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 105 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.
The development of hearing loss and concomitant cerebrospinal fluid (CSF) cytochemical changes in a model of pneumococcal meningitis were examined. Rabbits were injected intracisternally with 10(5) pneumococci. Auditory evoked potentials to clicks and to 10- and 1-kHz tone bursts were recorded hourly; CSF was analyzed every 4 h. Sensorineural hearing loss developed in all animals beginning 12 h after infection and progressed to severe deafness. The onset of hearing loss was preceded by a CSF leukocytosis of > 2000 cells/microL and elevation of CSF protein and lactate concentrations to > or = 1 mg/mL. Temporal bone histopathology showed pneumococci and leukocytes extending from the CSF to the perilymph via the cochlear aqueduct. Hearing loss can develop early in the course of meningitis and is preceded by the abrupt onset of inflammatory changes in CSF. Progression of hearing loss is rapid and proceeds from cochlear base to apex in parallel with the degree of inflammation.
Pneumococcal meningitis remains a significant cause of morbidity, particularly sensorineural hearing loss. Recent literature has suggested that a vigorous host immune response to Streptococcus [corrected] pneumoniae is responsible for much of the neurologic sequelae, including deafness, after bacterial meningitis. This study used a rabbit model of hearing loss in experimental pneumococcal meningitis to evaluate the therapeutic effect of two anti-inflammatory agents, dexamethasone and ketorolac, coadministered with ampicillin. Both adjunctive drugs minimized or prevented sensorineural hearing loss compared with placebo. Dexamethasone, administered 10 min before ampicillin, was particularly effective in minimizing mean hearing threshold change compared with placebo for both clicks (dexamethasone: 6.7-dB sound pressure level [SPL] vs. placebo: 33. 4-dB SPL, P=.0078) and 10-kHz tone bursts (dexamethasone: 8.4-dB SPL vs. placebo: 53.4-dB SPL, P=.0003). These findings support the beneficial role of anti-inflammatory agents in reducing the incidence of hearing loss from pneumococcal meningitis, especially if therapy is instituted early in the course of infection.
Malignant triton tumor is a rare, usually aggressive sarcoma consisting of a malignant schwannoma with rhabdomyoblastic differentiation. Although 20% of cases are located in the head and neck, this unusual tumor has not-to our knowledge-been described in the otolaryngology literature. We present the tenth reported case of triton tumor of the head and neck and the second involving the paranasal sinuses.'-9 An analysis of head and neck triton tumors suggests a possible subset of patients with lower-grade histology and improved survival, compared with triton tumors that occur elsewhere.
CASE REPORTA 66-ye=-old woman went to her physician with a 1-year history of left nasal airway obstruction. She was treated with antibiotics for a diagnosis of sinusitis, with no improvement. A few months later, profuse left-sided epistaxis developed. A bleeding granular mass of the left nasal cavity was noted and subsequently underwent wide biopsy. Pathology suggested a malignant spindle-cell tumor. A CT scan revealed a large mass of the left nasal cavity involving the left ethmoid sinus and orbit (Fig. 1). She was referred to the Massachusetts Eye and Ear Infirmary.The patient's history was otherwise unremarkable. She had noted no anosmia or visual symptoms. Examination revealed a patent left nasal cavity status after wide biopsy. A detailed ophthalmologic evaluation revealed 2.5 mm of proptosis of the left eye, but was otherwise normal. Review of the pathology specimen revealed polypoid spindle cells with foci consistent with skeletal muscle differentiation and rare mitoses, suggestive of an unusual benign neoplasm.A left external, extended ethmoidectomy approach was performed to excise what was thought to be a benign or lowgrade malignant tumor. A fleshy grey mass was found, centered on the left posterior ethmoid sinus, displacing, thinning, and eroding the lamina papyracea and floor of the anterior cranial fossa. Dura and periorbiturn abutted tumor, but were From the Departments of Otolaryngology and Pathology, The Mas-
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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