青光眼视神经保护的研究进展

青光眼是眼科临床中最常见的致盲眼病之一,目前的治疗方法主要是药物和手术控制眼压,单纯的降低眼压并不能有效地防止视网膜神经节细胞程序性死亡所引起的视神经进行性损害.自视网膜神经保护概念提出以来,对视网膜神经节细胞的损伤和保护研究取得了长足进展.文中就视网膜神经节细胞的损伤、死亡机制及对视网膜神经保护措施的研究进展加以综述.     

关注免疫炎症调控在青光眼全程诊疗中的作用

青光眼是由于病理性眼压升高引起视神经结构和功能损害而导致的不可逆性致盲眼病,具有多因性、强异质性的特点,长期以来降低并控制眼压以减轻视神经损害是青光眼主要的治疗策略。然而,临床实践中发现,尽管部分青光眼患者眼压得到控制,但视神经损害仍持续进展,因此非眼压依赖性的继发视神经损害仍为青光眼发生和发展病理机制中亟需解决的瓶颈...     

青光眼视神经保护的相关分析及研究进展

青光眼(glaucoma)是一组具有特征性视神经损害和视野缺损的眼病,在临床上常常表现为视力减退、眼部胀痛伴头痛等症状,是一种致盲率居第二位的不可逆性眼病.青光眼视神经损伤有一定的遗传倾向,造成视神经凹陷性萎缩及视野不同程度缺损这两种结局的危险因素有多种,其中致盲的主要原因包括进行性视神经节损害、病理性眼压升高等.所以在青光眼的治疗中一方面要考虑降低眼压,另一方面还要保护好视神经.本文将从视神经损害的机制、影响因素、分级方法、视神经相关检测指标及其在临床上相关仪器应用、治疗等方面进行综述.     

原发性开角型青光眼中枢视觉通路的改变

原发性开角型青光眼是临床上常见的一种不可逆性致盲眼病,对于青光眼所造成的视网膜神经节细胞水平及视神经水平的损害已得到广泛研究.最近研究表明,青光眼患者的上行视路部分,如外侧膝状体及枕叶视皮质等,存在损伤,提示青光眼可能同时也是一种中枢神经退行性疾病,早期对青光眼进行视神经保护治疗有助于减缓视神经节细胞的凋亡并阻止视功能的进一步损害.本文将从青光眼中枢损伤的发病机制、临床诊断及青光眼视神经保护治疗方面的研究进展进行综述,并对青光眼的研究前景进行展望.     

新型降眼压药物bimatoprost的药理作用及其临床疗效

青光眼治疗的主要目标是防止高眼压损害视神经导致视力丧失。理论上可以通过增强视神经对高眼压的耐受力或将眼压降到安全水平来达到这一目的。虽然实验研究已经证明某些药物有视神经保护作用，但在临床上，视神经保护治疗仍在探讨和验证之中，因此目前现代青光眼的治疗仍旨在降低眼压。     

青光眼视神经保护治疗的研究进展

青光眼是由于眼压升高引起视乳头损害和视野缺损的一种致盲性眼病,其病理基础是视网膜神经节细胞及其轴突的进行性丢失。过去大量的研究都集中在降低眼压方面,现在视神经保护治疗作为一种通过阻止神经元死亡治疗青光眼的新策略已被普遍接受。我们从NMDA受体拮抗剂、神经营养因子、热休克蛋白、免疫系统等方面,总结了目前青光眼视神经保护治疗的研究进展。     

重视青光眼性视神经保护的基础研究

青光眼是居世界首位的不可逆性致盲性眼病。虽然临床中唯一被认可的降眼压治疗可以延缓疾病进展,但大部分患者的视力损害仍日益加剧。针对这一棘手的问题,旨在直接保护视网膜终末受累细胞的"视神经保护"研究正如火如荼地开展。为进一步明确青光眼性视神经保护基础研究面临的问题,本文就目前该方面的研究现状进行简要总结,并主要针对基础研究中所遇到的关键性问题进行论述,以期提高研究工作者对青光眼性视神经保护的认识,为进一步有效的临床治疗干预靶点提供有力依据。     

