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。     

青光眼的视神经保护

青光眼是一种以特征性视野缺损、视盘凹陷病理性扩大为特点的致盲性眼病。到目前为止 ,青光眼的发病机理尚未完全明了。在众多的危险因子中 ,高眼压被认为是最重要的危险因素 ,该因素通过压迫筛板处的视神经纤维直接损害视神经和 /或影响视盘微循环间接损害视神经。虽然部分患者在整个病程中没有高眼压的表现 ,仍不能排除眼压在发病过程中的作用。因此 ,现有的治疗主要是以药物、手术或两者联合的途径降低眼压。眼压适当控制后 ,大部分患者的视功能损害能得以控制 ,但即使眼压低至 5～10mmHg仍有部分患者的青光眼性视野、视神经损害继续发…     

原发性闭角型青光眼角膜内皮观察

众所周知,高眼压、房角变窄、病理性视乳头凹陷及萎缩、视野缺损及视力下降是原发性闭角型青光眼的主要体征,但高眼压对角膜内皮细胞的损害,国外的研究报告甚少,国内尚未见报告。临床上经常可以看到闭角型青光眼在高眼压阶段可以导致角膜水肿,甚至在一次高眼压之后,个别病人可以     

我国正常人杯/盘的调查分析

高眼压、视野缺损和视乳头凹陷及萎缩构成了青光眼的三联征,特别是在单纯型青光眼中。但是在此三联征中,病理性视乳头凹陷和萎缩的形态学改变,多少年来一直被认为,只有当病程进展到中、后期时,才能显现出来。因而青光眼的早期病理性改变,只有依靠细微的视野检查才能发现。近些年来,相继有不少眼科学者对早期青光眼的视乳头凹陷进行了研究,从Armaly(1967)研究杯盘比开始,到Tomlinson(研究杯盘面积比)、Holm等     

下一步：一个成年人的青光眼患者的详细评估

青光眼青光眼是一组进行性的视神经病变，伴有视乳头特征性的结构改变和相应视野缺损的疾病。青光眼视神经病变的主要危险因素是眼压的升高。     

对青光眼诊治过程中眼压的评价

青光眼是一类严重威胁视功能的眼病,主要与病理性眼压升高相关。因患者眼压超过了自身眼球组织所能承受的限度,导致视功能损害。眼压升高的水平和视神经对压力损害的耐受性与青光眼性视神经萎缩和视野缺损的发生、发展密切相关。因此,临床眼科医师均将眼压作为诊治青光眼的重要指标之一。然而,我国眼科医师在评价眼压这一因素在青光眼诊治过程中的作用,尚存在一些模糊甚至不正确的认识,有必要引导眼科临床工作者重视。     

无特征性视野缺损青光眼的相对瞳孔传入障碍

青光眼可籍特征性视野缺损、视乳头凹陷及伴随的高眼压而得以确诊,然而早期确诊可能是困难的。当青光眼为非对称性者,常忽略相对瞳孔传入障碍(通常称为Gunn瞳孔)这一早期征象。Kaback等及Prywes(1976)分别注意到非对称性青光眼性视野缺损患者存在这种瞳孔异常,其中大多数患者同时有非对称性的视乳头凹陷。认为这一征象可以是高眼压性视神经损害(无视野缺损)的明确标志。就作者所知,无傍中心暗点或其它特征性青光眼视野缺损的非对称性青光眼视乳头凹陷及高眼压,而有相对瞳孔传     

婴幼儿性青光眼杯可逆性改变四例

婴幼儿性青光眼杯可逆性改变四例高殿文，李维昌，王　珏，李明，聂庆珠青光眼杯是由于病理性高眼压和／或血管因素等所致视乳头萎缩、凹陷。一般认为是一种不可逆改变。但在先天性青光眼可以有例外。当其眼压获得有效控制时，青光眼杯可出现缩小、甚至消失的可逆性改变［...     

