Carter C J, Brooks D E, Doyle D L, Drance S M
Department of Pathology, University of British Columbia, Vancouver, Canada.
Ophthalmology. 1990 Jan;97(1):49-55. doi: 10.1016/s0161-6420(90)32627-1.
Increased intraocular pressure is accepted as a primary etiologic factor for the atrophy of the optic nerve head and visual field defects of high-tension glaucoma. Other factors must be present to explain these findings in low-tension glaucoma. One of the current theories is that low-tension glaucoma is the result of decreased optic nerve perfusion on the basis of vascular disease or other factors such as altered blood viscosity. This study compared the non-invasive vascular profiles, coagulation tests, and rheological profiles of 46 consecutive cases of low-tension glaucoma with 69 similarly unselected cases of high-tension glaucoma and 47 age-matched controls. Despite the multifactorial approach and the use of previously validated objective tests, no significant group differences were detected with any of the above investigations. If vascular disease is important in the etiology of low-tension glaucoma, then it must be localized or vasospastic since this study does not support the concept of a generalized vascular etiology, either of an atheromatous or hyperviscous nature, for the genesis of low-tension glaucoma.
眼内压升高被认为是高眼压性青光眼视神经乳头萎缩和视野缺损的主要病因。在低眼压性青光眼中,必然存在其他因素来解释这些表现。当前的一种理论认为,低眼压性青光眼是基于血管疾病或其他因素(如血液粘度改变)导致视神经灌注减少的结果。本研究比较了46例连续的低眼压性青光眼患者、69例未经挑选的高眼压性青光眼患者以及47例年龄匹配的对照者的非侵入性血管特征、凝血试验和流变学特征。尽管采用了多因素研究方法并使用了先前验证过的客观检测方法,但上述任何一项研究均未发现显著的组间差异。如果血管疾病在低眼压性青光眼的病因中起重要作用,那么它必定是局限性的或血管痉挛性的,因为本研究不支持低眼压性青光眼的发生具有全身性血管病因(无论是动脉粥样硬化性还是高粘滞性)这一观点。