青光眼视神经损伤机制的研究进展

青光眼是目前全球范围内致盲性最高的疾病之一,是以进行性视网膜神经节细胞丧失、不可逆的视野损害等病理性改变为特征,最终导致视神经萎缩及视功能丧失的疾病。目前青光眼的发病机制并不完全清楚,其中视神经损伤的机制有多种学说,包括眼压因素及非眼压因素,非眼压因素包括血管因素、免疫作用、远端轴突病变、氧化应激作用、细胞因子的变化及自噬等机制。本文综述了有关青光眼视神经损伤机制的研究进展,为进一步研究青光眼视神经病变提供依据。     

Rho激酶抑制剂对青光眼的神经保护作用及研究进展

青光眼是全球主要的致盲眼病之一,以最终导致视网膜神经节细胞(RGCs)逐渐凋亡及其轴突丢失为主要特征.目前,降低眼压是控制青光眼发展的主要治疗方式,然而,并不是所有的患者都适用于该疗法,这与青光眼的病理生理过程并不只是由眼压升高引起有关.针对青光眼发病的多因素,迫切需要寻找新的治疗策略.新疗法的重点应放在预防或延缓RGCs的凋亡、修复损伤的轴突上,因此青光眼视神经保护治疗已成为目前研究的热点.Rho激酶(ROCK)抑制剂作为可以降低眼压、抑制抗青光眼术后瘢痕形成、改善眼部血液循环、提高RGCs存活率、防止轴突变性以及诱导轴突再生的实验阶段药物,已成为目前新药研究的热点.本文将重点对ROCK抑制剂的经典信号通路在青光眼视神经保护方面的研究现状及进展进行综述.     

颅内压与青光眼及其无创测量技术的研究进展

青光眼是世界上第二位致盲性眼病,第一位不可复性致盲性眼病。尽管眼压增高被认为是青光眼性视神经损害的主要危险因素,但是50%的原发性开角型青光眼患者的日常眼压正常,还有一些患者尽管眼压控制良好,但青光眼性视神经损害仍继续发展。这些现象无法用高眼压理论来解释,青光眼患者视神经损害的发病机制仍待探讨。目前国内外的一些研究表明：（1）视神经周围的生物力学的解剖结构包括眼内压,筛板和球后的脑脊液压力在原发性开角型青光眼的发病机制中发挥重要的作用;（2）正常眼压性青光眼患者的脑脊液压力比正常人低,而跨筛板压力差比正常人高;（3）高眼压症患者的脑脊液压力比正常人群高,而跨筛板压力差和正常人之间没有统计学意义。基于以上研究,本文就颅内压与青光眼性视神经损害之间关系的相关研究进展及临床上可行的无创颅内压测量方法作一综述。     

再论青光眼是否属于中枢神经系统疾病

青光眼是一种以眼压为主要危险因素的视神经疾病.近年来,随着对青光眼和视觉科学的深入研究以及眼科神经科交叉学科的发展,同时借助于神经影像技术的不断提高,关于青光眼本质的一些新问题随即产生,即青光眼仅仅是一种眼部疾病吗?它是原发于眼部但累及全视路的疾病吗?或者它是某种特殊中枢神经系统疾病在眼部的表现?这些问题在眼科界引起了争论.已有许多证据表明青光眼不仅仅累及视神经,而且引起外侧膝状体、视放射和视觉中枢的损伤,它是整个视路多层次损害的综合征群,其机制复杂.我们认为青光眼是一种中枢神经系统疾病.最近,有学者通过实验发现青光眼的首发损害在中枢神经系统而非眼部.将青光眼归为一种中枢神经系统疾病对认识青光眼的发病机制、建立系统全面的治疗策略、挽救患者视力具有一定意义.     

