TY - JOUR
T1 - A case of diffuse axonal injury in violent death
AU - Mochizuki, Kaori
AU - Ochi, Hiroshi
AU - Ogura, Yoshiaki
AU - Iino, Morio
AU - Kuroki, Hisanaga
AU - Matoba, Ryoji
PY - 2009/4
Y1 - 2009/4
N2 - A 59-year-old man was carried to the hospital by three men. The deceased was unconscious at admission and his face was severely swollen with many subcutaneous hemorrhages and extensive edema. His death was confirmed 17 min after resuscitation. A judicial autopsy was performed the next day. Findings showed that the victim's face and head were reddish and swollen, and that subscalp bleeding was ubiquitous, but no skull fracture, epi- and subdural hematoma or subarachnoidal bleeding was observed. The brain itself was severely edematous but no bleeding was found. Although small hemorrhages were seen in the limbs and back, there were no marked wounds except to the head. To determine the cause of death, we performed a microscopic histochemical examination. Conventional H.E. staining disclosed eosinophilic change, concentration of nuclei, edema, gliosis, and oozing at the corpus callosum. To identify further details of the cause of death, we used Bodian staining, Kluver-Barrera staining, anti-beta amyloid immunostaining, and anti-neurofilament immunostaining. We found sinusoidal swelling of axons and waving axons, which are typical findings of Diffuse Axonal Injury (DAI), but no positive staining of beta amyloid. Focal lesions of the corpus callosum and of the dorsolateral quadrant of the rostral brain stem, and diffuse damage to axons are considered to constitute the DAI triad. We therefore diagnosed the cause of death as DAI. Our experience shows that it is important to use several staining methods for diagnosis of a variety of neuronal degenerative disorders. Several days later, we were informed by the police that several men had hit and kicked the victim in an attempt to lynch him. To compare with this case, we also report two other cases in which DAI was observed.
AB - A 59-year-old man was carried to the hospital by three men. The deceased was unconscious at admission and his face was severely swollen with many subcutaneous hemorrhages and extensive edema. His death was confirmed 17 min after resuscitation. A judicial autopsy was performed the next day. Findings showed that the victim's face and head were reddish and swollen, and that subscalp bleeding was ubiquitous, but no skull fracture, epi- and subdural hematoma or subarachnoidal bleeding was observed. The brain itself was severely edematous but no bleeding was found. Although small hemorrhages were seen in the limbs and back, there were no marked wounds except to the head. To determine the cause of death, we performed a microscopic histochemical examination. Conventional H.E. staining disclosed eosinophilic change, concentration of nuclei, edema, gliosis, and oozing at the corpus callosum. To identify further details of the cause of death, we used Bodian staining, Kluver-Barrera staining, anti-beta amyloid immunostaining, and anti-neurofilament immunostaining. We found sinusoidal swelling of axons and waving axons, which are typical findings of Diffuse Axonal Injury (DAI), but no positive staining of beta amyloid. Focal lesions of the corpus callosum and of the dorsolateral quadrant of the rostral brain stem, and diffuse damage to axons are considered to constitute the DAI triad. We therefore diagnosed the cause of death as DAI. Our experience shows that it is important to use several staining methods for diagnosis of a variety of neuronal degenerative disorders. Several days later, we were informed by the police that several men had hit and kicked the victim in an attempt to lynch him. To compare with this case, we also report two other cases in which DAI was observed.
KW - Autopsy
KW - Case reports
KW - Corpus callosum
KW - Diffuse Axonal Injury
KW - Pathology
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U2 - 10.1016/j.legalmed.2009.02.039
DO - 10.1016/j.legalmed.2009.02.039
M3 - Article
C2 - 19345128
AN - SCOPUS:67349125392
VL - 11
SP - S518-S519
JO - Legal Medicine
JF - Legal Medicine
SN - 1344-6223
IS - SUPPL. 1
ER -