Neetens A
Dept. of Ophthalmology, University of Antwerp, Belgium.
Bull Soc Belge Ophtalmol. 1992;244:1-16.
Loss of mainly field in POAG is due to Schnabel's cavernous atrophy of the axons at their scleral passage, built up by aligned stacks of glial collagen (IV and I) tissue plates, which contain capillaries. Organisation, size and structural surroundings encircle isolated or grouped axons not evenly distributed. The stereotype pattern of fieldloss linked to a characteristic optic nerve lesion suggests POAG be considered a N.O. disease as raised IOP may be only one of the risk factors. Are cavernous atrophy (loss of field) and the trabecular spaces narrowing (rise of IOP) both the result of the same pathogenic mechanism acting on the collagen fiber (IV and I) of the scleral coat, resp. lamina cribrosa (posterior segment) and trabecular meshwork (anterior segment)? If so, IOP-rise only worsens the condition as will do a hemodynamic energy crisis at the level of the axons. Interactive dominance at any of both levels may explain unexpected discrepancies between IOP and fieldloss. Considering "to treat or not to treat" accurate field loss predictability testing, urgent research topic, are discussed.
开角型青光眼（POAG）主要视野缺损是由于轴突在巩膜通道处发生施纳贝尔海绵状萎缩，其由排列整齐的胶质胶原（IV型和I型）组织板堆叠形成，这些组织板含有毛细血管。组织结构、大小和结构环境围绕着孤立或成组的轴突，分布不均匀。与特征性视神经病变相关的典型视野缺损模式表明，POAG可被视为一种神经疾病，因为眼压升高可能只是危险因素之一。海绵状萎缩（视野缺损）和小梁间隙变窄（眼压升高）是否都是作用于巩膜外层、分别是筛板（后段）和小梁网（前段）的胶原纤维（IV型和I型）的同一致病机制的结果？如果是这样，眼压升高只会使病情恶化，轴突水平的血液动力学能量危机也会如此。这两个层面中任何一个层面的相互作用优势都可以解释眼压与视野缺损之间意想不到的差异。考虑到“治疗与否”这一准确的视野缺损预测性测试这一紧迫的研究课题，对此进行了讨论。
