普拉克索与溴隐亭治疗帕金森病患者疗效及安全性对照研究

目的观察普拉克索与溴隐亭治疗帕金森病的临床效果及安全性。方法选择我院收治的86例帕金森病患者为研究对象,随机分为对照组和观察组,2组均给予美多芭片治疗。观察组加用普拉克索治疗,对照组加用溴隐亭治疗。比较2组的治疗效果及不良反应发生情况。结果观察组治疗后UPDRSⅡ、UPDRSⅢ、UPDRSⅣ显著优于对照组,观察组治疗后HAMD评分显著优于对照组,观察组不良反应发生率显著低于对照组。结论普拉克索联合美多芭治疗帕金森病可显著改善患者运动评分、日常生活评分,可显著改善患者抑郁状况,降低患者不良反应发生率,值得临床推广应用。     

普拉克索添加治疗帕金森病临床随机对照研究

目的 评价新型多巴胺受体激动剂普拉克索联合美多巴与单用美多巴治疗帕金森病(PD)患者的疗效及安全性. 方法 采用随机对照开放式研究,将70例PD患者按照随机数字表法分为普拉克索+美多巴组和美多巴组,每组各35例.治疗12周后判断其疗效及安全性.疗效判定的主要指标为统一PD评定量表第Ⅲ部分(UPDRSⅢ)的运动检查总评分相对患者基线的变化和第Ⅱ部分(UPDRS Ⅱ)的日常生活活动能力总评分相对患者基线的变化;次要指标为第Ⅰ部分(UPDRS Ⅰ)的精神、行为和情感总评分相对患者基线的变化和第Ⅳ部分(UPDRS Ⅳ)的治疗并发症总评分相对患者基线的变化和美多巴药物每日剂量相对基线的变化.安全性指标依据药物的不良反应来判定. 结果 普拉克索+美多巴组患者UPDRS Ⅲ总评分均值与基线相比下降了11.40分,高于美多巴组(9.26分),比较差异有统计学意义(P<0.05);UPDRS Ⅱ总评分均值与基线相比下降了4.57分,高于美多巴组(4.50分),比较差异无统计学意义(P<0.05);UPDRS Ⅰ总评分均值与基线相比下降了0.66分,低于美多巴组(1.14分),差异无统计学意义(P0.05);UPDRS Ⅳ总评分均值与基线相比下降了0.22分,美多巴组则升高了0.06分,差异有统计学意义(P<0.05).与基线相比,治疗后12周普拉克索+美多巴组美多巴的日用量下降了163.57 mg/d,美多巴组升高了8.57 mg/d,差异有统计学意义(P<0.05).普拉克索+美多巴组在治疗后12周发生疗效减退、症状波动、异动症的例数均低于美多巴组,差异有统计学意义(P<0.05).美多巴组出现了明显的疗效减退、症状波动、异动症,而普拉克索+美多巴组无明显的上述症状,但有2例出现突然入睡发作、1例嗜睡、1例直立性低血压. 结论 普拉克索+美多巴组在改善PD运动功能方面优于美多巴组,在日常活动,精神、行为和情绪方面疗效相似.同时服用普拉克索可以明显减少美多巴的用量及其治疗后所引起的并发症(疗效减退、症状波动及异动症)的发生率.普拉克索可引起突然入睡发作、嗜睡、直立性低血压等副作用.     

