急性闭角型青光眼合并睫状体脉络膜脱离22例

目的分析原发性急性闭角型青光眼(acute prima-ry angle-closure glaucoma,APACG)高眼压状态患者并发睫状体脉络膜脱离的临床特征及治疗结果。方法回顾性研究经超声生物显微镜(ultrasound biomicroscopy,UBM)、B超等检查证实22例31眼高眼压状态合并睫状体、脉络膜上腔积液与脱离的APACG患者,对该组患者的眼前部结构、UBM、B超图像特征及治疗结果进行分析与评价。结果22例31眼首诊时眼压(37.61±10.94)mmHg(1kPa=7.5mmHg),中央前房深度(1.68±0.10)mm,眼轴长度(22.80±0.67)mm。UBM显示:睫状体脱离双眼9例、单眼13例;脱离分级:1级15眼,2级10眼,3级6眼;脱离范围:1/2象限6眼,3/4象限7眼,4个象限脱离18眼。4例(7眼)合并脉络膜脱离。临床治疗10眼作YAG激光虹膜切开术,21眼行巩膜瓣松解缝线小梁切除术,随访所有病例眼压控制良好。结论APACG高眼压患者可合并睫状体脉络膜脱离,常规抗青光眼及联合适量糖皮质激素治疗能有效控制该类患者眼压。     

PACG急性发作后继发睫状体脉络膜脱离的临床研究

目的:观察急性闭角型青光眼急性发作缓解后继发睫状体脉络膜脱离时眼压、前房深度的变化,探讨继发性睫状体脱离的原因、临床特征及治疗效果。方法:回顾性分析我院2011-08/11住院治疗的84例急性闭角型青光眼急性发作的患者,发作缓解后,经超声生物显微镜(UBM)及B超发现,19例出现睫状体脉络膜脱离,用非接触式眼压计及UBM测量急性发作前后和睫状体脉络膜脱离时的眼压和前房深度,并进行统计学分析。结果:急性发作期眼压50.4±6.5mmHg,中央前房深度1.65±0.12mm;发作缓解继发睫状体脉络膜脱离时眼压7.93±4.3mmHg,中央前房深度1.29±0.1mm。UBM及B超检查显示:继发单纯脉络膜脱离10例,单纯睫状体脱离4例,睫状体脉络膜脱离5例,给予常规抗青光眼手术联合适量糖皮质激素治疗,全部睫状体脉络膜脱离均复位。结论:急性闭角型青光眼急性发作缓解后常可合并睫状体及脉络膜脱离,且治疗前眼压越高,缓解时间越短,缓解后发生睫状体、脉络膜脱离的几率越高,其直接征象为眼压过低、前房更浅,UBM为其最可靠的检查方法,常规抗青光眼手术联合适量糖皮质激素为该类患者的有效治疗方法。     

急性闭角型青光眼并发睫状体脱离的观察与分析

目的分析原发性急性闭角型青光眼并发睫状体脱离的特点及治疗转归。方法对2006年5月至2008年5月治疗的163例（186眼）原发性急性闭角型青光眼,72h内经药物控制眼压后行超声生物显微镜（ultrasound biomicroscope,UBM）检查,并对这些病例的年龄、性别、UBM表现、中央前房深度及治疗结果进行分析。结果186眼中有26眼（13．98％）并发睫状体脱离,此类患者就诊时大多眼压较高（〉50mmHg,1mmHg=0．133kPa）,经治疗后迅速下降至正常甚至更低。脱离范围有全周也有部分,中央前房深度变浅。治疗后眼压控制良好,睫状体脱离复位。结论并发睫状体脱离是原发性急性闭角型青光眼的体征之一,UBM检查对其具有较高的诊断价值,并可为临床提供可靠依据。     

