P-2-196 - Epidemiologic transition of traumatic brain injury (TBI)

Abstract

We used β-amyloid precursor protein (β-APP) to investigate our own forensic neuropathological case material (n=252) in light of the current literature on the phenomenon “axonal injury” (AI) to determine the incidence, specificity and biomechanical significance of AI and its significance for determining vitality and survival time. The case material consisted of cases of fatal nonmissile closed-head injury (n=119), gunshot injury (n=30), fatal cerebral ischemia/hypoxia (n=51), brain death caused by mechanical trauma (n=14) or nonmechanical injury (n=18), and acute hemorrhagic shock (n=20). AI was observed in 65% to 100% of cases of closed-head injury, fatal cerebral ischemia/hypoxia, and brain death with a survival time of more than 3 h; AI could not be detected in the cases of acute hemorrhagic shock. A statistically significant difference between traumatically and nontraumatically induced (nondisruptive) AI was not found. There was no statistical evidence of a correlation between AI and the different types of external force, since AI could be demonstrated after both acceleration/deceleration injuries and traumatic impact. Therefore, biomechanical inferences for reconstruction purposes are not possible. On the other hand, β-APP was found to be a definite marker of vitality. In our material, cases with a posttraumatic interval of under 180 min did not express β-APP. Moreover, the literature shows that the posttraumatic interval can be determined by other methods for demonstration of AI such as by ubiquitin immunostaining (360 min), silver staining (15–18 h), hematoxylin and eosin staining (about 24 h), or by demonstration of a microglial reaction (about 4 to 10 days) or of a few remaining isolated bulbs, without accompanying fibers, which can be detected after a survival time of up to 17 months.