利培酮联合氟哌啶醇与单独氯氮平治疗以阳性症状为主的精神分裂症的效果比较

目的 探讨利培酮短期内联合小剂量氟哌啶醇治疗以阳性症状为主的精神分裂症患者的效果。方法 对80例精神分裂症患者随机分为利培酮联合小剂量氟哌啶醇组(n=40)及单独氯氮平(n=40)治疗组，并进行比较分析，疗程8周。采用简明精神病评定量表(BPRS)、阳性症状评定量表(SAPS)及副反应量表(TESS)分别于疗后第1周、2周、4周、6周、8周末进行评定。结果 利培酮联合小剂量氟哌啶醇组与单独氯氮平治疗组总体疗效相当，能较早、较好的出现治疗效果，而无严重副反应。结论 利培酮短期内联合小剂量氟哌啶醇治疗能有效治疗精神分裂症的阳性症状，值得推荐。     

自知力教育配合治疗精神分裂症对照研究

目的：探讨自知力教育在精神分裂症治疗中的作用。方法：对８２例精神分裂症患者随机分组,应用自知力教育配合氟哌啶醇（４０例）及单用氟哌啶醇（４２例）进行对照治疗,疗程１２周。采用简明精神病评定量表（ＢＰＲＳ）、阴性症状评定量表（ＳＡＮＳ）、阳性症状评定量表（ＳＡＰＳ）、及自知力与治疗态度问卷表（ＩＴＡＱ）进行测定。结果：自知力教育配合氟哌啶醇组疗效显著较好。结论：自知力教育配合治疗是治疗精神分裂症的有效方法,能较早、较好地出现治疗效果。     

银杏叶提取物对精神分裂症过氧化物歧化酶的作用

目的探讨银杏叶提取物（EGb）合并氟哌啶醇治疗对精神分裂症超氧化物歧化酶（SOD）的影响及其与临床疗效的关系。方法用固定剂量银杏叶提取物合并氟哌啶醇随机、双盲治疗82例患者12周，在治疗前后分别评定简明精神症状评定量表（BPRS）、阳性症状评定量表（SAPS）和阴性症状评定量表（SANS），并用双抗体放射免疫法测定SOD含量。结果（1）治疗前精神分裂症阳性症状与SOD值正相关（r=0．36，P＜0．01）；（2）EGb能提高抗精神病药的疗效，主要是治疗阳性症状的疗效；而且疗效与SOD值降低相关，表现为治疗前后SOD含量差值与BPRS、SAPS和SANS总分减分值分别呈正相关（r分别=0．38，0．45，0．29，P均＜0．01）；（3）治疗前患者SOD水平与疗效相关，表现为治疗前SOD值与BPRS、SAPS和SANS总分减分值分别呈正相关（r分别=0．37，0．42，0．34，P均＜0．01）。结论支持精神分裂症多巴胺功能亢进与阳性症状相关、并引起自由基生成增多的假说；银杏叶提取物提高抗精神病药疗效与其清除自由基、减轻过氧化损伤起作用相关。     

齐拉西酮与氟哌啶醇注射液治疗急性精神分裂症对照研究

目的:评价齐拉西酮注射液治疗急性精神分裂症的疗效和安全性. 方法:将120例精神分裂症患者随机分为齐拉西酮组和氟哌啶醇组,进行随机单盲对照研究.疗程3 d.采用简明精神病评定量表(BPRS)、Bech-Rafaelsen躁狂量表(BRMS)、治疗中出现的症状量表(TESS)及锥体外系反应量表(RSESE)分别评定疗效和不良反应. 结果:治疗后两组BPRS及BRMS评分均显著降低,两组间减分率及显效率的差异均无统计学意义.齐拉西酮组不良反应发生率明显低于氟哌啶醇组(P＜0.01). 结论:齐拉西酮注射液对急性精神分裂症治疗效果与氟哌啶醇注射液相当,而不良反应少于氟哌啶醇.     

