老年人眼外肌麻痹的原因分析

目的探讨老年人眼外肌麻痹的临床病因及特点。方法对113例以复视为首发症状的眼外肌麻痹患者的临床资料进行回顾性研究,依据病史、临床检查分析发病原因,并对其进行相关治疗。结果眼外肌麻痹的发病部位以核性及核下性眼球运动障碍为主,占83．19％。发病原因以血管性疾病为主,占49．56％。受累部位以动眼神经麻痹占首位为36．28％外展神经麻痹次之,占30．09％。单条眼外肌麻痹较多条肌肉麻痹多见,其中以内直肌受累居多。结论以复视为首发症状的老年人眼外肌麻痹多见,其中以内直肌受累居多。结论以复视为首发症状的老年人眼外肌麻痹病因复杂,以血管性疾病多见,以核及核下性损害为主,动眼神经麻痹占首位。必须及早检查,明确诊断,并给予相关治疗,以免误诊,应引起重视。     

80例以复视为首发症状的眼外肌麻痹病因分析

目的：探讨以复视为首发症状的眼肌麻痹患者的临床特征、鉴别诊断,探讨其病因及发病机制。方法回顾分析2008至2013年我院神经内科收治以复视症状为主症的眼肌麻痹患者80例,根据病史、详细的查体和眼部检查,分析其发病原因。结果80例病例中,糖尿病性眼肌麻痹24例（动眼神经麻痹16例,外展神经麻痹6例,合并动眼神经、外展神经麻痹2例）,脑血管病20例,动脉粥样硬化性动眼神经、外展神经麻痹18例,颅内动脉瘤者10例,重症肌无力眼肌型2例,躯体形式障碍1例,颅内肿瘤2例,多发性硬化1例,神经梅毒1例,脑干脑炎1例。结论很多神经系统疾病可引起复视的神经眼科体征,其中糖尿病性眼肌麻痹为最主要病因,脑血管病、动脉瘤眼肌麻痹、动脉粥样硬化也是重要原因,其他还有重症肌无力（眼肌型）、躯体形式障碍、颅内占位等。以复视为首发症状的急性眼外肌麻痹病因复杂,容易误诊,临床医生应高度重视,明确诊断,以达到正确治疗。     

动眼神经麻痹性斜视的手术方式探讨

目的 探讨动眼神经麻痹性斜视的手术方式.设计回顾性病例系列.研究对象单侧动眼神经麻痹性斜视患者13例.方法 动眼神经不完全麻痹者8例,行外直肌的超常量后退,同侧内直肌折叠,对侧外直肌后退术.动眼神经完全麻痹、上斜肌健康者3例,行外直肌的超常量后退,同侧内直肌折叠,上斜肌转位术,即将上斜肌移位至内直肌上方;动眼神经完全麻痹且伴上斜肌麻痹者2例,行外直肌的超常量后退,内直肌鼻侧眶缘固定术.主要指标手术前后的水平、垂直斜视度.结果 术前外斜视在80^△～120^△以上,5例伴有下斜视15^△～35^△,2例伴有上斜视15^△～20^△;术后随访6～27个月,残余外斜6^△～20^△,残余下斜视4^△～10^△.结论 根据动眼神经麻痹造成的眼外肌麻痹程度的不同,采取不同的手术方式,可获得眼位的美容正位.     

51例后天麻痹性斜视临床分析

后天麻痹性斜视为临床常见病 ,病人往往发病急骤 ,突然出现复视是其典型的症状。根据症状及眼部检查诊断某条肌肉麻痹并不困难 ,但由于导致眼外肌麻痹的病因较多 ,故寻找病因及时治疗 ,就很重要。现将我院 1 989～ 2 0 0 1年临床所见的 51例眼外肌麻痹报告如下 :临床资料1 一般资料　 51例中男 3 2例 ,女 1 9例 ;右眼 2 7例 ,左眼 2 4例 ;年龄最小 9岁 ,最大72岁。 2 3例为外直肌麻痹 ,1 5例为动眼神经支配的眼外肌麻痹 ,1 3例上斜肌麻痹 ;眼外肌麻痹程度为完全性和不完全性。 42例因复视首诊于眼科 ,3例因脑外伤后出现复视由神经外科转入 …     

