跨筛板压力差与青光眼发病机制的关系

原发性开角型青光眼及正常眼压青光眼患者脑脊液压力较正常人低,而高眼压症患者脑脊液压力较正常人高.跨筛板压力差增大可能导致青光眼损害,脑脊液压力升高是青光眼的保护因素.跨筛板压力差增大导致筛板向后弯曲变形变薄,视盘凹陷加深,杯盘比增大,导致青光眼病变发生发展.本文就跨筛板压力差的概念、测量方法、影响因素及其与青光眼的关系等方面综述.     

适用于大样本人群的无创脑脊液压力估算方法的标准与规范

最近的研究资料显示:视盘筛板前的眼压与筛板后的脑脊液压之间的差值(跨筛板压力梯度),而非眼压,是导致青光眼视神经损害的主要危险因素[1-2]。且已在单纯颅内脑脊液压力降低的动物模型发现了类似于青光眼视神经损害的结构性改变[3],提示脑脊液压力降低所致的跨筛板压力梯度增大与视神经损害之间存在因果关系。跨筛板压力梯度在原发性开角型青光眼     

谁动了我的视神经？ -正常眼压性青光眼视神经损害探因

正常眼压性青光眼和高眼压原发性开角型青光眼是一个“连续体”。本文基于病理生理学,探讨了正常眼压性青光眼中眼压与视神经损害的关系,认为视盘筛板是上述关系及其“连续体”概念的中间环节,眼压和筛板共同构成青光眼视神经损害的始动因素。（眼科,2020, 29： 87-89）     

原发性开角型青光眼与24h眼压及眼灌注压的研究进展

原发性开角型青光眼是一类早期无明显临床症状,但随病情进展将导致不可逆的视神经损害及视野缺损的致盲性眼病。眼压是原发性开角型青光眼诊断及评定治疗效果的简单而又重要的指标。临床上,一些治疗中的原发性开角型青光眼患者白天就诊时间所测眼压已达靶眼压,但视神经损害却仍在进展,研究表明可能与夜间眼压的升高、24 h较大的眼压波动及夜间眼灌注压的降低有关。因此,我们对原发性开角型青光眼与眼压及眼灌注压波动的相关文献予以综述,以更好的理解三者之间的关系。     

视神经筛板的生物力学研究

视神经筛板是一个生物力学结构,其受力应变引起青光眼视神经损伤.眼压被认为是引起筛板应变的主要因素,眼压升高引起筛板应变增加.相应的在青光眼用药或术后眼压下降的患者中,筛板会发生应变的消除.脑脊液压力作为跨筛板压力差的组成部分同样影响筛板,脑脊液压力降低增加了跨筛板压力差从而导致筛板应变增加.此外,眼球水平运动引起视神经...     

正常眼压性青光眼24小时眼压波动的研究进展

正常眼压性青光眼(normal-tension glaucoma, NTG)是一种慢性进行性视神经病变, 发病时眼压在正常范围内。NTG在开角型青光眼中的占比较高。在NTG的诊断中, 24 h眼压测量尤其重要, 是与原发性开角型青光眼相鉴别的主要体征。NTG患者24 h眼压监测通常表现为夜间出现眼压峰值, 且其眼压的昼夜波动幅度往往比正常人大。且24 h眼压的平均眼压、短期和长期眼压波动幅度、最小眼压值都显示为NTG疾病进展中的预测参数。这使得NTG患者24 h眼压监测及根据其24 h眼压波动特点进行个体化治疗变得尤为重要。(国际眼科纵览, 2023, 47:24-29)     

