舒必利治疗内源性抑郁

为研究低剂量舒必利对内源性抑郁的疗效,对39例内源性抑郁进行四周双盲对照,以汉密顿抑郁量表(HAMD)和副反应量表(TESS)评定。结果发现,舒必利组与阿米替林组相比HAMD因子分减分量在第二周、第四周末无差异;TESS量表植物神经系副反应较少。     

曲唑酮与阿米替林治疗抑郁症的对照观察

为比较曲唑酮与阿米替林治疗抑郁症的疗效和副反应,将符合CCMD-3抑郁症诊断标准的患者随机分为两组,分别给予曲唑酮和阿米替林治疗,并于治疗前及治疗后第1、2、4、6周分别用汉密尔顿抑郁量表(HAMD)、临床疗效总评量表(CGI-SI)及副反应量表(TESS)评定。结果,曲唑酮组显效率62.5％,总有效率为87.5％;阿米替林组分别为57.2％和86,7％。HAMD评分两组间疗效无显著差(P>0.05)。不良反应:曲唑酮表现为镇静,阿米替林为抗胆碱能症状。结论;曲唑酮是一种疗效与阿米替林相当,而副作用较轻的抗抑郁药。     

氟西汀与阿米替林改善精神分裂症后抑郁的对照观察

将符合中国精神疾病分类与诊断标准第二版修订版精神分裂症后抑郁诊断标准的66例患者随即分为两组，分别给予氟西汀和阿米替林治疗，疗程6周。采用汉密顿抑郁量表(HAMD)评定疗效，副反应量表(TESS)评定副反应。结果表明两组间治疗前后HAMD评分及减分比较差异均无显著性意义(P&;gt;0．05)。两组疗效接近，氟西汀组的副反应明显小于阿米替林组。     

氟西汀与阿米替林改善精神分裂症后抑郁的对照观察

将符合中国精神疾病分类与诊断标准第二版修订版精神分裂症后抑郁诊断标准的66例患者随即分为两组,分别给予氟西汀和阿米替林治疗,疗程6周。采用汉密顿抑郁量表(HAMD)评定疗效,副反应量表(TESS)评定副反应。结果表明两组间治疗前后HAMD评分及减分比较差异均无显著性意义(P>0.05)。两组疗效接近,氟西汀组的副反应明显小于阿米替林组。     

曲唑酮与阿米替林治疗伴有焦虑症状的抑郁症

目的比较曲唑酮与阿米替林治疗伴有焦虑症状的抑郁症的临床的疗效和副反应。方法68例符合CCMD-2-R诊断标准的抑郁症伴有焦虑症状的患者,随机分为两组,应用曲唑酮34例,阿米替林34例共治疗6周。采用汉密顿抑郁量表(HAMD)、焦虑量表(HAMA)和副反应量表(TESS)评定疗效和副反应。结果曲唑酮与阿米替林治疗伴有焦虑症状的抑郁症均有效,二者疗效相当(P>0.05)。曲唑酮的副反应明显少于阿米替林(P<0.01)。结论曲唑酮治疗伴有焦虑症状的抑郁性神经症是一种安全、有效的药物。     

西酞普兰和阿米替林治疗老年抑郁症的效果对照评价

目的:探讨西酞普兰与阿米替林治疗老年抑郁症的疗效与安全性。方法:将44例符合《中国精神障碍分类与诊断标准(第3版)》(CCMD-3)诊断标准的老年抑郁症患者随机分成两组,分别给予西酞普兰和阿米替林治疗6周。采用汉密顿抑郁量表(HAMD)和副反应量表(TESS)评定疗效和副反应。结果:西酞普兰组显效率为86%,阿米替林组显效率为82%,两者疗效相比差异无显著性意义(χ2=0.17,P>0.05),但西酞普兰起效快于阿米替林。西酞普兰组的副反应明显较阿米替林组轻。结论:西酞普兰治疗老年抑郁症起效快,副反应轻,安全有效。     

