Friede R L, Schachenmayr W
Am J Pathol. 1978 Jul;92(1):69-84.
A comparison of the fine structure of subdural neomembranes with the fine structural organization of the normal human dura-arachnoid interface discloses that neomembranes are not de novo proliferations of tissue from a smooth inner dural surface. Rather, a neomembrane is the result of proliferation and excessive thickening of the normal layer of dural border cells. On proliferation, the dural border cells form multilayered tiers and clusters of cells, transfixed by capillaries, with collagen fibrils and elastic fibers between them. Capillaries and collagen fibrils are absent from the normal interface layer. Pathogenetic concepts of chronic subdural hematoma need to be revised. Any pathologic condition inducing cleavage of tissue within the dural border layer at dura-arachnoid interface will be followed by proliferation of fural border cells with production of a neomembrane. There is no compelling reason to postulate that proliferation of the border cell layer is always secondary to traumatic hemorrhage.
将硬脑膜下新膜的精细结构与正常人类硬脑膜-蛛网膜界面的精细结构组织进行比较后发现,新膜并非来自光滑硬脑膜内表面的组织重新增殖。相反,新膜是硬脑膜边界细胞正常层增殖和过度增厚的结果。增殖时,硬脑膜边界细胞形成多层细胞层和细胞簇,有毛细血管贯穿其中,细胞之间有胶原纤维和弹性纤维。正常界面层中没有毛细血管和胶原纤维。慢性硬膜下血肿的发病机制概念需要修正。任何导致硬脑膜-蛛网膜界面硬脑膜边界层内组织分离的病理状况,随后都会伴有硬脑膜边界细胞的增殖并产生新膜。没有令人信服的理由假定边界细胞层的增殖总是继发于创伤性出血。