小儿眼外肌麻痹87例

儿童时期眼外肌麻痹并非少见，但其病因较为复杂，若能迅速查明原因，施以正确治疗，多数病例可获满意效果。为此，我们将近10a临床资料较完整的87例小儿眼外肌麻痹作一扼要分析。1临床资料1．1一般资料男54例，女33例；年龄3mo～14a；单侧眼外肌麻痹79例，双侧8例；完全性麻痹77例，不完全性麻痹10例；动眼神经麻痹72例，外展神经麻痹68例，滑车神经麻痹5例；其中2／3病例为2对或2对以上颅神经麻痹。1．2病因外伤所致者28例，均有明确的外伤史，其中2例上睑下垂为球壁骨折致单纯提上睑肌肌束损伤所致，3例颅内占位性病变，2例为脑肿瘤，1例…     

改良直肌交叉联结术治疗双眼麻痹性外斜视一例

单独的眼外肌麻痹中以外直肌麻痹和上斜肌麻痹最为常见,而不伴有动眼神经支配的其他肌肉麻痹的单独内直肌麻痹非常罕见。现对华西医院眼科中心一例双眼内直肌麻痹病例治疗报道如下。     

首发为动眼神经麻痹糖尿病的临床分析

目的 探讨以动眼神经麻痹为首发症状的糖尿病性动眼神经麻痹的临床特征，以提高对该病的重视，达到及早治疗。方法 对24例糖尿病性动眼神经麻痹的临床资料进行回顾性分析。结果 24例患者均以动眼神经麻痹为首发，缺乏糖尿病的典型症状，均为单眼受累，动眼神经眼外肌麻痹16例，合并跟内肌麻痹8例，其中不完全动跟神经麻痹16例（66．7％），完全性麻痹8例（33．3％），24例患者经过及时治疗均完全恢复。结论 1．本病突然发病，其发病机制与微血管病变及代谢障碍有关，多为单侧不完全性动眼神经麻痹。2．眼科医师要重视病因检查，及时诊治，有利于功能早期恢复。     

上直肌后徙术在眼性斜颈治疗中的应用

眼性斜颈的病因中,上斜肌麻痹较为常见,其次为上下直肌的麻痹。后天性眼外肌麻痹多数经药物治疗能见效,部分无效者可以手术矫治。先天性上斜肌麻痹所致的斜颈应早期作手术。其手术方法有:患眼下斜肌减弱术、患眼上斜肌加强术、健眼下直肌减弱术以及患眼上直肌减弱术等。作者自1984年3月至1988年10月,用上直肌后徒术治疗眼性斜颈13例,取得较满意的结果,现报告如下。     

上斜肌转位术治疗动眼神经全麻痹

对麻痹性斜视的治疗,一般认为动眼神经麻痹的手术治疗最为困难。自1907年Hummelscheim最初提倡用肌肉转位术治疗麻痹性斜视以后,相继出现了针对水平肌、垂直肌麻痹的各种手术。由于动眼神经完全麻痹而引起的外斜视,用内直肌短缩是不能治愈的,主要采用将上斜肌移位到内直肌部位的上斜肌转位术来治疗。关于上斜肌转位术治疗动眼神经完全麻痹病报告较少。本文对1例动眼神经完全麻痹的人采用上斜肌转位术,对其效果进行初步探讨。     

上斜肌转位治疗动眼神经麻痹

目的探讨上斜肌转位手术治疗动眼神经麻痹的临床效果。方法回顾我院1999年1月～2007年9月采用上斜肌转位术矫正动眼神经麻痹所致重度外斜视病例,并观察分析。结果20眼动眼神经麻痹行外直肌后退,内直肌折叠,上斜肌转位术。下斜视者3眼加下直肌后退术,上斜视6眼二次手术行上直肌超常量后退及下直肌超常量缩短术。患者外观取得满意效果,随访6月～3年眼位无明显改变。结论上斜肌转位术矫正动眼神经麻痹性斜视是可行的。     

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.