2型糖尿病患者合并周围神经病变相关危险因素分析

目的 探讨2型糖尿病周围神经病变的相关危险因素.方法 选取2型糖尿病（DM）患者114例为研究对象,根据有无合并周围神经病变将其分为糖尿病周围神经病变组（DPN组）和非糖尿病周围神经病变组（NDPN组）.分析患者临床资料,探讨2型糖尿病周围神经病变相关因素.结果 （1） DPN组与NDPN组病患年龄、病程、FPG、2hPG、HbA1C、尿 A/C 差异均有统计学意义（P〈0.05）.（2）Logistic分析显示糖尿病病程、年龄、糖化血红蛋白（HbA1C）是糖尿病周围神经病变的独立危险因素.结论 糖尿病病程、年龄、空腹血糖、餐后 2 h血糖、糖化血红蛋白等是 2 型糖尿病并周围神经病变的相关危险因素.其中年龄大、病程长、高HbA1C的糖尿病患者发生 DPN 的风险增加.提示临床医生应在糖尿病早期对DPN和相关危险因素进行预防和干预.     

2型糖尿病周围神经病变患者血清miR-155水平变化及相关研究

目的探究血清miR-155在2型糖尿病周围神经病变(DPN)患者的表达变化及其意义。方法收集160例2型糖尿病(T2DM)患者的临床资料,根据是否合并DPN,将其分为T2DM不伴周围神经病变(NDPN)组86例和DPN组74例。进行多伦多临床评分系统(TCSS)评估,检测血清生化指标、miR-155、TNF-α和IL-1β水平用于比较分析。采用Logistic回归分析T2DM患者发生DPN的危险因素,绘制ROC曲线进行分析。结果 DPN组患者年龄、体重指数、空腹血糖、糖化血红蛋白、糖尿病病程、低密度脂蛋白、TCSS评分和血清miR-155水平较NDPN组均明显升高(均P0.05)。血清miR-155与TCSS评分呈正相关(r=0.603,P0.01)。多因素Logistic回归分析显示,年龄、糖化血红蛋白、糖尿病病程、TCSS评分和血清miR-155均为DPN危险因素(均P0.05)。血清miR-155的ROC曲线下面积0.836,敏感性88.9%,特异性82.5%。联合年龄、糖化血红蛋白、糖尿病病程、TCSS评分和血清miR-155构建的ROC曲线曲线下面积0.912,灵敏性95.6%,特异性89.6%。DPN组血清miR-155分别与TNF-α和IL-1β呈正相关(r=0.675,r=0.701;均P0.01)。结论DPN患者血清miR-155水平表达异常,可用于辅助DPN患者临床病情评估和诊断,在DPN的炎性机制中发挥重要作用。     

糖尿病患者周围神经传导速度的研究

目的:通过周围神经传导速度(NCV)的研究,早期诊断糖尿病(DM)患者的糖尿病性周围神经病变。方法:应用上海海军医学研究所NDI-200F神经电检诊仪,对DM组95例患者行尺神经、正中神经、胫神经和腓神经运动传导速度(MCV)及尺神经、正中神经、腓肠神经感觉传导速度(SCV)检测与30例健康人组对照。结果:DM组95例, NCV异常率为77.89%(74/95)。共检测665条神经,MCV380条,异常率55.26%,SCV285条,异常率50.88%,差异无显著性意义(P>0.05)。上肢检测380条神经,异常率45.53%,下肢检测285条神经,异常率63.86%,差异有显著性意义(P<0.05)。DM组SCV波幅减低率为53.66%。DM组按病程分为三组,<5年,30例,异常率28.10%;≥5年,31 例,异常率为54.84%;≥10年,34例,异常率74.37%,组间差异均有非常显著性意义(P<0.01)。DM组中29例无周围神经病变症状与体征,NCV异常11例(37.93%)。结论:周围神经传导速度检测不但可以早期诊断糖尿病患者的糖尿病性周围神经病变,而且此方法可靠、简便、无创。     

