《青光眼视神经诊断图谱》（附光盘）出版

徐亮主编的《青光眼视神经诊断图谱》（附光盘）已由北京科学技术出版社出版。本书主要围绕青光眼视神经特征性改变,以眼底照片形式显示各类变化。不同类型的青光眼其发生机制各有不同,本书针对各种类型的青光眼包括老年慢性萎缩性开角型青光眼、高度近视合并开角型青光眼、青少年型青光眼、正常眼压性青光眼、继发性青光眼、急性闭角型青光眼等,     

《青光眼视神经诊断图谱》（附光盘）出版

徐亮主编的《青光眼视神经诊断图谱》（附光盘）已由北京科学技术出版社出版。本书主要围绕青光眼视神经特征性改变,以眼底照片形式显示各类变化。不同类型的青光眼其发生机制各有不同,本书针对各种类型的青光眼包括老年慢性萎缩性开角型青光眼、高度近视合并开角型青光眼、青少年型青光眼、正常眼压性青光眼、继发性青光眼、急性闭角型青光眼等,分别以图片的形式介绍其特征性视盘及眼底变化。     

《青光眼视神经诊断图谱》（附光盘）出版

徐亮主编的《青光眼视神经诊断图谱》（附光盘）已由北京科学技术出版社出版。本书主要围绕青光眼视神经特征性改变,以眼底照片形式显示各类变化。不同类型的青光眼其发生机制各有不同,本书针对各种类型的青光眼包括老年慢性萎缩性开角型青光眼、高度近视合并开角型青光眼、青少年型青光眼、正常眼压性青光眼、继发性青光眼、急性闭角型青光眼等,分别以图片的形式介绍其特征性视盘及眼底变化。     

牵牛花综合征伴中高度近视及急性闭角型青光眼一例

牵牛花综合征(morning glory syndrome,MGS)是一种较为罕见的特殊的先天性视乳头发育异常.本病患者可合并其他先天性眼部异常,但伴有急性闭角型青光眼发作的文献报告极少.2008年10月我院收治1例MGS合并急性闭角型青光眼及中高度近视患者,本例特殊之处在于急性闭角型青光眼发作在眼轴相对较长的MGS右眼,而眼轴相对较短的左眼未发作.     

高度近视合并原发性开角型青光眼的临床特点研究进展

许多研究显示高度近视与青光眼密切相关,高度近视因患者眼轴长、前房深、房角宽的特点,并发青光眼的类型常为原发性开角型青光眼.然而,由于高度近视可导致一系列的眼底病变,使青光眼的早期眼底改变易被高度近视造成的眼底病变所掩盖,所以,认识高度近视合并原发性开角型青光眼的临床特点及诊断要点,有利于疾病的早期诊断和减少漏诊、误诊.本文对高度近视合并原发性开角型青光眼的临床特点进行总结归纳,提高对疾病的认识,为疾病的早期诊断提供依据.     

轴性高度近视合并原发性闭角型青光眼

目的探讨轴性高度近视合并原发性闭角型青光眼的临床特点及发病机制。方法结合文献对一例（2眼）轴性高度近视合并原发性闭角型青光眼患者的临床资料进行分析。结果根据术前检查结果,右眼行虹膜周切术,左眼行复合式小梁切除术,术后矫正视力右眼0.4,左眼0.3;左眼上方结膜滤过泡扁平弥散;眼压：右眼14.57mmHg,左眼10.24mmHg。结论轴性高度近视发生的闭角型青光眼,可能与眼局部解剖结构的变异、脉络膜的神经血管因素以及高度近视患者的悬韧带松弛及晶状体的稳定性差等因素有关;常规抗青光眼手术可获得较好的治疗效果。     

选择不同手术方式治疗白内障合并青光眼

白内障合并青光眼是临床常见病，如何根据患者的具体情况作出较为妥善的处理，对临床工作很重要。我们根据青光眼的类型、病程、房角关闭和粘连程度，对４２例（４２眼）青光眼合并白内障患者选择不同的手术方式治疗，取得了满意效果，现报告如下： 资料和方法 １ 一般资料：白内障合并青光眼患者４２例（４２眼），男２５例，女１７例。年龄４８～７２岁，平均６２．１岁。原发性开角型青光眼合并白内障６例，原发性闭角型青光眼合并或并发白内障１２例，白内障膨胀期继发闭角型青光眼１５例，白内障成熟期继发闭角型青光眼９例。对闭角型…     

混合型青光眼住院病人的致病机制构成分析

目的 分析混合型青光眼(mixed glaucoma,MG)住院病人的致病机制.方法 收集 2005年~2009年连续住院患者MG 109只眼(76例)的临床资料,结合眼压、C/D、视野、前房角镜及超声生物显微镜(ultrasound biomicroscopy,UBM)等临床资料,分类分析其混合致病机制的构成.结果 (1)本组病例存在12个致病机制类型:原发性开角型青光眼(primary open-angle glaucoma,POAG、原发性闭角型青光眼(primary angle-closure glaucoma,PACG)、先天性青光眼、新生血管性青光眼、青睫综合征及以下因素:晶状体膨胀或脱位、睫状体囊肿、糖皮质激素、眼外伤或眼内手术、虹膜炎、Fuchs综合征和剥脱综合征继发性青光眼.(2) 本组病例存在7类混合机制致病:POAG合并PACG35只眼,占32.1%;PACG合并继发性闭角型青光眼32只眼(29.4%);PACG合并继发性开角型青光眼13只眼(11.9%);POAG合并继发性开角型青光眼11只眼(10.1%);POAG合并继发性闭角型青光眼10只眼(9.2%);先天性青光眼合并继发性青光眼5只眼(4.6%)及不同类型的继发性青光眼合并存在3只眼(2.8%).结论 注意对青光眼发病机制的全面分析,避免明确一种青光眼致病病机制而忽略混合致病机制的存在,以便采取恰当全面的治疗方案;UBM的应用有助于MG致病机制的分析;POAG 合并PACG是MG的主要类型.     

高度近视合并原发性开角型青光眼的早期诊断与研究

高度近视(high myopia,HM)是原发性开角型青光眼(primary open angle glaucoma,POAG)的高危人群。临床上我们发现原发性开角型青光眼与高度近视有着密切关联,所以认识高度近视合并原发性开角型青光眼时的临床特点,重视高度近视合并原发性开角型青光眼的早期诊断,避免漏诊或降低误诊率,有利于提高临床医师对该病的警惕性和早期诊断的水平。本文就高度近视合并原发性开角型的临床特征、早期诊断注意要点的研究进展等进行综述。     

原发性闭角型青光眼的临床类型

目前国际上对原发性闭角型青光眼的临床类型尚无一致通用的名称。本文描述3种临床类型:1.间歇性闭角型;2.急性和亚急性闭角型;3.潜移性闭角型,并提出分类命名的理由。慢性闭角型青光眼不是独立的一型,而是由各种闭角型青光眼晚期衍变而来的。     

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.