丙戊酸镁缓释片与碳酸锂治疗躁狂发作的临床对照研究

目的评价丙戊酸镁缓释片与碳酸锂治疗躁狂发作的临床疗效和不良反应。方法随机对60例躁狂发作患者分别给予丙戊酸镁释片与碳酸锂治疗,疗程6周。结果丙戊酸镁缓释片与碳酸锂治疗躁狂发作疗效相近,前者起效快,且不良反应显著低于后者,患者耐受性好。结论丙戊酸镁缓释片治疗躁狂发作疗效肯定,起效快,不良反应小,治疗安全性高,可作为治疗躁狂发作的首选药物。     

丙戊酸镁缓释片联合赛乐特片治疗脑卒中后抑郁

目的探讨丙戊酸镁缓释片辅助治疗脑卒中后抑郁的疗效。方法筛选出卒中后抑郁患者86例,随机分为治疗组(丙戊酸镁缓释片)和对照组各43例,治疗组:用丙戊酸镁缓释剂500mg/d,连用14d;赛乐特片20mg,每天早饭后顿服。对照组:单服赛乐特片20mg,每天早饭后顿服,对症处理(抗血小板聚集、改善循环、稳压、降糖)2组相同。结果丙戊酸镁缓释片组在治疗后6d,汉密尔顿(HAMD)抑郁量表评分开始下降,与治疗前比较差异有统计学意义(P<0.01);对照组在治疗后9d,HAMD评分开始下降,与治疗前比较差异有统计学意义(P<0.01)。2组疗效比较丙戊酸镁缓释片组有效率93.02%,对照组有效率79.07%,差异有统计学意义(P<0.01)。结论丙戊酸镁缓释片辅助抗抑郁药治疗卒中后抑郁效果更佳,起效时间早,不良反应少,故临床应用丙戊酸镁缓释片辅助治疗抑郁症,患者耐受性好,可以缩短病程,改善抑郁症状,解除患者病痛,效果令人满意。     

丙戊酸镁缓释片治疗精神分裂症的辅助作用

目的:探讨阿立哌唑合用丙戊酸镁缓释片治疗难治性精神分裂症患者的疗效及安全性。方法:60例难治性精神分裂症患者随机分为两组,分别给予阿立哌唑合用丙戊酸镁缓释片与阿立哌唑单用治疗,疗程8周。用阳性与阴性症状量表(PANSS)和治疗中出现的症状量表(TESS)评定疗效和不良反应。结果:阿立哌唑合用丙戊酸镁缓释片治疗难治性精神分裂症的疗效优于单用阿立哌唑(P<0.05);两组不良反应差异无统计学意义(P>0.05)。结论:阿立哌唑合用丙戊酸镁缓释片治疗难治性精神分裂症疗效好,安全性好。     

丙戊酸镁缓释片联合奥氮平治疗阿尔茨海默病的疗效观察

目的探讨丙戊酸镁缓释片联合奥氮平治疗阿尔茨海默病的临床疗效。方法阿尔茨海默病患者56例,随机分为观察组和对照组各28例,对照组给予奥氮平片治疗,观察组在对照组基础上加用丙戊酸镁缓释片,观察治疗前后患者BRMS评分和用药不良反应。结果治疗后2组不同时间BRMS评分均低于治疗前,差异具有统计学意义(P0.05);观察组治疗后1~4周末BRMS评分下降均优于对照组,差异具有统计学意义(P0.05);2组不良反应发生率差异无统计学意义(P0.05)。结论丙戊酸镁缓释片联合奥氮平治疗阿尔茨海默病疗效可靠,不良反应小,安全性好,值得临床推广应用。     

丙戊酸镁缓释片合并奥氮平治疗阿尔茨海默病伴精神行为症状的疗效观察

目的观察丙戊酸镁缓释片合并奥氮平治疗阿尔茨海默病（AD）伴精神行为症状（BPSD）的疗效及不良反应。方法将51例分为丙戊酸镁缓释片合并奥氮平组（合并组）及单用奥氮平组（单用组）,共治疗6周。以痴呆病理行为评定量表（BEHAVE-AD）、MMSE和TESS评定疗效及不良反应,分别于治疗前及治疗后2、6周各评定1次。结果两组均有效,治疗前后均有显著差异（P〈0.05）,合并组不良反应较单用组少4、（P〈0.05）。结论丙戊酸镁缓释片合并奥氮平可有效治疗阿尔茨海默病伴精神行为症状及减少不良反应的发生。     

丙戊酸镁中毒28例临床分析

丙戊酸镁中毒２８例临床分析河北省唐山市开滦精神病院（０６３００１）王树阳近年来报道用丙戊酸镁治疗情感性精神障碍效果颇佳，但该药引起中毒者，国内报道甚少，现将笔者近几年所遇丙戊酸镁引起中毒２８例总结分析如下。１临床资料１．１一般资料２８例病人中，男１２...     

