哌甲酯控释片联合认知行为治疗对儿童注意缺陷多动障碍疗效的对照研究

目的:探讨哌甲酯控释片联合认知行为治疗(CBT)对儿童注意缺陷多动障碍(ADHD)的疗效。方法:41例ADHD患者被随机分为研究组21例和对照组20例,两组均给予哌甲酯控释片口服12周。在此基础上,研究组联合每周1次的CBT,共12次。分别在基线、治疗后4、8、12周末对患者进行焦虑自评量表(SAS)、Conners简明症状问卷(ASQ)、ADHD筛查量表(SNAP-IV)-父母版的评估。结果:治疗后两组SNAP-IV总分、注意力因子分、多动冲动因子分均较基线显著下降(F=125.14,70.58,126.44;P均0.001);两组比较,研究组明显低于对照组(F=42.18,32.72,43.75;P均0.01)。治疗后各时间点两组SAS及ASQ评分均较基线时显著下降(P均0.01);治疗12周时研究组SAS评分及ASQ评分均显著低于对照组(P均0.01)。结论:哌甲酯控释片联合CBT较单一哌甲酯控释片能更有效地改善ADHD症状。     

二十二碳六烯酸对注意缺陷多动障碍儿童临床疗效、血清胶质源性神经营养因子及炎症因子水平的影响

目的:研究二十二碳六烯酸(DHA)对注意缺陷多动障碍(ADHD)儿童临床疗效、血清中胶质源性神经营养因子(GDNF)及炎症因子水平的影响。方法:118例ADHD儿童随机分为研究组(60例)与对照组(58例)。研究组给予盐酸哌甲酯与DHA 300 mg/d,对照组给予盐酸哌甲酯与空白安慰剂,治疗8周。在基线及治疗8周后,采用注意缺陷多动障碍SNAP-IV评定量表(中文版)(SNAP-IV)、美国康纳简易多动症行为评价量表(Conner)评估ADHD儿童病情,记录不良反应;检测两组DHA、GDNF、白介素(IL)-1β、IL-6、肿瘤坏死因子α(TNF-α)水平。结果:8周治疗后,两组SNAP-IV总分、注意缺陷分、Conner学习、心身、多动指数评分下降幅度差异具有统计学意义(P<0.05或P<0.01)。研究组DHA、GDNF水平显著高于对照组及治疗前,而IL-6、TNF-α水平显著低于对照组及治疗前(P<0.05或P<0.01)。研究组ΔDHA与ΔSNAP-IV总分呈负相关;ΔGDNF与ΔTNF-α、Δ注意缺陷分及Δ多动/冲动分呈负相关(P均<0.05)...     

脑电反馈治疗儿童注意缺陷多动障碍的对照研究

目的探讨脑电反馈治疗注意缺陷多动障碍(ADHD)的有效性及特点.方法将符合美国精神障碍诊断与统计手册第3版修订本标准的57例ADHD患儿,按就诊序号的奇偶数分为脑电反馈治疗(反馈组,28例)和哌甲酯(以下简称利他林)治疗(利他林组,29例),疗程为3～4个月,随访1～3个月;采用行为问卷、副作用量表、韦氏智力测查、注意变量检测(TOVA)、定量脑电图等工具于治疗前、中、后及随访时进行疗效评定.结果经过治疗两组行为问卷评分均明显减少(P＜0.05).其中利他林组减分更多,但停药后分值上升;反馈组为持续减分(治疗前、后及随访时的多动指数,利他林组分别为16.14±4.64,4.23±1.45,13.52±5.08;反馈组分别为16.04±6.31,9.26±3.09,8.76±3.79.TOVA亦有类似改变.利他林组的副作用出现率高(82%),而反馈组未发现明显副反应.随访时反馈组韦氏智测中C因子分增加[治疗前为(93.7±13.3)分,随访时为(106.3±14.1)分,P＜0.01],额区和右侧半球α波增多,δ波减少;利他林组尚无此现象.结论脑电反馈治疗ADHD的疗效肯定,与利他林治疗相比,虽起效较慢但作用相对持久,且无副作用,停止治疗后病情继续好转.     

