The cochlear lesion in experimental XXXX of the @entity95 .

@entity4008 @entity548 @entity327 @entity95 @entity693 @entity281 @entity1274 @entity393 @entity526
@entity1274 was studied in a @entity95 model of experimental @entity4008 using electrophysiological and ultrastructural techniques. Hearing impairment was monitored by auditory brain-stem evoked responses (ABERs) and concomitant structural lesions were identified by both transmission (TEM) and scanning (SEM) electron microscopy. @entity693 was induced by intra-cerebrospinal fluid injection of either @entity526 2073 and type K-12) or @entity327 type b. Auditory loss of approximately equal to 10 dB occurred in all @entity95 by about 10 hours post @entity281 and progressed in severity until by 20 h following @entity281 , @entity393 up to and > 60 dB were obtained. At levels of @entity393 < 20 dB ultrastructural damage to the organ of Corti was barely detectable. With greater levels of @entity393 , patchy structural damage to hair cells, synaptic nerve terminals, supporting cells and inner spiral sulcus cells and cells of the stria vascularis was clearly evident. Bacteria were found in scala tympani, the basilar membrane, the organ of Corti, scala media, the spiral ligament and at the margin of the stria vascularis. Evidence of @entity548 was found in some cochleas; erythrocytes were found in scala tympani, scala media, amongst hair cells and beneath the tectorial membrane. The results show that @entity393 is associated with bacterial invasion and damage to the organ of Corti and that the cause of @entity393 is likely to result from multiple lesions within the cochlea. Lesions to sensory cells almost certainly will produce permanent @entity393 . Lesions to supporting cells, nerve terminals and to stria vascularis may well produce only temporary @entity393 .
