睫状体光凝联合前房穿刺术对新生血管性青光眼的止痛效果观察

目的分析新生血管性青光眼半导体激光经巩膜睫状体光凝术后眼痛症状的成因及联合前房穿刺术后对减轻眼痛症状的效果。方法 35例（35眼）青光眼以半导体激光经巩膜的睫状体光凝联合前房穿刺术。术后随访眼压及疼痛6个月以上。结果术前平均眼压（56.73±21.62）mmHg,术后第2周平均眼压（28.36±11.01）mmHg（t=8.099,P=0.001）。术前轻度疼痛5眼,重度疼痛22眼,剧痛8眼;术后第2周无痛22眼,轻度疼痛11眼,重度疼痛2眼;术后1月只有1眼仍有轻度疼痛,2月后疼痛消失。结论新生血管性青光眼半导体激光经巩膜睫状体光凝联合前房穿刺术可以有效地减轻术后疼痛。     

睫状体光凝与视网膜消融术治疗新生血管性青光眼

目的观察半导体激光经巩膜睫状体光凝联合视网膜消融术(全视网膜光凝或前部视网膜冷凝)治疗新生血管性青光眼的临床效果。方法12例12眼药物不能控制的新生血管性青光眼接受治疗。8眼睫状体光凝和全视网膜光凝，4眼同时行睫状体光凝和前部视网膜冷凝。术后随访6～19月，对比分析6月时的眼压、视力及虹膜新生血管改变。结果睫状体光凝前眼压36～67mmHg(1mmHg=0．133kPa)，平均45．52mmHg。末次治疗后6月，在不用抗青光眼药物的情况下，6眼(50％)眼压在9～17mmHg；局部滴用0．5％噻吗心胺滴眼液后4眼(33．33％)眼压低于21mmHg，2眼(16．67％)眼压高于21mmHg。视力下降者2眼，提高者2眼，不变者8眼。虹膜新生血管完全消失8眼，部分消失4眼。结论半导体激光经巩膜睫状体光凝联合视网膜消融术治疗新生血管性青光眼，既能及时降低眼压，又能减少视网膜缺血，拯救现有或潜在视力。     

半导体激光经巩膜睫状体光凝治疗硅油填充术后难治性高眼压

目的　观察半导体激光经巩膜睫状体光凝 (transclera ciliary photocoagulation)治疗硅油填充术后高眼压的效果。方法　对 14例行玻璃体切割加硅油注入术后发生眼压升高的患者 ,在取出部分硅油和药物不能控制眼压时行半导体激光经巩膜睫状体光凝术 ,采用 810 nm波长激光 ,G-探头行巩膜睫状体光凝 ,每眼共光凝 15～ 2 0点。结果　行光凝术后随访 4～ 8个月 ,平均 5个月。 14只眼术前眼压为 (5 8m m± 17) mm Hg,术后平均眼压为(2 1m m± 10 ) mm Hg。经 t检验 ,P <0 .0 1,在所随访的患者中 ,1只眼因发生新生血管性青光眼 ,经多次光凝无效而行眼球摘除 ,其余 13只眼均保持一定的有用视力 ,无眼球萎缩的发生。结论　半导体激光经巩膜睫状体光凝对玻璃体切割硅油填充术后难治性高眼压具有较好的作用 ,能保持术眼的视功能 ,有效的避免冷冻术所带来并发症     

二极管激光经巩膜睫状体光凝术治疗先天性小眼球合并青光眼

目的：观察二极管激光经巩膜睫状体光凝术治疗先天性小眼球合并青光眼持续性高眼压的临床效果。 方法：回顾性自身对照研究,收集2009-01/2011-01在邢台眼科医院收治的先天性小眼球继发青光眼持续性高眼压并行二极管激光经巩膜睫状体光凝术的患者5例7眼。观察手术前后视力、眼压、并发症情况,并进行统计学处理。 结果：术后随访期间全部患者眼痛症状均缓解。术前平均眼压为52.56±7.31mmHg,术后1mo平均眼压17.8±47mmHg,6mo随访时平均眼压14.18±4.53mmHg,术后1mo及6mo眼压与术前相比,差异有显著统计学意义(P<0.01)。术后平均视力(0.127±0.165)较术前(0.0334±00322)提高,差异有显著统计学意义(P<0.01)。光凝术后5眼(71.4%)视力提高,2眼(28.6%)视力无变化,术后均有前房炎症反应伴前房渗出,药物治疗后消失。 结论：二极管激光经巩膜睫状体光凝术治疗先天性小眼球合并青光眼持续性高眼压,疗效确切,可降低眼压,缓解疼痛,并发症少。     

难治性青光眼半导体激光经巩膜睫状体光凝术

目的　评价半导体激光经巩膜睫状体光凝术治疗难治性青光眼的效果和安全性。方法　 68例 (69眼 )接受治疗 ,术后随访 6～ 17月。分析末次治疗后第 6月的眼压、视力和眼部症状。结果　无光感组 (3 6眼 ) :光凝术前眼压 (61.16± 12 .44 )mmHg(1mmHg =0 .13 3kPa) ,末次光凝术后第 6月后 3 3眼眼压 (2 9.67± 6.79)mmHg。 3眼眼球萎缩 ,12眼需 2次或多次治疗。光感及光感以上组 (3 3眼 ) :光凝术前眼压 (5 1.72± 13 .85 )mmHg ,末次光凝术后第 6月眼压 (2 1.42± 8.2 2 )mmHg。其中 11眼需要 2次或 3次光凝术 ,4眼 3次光凝术后眼压仍高于 2 1mmHg。结论　半导体激光经巩膜睫状体光凝术是一种简单、安全、有效的治疗难治性青光眼的方法 ,但常需要重复治疗。     