利培酮和氟哌啶醇治疗老年期精神障碍对照研究

目的 比较利培酮和氟哌啶醇治疗老年期精神障碍的疗效和安全性。方法 利培酮组22例,口服利培酮1.34±0.52mg/d;氟哌啶醇组20例,口服氟哌啶醇2.2±0.89mg/d,疗程均为8周。用临床疗效评定量表(CGI),简明精神症状检查量表(BPRS)、阴性症状评定量表(SANS)、汉密顿抑郁量表(HAMD)评价疗效。用药物副反应量表(TESS)评定不良反应。用简易智能量表(MMSE)评定对认知功能的影响。结果 临床总体疗效两组间无显著性差异(P>0.05),利培酮对BPRS各靶症状及阴性症状疗效显著,对阴性症状疗效优于氟哌啶醇(P<0.01),而且可提高MMSE的分值(P<0.01)。两组不良反应均以锥体外系症状和嗜睡为主。两组不良反应发生率无显著性差异(P>0.05)。结论 利培酮和氟哌啶醇对老年期精神障碍均有良好的疗效,利培酮对BPRS和SANS各常见靶症状疗效更显著,副反应小而安全,且不影响认知功能,更适宜于老年病人。     

利培酮治疗老年精神分裂症患者对照研究

目的 :评价利培酮和氟哌啶醇治疗老年精神分裂症患者的疗效和安全性。　方法 :对 10 5例老年精神分裂症患者分别给予利培酮、氟哌啶醇治疗 ,其中利培酮组 5 4例 ,氟哌啶醇组 5 1例。疗程12周。以简明精神病评定量表 (BPRS)评定临床疗效 ,以副反应量表 (TESS)和实验室检测评价安全性。　结果 :治疗结束时 ,两组BPRS总分较治疗前显著降低 (P <0 0 1) ,两组间差异无显著性 ,两组临床疗效 ,利培酮组有效率 87 0 % ,显效率 5 7 4 %。氟哌啶醇组有效率 84 3% ,显效率 5 4 9% ,两组差异无显著性。利培酮组不良反应总发生率较氟哌啶醇组少 (P <0 0 5 )。　结论 :利培酮治疗老年精神分裂症患者的疗效与氟哌啶醇相似 ,不良反应较氟哌啶醇轻而少。     

左旋咪唑涂布剂对精神分裂症患者免疫指标与疗效的关系

目的：探讨左旋咪唑涂布剂对精神分裂症患者免疫指标与疗效的关系。方法：将101例患者随机分成两组，均以固定剂量氟哌啶醇治疗，研究组辅以左旋咪唑涂布剂治疗，对照组予蒸馏水涂抹。治疗前后分别查免疫球蛋白及补体成分，用简明精神病评定量表(BPRS)、阳性症状量表(SAPS)、阴性症状量表(SANS)、临床疗效总评量表(CGI)和副反应量表(TESS)综合评定。结果：治疗后免疫球蛋白G(IgG)下降明显，且两组差异显著。各量表的减分率与治疗前IgG呈显著正相关。SANS减分率与治疗前后IgG差值呈显著正相关。结论：临床症状改善与IgG水平相关，且以阴性症状为主。     

氯硝西泮、氟哌啶醇及其联合治疗对精神分裂症激越症状疗效的比较

目的比较氯硝西泮、氟哌啶醇及其联合治疗对精神分裂症激越症状的疗效及安全性。方法本研究为随机、双盲、双模拟、平行活性对照研究,共分3组。氯硝西泮组15例,剂量范围（2-6）mg／d;氟哌啶醇组15例,剂量范围（5-15）mg／d;氟哌啶醇＋氯硝西泮组15例,氯硝西泮剂量范围（2-6）mg／d,氟哌啶醇剂量范围（5-15）mg／d。3组均以简明精神症状评定量表（BPRS）总分、BPRS兴奋激越项目分数、BPRS阳性症状项目分数及按临床疗效总评量表（CGI）标准评定观察24小时。结果3组的总体疗效大致相当,24h治疗后BPRS兴奋激越项目评分与基线分比较均具显著性差异（P〈0．01）,但各组之间无显著性差异（P〉0．05）;BPRS阳性症状项目评分与基线分比较均无显著性差异（P〉0．05）,各组之间也无显著性差异。结论氯硝西泮肌注对精神分裂症兴奋激越症状的疗效与氟哌啶醇或氟哌啶醇加氯硝西泮相当。     

