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Query: UMLS:C0085437 (bacterial meningitis)
 4,038 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Recent progress in magnetic resonance imaging (MRI) has made it possible to obtain detailed images of the inner ear by delineating the lymphatic fluid within the labyrinth. We analyzed CT scans and MR images in 70 ears manifesting profound deafness owing to inner ear lesions and compared their detective ability for inner ear lesions. The following results were obtained. 1) CT scan examination showed slight to extensive ossification of the labyrinth in six ears (9%), whereas MRI examination revealed low to absent signal intensity of the inner ear in nine ears (13%). Therefore, it was concluded that MRI is more sensitive in detecting abnormalities of the inner ear than CT scan. 2) MRI provided useful information as to whether the cochlear turn is filled with lymphatic fluid or obstructed. This point was one of the greatest advantages of MRI over CT scan. 3) Abnormal findings in either or both the CT scan and the MRI were detected in suppurative labyrinthitis occurring secondary to chronic otitis media, bacterial meningitis and in inner ear trauma. However, such abnormal findings were not detected in patients with idiopathic progressive sensorineural hearing loss, ototoxicity or sudden deafness. These findings should be taken into consideration in pre-operative assessment of cochlear implant candidates.
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PMID:[Image analysis of the inner ear with CT and MR imaging: pre-operative assessment for cochlear implant surgery]. 163 88

Clinical studies of predisposing factors in the development of hearing loss secondary to bacterial meningitis have produced conflicting results. An animal model of meningogenic labyrinthitis was developed for more precise study of these parameters. Rabbits were inoculated intrathecally with 10(5) pneumococci to induce meningitis. Hearing thresholds were measured using auditory-evoked responses to 1 kHz, 10 kHz, and click stimuli before infection and every 12 hours thereafter. Profound deafness occurred in all subjects at an average of 48 hours following infection. The incidence and severity of hearing loss was strongly correlated with the duration of meningitis. Temporal bone histology revealed acute inflammation of all perilymphatic spaces including the cochlear aqueduct. This model demonstrated that the risk and severity of hearing loss increase with the duration of meningitis and suggested that the cochlear aqueduct is an anatomic pathway for the extension of infection from the cerebrospinal fluid to the cochlea. The implications for therapy in humans is discussed.
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PMID:Hearing loss and pneumococcal meningitis: an animal model. 176 98

The pathological basis of hearing loss in bacterial meningitis was investigated using an animal model of Streptococcus suis meningitis. Forty guinea-pigs were infected after their hearing had been assessed by brain stem auditory evoked potentials. In 17 animals, it was possible to repeat the procedure at the onset of meningitis; this included one animal with subclinical disease. Fifteen animals showed evidence of hearing loss, which on subsequent histological examination was found to be associated invariably with suppurative labyrinthitis. The remaining two animals without hearing loss had normal cochleas. It is suggested that cochlear sepsis rather than eighth cranial nerve involvement by meningeal sepsis is primarily responsible for hearing loss in bacterial meningitis, and that bacteria enter the cochlea via the cochlear aqueduct and not the internal auditory canal. The tissue within the lumen of the cochlear aqueduct may act as a barrier against invasion by micro-organisms, and haemolytic streptococci could cause lysis of this barrier by the exotoxins they produce.
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PMID:The site of the lesion causing hearing loss in bacterial meningitis: a study of experimental streptococcal meningitis in guinea-pigs. 180 Sep 12

Bacterial meningitis is a common cause of profound deafness and, hence, a common cause of deafness in published series of patients treated with a cochlear prosthesis. Labyrinthitis ossificans is a common finding in meningogenic labyrinthitis and has been considered a relative contraindication to cochlear implantation. In the present study, the numbers of remaining spiral ganglion cells in cases of meningogenic labyrinthitis were correlated with the severity of new bone formation within the inner ear. Six temporal bones in which profound sensorineural hearing loss occurred in life secondary to meningogenic labyrinthitis were studied by serial section light microscopy. Some degree of labyrinthitis ossificans was found in four of six. There was a moderately strong negative correlation between the number of years of total deafness and the percentage of normal of the remaining spiral ganglion cell count. There was a strong negative correlation between the degree of bony occlusion by labyrinthitis ossificans and the normality of the spiral ganglion cell count. The percentage of bony occlusion of the membranous labyrinth increased with the years of total deafness. The significance of these findings for cochlear implantation of individuals with meningogenic labyrinthitis is discussed.
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PMID:Histopathologic correlation of spiral ganglion cell count and new bone formation in the cochlea following meningogenic labyrinthitis and deafness. 195 61

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.
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PMID:Pathogenesis of labyrinthitis associated with Haemophilus influenzae type b meningitis in infant rats. 351 Feb 60

The objectives of the present investigation are as follows: to prospectively assess the incidence of sensorineural hearing loss (SHL) associated with bacterial meningitis; to evaluate the onset and degree of SHL; and to describe the audiometric pattern. Forty-seven patients were studied otologically and audiologically. The incidence of SHL was 11%. Late onset of SHL was not observed, however, one patient demonstrated a probable progressive hearing loss. Both bilateral and unilateral hearing loss were noted. The degree of hearing loss varied from mild to profound, with no consistent audiometric pattern. Intensive follow-up on one hearing-impaired patient included temporal bone polytomograms. Obliterative labyrinthitis is detailed. Antibiotic treatment and laboratory data are evaluated. Suggestions are provided for the post-meningitic course.
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PMID:Bacterial meningitis and sensorineural hearing loss: a prospective investigation. 740 46

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.
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PMID:A human temporal bone study of acute bacterial meningogenic labyrinthitis. 881 13

