PMID- 10433037
OWN - NLM
STAT- MEDLINE
DCOM- 19990924
LR  - 20191024
IS  - 0937-9827 (Print)
IS  - 0937-9827 (Linking)
VI  - 112
IP  - 4
DP  - 1999
TI  - Pontine axonal injury after brain trauma and nontraumatic hypoxic-ischemic brain 
      damage.
PG  - 261-7
AB  - 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.
FAU - Oehmichen, M
AU  - Oehmichen M
AD  - Department of Legal Medicine, Medical University of Lubeck, Germany.
FAU - Meissner, C
AU  - Meissner C
FAU - Schmidt, V
AU  - Schmidt V
FAU - Pedal, I
AU  - Pedal I
FAU - Konig, H G
AU  - Konig HG
LA  - eng
PT  - Journal Article
PL  - Germany
TA  - Int J Legal Med
JT  - International journal of legal medicine
JID - 9101456
RN  - 0 (Amyloid beta-Protein Precursor)
SB  - IM
MH  - Adolescent
MH  - Adult
MH  - Amyloid beta-Protein Precursor/analysis
MH  - Axons/*pathology
MH  - Biomechanical Phenomena
MH  - Brain Damage, Chronic/*pathology
MH  - Brain Death/pathology
MH  - Brain Injuries/*pathology
MH  - Cerebral Hemorrhage/pathology
MH  - Child
MH  - Child, Preschool
MH  - Female
MH  - Head Injuries, Closed/*pathology
MH  - Hematoma, Subdural/pathology
MH  - Humans
MH  - Hypoxia, Brain/*pathology
MH  - Infant
MH  - Male
MH  - Middle Aged
MH  - Pons/*injuries/pathology
MH  - Postmortem Changes
MH  - Retrograde Degeneration/pathology
EDAT- 1999/08/05 00:00
MHDA- 1999/08/05 00:01
CRDT- 1999/08/05 00:00
PHST- 1999/08/05 00:00 [pubmed]
PHST- 1999/08/05 00:01 [medline]
PHST- 1999/08/05 00:00 [entrez]
AID - 10.1007/s004140050246 [doi]
PST - ppublish
SO  - Int J Legal Med. 1999;112(4):261-7. doi: 10.1007/s004140050246.