多波长激光治疗糖尿病性视网膜病变的临床研究

目的探讨多波长激光治疗糖尿病性视网病变的临床疗效.方法对50例(80眼)患有糖尿病性视网膜病变和黄斑水肿的Ⅱ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NPDR25例42眼,增殖期糖尿病视网膜病变PDR25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±0.29,光凝后的视力均值为0.47±0.31,P＜0.05黄斑水肿消减率达71.25%.NPDR的视力提高或不变值为92.85%,PDR者为76.31%,P＜0.05.结论多波长激光治疗视网膜病变有效,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.     

氪黄激光治疗糖尿病性视网膜病变黄斑水肿

目的：评价氪黄激光治疗糖尿病性视网膜病变黄斑水肿的临床疗效。方法：用氪黄激光治疗糖尿病性视网膜病变黄斑水肿共34例（48眼）,氪黄激光波长568nm,对黄斑区局部水肿采用局部光凝,弥漫性水肿采用C形格栅状光凝,光凝距黄斑中心小凹300um,避开视盘黄斑束,功率60～20mw,光斑直径100um,曝光时间0.1s,光凝68～189点,光斑反应I-Ⅱ级。术后平均随访10个月。结果：术后视力提高者33眼（68.8%）,不变者13眼（27.1%）,下降者2眼（4.2%）。光凝后黄斑水肿完全消退者15眼（31.3%）,部分消退者28眼（58.3%）,不变者5眼（10.4%）。无明显并发症。结论：氪黄激光治疗糖尿病性视网膜病变黄斑水肿安全、有效。     

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。     

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.     

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。     

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。     

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。     

老年人非增殖性糖尿病视网膜病变的氩激光治疗

的　探讨老年人非增殖性糖尿病视网膜病变氩激光光凝的临床特点、时效性和疗效。方法　老年人非增殖性糖尿病视网膜病变 ,黄斑水肿组 32只眼 ,非黄斑水肿 2 7只眼。行氩离子兰绿激光光凝。结果　治疗 5 9只眼 (44例 ) ,随访 2 9.98± 11.75个月。激光光凝有效 5 4只眼 (91% ) ,视力进步 7只眼 ,视力不变 42只眼。 0 .2以上视力 42只眼 (71% )。随访期间 5只眼行老年性白内障手术 ,均恢复有用视力 ,眼底无黄斑水肿。结论　老年人非增殖性糖尿病视网膜病变者血糖控制不良及全身性疾病等 ,发生黄斑水肿比例较高 ,应及时施行激光光凝治疗。同时 ,因对侧眼增殖性糖尿病视网膜病变或其它眼底病致低视力时 ,适当放宽激光光凝标准 ,对保护老年人糖尿病患者视力有益     

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.     

轻型播散性光凝治疗非增殖性糖尿病视网膜病变的回顾性研究

目的 观察对非增殖性糖尿病视网膜病变进行轻型播散性光凝的治疗效果。设计 回顾性病例系列。研究对象 背景型糖尿病视网膜病变（BDR）Ⅲ期，且病变未进入增殖前期（PPDR）的病例100例（178眼），其中合并黄斑水肿者156眼。方法 对BDR-Ⅲ期患者100例（178眼）进行规定治疗标准的轻型播散性光凝，其中合并黄斑水肿的156眼同时进行局部光凝治疗。随诊观察至光凝治疗后2年，对光凝治疗前后的视力、视网膜病变进展程度（通过荧光素眼底血管造影和眼底照相）进行评价。主要指标 视力，糖尿病视网膜病变进展程度。结果 本组病例在接受早期光凝治疗后2年内，视力变化差异有统计学意义（P=0．017），以光凝后2年的视力变化最为显著。但视力〉0-3者的比例变化不大，在光凝前为53．9％，光凝后1年、2年分别为55．1％、52．8％。黄斑水肿通过局部光凝治疗2年内视力稳定或改善的病例达到70．5％。早期光凝术后1年、2年视网膜病变稳定者分别占91．0％、80．9％。结论 对于BDR Ⅲ期，且病变未进入PPDR的病例行早期轻型播散性光凝治疗，对合并黄斑水肿的病例同时进行黄斑局部光凝，可使多数患者达到稳定视网膜病变进展的作用。     

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.