玻璃体腔注射曲安奈德联合激光治疗视网膜黄斑分支静脉阻塞黄斑水肿

目的:观察玻璃体腔注射曲安奈德(triamcinolone ace-tonide,TA)联合激光治疗视网膜黄斑分支静脉阻塞黄斑水肿的临床疗效。方法:将经过视力、眼压、眼底检查、眼底彩色照相、荧光素眼底血管造影(FFA)、光相干断层扫描(OCT)检查确诊的164例164眼视网膜黄斑分支静脉阻塞伴黄斑水肿患者纳入治疗。男90例90眼,女74例74眼,年龄20～80(平均59.7)岁。矫正视力0.02～0.6,logMAR视力为0.778±0.347。病程3d～2a。平均眼压15.22mmHg(1mmHg=0.133kPa)。FFA检查黄斑区晚期均有荧光素蓄积;OCT示平均黄斑中心凹视网膜厚度442.41±74.07μm。表面麻醉下给予4mgTA玻璃体腔注射,2wk后进行黄斑区光凝治疗。治疗后第1,3,6mo随访。结果:164例患者治疗后1,3,6mo的平均logMAR最佳矫正视力(BCVA)分别提高至0.49±0.34,0.44±0.34,0.43±0.33,与治疗前比较,差异均有统计学意义。治疗后6mo视力提高135眼(82.3%),其中视力提高≥2者103眼(62.8%);治疗后1,3,6moFFA检查黄斑区晚期荧光素蓄积均有减轻或消失,治疗后1,3,6mo,OCT检查平均黄斑中心凹视网膜厚度分别为253.99±63.99μm,239.84±53.74μm,234.55±51.32μm;与治疗前比较,差异均有统计学意义。治疗后6mo,黄斑水肿改善者147眼(89.6%)。玻璃体腔注药后3d之内有4眼发生假性眼内炎,观察及治疗后恢复至可行激光治疗,治疗后3mo时有11眼眼压高于正常,用药后均恢复至正常范围。结论:玻璃体腔注射TA联合激光治疗视网膜黄斑分支静脉阻塞引起的黄斑水肿疗效较好,明显提高视力,改善视功能,促使黄斑水肿消退或减轻。     

PDT联合ranibizumab玻璃体腔注射治疗年龄相关性黄斑变性合并CNV

目的：观察 PDT 联合玻璃体腔注射 ranibizumab (雷珠单抗)治疗老年性黄斑变性脉络膜新生血管( choroidal neovascularization,CNV)的疗效。
　　方法：将符合纳入标准,经吲哚青绿脉络膜血管造影(indocyanine green angiography, ICGA)、光学相干断层扫描( optical coherence tomography, OCT)检查确诊为黄斑区脉络膜新生血管( CNV)患者27例27眼,经PDT治疗后3~7 d内行 ranibizumab 玻璃体腔注射。观察治疗后1,3,6 mo、末次随访时行最佳矫正视力、FFA、ICGA、OCT 检查及有无并发症发生情况。
　　结果：最佳矫正视力提高17眼(63%),最佳矫正视力稳定6眼(22%),最佳矫正视力下降4眼(15%)。27例27眼治疗前平均渗漏面积为1005.69±105.47μm,治疗后1,3mo后平均875.54±103.27,423.37±79.68μm,与治疗前比较差异有统计学意义(P<0.01),视网膜黄斑中央厚度27例27眼治疗前平均厚度为485.58±122.59μm,治疗后1,3mo后平均398.84±105.32,297.74±89.18μm,与治疗前比较差异有统计学意义(P<0.01)。
　　结论：PDT 封闭 CNV 后,联合玻璃体内腔内注射ranibizumab,有效阻断新生血管复发,减少PDT再次治疗次数和并发症,可提高治疗效果。     