小梁消融术治疗开角型青光眼的研究进展

防止眼压升高对视神经的不可逆性损伤是治疗开角型青光眼的关键.手术治疗目前仍是临床控制眼压的重要措施.近年来,微创青光眼手术逐渐应用于临床,小梁消融术通过增加生理性小梁网房水引流途径而达到降眼压作用.与传统的滤过性手术相比,小梁消融术以其创伤小、手术时间短、术中及术后并发症少、术后恢复快、降眼压效果良好、术后护理简单等特点成为近年来应用于临床的新颖术式.本文对小梁消融术治疗开角型青光眼的原理、适应证、疗效、并发症等进行综述.     

青光眼视神经保护研究进展

青光眼是以视网膜神经节细胞进行性死亡为特征的一类疾病,其病理学机制包括慢性缺血、氧自由基损害、谷氨酸兴奋性毒素导致神经变性、轴突运输障碍、神经营养因子缺乏、电活动消失等。临床上主要通过降眼压治疗青光眼,但往往有一部分患者控制眼压后仍不能有效减少视网膜神经节细胞的死亡。因此,合理的青光眼治疗应包括视神经保护,本文就近几年青光眼视神经保护治疗的研究进展作一综述。     

Elevated intraocular pressure and optic nerve injury models in the rat

Models of experimentally elevated intraocular pressure in rats provide valuable opportunities to discover and study mechanisms of pressure-induced optic nerve damage. The structure and vasculature of the rat optic nerve head have several anatomic similarities and differences from the primate that allow useful comparisons and insights into human glaucoma. Specifically, the ultrastructural relationship between astrocytes, retinal ganglion cell axons and the connective tissues of the optic nerve head appear quite similar to the primate, and have a high potential for revealing cellular mechanisms of axonal injury. Three widely used models of creating elevated IOP in rats exist. However, they are not all equivalent and appear to differ in the relationship they exhibit between the level of pressure and extent of optic nerve damage. This indicates that these models may differ in the mechanisms by which they produce elevated eye pressure. All of these models are amenable to a variety of methods for evaluating damage. These include objective and subjective histologic assessment of the optic nerve, counting cells in the retinal ganglion cell layer of the retina and the use of retinal whole mounts to count retinal ganglion cells that have been back-labeled with dye applied to the superior colliculus. In the decade since their introduction, these versatile models have provided important insights into mechanisms of pressure-induced optic nerve damage using sensitive molecular biology techniques. They have also allowed the evaluation of several potential strategies for neuroprotection in glaucoma, ranging from currently available drugs to gene transfer studies.     

Normal tension glaucoma, sleep apnea syndrome and nasal continuous positive airway pressure therapy--case report with a review of literature

BACKGROUND: In the pathogenesis of glaucoma, besides an elevated intraocular pressure (IOP), cardiovascular risk factors, such as arterial hypotension and hypertension, vasospasms, autoregulatory defects, atherosclerosis, and diabetes mellitus are of increasing importance, especially in normal tension glaucoma. Recently, there have been several reports of an additional risk factor: obstructive sleep apnea syndrome. METHODS: Literature review (Medline) and case report. RESULTS: The authors report on a 8 1/2 years follow-up of a 60-year-old patient with normal tension glaucoma. Despite successful pharmacological and surgical lowering of intraocular pressure a progressive glaucomatous damage with optic nerve atrophy and increasing visual field defects occurred. As a result of intensive investigations of possible cardiovascular risk factors, an obstructive sleep apnea syndrome was diagnosed. Since the beginning of therapy with nCPAP (nasal continuous positive airway pressure) more than 3 1/2 years ago, no further progression of glaucomatous optic nerve damage or visual field defects have been observed. CONCLUSIONS: In clinical practice, obstructive sleep apnea syndrome often is underdiagnosed. In patients suffering from glaucoma and obstructive sleep apnea syndrome, intraocular pressure lowering therapy may not be enough, whereas an additional nCPAP-therapy potentially could prevent the beginning/progression of glaucomatous optic nerve damage.     

