结膜松弛症诊断治疗技术

结膜松弛症是由于球结膜过度松弛和/或下睑缘张力高,造成松弛球结膜堆积在眼球与下睑缘、内、外眦部之间形成皱褶,引起眼表泪液学异常,并伴有眼部不适等症状的疾病。结膜松弛症多发生于老年人,常主诉眼部干涩、异物感、泪溢。诊断结膜松弛症的关键是裂隙灯检查见松弛的球结膜堆积在眼球与下睑缘、内眦部、外眦部之间。结膜松弛症根据症状和体征在临床上分为四级。结膜松弛症的球结膜组织发生以弹力纤维减少、胶原纤维溶解为主要的组织病理改变,泪液中出现蛋白质及酶的异常表达,泪液排泄出现障碍。结膜成纤维细胞中基质金属蛋白酶MMP-1及MMP-3过度表达,使得MMPs与TIMPs之间失去平衡,可能使胶原纤维溶解,弹力纤维变性,导致球结膜基质和Tenon’s的过度降解,引起眼表泪液学异常的病理循环,而发生结膜松弛症。结膜松弛症眼部刺激症状严重者,可以给予泪液制剂、润滑剂和皮质类固醇或抗组胺等药物。上述方法无效,选择手术治疗:(1)结膜新月形切除术;(2)结膜缝线固定术;(3)结膜切除羊膜移植术;(4)角膜缘结膜梯形切除术;(5)双极电凝治疗术;(6)下睑缘高张力减弱术。上述手术方法对治疗结膜松弛症都有效,但各有缺点,且有不同适应证。     

结膜松弛症手术治疗临床观察

结膜松弛症可由于球结膜过度松弛和／或下睑缘张力高，导致松弛的球结膜堆积在眼球与下睑缘、内外眦部之间而引起眼表泪液学异常。我科采用手术治疗结膜松弛症效果良好，报告如下。     

结膜松弛症泪液功能改变的观察

结膜松弛症(conjunctivochalasis)是由于球结膜过度松弛和(或)下睑张力高,造成松弛球结膜堆积在眼球与下睑缘,内、外眦部之间形成皱褶引起眼表泪液学异常,并伴有眼部不适(如流泪、干涩、异物感等)症状的疾病[1].有学者发现结膜松弛症可引起泪液动力学异常型干眼[2-5],泪液功能的改变在结膜松弛症的发生与发展中可能起一定的作用,但机制尚不明.因此,本研究对结膜松弛症的泪液功能改变进行检测,以探讨结膜松弛症的发病机制.     

结膜松弛症泪液功能改变的观察

结膜松弛症(conjunctivochalasis)是由于球结膜过度松弛和(或)下睑张力高,造成松弛球结膜堆积在眼球与下睑缘,内、外眦部之间形成皱褶引起眼表泪液学异常,并伴有眼部不适(如流泪、干涩、异物感等)症状的疾病[1].有学者发现结膜松弛症可引起泪液动力学异常型干眼[2-5],泪液功能的改变在结膜松弛症的发生与发展中可能起一定的作用,但机制尚不明.因此,本研究对结膜松弛症的泪液功能改变进行检测,以探讨结膜松弛症的发病机制.     

结膜松弛症泪液功能改变的观察

结膜松弛症(conjunctivochalasis)是由于球结膜过度松弛和(或)下睑张力高,造成松弛球结膜堆积在眼球与下睑缘,内、外眦部之间形成皱褶引起眼表泪液学异常,并伴有眼部不适(如流泪、干涩、异物感等)症状的疾病[1].有学者发现结膜松弛症可引起泪液动力学异常型干眼[2-5],泪液功能的改变在结膜松弛症的发生与发展中可能起一定的作用,但机制尚不明.因此,本研究对结膜松弛症的泪液功能改变进行检测,以探讨结膜松弛症的发病机制.     

结膜松弛症泪液功能改变的观察

结膜松弛症(conjunctivochalasis)是由于球结膜过度松弛和(或)下睑张力高,造成松弛球结膜堆积在眼球与下睑缘,内、外眦部之间形成皱褶引起眼表泪液学异常,并伴有眼部不适(如流泪、干涩、异物感等)症状的疾病[1].有学者发现结膜松弛症可引起泪液动力学异常型干眼[2-5],泪液功能的改变在结膜松弛症的发生与发展中可能起一定的作用,但机制尚不明.因此,本研究对结膜松弛症的泪液功能改变进行检测,以探讨结膜松弛症的发病机制.     

结膜松弛症泪液功能改变的观察

结膜松弛症(conjunctivochalasis)是由于球结膜过度松弛和(或)下睑张力高,造成松弛球结膜堆积在眼球与下睑缘,内、外眦部之间形成皱褶引起眼表泪液学异常,并伴有眼部不适(如流泪、干涩、异物感等)症状的疾病[1].有学者发现结膜松弛症可引起泪液动力学异常型干眼[2-5],泪液功能的改变在结膜松弛症的发生与发展中可能起一定的作用,但机制尚不明.因此,本研究对结膜松弛症的泪液功能改变进行检测,以探讨结膜松弛症的发病机制.     

结膜松弛症泪液功能改变的观察

结膜松弛症(conjunctivochalasis)是由于球结膜过度松弛和(或)下睑张力高,造成松弛球结膜堆积在眼球与下睑缘,内、外眦部之间形成皱褶引起眼表泪液学异常,并伴有眼部不适(如流泪、干涩、异物感等)症状的疾病[1].有学者发现结膜松弛症可引起泪液动力学异常型干眼[2-5],泪液功能的改变在结膜松弛症的发生与发展中可能起一定的作用,但机制尚不明.因此,本研究对结膜松弛症的泪液功能改变进行检测,以探讨结膜松弛症的发病机制.     

结膜松弛症泪液功能改变的观察

结膜松弛症(conjunctivochalasis)是由于球结膜过度松弛和(或)下睑张力高,造成松弛球结膜堆积在眼球与下睑缘,内、外眦部之间形成皱褶引起眼表泪液学异常,并伴有眼部不适(如流泪、干涩、异物感等)症状的疾病[1].有学者发现结膜松弛症可引起泪液动力学异常型干眼[2-5],泪液功能的改变在结膜松弛症的发生与发展中可能起一定的作用,但机制尚不明.因此,本研究对结膜松弛症的泪液功能改变进行检测,以探讨结膜松弛症的发病机制.     

结膜松弛症泪液功能改变的观察

结膜松弛症(conjunctivochalasis)是由于球结膜过度松弛和(或)下睑张力高,造成松弛球结膜堆积在眼球与下睑缘,内、外眦部之间形成皱褶引起眼表泪液学异常,并伴有眼部不适(如流泪、干涩、异物感等)症状的疾病[1].有学者发现结膜松弛症可引起泪液动力学异常型干眼[2-5],泪液功能的改变在结膜松弛症的发生与发展中可能起一定的作用,但机制尚不明.因此,本研究对结膜松弛症的泪液功能改变进行检测,以探讨结膜松弛症的发病机制.     

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.