Labadie E L, Glover D
Can J Neurol Sci. 1974 Nov;1(4):222-5. doi: 10.1017/s0317167100019806.
From the present review it seems clear that the physiopathogenesis of the chronic subdural hematoma is far from being completely understood. However, an analysis of the known data can be summarized as follows: The development of subdural hematomas most likely occurs following minimal trauma in those patients with predisposing factors. Experimental data substantiates the fact that an accumulation of clotted blood in the subdural or subcutaneous space induced the formation of the fibroplastic neomembrane. The hypothesis that blood must come in contact with cerebrospinal fluid in order for the growth to occur, is still controversial. It has been virtually disproven that osmosis, referring to the electrolyte gradient as measured by freezing point depression, has any significance as a growth inducing factor. The protein oncotic gradient theory, having been the most widely accepted explanation as to the progressive enlargement of the subdural hematoma sac, has little experimental data supporting it. A larger body of clinical evidence exists supporting the concept that plasma and/or erythrocytes continuously penetrate into the subdural cavity, where enhanced fibrinolytic activity is present. However, this chronic rebleeding cannot fully explain the observed growth, because the composition of the hematoma fluid is smoewhat different from serum or plasma, and the protein content is also progressively diluted by fluid arising from an unknown source. There is some clinical and experimental evidence to suggest that a production-reabsorption balance may be a significant growth variable. No work has been done to define the role, if any, of local inflammatory mechanisms in the chronic subdural hematoma. Sound clinical evidence has shown that after the initial formation of the subdural clot, growth follows, than a slow, complete reabsorption usually occurs. Aside from the plausible production-reabsorption balance concept, it is not known why the evolution proceeds in this manner.
从目前的综述来看，慢性硬膜下血肿的病理生理机制显然远未被完全理解。然而，对已知数据的分析可总结如下：硬膜下血肿最有可能在有易感因素的患者遭受轻微创伤后发生。实验数据证实了这样一个事实，即硬膜下或皮下空间内凝血块的积聚可诱导纤维增生性新膜的形成。血液必须与脑脊液接触才能生长这一假说仍存在争议。关于渗透压（通过冰点降低法测量的电解质梯度）作为生长诱导因素的任何意义实际上已被否定。蛋白质胶体渗透压梯度理论曾是关于硬膜下血肿囊渐进性增大最被广泛接受的解释，但几乎没有实验数据支持它。有更多临床证据支持血浆和/或红细胞持续渗入存在增强纤维蛋白溶解活性的硬膜下腔这一概念。然而，这种慢性再出血不能完全解释所观察到的血肿增大，因为血肿液的成分与血清或血浆略有不同，并且蛋白质含量也会被来自未知来源的液体逐渐稀释。有一些临床和实验证据表明，产生 - 吸收平衡可能是一个重要的生长变量。尚未开展工作来确定局部炎症机制在慢性硬膜下血肿中是否起作用（若有作用的话）。可靠的临床证据表明，硬膜下血凝块最初形成后会继续增大，随后通常会缓慢、完全吸收。除了看似合理的产生 - 吸收平衡概念外，尚不清楚为何会以这种方式发展。
