M. Oehmichen et al., Brain injury after survived gunshot to the head: reactive alterations at sites remote from the missile track, FOREN SCI I, 115(3), 2001, pp. 189-197
Gunshot wounds to the brain usually lead to acute respiratory arrest or dea
th after a brief survival period, even in cases involving only slight direc
t tissue damage. It can be assumed therefore that the damage extends beyond
the zone of recognizable destruction and hemorrhages. To determine the tru
e extent of the tissue injury resulting from gunshot wounds to the brain, w
e carried out microscopic investigations for reactive changes (emigration o
f leukocytes and macrophages, axonal expression of beta -amyloid precursor
protein (beta -APP) in 10 cases of gunshot wound to the narrow channel of t
he brain with survival times >2 h. Demonstration of leukocytes expressing n
aphthol AS-D chloroacetate esterase activity in the brain tissue at the bor
der of the missile track established the vitality of the gunshot effect. Th
e presence of macrophages (CD68-epitope) allowed demarcation of a 1-2 mm wi
de necrotic zone around the permanent cavity. Within this zone and beyond,
beta -APP showed an initial increase followed by a decline in the number of
injured axons. Three types of beta -APP positive staining could be differe
ntiated. In the immediate vicinity of the missile track beta -APP positive
neurons were present at a distance of 2-4 mm from the margin of the permane
nt cavity (type 1) as a result of primary injured neuronal tissue by the gu
nshot itself. At longer distances from the narrow channel and the permanent
cavity single beta -APP positive axons or axon fragments and two additiona
l types were found; type 2 shows a parallel, wave-like arrangement of the d
amaged fibers, which suggests that the injury was produced by mechanical ac
celeration of the brain tissue created by the energy the projectile expende
d within the brain; irregular aggregation of beta -APP positive axons or ax
on fragments within a local edema represents type 3, which may be attribute
d to secondary ischemia or edema. (C) 2001 Elsevier Science Ireland Ltd. Al
l rights reserved.