准分子激光治疗屈光参差的临床观察

目的　评价准分子激光原位磨镶术 (LASIK)治疗不同程度近视性屈光参差的效果。方法　对 13 0例 (2 16眼 )屈光参差进行LASIK治疗。术前近视为 -2 .5 0～ -18.0 0D ,平均 (-6.10± 3 .3 4)D ;散光为 0～ -5 .0 0D ,平均 (-1.70± 0 .88)D。屈光参差 :近视为 2 .5 0～ 18.0 0D ,平均 (5 .65± 3 .2 8)D ;散光为 0～ 4.5 0D ,平均 (1.3 0± 1.2 2 )D。术后随访 3月～ 3年。结果　术后所有 13 0例的屈光参差均好转。两眼近视之差降至 0～ 2 .0 0D ,平均 (0 .5 7± 0 .5 6)D ;散光之差降至 0～ 1.2 5D ,平均 (0 .3 0± 0 .2 6)D。 14 6眼 (67.5 9% )术后最佳矫正视力较术前最佳矫正视力有显著提高。术前弱视 46眼 (2 1.3 0 % ) ,术后减少至 2 8眼(12 .3 0 % )。结论　LASIK是安全有效的治疗屈光参差的手术方法。     

LASIK治疗近视性屈光参差性弱视

目的 评价准分子激光原位角膜磨镶术(laser in situ keratomileusis;LASIK)治疗近视性屈光参差性弱视的临床疗效.方法 用LASIK手术矫正8位近视性屈光参差性弱视患者,比较手术前后屈光不正的度数和立体视锐度的改变,并将术前的最佳矫正视力和术后第1天,第3天,第10天的裸眼视力以及6～9个月随访的裸眼视力和最佳矫正视力进行比较和分析.结果 术前屈光度数高眼的屈光不正的等效球镜平均为(-10.06±1.50)D,术后该眼屈光不正的等效球镜平均为(0.19±0.32)D.手术前后立体视锐度差别有统计学意义(z=-2.207,P=0.027).术前屈光度数高眼矫正视力和术后该眼矫正视力相比,差别有统计学意义(F=11.431;P=0.000).结论 LASIK手术能安全,有效地减少近视性屈光参差,提高患者的视力和立体视功能.     

LASIK治疗小儿屈光参差性弱视初步报告

目的探讨用LASIK治疗小儿屈光参差性弱视的可能性.方法对1 7例4～1 2岁的屈光参差患儿进行LASIK手术治疗,术前屈光度从+5.50～-11.00D不等,且两眼屈光参差超过5D.对屈光度较大的患眼施行手术.手术在表面麻醉或基础麻醉下施行,术后再进行弱视治疗.结果经术后6～13个月随访,17眼裸眼视力均较术前提高,6眼裸眼视力超过术前矫正视力,7眼达术前矫正视力;12眼屈光度在±1.00D之间.结论对屈光参差性弱视小儿施行LASIK,可矫正屈光不正,提高视力,为弱视治疗提供保障.     

LASIK治疗屈光参差

目的总结激光原位角膜磨镶术(LaserinsituKeratomileusis,LASIK)治疗屈光参差后病人的屈光和视力结果,评价此疗法的效果、安全性和可预测性.方法25例屈光参差病人的40只眼接受了LASIK治疗.术前,40只术眼的平均球镜和柱镜分别为-11.7±4.78D(-3.75～-22.0D)和1.98±1.48D(0.0～6.0D),最佳矫正视力为眼前数指到1.0(平均0.6).25例病人的双眼平均球镜和柱镜之差分别为7.47±3.76D(2.5～16.5D)和1.21±1.44D(0.0～5.75D).术后随访时间是1天,1周,1、3、6月,1、2、3年.结果术后,所有病人的屈光参差都有显著好转,双眼的平均球镜和柱镜之差分别下降到1.49±1.361D(0.0～5.75D)和0.5±0.71D(0.0～2.25D).术眼的平均球镜和柱镜分别下降到-1.24±2.02D(1.5～11.0D)和0.58±0.62D(0～2.25D),平均最佳矫正视力上升到0.9,31只眼(77.5%)的最佳矫正视力增加了1至7行.22只弱视眼中,14眼(63.6%)的最佳矫正视力可达到0.8或1.0.未发生明显的术中和术后并发症.结论LASIK是一种安全、有效、预测性好的治疗成人屈光参差的手术方法.     