青光眼昼夜眼压波动

病理性高眼压和较大的昼夜眼压波动是青光眼视神经损害进展的重要危险因素.眼压具有波动性,正常人眼压波动的峰值多出现于凌晨,这种波动与体位、眼灌注压、眼轴等有关.正常眼压性青光眼患者眼压波动是视野进展的重要危险因素,且经24小时眼压监测发现大部分眼压是存在异常的,因此需根据其昼夜眼压曲线明确诊断和针对性治疗;原发性开角型青光眼患者昼夜眼压波动规律与正常人相似,眼压高峰多在夜间,但波动范围可能比正常人大,且双眼的波动呈明显的一致性;激光周边虹膜切开术后的慢性闭角型青光眼患者的昼夜眼压波动较大,其眼压波动与基线眼压和房角粘连程度呈正相关.与激光和药物相比,小梁切除术更有利于控制长期和昼夜的眼压波动.抗青光眼药物中前列腺素类药物是控制昼夜眼压波动效果最好的滴眼剂.     

跨筛板压力差与青光眼相关关系的研究:邯郸眼病研究

目的评价中国农村成年人群估算跨筛板压力差(TLCPD)与青光眼视神经损害的相关关系。设计以人群为基础的横断面研究。研究对象中国农村30岁及以上成年人群。方法对邯郸眼病研究I期6830例30岁以上受试者进行问卷、全身及眼部检查和血液、尿液实验室检查。眼科检查包括:视力检查、验光、裂隙灯检查、眼压、视野、晶状体、眼底检查、散瞳下眼底视神经立体照相,眼部A超,HRT-Ⅱ等。利用HRT-Ⅱ获得视盘的全周参数;引入非侵入测量颅内压(CSFP)研究得出的CSFP估算公式:CSFP(mmHg)=0.44×体质指数(BMI)(kg/m~2)+0.16×舒张压(DBP)(mmHg)-18×年龄(岁)-1.91。TLCPD:眼压-估算的CSFP。单因素及多因素分析分析非青光眼人群及原发性开角型青光眼(POAG)人群中估算筛板压力差、估算CSFP与全身系统及眼部参数的相关关系;评价该人群青光眼患病或青光眼特征性视神经损害定量参数与筛板压力差的关系。主要指标POAG及原发性闭角型青光眼(PACG)患者估算CSFP,估算TLCPD。结果 6450人(87.5%)的血压、身高、体重数据可用于数据分析。原发性开角型青光眼(POAG)组及非青光眼组相比,POAG组估算CSFP明显偏低,眼压、估算TLCPD明显偏高(P<0.001)。多因素分析中,校准其他混杂因素,POAG患病分别与较高的TLCPD(P<0.001;β:0.08;B:4.12;95%CI:2.24,6.02)、较低的估算CSFP(P=0.01;β:-0.05;B:-2.37;95%CI:-4.23,-0.51)显著相关。将TLCPD与眼压置于同一模型中,POAG患病与TLCPD增高显著相关(P<0.001;OR:1.290;95%CI:1.204,1.383),而非眼压(P=0.321);盘沿面积与TLCPD相关(P=0.028;β:-0.034;B:-0.003;95%CI:-0.005~-0.000),眼压被剔除(P=0.398);原发性闭角型青光眼(PACG)患病与眼压显著相关(P=0.02;OR:1.38;95%CI:1.05,1.71),而非TLCPD(P=0.46)。结论与PACG相比,TLCPD与POAG患病及视神经损害的关联强于眼压。这表明较低的CSFP在POAG发病机制中可能起到重要作用。     

低颅压与正常眼压性青光眼的关系

青光眼作为导致人类不可逆性盲的头号杀手,是一组慢性进行性视神经病变疾病。虽然病理性眼压增高是青光眼发展的主要危险因素,但是其视神经病变机制始终不明。而且有部分患者眼压处于正常值范围内,却依然发生了青光眼性视神经损害,被称为“正常眼压性青光眼”。因此,我们不得不考虑,除眼压外还有其他因素参与青光眼视神经的损害。近年来有研究表明:颅内压与眼压的失衡有可能是正常眼压性青光眼的原因之一,本文就颅内压与正常眼压性青光眼的关系做一综述。     

