Rovegno M, Soto P A, Sáez J C, von Bernhardi R
Laboratorio de Neurociencias y Departamento de Medicina Intensiva, Facultad de Medicina, Pontificia Universidad Católica de Chile, Chile.
Med Intensiva. 2012 Jan-Feb;36(1):37-44. doi: 10.1016/j.medin.2011.06.008. Epub 2011 Sep 7.
Traumatic brain injury (TBI) is a worldwide health problem that is especially prevalent in young adults. It is characterized by one or more primary injury foci, with secondary spread to initially not compromised areas via cascades of inflammatory response, excitotoxicity, energy failure conditions, and amplification of the original tissue injury by glia. In theory, such progression of injury should be amenable to management. However, all neuroprotective drug trials have failed, and specific treatments remain lacking. These negative results can be explained by a neuron centered approach, excluding the participation of other cell types and pathogenic mechanisms. To change this situation, it is necessary to secure a better understanding of the biological mechanisms determining damage progression or spread. We discuss the biological mechanisms involved in the progression of post-trauma tissue damage, including the general physiopathology of TBI and cellular mechanisms of secondary damage such as inflammation, apoptosis, cell tumefaction, excitotoxicity, and the role of glia in damage propagation. We highlight the role of glia in each cellular mechanism discussed. Therapeutic approaches related to the described mechanisms have been included. The discussion is completed with a working model showing the convergence of the main topics.
创伤性脑损伤（TBI）是一个全球性的健康问题，在年轻人中尤为普遍。它的特征是存在一个或多个原发性损伤灶，并通过炎症反应、兴奋性毒性、能量衰竭状态的级联反应以及胶质细胞对原始组织损伤的放大作用，继发扩散至最初未受影响的区域。从理论上讲，这种损伤进展应该是可以控制的。然而，所有神经保护药物试验均告失败，目前仍缺乏特效治疗方法。这些负面结果可以用一种以神经元为中心的方法来解释，该方法排除了其他细胞类型和致病机制的参与。为改变这种状况，有必要更好地了解决定损伤进展或扩散的生物学机制。我们讨论了创伤后组织损伤进展过程中涉及的生物学机制，包括TBI的一般病理生理学以及继发性损伤的细胞机制，如炎症、凋亡、细胞肿胀、兴奋性毒性，以及胶质细胞在损伤传播中的作用。我们强调了胶质细胞在上述每种细胞机制中的作用。文中还纳入了与所描述机制相关的治疗方法。最后通过一个工作模型展示了主要主题的融合，从而完成了本次讨论。