白内障超声乳化联合房角粘连分离术治疗慢性闭角型青光眼

目的观察白内障超声乳化人工晶体植入联合房角粘连分离术治疗慢性闭角型青光眼的疗效以及术后房角形态的改变。方法白内障超声乳化联合房角粘连分离术治疗慢性闭角型青光眼32例(36只眼),对其手术前后的视力、眼压、视野、中央前房深度、房角形态进行对照观察。结果术后随访3~7个月,32例(36只眼)有31例(35只眼)视力较术前明显提高。36只眼术后中央前房深度均加深,术前前房深度(1.557±0.338)mm,术后前房深度(3.382±0.197)mm。35只眼术后眼压明显降低,术前眼压(26.655±3.274)mmHg,术后眼压(13.96±4.045)mmHg。房角镜和UBM术后1月检查32例(36只眼)房角均开放,术后3月房角镜和UBM检查未发现房角再次粘连。26例(28只眼)术后6月复查视野无缩小。结论白内障超声乳化房角分离术可有效治疗合并白内障的慢性闭角型青光眼。     

原发性视网膜色素变性并发急性闭角型青光眼临床分析

目的探讨原复性视网膜色素变性（PRP）并发急性闭角型青光眼的治疗。方法对8例PRP并发急性闭角型青光眼（单眼发作5例、双眼发作3例）患者行常规眼部检查，部分患者行视野、A型和B型超声波检查、超声生物显微镜检查（UBM）检查、角膜内皮细胞镜检查及眼部电生理检查。结果男女发病比例1：3。青光眼发作期11只眼，其中1只眼并发自发性晶状体半脱位，临床前期5只眼。发作眼平均眼压（52．63±11．22）mmHg，临床前期平均眼压（15．75±2．43）mmHg。A型超声波检查：眼轴长度平均（22．28±1．04）mm。UBM检查：前房中轴部深度平均（1．50±0．46）mm。手术治疗11只眼，其中小梁切除术7只眼，白内障摘除联合小粱切除术3只眼，二极管激光经巩膜睫状体光凝术1眼。术后并发症：前房葡萄膜炎性反应絮状渗出多见于青光眼自内障联合手术，小梁切除术后浅前房发生率为57．14％。结论PRP并发急性闭角型青光眼患者具有与原发性闭角型青光眼一致的解剖结构，小梁切除术术后浅前房发生率较高。并发自发性晶状体脱位者较为少见。     

急性闭角型青光眼降眼压治疗中继发脉络膜脱离的临床观察

目的量化观察急性闭角型青光眼降眼压治疗中继发脉络膜脱离的眼压和前房深度的变化,总结临床特点。方法回顾分析2005年1月至2006年4月,107例114只眼急性闭角型青光眼在降眼压治疗中,34例36只眼(31.8%)经超声生物显微镜(UBM)检查诊断继发脉络膜脱离,用Goldmann压平眼压计和UBM分别测量这组病例降眼压治疗前和发现脉络膜脱离时的眼压和前房深度,观察总结其临床特点。结果降眼压治疗前眼压平均(51.6±7.5)mmHg(1mmHg=0.133kPa),前房中央深度平均(1.763±0.285)mm;脉络膜脱离时眼压平均(7.6±3.2)mmHg,前房中央深度平均(1.547±0.334)mm;眼压变化平均(42.9±6.7)mmHg,前房中央深度变化平均(0.162±0.136)mm。继发脉络膜脱离无须特殊治疗,予减少或停用降眼压药物(尤其是缩瞳剂),2-7(3.5±1.4)天自愈,给予皮质类固醇类药物可缩短疗程。结论急性闭角型青光眼降眼压抢救治疗时,继发性脉络膜脱离的发生与眼压降低过快过低有关;UBM具有较高的诊断价值,并可为临床提供可靠依据。     

急性闭角型青光眼急性发作期缓解后并发睫状体脱离的临床观察

目的:探讨急性闭角型青光眼急性发作期缓解后并发睫状体脱离的临床变化过程,并评价超声生物显微镜(ultra-sound biom icroscopy,UBM)在其诊断中的应用价值。方法:选择急性闭角型青光眼急性发作期缓解后并发睫状体脱离的患者34例,给予皮质类固醇治疗,治疗前后检查眼压、裂隙灯和UBM,分析睫状体脱离的动态变化。结果:治疗前眼压为6.75±3.12mmHg,UBM显示睫状体脱离,其中1级53%,2级32%,3级15%。经治疗33例眼压正常,平均末次眼压为12.67±5.52mmHg。UBM检查发生明显的变化,ACD,AOD,θ1增加(P<0.01),TCPD,ICPD增大(P<0.05)。睫状体脱离随治疗时间的延长逐渐恢复。结论:药物治疗急性闭角型青光眼急性发作期缓解后并发睫状体脱离可获得理想的疗效,UBM检查对其诊断具有较高的价值。     

