多波长激光治疗糖尿病性黄斑水肿

目的　探讨多波长激光治疗糖尿病性黄斑水肿的临床疗效。方法　对 5 0例 (80眼 )患有糖尿病性视网膜病变和黄斑水肿的 型糖尿病患者进行多波长激光治疗 ,其中非增殖期糖尿病性视网膜病变 2 5例 4 2眼 ,增殖期糖尿病视网膜病变 2 5例 38眼。治疗中 ,黄斑区治疗 ,以黄光治疗为主 ,包括局灶性光凝和弥漫性格栅样光凝。周边光凝则以黄绿混合光、绿光或红光进行治疗。在一些复杂的病例治疗中 ,则采用几种波长激光随时切换使用 ,达到以最低能量最低损害 ,产生有效光斑和最大治疗效果的目的。结果　本组病例治疗前视力均值为 0 .36± 0 . 2 9,光凝后的视力均值为 0 .4 7± 0 .31,P<0 .0 5 ,光斑水肿消减率达 71.2 5 % .非增殖期糖尿病性视网膜病变的视力提高或不变值为 92 .85 % ,增殖期糖尿病视网膜病变者为 76 .31% ,P<0 .0 5。结论　多波长激光治疗黄斑水肿有效 ,且早期治疗效果好 ,氪黄激光治疗糖尿病性黄斑水肿疗效较好。     

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.     

糖尿病视网膜病变激光治疗技术标准探讨

目的：探讨糖尿病视网膜病变激光治疗技术标准及疗效。方法：根据DRPSG（DiabeticRetinopathy Photocoagulation dStudy Group)制订的治疗技术规定。对70例105眼分别为增殖前期糖尿病视网膜病变（PPDR）、增殖期糖尿病视网膜病变（PDR）及糖尿病性黄斑水肿患者行激光治疗,按技术规定垢光产张范围和光凝参数行标准全视网膜光凝（S-PRP）和超全视网膜光凝（E-PRP）及黄斑水肿行局限光凝或格栅光凝。激光后3个月、6个月、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3-12个月（平均8.91个月）。结果：20眼弥漫性黄斑水肿格栅光凝后,13眼（约65.0%)水肿减轻或消失,102眼行全视网膜光凝,新生血管部分或全部消退73眼（约71.6%),105眼中视力不变和增进81眼（约77.1%)。结论：按DRPSG制订的治疗技术规定治疗糖尿病视网膜病变是行之有效的,激光治疗糖尿病视网膜病变更规范化。     

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.     

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。     

多波长激光治疗糖尿病性视网膜病变临床观察

目的探讨多波长激光光凝对糖尿病性视网膜病变的疗效。方法30例（52只眼）糖尿病性视网膜病变行荧光素眼底血管造影（FFA）及黄斑区相干光断层扫描（OCT）,对重度非增生性及增生性糖尿病性视网膜病变分别进行绿光、黄光、红光激光光凝。黄斑水肿患者同时行黄斑格栅光凝,分4次进行泛视网膜光凝。光凝后观察视力、黄斑中心凹厚度及FFA情况。结果随访6个月,35只眼视力不同程度提高,14只眼视力维持激光治疗前的水平,3只眼因黄斑水肿加重视力下降,激光治疗前OCT显示黄斑部中央凹平均厚度为（430．35±98．53）μm,治疗后6个月平均厚度（178．48±42．56）μm。结论多波长激光治疗糖尿病视网膜病变能有效提高或保存患眼视功能。     

多波长氪激光治疗糖尿病视网膜病变的观察

目的 探讨多波长氪离子激光治疗糖尿病视网膜病变的长期疗效.方法 对278例（451眼）分为非增生性糖尿病视网膜病变（NPDR）,增生前期糖尿病视网膜病变（PPDR）,增生性糖尿病视网膜病变（PDR）.行局部、象限、广泛视网膜光凝或超广泛视网膜光凝治疗.分别于激光治疗前、激光治疗后3个月、6个月、12个月、24个月随访,行视力、眼压、散瞳后眼底检查、荧光眼底血管造影（FFA）.复查时如发现仍有毛细血管渗漏、无灌注区或新生血管未消退者则追加光凝.结果 NPDR随访2年,218眼（86.1％）视力稳定,其中5眼发生玻璃体积血,随访期间均逐渐吸收好转.PPDR随访2年,93眼（74.4％）视力稳定,其中有2眼因玻璃体积血难以吸收而接受玻璃体切除手术.PDR随访2年,40眼（54.8％）视力稳定,4眼因玻璃体积血难以吸收而行玻璃体手术.光凝可以减少玻璃体积血的发生,也有助于玻璃体内积血不能吸收的患者进行手术治疗.结论 应根据糖尿病视网膜病变的严重程度,选择合适的激光治疗方式,病情较轻、原视力较好者预后较好.     

氪绿激光治疗糖尿病性黄斑水肿

目的：评价氪绿激光治疗糖尿病性黄斑水肿的临床效果。方法：对50例72眼非增殖期或增殖早期糖尿病视网膜病变合并黄斑水肿患者根据黄斑水肿形态行局部或格栅状光凝,观察光凝后视力及黄斑水肿的变化,并进行统计学分析。结果：光凝后视力提高14眼（19.4%),下降16眼（22.2%),不变42眼（58.4%)。黄斑水肿完全消退15眼（20.8%),部分消退37眼（51.4%),不变或加重20眼（27.8%)。结论：氪绿激光治疗糖尿病性黄斑水肿效果显著。     

糖尿病视网膜病变的激光光凝治疗

目的:探讨532 nm半导体激光光凝术治疗糖尿病性视网膜病变的效果.方法:应用美国IRIS公司生产的Oculighht GL激光治疗机,对视网膜病变达Ⅲ期以上者,行全视网膜光凝术,分3～4次完成.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.伴黄斑水肿者先行黄斑区"C"型光凝,然后行全视网膜光凝术治疗.结果:糖尿病性视网膜病变患者87例(153眼),光凝后视力提高及保持不变者127眼,视力降低者26眼,光凝前后视力比较,差异有非常显著意义.黄斑水肿大部分减轻,微血管瘤逐渐消退.结论:532 nm激光治疗糖尿病性视网膜病变安全有效.     

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.