激光虹膜成形术治疗急性闭角型青光眼

目的　观察激光周边虹膜成形术在治疗急性闭角型青光眼持续性高眼压中的作用 ,证实该治疗方法的有效性和安全性。方法　原发性急性闭角型青光眼第 1次急性发作者 2 0例 (2 0眼 ) ,联合应用可耐受最大剂量降眼压药物 3～ 6小时 ,均不能将眼压控制在 3 0mmHg(1mmHg =0 . 13 3kPa)以下 ,立即行激光周边虹膜成形术。观察激光治疗前后的视力、眼压及前房角变化。结果　激光术后 2小时全组 2 0眼眼压从 3 2～ 68mmHg降至 12～ 2 8mmHg ,视力均有提高 ,房角均有不同程度的加宽。结论　激光周边虹膜成形术是快速降低急性闭角型青光眼发作期眼压的一种有效的方法。     

激光虹膜成形联合白内障超声乳化吸除术治疗急性闭角型青光眼

目的 分析激光虹膜成形术联合白内障超声乳化吸除术,对药物治疗不能迅速缓解的合并白内障的原发性闭角型青光眼急性发作的治疗效果.方法 对药物治疗不能迅速缓解的合并不同程度白内障的原发性闭角型青光眼急性发作患者12例(14只眼)行激光虹膜成形术以开放房角、控制眼压,而后行白内障超声乳化吸除联合人工晶状体植人术,随访(3～12)月,观察房角、眼压、视力变化及并发症情况.结果 激光虹膜成形术后超声生物显微镜检查示所有术眼房角开放;激光虹膜成形术前眼压(44.5±6.3)mmHg,术后2h、4h的眼压分别为(20.5 4±3.5)mmHg、(11.9 4±2.9)mmHg,与光凝前眼压的差异均有统计学意义(t=21.4956,P=0.000;t=241.5631,P=0.000);白内障超声乳化术后2周、3月的眼压均低于21mmHg,平均分别为(16.54±2.7)mmHg、(15.84±2.6)mmHg;激光虹膜成形术后和白内障超声乳化吸除术后视力不同程度提高;无严重并发症.结论 激光虹膜成形术能有效缓解药物治疗无效的原发性闭角型青光眼急性发作,并可作为白内障超声乳化吸除术治疗急性闭角型青光眼的前期治疗.     

激光周边虹膜成形及切除术治疗药物难控制的急性闭角型青光眼

目的：探讨激光周边虹膜成形联合周边虹膜切除术,治疗药物难控制的急性闭角型青光眼的效果和安全性。方法：选取药物治疗24h后眼压仍高于21mmHg的原发性急性闭角型青光眼15例17眼和白内障膨胀期继发的急性闭角型青光眼4例4眼,共19例21眼,采用激光周边虹膜成形联合周边虹膜切除术,术后24h观察视力、眼压、角膜、周边前房深度、房角及并发症。结果：所有患者激光术后24h眼压均有大幅度的下降,术前眼压53.09±11.01mmHg,术后24h眼压下降至14.98±4.21mmHg,治疗前后差异有统计学意义（P〈0.01 ）。术后视力由术前手动～0.3提高至0.1～1.0。所有患者角膜水肿减轻或消退,周边前房深度增加,房角不同程度开放。其中虹膜出血11眼（52.4%）,轻度反应性虹膜炎21眼（100%）,无1眼发生角膜灼伤。结论：激光周边虹膜切除联合周边虹膜成形术,是降低药物难控制的急性闭角型青光眼眼压的一种安全有效的方法。     

晶状体乳化术治疗急性闭角型青光眼并白内障

目的探讨晶状体超声乳化吸出并人工晶状体植入治疗原发性急性闭角型青光眼合并白内障的疗效。方法原发性急性闭角型青光眼12例(14眼),视力<0.4,晶状体不同程度浑浊,行晶状体超声乳化联合人工晶状体植入术,随访3月~3年。观察术前、术后视力、眼压、前房深度及前房角的变化。结果12眼(房角关闭<1/2周)术后眼压控制正常;2眼(房角关闭>3/4周)需滴降眼压滴眼液。其中1眼在1月后再次眼压急性升高,经YAG激光虹膜造孔后好转。视力均有不同程度提高。结论晶状体超声乳化并人工晶状体植入术治疗急性闭角型青光眼合并白内障,房角关闭小于1/2周者手术有效;房角关闭大于3/4周的病例需进一步随访观察。     

窄角型慢性单纯性青光眼：附9例报告

本文对9例(16眼)窄角型慢性单纯性青光眼(简称“窄角慢单”)的诊断治疗进行了分析,指出窄角慢单是原发性开角型青光眼的一种特殊类型。其诊断的建立,除了符合原发性开角型青光眼的一般定义外,低眼压及高眼压状态下,房角形态无明显差异,均呈窄房角开放状态为其特征.激光周边虹膜切除术可作为鉴别诊断手段之一,亦可防止这类患者随年龄增长,晶体增大导致瞳孔阻滞而引起的急性闭角型青光眼样的发作。窄角慢单的治疗,作者主张首选药物治疗,对于药物不能控制者宜及时采用滤过性手术。     

