532半导体激光光凝术治疗糖尿病性视网膜病变

目的探讨532半导体激光光凝术治疗糖尿病性视网膜病变的效果。方法应用法国莱特532半导体纯绿激光,对黄斑局限性水肿行局部光凝、弥漫型水肿或囊样水肿者作“C”型光凝。对于视网膜病变达期以上者,行广泛视网膜光凝术(PRP),分3～4次完成。伴黄斑水肿者先行黄斑区“C”型光凝,然后行PRP治疗。结果830例(1560只眼)糖尿病性视网膜病变患者,其中非增殖期369例(721只眼),光凝后视力提高及保持不变者701只眼,视力降低者20只眼(u=19.75,P<0.001);增殖期461例(839只眼),光凝后视力提高及保持不变者818只眼,降低者21只眼(u=18.51,P<0.001),两组差异均有非常显著意义。黄斑水肿大部分减轻,微血管瘤逐渐消退。结论532激光治疗糖尿病性视网膜病变安全有效。     

眼底激光联合玻璃体腔注药治疗合并黄斑水肿的糖尿病性视网膜病变的临床观察

目的:探讨全视网膜光凝术联合玻璃体腔注药术治疗合并黄斑水肿的糖尿病性视网膜病变的效果。方法:应用532半导体绿激光治疗机对视网膜病变达Ⅲ期以上同时合并黄斑水肿的糖尿病性视网膜病变患者,行全视网膜光凝术,术后1wk行曲安奈德玻璃体腔注射。结果:治疗后241眼中视力提高及无下降者218眼,有效率占90.5%,视力下降及玻璃体出血23眼,占9.5%,治疗前后有非常显著的临床意义。结论:全视网膜光凝术联合玻璃体腔注药术治疗合并黄斑水肿的糖尿病性视网膜病变安全有效。     

倍频532nm激光治疗视网膜血管性疾病所致黄斑水肿

目的:探讨倍频532nm激光治疗视网膜血管性疾病所致黄斑水肿的临床效果。方法:对89例112眼视网膜血管性疾病所致黄斑水肿患者(糖尿病性视网膜病变53例75眼,视网膜静脉阻塞34例35眼,Coats病1例1眼,旁中心凹视网膜毛细血管扩张症1例1眼),采用倍频532nm激光行黄斑区局部或格栅样光凝治疗黄斑部的局部或弥漫性水肿。术后随访1a观察患者黄斑水肿消退情况和视力变化。结果:光凝治疗后视力提高者21眼(18.7%),不变者84眼(75.0%),下降者7眼(6.3%)。光凝后黄斑水肿完全吸收40眼(35.7%),部分吸收60眼(53.6%),无吸收12眼(10.7%)。且局限性黄斑水肿的治疗效果优于弥漫水肿及囊样水肿(P<0.01)。结论:倍频532nm激光光凝术是治疗视网膜血管性疾病所致黄斑水肿的有效、安全方法。     

532nm激光治疗糖尿病视网膜病变的临床观察

目的:评估532nm激光治疗糖尿病视网膜病变(diabetic retinopathy,DR)的治疗效果。方法:应用532nm激光对糖尿病患者48例96眼[包括增殖前期糖尿病视网膜病变(PPDR)54眼,增殖期糖尿病视网膜病变(PDR)42眼(包括高危PDR20眼,非高危PDR22眼),合并黄斑水肿21眼]行视网膜光凝术。根据DR分期及病变严重程度行次全视网膜光凝(Sub-PRP)、标准全视网膜光凝(S-PRP)和超全视网膜光凝(E-PRP)及局限光凝和格栅样光凝,随访3mo～4a,观察视力和视网膜病变进展情况。必要时再补充激光治疗。结果:视力:提高或不变为有效,其中PPDR组有效45眼(83%),非高危PDR组有效18眼(82%),高危PDR组有效12眼(60%)。视网膜病变进展情况:视网膜水肿、渗出、出血部吸收,视网膜新生血管部分或全部消退为有效,其中PPDR组有效50眼(93%),非高危PDR组有效19眼(86%),高危PDR组有效13眼(65%)。结论:倍频532nm激光治疗DR安全有效,早期病变治疗效果好。及早发现和治疗病变,注意光凝方法和技巧,以及随访和跟踪治疗,是提高视网膜光凝疗效的关键。     

倍频532激光光凝治疗糖尿病视网膜病变的临床观察

目的观察倍频532nm激光视网膜光凝术治疗糖尿病视网膜病变（DR）的临床效果。方法用倍频532nm激光对30例（54只眼）增生前期和增生期DR患者进行全视网膜光凝治疗,伴有临床意义黄斑水肿者,先行黄斑部光凝治疗。术前行视力、眼压、裂隙灯、眼底、荧光素眼底血管造影（FFA）检查。术后定期复查,并记录视力变化及视网膜病变进展程度。光凝术后平均随访10个月。结果治疗后18只眼（33．3％）视力提高,视力无变化32只眼（59．3％）,视力下降4只眼（7．4％）,有效45只眼（83．3％）,随病变程度加重疗效降低。经FFA检查,有临床意义黄斑水肿者16只眼,经光凝后水肿完全消退者10只眼（62．5％）,部分消退者5只眼（31．3％）,不变者1只眼（6．3％）。结论倍频532nm激光视网膜光凝术是治疗DR安全、有效的方法。     

