甲钴胺联合复方血栓通及维生素B1治疗糖尿病性眼肌麻痹临床观察

目的:观察甲钴胺联合复方血栓及维生素B1通治疗糖尿病性眼肌麻痹的临床疗效。方法:收集近4a来我院就诊的糖尿病性眼肌麻痹患者64例,在控制原发病基础上口服甲钴胺联合复方血栓通及维生素B1治疗糖尿病性眼肌麻痹,并设立复方血栓通联合维生素B1治疗为对照组。结果:两组患者在良好控制血糖的情况下,眼科治疗2～16wk后症状及体征均有不同程度的减轻及消失;治疗3mo后,甲钴胺组治愈率优于对照组。结论:在控制血糖的情况下,甲钴胺联合维生素B1及复方血栓通治疗糖尿病性眼肌麻痹安全有效。     

老年人糖尿病性眼肌麻痹的临床分析

目的：探讨老年人糖尿病性眼肌麻痹的临床特点和发病机制。方法：常规的眼科检查和眼肌专科检查，内科行全身检查及实验室血生化检查以确诊糖尿病；部分病例辅以影像学检查。结果：３９例老年人糖尿病患者多数为单眼患病；受累颅神经以动眼神经最多２１例２３只眼，以后依次为外展神经１２例，滑车神经和复合神经麻痹各３例。动眼神经麻痹中５例为伴随上睑下垂和瞳孔变化的完全性动眼神经麻痹。大多数患者合并有高血压，近半数患者有     

糖尿病性眼肌麻痹临床分析

目的 探讨糖尿病性眼肌麻痹的临床特点.方法 对25例(25只眼)经常规眼科检查,眼肌检查及实验室生化检查后,确诊为糖尿病性眼肌麻痹进行分析.结果 25只眼均单眼发病,受累神经以动眼神经麻痹多见,为15例,其次外展神经麻痹6例,滑车神经麻痹3例,复合神经(Ⅲ+Ⅳ)麻痹1例.结论 中老年糖尿病患者易并发眼肌麻痹,糖尿病性微循环病变是导致神经缺血缺氧以致变性的病理基础.     

糖尿病性眼肌麻痹临床分析

目的　探讨老年人糖尿病性眼肌麻痹的临床特点和发病机制。方法　常规眼科检查和眼肌专科检查及实验室生化检查确诊为糖尿病性眼肌麻痹 2 4例 (2 4只眼 ) ,部分病例辅以影像学检查。结果　 2 4例均匀单眼发病 ,受累颅神经以动眼神经最多见 13例 (13只眼 ) ,其次为外展神经 9只眼 ,滑车神经 1只眼。结论　老年人糖尿病患者易合并眼肌麻痹 ,其发病可能与微血管病变有关     

糖尿病性眼肌麻痹9例报告

随着人民生活水平的不断提高 ,我国糖尿病患者与日俱增 ,糖尿病已成为我国主要的公共卫生问题 ,随之而来的糖尿病性眼病日益成为危及患者视力、影响患者生活质量的重要问题 ,糖尿病视网膜病变较为多见 ,但糖尿病性眼肌麻痹则比较少见 ,笔者自 1991～ 2 0 0 0年 10年间共收集 9例 ,现报告如下。一、资料与方法1.本文 9例 (9眼 )中男 4例 ,女 5例 ,年龄 36～ 6 2岁 ,平均 49岁。 40岁以上者 8例 ,占 88.89% ,眼肌麻痹分别发生在患糖尿病后 4～ 8年。自述糖尿病史者 4例 ,经实验检查确诊为糖尿病者 5例 ,本组病例均为 型糖尿病。2 .诊断依据 :…     

50例眼肌麻痹病因与临床诊治分析

目的探讨眼肌麻痹的病因、临床特点及治疗效果。方法回顾性分析了50例（50只眼）眼肌麻痹患者的临床资料,根据病史、红玻片复视像检查、眼科检查、实验室检查、影像学诊断,分析发病原因,并对其进行相关治疗。结果 50例中神经血管源性眼肌麻痹42例（84%）,肌源性麻痹3例（6%）,全身免疫性麻痹3例（6%）,机械性麻痹2例（4%）。结论眼肌麻痹病因复杂,仔细分析临床特征,进行全面细致的眼科检查、影像学检查有助于病因诊断及有效的治疗。     

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。     

疼痛性眼肌麻痹的临床特征及治疗

目的 探讨疼痛性眼肌麻痹的临床特征和治疗效果。方法 综合国内外文献和本文１０例病人的临床表现,应用皮质类固醇药物治疗。结果 随访３月至６年。９例４８ｈ～７２ｈ治愈,１例遗留视神经萎缩。４例复发２次１例复发３次,复发间隔时间数月至数年。结论疼痛性眼肌麻痹应以眼球后持续性疼痛并向前额和颞部放射;第３脑神经或合并第４、６脑神经麻痹及第５脑神经１、２支麻痹;角膜和前额部皮肤知觉异常;皮质类固醇药物治疗效果明显作为诊断依据。     

眼肌麻痹的病因及治疗

目的探讨眼肌麻痹患者的病因及治疗。方法回顾性分析46例有眼肌麻痹症状，且经眼科、神经内外科检查、实验室和影像学检查的住院病例。结果眼肌麻痹的病因以动脉瘤最多（34．8％，16／46），其次为痛性眼肌麻痹（17．4％，8／46）及糖尿病性眼肌麻痹（17．4％，8／46），其它依次为：颅脑外伤（13．0％。6／46）、颅内感染（8．6％，4／46）、内直肌损伤（4．3％，2／46）。累及的神经以动眼神经最多（73．9％，34／46）。其次为外展神经（30．4％，14／46），滑车神经受累及较少（4．3％，2／46）。明确诊断后，针对原发病治疗可取得较好效果。结论眼肌麻痹的病因复杂，应仔细分析临床特点，并针对原发病进行积极治疗。     

糖尿病性眼肌麻痹36例临床分析

目的探讨糖尿病性眼肌麻痹的临床特点、治疗方法并观察其疗效。方法回顾对36例糖尿病性眼肌麻痹患者采用中西医结合治疗的方法及疗效。结果治愈率80.55%;好转率13.89%;未愈率5.56%;总有效率为94.44%。结论糖尿病性眼肌麻痹中动眼神经麻痹最多,其次是外展神经,中西医结合治疗对其有显著疗效。     

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.