准分子激光散光性角膜切削术治疗复合近视散光

为评价准分子激光散光性角膜切削术（ｐｈｏｔｏａｓｔｉｇｍａｔｉｃ－ｒｅｆｒａｃｔｉｖｅｋｅｒａｔｅｃｔｏｍｙ，ＰＡＲＫ）治疗复合性近视散光的效果，采用ｋｅｒ－ａｔｏｍⅠ型准分子激光机，利用准分子激光对角膜浅表层的椭圆形切削，共对５７例８２只复合近视散光眼行治疗，随访１年以上。术前近视球镜平均为－６．２３±２．５０Ｄ，散光为－１．４７±０．８２Ｄ，角膜散光为１．２１±０．４８Ｄ，最佳矫正视力为０．９７±０．１５。结果：术后视力和屈光状态在３～６个月趋于稳定，术后１年随访，近视平均为－０．５２±１．００Ｄ，散光为－０．４３±０．４３Ｄ，相比术前散光平均降低７０．７％；在术前散光≤０．７５Ｄ、１．００～１．７５Ｄ及≥２．００Ｄ三组中，其术后散光分别比术前降低６０．３％、７０．０％和７４．９％，术后角膜散光平均为０．７２±０．２７Ｄ，比术前降低４０．５％；术后裸眼视力：９０．２％达到０．５或以上，７２％达到０．８或以上。无严重手术并发症。结论：ＰＡＲＫ是矫治散光的有效安全方法，主要用于矫正由规则对称角膜散光引起的复合近视散光     

固体激光角膜切削术治疗近视散光的疗效观察

为评价固体激光角膜切削术治疗近视散光的疗效，采用ＬｉｇｈｔＢｌａｄｅ固体激光手术系统对４４例６０眼复性近视散光同时竟性进行近视和散光角膜切削术，随访６～１２个月，对手术前后屈光度变化，视力结果统计分析，并与同期手术的单纯近视进行比较。结果：６０眼平均球镜屈光度从－６．７４±２．１４（－０．７５－１６．００）Ｄ降到－０．１４７±０．２３（－０．２５－０．７５）Ｄ柱镜度从１．６２±０．５３（０．７５－４．７５）Ｄ降到０．０６４±０．２７（０－０．７５）Ｄ。裸眼视力０．５，５７眼９５％，裸视力１．０４者７眼７３．３３％。单纯近视术后裸视力０．５和１．０的分别是９４．２３％和７５％，复性近视散光和单纯近视的固体激光疗效无明显差别（Ｐ＞０．１）。结论：ＬｉｇｈｔＢｌａｄｅ固体激光手术系统治疗近视散光安全有效，预测性好。     

准分子激光屈光性角膜切削术治疗近视,近视散光2年结果分析

为了评价准分子激光屈光性角膜切削术治疗近视、近视散光的疗效。应用美国ＶＩＳＸ２０／２０型准分子激光仪,采用多削区治疗近视屈光度为－１．７５～－１６．００Ｄ的患者,观察２年以上,按术前球镜屈光度分为二组,Ⅰ组为－１．７５～６．００Ｄ（１２１眼）,Ⅱ组为－６．２５～－１６．００Ｄ（８６眼）。术后２年裸眼视力≥０．５者在Ⅰ、Ⅱ组中分别为９５．９％、７０．９％,≥１．０者分别为７３．６％、３４．９％。Ⅰ、Ⅱ组中屈光度在±１．００Ｄ以内者分别为９１．７％、６２．８％。角膜上皮下混浊０度在Ⅰ、Ⅱ组中分别为８７．６％、６６．３％,２级以上分别为０、１．２％。眼压均正常。结论：准分子激光屈光性角膜切削术对低、中、高度近视、近视散光均取得良好的远期效果,但对低、中度近视效果更佳,对高度近视预测性较差。     

角膜地形图对准分子激光屈光性角膜手术后散光变化的判断作用

目的 探讨准分子激光我性角膜手术前后角膜地形图△ＳｉｎＫ变化值在散光度数变化判断中的作用。方法 对近视度为－１．５０～－２４．００Ｄ,散光度数－０．７５～－５．５０Ｄ的患者８９例１５０眼行准分子激光屈光性角膜切削术（ＰＲＫ）或分子激光原位角膜磨削术（ＬＡＳＩＫ）,观察６个月以上,经计算机得出角膜曲率△ＳｉｎＫ变化值Ｘ与临床散光度数变化 值Ｙ的散点图及相关系数ｒ值。结果 手术前后Ｘ与Ｙ的关系：Ｙ＝１     

