准分子激光角膜切削术矫正RK术后近视22例

目的:探讨准分子激光角膜切削术(PRK)矫正角膜放射状切开术(RK)后残留近视及近视散光的有效性和安全性。方法:应用波长193nm的ArF准分子激光对22例39眼RK术后残留的近视及近视散光进行准分子激光屈光手术治疗。结果:随访5a,平均屈光度由术前-4.21±1.42D下降至术后的-0.41±0.31D,34眼≥术前最佳矫正视力,术前裸眼视力≥1.0者32眼,术后裸眼视力≥1.0者30眼,回退4眼(10%),回退度数<-1.25D。术前矫正视力≤0.9者,术后5a时仅2眼裸眼视力≥1.0。结论:PRK是一种有效和安全的矫正RK术后残留近视的方法。     

影响近视眼角膜屈光力多因素分析

目的:探讨影响近视眼角膜屈光力的相关因素。方法:分别测量227例(452眼)近视及近视散光患者角膜地形图、角膜中央厚度、眼压、A超及屈光度,将所得结果进行统计学分析。结果:①不同程度屈光度,角膜顶点屈光力低度近视组与中、高、重度近视组比较有显著性差异(P <0.05),角膜中央3mm屈光力,低、中度近视组与重度近视组比较有显著性差异(P <0.05),角膜中央5mm屈光力低度近视眼组与重度近视组比较有显著性差异(P <0.01),角膜中央7mm屈光力各组之间比较无显著性差异(P >0.05);②角膜中央3,5,7mm的屈光力与年龄、前房深度呈正相关(年龄:r分别为:0.398,0.387,0.342,P =0.000;前房深度:r分别为:0.277,0.310,0.288,P =0.000);③角膜中央3,5,7mm的屈光力均与等效球镜屈光度、眼轴、晶状体厚度呈负相关(等效球镜屈光度:r分别为-0.80,-0.782,-0.710,P =0.000;眼轴:r分别为:-0.670,-0.668,-0.598,P =0.000;晶状体厚度r分别为-0.318,-0.282,-0.232,P值分别为0.000,0.000,0.001);④将角膜不同区域屈光力为应变量,分别建立多元线性回归方程:Y 3=77.571-1.432X 1-0.554X 2 0.964X 3 0.067X 4-1.205X 5;(F =101.356,P =0.000);Y 5=76.538-1.424X 1-0.538X 2 1.063X 3 0.067X 4-1.122X 5;(F =92.395,P =0.000);Y 7=72.563-1.     

PRK治疗RK术后残余近视、散光7年观察

目的　评价 PRK治疗 RK术后残余近视、散光的远期疗效。方法　应用日本 NIDEK EC- 5 0 0 0型准分子激光仪对 3例 (5只眼 ) RK术后残余近视、散光施行 PRK治疗 ,5只眼术前平均球镜度为 - 2 .5 5 D,平均柱镜度为 - 2 .5 5 D。术后随访 7年。结果　术后 1年时 ,5只眼平均球镜度为 +0 .35 D,无散光 ,屈光度均在预定矫正度± 0 .5 0 D以内 ,裸眼视力均≥ 1 .0 ,最佳矫正视力均大于或等于术前最佳矫正视力 ,角膜透明。术后 7年时 ,5只眼平均球镜度为 - 0 .9D,平均柱镜度为 - 0 .5 5 D。 3只眼屈光度在预定矫正度± 0 .5 0 D以内 ,4只眼裸眼视力≥ 0 .5 ,3只眼裸眼视力≥ 1 .0 ,5只眼最佳矫正视力均大于或等于术前最佳矫正视力 ,3只眼角膜透明 ,2只眼有 3级 haze。结论　PRK治疗 RK术后残余近视、散光安全 ,有效 ,有良好的预测性、准确性及稳定性 ,是 RK术后残余近视、散光补救治疗的有效方法。但对 RK术后切口愈合不良、疤痕粗大的病例却应慎重     