联合激光手术治疗原发性闭角型青光眼急性发作

目的探讨用联合激光手术治疗原发性闭角型青光眼急性发作。方法21眼原发性闭角型青光眼第1次急性发作时行激光周边虹膜成形术(160~240mW,500μm,0.4s)和激光周边虹膜切除术(能量:2.0~7.8mJ)治疗。结果联合激光手术前眼压为39~68mmHg(1kPa=7.5mmHg,平均51.5mmHg±9.4mmHg),术后眼压为10~29mmHg(平均15.3mmHg±6.4mmHg),15眼不用药物眼压≤21mmHg,4眼加用局部降眼压药物眼压≤21mmHg。结论联合激光手术治疗原发性闭角型青光眼急性发作是有效的。     

氩激光周边虹膜成形术联合YAG和氩激光周边虹膜切除术治疗原发性闭角型青光眼

我们应用氩激光周边虹膜成形术联合 YAG和氩激光周边虹膜切除术治疗原发性闭角型青光眼取得良好效果 ,现报告如下 :资料与方法 :1998年 9月～ 2 0 0 0年 9月应用氩激光周边虹膜成形术联合 YAG和氩激光周边虹膜切除术治疗原发性闭角型青光眼 42例 5 1眼 ,女性 33例 ,男性 9例 ,年龄 5 3～ 73岁 ,平均 6 4岁。临床前期 38眼 ,间歇期 6眼 ,发作期 3眼 ,慢性闭角型青光眼 4眼。慢性闭角型青光眼作暗室试验。随访观察时间 3个月～ 2 4个月。常规作视力、裂隙灯、房角镜、暗室试验和视野检查。眼压控制标准为停用降眼压药物后眼压≤2 .79k Pa,…     

超声乳化晶状体吸除术治疗闭角型青光眼

目的：观察超声乳化晶状体吸除加人工晶状体植入治疗闭角型青光眼的临床疗效。方法：对31只闭角型青光眼行白内障吸出加人工晶状体植入术，术前眼压经药物治疗后为21～50mmHg；原发性急性闭角型青光眼27眼，慢性闭角型青光眼1眼，老年性白内障膨胀期继发青光眼3眼，晶状体透明15眼，晶状体不同程度混浊11眼，虹膜节段性萎缩5眼；术后观察患眼压、视力、前房深度，随访1a以上。结果：术后视力31眼均有提高。术后眼压均正常(12～20mmHg)30眼；术后8mo发生恶性青光眼1眼(慢性闭角型青光眼)，行小梁切除术加前节玻璃体切割后眼压控制正常。结论：晶状体超声乳化吸出术可使前房加深，房角开放，眼压得到控制，无青光眼小梁切除术的并发症，是治疗某些闭角型青光眼的首选方法。     

小梁切开联合虹膜根切术治疗原发性闭角型青光眼

目的 观察外路小梁切开术联合虹膜周边切除治疗原发性闭角型青光眼的疗效.方法 对31例(31眼)原发性闭角型青光眼行外路小梁切开及虹膜周边切除术.其中急性闭角型青光眼22例,慢性闭角型青光眼9例.术后1周,1、3、6个月观察患者眼压和房角情况.结果 术后1个月和3个月,不用降眼压药眼压≤21 mm Hg(1 mm Hg=0.133 kPa)者分别为29例和27例,完全成功率分别为93.5%和87.1%.19例(19眼)随访6个月,不用降眼压药眼压≤21 mm Hg者16例(84.2%).术后房角检查显示上方120°范围房角开放和小梁组织切开的裂隙.术后并发症:前房出血31眼,均自行吸收,后弹力层损伤6眼、虹膜根部断离2眼、虹膜后粘连4眼.结论 外路小梁切开联合周边虹膜切除术能有效治疗原发性闭角型青光眼.     

原发性急性闭角型青光眼合并白内障的联合治疗

目的探讨氪激光及Nd：YAG激光虹膜成形加打孔术联合超声乳化手术治疗原发性急性闭角型青光眼合并白内障的临床意义。方法对25例（25眼）急性闭角型青光眼合并白内障首次发作者,药物控制眼压后即行Nd：YAG激光及氪激光虹膜成型及打孔术,术后3～14d行超声乳化吸出联合人工晶状体植入术,观察治疗前及术后眼压、前房深度及视力,并用StratusOCT观察房角情况。随访3～12个月,结果采用配对t检验,SPSS10．0统计学方法分析。结果眼压由术前的（62．17±14．12）mmHg降至（14．32±3．17）mmHg,前房深度由术前（1．67±0．32）mm加深至（2．86±0．40）mm,房角明显加宽,术后视力明显提高。结论对首次发作的急性闭角型青光眼合并白内障,激光虹膜成形及打孔术联合白内障超声乳化手术可以有效的控制眼压,开放房角,提高视力。减少青光眼外滤过手术的并发症,减少创伤,改善视力,提高生活质量。     

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.

---

     

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.