准分子激光角膜切削术治疗近视散光的临床分析

目的评价准分子激光屈光性角膜切削术（ｐｈｏｔｏｒｅｆｒａｃｔｉｖｅｋｅｒａｔｅｃｔｏｍｙ，ＰＲＫ）矫正近视性角膜散光的结果。方法对２３１例（３８７只眼）近视患者按术前散光度分为Ａ（无散光）、Ｂ（散光＜２．００Ｄ）及Ｃ（散光＞２．００Ｄ）三组，并用ＰＲＫ对其近视和散光进行治疗。对手术前、后散光的变化进行比较，采用矢量分析方法，对手术矫正效应的量和方向进行分析。结果Ｂ、Ｃ两组术前散光分别为１．２９±０．４８Ｄ和３．０７±０．７２Ｄ，按术后６个月时残留散光计算，手术矫正效应分别为１．１０±０．６７Ｄ和２．４２±０．９３Ｄ，而手术效应与术前散光轴之间的夹角分别为５．８°±２．１°和４．９°±２．４°。结论ＰＲＫ治疗散光效果明显，轴向准确，但在高度散光组有一定的回退现象。     

准分子激光角膜切削术治疗角膜表面镜片术后散光

评价准分子激光角膜切削术治疗角膜表面镜片术后散光的效果。采用Ｃｏｈｅｒｅｎｔ产ＳＣＨＷＩＮＤＫＥＲＡＴＯＭ准分子激光治疗系统对８例１２只眼角膜表面镜片术后散光进行治疗，均为圆锥角膜术后病例，术前柱镜屈光度为－１．７５—－１０．００Ｄ，平均－５．４９Ｄ±３．２１Ｄ。术后随访６—１５月，平均１１．８月，显示裸眼视力均明显提高，矫正视力与术前相比提高者７只眼（５８．３３％）。柱镜平均屈光度由－５．４９Ｄ下降至－２．７７Ｄ，均无明显术后痛疼，术后角膜雾状混浊均不显著。说明准分子激光角膜切削术可有效地治疗角膜表面镜片术后的角膜散光，能显著地提高角膜表面镜片术治疗圆锥角膜的最终效果。     

准分子激光屈光性角膜切削术矫正散光的准确性及预测性

目的 探讨准分子激光屈光性角膜切削术（ｅｘｃｉｍｅｒ ｌａｓｅｒ ｐｈｏｔｏｒｅｆｒａｃｔｉｖｅ ｋｅｒｅｃｔｏｍｙ,ＰＲＫ）矫正散光的准确性及预测性。方法 根据角膜地形图提供的角膜屈光力数值,用Ｈｏｌｌａｄａｙ法计算复性近视散光３０例（５３只眼）和单纯近视２３例（３３只眼）患者术前与术后６个月角膜屈光力的差值,确定实际矫正散光度及轴位,及预期矫正散光度及轴位进行对比分析。结果 复性近视散光组５３     

PRK与LASIK治疗PK术后残留近视的临床研究

目的 探讨准分子激光角膜切削术（ＰＲＫ）及准分子激光原位角膜磨镶术（ＬＡＳＩＫ）矫治角膜放射状切开术（ＲＫ）后残留近视的安全性、稳定性和可靠性。方法 采用美国ＣＯＭＰＡＫ－２００型准分子激光治疗仪帮ＳＣＭＤ公司的可调节器气动微型角膜刀,分别对ＲＫ后残留近视的３８眼和９眼行ＰＲＫ和ＬＡＳＩＫ术,并随访半年以上。ＰＲＫ组根据屈光状态分为３组：Ⅰ组〈－３．００Ｄ;Ⅱ组－３．００～５．７５Ｄ,Ⅲ组－６．０     

LASIK治疗近视散光临床分析

为评价准分子激光原位角膜磨镶术（ＬＡＳＩＫ）治疗近视散光的疗效，对３６例（７２只眼）近视患者按术前散光度数分为３组，Ａ组（无散光），Ｂ组（散光＜２．０Ｄ），Ｃ组（散光＞２．０Ｄ），三组术前等量球镜差异无显著性（Ｐ＞０．０５），范围２．２５～１０．０Ｄ，并用ｌａｓｉｋ对其近视及散光治疗，平均随访时间８．１±１．７个月，对手术前后散光的变化比较分析。结果Ｂ、Ｃ两组术前散光分别为１．３７±０．３９Ｄ和２．９９±０．８２Ｄ，术后７个月残留散光分别为０．１９±０．５７Ｄ和０．３４±０．４６Ｄ，术前、术后散光轴夹角分别为４．９°±２．２°和３．７°±２．５°。结论：ｌａｓｉｋ治疗散光疗效确切，轴向准确，显示出较好的预测性、安全性、稳定性     

准分子激光角膜切削术治疗混合性散光

准分子激光角膜切削术治疗混合性散光严宗辉朱圣练胡建荣丁克西古洵清近年来，准分子激光散光性角膜切削术（ｐｈｏｔｏａｓｔｉｇｍａｔｉｃｒｅｆｒａｃｔｉｖｅｋｅｒａｔｅｃｔｏｍｙ，ＰＡＲＫ）治疗散光主要为复合近视散光，目前已在国内外开展，疗效令人鼓舞［１...     

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.