Cernak Ibolja
Biomedicine Business Area, National Security Technology Department, Johns Hopkins University Applied Physics Laboratory Laurel, MD, USA.
Front Neurol. 2010 Dec 10;1:151. doi: 10.3389/fneur.2010.00151. eCollection 2010.
Due to complex injurious environment where multiple blast effects interact with the body parallel, blast-induced neurotrauma is a unique clinical entity induced by systemic, local, and cerebral responses. Activation of autonomous nervous system; sudden pressure increase in vital organs such as lungs and liver; and activation of neuroendocrine-immune system are among the most important mechanisms that contribute significantly to molecular changes and cascading injury mechanisms in the brain. It has been hypothesized that vagally mediated cerebral effects play a vital role in the early response to blast: this assumption has been supported by experiments where bilateral vagotomy mitigated bradycardia, hypotension, and apnea, and also prevented excessive metabolic alterations in the brain of animals exposed to blast. Clinical experience suggests specific blast-body-nervous system interactions such as (1) direct interaction with the head either through direct passage of the blast wave through the skull or by causing acceleration and/or rotation of the head; and (2) via hydraulic interaction, when the blast overpressure compresses the abdomen and chest, and transfers its kinetic energy to the body's fluid phase, initiating oscillating waves that traverse the body and reach the brain. Accumulating evidence suggests that inflammation plays important role in the pathogenesis of long-term neurological deficits due to blast. These include memory decline, motor function and balance impairments, and behavioral alterations, among others. Experiments using rigid body- or head protection in animals subjected to blast showed that head protection failed to prevent inflammation in the brain or reduce neurological deficits, whereas body protection was successful in alleviating the blast-induced functional and morphological impairments in the brain.
由于存在多种爆炸效应与身体并行相互作用的复杂致伤环境，爆炸所致神经创伤是一种由全身、局部和脑部反应引起的独特临床实体。自主神经系统的激活；肺和肝等重要器官的突然压力升高；以及神经内分泌免疫系统的激活，是对大脑分子变化和级联损伤机制有重大贡献的最重要机制。据推测，迷走神经介导的脑部效应在爆炸的早期反应中起关键作用：双侧迷走神经切断术减轻心动过缓、低血压和呼吸暂停，并防止暴露于爆炸的动物大脑中过度的代谢改变，这些实验支持了这一假设。临床经验表明存在特定的爆炸-身体-神经系统相互作用，例如：(1) 通过爆炸波直接穿过颅骨或通过引起头部加速和/或旋转与头部直接相互作用；以及(2) 通过液压相互作用，当爆炸超压压缩腹部和胸部并将其动能传递到身体的液相时，引发穿过身体并到达大脑的振荡波。越来越多的证据表明，炎症在爆炸所致长期神经功能缺损的发病机制中起重要作用。这些包括记忆衰退、运动功能和平衡受损以及行为改变等。在遭受爆炸的动物中使用刚体或头部保护的实验表明，头部保护未能预防脑部炎症或减少神经功能缺损，而身体保护成功减轻了爆炸所致的大脑功能和形态损伤。
