A HUMAN TEMPORAL BONE STUDY OF ACUTE BACTERIAL MENINGOGENIC LABYRINTHITIS

It is well established that sensorineural hearing loss (SNHL) is an im portant sequela of acute bacterial menin gitis. Previous human tempora l bone histopathologic studies have suggested that such hearing loss i s due to labyrinthitis. This study involved a detailed and systematic evaluation of the auditory and vestibular end-organs in 41 human tempo ral bones from patients with acute bacterial meningitis, aimed at desc ribing the spectrum of histopathologic changes within the labyrinth, a scertaining likely routes for spread of infection from the meninges to the inner ear, and comparing the data from humans with those describe d in a rabbit model of meningogenic labyrinthitis. Our study revealed the following: (a) Suppurative labyrinthitis occurred in 20 (49%) bone s. Of these 20 bones, the cochlea was affected in all, whereas the ves tibular 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 stain ing 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 stai ning of inner ear fluids. This finding raises the possibility of preve nting or reversing SNHL by therapeutic intervention. Spiral ganglion c ells were severely degenerated in 12% of bones, Indicating a retrococh lear site of hearing loss in addition to the cochlea. This subset of p atients may perform poorly after cochlear implantation; (c) It has bee n traditionally assumed that irreversible and permanent SNHL is caused by suppurative labyrinthitis, whereas reversible SNHL is caused by se rous labyrinthitis. Our findings question the validity of these assump tions; (d) The data were consistent with the hypothesis that both the cochlear modiolus and cochlear aqueduct can serve as potential pathway s for spread of infection from the meninges to the inner ear; (e) Ther e were many similarities in the histopathology of the inner ear in hum ans when compared with the rabbit model of meningogenic labyrinthitis. A notable difference was that the cochlear aqueduct appeared to be th e sole pathway for spread of infection in the rabbit, whereas in the h uman, both the modiolus and aqueduct were possible pathways.