普拉克索治疗帕金森病运动并发症的临床研究

目的 探讨普拉克索对经复方左旋多巴治疗并且已经出现运动并发症的中晚期帕金森病(PD)患者的疗效和安全性.方法 42例PD患者在原有复方左旋多巴治疗的基础上加用普拉克索1.5～3.0mg/d,为期12周.疗效指标为治疗前后统一PD评定量表(Unified Parkinson's Disease Rating Scale,UPDRS)及汉密尔顿抑郁量表(Hamilton Depression Scale,HAMD)评分,其中UPDBS Ⅰ及HAMD用于评价精神、行为、情绪等非运动症状;UPDRS Ⅱ评价日常生活活动能力;UPDRS Ⅲ、Ⅳ及"开"期和"关"期时间的变化用于评价运动功能,并对患者的临床疗效进行整体评价.安全性指标为不良反应、血压、脉搏、实验室检查、心电图及对认知功能的影响.结果 治疗12周后,UPDRS各项评分均减少,差异具有统计学意义(UPDRS总分:52.05±7.69与39.26±7.64,t=25.378,P＜0.05).UPDRS运动评分改善22.61%,"开"期持续时间增加约1.64 h;复方左旋多巴用最平均减少129.46 mg/d;治疗并发症评分变化均值下降1.45分;HAMD评分均值下降6.14分.不良反应主要有头晕、嗜睡、恶心、便秘、厌食等.结论 普拉克索对运动症状和非运动症状均有较好的疗效,不良反应发生率低,中晚期PD患者加用普拉克索是安全而有效的.     

普拉克索治疗帕金森病运动并发症的临床疗效观察

目的 评估普拉克索治疗帕金森病运动并发症的临床疗效及安全性.方法 收集92例晚期帕金森病患者并随机分为治疗组和对照组,每组46例.对照组给予多巴丝肼治疗,治疗组在对照组的基础上给予普拉克索,疗程均为12周.两组患者于治疗前后分时间点进行统一帕金森病评定量表修正(UPDRSⅣ-)的评分、不良反应的记录,疗程结束后评估疗效.结果 治疗后对照组和治疗组UPDRSⅣ-评分与基线比较均有下降,治疗组下降更显著,两组比较差异有统计学意义(P＜0.01).治疗组第12周剂末现象(93.75％vs 70.59％)、开关现象(91.67％ vs 63.64％)以及异动症(84.62％ vs48.00％)的总有效率优于对照组,差异均有统计学意义(P＜0.05).两组不良反应发生率差异无统计学意义(P＞0.05).结论 普拉克索治疗帕金森病运动并发症有效,安全性好.     

普拉克索治疗帕金森病伴抑郁的临床疗效观察

目的：评价普拉克索治疗帕金森病（PD）伴抑郁的临床疗效。方法：采用随机对照研究,将68例PD伴抑郁患者随机分为对照组、帕罗西汀组和普拉克索组。冶疗12周后评价其疗效,评价指标包括Hamilton抑郁量表（HAM—D）、Zung抑郁自评量表和统一帕金森病评分量表（UPDRS）,观察各量表评分相对于基线值的变化情况。结果：普拉克索组HAM—D和Zung总评分第4周时与基线值相比已有下降趋势,而在第8周时与对照组相比差异有统计学意义（P〈0．05）,其作用与帕罗西汀组相比差异无统计学意义（P〉0．05）,而UPDRS评分均差异无统计学意义（P〉0．05）。结果：普拉克索具有抗抑郁作用,可能在治疗后4～8周时开始发挥比较明显的抗抑郁作用,治疗8周时其抗抑郁作用强度似平接近于帕罗西汀,抗抑郁作用可能小依赖于其对于运动症状的改善。     

普拉克索联合左旋多巴对晚期帕金森病患者临床症状及负性情绪的影响

目的探讨普拉克索联合左旋多巴对晚期帕金森病患者临床症状及负性情绪的影响。方法采用抽签法将我院神经内科收治的125例晚期帕金森病患者进行分组,对照组62例给予左旋多巴治疗,观察组63例给予普拉克索联合左旋多巴治疗,观察比较2组治疗后的临床症状及负性情绪的。结果观察组治疗后改善UPDRS评分优于对照组(P0.05);观察组降低HAMA及HAMD评分优于对照组(P0.05);观察组不良反应发生率为6.35%低于对照组的19.35%(P0.05)。结论普拉克索联合左旋多巴通过兴奋纹状体,恢复多巴胺,以改善晚期帕金森病患者的临床症状及负性情绪效果确切,安全性高,值得临床应用及推广。     