青光眼的眼压及眼脉动幅度比较分析

目的:观察比较慢性闭角型青光眼、原发性开角型青光眼、正常眼压性青光眼以及正常人的眼压,眼脉动幅度特征及其相关性。方法:收集临床确诊为慢性闭角型青光眼患者19例,原发性开角型青光眼18例,正常眼压性青光眼15例,正常人20例,用动态轮廓眼压计测量其眼压及眼脉动幅度,同时测量患者的血压及心率。运用SPSS14.0进行统计学分析。结果:慢性闭角型青光眼组的平均眼压为25.42±9.95mmHg,OPA为3.84±0.88mmHg;原发性开角型青光眼组的平均眼压为23.12±5.47mmHg,OPA为3.29±0.90mmHg;正常眼压性青光眼组的平均眼压为16.52±2.23mmHg,OPA为1.85±0.47mmHg;正常人组的平均眼压为16.31±2.67mmHg,OPA为2.47±0.80mmHg。前两组与后两组之间的眼压存在着显著性差异,四组之间的OPA均存在统计学差异。四组患者的眼压及眼脉动幅度之间存在着弱相关性,但无统计学意义。结论:慢性闭角型青光眼、原发性开角型青光眼及正常眼压性青光眼的OPA之间存在统计学差异,眼压与OPA之间存在弱相关性,但无统计学意义。     

Role of cerebrospinal fluid pressure in the pathogenesis of glaucoma

The pathogenesis of normal (intraocular) pressure glaucoma has remained unclear so far. As hospital‐based studies showed an association of normal‐pressure glaucoma with low systemic blood pressure, particularly at night, and with vasospastic symptoms, it has been hypothesized that a vascular factor may play a primary role in the pathogenesis of normal‐pressure glaucoma. That assumption may, however, be contradicted by the morphology of the optic nerve head. Eyes with normal‐pressure glaucoma and glaucomatous eyes with high‐intraocular pressure can show a strikingly similar appearance of the optic nerve head, including a loss of neuroretinal rim, a deepening of the optic cup, and an enlargement of parapapillary atrophy. These features, however, are not found in any (other) vascular optic neuropathy, with the exception of an enlargement and deepening of the optic cup in arteritic anterior ischaemic optic neuropathy. One may additionally take into account (i) that it is the trans‐lamina cribrosa pressure difference (and not the trans‐corneal pressure difference, i.e. the so‐called intraocular pressure) which is of importance for the physiology and pathophysiology of the optic nerve head; (ii) that studies have shown that the anatomy of the optic nerve head including the intraocular pressure, the anatomy and biomechanics of the lamina cribrosa and peripapillary sclera, retrobulbar orbital cerebrospinal fluid pressure and the retrobulbar optic nerve tissue pressure may be of importance for the pathogenesis of the highly myopic type of chronic open‐angle glaucoma; (iii) that studies have suggested a physiological association between the pressure in all three fluid filled compartments, i.e. the systemic arterial blood pressure, the cerebrospinal fluid pressure and the intraocular pressure; (iv) that an experimental investigation suggested that a low cerebrospinal fluid pressure may play a role in the pathogenesis of normal (intraocular) pressure glaucoma; and (v) that recent clinical studies reported that patients with normal (intraocular) pressure glaucoma had significantly lower cerebrospinal fluid pressure and a higher trans‐lamina cribrosa pressure difference when compared to normal subjects. One may, therefore, postulate that a low cerebrospinal fluid pressure may be associated with normal (intraocular) pressure glaucoma. A low systemic blood pressure, particularly at night, could physiologically be associated with a low cerebrospinal fluid pressure, which leads to an abnormally high trans‐lamina cribrosa pressure difference and as such to a similar situation as if the cerebrospinal fluid pressure is normal and the intraocular pressure is elevated. This model could explain why patients with normal (intraocular) pressure glaucoma tend to have a low systemic blood pressure, and why eyes with normal (intraocular) pressure glaucoma and eyes with high‐pressure glaucoma, in contrast to eyes with a direct vascular optic neuropathy, show profound similarities in the appearance of the optic nerve head.     

