Pontine axonal injury after brain trauma and nontraumatic hypoxic-ischemic brain damage

• Verfasst von: Oehmichen, Manfred [VerfasserIn]
• Verfasst von: Meißner, C. [VerfasserIn]
• Verfasst von: Schmidt, V. [VerfasserIn]
• Verfasst von: Pedal, Ingo [VerfasserIn]
• Verfasst von: König, H. G. [VerfasserIn]
• Titel: Pontine axonal injury after brain trauma and nontraumatic hypoxic-ischemic brain damage
• Verf.angabe: M. Oehmichen, C. Meißner, V. Schmidt, I. Pedal, H.G. König
• E-Jahr: 1999
• Jahr: June 1999
• Umfang: 7 S.
• Teil: volume:112
• Teil: year:1999
• Teil: number:4
• Teil: pages:261-267
• Teil: extent:7
• Fussnoten: Gesehen am 27.04.2021
• Titel Quelle: Enthalten in: International journal of legal medicine
• Ort Quelle: Berlin : Springer, 1922
• Jahr Quelle: 1999
• Band/Heft Quelle: 112(1999), 4, Seite 261-267
• ISSN Quelle: 1437-1596
• DOI: doi:10.1007/s004140050246
• Datenträger: Online-Ressource
• Sprache: eng
• K10plus-PPN: 1756041601

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 β-amyloid precursor protein (β-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 β-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.