单眼LASIK矫正近视性屈光参差疗效分析

目的探讨单眼准分子激光原位角膜磨镶术（LASIK）治疗单眼近视所致屈光参差的效果。方法采用对单跟等效球镜度-2．50D以上的近视性屈光参差42例，进行单眼LASIK手术前后平均屈光度、屈光参差度数、最佳矫正视力和裸眼视力进行评价，术后随访6～12月。结果术前平均等值球镜度数为-4．66D（-2．50D--9．25D），术后减少至-0．62D（0～-1．70D），LASIK对平均等值球镜改变为-4．38D（-2．00D～-8．00D）。术前两眼平均屈光参差为-5．23D（-2．5D～-9．25D），术后减少至-0．50D（0～-1．25D）。术前术后BCVA（最佳矫正视力）范围均为0．6～1．0，平均最佳矫正视力从术前1．0提高到1．04；术后裸眼视力≥1．0者39跟，平均裸跟视力从术前的0．13术后提高至1．0。结论单眼LASIK治疗近视性届光参差不仅能提高患眼的最佳矫正视力和裸眼视力，解除单眼近视、散光所致的屈光参差对眼镜或角膜接触镜不能耐受的痛苦，而且对恢复双眼单视功能具有积极意义。     

LASIK手术在治疗成年人屈光参差性弱视中的作用

目的探讨准分子激光原位角膜磨镶术(LASIK)在治疗成年人屈光参差性弱视中的作用。设计前瞻性病例系列。研究对象临床已确诊为屈光参差性弱视并自愿接受LASIK治疗的成年患者11例(11眼)。方法对上述患者行常规角膜屈光手术前检查,行LASIK手术治疗后随访3～12个月,观察患者裸眼视力、最佳矫正视力、屈光状态、角膜地形图等,并进行比较。主要指标手术前后患者的裸眼视力、最佳矫正视力、屈光状态、角膜地形图。结果术前裸眼视力(0.04±0.01),最佳矫正视力(0.54±0.14),术后平均4个月裸眼视力(0.64±0.22),最佳矫正视力(0.65±0.21)。术前屈光度(-10.52±6.07)D,术后屈光度(-0.25±2.26)D,11眼手术后裸眼视力和屈光度与术前相比均得到明显改善,其中7眼(63.64%)术后裸眼视力(0.76±0.18)好于术前最佳矫正视力(0.60±0.13)。结论本文的小样本资料显示,LASIK在治疗成年人屈光参差性弱视中有一定的作用。     

LASIK治疗RK后屈光欠矫临床观察

目的评价准分子激光原位角膜磨削术(LASIK)治疗放射状角膜切开术(RK)术后屈光欠矫的临床效果。方法对34眼(21人)RK术后残余近视、散光患者行LASIK治疗,年龄20～38岁,残余球镜屈光度-2.00～-13.00D(-5.87D±2.65D),柱镜屈光度0～3.5D(-1.15D±0.94D)。结果术后6个月屈光稳定,裸眼视力≥术前矫正视力32眼(94.12％),所有眼屈光度在术前预期矫正±1.00D以内。1眼最佳矫正视力较术前下降l行。无角膜瓣移位、脱失、角膜混浊等并发症。结论LASIK治疗RK后屈光欠矫安全、有效、预测性好。     

