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Results for “LABYRINTH DISEASES”

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At least 127 records · Page 7Linked to original sources
PubMed1984

Immunologic and electrophysiological response to cytomegaloviral inner ear infection in the guinea pig.

We investigated the development of labyrinthitis in animals inoculated with guinea pig cytomegalovirus (GPCMV). These animals all became deaf eight days after inoculation into the perilymphatic compartment and showed severe inflammatory changes within the inner ear. Animals that received inactivated virus maintained their hearing throughout the observation period and exhibited normal cochlear morphology. Neither group had serum or perilymph antibody to GPCMV eight days after viral inoculation. We then investigated the effect of systemic immunity to GPCMV on inner ear viral challenge in animals with high levels of serum antibodies to GPCMV. No significant hearing loss could be detected eight days after inner ear inoculation. Seropositive animals that received live virus demonstrated a significant rise in perilymph antibody titer to GPCMV and showed preservation of normal cochlear morphology. Thus, systemic and inner ear immunity to GPCMV afforded protection against damage caused after direct perilymphatic inoculation of live virus.

Action Potentials↗
PubMed1986

Pathogenesis of labyrinthitis associated with Haemophilus influenzae type b meningitis in infant rats.

The pathogenesis of labyrinthitis associated with bacterial meningitis was studied by histopathologic examination of inner ears of 114 rats with Haemophilus influenzae type b meningitis produced by ip inoculation of one of 13 clinical isolates. Findings consisted of inflammation of the perilymphatic spaces of the cochlea and semicircular canals with sparing of the endolymphatic space, cochlear nerve fibers, and middle ear. The degree of inflammation peaked at 48 hr after inoculation, then declined by 96 to 144 hr. No interstrain differences in type or degree of pathology were observed. Immunofluorescent staining of cochleae from 15 animals demonstrated that bacteria were present in areas of inflammation and also in the endolymphatic space and organ of Corti. One isolate displayed a tendency to accumulate in the perilymphatic spaces in larger numbers than those seen with three other isolates. These findings suggest that, in this model, inflammation reaches the inner ear by spreading from the subarachnoid space. Bacterial invasion of the organ of Corti may be one mechanism by which deafness occurs in bacterial meningitis.

Animals↗
PubMed1980

Round window membrane rupture and acquired sensorineural hearing loss in children.

The aetiology of acquired sensorineural hearing loss includes many conditions. The disparity between the number of children affected by the conditions which are supposed to cause hearing loss and the number of children who are actually deaf, has never been satisfactorily explained. Clinical features observed in children with surgically proven round window membrane rupture have been noted in all conventional aetiological groups. These features include otitis media, doubt about the hearing status in early life, disturbance of balance and other occasional neurological phenomena. Wide variation in the appearance of round window niche has been observed in children with secretory otitis and similar appearances have been observed in children with proven round window membrane rupture. The appearances may represent a reaction to perilymph. Round window membrane rupture is probably common and may prove to be a unifying factor for many cases of acquired sensorineural hearing loss. Occasional neurological phenomena may be related to it.

Adolescent↗
PubMed1987

Cumulative and acute toxicity of repeated high-dose tobramycin treatment in cystic fibrosis.

Forty-six patients with cystic fibrosis and chronic bronchopulmonary Pseudomonas aeruginosa infection entered a study of tobramycin-related chronic and acute nephro- and acousticovestibular toxicity. The patients (mean age, 15.7 years) had previously received 2-week courses of tobramycin therapy, for a mean cumulative total of 279 days each. The cumulative tobramycin dose ranged from 632 to 7,644 mg/kg. The patients were studied before and at the end of a 2-week course of treatment with tobramycin (10 to 20 mg/kg per day) to discriminate between acute and chronic toxicity. In patients studied at the beginning of the present course of treatment, the glomerular filtration rate, measured as 24-h creatinine clearance, did not correlate with the cumulative dose of tobramycin received during previous courses. Eighteen patients (39%) had a reduced glomerular filtration rate compared with normal values (mean, 12.5% reduction) but normal serum creatinine values. Two patients (5%) had a high-frequency hearing deficit (above 8 kHz), but only one deficit was possibly related to tobramycin. No chronic vestibular toxicity was observed. During the course of treatment, no patients developed acute nephrotoxicity. After 2 weeks of treatment 32% had a slightly reduced hearing threshold (15 to 30 dB) in two or more high frequencies, and 28% had a fall in vestibular response greater than 25% of the initial value but remained within normal limits. Thus, the acute and chronic toxicity of repeated high-dose tobramycin treatment in cystic fibrosis patients seems to be very mild.

Adolescent↗
PubMed1988

Ganciclovir prophylaxis for cochlear pathophysiology during experimental guinea pig cytomegalovirus labyrinthitis.