精神分裂症患者的自知力及其对精神症状认识的研究

目的研究精神分裂症患者对症状的认识及其与自知力、精神病理症状及疾病严重程度的关系.方法由患者和医生分别评定4个阳性症状和4个阴性症状在患者身上的表现程度.同时由医生对患者进行ITAQ、BPRS、SANS、SAPS、CGI评定.结果患者对自身阳性和阴性症状的总评分分别为(16.79±3.67)和(16.02±3.81),明显高于医生评定的(15.46±4.25)和(13.22±4.22),患者对自身症状的评分ITAQ、BPRS、SANS、SAPS、CGI均具有一定程度的相关.结论患者对自身症状的认识明显不足,特别是阴性症状.患者对症状的认识与其自知力、疾病严重程度、精神病理症状有关.     

首发青少年精神分裂症患者认知自知力相关研究

目的探索首发青少年精神分裂症患者认知自知力受损情况及其与临床症状的关系。方法对37例符合《精神障碍诊断与统计手册(第5版)》(DSM-5)诊断标准的首发青少年精神分裂症患者在入院时进行贝克认知自知力量表(BCIS)、阳性症状量表(SAPS)、阴性症状量表(SANS)和精神症状评定量表(PSYRAT)评定,分析患者认知自知力受损情况及其与临床症状的关系,同时对37名正常对照组进行BCIS评定。结果首发青少年精神分裂症患者BCIS的自我肯定(SC)评分高于对照组(t=2.051,P0.05),且SC评分与SANS评分呈负相关(r=-0.465,P0.05),自省能力(SR)评分与SAPS评分呈负相关(r=-0.447,P0.05)。结论首发青少年精神分裂症患者存在明显的认知自知力受损,且阳性症状越重者,其自省能力越弱,阴性症状越重者,自我肯定程度越低。     

Reduced haloperidol/haloperidol ratios after oral haloperidol and decanoate administration in schizophrenics

1. Haloperidol and reduced haloperidol plasma concentrations were measured in thirteen stable schizophrenic patients that received both oral haloperidol and haloperidol decanoate.2. Significant correlations between reduced haloperidol/haloperidol ratios from oral haloperidol and haloperidol decanoate occurred at week two and week 16, respectively.3. The formation of RH was consistent during haloperidol decanoate treatment.     

Dose-dependent reduced haloperidol/haloperidol ratios in schizophrenic patients.

Plasma haloperidol (HAL) and reduced HAL (RHAL) concentrations were measured in 113 Chinese schizophrenic patients. Daily doses of HAL ranged from 8 to 65 mg. Samples were obtained under steady-state conditions and drawn 10-12 hours after the bedtime dose and before the morning dose. In all, 313 blood samples were collected. Multiple samples were obtained at the same doses in 63 patients and at two or three different doses in 31 patients. HAL and RHAL concentrations were assayed by high performance liquid chromatography. Interpatient variation in plasma HAL levels at a given dosage was up to sixfold. However, there was a high positive correlation between plasma levels and daily dosages with the equation of HAL plasma level (ng/ml) = 0.88 x dosage (mg/day) -0.56 or 46.0 x dosage (mg/day/kg) + 0.28. The expected values are about 15-55% higher than those obtained from non-Chinese patients as reported in the literature. The RHAL/HAL ratios were dose-dependent. The greater the dose used, the higher the ratio. An upper therapeutic limit of plasma HAL level is suggested to be 25 ng/ml, which can be achieved at dosages about 30 mg/day in most Chinese patients. Based upon the dose-dependent increase in RHAL/HAL ratios, the importance of RHAL in determining the therapeutic benefit of HAL treatment is discussed.     