Hcy和Cys-C水平与糖尿病周围神经病变的相关性研究

目的 探讨2型糖尿病(T2DM)周围神经病变患者血浆同型半胱氨酸(Hcy)、胱抑素C(Cys-C)的水平变化及其意义。方法 选取2016年1月～2016年12月本院确诊的T2DM周围神经病变患者88例(DPN组),另选88例年龄、性别与之匹配的单纯T2DM患者(对照组),检测并比较2组的血浆Hcy、Cys-C的水平,采用非条件Logistic回归分析T2DM患者并发周围神经病变的危险因素。结果 DPN组的糖尿病病程、HbA1c测定值均高于对照组(P<0.05); DPN组的HDL-C水平低于对照组(P<0.05); DPN组的血浆Hcy、Cys-C的水平均高于对照组(P<0.05); 糖尿病患者并发周围神经病变的危险因素为糖尿病病程(OR=1.829)、HbA1c(OR=1.558)、Hcy(OR=1.629)、Cys-C(OR=1.733)(P<0.05)。结论 血浆Hcy、Cys-C高水平是糖尿病患者并发周围神经病变的独立危险因素。     

分析2型糖尿病周围神经病变的临床危险因素

目的 分析2型糖尿病周围神经病变的临床危险因素.方法 回顾性分析我院2015-03—2016-03收治的268例2型糖尿病患者,按其病情分为2型糖尿病合并周围神经病变组(n=159)和2型糖尿病非合并周围神经病变组(n=109),对比2组患者各项指标.结果 单因素分析显示,合并周围神经病变组患者的年龄、病程、空腹血糖值、餐后2h血糖值、糖化血红蛋白值、尿白蛋白和肌酐比值等指标均高于非合并周围神经病变组,2组患者2 h胰岛素对比有明显差异(P<0.05);2组患者在性别、体重指数、收缩压、舒张压、空腹胰岛素、甘油三酯、低密度脂蛋白、高密度脂蛋白和总胆固醇等方面比较无显著差异(P>0.05).以患者是否发生周围神经病变为应变量,以单因素对比存在明显差异的指标为自变量,多元回顾性分析结果显示,病程长短、尿白蛋白与肌酐比值和糖化血红蛋白是2型糖尿病周围神经病变的危险因素.结论 2型糖尿病周围神经病变的危险因素为病程长短、尿白蛋白与肌酐比值、糖化血红蛋白,应对上述危险因素进行积极有效的预防.     

2型糖尿病患者肌电图临床分析

目的探讨肌电图对糖尿病患者周围神经测试的临床价值及周围神经病变的影响因素。方法对我院门诊和住院的140例2型糖尿病患者采用肌电图仪对腓总神经、腓浅神经进行测定,结合临床资料分析病史、血糖、糖化血红蛋白(HbA1c)与周围神经病变的关系。结果肌电图测试结果与临床症状相符,具有神经症状的糖尿病患者轻收缩峰电压明显高于无神经症状的糖尿病患者,轻收缩峰平均时限延长,多相电位比数增大,病程长,血糖控制不佳,差异有统计学意义(P<0.05)。结论随着病程延长,周围神经传导速度下降,控制空腹血糖及HbA1c有助于延缓周围神经病变的进展。肌电图检测适用于临床检测糖尿病患者的神经功能。     

2型糖尿病认知障碍的相关因素分析

目的 探讨2型糖尿病(T2DM)认知障碍(CI)的相关因素,为其预防措施的制定提供依据.方法 对229例T2DM患者行蒙特利尔认知量表(MOCA)评估,采集年龄、DM病程等临床指标,分别进行单因素和多因素Logistic回归分析,筛选CI的相关因素.结果 MOCA总分＜26分者64例(CI组),MOCA总分≥26分者165例(非CI组).CI组应用胰岛素增敏剂(INS)治疗,坚持运动锻炼的构成比低于非CI组,而合并糖尿病周围神经病变(DPN)、糖尿病肾病(DN)的构成比以及DM病程、空腹血糖(FPG)、餐后2 h血糖(2hPG)、糖化血红蛋白(HbA1C)水平高于非CI组.多因素分析入选Logistic回归模型的变量是:DM病程(OR=1.335,95CI%:1.178-1.514),HbA1C(OR=2.373,95CI%:1.753-3.214),INS治疗(OR=0.242,95CI%:0.088-0.660),坚持运动锻炼(OR=0.308,95CI%:0.130-0.728).结论 DM病程,HbA1C是导致T2DM患者CI的危险因素,INS治疗和坚持运动锻炼是保护因素.严格控制血糖、改善胰岛素抵抗(IR)和体育锻炼是防治CI的重要措施.     