左旋多巴联合普拉克索对帕金森病患者应激反应的影响

目的探讨左旋多巴联合普拉克索对帕金森病患者运动功能调节及机体氧化应激反应的影响。方法选取濮阳市中医院2014-10—2016-09收治的63例帕金森病患者,随机分为对照组31例,观察组32例;对照组予以单一左旋多巴治疗,观察组予以左旋多巴联合普拉克索治疗,观察比较2组运动功能评分(UPDRSⅢ)、氧化应激反应各指标[血浆谷胱甘肽(GSH)、谷胱甘肽过氧化物酶(GSH-Px)、过氧化氢酶(CAT)、超氧化物歧化酶(SOD)]水平及不良反应发生情况。结果治疗后观察组UPDRSⅢ评分低于对照组,GSH、GSH-Px、CAT及SOD水平均高于对照组,差异具有统计学意义(P0.05);观察组不良反应发生率为21.88%(7/32),对照组为19.35%(6/31),差异无统计学意义(P0.05)。结论左旋多巴联合普拉克索治疗可改善帕金森病患者机体氧化应激反应及运动功能,安全性高。     

多巴丝肼联合多巴胺受体激动剂治疗帕金森病的疗效观察

目的：探讨多巴丝肼联合普拉克索治疗帕金森病的临床疗效及安全性。方法60例帕金森病患者根据治疗方式分为观察组及对照组各30例。2组均采用多巴丝肼治疗,观察组加用多巴胺受体普拉克索,连续治疗12周,采用帕金森统一评分量表（UPDRS）对患者治疗效果进行评价,同时观察用药过程中的不良反应。结果观察组 UDPRS各单项评分降低明显,与对照组比较差异有统计学意义（P＜0.05）。2组不良反应差异无统计学意义（P＞0.05）。结论多巴丝肼联合普拉克索治疗帕金森病能明显改善患者的临床症状,值得临床推广。     

金刚烷胺治疗帕金森病异动症的疗效观察

目的探讨金刚烷胺治疗帕金森病(PD)左旋多巴诱导异动症(LID)的临床疗效。方法将42例帕金森病患者随机分为金刚烷胺组与恩托卡朋组,每组21例,每组均应用美多巴和普拉克索作为帕金森病基础治疗。经12 w联合用药治疗后,以统一帕金森病评定量表(UPDRS)各部分评分相对于基线(治疗前评分)的变化为指标评估疗效。同时监测血压,观察患者不良反应,比较两组治疗方案的安全性。结果经12 w治疗后金刚烷胺组UPDRS.IV(治疗的并发症)评分相对基线有显著下降.差异有统计学意义(P<0.05)。金刚烷胺组UPDRS.IV(治疗的并发症)评分较恩托卡朋组评分下降更多,差异有统计学意义(P<0.05)。金刚烷胺组临床总有效率为86%,恩托卡朋组临床总有效率为32%,差异有显著统计学意义(P<0.05)。两组药品不良反应发生率分别为19%和23%。差异无统计学意义(P>0.05)。结论金刚烷胺治疗左旋多巴诱导的帕金森病异动症可获得较显著的近期疗效。     

添加普拉克索治疗对帕金森病患者UPDRS评分及非运动症状的影响分析

目的探讨添加普拉克索治疗对帕金森病患者的统一帕金森病量表(UPDRS)评分及非运动症状的影响,同时观察治疗安全性。方法按照随机数字法分为对照组(71例)和观察组(74例),对照组患者给予复方左旋多巴治疗,观察组患者在使用复方左旋多巴的基础上添加普拉克索治疗,比较两组患者治疗前后UPDRSⅡ、Ⅲ评分及汉密尔顿抑郁量表(HAMD)及简易精神状态检查(MMSE)量表评分,比较两组患者的睡眠障碍,感觉异常,尿频尿急,便秘和流涎等非运动症状改善情况,及治疗后各种不良反应发生率。结果治疗后两组患者UPDRSⅡ、Ⅲ评分明显低于治疗前,且观察组显著优于对照组(P0.05)。治疗后,观察组与对照组相比HAMD评分有明显降低(P0.05),而MMSE评分无明显差异(P0.05)。治疗后,两组患者睡眠障碍、感觉异常和尿频尿急的发生率有明显下降、且观察组低于对照组(P0.05),而便秘和流涎的发生率无明显变化(P0.05)。观察组患者的不良反应发生率为(9.46%),对照组患者的不良反应发生率为(16.90%),两组患者差异明显(P0.05)。结论添加普拉克索治疗帕金森病的疗效明显,能提高PD患者的运动功能和日常生活能力,缓解忧郁、焦虑等不良情绪的发生,同时能有效改善患者的部分非部分运动症状,不良反应发生率较低。     