Although the identity of all the variables that may influence speech recognition after cochlear implantation is unknown, the degree of preservation of spiral ganglion cells is generally considered to be of primary importance. A series of experiments in our laboratories, directed at quantification of surviving spiral ganglion cells in the profoundly deaf, evaluation of the predictive value of a variety of clinical parameters, and the evaluation of the consequences of implantation in the inner ear, is summarized. Histologic study of the inner ears of patients who were deafened during life demonstrated that the cause of deafness accounted for 57% of the variability of spiral ganglion cell counts. Spiral ganglion cell counts were highest in individuals deafened by aminoglycoside toxicity or sudden idiopathic deafness and lowest in those deafened by postnatal viral labyrinthitis, congenital or genetic deafness, or bacterial meningitis. Study of the determinants of degeneration of the spiral ganglion revealed that degeneration is most severe in the basal compared with the apical turn and more severe when both inner and outer hair cells are absent. Unlike the findings in some experimental animal studies, no survival advantage of type II ganglion cells could be identified. There was a strong negative correlation between the degree of bony occlusion of the cochlea and the normality of the spiral ganglion cell count. However, even in specimens in which there was severe bony occlusion, significant numbers of spiral ganglion cells survived. A strong positive correlation between the diameter of the cochlear, vestibular, and eighth cranial nerves with the total spiral ganglion cell count (p < 0.001) was found. This would suggest that modern imaging techniques may be used to predict residual spiral ganglion cell population in cochlear implant candidates. Trauma from implantation of the electrode array was studied in both cadaveric human temporal bone models and temporal bones from individuals who received implants during life. A characteristic pattern of damage to the lateral cochlear wall and basilar membrane was identified in the upper basal turn. New bone formation and perielectrode fibrosis was common after cochlear implantation. Despite this significant trauma and reaction, there is no firm evidence that further degeneration of the spiral ganglion can be predicted as a consequence.
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PMID:Patterns of neural degeneration in the human cochlea and auditory nerve: implications for cochlear implantation. 933 69

The progressive sensorineural hearing loss due to infectious causes can involve different etiological agents like bacteria, viruses, protozoons or mycetes. These infectious agents can act in various ways: directly through a labyrinthitis that may destroy the neuroepithelium; through an ischaemic process secondary to a septic embolus; or through a thrombus. In some cases the damage can occur in a meningitis context, because of the passage of the germ in the inner through the nerves, the vases or the labyrinthine liquids. Bacterial meningitis is one of the causes of progressive sensorinueral hearing loss. Among bacteria, the Mycobacterium Tuberculosis has nowadays acquired a remarkable importance which is also due to its considerable diffusion, despite modern therapy, and to its association with HIV infection. Bacteria can also cause a labyrinthitis acting directly on the inner ear: among these, Treponemas Pallidum, a spirochaete which causes syphilis and Borrelia Burgdorferi, a spirochaete that causes Lyme Disease, must be mentioned. The viruses that are certainly involved in the etiology of progressive sensorineural hearing loss are Cytomegalovirus and Rubella virus. The virus usually causes a labyrinthitis after the viraemia, wich may be due to the passage of the virus from the blood to the endolymph, through the stria vascularis with the consequent infection of the sensorial cells of the organ of Corti. Less frequently the viral damage to the inner ear can occur after a vasculitis, a meningitis or an alteration of the cell-mediated immunity. Progressive sensorineural hearing loss can also occur because of some congenital viral infections such as those caused by Cytomegalovirus and Rubella virus. More recently even the Human Parvovirus B19 seems to have been involved. This virus seems to act through autoimmune and/or immunologic processes, like that causing sudden hearing loss in Lassa fever. Another viral infection which can nowadays more frequently be considered among the cause of progressive hearing loss is HIV. In the HIV infection the neurological toxic lesions due to the administered ototoxic drugs are added up to the damages caused by the opportunistic infectious agents (virus, bacterium, protozoon mycete). However, in these patients HIV itself could be the cause of the auditory and vestibular lesions. More rarely, a progressive hearing loss may be due to the action of a protozoon or mycete only.
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PMID:[Progressive sensorineural hearing loss from infectious agents]. 1020 33

Bacterial meningitis is one of the most common causes of acquired profound sensorineural deafness in children. Measurement of hearing and examination of the cochlea is limited in patients suffering from acute meningitis. A rabbit model of pneumococcal meningitis was developed to identify the temporal bone histopathologic changes that occur in meningogenic labyrinthitis caused by Streptococcus pneumoniae. Light microscopy was previously performed on temporal bones from acutely meningitic rabbits with profound hearing loss as determined electrophysiologically. Extensive inflammation of the cochlea with endolymphatic hydrops was observed. The organ of Corti, however, showed preserved architecture in the majority of these animals. In order to further investigate these findings, a protocol was used to create meningitic rabbits with hearing loss ranging from early high-frequency loss to profound deafness. The temporal bones from 7 rabbits were examined by transmission electron microscopy. In cases of mild hearing loss, partial degeneration of the inner row of outer hair cells, as well as edema of efferent cochlear nerve endings and marginal cells of the stria vascularis, was seen. With increasing degrees of hearing loss, the remainder of the organ of Corti and intermediate cells of the stria showed ultrastructural abnormalities. Spiral ganglion cells and basal cells of the stria vascularis remained intact in all subjects. This study provides unique information regarding the histology and pathophysiology of meningogenic deafness. The clinical implications of these findings are discussed, with an emphasis on potentially reversible changes and therapeutic intervention.
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PMID:Electron microscopic temporal bone histopathology in experimental pneumococcal meningitis. 1037 20


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