准分子激光治疗高度和超高度近视的远期疗效

目的:比较准分子激光屈光性角膜切削术(PRK)和激光原位角膜磨镶术(LASIK)治疗高度和超高度近视的远期临床效果及其影响疗效的因素。方法:高度近视眼163例(294眼),其中PRK组84例(139眼),平均等效球镜屈光度-8.68±2.08D,LASIK组79例(155眼),平均等效球镜-9.17±2.92D。按术前屈光度分2组,Ⅰ组-6.25～-10.00D,Ⅱ组≥-10.00D,随访2a。结果:2a时,裸眼视力≥0.5者,Ⅰ组中PRK占89.5%,LASIK占96.8%;Ⅱ组中PRK占35.3%,LASIK占83.9%。裸眼视力≥1.0者,Ⅰ组中PRK为51.4%,LASIK为80.6%;Ⅱ组中PRK为2.9%,LASIK为46.8%。术后屈光度在预期矫正屈光度±1.00D范围以内者:Ⅰ组中PRK为62.8%,LASIK为88.2%;Ⅱ组中PRK为17.6%,LASIK为61.3%。角膜上皮下混浊(Haze)发生率,PRK组0级53.2%,0.5级25.3%,1级13.0%,2级8.6%。其中Ⅰ组发生率为39.0%,Ⅱ组发生率为70.5%。LASIK组均无上皮下或层间混浊发生。术后2a的等效球镜屈光度(Y)PRK组与术前等效球镜(X1雪,角膜屈光力(X 2)建立多元回归方程为Y =-8.645 0.444X1 0.265X 2(P <0.001)。LASIK组与术前等效球镜(X 1)、术中角膜切削深度(X 3)建立多元回归方程Y =-0.703 0.52X 1 0.0437X 3(P <0.001)。结论:准分子激光治疗高度和超高度近视眼的临床效果LASIK术式较PRK术式具有明显的优势。     

PRK治疗复性近视散光效果分析

目的探讨PRK治疗复性近视散光的临床疗效.方法按术前欲矫正球镜屈光度将88眼分为A(≤-6D,62眼)、B(≥-6.25D,26眼)两组,回顾性分析随访1年后的残留球镜度、散光度和非矫正视力情况.结果术后B组球镜度仍高于A组(-0.83D和-0.44D,P=0.0005).两组除术后3个月时,手术前后散光度均无明显差别(P>0.05).两组间非矫正视力在整个随访期间差别均有非常显著性意义(P<0.01).结论由于对高度近视矫正得不够彻底,PRK仅对球镜度低于-6D以下的复性近视散光疗效确切.     

角膜塑形镜控制青少年近视进展的效果和影响因素分析

目的:评价角膜塑形镜对青少年近视的控制效果和相关影响因素.方法:选择2012-01/2014-12在我院眼科门诊就诊的8~17岁低中度近视的患者97例189眼,配镜后随访2a,观察患者视力、角膜曲率、屈光度、眼轴长度的变化,并分析青少年近视进展的影响因素.结果:患者裸眼视力、角膜水平曲率及角膜垂直曲率戴镜1mo后与戴镜前相比,差异均有统计学意义(P<0.001).配戴角膜塑形镜的患者在戴镜2a后等效球镜变化量(-0.51±0.64D,t=10.864,P<0.001),眼轴长度增加(0.33±0.31mm,t=14.879,P<0.001),角膜散光变化量(-0.25±0.43D,t=5.375,P<0.001),差异均有统计学意义.等效球镜变化量相关因素分析显示,年龄、戴镜前球镜、戴镜前等效球镜、基础眼轴与等效球镜变化量均呈负相关(P<0.05).结论:角膜塑形镜可有效提高患者裸眼视力.虽然配戴角膜塑形镜患者的眼轴和屈光度有小幅增加,但仍是一种有效控制近视发展的矫治方法.角膜塑形术对于年龄较大,基础眼轴长,近视度数高的患者,其近视控制效果更好.     

近视眼LASIK术后屈光回退的相关因素分析

目的 探讨影响准分子激光原位角膜磨镶术(LASIK)治疗近视术后疗效的相关因素.方法 采用LASIK对72例(141只眼)近视眼患者进行治疗.分别记录术前、术后第1周、第1个月、第3个月、第6个月和第12个月视力、屈光度、眼压、角膜厚度、角膜地形图检查所得的角膜后表面数据.根据术后第12个月裸眼视力和等效球镜屈光度分2组,Ⅰ组屈光回退组视力＜5.0且术后近视等效球镜屈光度＞1.00I),计35只眼;Ⅱ组视力正常组视力≥5.0,计106只眼.分析术后裸眼视力与i者多因素关系.结果 术后第12个月裸眼视力4.4～5.1,平均4.97±0.13,以术后第12个月裸眼视力为因变量(Y)与术前近视屈光度(X1)、角膜切削比(X2),术后第12个月角膜后表面最高点Diff值(X3),术后第12个月和术后第1周角膜厚度差(X4),术后第12个月和术后第1周角膜后表面屈光度差(X5)等进行逐步回归分析建立多元同归方程Y=5.09-0.034X1+1.785X2-2.216X3-0.002X4+0.081X5(F=21.474,19＜0.01).术后随访角膜厚度有不同程度增加,角膜后表面屈光度降低,角膜后表面Diff值增高,屈光回退组各指标不同阶段比较差异有统计学意义(分别F=8.56、4.68、2.49;均P＜0.05),变化尤以术后3个月内明显;正常眼组各指标不同阶段比较除角膜最薄处厚度有差异外,余均无统计学意义(角膜最薄厚度F=7.27,P＜0.01;其余均P＞0.05).结论 LASIK治疗近视是一种安全、有效的方法,但欲取得较好疗效,应考虑不同因素如术前近视屈光度、角膜切削比、术后角膜增殖、术后角膜后表面改变等因素的影响.     