Pregabalin effect on steady-state pharmacokinetics of carbamazepine, lamotrigine, phenobarbital, phenytoin, topiramate, valproate, and tiagabine

By reducing neuronal excitability through selective binding to the α(2)δ subunit of voltage-dependent calcium channels, pregabalin effectively treats epilepsy, chronic pain, and anxiety disorders. To evaluate if pregabalin coadministration affects pharmacokinetics of other antiepileptic drugs, population pharmacokinetic analyses using NONMEM software were performed on data from three epilepsy trials involving seven antiepileptic drugs with pregabalin as add-on therapy. Results demonstrated that pregabalin did not alter the steady-state plasma concentrations of carbamazepine, lamotrigine, phenobarbital, phenytoin, tiagabine, topiramate, and valproate. Furthermore, the small percent change in the population estimate of antiepileptic drug plasma clearance values (-2% to +7%) suggests that pregabalin coadministration exerted no significant effect on the pharmacokinetics of these antiepileptic drugs, with the possible exception of tiagabine (+34.9%). These findings are in agreement with those of previously published reports. A further clarification study is necessary for tiagabine. In conclusion, it appears that pregabalin can be coadministered with other antiepileptic drugs without concern for significantly altering their pharmacokinetic profiles.     

Mass spectrometric identification of Cu, Zn, Fe, Co, Mn, Mg, and Pb in mammalian brain.

Combining the techniques of thin-layer chromatography (TLC) and mass spectrometry, we unambiguously identified the trace metals Cu, Zn, Fe, Pb, Mn, Co, and Mg in the brain of a female human who had no evidence of any pathologic disease in the central nervous system, and in brains from mouse, rat, guinea pig, and rabbit. These trace metals were also found in anatomic regions of human brain: cortex (gray), cortex (white), caudate nucleus, putamen, hippocampus, and thalamus, and in anatomic regions of rat brain: hypothalamus, cerebellum, stem striatum, and "the rest." The metals were characterized from the color and Rf values of their tetraphenylporphyrin chelates on TLC and from the mass and pattern of molecule ion cluster of the mass spectrum. The unexpected presence of lead in the brain is discussed.     

Alteration of proteins regulating apoptosis, Bcl-2, Bcl-x, Bax, Bak, Bad, ICH-1 and CPP32, in Alzheimer''s disease

Recently, apoptosis has been implicated in the selective neuronal loss of Alzheimer's disease (AD). Apoptosis is regulated by the B cell leukemia-2 gene product (Bcl-2) family (Bcl-2, Bcl-x, Bax, Bak and Bad) and the caspase family (ICH-1 and CPP32), with apoptosis being prevented by Bcl-2 and Bcl-x, and promoted by Bax, Bak, Bad, ICH-1 and CPP32. In the present study, we examined the levels of these proteins in the membranous and cytosolic fractions of temporal cortex in AD and control brain. In the membranous fraction, the levels of Bcl-2, Bcl-x_L, Bcl-x_β, Bak and Bad were increased in AD. In the cytosolic fractions, the level of Bcl-x_β was increased, while Bcl-x_L, Bax, Bak, Bad and ICH-1_L were unchanged. CPP32 was not detected in AD or control brain. These findings demonstrate a differential involvement of cell death-regulatory proteins in AD and suggest that Bak, Bad, Bcl-2 and Bcl-x are upregulated in AD brains.     