盐酸哌甲酯控释片联合生物反馈治疗注意缺陷多动障碍患儿对临床症状、脑电θ/β比值的影响

目的:探讨盐酸哌甲酯控释片联合生物反馈治疗注意缺陷多动障碍(ADHD)患儿对临床症状、脑电慢波(θ)/快波(β)比值的影响.方法:选取在我院诊治的ADHD患儿86例作为研究对象,以随机数字表法简单随机分组为对照组与研究组各43例,对照组给予脑电生物反馈治疗,研究组在同样治疗的基础上加予盐酸哌甲酯控释片.采用中文版注意缺...     

感觉统合训练与匹莫林治疗注意缺陷多动障碍患儿的对照研究

目的　探讨感觉统合训练治疗注意缺陷多动障碍的疗效及其可能的机制。方法　将1 2 6例注意缺陷多动障碍患儿按就诊顺序编号分为两组 ,奇数者为感觉统合训练 (训练组 ,63例 ) ,不应用任何药物 ;偶数者为匹莫林 [平均日剂量 (2 8 1± 9 3)mg]治疗 (匹莫林组 ,63例 ) ,开放治疗 1 2周。于治疗前和治疗后第 2 ,4,8,1 2周末进行Conners多动指数和儿童感觉统合能力评定 ,1 2周末用临床总体印象量表 (CGI)评定总体疗效。结果　治疗前训练组和匹莫林组多动指数分别为 (1 8 2± 4 3)分和 (1 8 3± 4 5)分 ,治疗后下降值为 (8 5± 4 9)分和 (8 9± 4 7)分 ,两组疗效近似 (P >0 0 5)。训练组和匹莫林组感觉统合能力增加值分别为 :前庭功能 (7 8± 6 6)分和 (0 9± 3 6)分 ,触觉防御 (8 5±7 6)分和 (0 6± 3 0 )分 ,本体感 (8 4± 8 8)分和 (0 5± 2 2 )分 ,学习能力 (6 4± 4 6)分和 (3 2± 2 5)分 ,前者显著优于后者 (P <0 0 1 )。训练组的多动指数下降值与感觉统合能力增加值均呈显著正相关(r>0 99,P <0 0 0 1 )。结论　感觉统合训练可通过纠正患儿的感觉统合能力低下而改善注意缺陷多动障碍的症状 ,疗效与匹莫林相当。     

重复经颅磁刺激对注意缺陷多动障碍儿童临床症状及血清脑源性神经营养因子的影响

目的:探讨高频重复经颅磁刺激(rTMS)对注意缺陷多动障碍(ADHD)儿童临床症状及血清脑源性神经营养因子(BDNF)水平的影响.方法:30例ADHD患儿随机分为真、伪刺激组;两组在接受盐酸哌甲酯控释片(18 mg/d)治疗的同时分别给予真、伪高频(10 Hz)rTMS治疗4周,刺激部位为右侧前额叶皮质;治疗前后采用中...     

电针与氟西汀治疗抑郁症疗效的对照研究

目的　对比电针与氟西汀治疗抑郁症的疗效。方法　将 95例抑郁症患者随机分为电针组 ( 31例 )、氟西汀组 ( 32例 )及安慰剂组 ( 32例 )。电针组采用智能电针仪治疗 ,用抗抑郁波型 ,以毫针针刺百会、印堂穴 ,强度 2～ 3V ,4 5min/次 ,1次 /d ,每周 5次 ,同时服安慰剂 ;氟西汀组予氟西汀胶囊 2 0mg/d ,并接受模拟电针 ;安慰剂组用安慰剂并接受模拟电针 ;疗程 6周。于治疗前及治疗中每 2周评定 1次汉密尔顿抑郁量表 (HAMD)、Asberg抗抑郁药副作用量表、抑郁自评量表 (SDS)、临床总体印象量表 (CGI)。结果　治疗第 6周末 ,电针组的HAMD总分 [( 10 19± 5 88)分 ]低于安慰剂组[( 13 88± 8 2 9)分 ;P <0 0 5 ],SDS评分 [( 5 3 0 2± 9 6 7)分 ]亦低于安慰剂组 [( 6 0 0 0± 12 89)分 ;P <0 0 5 ];安慰剂组CGI中的病情严重程度 [( 3 16± 1 32 )分 ]重于电针组 [( 2 4 2± 1 0 3)分 ]和氟西汀组[( 2 5 6± 1 13)分 ;P <0 0 5 ],总体进步分 [( 2 84± 1 2 7)分 ]低于电针组 [( 2 10± 0 94 )分 ;P <0 0 1]和氟西汀组 [( 2 2 5± 1 0 8)分 ;P <0 0 5 ];电针组与氟西汀组各项评分的差异均无显著性。三组Asberg量表评分差异无显著性。结论　电针与氟西汀治疗重性抑郁症的疗效基本相同     