114例糖尿病患者神经电生理特征与相关因素分析

目的观察糖尿病患者神经电生理特征,分析糖尿病周围神经病变的相关危险因素。方法对114例糖尿病患者进行神经传导检测,并对糖尿病周围神经病变组(DPN)及神经传导正常(NDPN)组年龄、病程、空腹血糖(FBG)、糖化血红蛋白(HbA1c)、低密度脂蛋白胆固醇(LDL-C)、血压及血同型半胱胺酸等进行分析。结果 114例2型糖尿病患者中94例出现周围神经病变,20例神经传导正常,总异常率82.5%。其中运动神经纤维受损:正中神经纤维异常率右侧31%,左侧19%;尺神经纤维异常率右侧9%,左侧9%;胫后神经纤维异常率右侧16%,左侧23%;腓总神经纤维异常率右侧28%,左侧29%。感觉神经纤维受损:正中神经纤维异常率右侧63%,左侧49%;尺神经纤维异常率右侧26%,左侧27%;胫后神经纤维异常率右侧70%,左侧67%;腓浅神经纤维异常率右侧67%,左侧61%;腓肠神经异常率右侧50%,左侧47%。DPN组较NDPN组病程更长,血HbA1c、FBG、LDL-C、同型半胱胺酸更高,差异均有统计学意义(P0.05)。结论糖尿病周围神经病变以感觉纤维受损为主,下肢重于上肢,病程、FBG、HbA1c、LDL-C、同型半胱胺酸等为糖尿病周围神经病变的危险因素。     

皮肤交感反应与2型糖尿病自主神经病变相关性研究

目的 探讨皮肤交感反应(sympathetic skin response,SSR)对2型糖尿病自主神经病变的诊断价值.方法 对111例2型糖尿病患者及30例健康体检者进行SSR及神经传导速度测定,检测糖化血红蛋白(hemoglobin A1c,HbAlc)等多项生化指标,同时分析与SSR异常有关的因素.结果 与对照组比较,病例组SSR潜伏期延长,波幅降低(P＜0.05).与病程＜5年组比较,5～10年组、病程≥10年组上肢SSR潜伏期延长(P＜0.05),而波幅变化无统计学差异(P＞0.05).各不同病程组间SSR异常率比较无统计学差异(P＞0.05).周围神经病变组SSR异常率高于无周围神经病变组(P＜0.05),自主神经症状的有无对SSR异常率无影响(P＞0.05).Logistic回归分析结果显示,HbAlc是2型糖尿病患者SSR异常的相关因素.结论 SSR可早期发现糖尿病患者自主神经功能损害,HbAlc是2型糖尿病患者SSR异常的相关因素.     

2型糖尿病患者视觉诱发电位改变及其相关因素分析

目的探讨2型糖尿病患者视觉诱发电位(pattern visual evoked potential,P-VEP)改变的特点及其与各临床因素之间的关系。方法对109例2型糖尿病患者及40例健康体检者进行P-VEP的检测,病例组按病程分为病程<5年组、5年≤病程<10年组、病程≥10年组。回顾性分析各组生化指标、肌电图等临床资料与P-VEP改变的相关性。应用SPSS统计软件进行统计学处理。结果病例组P-VEP总异常率为27.52%,病程<5年组P-VEP异常8例(20.00%),5年≤病程<10年组P-VEP异常8例(25.81%),病程≥10年组P-VEP异常14例(36.84%),各组间其异常率比较差异无统计学意义(P>0.05)。P100潜伏期的改变:病程≥10年组的P100潜伏期较对照组明显延长(P<0.05),病程<5年组、5年≤病程<10年组的P100潜伏期较对照组无明显变化(P>0.05)。P100枕中波幅改变:5年≤病程<10年组,病程≥10年组的枕中波幅较对照组明显降低(P<0.05),病程<5年组的枕中波幅较对照组无明显变化(P>0.05)。周围神经病变严重组(病变神经数>4条)的枕中波幅较周围神经病变较轻组(病变神经数≤4条)明显降低(P<0.05)。非条件Logistic逐步回归分析显示病程和糖化血红蛋白是2型糖尿病患者视力损害的相关因素。结论 P-VEP是早期发现2型糖尿病患者视神经病变的无创检测手段。病程和糖化血红蛋白是2型糖尿病患者视神经病变的相关因素。     

