Neuropathophysiology of Brain Injury.
Neuropathophysiology of Brain Injury.
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DOI：
10.1016/j.anclin.2016.04.011
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发表时间：
2016-09
影响因子：
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通讯作者：
Traystman, Richard J
中科院分区：
文献类型：
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作者：
Quillinan, Nidia;Herson, Paco S;Traystman, Richard J
在美国，每年有数百万人因中风、心脏骤停或创伤性脑损伤（TBI）而遭受缺血性脑损伤。这些形式的后天性脑损伤可能导致死亡，或在许多情况下导致长期的神经和神经心理障碍。导致这些缺陷的缺血性和创伤性脑损伤的机制是由多个相互依赖的分子通路的复杂相互作用引起的，所述分子通路包括兴奋性毒性、酸毒性、离子失衡、氧化应激、炎症和细胞凋亡。本文简要回顾了几个传统的，众所周知的脑损伤机制，然后讨论了最近的发展和更新的机制。尽管关于损伤机制和操纵这些机制以导致损伤动物模型中神经元的保护和行为表现的增加的已知很多，但是难以将这些效果转化为人类。注意力是给予为什么这是如此和新的结果伤害的措施进行了讨论。
Every year in the United States, millions of individuals incur ischemic brain injury from stroke, cardiac arrest, or traumatic brain injury (TBI). These forms of acquired brain injury can lead to death, or in many cases long-term neurologic and neuropsychological impairments. The mechanisms of ischemic and traumatic brain injuries that lead to these deficiencies result from a complex interplay of multiple interdependent molecular pathways that include excitotoxicity, acidotoxicity, ionic imbalance, oxidative stress, inflammation, and apoptosis. This article briefly reviews several of the traditional, well-known mechanisms of brain injury and then discusses more recent developments and newer mechanisms. Although much is known concerning mechanisms of injury and the manipulation of these mechanisms to result in protection of neurons and increased behavioral performance in animal models of injury, it has been difficult to translate these effects to humans. Attention is given to why this is so and newer outcome measures of injury are discussed.