DIFFUSE AXONAL INJURY AND TRAUMATIC COMA IN THE PRIMATE
DIFFUSE AXONAL INJURY AND TRAUMATIC COMA IN THE PRIMATE
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DOI：
10.1002/ana.410120611
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发表时间：
1982-01-01
影响因子：
11.2
通讯作者：
MARCINCIN, RP
中科院分区：
文献类型：
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作者：
GENNARELLI, TA;THIBAULT, LE;MARCINCIN, RP
在45只猴子中，通过在三个方向中的一个方向上加速头部而不产生冲击，造成了创伤性昏迷。昏迷持续时间、神经功能损害程度、脑弥漫性轴索损伤（DAI）量与冠状头运动量直接相关。13只头矢状位运动动物中有11只出现15分钟以内的昏迷（脑震荡），6只头斜位运动动物中有2只出现昏迷，26只头完全侧位运动动物中有2只出现昏迷。15只脑震荡动物均恢复良好，无DAI。相反，在矢状或斜向损伤组中没有出现昏迷持续6小时以上的情况，但在侧向损伤组中有20只动物出现昏迷，这些动物后来都严重残疾。所有侧伤动物的DAI程度与严重的人类头部损伤相似。矢状位组13例中有2例昏迷16分钟至6小时，斜位组6例中有4例，侧卧位组26例中有4例；与昏迷时间超过6小时的动物相比，这些动物的神经功能障碍和DAI较少。这些实验结果重复了人类创伤性昏迷的频谱，包括与人类严重头部损伤相同的轴突损伤。由于DAI的数量与损伤的严重程度（昏迷持续时间和结果质量）成正比，我们得出结论，冠状头部加速造成的轴突损伤是外伤性昏迷及其后遗症的主要原因。
Traumatic coma was produced in 45 monkeys by accelerating the head without impact in one of three directions. The duration of coma, degree of neurological impariment, and amount of diffuse axonal injury (DAI) in the brain were directly related to the amount of coronal head motion used. Coma of less than 15 minutes (concussion) occurred in 11 of 13 animals subjected to sagittal head motion, in 2 of 6 animals with oblique head motion, and in 2 of 26 animals with full lateral head motion. All 15 concussed animals had good recovery, and none had DAI. Conversely, coma lasting more than 6 hours occurred in none of the sagittal or oblique injury groups but was present in 20 of the laterally injured animals, all of which were severely disabled afterward. All laterally injured animals had a degree of DAI similar to that found in severe human head injury. Coma lasting 16 minutes to 6 hours occurred in 2 of 13 in the sagittal group, 4 of 6 in the oblique group, and 4 of 26 in the lateral group; these animals had less neurological disability and less DAI than when coma lasted longer than 6 hours. These experimental findings duplicate the spectrum of traumatic coma seen in human beings and include axonal damage identical to that seen in severe head injury in humans. Since the amount of DAI was directly proportional to the severity of injury (duration of coma and quality of outcome), we conclude that axonal damage produced by coronal head acceleration is a major cause of prolonged traumatic coma and its sequelae.