Department of Pathology and Laboratory Medicine, University of British Columbia, Vancouver BC, Canada.
Curr Opin Neurol. 2010 Jun;23(3):293-9. doi: 10.1097/WCO.0b013e328337f451.
Although a number of factors contribute to the high mortality and morbidity associated with traumatic brain injury (TBI), the development of cerebral edema with brain swelling remains the most significant predictor of outcome. The present review summarizes the most recent advances in the understanding of mechanisms associated with development of posttraumatic cerebral edema, and highlights areas of therapeutic promise.
Despite the predominance of cytotoxic (or cellular) edema in the first week after traumatic brain injury, brain swelling can only occur with addition of water to the cranial vault from the vasculature. As such, regulation of blood-brain barrier permeability has become a focus of recent research seeking to manage brain edema. Aquaporins, matrix metalloproteinases and vasoactive inflammatory agents have emerged as potential mediators of cerebral edema following traumatic brain injury. In particular, kinins (bradykinins) and tachykinins (substance P) seem to play an active physiological role in modulating blood-brain barrier permeability after trauma. Substance P neurokinin-1 receptor antagonists show particular promise as novel therapeutic agents.
Attenuating blood-brain barrier permeability has become a promising approach to managing brain edema and associated swelling given that increases in cranial water content can only be derived from the vasculature. Inflammation, both classical and neurogenic, offers a number of attractive targets.
尽管许多因素导致与创伤性脑损伤（TBI）相关的高死亡率和高发病率，但脑水肿导致的脑肿胀仍然是预后的最显著预测因素。本综述总结了目前对创伤性脑水肿相关机制的最新认识进展，并突出了有治疗前景的领域。
尽管在创伤性脑损伤后的第一周，细胞毒性（或细胞）水肿占主导地位，但只有当血管中的水进入颅腔时，脑肿胀才会发生。因此，调节血脑屏障通透性已成为寻求管理脑水肿的近期研究重点。水通道蛋白、基质金属蛋白酶和血管活性炎症介质已成为创伤性脑损伤后脑水肿的潜在介质。特别是激肽（缓激肽）和神经激肽（P 物质）似乎在创伤后调节血脑屏障通透性方面发挥着积极的生理作用。P 物质神经激肽-1 受体拮抗剂作为新型治疗药物具有特殊的应用前景。
鉴于颅内容量的增加只能来源于血管，因此降低血脑屏障通透性已成为管理脑水肿和相关肿胀的一种有前途的方法。经典和神经源性炎症提供了许多有吸引力的靶点。
