Li Dong-Ri, Zhang Fu, Wang Yao, Tan Xiao-Hui, Qiao Dong-Fang, Wang Hui-Jun, Michiue Tomomi, Maeda Hitoshi
Department of Forensic Medicine, Southern Medical University, Guangzhou, Guangdong Province, PR China.
Leg Med (Tokyo). 2012 Mar;14(2):84-92. doi: 10.1016/j.legalmed.2011.12.007. Epub 2012 Feb 1.
Previous studies have shown that diffuse cortical astrocyte damage is seen in acute deaths due to brain injury and mechanical asphyxiation. The present study quantitatively investigated the number of astrocytes that showed GFAP- and S100-protein immunopositivity in the cerebral white matter and hippocampus at the sites distant from primary injury with regard to survival time, complication, and the immediate cause of death of brain injury cases. Autopsy cases of brain injury (8-48 h postmortem) comprising acute/subacute deaths (survival time, <3/6 h-3 days; n=27/42) and delayed deaths (survival time >3 days) with/without complications (n=30/22) were examined. Delayed death cases with complications were subdivided into those in which the immediate cause of death had been determined as cerebral dysfunction (n=22) and those that had been determined as due to fatal complications (n=8). For controls, natural deaths from pneumonias (n=12) and sudden cardiac deaths (n=27) were used. In brain injury cases, the numbers of astrocytes in the cerebral white matter and hippocampal CA4 region were significantly lower for subacute death and delayed death without complications (p<0.05-0.001). Delayed death with fatal complications showed a significant increase in the number of astrocytes (p<0.05). Among delayed death cases, the numbers of astrocytes were higher in the cases with fatal complications than in those without complications and with non-fatal complications, although the latter cases showed large variations in the numbers of these astrocytes. These findings suggest that critical brain injury causes acute death without evident astrocyte pathology and that subacute death is associated with progressive brain damage accompanied by an astrocyte loss. In delayed death cases, the numbers astrocytes might be closely related to the severity of posttraumatic brain injury. GFAP and S100-immunopositivity might be useful for elucidating the cause and process of deaths due to brain injury.
先前的研究表明，在因脑损伤和机械性窒息导致的急性死亡中可见弥漫性皮质星形胶质细胞损伤。本研究定量调查了脑损伤病例在远离原发性损伤部位的脑白质和海马中显示胶质纤维酸性蛋白（GFAP）和S100蛋白免疫阳性的星形胶质细胞数量，涉及生存时间、并发症以及脑损伤病例的直接死因。对脑损伤尸检病例（死后8 - 48小时）进行了检查，这些病例包括急性/亚急性死亡（生存时间，<3/6小时 - 3天；n = 27/42）和有/无并发症的延迟死亡（生存时间>3天）（n = 30/22）。有并发症的延迟死亡病例又细分为直接死因被确定为脑功能障碍的病例（n = 22）和被确定为因致命并发症导致的病例（n = 8）。作为对照，使用了因肺炎自然死亡的病例（n = 12）和心源性猝死的病例（n = 27）。在脑损伤病例中，亚急性死亡和无并发症的延迟死亡时，脑白质和海马CA4区的星形胶质细胞数量显著减少（p<0.05 - 0.001）。因致命并发症导致的延迟死亡显示星形胶质细胞数量显著增加（p<0.05）。在延迟死亡病例中，有致命并发症的病例中星形胶质细胞数量高于无并发症和有非致命并发症的病例，尽管后一类病例中这些星形胶质细胞的数量变化很大。这些发现表明，严重脑损伤导致急性死亡时无明显的星形胶质细胞病变，而亚急性死亡与伴有星形胶质细胞丢失的进行性脑损伤有关。在延迟死亡病例中，星形胶质细胞数量可能与创伤后脑损伤的严重程度密切相关。GFAP和S100免疫阳性可能有助于阐明脑损伤死亡的原因和过程。
