Brain injury after survived gunshot to the head: reactive alterations at sites remote from the missile track.
Gunshot wounds to the brain usually lead to acute respiratory arrest or death after a brief survival period, even in cases involving only slight direct tissue damage. It can be assumed therefore that the damage extends beyond the zone of recognizable destruction and hemorrhages. To determine the true extent of the tissue injury resulting from gunshot wounds to the brain, we carried out microscopic investigations for reactive changes (emigration of leukocytes and macrophages, axonal expression of beta-amyloid precursor protein (beta-APP) in 10 cases of gunshot wound to the narrow channel of the brain with survival times >2h. Demonstration of leukocytes expressing naphthol AS-D chloroacetate esterase activity in the brain tissue at the border of the missile track established the vitality of the gunshot effect. The presence of macrophages (CD68-epitope) allowed demarcation of a 1-2mm wide 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 differentiated. In the immediate vicinity of the missile track beta-APP positive neurons were present at a distance of 2-4mm from the margin of the permanent cavity (type 1) as a result of primary injured neuronal tissue by the gunshot itself. At longer distances from the narrow channel and the permanent cavity single beta-APP positive axons or axon fragments and two additional types were found; type 2 shows a parallel, wave-like arrangement of the damaged fibers, which suggests that the injury was produced by mechanical acceleration of the brain tissue created by the energy the projectile expended within the brain; irregular aggregation of beta-APP positive axons or axon fragments within a local edema represents type 3, which may be attributed to secondary ischemia or edema.
Oehmichen
M
M
Department of Legal Medicine, Medical University of Lübeck, Kahlhorststrasse 31-35, D-23562, Lübeck, Germany. oehmich@rmed.mu-luebeck.de
Meissner
C
C
König
H G
HG
D000328:Adult; D000368:Aged; D016564:Amyloid beta-Protein Precursor / Q000032:analysis; D015703:Antigens, CD / Q000032:analysis; D015214:Antigens, Differentiation, Myelomonocytic / Q000032:analysis; D001344:Autopsy / Q000379:methods*; D001696:Biomechanical Phenomena; D001706:Biopsy / Q000379:methods*; D001926:Brain Death; D001930:Brain Injuries / Q000150:complications* / Q000473:pathology* / Q000628:therapy; D020833:Diffuse Axonal Injury / Q000209:etiology* / Q000473:pathology*; D005260:Female; D006801:Humans; D007150:Immunohistochemistry; D007962:Leukocytes / Q000473:pathology; D008264:Macrophages / Q000473:pathology; D008297:Male; D008875:Middle Aged; D009336:Necrosis; D012121:Respiration, Artificial; D013997:Time Factors; D014948:Wounds, Gunshot / Q000150:complications* / Q000473:pathology* / Q000628:therapy; D000097382:CD68 Molecule
D016564:Amyloid beta-Protein Precursor; D015703:Antigens, CD; D015214:Antigens, Differentiation, Myelomonocytic; C067980:CD68 antigen, human; D000097382:CD68 Molecule