The effectiveness of the antiviral agent ganciclovir (9-[1,3-dihydroxy-2-propoxymethyl]guanine) against guinea pig cytomegalovirus was tested in vitro in guinea pig embryonic fibroblasts and in vivo in an experimental guinea pig cytomegalovirus labyrinthitis model. In vitro, ganciclovir completely prevented guinea pig cytomegalovirus infection of guinea pig embryonic fibroblasts at concentrations above 32.6 micrograms/ml. In vivo, antibody-negative animals had an average 17-dB elevation in their auditory nerve compound action potential thresholds (P less than 0.01, t test) and showed signs bilaterally of guinea pig cytomegalovirus labyrinthitis 8 days after intrathecal inoculation of virus. Ganciclovir administration starting 1 day before inoculation prevented the development of both cochlear histopathologic change and hearing loss. Guinea pig cytomegalovirus meningitis was observed in both the drug-treated and untreated groups. High-pressure liquid chromatography confirmed the presence of ganciclovir in the serum, perilymph, and cerebrospinal fluid of the drug recipients. Prophylactic ganciclovir thus can protect the cochlea from the histopathologic changes and hearing loss normally associated with experimental guinea pig cytomegalovirus labyrinthitis.

Acoustic Stimulation↗
PubMed1969

Comparison of the pathogenicity for mice of Mycobacterium fortuitum and Mycobacterium abscessus.

The pathogenicity for mice of 12 strains of Mycobacterium abscessus was compared with that for 8 strains of M. fortuitum. Both species caused lesions in kidneys and produced "spinning disease" resulting from inner ear infections. No major differences in pathogenicity of these two species were demonstrated. Strain to strain variation was marked, especially with M. abscessus. For example, 1.6 x 10(6) organisms of strain 11188 of M. abscessus produced death in four of five animals within 42 days, whereas strain 380 of M. abscessus failed to produce any deaths within 42 days. In the case of M. fortuitum, the greatest mortality observed was one of five animals, yet the incidence of spinning disease and kidney disease occurred earlier postinfection than in mice infected with M. abscessus. Histologically, abscess formation by a strain of M. abscessus was greater than by a strain of M. fortuitum, but this difference cannot be interpreted as a species difference.

Animals↗
PubMed1986

Detection of pseudorabies virus DNA in the inner ear of intranasally infected BALB/c mice with nucleic acid hybridization in situ.

Evidence for the pathogenicity of pseudorabies virus for the auditory and vestibular organs of experimentally infected mice is presented. We demonstrate viral genomes in cells of the peripheral sensory organs, the nerve structures, and the affected areas of the brain in single sections from an entire cranium of an adult mouse. The data were obtained by an in situ hybridization technique adapted for use with fixed, plastic-embedded materials. In contrast to conventional methods which use frozen sections, we were able to analyze cartilaginous and bony materials with high resolution.

Animals↗
PubMed1985

Labyrinthine ossification: etiologies and CT findings.

Ossification of the membranous labyrinth (labyrinthitis ossificans) develops as the final result of many inflammatory processes, for example, meningitis, blood-borne septic emboli, middle ear infection, and cholesteatoma. Labyrinthine ossification may also occur as a result of previous labyrinthectomy or secondary to trauma. Seven cases of labyrinthine ossification accompanied by severe vertigo and total hearing loss in the affected ear are discussed. The computed tomographic appearance of varying degrees of ossification, the clinical and surgical circumstances from which this disorder may develop, and the various approaches to labyrinthectomy are described.

Adult↗
PubMed1976

[Meningitis and labyrinthitis in childhood].

The Haemophilus influenzae meningitis is the most common cause of deafness following meningitis. Five of 22 children (23%) had this complication in spite of antibiotic treatment (ampicillin). The question must be raised whether a different antibiotic treatment could avoid the inner-ear problems occurring in Haemophilus influenzae meningitis. Early decompression of the internal auditory canal has reversed deafness in one of four children.

Adolescent↗
PubMed1985

Protective effect of fosfomycin against aminoglycoside ototoxicity.

The protective effect of fosfomycin against aminoglycoside (dibekacin)-induced ototoxicity was studied in rats. Rats were injected with 100 or 50 mg/kg of dibekacin with or without 500 mg/kg of fosfomycin for 60 or 120 consecutive days. Inner ear damage appeared to be more reduced histopathologically in animals given both dibekacin and fosfomycin than in animals given dibekacin alone. Similarly, renal damage appeared to be reduced histopathologically and functionally by the combined administration of dibekacin and fosfomycin. The mechanism of reduced ototoxicity may be as follows: fosfomycin inhibits the accumulation of dibekacin in the kidney, and reduces its concentration in the kidney and serum. Consequently, the amounts of dibekacin reaching the inner ear are decreased, and ototoxicity is reduced.

Acetylglucosaminidase↗