丙戊酸镁、丙戊酸镁缓释片与德巴金缓释片药效时效关系的比较研究

目的探讨丙戊酸镁片、丙戊酸镁缓释片与德巴金缓释片在药效、时效、副反应方面的差异。方法利用大鼠抗电刺激皮层惊厥阈值模型,观察三种药物组及假阳性对照组单次及重复给药后大鼠惊厥阈值动态变化趋势,连续给药一个月后取其肝肾做病理学检查。并监测人单次口服三种药物后体内血药浓度变化趋势。结果对照组24h内惊厥阈值稳定在860±40μA,丙戊酸镁单次给药后1~2h达药效高峰,大鼠惊厥阈值升高至1100μA,较其它三组明显升高(P<0.05),给药后3h其药效开始下降,至12h其惊厥阈值下降至950μA。丙戊酸镁缓释片及德巴金给药后7h左右达峰,惊厥阈值分别升高至1085μA及1000μA,显著高于对照组(P<0.05),给药后12h两组惊厥阈值均保持在1023μA左右。三种药物药效变化趋势与人体单次服药后体内血药浓度变化相吻合。重复给药过程中丙戊酸镁组的惊厥阈值的峰谷平均差值为120~150μA,是丙戊酸镁缓释片和德巴金峰谷差值的2倍和2.5倍。重复给药10次后,丙戊酸镁缓释片组惊厥阈值较给药前升高430μA,德巴金缓释片组升高230μA。连续给药一个月后,三者肝肾损害较对照组无明显差异。结论丙戊酸镁片起效快、持续时间短,波动大。丙戊酸镁缓释片起效慢,作用力维持时间比丙戊酸镁片长。德巴金吸收较好,药效更平稳,但长时程的抗惊厥效果不如丙戊酸镁缓释片显著。     

丙戊酸镁治疗癫痫

丙戊酸镁治疗癫痫张敬军，陈青，孙思琴丙戊酸镁是继丙戊酸钠、癫痫安之后合成的另一丙戊酸类药，国外７０年代开始用于临床，国内应用尚少，本文单用丙戊酸镁治疗各型癫痫８３例，并监测血浓度，现就临床疗效、血浓度测定、脑电图变化及其不良反应加以分析及讨论。１资料...     

奎硫平合并丙戊酸镁缓释片治疗精神分裂症兴奋激越研究

目的：比较奎硫平合并丙戊酸镁缓释片与氟哌啶醇治疗精神分裂症患者伴有兴奋、激越症状的疗效及不良反应.方法：对精神分裂症住院患者采用随机对照、开放性研究治疗2周.以阳性与阴性症状量表（PANSS）及临床疗效总评量表（CGI）评估疗效,以治疗中出现的症状量表（TESS）评估不良反应.结果：合用组与对照组的总体疗效相当,兴奋、激越症状的控制前者优于后者（P＜0.05）;不良反应方面,氟哌啶醇引起的锥体外系不良反应较奎硫平合并丙戊酸镁缓释片高.结论：奎硫平合并丙戊酸镁缓释片对精神分裂症兴奋、激越症状的疗效优于氟哌啶醇,且不良反应较小.     

丙戊酸镁缓释片与碳酸锂对躁狂发作的疗效及生存质量的对照研究

目的比较丙戊酸镁缓释片与碳酸锂治疗对躁狂发作患者的疗效及对生存质量的影响。方法采用入院顺序分层随机法,将120例躁狂发作患者平均分为研究组(丙戊酸镁)和对照组(碳酸锂),在治疗前,治疗后1、3、6、12月末分别用Bech-Rafaelsen躁狂量表(BRMS)和临床疗效总评量表(CGI)及不良反应表(TESS)评定疗效和副作用,用世界卫生组织生存质量测定量表(WHOQOL-BREF)评估患者的生存质量,分析量表中各领域的计分。结果两组BRMS总分在治疗后与治疗前比较有显著性差异(P<0.01),及各因子分比治疗前明显降低(P<0.01),研究组有效率96.7%,显效率70%;对照组有效率93.3%,显效率66.7%。两组间疗效无显著性差异(P>0.05),研究组副作用比对照组少。经12个月治疗,研究组与对照组两组生存质量各分指标均较治疗前有显著改善(P<0.01),在心理领域、社会关系和环境领域三方面,丙戊酸镁优于碳酸锂(P<0.01)。结论丙戊酸镁缓释片和碳酸锂对治疗躁狂发作均有效。丙戊酸镁缓释片由于副作用小,对生存质量的改善更彻底,而优于碳酸锂。     