闭角型青光眼的超声生物显微镜观察

目的　应用超声生物显微镜 (UBM )探讨闭角型青光眼的解剖结构特点及其与滤过性手术后浅前房并发症的关系。方法　对 71例 14 0只闭角型青光眼应用美国Paradigm -P40型UBM和中国BEM -2 0 0眼科A/B型超声诊断仪进行眼前节及眼轴生物测量。包括前房深度 (AD)、各象限的房角开放距离 (AOD)、小梁睫状体距离 (TCPD)及眼轴长度 (AL)的测量 ,使用SPSS软件进行数据统计。结果　 1 14 0只闭角型青光眼患者的生物测量值 :前房深度 1 662 0± 0 2 74mm ,眼轴长度2 2 85 5 4± 1 1772mm ,AOD 0 0 5 60± 0 0 60 7mm ,TCPD 0 5 670± 0 0 985mm。急性和慢性闭角型青光眼患者的年龄、房角开放距离和小梁睫状体距离无显著性差异 ;但是急闭青光眼发生房角关闭 (AOD= 0 )的眼数和象限范围多于慢闭青光眼 ,急闭青光眼患者的前房深度和眼轴长度短于慢闭青光眼 ,而慢闭青光眼虹膜呈膨隆状态的则较多。 2 小梁切除术后发生浅前房并发症与患者眼轴 <2 2 5mm、TCPD <0 5mm、全周房角关闭 (AOD =0 )有关。结论　超声生物显微镜对研究闭角型青光眼解剖特点及评估滤过性手术并发症是非常有价值的     

超声生物显微镜评价小梁切除术治疗急性闭角型青光眼

目的:应用超声生物显微镜观察急性闭角型青光眼小梁切除术的有效性和安全性。方法:选取80例80眼急性闭角型青光眼病例按手术前眼压水平分为高眼压组(30例30眼,眼压≥30mmHg)和对照组(50例50眼,眼压<30mmHg),对两组病例小梁切除术后眼压、视力以及超声生物显微镜(ultrasound biomicroscopy,UBM)情况等进行统计比较。结果:高眼压组术后大多数保留了较好的视力;两组病例术后眼压大多控制在8～15mmHg;UBM检测结果,高眼压组术后发生1例睫状体脱离,1例恶性青光眼,1例浅前房,对照组术后发生1例浅前房,两组比较差异无显著性(P>0.05);两组患者手术后ACD,AOD,TCPD术前术后比较差异均无显著性。结论:急性闭角型青光眼高眼压下小梁切除术是有效、安全的,在充分药物治疗后,应及时采取手术治疗。UBM检查可发现小梁切除术后睫状体脱离、恶性青光眼等严重并发症,在急性闭角型青光眼诊治过程中发挥重要作用。     

白内障超声乳化术治疗急性闭角型青光眼合并白内障

了解白内障超声乳化术治疗急性闭角型青光眼合并白内障的有效性。 方法:对2006-03-01/2010-10-31收治的急性闭角型青光眼合并白内障患者47例51眼,眼压稳定后行超声乳化联合人工晶状体植入术,术后均随访1~3a。 结果:术后47例51眼中44例48眼眼压下降,术前眼压22.98±3.22mmHg,术后眼压13.24±3.17mmHg(P<005),45例49眼视力较术前明显提高(P<0.05)。47例51眼术后前房深度加深,由术前1.542±0.314mm转为术后3.157±0.243mm(P<0.05)。 结论:白内障超声乳化术可以使急性闭角型青光眼前房加深,不同程度地开放已关闭的房角,改善周边窄房角的解剖状态,降低瞳孔阻滞后周边前房关闭的可能性,可以使升高的眼压下降,提高视力,是闭角型青光眼合并白内障患者安全有效的治疗途径。     

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.