LASIK矫治儿童高度复性近视散光性屈光参差

目的　评价LASIK联合散光MASK盘 (M盘 )矫治儿童高度复性近视散光性屈光参差的安全性、有效性、可预测性和稳定性。方法　使用Summit公司的SVSApexPlus准分子激光系统、MASK盘 (M盘 )及Moria公司的板层刀 ,对 2 1例 7～ 1 5岁患儿 2 3只高度复性近视散光性屈光参差眼行LASIK手术 ,术后托百士、艾氟龙眼液点眼。随访时间 1 2个月。结果　术前球镜均值 :-9 1 0± 3 3 7DS ( -4 5 0～ -1 7 2 5DS) ,柱镜均值 :-2 3 7± 0 47DC ( -1 2 5～ -4 5 0DC)。裸眼视力均值 :0 0 7± 0 0 4( 0 0 4～ 0 1 ) ,矫正视力均值 :0 5 1± 0 3 1 ( 0 1～ 1 0 )。术后 1 2月球镜均值 :-1 1 0± 1 1 5DS ( +0 5 0～ -3 2 5DS) ,柱镜均值 :-0 1 0± 0 1 4DC ( +0 2 5～ -1 2 5DC)。裸眼视力均值 :0 5 8± 0 41 ( 0 2～ 1 0 ) ,矫正视力均值 :0 67± 0 40 ( 0 3～ 1 2 )。结论　LASIK矫治儿童高度复性近视散光性屈光参差是安全、有效的 ,且可预测性及稳定性均较好。这一手术的开展为不能耐受戴镜的高度复性近视散光性屈光参差眼提供了一种有效的矫治手段。     

单眼行LASIK或LASEK术后疗效观察

目的:探讨单眼行准分子激光原位角膜磨镶术(laserin situkeratomileusis,LASIK)或准分子激光上皮下角膜磨镶术(laser epithelial keratomileusis,LASEK)治疗单眼近视所致屈光参差的效果。方法:采用对单眼等效球镜度>-2.50D的近视性屈光参差患者62例,进行单眼LASIK或LASEK手术。术眼及非术眼手术前后平均屈光度、屈光参差度数、最佳矫正视力和裸眼视力进行评价,术后随访6~24mo。结果:术眼术前平均等值球镜度数为-3.66(-2.50~-6.25)D,术后减少至-0.62(0.00~-1.00)D。LASIK或LASEK对平均等值球镜改变为-3.38(-2.50~-5.50)D。术前两眼平均屈光参差为-3.25(-2.50~-6.25)D,术后减少至-0.85(0.00~-1.75)D。术前术后最佳矫正视力(BCVA)范围均为0.6~1.0,平均最佳矫正视力从术前0.8提高到1.04;术后裸眼视力≥1.0者59眼,平均裸眼视力从术前的0.1提高至术后的1.0。非术眼术前平均等值球镜度数为-0.85(+0.25~-1.50)D,术后平均等值球镜度数为-1.85(-0.50~-3.50)D,平均裸眼视力从术前的0.5术后下降至0.1。结论:单眼LASIK或LASEK治疗近视性屈光参差虽然能提高患眼的最佳矫正视力和裸眼视力,解除单眼近视、散光所致的屈光参差对眼镜或角膜接触镜不能耐受的痛苦,而且对恢复双眼单视功能具有积极意义,但是同时我们也发现术后非术眼有近视加深的趋势,而且非术眼原近视度数越高近视加深越快越多。     

近视准分子激光原位角膜磨镶术后的再次手术

目的　评估准分子激光原位角膜磨镶术 (LASIK)治疗近视术后再次手术的有效性及安全性。方法　对近视LASIK术后有残留近视的 5 6例 80眼 ,掀开原角膜瓣 ,再次对瓣下基质床进行准分子激光切削。术后随访 1～ 3 .5年 ,观察视力、屈光度及手术并发症。结果　再次术后 3、6、12、2 4月 ,平均裸眼视力从术前的 0 .43± 0 .2 1,分别提高为 0 .93± 0 .3 2、0 .94± 0 .3 1、0 .94± 0 .3 1及 0 .93± 0 .3 2。平均屈光度等值球镜从术前的 (-2 .84± 1.2 )D变为 (-0 .44± 1.3 4)D、(-0 .60± 1.3 7)D、(-0 82± 1.3 3 )D及 (-1.2 6± 2 .76)D。再次术后 2 4月最佳矫正视力与再次术前相比下降 2行以上的 3眼占 3 .8%。再次术后 12及2 4月 ,分别有 1眼和 2眼形成继发性圆锥角膜。结论　LASIK治疗近视术后再次手术 ,对于消除残留近视有效 ,但术后角膜瓣下必须保留 2 5 0 μm以上的基质厚度 ,以尽量避免术后继发圆锥角膜     

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.