The interaction between intracranial pressure,intraocular pressure and lamina cribrosal compression in glaucoma

This review examines some of the biomechanical consequences associated with the opposing intraocular and intracranial forces. These forces compress the lamina cribrosa and are a potential source of glaucomatous pathology. A difference between them creates a displacement force on the lamina cribrosa. Increasing intraocular pressure and/or decreasing intracranial pressure will increase the trans‐lamina cribrosa pressure difference and the risk of its posterior displacement, canal expansion and the formation of pathological cupping. Both intraocular pressure and intracranial pressure can be elevated during a Valsalva manoeuvre with associated increases in both anterior and posterior lamina cribrosa loading as well as its compression. Any resulting thinning of or damage to the lamina cribrosa and/or retinal ganglion cell axons and/or astrocyte and glial cells attached to the matrix of the lamina cribrosa and/or reduction in blood flow to the lamina cribrosa may contribute to glaucomatous neuropathy. Thinning of the lamina cribrosa reduces its stiffness and increases the risk of its posterior displacement. Optic nerve head posterior displacement warrants medical or surgical lowering of intraocular pressure; however, compared to intraocular pressure, the trans‐lamina cribrosa pressure difference may be more important in pressure‐related pathology of the optic nerve head region. Similarly important could be increased compression loading of the lamina cribrosa. Reducing participation in activities which elevate intraocular and intracranial pressure will decrease lamina cribrosa compression exposure and may contribute to glaucoma management and may have prognostic significance for glaucoma suspects.     

The role of cerebrospinal fluid pressure in glaucoma and other ophthalmic diseases: A review

Glaucoma is one of the most common causes of blindness in the world. Well-known risk factors include age, race, a positive family history and elevated intraocular pressures. A newly proposed risk factor is decreased cerebrospinal fluid pressure (CSFP). This concept is based on the notion that a pressure differential exists across the lamina cribrosa, which separates the intraocular space from the subarachnoid fluid space. In this construct, an increased translaminar pressure difference will occur with a relative increase in elevated intraocular pressure or a reduction in CSFP. This net change in pressure is proposed to act on the tissues within the optic nerve head, potentially contributing to glaucomatous optic neuropathy. Similarly, patients with ocular hypertension who have elevated CSFPs, would enjoy a relatively protective effect from glaucomatous damage. This review will focus on the current literature pertaining to the role of CSFP in glaucoma. Additionally, the authors examine the relationship between glaucoma and other known CSFP-related ophthalmic disorders.     

Facts and myths of cerebrospinal fluid pressure for the physiology of the eye

The orbital cerebrospinal fluid pressure (CSFP) represents the true counter-pressure against the intraocular pressure (IOP) across the lamina cribrosa and is, therefore, one of the two determinants of the trans-lamina cribrosa pressure difference (TLPD). From this anatomic point of view, an elevated TLPD could be due to elevated IOP or abnormally low orbital CSFP. Both experimental and clinical studies have suggested that a low CSFP could be associated with glaucomatous optic neuropathy in normal-pressure glaucoma. These included monkey studies with an experimental long-term reduction in CSFP, and clinical retrospective and prospective studies on patients with normal-pressure glaucoma. Since the choroidal blood drains via the vortex veins through the superior ophthalmic vein into the intracranial cavernous sinus, anatomy suggests that the CSFP could influence choroidal thickness. A population-based study revealed that thicker subfoveal choroidal thickness was associated with higher CSFP. Since the central retinal vein passes through the orbital CSF space, anatomy suggests that the retinal venous pressure should be at least as high as the orbital CSFP. Other experimental, clinical or population-based studies suggested an association between higher CSFP and higher retinal venous pressure and wider retinal veins. Consequently, a higher estimated CSFP was associated with arterial hypertensive retinopathy (with respect to the dilated retinal vein diameter and higher arterial-to-venous diameter) and with the prevalence, severity and incidence of diabetic retinopathy. Physiologically, CSFP was related with higher IOP. The influence of the CSFP on the episcleral venous pressure and/or a regulation of both CSFP and IOP by a center in the dorsomedial/perifornical hypothalamus may be responsible for this. In summary, the CSFP may be an overlooked parameter in ocular physiology and pathology. Abnormal changes in the CSFP, in particular in relationship to the IOP, may have pathophysiologic importance.     

