title: Pontine axonal injury after brain trauma and nontraumatic hypoxic-ischemic brain damage.
abstract: Experimental studies have shown that diffuse axonal injury is usually induced by positive or negative acceleration mechanisms. In order to determine the reliability of axonal injury (AI) as a marker of this type of traumatic insult, we compared cases of trauma-induced focal cortical hemorrhage without dural involvement (n = 67) with cases of trauma-induced subdural bleeding without cortical hemorrhage (n = 26). Both groups exhibited a wide range of post-traumatic survival times. The injuries in the first group were caused mainly by direct impact to the head, those in the second by acceleration/deceleration mechanisms. The investigations were based primarily on immunohistochemical demonstration of antibodies targeted to beta-amyloid precursor protein (beta-APP) in the pons as a marker of AI and the results were assessed semiquantitatively. No significant differences were found between the two groups. In both groups AI was detected in 80-100% of cases with survival times of more than 3 h and two thirds of all positive cases showed pronounced positivity. Additional comparison of cases of brain death due to mechanical trauma (n = 14) with cases of brain death due to non-mechanical trauma (n = 18) also disclosed no significant intergroup differences. Finally, investigations of the pons in cases of non-traumatic death due to cerebral hypoxia/ischemia (n = 51) demonstrated AI with the same frequency as in the other groups, although the expression tended to be less pronounced. Our results confirm that beta-APP expression in the pons is a reliable indicator of AI but does not discriminate between injuries caused by traumatic strain or shearing mechanisms and secondary damage due to cerebral hypoxia/ischemia or edema. In the large majority of cases with prolonged post-traumatic survival, it can therefore be assumed that AI in the pons is the consequence of primary and/or secondary events or a combination of both, as is common in non-missile head injury survived for more than 90-120 min. Therefore, positive differentiation of the type of biomechanical event based on this criterion alone is not possible.
authors.affiliation: Department of Legal Medicine, Medical University of Lübeck, Germany.
authors.forename: M
authors.initials: M
authors.lastname: Oehmichen
authors.forename: C
authors.initials: C
authors.lastname: Meissner
authors.forename: V
authors.initials: V
authors.lastname: Schmidt
authors.forename: I
authors.initials: I
authors.lastname: Pedal
authors.forename: H G
authors.initials: HG
authors.lastname: König
mesh_terms: D000293:Adolescent; D000328:Adult; D016564:Amyloid beta-Protein Precursor / Q000032:analysis; D001369:Axons / Q000473:pathology*; D001696:Biomechanical Phenomena; D001925:Brain Damage, Chronic / Q000473:pathology*; D001926:Brain Death / Q000473:pathology; D001930:Brain Injuries / Q000473:pathology*; D002543:Cerebral Hemorrhage / Q000473:pathology; D002648:Child; D002675:Child, Preschool; D005260:Female; D016489:Head Injuries, Closed / Q000473:pathology*; D006408:Hematoma, Subdural / Q000473:pathology; D006801:Humans; D002534:Hypoxia, Brain / Q000473:pathology*; D007223:Infant; D008297:Male; D008875:Middle Aged; D011149:Pons / Q000293:injuries* / Q000473:pathology; D011180:Postmortem Changes; D012183:Retrograde Degeneration / Q000473:pathology
chemical_list: D016564:Amyloid beta-Protein Precursor