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脊髓损伤的病理生理学及其临床意义。

The pathophysiology of spinal cord injury and its clinical implications.

作者信息

Kraus K H

机构信息

Tufts University School of Veterinary Medicine, North Grafton, MA 01536, USA.

出版信息

Semin Vet Med Surg Small Anim. 1996 Nov;11(4):201-7. doi: 10.1016/s1096-2867(96)80013-2.

DOI:10.1016/s1096-2867(96)80013-2
PMID:9020573
Abstract

The pathophysiology of spinal cord injury can be categorized as acute impact or compression. Acute impact injury is a concussion of the spinal cord. This type of injury initiates a cascade of events focused in the gray matter, and results in hemorrhagic necrosis. The initiating event is a hypoperfusion of the gray matter. Increases in intracellular calcium and reperfusion injury play key roles in cellular injury, and occur early after injury. The extent of necrosis is contingent on the amount of initial force of trauma, but also involves concomitant compression, perfusion pressures and blood flow, and administration of pharmacological agents. Preventing or quelling this cascade of events must involve mechanisms occurring in the initial stages. Spinal cord compression occurs when a mass impinges on the spinal cord causing increased parenchymal pressure. The tissue response is gliosis, demyelination, and axonal loss. This occurs in the white matter, whereas gray matter structures are preserved. Rapid or a critical degree of compression will result in collapse of the venous side of the microvasculature, resulting in vasogenic edema. Vasogenic edema exacerbates parenchymal pressure, and may lead to rapid progression of disfunction. Treatment of compression should focus on removal of the offending mass.

摘要

脊髓损伤的病理生理学可分为急性撞击伤或压迫伤。急性撞击伤是脊髓的震荡。这种类型的损伤引发了一系列集中在灰质的事件,并导致出血性坏死。起始事件是灰质灌注不足。细胞内钙的增加和再灌注损伤在细胞损伤中起关键作用,且在损伤后早期发生。坏死的程度取决于初始创伤力的大小,但也涉及伴随的压迫、灌注压力和血流量,以及药物的使用。预防或平息这一系列事件必须涉及初始阶段发生的机制。当一个肿块压迫脊髓导致实质压力增加时,就会发生脊髓压迫。组织反应是胶质增生、脱髓鞘和轴突丧失。这发生在白质中,而灰质结构得以保留。快速或严重程度的压迫将导致微血管系统静脉侧塌陷,从而导致血管源性水肿。血管源性水肿会加剧实质压力,并可能导致功能障碍迅速进展。压迫的治疗应集中于去除致病肿块。

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