玻璃体腔注射Bevacizumab联合视网膜光凝治疗糖尿病性黄斑水肿

目的: 评价玻璃体腔注射1.25mg贝伐单抗(Bevacizum ab)注射液后行黄斑区激光光凝治疗糖尿病性弥漫性黄斑水肿的临床效果。方法: 随机将74例86眼糖尿病性黄斑水肿引起视力下降的患者分成两组,即治疗组和对照组。治疗组43例48眼玻璃体腔注射Bevacizum ab注射液1.25mg,3wk后进行局部或格栅样视网膜光凝。对照组31例38眼单纯玻璃体腔注射Bevacizum ab注射液1.25mg,跟踪观察治疗前、治疗后3,6wk;3mo两组视力情况与视网膜厚度的变化。结果: 两组视力比较,治疗前、治疗后3wk时无统计学意义,两组间治疗后6wk;3mo比较差异有显著性。治疗组黄斑中心凹厚度在治疗前,治疗后3,6wk;3mo分别为395.933±119.784,292.617±39.131,302.350±55.272,314.200±60.528μm。对照组治疗前,治疗后3,6wk;3mo分别为398.734±111.764,301.217±34.231,312.120±53.170,395.145±108.687μm。两组在治疗前、治疗后3wk视网膜厚度无统计学意义,但在治疗后6wk和3mo时差异有统计学意义。结论: 玻璃体腔注射Bevacizum ab后联合黄斑激光光凝治疗糖尿病性弥漫性黄斑水肿更有效,有利于视网膜光凝,并且能提高糖尿病性黄斑水肿患者的视力。     

激光联合曲安奈德治疗糖尿病黄斑水肿的疗效

目的:评价激光联合曲安奈德玻璃体腔注射治疗黄斑水肿的疗效及安全性。方法:对37例55眼糖尿病黄斑水肿(diabetic macular edema,DME)患者首先采用玻璃体腔注射曲安奈德4mg,术后3wk采用眼底激光对黄斑水肿进行局部直接光凝或格栅样光凝,分别在激光治疗术后1,3,6mo行最佳矫正视力、眼压、眼底检查,术后3mo行光学相干断层扫描(OCT)、荧光素眼底血管造影(FFA)检查,术后6mo行OCT检查,将术后各时间点检测结果与术前值进行比较,做出客观评价。结果:与治疗前相比,术后3wk,激光治疗后1mo,术后3mo,术后6mo视力提高者分别占34.2%,84.6%,87.9%,79.6%;术前、术后3mo和术后6mo平均视力分别为0.1627±0.1016,0.2743±0.1617,0.2615±0.1833,术前视力与术后3mo和6mo视力有显著统计学差异(P<0.01),术后3mo视力提高有效率为83.6%。OCT测量黄斑区视网膜厚度显示,术前、术后3mo和术后6mo黄斑区平均视网膜厚度分别为467.5±150.9,272.7±120.1,308.1±136.2μm,术前黄斑区厚度与术后3mo及6mo有显著统计学差异(P<0.01)。治疗前后FFA显示黄斑区及相关血管的荧光素渗漏较术前明显减少。结论:激光联合曲安奈德玻璃体腔注射治疗黄斑水肿疗效好,并发症少,术后3mo效果最为显著。     

玻璃体腔注射Ranibizumab联合视网膜光凝治疗视网膜分支静脉阻塞继发黄斑水肿

目的：观察玻璃体腔注射Ranibizumab(雷珠单抗)联合视网膜光凝术对视网膜分支静脉阻塞( branch retinal vein occlusion,BRVO)继发黄斑水肿的治疗效果。
　　方法：确诊为视网膜分支静脉阻塞继发性黄斑水肿的患者42例42眼,随机分为三组,每组14眼。单纯注药组给予玻璃体腔注射Ranibizumab 0.05 mL;单纯光凝组行黄斑格栅样光凝;联合治疗组先行玻璃体腔内注射Ranibizumab,再于注药1wk 后行黄斑格栅样光凝。观察三组治疗前和治疗后1,3,6 mo时患者的最佳矫正视力( BCVA)、黄斑区中心凹厚度( CMT)。
　　结果：三组在治疗前BCVA和CMT组间差异无显著性( P>0.05)。各组在治疗后1,3,6 mo的BCVA和CMT均优于治疗前,差异有统计学意义(P<0.05)。单纯注药组治疗后1,3,6mo 的 BCVA 和 CMT 变化有显著性差异( P<0.05),BCVA呈下降趋势,CMT呈增厚趋势;单纯光凝组和联合治疗组治疗后1,3,6 mo BCVA及CMT变化无显著性差异(P>0.05)。治疗后1,3,6mo,联合治疗组BCVA和CMT优于单纯注药组和单纯光凝组(P<0.05),治疗后3,6 mo,单纯光凝组BCVA和CMT优于单纯注药组(P<0.05)。
　　结论：玻璃体腔注射Ranibizumab联合视网膜光凝可以有效治疗视网膜分支静脉阻塞继发黄斑水肿,提高视力,相比单纯注药或者单纯光凝效果更稳定可靠。     