巩膜睫状体光凝术对难治性青光眼的中长期疗效

目的　评价经巩膜 810nm半导体激光睫状体光凝术对难治性青光眼的中长期疗效。方法　回顾性地分析了 65例 (65只眼 )经巩膜睫状体光凝的难治性晚期青光眼 ,时间从 1998年 10月至 2 0 0 0年 10月 ,随访 2 4m～ 46m (平均 3 4 1m± 5 8m ) ,观察指标包括包括眼压、视力、用药数量、眼痛情况和眼球萎缩发生率。结果　术前平均眼压 5 1 2mmHg± 14 3mmHg ;最后一次随访 ,平均眼压 16 1mmHg± 11 2mmHg ;最后眼压在 6mmHg～ 2 1mmHg之间者有 41眼 (63 1% ) ,经配对资料T检验 ,术前眼压与术后眼压相比 ,差异有显著性 ,P <0 0 1。术后 46只眼 (70 8% )视力保持不变 ;18只眼 (2 7 7% )视力下降 ;1只眼 (1 5 % )视力增加。抗青光眼用药种类从治疗前的平均3 1种降至治疗后平均 0 4种 (P <0 0 1)。术前有眼痛的患者中 93 3 %的眼痛症状显著缓解或消失。7只眼 (10 8% )发生眼球萎缩。结论　经中长期随访观察 ,810nm半导体激光经巩膜睫状体光凝术仍是治疗难治性青光眼的有效方法。     

接觸式二極管激光治瘵新生血管性青光眼97例

目的 评价二机管激光经巩膜睫状体光凝治疗新生血管性青光眼的有效性和安全性,同时观察近期和远期疗效。方法对97例98眼新生血管性青光眼施行接触式二机管激光以巩膜睫状体光凝,术后观察并记录视力、眼压、结膜、角膜、前房、虹膜、晶状体等情况,随访时间3月～4年。结果 术后眼压近期平均为27.12mmHg,远期为31.24mmHg,与术前相比均有显著性差异(P<0.01)。并发症有色素膜炎、前房出血等。结论 接触式二机管激光经巩膜睫状体光凝是治疗新生血管性青光眼有效、安全、简便的方法。     

新生血管性青光眼不同手术疗法的疗效对比

目的:对比经巩膜睫状体光凝术和睫状体冷凝术对于新生血管性青光眼的疗效。方法:选取2006年在我院住院的38例43眼新生血管性青光眼患者,一组采用常规睫状体冷凝术18眼,另一组采用810nm激光经巩膜睫状体光凝术治疗25眼,术后处理相同,术后12wk随诊期内观察患者眼部表现、视力、眼压情况。结果:睫状体冷凝组11眼(61%)、睫状体光凝组20眼(80%)术后3mo眼压稳定于11~24mmHg之间,各组术前、后眼压对比,差异均有高度统计学意义(P=0.000);组间术后眼压对比,差异无统计学意义(P=0.669)。睫状体冷凝组10眼(56%)、睫状体光凝组21眼(84%)视力保存,差异有统计学意义(P=0.040)。所有患者术后2wk虹膜新生血管开始逐渐减少,睫状体冷凝患者术后均有明显球结膜充血水肿,并颜面浮肿、眼痛、头痛;睫状体光凝患者术后仅有轻度球结膜混合充血,无颜面部浮肿、头痛及眼痛、前房出血。结论:治疗新生血管性青光眼,睫状体冷凝术及经睫状体激光光凝术控制眼压效果确切;而睫状体激光光凝术手术具有视力保存率高、并发症少,患者术后痛苦少等优点。     

NVG经巩膜睫状体光凝联合布洛芬口服的疗效

目的:分析晚期新生血管性青光眼(neovascular glaucoma,NVG)以半导体激光经巩膜睫状体光凝术后眼痛症状的成因及联合布洛芬口服后对减轻眼痛症状及降低眼压的效果。方法:NVG患者30例30眼以半导体激光经巩膜的睫状体光凝联合布洛芬口服。术后对眼压及疼痛情况随访6mo以上。结果:术前平均眼压56.23±21.62mmHg,术后1d平均眼压31.36±10.01mmHg(t=8.099,P=0.001)。术前轻度疼痛3眼,重度疼痛18眼,剧痛9眼;术后24h内无痛14眼,轻度疼痛9眼,重度疼痛7眼;术后72h内无痛21眼,轻度疼痛8眼,重度疼痛1眼。结论:晚期NVG半导体激光经巩膜睫状体光凝联合布洛芬口服可以有效地减轻术后早期疼痛及降低眼压。     

经巩膜睫状体光凝治疗难治性青光眼的临床观察

目的:评价半导体激光经巩膜睫状体光凝术治疗难治性青光眼的效果。方法:回顾性分析55例56眼难治性青光眼的临床资料,均行睫状体光凝,术后随访观察并记录眼压、视力、眼部自觉症状以及并发症,随访时间3mo以上。结果:术前平均眼压53.5±18.7mmHg,末次随访平均眼压为19.4±9.6mmHg,术后眼压与术前眼压相比,差别具有统计学意义(P<0.01)。术后44眼视力无变化,2眼视力提高,10眼视力下降;眼痛均消失或缓解;并发症少,主要有葡萄膜炎、前房出血等。结论:睫状体光凝能有效降低难治性青光眼患者的眼压,且并发症少。     

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.