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自从1853年由Tuvck和Coccius首先分别叙述颅内占位性病变所致视乳头水肿以来,这个问题仍是一个谜。作者复习了近十年的文献,由于实验性颅内占位性病变所致视乳头水肿实验方法的发展和新近出现尖端的检查视乳头水肿方法(如萤光素眼底血管照相、立体镜眼底照相、电子显微镜和辣根过氧化物酶以及轴浆流动的研究等),对于阐明这个高度复杂的问题很有帮助。作者曾用恒河猴做实验研究,将气球放入蛛网膜下腔,产生类似进行性生长的颅内占位病变,对已充分确认以解释视乳头水肿发病机理的假说引起怀疑。现将有关的研究结果简略摘要如下; (1)视乳头水肿的发生和发展取决于脑蛛网膜下腔脑脊液压力升高及其直接传送到视神经的硬膜鞘内。当视神经鞘减压则视乳头水肿消失。(2)视乳头水肿是由于颅内蛛网膜下腔脑脊液压力升高所致,而不是单独由于脑室
This problem has remained a mystery since Tuvck and Coccius first described papilledema in the intracranial lesions in 1853, respectively. The authors reviewed nearly a decade of literature on the development of experimental methods for papilledema due to experimental intracranial space-occupying lesions and the recent emergence of sophisticated methods for examining papilledema (fluorescein angiography, stereoscopic fundus photography , Electron microscopy and horseradish peroxidase and the study of axoplasm flow, etc.) are helpful in elucidating this highly complex issue. The authors have used rhesus monkeys to do experimental research, put the balloon into the subarachnoid space, produce intracranial space-occupying lesions similar to progressive growth, and cast doubt on the hypothesis that the mechanism of papilledema has been well established to explain the pathogenesis of papilledema. The relevant summary of the results are as follows; (1) The occurrence and development of papilledema depends on the elevated cerebrospinal fluid pressure in the subarachnoid space and its direct transmission to the dural sheath of the optic nerve. When optic nerve sheath decompression papillede disappeared. (2) papilledema is due to intracranial subarachnoid cerebrospinal fluid pressure due to, rather than alone due to ventricular