玻璃体腔注射雷珠单抗联合激光治疗视网膜分支静脉阻塞

目的:观察玻璃体腔注射雷珠单抗联合黄斑区格栅样光凝治疗视网膜分支静脉阻塞(branch retinal vein occlusion BRVO)继发黄斑水肿的疗效和安全性。方法:据荧光素眼底血管造影(FFA)对30例30眼视网膜分支静脉阻塞继发黄斑水肿患者随机分为2组:第1组(14眼)单纯行黄斑区格栅样光凝(GLP);第2组(16眼)玻璃体腔连续注射3次雷珠单抗0.05mL/(0.5mg),每次间隔1mo,第1次注射雷珠单抗7d后行GLP治疗。随访6mo,观察最佳矫正视力(BCVA)及光学相关断层扫描(OCT)检查黄斑中心凹厚度(CMT)的变化。结果:治疗6mo后两组患者最佳矫正视力(BCVA)均提高,联合治疗组优于单纯GLP组(P<0.05)。OCT显示第1组黄斑中心凹厚度平均降低236.4±113.0μm,第2组平均降低386.6±195.5μm,联合治疗组优于单纯GLP组(P<0.05)。结论:联合治疗的效果明显优于单纯GLP治疗的效果,玻璃体腔内注射雷珠单抗联合黄斑区格栅样光凝术治疗视网膜分支静脉阻塞继发黄斑水肿安全有效。     

地奥司明治疗非缺血型RVO的疗效观察

目的:探讨地奥司明治疗非缺血型视网膜静脉阻塞(retinal vein occlusion,RVO)的临床疗效。方法:将符合非缺血型RVO诊断的48例48眼随机分为治疗组和对照组。治疗组27例27眼,给予地奥司明0.9g,po,bid,4wk为一疗程,连续三个疗程。对照组21例21眼,先给予丹香冠心注射液16mL加入5g/L葡萄糖注射液(或者9g/L氯化钠注射液)500mL中,iv,qd,1wk后改为丹参片3片,po,tid,连续服用11wk。观察治疗前后最佳矫正视力和眼底病变的动态改变、视网膜电流图的变化、黄斑水肿的发生率及黄斑水肿厚度变化。结果:治疗后4,8,12wk治疗组最佳矫正视力提高均显著高于对照组(P<0.05)。治疗后4wk,治疗组渗出、出血吸收率为63%,高于对照组的33%(P<0.05)。治疗后12wk,治疗组暗适应眼最大电反应的b波振幅(231±39)μV与治疗前(184±65)μV相比明显提高(P<0.05),且与对照组(207±49)μV相比有差异(P<0.05)。治疗组并发黄斑水肿17例,对照组14例,治疗组黄斑水肿的发生率与对照组相比没有明显差异(P>0.05)。治疗后12wk黄斑中心凹厚度,治疗组为298±54μm,低于对照组的369±76μm(P<0.05)。结论:对于非缺血型RVO,地奥司明能够有效的减轻黄斑水肿,降低视网膜的功能损伤,从而改善视功能,效果优于丹参治疗。     

曲安奈德玻璃体腔注射治疗弥漫性糖尿病黄斑水肿的临床观察

目的:研究曲安奈德玻璃体腔注射联合黄斑部格栅样光凝治疗弥漫性糖尿病黄斑水肿效果。方法:对35例37眼弥漫性糖尿病黄斑水肿患者随机分为两组单纯玻璃体腔曲安奈德注射组及联合黄斑部格栅样光凝治疗组,其中光凝组在注药后1mo行黄斑部格栅样光凝,分别对比各组治疗前及治疗后1,3,6mo视力及黄斑厚度进行统计分析。结果:单纯曲安奈德注射组注药后1,3mo视力分别为0.28±0.19、0.22±0.14较注射前视力0.15±0.13提高,有统计学意义(P<0.05),治疗后6mo视力为0.17±0.10与治疗前视力无统计差异(P>0.05),黄斑厚度注药后1,3,6mo分别为231.82±61.02μm、255.12±92.66μm、349.06±116.19μm均较注药前469±136.60μm减轻(P<0.01),但治疗后6mo较3mo黄斑厚度明显增加有统计学意义(P<0.01),提示黄斑水肿复发;联合治疗组注药后1,3,6mo视力为0.27±0.17、0.25±0.15,0.23±0.13,与治疗前视力0.14±0.11对比均明显提高(P<0.01),黄斑厚度治疗后1,3,6mo分别为245.68±74.85μm、257.36±79.44μm、276.57±99.64μm较治疗前黄斑厚度473.33±123.22μm显著减轻(P<0.01),但6mo与3mo黄斑厚度对比无显著增加(P>0.05)。观察期间29%患眼出现眼压升高,经局部降眼压药物治疗后得到控制。结论:曲安奈德玻璃体腔注射联合黄斑部格栅样光凝治疗弥漫性糖尿病黄斑水肿,能减轻黄斑水肿,提高患者视力,但仍需进一步长期临床观察。     