Prevalence, knowledge, attitude, and practice of epilepsy in Kerala, South India

PURPOSE: To ascertain the prevalence and pattern of epilepsy and to characterize and quantify knowledge, attitude, and practice (KAP) toward epilepsy among the people of the state of Kerala, which is distinguished from the rest of India by a high level of literacy and health awareness of its population. METHODS: We conducted a door-to-door survey covering the entire population of 238,102 people residing in 43,681 households in a semiurban area of central Kerala. The screening questionnaire administered by medical social workers had a sensitivity of 100% for identifying persons with epilepsy. Neurologists examined all the individuals suspected of having epilepsy. We evaluated KAP toward epilepsy among 1,118 subjects (439 males and 679 females; mean age, 33.3 years; age range, 15-85 years) from households without epilepsy in the study area. RESULTS: Through a three-phased survey, we ascertained 1,175 cases (616 males and 559 females) with active epilepsy, providing a crude point prevalence ratio of 4.9 cases per 1,000 people and an age-adjusted prevalence ratio of 4.7 cases per 1,000 population. The highest age-specific prevalence rate of 6.5 per 1,000 occurred in the 10- to 19-year-old age group. Sex-specific prevalence rates did not significantly differ. The proportion of generalized and localization-related epilepsies was 58.8% and 30.6%, respectively. Ninety-nine percent of the KAP respondents had read or heard about epilepsy. Thirty-one percent and 27% thought epilepsy was a hereditary disorder and a form of insanity, respectively. About 40% of the respondents felt that individuals with epilepsy could not be properly educated or employed. Eleven percent would object to their children having contact with epileptic children. CONCLUSIONS: The prevalence and pattern of epilepsy in central Kerala, South India, do not differ from that of developed countries. Although the awareness of epilepsy among the people of Kerala was comparable to that of developed countries, the attitudes were much more negative. The need for educating the people of Kerala on epilepsy and for incorporating an adequate knowledge of epilepsy in the school curricula cannot be overemphasized.     

Consecutive Gas Chromatographic Determination of Phenytoin, Phenobarbital, Primidone, Phenylethylmalondiamide, Carbamazepine, Trimethadione, Dimethadione, Ethosuximide, and Valproate from the Same Serum Specimen

A quantitative gas-liquid chromatographic procedure is described for the consecutive determination of phenytoin, phenobarbital, primidone, phenylethylmalondiamide, carbamazepine, trimethadione, dimethadione, ethosuximide and valproate from a single serum specimen of 1.2 ml. After extraction from serum by two different procedures, the anticonvulsants are chromatographed without further purification on a 3% OV 17 column either with or without derivative formation by means of "on-column" methylation. Multiple internal standards are employed in order to enhance the reproducibility of drug-concentration measurement.     

中国汉族人群SCA1、2、3、6、7、8、10、12、17亚型和齿状核-红核-苍白球-路易体萎缩亚型频率分布

目的 研究中国汉族人群中脊髓小脑性共济失调(SCAs)不同基因亚型的频率分布.方法 运用聚合酶链反应、变性聚丙烯酰胺凝胶电泳、Southern blot、T载体克隆重组DNA技术结合直接测序等技术对559例临床诊断为SCA的患者(363例常染色体显性遗传先证者,196例散发患者)进行了SCA1、SCA2、SCA3/MJD、SCA6、SCA7、SCA8、SCA10、SCA12、SCA17和齿状核-红核-苍白球-路易体萎缩(DRPLA)致病基因多核苷酸病理重复突变检测分析.结果 在363个常染色体显性遗传的SCA(AD-SCA)家系中,发现有15个SCA1家系(4.13%),26个SCA2家系(7.16%),187个SCA3/MJD家系(51.52%),6个SCA6家系(1.65%),7个SCA7家系(1.93%),1个SCA12家系(0.28%)和1个SCA17家系(0.28%),120个SCA家系未明确基因分型(33.06%);在196例散发SCA患者中,发现有2例SCAI患者(1.02%),3例SCA2患者(1.53%),15例SCA3/MJD患者(7.65%),3例SCA6患者(1.53%),173例SCA患者未明确基因分型(88.27%);未发现SCA8、SCA10和DRPLA型患者.结论 在中国汉族人群中SCA3/MJD为最常见的SCA亚型,其次为SCA2、SCA1、SCA7和SCA6,SCA12和SCA17比较少见,SCA8、SCA10和DRPLA罕见,SCA17亚型为国内首次报道.部分AD-SCA家系存在其他致病基因的作用,大部分散发SCA患者除遗传因素外还存在其他致病因素.