Jonas Jost B, Wang Ningli
Department of Ophthalmology, Medical Faculty Mannheim, University of Heidelberg, Germany.
Beijing Tongren Eye Center, Beijing Tongren Hospital, Capital Medical University; Beijing Ophthalmology and Visual Sciences Key Laboratory, Beijing, China.
J Ophthalmic Vis Res. 2013 Jul;8(3):257-63.
Eyes with normal-pressure glaucoma and those with high-pressure glaucoma can show a similar optic nerve head appearance, while eyes with vascular optic neuropathies show a markedly different optic disc appearance. Factors in addition to intraocular pressure (IOP) may thus play a role in the pathogenesis of glaucomatous optic neuropathy. Clinical and experimental studies showed that (1) physiologic associations between cerebrospinal fluid (CSF) pressure, systemic arterial blood pressure, IOP and body mass index exist; (2) a low CSF pressure was associated with the development of glaucomatous optic nerve damage in cats; (3) patients with normal (intraocular) pressure glaucoma had significantly lower CSF pressure and a higher trans lamina cribrosa pressure difference when compared to normal subjects; and (4) patients with normal- pressure glaucoma as compared with patients with high-pressure glaucoma have a significantly narrower orbital CSF space. A shallow orbital CSF space has been shown to be associated with a low CSF pressure. Due to anatomic reasons, the orbital CSF pressure and the optic nerve tissue pressure (and not the atmospheric pressure) form the retro-laminar counter-pressure against the IOP and are thus part of the trans-lamina cribrosa pressure difference and gradient. Assuming that an elevated trans-lamina cribrosa pressure difference and a steeper trans-lamina cribrosa pressure gradient are important for glaucomatous optic nerve damage, a low orbital CSF pressure would therefore play a role in the pathogenesis of normal-(intraocular) pressure glaucoma. Due to the association between CSF pressure and blood pressure, a low blood pressure could be indirectly involved.
眼压正常的青光眼患者和高眼压青光眼患者的视神经乳头外观可能相似,而血管性视神经病变患者的视盘外观则明显不同。因此,除眼压(IOP)外的其他因素可能在青光眼性视神经病变的发病机制中起作用。临床和实验研究表明:(1)脑脊液(CSF)压力、体循环动脉血压、眼压和体重指数之间存在生理关联;(2)低脑脊液压力与猫青光眼性视神经损伤的发生有关;(3)与正常受试者相比,正常(眼内)压青光眼患者的脑脊液压力显著更低,且跨筛板压力差更高;(4)与高眼压青光眼患者相比,正常眼压青光眼患者的眼眶脑脊液间隙明显更窄。已表明眼眶脑脊液间隙浅与脑脊液压力低有关。由于解剖学原因,眼眶脑脊液压力和视神经组织压力(而非大气压力)形成对抗眼压的视网膜后反压力,因此是跨筛板压力差和梯度的一部分。假设跨筛板压力差升高和跨筛板压力梯度更陡对青光眼性视神经损伤很重要,那么低眼眶脑脊液压力因此会在正常(眼内)压青光眼的发病机制中起作用。由于脑脊液压力和血压之间的关联,低血压可能间接参与其中。