智慧型光斑LASIK治疗近视临床分析

目的:探讨智慧型光斑LASIK治疗近视或近视散光可预测性、稳定性、有效性及术后残留屈光度危险因素分析。方法:回顾性分析2008-10/2009-10在我中心行LASIK病例,术前最佳矫正视力(BCVA)≥0.8,随访时间>1mo,球镜<-10.00D纳入统计分析病例,共768例。按激光切削模式及屈光度分组,对术后裸眼视力,术后1,3,6mo;1a残留等效球镜,屈光回退患者术前术后数据行统计学分析。结果:10例BCVA术后未达术前;预测性:术后常规组98.0%SE<0.50D,99.2%SE<1.00D;波前组97.4%SE<0.50D,99.3%SE<1.00D;术后残留屈光度,常规组:1mo:-0.01±0.10D;3mo:-0.02±0.20D;6mo:-0.07±0·31D;1a:-0.15±0.38D。波前组:1mo:-0.01±0.08D;3mo:-0.01±0.09D;6mo:-0.03±0.15D;1a:-0.08±0.19D;视力改变,常规组:0±0.05,波前组:0.01±0.04。23例术后残留屈光度危险因素分析,术后残留球镜与年龄,术前球镜有关,术后球镜=1.355-0.034年龄+0.142术前球镜;术后残留柱镜与术前柱镜,术前中央角膜厚度有关,术后柱镜=3.489+0.238术前柱镜-0.007术前中央角膜厚度。结论:智慧型光斑LASIK预测性,稳定性,有效性均较好,波前像差引导LASIK在预测性及有效性方面更优,两种术式均有较好的稳定性;术后残留球镜危险因素:年龄、术前球镜,术后残留柱镜危险因素:术前柱镜、术前中央角膜厚度。     

PRK治疗近视术后远期疗效分析

目的:评价PRK治疗近视及散光的远期疗效。方法:选取1996-11/1998-01PRK手术116例(219眼),按术前等值球镜度分为3组,A组:-1.00D~-3.00D53眼;B组:-3.125D~-6.00D125眼;C组:-6.125D~-16.00D41眼。术后随访10a。结果:术后10a裸眼视力≥0.5、≥1.0者,A组分别为100%、84.9%;B组分别为100%、80.8%;C组分别为92.7%、31.7%。术后10a屈光度在预定矫正度±1.00D以内者,A、B、C组依次为92.5%,74.4%,34.2%。术后10a最佳矫正视力达到或超过术前最佳矫正视力者依次98.1%、98.4%、92.2%。无1例有1级以上角膜上皮下雾状浑浊(Haze)者。结论:PRK是治疗近视安全有效的方法,其预测性及稳定性与近视度呈负相关。     

准分子激光角膜切削术随访十年结果分析

目的评价准分子激光角膜切削术（PRK）远期疗效。方法收集在我院施行PRK手术随访10年近视156例（308眼）。根据术前屈光度（等值球镜）分为A、B两组，A组屈光度-1．50D～-6．00D者224眼，B组-6．12D--10．00D者84眼。术后随访视力、屈光度、眼前段及眼底表现，眼压、角膜地形图等。6个月后每年复查1次，以1、5、10年检查情况为准。结果PRK术后随访10年，裸眼视力达预期矫正视力A组为91．96％、B组为76．19％，屈光度±0．75D正视范围内比率A组为90．18％，B组为75．00％。近视屈光回退-1．00D以上在5年和10年时A组为7．14％和6．70％，B组为22．62％和23．81％，屈光回退率相比，相同时间两组间P〈0．01，同一组5年和10年相比P〉0．05。随时间延长haze逐渐吸收，无角膜感染、角膜扩张及变性样角膜病变等发生。结论PRK矫正近视远期效果稳定，预测性、安全性好，中低度近视优于高度近视。随时间延长haze逐渐吸收，回退的屈光度稳定。     

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.