低眼压性青光眼

低眼压性青光眼系指具有青光眼性视乳头凹陷和视野损害,而眼压却在统计学正常范围内的一类青光眼。患病早期中心视力影响较少,受累多在中晚期。诊断本病的关键,在于除外可致视乳头萎缩凹陷和视野缺损的其它原因,因而鉴别诊断特别重要。由于病因尚不明了,至今还无根治办法。但大部分患者病程进展缓慢,视功能可维持一段较长的时间,其最终结局与慢性单纯性青光眼类似。     

视神经萎缩和青光眼性视乳头凹陷

青光眼的特点为进行性视神经萎缩、视乳头凹陷和视野缺损,其发生的原因仍然不能肯定。目前盛行的一种假说,认为是由于巩膜筛板的神经轴索受高眼压直接压迫而死亡所引起的;另一则认为因眼压高,视乳头的眼灌注压降低,发生慢性缺血,神经轴索和胶质消失所致。     

Strabisme Alternant - Etude clinique - traitement

The author defines motor and sensory alternation: the term alternation should not be used in isolation, it should always be accompanied by the name of the parameter concerned. Sensory alternation is always found together with motor alternation but the reverse is not true.The examining criteria for a diagnosis of sensory alternation are given, sensory alternation must not be confused with alternating inhibition. Working from clinical observations of cases of motor alternating strabismus, the author selects 2 types of binocular sensory relations which allow one to differentiate between:- cases of primary alternating strabismus- cases of secondary alternating strabismusThese forms will develop in different ways; in both cases a cure is possible providing that the right treatment is prescribed and once prescribed carefully followed, etc. It is always a case of serious forms of strabismus whose developmental period is spread over several years.According to the authors, the frequency of cases of true primary strabismus is from 1–3%, the frequency of cases of secondary alternating strabismus varies according to the type of therapy practised on cases of monocular strabismus with amblyopia. These latter will become cases of alternating strabismus under the influence of certain types of therapy carried out over several years (penalization, rocking, alternated occlusion, etc...).Experimental data on kittens confirm clinical data; kittens placed in abnormal environments during the sensitive period will show modification in the distribution of cortical cells and the absence of binocular cells (either because the excitation of the two eyes was not simultaneous, or not identical: artificial strabismus, occlusion, opaque glasses). This disturbances become irreversible after a certain period of exposure (a function of age, length of exposure, etc...).It is thus necessary to bear in mind: 1) the iatrogenic risks of certain orthoptic treatments, 2) the necessity for a binocular form of treatment as soon as possible, as once a certain stage is passed, cortical plasticity diminishes and the elaboration of normal binocular relations becomes impossible.

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Effects of Adenosine Agonists on Intraocular Pressure and Aqueous Humor Dynamics in Cynomolgus Monkeys

The effects of single or multiple topical doses of the relatively selective A₁adenosine receptor agonists (R)-phenylisopropyladenosine (R-PIA) and N⁶-cyclohexyladenosine (CHA) on intraocular pressure (IOP), aqueous humor flow (AHF) and outflow facility were investigated in ocular normotensive cynomolgus monkeys. IOP and AHF were determined, under ketamine anesthesia, by Goldmann applanation tonometry and fluorophotometry, respectively. Total outflow facility was determined by anterior chamber perfusion under pentobarbital anesthesia. A single unilateral topical application of R-PIA (20–250 μg) or CHA (20–500 μg) produced ocular hypertension (maximum rise=4.9 or 3.5 mmHg) within 30 min, followed by ocular hypotension (maximum fall=2.1 or 3.6 mmHg) from 2–6 hr. The relatively selective adenosine A₂antagonist 3,7-dimethyl-1-propargylxanthine (DMPX, 320 μg) inhibited the early hypertension, without influencing the hypotension. Neither 100 μg R-PIA nor 500 μg CHA clearly altered AHF. Total outflow facility was increased by 71% 3 hr after 100 μg R-PIA. In conclusion, the early ocular hypertension produced by topical adenosine agonists in cynomolgus monkeys is associated with the activation of adenosine A₂receptors, while the subsequent hypotension appears to be mediated by adenosine A₁receptors and results primarily from increased outflow facility.