康柏西普治疗湿性老年黄斑变性的初步研究

目的:探讨康柏西普(conbercept)玻璃体腔内注射治疗湿性老年性黄斑变性的初步疗效.方法:研究共纳入17例18眼确诊为湿性老年性黄斑变性的患者,给予康柏西普玻璃体腔内注射治疗,初始治疗3mo,每个月给药1次.评估康柏西普玻璃体内注射前后的最佳矫正视力、眼压、散瞳后眼底照相、眼底荧光素血管造影和吲哚菁绿血管造影结果,观察并对比分析治疗前和治疗后1、2、3mo的最佳矫正视力、眼压、黄斑区的渗漏情况以及视网膜黄斑中心凹的厚度.结果:患者17例18眼接受玻璃体注射康柏西普治疗后3mo随诊时,15眼(83%)的最佳矫正视力不同程度提高,3眼(17%)最佳矫正视力稳定.以Optovue OCT测量18眼治疗前的视网膜黄斑中心凹厚度平均为421.72±54.43μm,治疗后1、2、3mo平均为337.89±25.88、293.56±26.87、266.89±19.10μm,与治疗前相比差异具有统计学意义(P<0.05).末次随访时,FFA和ICG检查结果显示,15眼(83%)黄斑区渗漏消失,3眼(17%)黄斑区仍存在渗漏,随后再次行康柏西普玻璃体腔内注射1~2次至黄斑区渗漏消失.患者18眼中,有2眼出现了眼压升高(26,23mmHg),留院观察1d后,眼压恢复至正常水平.1眼接受玻璃体注射后出现球结膜轻度的充血,给予左氧氟沙星滴眼液2d后充血消失.使用该药后未出现与药物相关的严重不良反应.结论:对于湿性老年性黄斑变性的患者,采用玻璃体腔内注射康柏西普能够有效改善患者的视力,疗效好,见效快,副作用少,安全性也较高.     

曲安奈德玻璃体腔注射治疗视网膜分支静脉阻塞继发黄斑水肿

目的:观察玻璃体腔注射曲安奈德(tviamcinolone ace-tonide,TA)治疗视网膜分支静脉阻塞(branch retinal vein occusion,BRVO)继发黄斑水肿的疗效。方法:经眼底检查、荧光眼底血管造影(FFA)、光学相干断层扫描(OCT)检查确诊的BRVO继发黄斑水肿22例(22眼)行玻璃体腔曲安奈德注射,治疗后随访(4.2±0.4)mo,对比治疗前及治疗后1,3mo视力、眼压、眼底、FFA表现、OCT所显示黄斑水肿高度以及黄斑中心凹阈值。结果:治疗的22眼中19眼(82%)视力明显提高,3眼(14%)视力不变,治疗前平均视力0.10±0.06,治疗后1,3mo平均视力分别为0.25±0.12、0.28±0.13,黄斑中心凹厚度(OCT)治疗前平均厚度(519.0±137.5)μm,治疗后1,3mo平均厚度分别为(256.4±68.3)μm、(239.4±52.2)μm,黄斑中心凹阈值(dB):治疗前(18.8±4.2)dB,治疗后1,3mo分别为(24.0±6.0)dB、(24.6±5.2)dB,治疗前后比较差异有统计学意义(P<0.01)。22眼中有6眼(27%)治疗后暂时性眼压升高,经局部抗青光眼药物治疗后恢复正常。5例(23%)患者2次注药。结论:玻璃体腔注射TA在短期内可有效改善BRVO继发黄斑水肿,但也要注意对原发病治疗。     

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.