准分子激光术前眼底检查结果及预防性光凝治疗

目的 研究准分子激光术前中高度近视眼眼底情况及术前眼底激光预防性治疗的意义.方法 对2686例(5316只眼)准备接受LASIK手术的患者进行术前常规检查,并采用散瞳三面镜检查眼底.对发现视网膜裂孔、变性、脱离的病人进行预防性眼底激光治疗.结果 有45例(49只眼)发现裂孔,发生率为0.9%,视网膜变性有526只眼(9.89%),其中格子样变性132只眼(2.48%),囊样变性97只眼(1.82%),霜样变性57只眼(1.07%)、非压迫白变性192只眼(4.42%),其他变性48只眼(0.90%).结论 高度近视患者在接受LASIK术前行散瞳三面镜眼底检查是必要的,避免和减少术后并发视网膜脱离的可能.对于有视网膜脱离者可及时行手术复位,从而提高LASIK手术的安全性.     

LASIK前眼底三面镜检查及其意义

目的：探讨散瞳眼底三面镜检查在LASIK术前的重要意义。方法：对385例（721眼）LASIK术前患者行散瞳眼底三面镜检查并作详细眼底记录。结果：发现各种视网膜变性136眼（18.86%),视网膜干性裂孔（干孔）16眼（2.22%）,亚临床视网膜脱离（RD）5眼（0.69%)。其中37眼严重视网膜变性、16眼干孔和4眼亚临床RD行氩激光光凝治疗,仅1例亚临床RD需行视网膜脱离手术。结论：将散瞳眼底三面镜检查作为LASIK术前常规检查是必要的,同时提出眼底病变光凝的指征。     

LASIK术前高度近视眼底病变临床分析及处理

目的探讨准分子激光原位角膜磨镶术（LASIK）术前高度近视眼底病变病情及治疗方法。方法对264例（496只眼）LASIK术前高度近视患者行散瞳眼底检查并作详细眼底检查记录。结果 496只眼中11只眼有干性视网膜裂孔（占2.2%）,9只眼有玻璃体牵引,4只眼伴视网膜脱离,14只眼有严重视网膜变性。11只眼干性视网膜裂孔和2只眼视网膜浅脱离行氩激光光凝治疗,2只眼视网膜脱离行巩膜外硅压术。结论高度近视眼LASIK术前常规散瞳检查眼底对发现病变并及时治疗是非常必要的。     

激光光凝辅助角膜原位磨镶术前眼底

目的：探讨近视LASIK术前眼底病变及治疗方法。方法：对385例（721只眼）LASIK术前患者行散瞳眼底三面镜检查并作详细眼底记录,结果：发现各种视网膜变性136只眼（18.86%),视网膜干性裂孔16只眼（2.22%),亚临床视网膜脱离（RD）5只眼（0.69%)。其中37只眼严重视网膜变性、16只眼干孔和4只眼亚临床RD行氩激光光凝治疗,仅1例亚临床RD需行视网膜脱离手术,结论：近视LASIK术前及术后眼底常规检查和病变治疗是必要的,同时本文提出眼底病变光凝的指征。     

90D前置镜在准分子激光原位角膜磨镶术术前眼底检查中的应用

目的探讨使用90D前置镜进行准分子激光原位角膜磨镶术（LASIK）术前检查的意义。方法对准备施行LASIK术前检查的患者充分扩瞳后,分别使用90D前置镜和双目间接眼底镜检查眼底,详细记录检查结果。对比检查结果。结果 276眼（138例）中,90D前置镜组发现视网膜干性裂孔12眼4.35%,视网膜裂孔伴有浅脱离3眼1.09%,格子样变性23眼8.33%;双目间接检眼镜组发现视网膜干性裂孔11眼3.99%,视网膜裂孔伴有浅脱离2眼0.72%,格子样变性23眼8.33%,对两种检查法的视网膜裂孔发现率采用x~2检验分析,P〉0.05。1眼视网膜裂孔浅脱离行巩膜外冷凝＋外填压术。其余病例均行氩离子激光光凝术封闭裂孔。结论使用90D前置镜进行LASIK术前眼底检查检出率高,且安全无创伤,方便和快速。     