丙戊酸镁缓释片对精神分裂症暴力攻击行为的疗效观察

目的:探讨丙戊酸镁缓释片联合抗精神病药治疗精神分裂症暴力攻击行为疗效及安全性.方法:将64例有暴力攻击行为的精神分裂症患者随机分为两组,丙戊酸镁缓释片联合抗精神病药组(合用组)32例,单用抗精神病药组(单用组)32例治疗4周.采用简明精神病量表(BPRS)、外显攻击行为量表(MOAS )和治疗中出现的症状量表(TESS...     

度洛西汀联合丙戊酸镁缓释片治疗伴有疼痛的抑郁症疗效观察

目的探讨度洛西汀联合丙戊酸镁缓释片治疗伴有疼痛的抑郁症疗效及安全性。方法将104例伴有疼痛的抑郁症患者随机分成两组,合用组52例,应用度洛西汀联合丙戊酸镁缓释片;单用组52例,单用度洛西汀,疗程为8周。采用McGILL疼痛评分表（McGILL）,汉密尔顿抑郁量表（HAMD）,汉密尔顿焦虑量表（HAMA）,临床总体疗效量表（CGI）,不良反应量表（TESS）,评定疗效及用药不良反应。结果两组患者的McGILL总分、HAMD总分、HAMA总分、CGI—SI、CGI—GI较治疗前显著下降,差异有统计学意义（P〈0．05）,合用组疗效明显优于单用组,差异有统计学意义（P〈0．05）,两组不良反应差异无统计学意义（P〉0．05）。结论度洛西汀联合丙戊酸镁缓释片治疗伴有疼痛的抑郁症疗效好,疼痛缓解明显,安全性高。     

奥氮平联合丙戊酸镁缓释片治疗难治性精神分裂症的随机对照试验

目的探讨奥氮平片联用丙戊酸镁缓释片对难治性精神分裂症的临床疗效和认知功能的影响。方法选择2014年6月-2015年12月湖北科技学院附属第二医院精神科收治的符合《国际疾病分类第10版》(ICD-10)诊断标准的住院难治性精神分裂症患者为研究对象,共100例,按照随机数字表法分为研究组和对照组各50例,研究组给予奥氮平联合丙戊酸镁缓释片治疗,对照组给予奥氮平联合安慰剂治疗,两组疗程均为3个月。在治疗前、治疗后半月、1月、2月、3月采用改良版威斯康星卡片分类测试(M-WCST)、阳性和阴性症状量表(PANSS)和副反应量表(TESS)分别评定患者的认知功能改善、临床疗效和不良反应。结果治疗3月后,研究组PANSS总评分、阴性症状评分较治疗前低(t=2.364、1.268,P均0.01),M-WCST错误数、持续错误数、非持续错误数各因子评分和总评分均较治疗前低(t=0.365~4.116,P均0.01);对照组PANSS总评分、各条目评分、M-WSCT各项目评分与治疗前比较差异无统计学意义(P均0.05)。治疗3月后,研究组M-WCST正确数、正确分类数高于对照组(t=2.369、5.118,P均0.01),M-WCST错误数、持续错误数、非持续错误数低于对照组(t=1.368~5.118,P均0.01)。两组不良反应发生率差异无统计学意义(t=-1.261,P0.05)。结论奥氮平联合丙戊酸镁缓释片对长期住院难治性精神分裂症患者的疗效优于奥氮平联合安慰剂,前者能改善认知功能。     

Valproate as psychotropic agent. Interactions and adverse cerebral reactions

Recent data stress the psychotropic actions of valproate in schizo-affective disorder. Four patients are reported presenting an altered state of consciousness and prominent EEG dysfunction following combined valproate/neuroleptic drug treatment. Similar cerebral reactions have been reported in anti-epileptic poly- and monotherapy, and the pathogenetic considerations are discussed. Further investigations of the interactions of valproate with other psychotropic agents are highly mandatory.     