Cerebrospinal fluid pressure in ocular hypertension

Background: To assess the lumbar cerebrospinal fluid pressure (CSF‐P) in ocular hypertensive subjects with elevated intraocular pressure (IOP) but without development of glaucomatous optic nerve damage. Methods: The prospective interventional study included 17 patients with ocular hypertension and 71 subjects of a nonglaucomatous control group. All patients underwent a standardized ophthalmologic and neurological examination including measurement of lumbar CSF‐P. In the ocular hypertensive group, the IOP was corrected for its dependence on central corneal thickness (IOP_corrected). The trans‐lamina cribrosa pressure difference (Trans‐LCPD) was calculated as IOP_corrected ? CSF‐P. Results: CSF‐P was significantly (p < 0.001) higher in the ocular hypertensive group (16.0 ± 2.5 mmHg) than in the control group (12.9 ± 1.9 mmHg). CSF‐P was significantly associated with IOP_corrected (p < 0.001; r = 0.82). In multivariate analysis, CSF‐P was significantly correlated with IOP_corrected (p < 0.001) and marginally significantly with mean blood pressure (p = 0.05). Trans‐LCPD was not associated significantly with blood pressure (p = 0.69). Conclusion: Some ocular hypertensive subjects with increased intraocular pressure measurements (after correction for their dependence on central corneal thickness) had an abnormally high lumbar cerebrospinal fluid pressure. Assuming that lumbar cerebrospinal fluid pressure correlated with orbital cerebrospinal fluid pressure, one may postulate that the elevated retro‐lamina cribrosa pressure compensated for an increased intraocular pressure. The elevated retro‐lamina cribrosa pressure may have led to a normal trans‐laminar pressure difference in the eyes with elevated intraocular pressure, so that glaucomatous optic nerve damage did not develop. Intraocular pressure, cerebrospinal fluid pressure and arterial blood pressure were correlated with each other.     

Einfluss des Liquordrucks auf die glaukomatöse Schädigung des Nervus opticus

Eyes with normal pressure glaucoma and eyes with high pressure glaucoma show a similar optic disc appearance with marked differences to eyes with vascular optic neuropathy. Non-vascular, potentially barotraumatic factors in addition to intraocular pressure (IOP) may thus play a role in glaucoma. Recent studies have shown that cerebrospinal fluid pressure (CSFP), arterial blood pressure and IOP are correlated with each other, higher CSFP is associated with younger age, higher blood pressure and higher body mass index, some patients with normal (IOP) pressure glaucoma have abnormally low CSFP and thus an abnormally high trans-lamina cribrosa pressure difference and a small orbital CSF space, the orbital CSF space width is associated with CSFP and the estimated CSFP correlated better with open-angle glaucoma-related parameters than IOP. The orbital CSFP as counter-pressure against IOP may play a role in the pathogenesis of glaucoma.     

局灶性筛板缺损对青光眼进展的影响

筛板一直被认为是青光眼视网膜神经节细胞和轴突发生损伤的初始部位,观察筛板的形态学改变有助于认识青光眼的病理机制。以往研究结果显示局灶性筛板缺损与青光眼进展相关,但两者的因果关系和作用机制并不清楚。本文指出相干光层析成像术发展,首次揭示了青光眼局灶性筛板缺损可以平衡跨筛板压力梯度,从而起到延缓或终止青光眼视神经损伤进展的作用,该发现为跨筛板压力梯度学说在青光眼发病机制中的作用提供了直接的临床依据,深化了临床对局灶性筛板缺损与青光眼进展的认识,从另一角度阐述了原发性开角型青光眼的发病机制,为该疾病的治疗和预后判断提供了新的思路。