Quantitative neuropathology of a focal @entity128 causing XXXX .

@entity1 @entity1931 @entity714 @entity4 @entity16 @entity128 @entity158 @entity6441 @entity35 @entity8638
The @entity8638 ( @entity8638 ) model of @entity16 in the @entity35 produces @entity1931 and @entity1931 in the sciatic distribution of one hindlimb. We previously described the pathology of the affected nerves at the light microscopic and electron microscopic levels and in this report quantify the morphological changes of the nerves. This analysis gives new insights into the pathophysiology and @entity158 -related mechanisms in this model of @entity1 @entity16 . We observed that total @entity714 increased up to fourfold due to an initial massive increase in @entity4 and, later, endoneurial cells. Intact myelinated nerve fibers were reduced from 75% of @entity714 to 29.7% on day 1 and to a minimum of less than 0.5% on day 14 when @entity4 had resolved. The few surviving myelinated fibers were in the small to medium size range. Fiber size histograms revealed an increase in fiber size early on, corresponding to fiber swelling, and the later loss of large as well as small myelinated fibers. Unmyelinated nerve fibers dropped from 19.36/1,000 microns 2 to 6.08/1,000 microns 2 on day 5, and increased from there on. Sprouts were first visible on light micrographs on day 7, occupying 6.8% of @entity714 , while regenerating fibers that were undergoing myelination reached 42.6% of @entity714 by day 42. Macrophage numbers were maximal on day 14 and were still increased on day 42. These data support the hypothesis that the pathogenesis of the extended @entity1931 following chronic @entity128 is temporally linked with @entity6441 and macrophage activation.(ABSTRACT TRUNCATED AT 250 WORDS)