Valproate sustained release in the treatment of epilepsy

In an observational study under routine clinical setting data after administration of once daily evening dosing of valproate sustained release minitablets were recorded in 359 patients with epilepsy aged between 12 and 86 years. Patients were either newly treated with valproate sustained release minitablets (N = 58) or switched from conventional valproate (N = 124) or from sustained release valproate (N = 138) to the once daily evening dosing. In 39 patients other antiepileptic drugs were replaced. At the end of the 7-week observational period most patients (65.4 %) received a daily dose of 10 to less than 18 mg/kg body weight followed by 17.4 % receiving doses in the therapeutically recommended range of 18 - 24 mg/kg. 8.6 % and 7.4 % of patients received more than 24 mg/kg or less than 10 mg/kg body weight, respectively. As expected, in both groups with valproate pre-treatment the mean morning valproate plasma levels increased by approximately 10 microg/ml after switch to once evening dosing with sustained release minitablets. The mean seizure frequency decreased from 2.1 to 0.5 in the 318 patients with data before the beginning and at the end of the investigation. At the final examination 137 patients (62.3 %) were seizure free, and further 60 patients (27.3 %) experienced a seizure reduction of more than 50 % (responder) of those 220 patients who experienced seizures in the last 7 weeks before the study. The efficacy and tolerability was rated in more than 95 % of the cases by the patient and the investigator as good or very good. The compliance/acceptance of the valproate sustained release minitablets was rated as good or very good in almost all patients. These results confirm the excellent benefit-risk ratio of the valproate sustained release minitablets and underline the importance of a simple compliance-improving dose regimen for effective seizure control.     

Lamotrigine-associated anticonvulsant hypersensitivity syndrome in bipolar disorder

Anticonvulsant hypersensitivity syndrome (AHS) is a rare but life-threatening adverse effect of aromatic anticonvulsants such as phenytoin, phenobarbital and carbamazepine, although there is extensive experience with AHS related to these anticonvulsants. Very few cases of lamotrigine-associated AHS have been reported in bipolar patients and most reported cases were published in non-psychiatric journals. The authors describe here the occurrence of an AHS in a 48-year-old bipolar woman who was treated with lamotrigine, valproic acid and venlafaxine for her depressive symptoms. She developed a high fever, generalized maculopapular rash, pancytopenia, pneumonitis and hepatitis after we added lamotrigine to valproate and venlafaxine. These adverse drug reactions resolved after the discontinuation of lamotrigine and valproate, and the administration of oral antihistamine and corticosteroid. Our case demonstrates that the most important steps in the management of lamotrigine-associated AHS are to recognize the disorder, discontinue the offending anticonvulsants, provide supportive care in an inpatient setting, and treat with antihistamine and steroids when appropriate.     

Valproate-induced panhypogammaglobulinemia

Valproate is one of the most used anti-epileptic drugs. Its common side effects are nausea, vomiting, weight gain, hair loss, tremor, changes in behavior, slowed thinking and impaired liver function. Blood dyscrasias are also relatively frequent and a few studies reported changes in serum immunoglobulin concentrations with valproate treatment. We describe a case of panhypogammaglobulinemia with transient pancytopenia due to valproate. Pancytopenia was recovered after discontinuation of valproate but panhypogammaglobulinemia has been persisting. Intravenous immunoglobulin is being administrated monthly. Previous reports describe that other sodium channel blockers, such as phenytoin and carbamazepine, have been associated with hypogammaglobulinemia. This report also suggests that immunodeficiencies can be caused by valproate.     

Comparison of valproate concentrations in human plasma, CSF and brain tissue after administration of different formulations of valproate or valpromide.

The concentration of valproate was measured in plasma, CSF and brain tissue of patients who underwent resective surgical treatment because of severe temporal lobe epilepsy after pretreatment with either a sustained release formulation of valproate (Depakine Chrono; 5 patients), the conventional formulation of valproate (Depakine; 6 patients) or valpromide (Depamide; 2 patients). With a mean serum value for all 13 patients of 32.3 micrograms/g valproate, the mean brain/serum ratio was 15.1% (SD 6.1%). The valproate concentration of the hippocampus was significantly higher than that of the amygdala and patients who had the sustained release formulation had significantly higher valproate concentration in the CSF and in the hippocampal formation than those patients who had the conventional valproate. Since a few patients had tumors, whereas others had varying degrees of gliosis, it cannot be ruled out that these differences are the result of different histopathological conditions with related differences in blood-brain barrier functions.