托莫西汀治疗儿童注意力缺陷多动障碍研究进展

为探讨托莫西汀对儿童注意力缺陷多动障碍(ADHD)的疗效,本文对托莫西汀治疗儿童ADHD的研究进行综述。通过阐述ADHD发病机制和治疗方案,总结托莫西汀治疗儿童ADHD的效果和安全性,并与哌甲酯、安慰剂治疗的效果进行比较,为ADHD临床治疗提供参考。     

哌甲酯治疗注意缺陷多动障碍疗效影响因素

目的分析临床特征对哌甲酯治疗注意缺陷多动障碍(attention deficit hyperactivity disorder,ADHD)患儿疗效的影响。方法对110例ADHD汉族患儿给予哌甲酯速释剂型6周滴定治疗。以ADHD症状分级父母评量表(ADHD rating scale-IV home version,ADHD-RS-IV)为临床疗效指标,持续操作测验(continuous performance task,CPT)各单项T分为认知功能疗效指标,对可能影响疗效的人口学资料、基线临床特征和认知因素进行分析。结果临床疗效指标治疗有效65例(59.1%),无效45例(40.9%)。87例患儿接受CPT测验,错误数单项有效35例(40.2%),漏报数单项有效31例(35.6%),反应时间单项有效10例(11.5%)。logistic回归提示父母关系好(OR=3.516,95%CI:1.087~11.375)和基线ADHD-RS-IV量表分高于35分(OR=3.075,95%CI:1.131~8.359)是临床疗效指标治疗有效的预测因素(P0.05)。智商分较高是认知功能指标CPT错误数T分(OR=1.085,95%CI:1.013~1.162)和漏报数T分(OR=1.078,95%CI:1.008~1.153)有效的预测因素(P0.05)。结论治疗前临床症状严重和CPT测验结果差、父母关系好、智商较高的患者有可能哌甲酯治疗效果更好。     

卡马西平联用盐酸哌甲酯控释片治疗小儿癫痫合并注意缺陷多动障碍的疗效观察

目的探讨卡马西平联合盐酸哌甲酯控释片治疗小儿良性癫痫(benign epilepsy with centro-temporal spikes.BECTS)伴中央颞区棘波合并注意缺陷多动障碍(attention deficit hyperactivity disorder.ADHD)的临床疗效。方法选择2011年1月至2016年1月于本院精神内科治疗且确诊BECTS伴ADHD的患儿80例作为研究对象,首先采用卡马西平单药治疗,若6个月内复查脑电图稳定,联用盐酸哌甲酯控释片进行继续治疗。观察盐酸哌甲酯控释片治疗前后患儿注意力和行为改善情况、癫痫发作情况、不良反应和治疗效果。结果卡马西平治疗3个月后有效的56例患儿联合盐酸哌甲酯治疗6个月治疗后,ADHD治疗总有效率为92.73%(51/55),且与联合治疗前相比,Conner儿童行为的问卷评分显著降低。1例(1.82%)患儿在治疗2个月后癫痫发作频率和EEG异常放电频率增加,停药后即未发作,停药4周后再服药,未再出现癫痫发作增加现象。结论卡马西平联用盐酸哌甲酯控释片能够有效的控制BECTS伴ADHD患儿的临床症状,明显改善患儿的注意力及其社会功能,且具有一定的临床安全性。     

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.     

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.     

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.     

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.     

Plant inhibitors of serine proteinases: Hageman factor fragment, kallikreins, plasmin, thrombin, factor Xa, trypsin, and chymotrypsin

Numerous plants were tested for inhibitors of human Hageman factor fragment (HF_f), plasma kallikrein, urinary kallikrein, plasmin, thrombin, porcine pancreatic kallikrein, and bovine Factor X_a, trypsin, and chymotrypsin. Pumpkin seeds and iris bulbs contain trypsin inhibitors which specifically inhibit HF_f. Flower bulbs—especially those of tulip, lily, hyacinth, and calla—are hitherto unrecognized rich sources of inhibitors with different inhibitory spectrums and physicochemical properties.     

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.