应用OCT探究眼压与筛板参数的关系

筛板的变形与血流减少一直被视作青光眼视神经轴突损伤的首发因素.病理性眼压升高与青光眼的发生发展间有紧密关系.通过OCT技术衡量筛板及周边参数随眼压变化来研究青光眼发病机制受到了广泛关注.研究表明筛板深度(LCD)、筛板前表面厚度(PTT)、筛板曲率指数(LCCI)以及视盘血管密度等参数均与眼压具有相关性.眼压升高可对筛...     

Neuroprotection in glaucoma: a model for neuroprotection in optic neuropathies

PURPOSE OF REVIEW: Efforts to discover modalities and pathophysiologies that might afford successful neurorescue, neurorestoration, and neuroprotection of cells of the central nervous system have focused on processes that affect the central nervous system proper, that is, the brain. Often overlooked in the search for neural protection is the fact that the mammalian optic nerve behaves in many ways as an integral part of the central nervous system. As such, the eye--the optic nerve and retina--affords an ideal clinical model for neuroprotection and neuroprotective agents. Glaucomatous optic neuropathy is the most prevalent of all adult optic neuropathies, and offers an ideal primate and lower mammalian animal model for investigations of neuroprotection. RECENT FINDINGS: This is especially compelling because while recent studies in glaucoma have shown reduction of intraocular pressure (IOP) to be an effective modality in the treatment of glaucomatous optic neuropathy, not all patients respond to or can achieve meaningful IOP reductions. Therefore much attention has now been focused on neuroprotection as a strategy in therapies for glaucomatous optic neuropathy as a means of preserving retinal ganglion cells and their axonal projections. SUMMARY: This review discusses the latest studies on various mechanisms of neuroprotection in the treatment of glaucomatous optic neuropathy.     

Medical therapy of primitive hypertensive glaucoma-therapeutic principles, perspectives

The present-day glaucoma therapy is aiming to preserve visual function by decreasing the intraocular pressure below a certain level, that prevents the optic nerve damage to occur. The target IOP must be individualized, considering the IOP level at presentation, the severity of the optic nerve damage, life expectancy and associated risk factors. In order to prevent the glaucoma progression, the more serious the damages are at presentation, the lower the target IOP level must be. New ocular hypotensive agents that have been created during the last few years allowed a more efficient control of the glaucoma progression.     

Predictive factors for progressive optic nerve damage in various types of chronic open-angle glaucoma

PURPOSE: To evaluate whether various types of chronic open-angle glaucoma differ in predictive factors for progression of glaucomatous optic nerve damage. DESIGN: Observational cohort study. METHODS: SETTING: Prospective observational clinical study. PATIENTS: 517 eyes of 300 Caucasian patients with chronic open-angle glaucoma with elevated intraocular pressure (primary open-angle glaucoma, n = 289; secondary open-angle glaucoma, n = 50) and with normal intraocular pressure (n = 178). OBSERVATION PROCEDURE: During follow-up (median: 49 months, 6 months-130 months), all patients underwent repeated evaluation of color stereo optic disk photographs and white-on-white visual field examination. MAIN OUTCOME MEASURES: Progression of glaucoma was defined as neuroretinal rim loss during the study period. RESULTS: For patients with elevated intraocular pressure, significantly predictive factors for eventual progression were older age, advanced perimetric damage, smaller neuroretinal rim, and larger area of beta zone of parapapillary atrophy. In contrast, in the normal intraocular pressure group, a significant predictive factor was presence of disk hemorrhages at baseline. Within the patients with elevated intraocular pressure, the primary open-angle glaucoma group and the secondary open-angle glaucoma group did not differ in predictive factors for progression of glaucoma. CONCLUSIONS: Open-angle glaucoma patients with normal intraocular pressure and open-angle glaucoma patients with elevated intraocular pressure differ in predictive factors for eventual progression of glaucomatous optic nerve damage. It may have clinical importance and may be helpful in the discussion of the pathogenesis of the glaucomas.