Hamberger Anders, Viano David C, Säljö Annette, Bolouri Hayde
Institute of Biomedicine, Section of Anatomy and Cell Biology, University of Göteborg, Göteborg, Sweden.
Neurosurgery. 2009 Jun;64(6):1174-82; discussion 1182. doi: 10.1227/01.NEU.0000316855.40986.2A.
An animal model of concussions in National Football League players has been described in a previous study. It involves a freely moving 300-g Wistar rat impacted on the side of the head at velocities of 7.4 to 11.2 m/s with a 50-g impactor. The impact causes a 6% to 28% incidence of meningeal hemorrhages and 0.1- to 0.3-mm focal petechiae depending on the impact velocity. This study addresses the immunohistochemical responses of the brain.
Twenty-seven tests were conducted with a 50-g impactor and velocities of 7.4, 9.3, or 11.2 m/s. The left temporal region of the helmet-protected head was hit 1 or 3 times. Thirty-one additional tests were conducted with a 100-g impactor. Diffuse axonal injury in distant regions of the brain was assessed with immunohistochemistry for NF-200, the heaviest neurofilament subunit, and glial fibrillary acidic protein, an intermediate filament protein in astrocytes. Hemorrhages were analyzed by unspecific peroxidase. There were 10 controls.
A single impact at 7.4 and 9.3 m/s velocity with the 50-g impactor causes minimal neuronal injury and astrocytosis. Repeat impacts with 11.2 m/s velocity and more than 9.3-m/s impacts with 100 g cause diffuse axonal injury and distant injury bilaterally in the cerebral cortex, the subcortical, the white matter, the hippocampus CA1, the corpus callosum, and the striatum, as indicated by NF-200 accumulation in neuronal perikarya 10 days after impact. It also causes reactive astrocytosis in the midline regions of the cerebral cortex and periventricularly. Regions with erythrocyte-loaded blood capillaries indicated brain edema in regions of the cerebral cortex, the brainstem, and the cerebellum.
When the immunohistochemical results are extrapolated to professional football players, concussions result in no or minimal brain injury. Repeat impacts at higher velocity or with a heavier mass impactor cause extensive and distant diffuse axonal injury. Based on this model, the threshold for diffuse axonal injury is above even the most severe conditions for National Football League concussion.
先前的一项研究描述了美国国家橄榄球联盟(National Football League)球员脑震荡的动物模型。该模型使用一只重50克的撞击器,以7.4至11.2米/秒的速度撞击一只自由活动的300克Wistar大鼠的头部侧面。根据撞击速度的不同,撞击会导致6%至28%的脑膜出血发生率以及0.1至0.3毫米的局灶性瘀点。本研究探讨了大脑的免疫组化反应。
使用50克撞击器,以7.4、9.3或11.2米/秒的速度进行了27次测试。对头盔保护的头部左侧颞区进行1次或3次撞击。另外使用100克撞击器进行了31次测试。通过免疫组化检测NF-200(最重的神经丝亚基)和胶质纤维酸性蛋白(星形胶质细胞中的一种中间丝蛋白),评估大脑远处区域的弥漫性轴索损伤。通过非特异性过氧化物酶分析出血情况。设置了10个对照组。
使用50克撞击器,以7.4和9.3米/秒的速度单次撞击会导致最小程度的神经元损伤和星形细胞增多。以11.2米/秒的速度重复撞击以及使用100克撞击器以超过9.3米/秒的速度撞击,会导致大脑皮质、皮质下、白质、海马CA1区、胼胝体和纹状体双侧出现弥漫性轴索损伤和远处损伤,这在撞击后10天神经元胞体中NF-200的积累情况中得到体现。它还会导致大脑皮质中线区域和脑室周围出现反应性星形细胞增多。大脑皮质、脑干和小脑区域有红细胞填充的毛细血管表明存在脑水肿。
当将免疫组化结果外推至职业橄榄球运动员时,脑震荡导致的脑损伤无或极小。更高速度或更重质量的撞击器重复撞击会导致广泛的远处弥漫性轴索损伤。基于此模型,弥漫性轴索损伤的阈值甚至高于美国国家橄榄球联盟脑震荡最严重的情况。