自体板层角膜转位联合层间烧灼及羊膜移植术治疗大泡性角膜病变

目的 探讨自体板层角膜转位联合层间烧灼及羊膜移植术在大泡性角膜病变治疗中的临床效果.方法 选取大泡性角膜病变患者6例(6眼),均有明显刺痛、流泪症状.其中白内障术后3例;白内障术后继发青光眼1例:青光眼术后并发白内障1例:角膜异物取出术后1例.6例患者均行自体板层角膜转位联合层间烧灼及羊膜移植术治疗.结果 6例患者术后眼病等刺激症状基本消失,角膜上皮完整,随访3～12个月均未发现大泡性角膜病变复发及并发症出现,视力有轻度提高.结论 自体板层角膜转位联合层间烧灼及羊膜移植术可有效缓解大泡性角膜病变的症状,是解除视功能不佳的大泡性角膜病变患者临床症状的有效方法.     

角膜表面及层间联合生物羊膜移植治疗大泡性角膜病变

目的探讨生物羊膜移植治疗大泡性角膜病变的方法和疗效。方法对13例(13只眼)大泡性角膜病变患者行角膜表面及层间联合生物羊膜移植术,并对其进行近期和远期的疗效观察。结果13例(13只眼)患者角膜愈合好,眼部症状消失,无复发、无不良反应。结论角膜表面及层间联合生物羊膜移植术对减轻大泡性角膜病变炎症反应和疼痛,重建角膜表面,防止大泡性角膜病变复发有非常好的治疗效果,且手术安全、简单易行、取材容易、疗效可靠,值得临床应用。     

大泡性角膜病变18例手术治疗效果回顾性分析

目的:评价羊膜移植几种手术方法治疗大泡性角膜病变的临床效果。方法:对18例大泡性角膜病变患者,分别采取角膜层间烧烙术、新鲜羊膜移植术、角膜灼烙联合羊膜嵌入移植手术。结果:18例大泡性角膜病变患者,术后1～5d疼痛消失,7～12d角膜上皮修复,7～21d后羊膜植片常规溶解。角膜层间烧烙术1眼、新鲜羊膜移植术3眼术后1～2mo再次出现角膜大泡及角膜刺激症状而再次手术。角膜灼烙联合羊膜嵌入移植术,术后当天疼痛消失,14d角膜上皮光滑,角膜大泡消失。随访6～18mo无1例复发,部分患者视力有不同程度的提高。结论:角膜灼烙联合羊膜嵌入移植对大泡性角膜病变具有明显的治疗效果。     

角膜层间晶状体前囊植入联合羊膜移植治疗大泡性角膜病变

目的 探讨角膜层间晶状体前囊植入联合羊膜移植治疗大泡性角膜病变的效果.方法 对内眼手术后大泡性角膜病变11例（11眼）施行角膜层间晶状体前囊植入联合羊膜移植术.术后随诊12个月,观察治疗后疼痛等症状缓解情况、角膜水泡消退、角膜上皮愈合情况,以及有无眼部并发症.结果 11例中,9例术后疼痛症状减轻,6例术后视力提高,8例角膜缺损区3周内愈合.结论 在基层医院缺乏角膜材料的情况下,应用角膜层间晶状体前囊植入联合羊膜移植治疗大泡性角膜病变,可缓解大泡性角膜病患者的痛苦,提高部分患者视力,达到治疗的效果.     

羊膜移植术治疗大泡性角膜病变

目的：探讨施行羊膜移植术治疗大泡性角膜病变的临床效果。方法：对11例（11只眼）大泡性角膜病变患者施行羊膜移植术,结果：羊膜移植术后随访1-7个月间,术前难以忍受疼痛的11例中10例（91%）术后疼痛消失,1例疼痛减轻。有4例（36%）术后视力提高,9例（82%）角膜上皮在5周内迅速愈合,另2例角膜大泡局限于小区域。结论：羊膜移植术为治疗大泡性角膜病变的有效方法,与继往其他治疗方法比较具有明显优越性。     

角膜层间羊膜植入术治疗大泡性角膜病变

目的探讨角膜层间羊膜植入术治疗大泡性角膜病变的中远期临床效果。方法9例(9眼)大泡性角膜病变,根据病史、年龄和视力恢复的可能性,实施了角膜层间羊膜植入术。结果术后眼部刺激症状、角膜大泡均于2~5 d消失,角膜基质水肿于5~10 d消失。术后视力增进4例,无改变5例。随访2~27个月,平均(16.8±11.7)月无并发症发生,无复发者。结论对于症状明显、病情顽固、难以恢复有效视力或不具备角膜移植手术条件的大泡性角膜病变,角膜层间羊膜植入术不失为一种安全可靠的治疗方法。     

角膜层间灼烙联合羊膜移植治疗疼痛性大泡性角膜病变

目的：：观察角膜层间灼烙联合羊膜移植治疗疼痛性大泡性角膜病变的手术疗效。方法：选取疼痛性大泡性角膜病( PBK )患者156例156眼(均为单眼),行角膜层间灼烙联合羊膜移植术,术后随访2~3mo,观察患者术眼疼痛症状、角膜上皮水泡、异物感、术后并发症等指标。结果：疼痛症状全部消失,角膜上皮不再出现水泡130例(83.3%);患者剧烈眼疼消失,但偶有异物感等不适,角膜上皮偶有小水泡24例(15.4%);术后2wk内角膜基质发生溶解,再行结膜瓣覆盖后治愈2例(1.3%)。结论：角膜层间灼烙联合羊膜移植术能解除98.7%的PBK患者的痛苦且手术操作简单,值得提倡。     

角膜板层错位切开联合羊膜移植治疗大泡性角膜病变

目的探讨一种治疗大泡性角膜病变的新方法。方法对不具备行角膜移植的大泡性角膜病变患者行角膜板层错位切开＋羊膜移植术,观察其疗效。结果本组8例（8只眼）患者行手术治疗后,眼痛、流泪症状消失,角膜上皮修复,缓解了症状,保留了眼球。结论角膜板层错位切开联合羊膜移植对于不具备行角膜移植的大泡性角膜病变患者可有效缓解症状,减轻患者痛苦,且操作简单,值得基层推广。     

角膜层间烧灼术治疗大泡性角膜病变

目的 探讨角膜层间烧灼术对大泡性角膜病变的治疗效果.方法 对7例(7眼)大泡性角膜病变施行角膜层间烧灼术.结果 6眼角膜大泡完全消失,角膜无水肿,症状完全改善,1眼仍发生局部的大泡性病变,重复行角膜层间烧灼术后获得良好效果.结论 对于不能实行穿透性角膜移植术或角膜内皮移植术的大泡性角膜病变,视力严重受损,角膜刺激症状明显者,角膜层间烧灼术是一种有效的方法.     

角膜基质层烧烙联合羊膜移植治疗大泡性角膜病变

目的探讨角膜基质层烧烙联合羊膜移植治疗大泡性角膜病变（BK）的临床疗效。方法对9例（9只眼）大泡性角膜病变的患者行角膜基质层烧烙联合羊膜移植,其中白内障联合人工晶状体植入术后5例,抗青光眼术后3例,角膜穿通伤1例。结果术后眼部刺激症状、角膜上皮大泡均于1周内消退,角膜基质水肿7～10d消失。术后随访3～24个月,均未发现BK复发及并发症的发生。结论对于症状明显、病情顽固、难以恢复有效视力且不具备角膜移植条件的BK患者,角膜基质层烧烙联合羊膜移植可有效控制BK的症状,防止BK的复发,是治疗BK可供选择的有效方法。     

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.