飞秒激光制瓣LASIK术前预防性视网膜光凝

目的观察低、中、高度近视飞秒激光制瓣准分子激光原位角膜磨镶术（LASIK）术前周边视网膜变性和裂孔进行预防性光凝的效果。方法近视1000例（2000眼）,年龄18—50岁,屈光度-1．00～-13．00D,散光-0．50～-4．00D。术前按屈光度分组：组I,-1．00～-3．00D,350例（700眼）;组Ⅱ,-3．25～-6．00D,360例（720眼）;组Ⅲ,-6．25～-13．00D,290例（580眼）。LASIK术前常规散瞳行90D前置镜眼底检查。结果发现严重周边视网膜变性和裂孔100眼,其中组I20眼,组Ⅱ44眼,组Ⅲ36眼,多发生于颞侧。组Ⅱ和组Ⅲ发生率高于组I。对此100眼进行532nm激光预防性光凝。光凝术后1个月复查,变性和裂孔区激光封闭良好,色素斑形成,遂行飞秒激光制瓣LASIK。术后6个月-1年随访,未发现孔源性视网膜脱离。结论LASIK术前眼底检查,对明确有严重视网膜变性或有裂孔者预防性激光光凝是安全有效的,能够减少或避免术后视网膜脱离的发生,保障术后效果。     

激光光凝辅助角膜原位磨镶术前眼底病变分析及治疗

目的探讨近视LASIK术前眼底病变及治疗方法.方法对385例(721只眼)LASIK术前患者行散瞳眼底三面镜检查并作详细眼底记录.结果发现各种视网膜变性136只眼(18.86%),视网膜干性裂孔16只眼(2.22%),亚临床视网膜脱离(RD)5只眼(0.69%).其中37只眼严重视网膜变性、16只眼干孔和4只眼亚临床RD行氩激光光凝治疗,仅1例亚临床RD需行视网膜脱离手术.结论近视LASIK术前及术后眼底常规检查和病变治疗是必要的.同时本文提出眼底病变光凝的指征.     

LASIK术前眼底周边视网膜病变检查及处理的价值

目的观察准分子激光原位角膜磨镶术（LASIK）术前对视网膜变性或伴裂孔等进行预防性治疗的价值。方法对LASIK术前1260只眼扩瞳后行眼底检查并作详细记录,对明显视网膜变性或伴裂孔15只眼进行视网膜光凝治疗。结果15只眼光凝3～4周,行LASIK手术,术后随访6个月,无1例发生视网膜脱离。结论对拟行LASIK手术的患者进行详细眼底检查,并对周边视网膜变性严重和视网膜裂孔者实施预防性光凝治疗可大大降低术后视网膜脱离的发生率。     

LASIK术前近视性视网膜病变特征分析与氩激光疗效评价

目的:分析LASIK术前检查发现的近视患者视网膜病变的特征,评价眼底氩激光光凝治疗的疗效与安全性。方法:回顾性研究,分析了施行LASIK术的连续性病例1 100例(2 190眼)的术前资料,在对所有患者术前扩瞳后以检眼镜、三面镜详细检查眼底周边视网膜情况并记录,对严重的视网膜病变如格变、囊样变、干性裂孔、视网膜浅脱离等予以氩离子激光光凝治疗,经随访稳定有效后再择期行LASIK手术。结果:视网膜病变及视网膜裂孔的发生率均随屈光度增加而提高,组间有显著性差异(P<0.05),颞侧病变比例高于鼻侧。在全部患眼的检查中,发现各类视网膜变性132眼,64眼发现格子样变性(48.48%)、37眼发现囊样变性(28.03%)、54眼发现霜样变性(40.91%)、34眼发现不压白变(25.76%)、12眼发现铺路石样变性(9.09%)、14眼发现干性裂孔(10.61%)、4眼发现裂孔伴局限性浅脱离(3.03%)。对出现较严重视网膜病变的43例患者(78眼)施行了眼底氩激光治疗。复诊时见激光斑反应明显、干性裂孔稳定,局限性浅脱离患者经2～4次激光,光凝后视网膜完全平复。对眼底经光凝后行LASIK的患者,在3～6mo复诊中无1例视网膜脱离发生。结论:LASIK术前对全部患者进行常规三面镜详查眼底是十分有必要,对发现的周边视网膜严重变性及时予以激光光凝能够有效防止视网膜脱离的发生。     

LASIK术前周边视网膜变性的干预性光凝

目的探讨准分子激光原位角膜磨镶术（LASIK）术前对周边视网膜变性干预性激光光凝的方法和疗效。方法LASIK术前对近视眼常规行直接检眼镜、三面镜和间接检眼镜检查,对合并有明届的周边视网膜变性的近视眼行532nm激光干预性光凝渝疗。在变性区外光凝2～3排,光斑直径200～300μm,时间0．15～0．20s,光斑间距1．0～1．5个光斑,出现三级光斑为准。结果197例（231眼）视网膜变性,其中格子样变性163眼（70．56％）,霜样变性64眼（27．71％）,囊样变性4眼（1．73％）。激光光凝术后,视网膜变性及干性裂孔区封闭良好,色素斑形成明显。LASIK术后随访6～18个月,无发生视网膜脱离者。结论LASIK术前对周边部视网膜变性进行干预性光凝,是预防LASIK术后发生视网膜脱离的重要方法。     

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.