透明角膜小切口白内障手术后角膜散光变化

目的　评价透明角膜小切口超声乳化白内障吸除折叠式人工晶状体植入术后角膜散光的变化。方法　将62例(78只眼)白内障患者,按照切口位置位于颞上方及鼻上方或角膜曲率最大子午线轴位分为A、B两组,行透明角膜小切口超声乳化白内障吸除折叠式人工晶状体植入术,比较术后角膜散光的变化情况。结果　A、B两组术后3个月平均手术性角膜散光度分别为（0.83±0.65）D和（0.72±0.55）D,差异无显著性(P>0.05);平均角膜散光度分别较术前减少0.11D和0.39D,两者比较差异有显著性（P<0.05）。结论　以透明角膜小切口行超声乳化白内障吸除折叠式人工晶状体植入术,术后角膜散光度小;结合散光轴位选择切口位置,术后可明显减小角膜散光度。     

两种透明角膜切口白内障超声乳化术后角膜散光比较

目的 评价2.6mm与3.0mm两种透明角膜小切口超声乳化白内障吸除联合折叠式人工晶状体植入术对角膜散光的影响.方法 将69例(69只眼)白内障患者,按照2.6mm与3.0mm两种不同大小透明角膜切口随机分为A、B两组,行透明角膜小切口超声乳化白内障吸除联合折叠式人工晶状体植入术,比较两组手术性角膜散光的情况.结果 A组(3.0mm组)术后1周、术后1个月、术后3个月平均手术性角膜散光度分别为(0.6347±0.57773)D、(0.6029±0.52986)D和(0.6471±0.51902)D;B组(2.6mm组)术后1周、术后1个月、术后3个月平均手术性角膜散光度分别为(0.7286±0.62241)D、(0.6286±0.45927)D和(0.5714±0.49472)D;差异无统计学意义(P>0.05).结论 在同轴白内障超声乳化吸除联合折叠式人工晶状体植入术中,2.6mm透明角膜切口是一种安全有效的手术切口.     

透明角膜切口超声乳化折叠人工晶状体术后角膜散光的临床观察

目的:探讨透明角膜切口白内障超声乳化吸除联合折叠人工晶状体植入术后角膜散光的变化情况。方法:收集年龄相关性白内障患者58例79眼,全部实施透明角膜小切口超声乳化吸除联合折叠人工晶状体植入术。观察术前,术后3d;1wk;1mo视力及角膜散光情况。结果:术后1mo视力提高明显且趋于稳定。平均角膜散光度,术后1mo较1wk明显减少,二者比较差异有显著性。结论:3.2mm透明角膜切口白内障超声乳化吸除联合折叠人工晶状体植入术,术后角膜散光小,视力恢复快,稳定时间短,是理想的白内障手术切口方法。     

透明角膜小切口白内障术后的屈光稳定时间分析

目的　观察分析透明角膜切口超声乳化白内障吸除联合折叠人工晶状体植入术后屈光状态趋于稳定的时间。方法　计算并比较73例(82只眼)施行透明角膜切口超声乳化白内障吸除联合折叠人工晶状体植入术患者术后不同时间的手术性角膜散光度。结果　比较白内障患者术后1周与1个月的手术性角膜散光度,差异无显著性(P =0 .312 ,>0 .0 5 ) ;术后1周与3个月比较,差异有显著性(P =0 .0 0 0 ,<0 .0 5 ) ;术后1个月与3个月比较,差异有显著性(P =0 .0 5 0 )。结论　透明角膜小切口白内障术后早期角膜散光即基本稳定,至术后3个月时角膜散光还会较前有少许改变。     

小切口非超声乳化白内障手术中选择性切口矫正术前散光的临床观察

目的:评价小切口白内障非超声乳化手术中根据角膜散光轴位选择不同切口位置矫正术前散光的疗效。方法:对角膜散光>1.00D的39例39眼老年性白内障患者进行研究,随机分为A,B两组。A组20例患者,术前根据患者散光轴位行12∶00(顺规)及9∶00(逆规)位的角膜切口小切口白内障非超声乳化吸除人工晶状体植入术;B组19例患者行常规上方角膜切口小切口白内障非超声乳化摘除人工晶状体植入术。术前及术后记录最佳矫正视力、角膜屈光度及散光轴位,比较两组术后角膜散光的变化。结果:术后A组视力平均提高0.66,B组平均提高0.57,两组比较差异无统计学意义。A组平均矫正散光1.10D,B组矫正0.40D,两组差异显著。在随访过程中未出现并发症。结论:根据术前散光轴位,在小切口白内障非超声乳化摘除人工晶状体植入术中选择不同位置的切口,可安全有效地矫正术前散光。     