Denervation study of synapses of organ of corti of old world monkeys

Fine structural characteristics of synapses in the spiral organ of Corti were examined, with reference to differences between inner and outer haircell systems, and to location of neurons of origin of efferent axons. Surgical interruption of crossed olivocochlear bundle, of vestibular nerve, of facial nerve, and excision of superior cervical ganglia were used to determine the pathways of efferent axons. Interruption of the vestibular nerve near the brainstem results in degeneration of all efferent terminals on outer hair cells. Mid-line lesions at, and caudal to, the facial colliculus result in degeneration of about half of these efferent terminals. Efferent synaptic bulbs to the inner hair-cell system are small, of the order of one micron, and form type 2 junctions with afferent dendrites. They tend to have more large dense-core vesicles (about 80 nm) than the large efferent terminals of the outer hair-cell system, and appear to be the terminals of axons in the habenula perforata, which exhibit varicosities laden with large dense core vesicles. The varicosities are unaffected by excision of the superior cervical ganglia. So far as our material can reveal, it appears that the varicosities in the habenula perforata do not survive vestibular root interruption, nor do the efferent processes in the internal spiral bundle or at the base of inner hair cells. Most interestingly, the afferent processes of the inner hair-cell system, as identified for example by their relation to pre-synaptic bodies in the inner hair cells, are subject to a trans-synaptic reaction after severance of the vestibular root. They undergo a dramatic cytological transformation, characterized by increase of volume, engorgement with microtubules, microfilaments, microvesicles of various sizes, and clusters of lysosomes. Thus, both the efferent and afferent terminals of the inner hair-cell system show marked cytological differences from the corresponding terminals of the outer hair cell system.     

Mechanism of action of tubocurarine on nicotinic cholinoreceptors of neurons of the sympathetic ganglia of rats

Tubocurarine (Tc) effect on membrane currents elicited by acetylcholine (ACh) was studied in isolated superior cervical ganglion neurons of rat using patch-clamp method in the whole-cell recording mode. The "use-dependent" block of ACh current by Tc was revealed in the experiments with ACh applications, indicating that Tc blocked the channels opened by ACh. Mean lifetime of Tc-open channel complex, tau, was found to be 9.8 +/- 0.5 s (n = 7) at -50 mV and 20-24 degrees C. tau exponentially increased with membrane hyperpolarization (e-fold change in tau corresponded to the membrane potential shift by 61 mV). Inhibition of the ACh-induced current by Tc (3-30 microM/1) was completely abolished by membrane depolarization to the level of 80-100 mV. Inhibition of ACh-induced current was augmented at increased ACh doses. It is concluded that the open channel block produced by Tc is likely to be the only mechanism for Tc action on nicotinic acetylcholine receptors in superior cervical ganglion neurons of rat.     

The effect of age of onset of PD on risk of dementia

Background Dementia occurs in the majority of patients with Parkinson’s disease (PD). Late onset of PD has been reported to be associated with a higher risk for dementia. However, age at onset (AAO) and age at baseline assessment are often correlated. The aim of this study was to explore whether AAO of PD symptoms is a risk factor for dementia independent of the general effect of age. Methods Two community-based studies of PD in New York (n = 281) and Rogaland county, Norway (n = 227) and two population-based groups of healthy elderly from New York (n = 180) and Odense, Denmark (n = 2414) were followed prospectively for 3–4 years and assessed for dementia according to DSM-IIIR. All PD and control cases underwent neurological examination and were followed with neurological and neuropsychological assessments. We used Cox proportional hazards regression based on three different time scales to explore the effect of AAO of PD on risk of dementia, adjusting for age at baseline and other demographic and clinical variables. Findings In both PD groups and in the pooled analyses, there was a significant effect of age at baseline assessment on the time to develop dementia, but there was no effect of AAO independent of age itself. Consistent with these results, there was no increased relative effect of age on the time to develop dementia in PD cases compared with controls. Interpretation This study shows that it is the general effect of age, rather than AAO that is associated with incident dementia in subjects with PD. Received in revised form: 22 December 2005     

Limits of deinstitutionalization--perspectives of relatives of psychiatric patients

After a hopeful beginning, the social process of the reintegration of those with severe mental illness has come to a standstill. I am led to wonder whether "the community" really wants to live together with people suffering from severe mental illness, and if so, how closely? As long as the medical treatment of mental illness provided by the general practitioners is fundamentally deficient, as they are not able to prescribe the necessary interventions--such as out-patient psychiatric nursing, and service providers in the out-patient sector are content with offering increasingly intensive forms of care for the less seriously ill at the cost of the Social Welfare System--the reintegration of those with serious mental illness remains an illusion--which is mainly to the benefit of providers of residential care in homes and hostels.     

Summary of Legislation of 1933 of interest to the Department of Mental Hygiene

Psychiatric Quarterly -