Motohashi O, Suzuki M, Shida N, Umezawa K, Ohtoh T, Sakurai Y, Yoshimoto T
Division of Neurosurgery, School of Medicine, Tohoku University, Sendai, Japan.
Acta Neurochir (Wien). 1995;136(1-2):88-91. doi: 10.1007/BF01411441.
Subarachnoid haemorrhage (SAH) often leads to subarachnoid fibrosis and resultant normal pressure hydrocephalus; however, how subarachnoid fibrosis occurs is unknown. We examined the changes within arachnoid granulations (AGs) and the subarachnoid space (SAS) chronologically at the parasagittal region obtained from patients with SAH at autopsy and made comparison with controls by immunostaining for cytokeratin, specific marker for leptomeningeal cells and by the elastica Masson-Goldner methods. Within a week some AGs were torn, and many inflammatory cells filled the AGs and SAS. Cytokeratin positive cells were scarce. During the next two weeks cytokeratin positive cells increased. After three weeks, AGs and SAS were filled by dense deposits of extracellular matrices surrounded by multiple layers of leptomeningeal cells.
蛛网膜下腔出血(SAH)常导致蛛网膜下腔纤维化及由此引发的正常压力脑积水;然而,蛛网膜下腔纤维化的发生机制尚不清楚。我们对尸检时获取的SAH患者矢状旁区蛛网膜颗粒(AGs)和蛛网膜下腔(SAS)内的变化进行了时序性检查,并通过细胞角蛋白免疫染色(软脑膜细胞的特异性标志物)以及弹性马松-戈德纳方法与对照组进行比较。在一周内,一些AGs破裂,许多炎性细胞充斥于AGs和SAS内。细胞角蛋白阳性细胞稀少。在接下来的两周内,细胞角蛋白阳性细胞增多。三周后,AGs和SAS被多层软脑膜细胞包绕的细胞外基质致密沉积物所填充。