistula. In most cases, reactive inner ear
changes do not occur at the fistula site. Occasionally, there is
thickening of the endosteum or chronic localized labyrinthitis. (c)
Most bones do not show any alterations of the vestibular and
cochlear sense organs. Occasionally, there is serous labyrinthitis,
which might lead to partial sensorineural hearing loss. (d) A
protective "walling-off" phenomenon in the labyrinth is
not common. Therefore, if overwhelming infection or surgical trauma
breaches the natural barriers of the endosteum/membranous labyrinth,
then the fistula may allow rapid dissemination of infection
throughout the inner ear.
A human temporal
bone study of acute bacterial meningogenic labyrinthitis. Am
J Otol. 1996 May;17(3):375-85.
It is well
established that sensorineural hearing loss (SNHL) is an important
sequela of acute bacterial meningitis. Previous human temporal bone
histopathologic studies have suggested that such hearing loss is due
to labyrinthitis. This study involved a detailed and systematic
evaluation of the auditory and vestibular end-organs in 41 human
temporal bones from patients with acute bacterial meningitis, aimed
at describing the spectrum of histopathologic changes within the
labyrinth, ascertaining likely routes for spread of infection from
the meninges to the inner ear, and comparing the data from humans
with those described in a rabbit model of meningogenic labyrinthitis.
Our study revealed the following: (a) Suppurative labyrinthitis
occurred in 20 (49%) bones. Of these 20 bones, the cochlea was
affected in all, whereas the vestibular organs were involved in 10.
Eosinophilic staining of inner ear fluids without the presence of
inflammatory cells (so-called "serous" labyrinthitis)
occurred in 14 of the remaining 21 bones. This staining occurred
primarily within the vestibular system. Its significance and
pathogenesis remains unknown; (b) Sensory and neural structures of
the inner ear appeared intact in the majority of specimens,
including bones with suppurative labyrinthitis and those with
eosinophilic staining of inner ear fluids. This finding raises the
possibility of preventing or reversing SNHL by therapeutic
intervention. Spiral ganglion cells were severely degenerated in 12%
of bones, indicating a retrocochlear site of hearing loss in
addition to the cochlea. This subset of patients may perform poorly
after cochlear implantation; (c) It has been traditionally assumed
that irreversible and permanent SNHL is caused by suppurative
labyrinthitis, whereas reversible SNHL is caused by serous
labyrinthitis. Our findings question the validity of these
assumptions; (d) The data were consistent with the hypothesis that
both the cochlear modiolus and cochlear aqueduct can serve as
potential pathways for spread of infection from the meninges to the
inner ear; (e) There were many similarities in the histopathology of
the inner ear in humans when compared with the rabbit model of
meningogenic labyrinthitis. A notable difference was that the
cochlear aqueduct appeared to be the sole pathway for spread of
infection in the rabbit, whereas in the human, both the modiolus and
aqueduct were possible pathways.
Cytomegalovirus
endolabyrinthitis. Arch. Pathol Lab Med.1977 Mar;101 (3):118-21.
A premature
male infant, who died 22 days after birth with hyaline membrane
disease, was found to have had cytomegalic inclusion disease at
autopsy. Histopathologic examination of the temporal bones showed
cytomegalovirus (CMV) infection of the entire endolabyrinth without
involvement of the neural and sensory structures. These findings
support the thesis that late gestational or perinatal fetal CMV
infection results in an endolymphatic labyrinthitis. We hypothesize
that blood-borne virus passes from the stria vascularis into the
endolymphatic spaces and infects the nonneurosensory epithelium.
This pattern of infection differs from the perilabyrinthitis of
human varicellazoster and experimentally produced mouse CMV.
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