角膜切口对白内障手术后散光的影响

目的:观察沿角膜散光陡峭轴方向做透明角膜切口行白内障超声乳化联合人工晶状体植入术后散光和视力的变化。方法:根据IOL-Master检测结果选择角膜最大屈光力轴行3.0mm透明角膜切口做白内障超声乳化术42眼作为观察组(A组),常规颞上(右眼)、鼻上(左眼)3.0mm透明角膜切口白内障超声乳化术68眼作为对照组(B组)。检测术前、术后1d;1wk;1,3mo角膜散光和视力变化。结果:A组术前、术后1d;1wk;1,3mo视力分别为0.2±0.24,0.73±0.37,0.78±0.38,0.94±0.36,0.76±0.13;B组为0.17±0.2,0.82±0.3,0.84±0.2,0.77±0.26,0.8±0.36;差异无统计学意义(P>0.05)。A组术前、术后1d;1wk;1,3mo角膜散光度分别为1.01±0.10D,1.33±0.13D,1.15±0.14D,0.90±0.13D,0.89±0.12D;B组为0.95±0.13D,1.25±0.15D,1.07±0.13D,0.87±0.12D,0.82±0.11D。术后1d;1wk;1mo与术前相比散光度均无统计学意义(P>0.05)。两组术后3mo散光度与术前相比差异有统计学意义(P<0.05)。两组术后3mo裸眼视力≥0.8者分别为21眼(50%)和32眼(47%),两者相比有统计学意义(P<0.05)。结论:沿陡轴透明角膜切口白内障超声乳化联合人工晶状体植入术有助于患者视力提高及减少术后角膜散光。     

白内障超声乳化术不同子午线切口对术后角膜散光的影响

目的　评价在角巩缘切口白内障超声乳化术中不同子午线切口对术后角膜散光的影响。方法　 76例(10 2眼 )白内障患者被随机分为 A、B两组 ,A组根据手术者的习惯切口位置选择颞上方 (右眼 )或鼻上方 (左眼 )的切口 ,B组按照角膜曲率最大子午线轴向做手术切口。通过行角巩缘切口白内障超声乳化折叠式人工晶状体植入术 ,比较两组术后角膜散光的变化情况。结果　 A、B两组术后平均角膜散光度分别较术前减少 0 .13D和 0 .32 D,两者比较差异有显著性 (t=2 .185 ,P <0 .0 5 ) ;平均手术性角膜散光度为 (0 .95± 0 .89) D和 (0 .83± 0 .75 ) D,差异无显著性 (t=0 .314 ,P >0 .0 5 )。结论　在角巩缘切口白内障超声乳化术中结合术前角膜散光轴向选择切口位置可进一步降低术后角膜散光。     

透明角膜切口超声乳化白内障吸除折叠式人工晶状体植入术临床分析

目的探讨透明角膜切口超声乳化白内障吸除可折叠人工晶状体植入术后的临床效果。方法采用上方3.2mm阶梯状透明角膜切口,对101例123眼白内障行超声乳化白内障吸除折叠人工晶体植人。术后观察手术反应,角膜散光,视力和并发症。结果术后第一天裸眼或球镜矫正视力≥0.5者占79.68%;术后1周,1个月和3个月裸眼或球镜矫正视力≥0.5者分别占87.00%,91.87%和95.12%。术后3个月平均角膜散光与术前两者相比较差异无统计学意义(>0.05)。术后常见的炎症反应主要与核的硬度,超声乳化的时间及能量的大小有关。结论透明角膜切口的超声乳化白内障吸除折叠式人工晶状体植入术具有角膜散光小、术后视力恢复快、术后反应轻、无严重并发症发生的优点。     

角膜地形图引导下白内障手术切口对角膜散光的矫正

目的:比较不同位置和形态的手术切口对白内障摘除术后角膜散光及裸眼视力的影响。方法:选取术前角膜散光值>1.00D的白内障患者43例52眼,将患者随机分成两组,A组患者采用超声乳化白内障吸除联合人工晶状体植入术,手术切口为位于上方10∶30～11∶30的透明角膜隧道切口。B组患者采用手法碎核白内障摘除联合人工晶状体植入术,其中角膜散光值为1.00～2.00D的患者,切口为位于角膜最大屈光度径线的直线形巩膜隧道切口,长度为6.0～7.0mm,角膜散光值>2.00D的患者,在上述直线形切口对侧角膜缘处,另作一弧形板层松解切口。分别于术后2wk,3mo随访患者,检查裸眼视力及行角膜地形图检查。结果:B组患者术后2wk,3mo裸眼视力好于A组。B组患者术后角膜散光度在术后2wk,3mo时均小于A组。结论:位于角膜最大屈光度径线的6.0～7.0mm直线形巩膜隧道切口,及此切口联合作对侧弧形板层松解切口均能有效矫正白内障术前存在的角膜散光,能够使患者获得更好的术后裸眼视力。     

白内障切口对角膜散光的影响

目的:研究不同方位3.2mm切口超声乳化白内障术对角膜散光25度以内患者的影响。方法:收集Orbscan检测出角膜散光在25度以内白内障患者共40例,随机分成A,B两组。在Orbscan引导下,A组20例20眼行3.2mm角膜散光轴向切口,B组20例20眼在90度轴上行3.2mm透明角膜切口,并由同一位手术医师行超声乳化白内障吸除人工晶状体植入术。观察患者术前及术后Orbscan检测的角膜Simk值及PolarK的变化。结果:各组内术前与术后各个时间点PolarK比较,差异有显著统计学意义;两组之间术后各个时间点PolarK比较,差异无统计学意义,两种切口术后3mo都会增加角膜PolarK0.3D左右。结论:对于角膜散光25度以内白内障患者,3.2mm透明角膜切口可能引起角膜PolarK0.3D左右散光。     

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.