@entity7181 : a pathophysiological model in the XXXX .

@entity1690 @entity1333 @entity4 @entity602 @entity95 @entity794 @entity1746 @entity51 @entity1745 @entity1188 @entity14159 @entity451 @entity7181 @entity715
To define the pathophysiology of @entity602 associated with @entity7181 formation, we developed an experimental model. Spinal epidural abscesses were produced in @entity95 by injecting @entity794 into the posterior thoracolumbar epidural space under direct vision. Progressive @entity51 were detected in 18 of 20 animals; severe @entity1746 or @entity451 occurred in 75%, and @entity1690 occurred in 55%. Clinical data, including the results of plain spine roentgenography, myelography, and biochemical and bacteriological examination of the cerebrospinal fluid, were recorded. Epidural abscesses with varying degrees of @entity1745 were confirmed pathologically in 95% of the experimental group. Spinal cord white matter changes included vacuolization, loss of myelin, and @entity4 . The gray matter of the spinal cords was relatively preserved. There was no microscopic evidence of @entity715 or @entity1333 in the major blood vessels supplying the spinal cords. Histopathological changes detected in the spinal cords were more consistent with direct compression of neural tissue than with @entity1188 . The progressive clinical course and the histopathological changes in the spinal cord after compression by abscess closely resembled those of experimental compression of the spinal cord by @entity14159 .