增生性糖尿病视网膜病变弥漫性黄斑水肿的激光治疗

目的　评价全视网膜光凝联合黄斑格栅样光凝治疗伴有弥漫性黄斑水肿的增生性糖尿病视网膜病变的疗效。方法　 4 0例 5 0眼伴有弥漫性黄斑水肿的增生性糖尿病视网膜病变患者 ,采用氩绿激光进行黄斑格栅样光凝联合全视网膜光凝。分析视力、黄斑水肿和新生血管的变化。结果　激光治疗后随访 6～ 30个月 ,5 0眼中 36眼治疗有效 ;76 %患眼的视力稳定 ,视力进步者占 12 % ;6 2 %患眼黄斑水肿明显减少 ,黄斑水肿完全消退者占 10 % ;视网膜新生血管或视盘新生血管完全消退者为 12 % ,部分消退者为 5 6 % ,余 14眼 (2 8% )治疗无效。结论　全视网膜光凝联合黄斑格栅样光凝是治疗伴有弥漫性黄斑水肿的增生性糖尿病视网膜病变的有效措施。     

倍频532nm激光治疗糖尿病视网膜病变50例

目的观察倍频532nm激光视网膜光凝术治疗糖尿病视网膜病变(diabeticretinopathy,DR)的疗效。方法用倍频532nm激光对50例(89眼)增生前期和增生早期DR患者进行视网膜光凝治疗。光凝3～8次,术后平均随访16月。结果治疗后29眼(32.6%)视力提高,视力无变化55眼(61.8%),视力下降5眼(5.6%)。随病变程度增加疗效降低(P<0.01)。荧光素眼底血管造影检查,有黄斑水肿的58眼中,光凝后水肿完全消退者32眼(55.2%),部分消退者24眼(41.4%),不变者2眼(3.4%)。5眼晶状体混浊加重。结论倍频532nm激光视网膜光凝术治疗DR有效,在增生前期治疗效果好。     

次全视网膜光凝治疗中度非增殖性糖尿病视网膜病变的临床观察

目的 观察次全视网膜光凝治疗中度非增殖性糖尿病视网膜病变(NPDR)的临床效果.方法 对中度非增殖性糖尿病视网膜病变患者42例(62只眼)进行次全视网膜光凝,对其中合并有临床意义黄斑水肿的22只眼同时进行局部光凝.光凝后平均随访20个月,对光凝前、后的视力变化及视网膜病变进展程度进行评价.结果 激光治疗后绝大多数病眼的视力得以维持或有所提高.合并黄斑水肿的22只眼中有21只眼(95.45%)视力得以维持或有所提高.糖尿病视网膜病变的发展在激光治疗后大部分病变表现稳定(87.10%),加重者仅为12.90%.结论 对中度非增殖性糖尿病视网膜病变患者早期进行次全视网膜光凝,对合并有临床意义的黄斑水肿者同时进行局部光凝,可使大多数病眼的视力得以维持或提高,并具有稳定视网膜病变进展的作用.     

激光治疗糖尿病视网膜病变的疗效观察

目的 探讨激光治疗糖尿病视网膜病变的效果.方法 根据DRPSG(Diabetic Retinopathy Photocoagulation Study Group)制定的治疗技术规定,对280例365只眼分别为增殖前期糖尿病视网膜病变(Preproliferative diabetic retinopathy,PPDR)、增殖期糖尿病视网膜病变(Proliferative diabetic retinopathy,PDR)及糖尿病性黄斑水肿(Diabetic macular edema,DME)患者,分别行标准全视网膜光凝(S-PRP)、超全视网膜光凝(E-PRP)、局限或格栅光凝.术后3、6、12个月行FFA及彩色眼底像,新生血管未消退者和无灌注区尚存者追加光凝,随访3～36个月.结果 355只眼行全视网膜光凝,新生血管或无灌注区全部或部分消退256只眼,有效率为72.1%:视力不变和增进292只眼,占82.3%;35只黄斑水肿眼局限或格栅光凝后,26只眼水肿减轻或消失,有效率74.3%.结论 激光治疗糖尿病性视网膜病变安全有效.     

糖尿病视网膜病变激光术后视野的改变

目的报告增殖性糖尿病视网膜病变(proliferative diabetic retinopathy PDR)、严重非增殖性糖尿病视网膜病变(severe nonproliferative diabetic retinopathy severe NPDR)、糖尿病性黄斑水肿患者激光治疗后视野的改变.方法52眼分A、B、C三组.A组为无黄斑水肿的PDR及严重NPDR,行全视网膜光凝术(panretinal photocoagulation PRP).B组为PDR合并黄斑水肿者,行PRP联合黄斑区光凝.C组为单纯黄斑水肿者,行黄斑区光凝.结果A组光凝后,30°内视野平均光阈值敏感度下降(P＜0.01),周边视野暗点增多或增大.B组光凝后,30°视野平均光阈值敏感度下降(P＜0.01),周边视野暗点增大增多,10°内光阈值敏感度下降(P＜0.05).C组10°内视野平均光阈值敏感度下降(P＜0.05).三组激光治疗前后视力无显著区别,新生血管明显消退,黄斑水肿消退.结论全视网膜光凝可有效阻止PDR的进一步发展,防止病人视力进一步下降,但降低了视网膜光敏感度,且周边部视野暗点增多.黄斑区光凝不损伤黄斑中心视功能,对糖尿病黄斑部病变局部代谢的改善,促进组织修复有一定临床意义.     

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.