Savoxepine versus haloperidol

Savoxepine, an atypical neuroleptic compound developed in the 1980s, was believed to act via selective limbic dopamine D₂-receptor blockade. The results of the presented double-blind, randomised, controlled clinical trial comparing savoxepine (n = 58) with haloperidol (n = 29) did not confirm the preclinical data suggesting that savoxepine would produce fewer extrapyramidal symptoms than the comparator. Animal data and PET-results obtained a posteriori suggested that this unfavourable outcome may have been due to the conventional, step-wise dose increase strategy used in the study leading to a high dopamine D₂-receptor occupancy in the striatum thus eliciting EPS. Using either a slower dose-titration or a high, single loading dose followed by a low maintenance dosing may have offered the possibility to obtain a good antipsychotic effect together with low incidence of EPS. In future clinical trials with new neuroleptics, the preclinical data should be carefully evaluated, and drug brain kinetic parameters taken into consideration. Received: 4 December 2001 / Accepted: 5 April 2002     

Pharmacodynamics and pharmacokinetics of haloperidol and reduced haloperidol in schizophrenic patients

Twelve male chronic schizophrenic inpatients, neuroleptic-free for at least 4 weeks, were given an oral test dose of 10 mg haloperidol (HAL) and reduced HAL (RHAL) in a random order, with a 2-week interval. Two weeks after the last test dose, the patients were given HAL, 5 mg orally twice daily for 7 days. Blood samples were drawn at baseline and between 0.5 and 24 hr after the test doses, and during HAL treatment as well. Plasma drug concentrations and homovanillic acid (HVA) levels were measured with high-performance liquid chromatography using electrochemical detection. HAL, but not RHAL, produced increments in plasma HVA (pHVA) levels at 24 hr after a test dose. pHVA levels remained higher than baseline during HAL treatment. Detectable interconversion between HAL and RHAL was observed in eight patients. The capacity of the reductive drug-metabolizing enzyme system, however, was greater than that of the oxidative processes. The plasma RHAL:HAL ratios on days 6 and 7 were higher than and positively correlated with those at Tmax after a single dose of HAL and were negatively correlated with the HAL:RHAL ratios at Tmax after a single dose of RHAL. Thus, both reductive and oxidative drug-metabolizing systems probably contribute to individual differences in plasma RHAL:HAL ratios in HAL-treated schizophrenic patients.     

The discovery of haloperidol

Haloperidol was synthesized on the 11th of February 1958 by Bert Hermans at the Janssen Laboratories, Beerse, Belgium. Simple but ingenuous methods of animal pharmacology suggested to Paul Janssen and his collegues that this butyrophenone derivative, called R1625, then halop-peridol, would be of great interest: qualitatively, the pharmacological action of R1625 was similar to chlorpromazine, but R1625 was very more powerful since it produced effects with much smaller doses than chlorpromazine. Soon after the synthesis and animal studies, haloperidol was administered in humans by Divry, Bobon et Collard, psychiatrists at the Liege Hospital. The first clinical publication, on the 28th of October, 1958, described the effects of haloperidol in agitation states. The subsequent clinical studies, including those of the prestigious French school of Sainte-Anne hospital, confirmed that haloperidol belongs to the pharmacological family of neuroleptics, as it was defined by J. Delay and P. Deniker in 1955. These clinical studies demonstrated also that haloperidol was particularly active against delusions and hallucinations. Numbers of chronically inpatients were able to leave hospital and to live home thanks to this new drug, which remains one of the more prescribed neuroleptics 40 years after its discovery.     

The haloperidol story.

Haloperidol was synthesized on the 11th of February 1958 at the Janssen Laboratories, in Belgium. Soon after its synthesis and animal studies, which suggested to Paul Janssen and his colleagues that this butyrophenone drug would be of great interest as its action was similar but much more powerful than that of chlorpromazine, haloperidol was administered to humans at the Liege hospital. The subsequent clinical studies confirmed that this new drug was particularly active against delusions and hallucinations. The introduction of haloperidol in the United States of America was difficult for clinical and legal reasons. For many years, haloperidol had been widely used in western countries, until the introduction of "new antipsychotics."