氟伏沙明与阿米替林治疗老年期抑郁症疗效分析

目的:比较氟伏沙明与阿米替林治疗老年期抑郁症的疗效及副反应.方法:将65例老年期抑郁症患者随机分为研究组(33例)给予氟伏沙明治疗6周,对照组(32例)给予阿米替林治疗6周.采用Hamilton抑郁量表(HAMD)和副反应量表(TESS)评定疗效及不良反应.结果:氟伏沙明总有效率为83.87%,阿米替林总有效率为78.57%,两者差异无统计学意义(P>0.05).但氟伏沙明副反应轻微,两者比较差异有显著性.结论:氟伏沙明治疗抑郁症效果肯定且副反应少,特别适合治疗老年期抑郁症患者.     

西酞普兰和阿米替林治疗老年抑郁症的效果对照评价

目的：探讨西酞普兰与阿米替林治疗老年抑郁症的疗效与安全性。方法：将44例符合《中国精神障碍分类与诊断标准(第3版)》(CCMD-3)诊断标准的老年抑郁症患者随机分成两组，分别给予西酞普兰和阿米替林治疗6周。采用汉密顿抑郁量表(HAMD)和副反应量表(TESS)评定疗效和副反应。结果：西酞普兰组显效率为86％，阿米替林组显效率为82％，两者疗效相比差异无显著性意义(x^2=0．17，P&;gt;0．05)，但西酞普兰起效快于阿米替林。西酞普兰组的副反应明显较阿米替林组轻。结论：西酞普兰治疗老年抑郁症起效快，副反应轻，安全有效。     

文拉法辛与阿米替林治疗抑郁症临床对照分析

目的：了解文拉法辛与阿米替林治疗抑郁症的临床疗效及不良反应。方法：将门诊就诊60例患者随机分为两组,分别给予文拉法辛和阿米替林治疗,疗程6周,采用汉米尔顿抑郁量表（HAMD）和副反应量表（TESS）评定疗效与不良反应。结果：文拉法辛组在治疗1、2周末HAMD评分明显低于阿米替林组,P〈0.05,治疗6周两组HAMD评分无显著性差异,不良反应小。结论：文拉法辛治疗抑郁症起效快,疗效与阿米替林相当,是一种安全有效的抗抑郁药物。     

抗抑郁剂治疗脑卒中后抑郁障碍

目的:探讨抗抑郁剂的应用对脑卒中后抑郁障碍患者的影响.方法:汉密顿抑郁量表(HAMD)总分≥14的脑卒中患者72例,随机分为3组各24例,在按脑卒中常规治疗基础上,A组给予10-30 mg/d帕罗西汀治疗,B组50-150 mg/d阿米替林治疗,C组为空白对照.治疗6及12周后采用HAMD、神经功能缺损评分及副反应量表(TESS)评定.结果:与治疗前及C组比较,A、B组治疗6及12周后HAMD总分及神经功能缺损评分均显著下降(P＜0.05),A组优于B组(P＜0.05);TESS总分,A组明显低于B组(P＜0.001).结论:帕罗西汀及阿米替林能显著改善脑卒中后合并抑郁障碍患者的抑郁症状及神经功能,且帕罗西汀对神经功能的恢复及减少药物副作用等方面优于阿米替林.     

氟西汀联合小剂量舒必利治疗抑郁症对照研究

目的探讨氟西汀联合小剂量舒必利治疗抑郁症的临床疗效及安全性。方法将60例抑郁症患者随机分为研究组和对照组各30例,研究组给予氟西汀联合小剂量舒必利治疗,对照组单用氟西汀治疗,疗程均为8w。与治疗前和治疗2w,4W,6w,8w末采用汉密顿抑郁量表评定临床疗效,副反应量表评定不良反应,并进行比较分析。结果两组治疗后各周汉密顿抑郁量表评分均较治疗前显著下降（P〈0.01）;研究组较对照组下降显著（P〈0.05或0．01）;两组副反应量表评分差异无显著性（P〉0.05）。结论氟西汀联合小剂量舒必利治疗抑郁症较单用氟西汀治疗起效快,疗效显著,安全性高。     

舍曲林联合小剂量舒必利治疗抑郁症临床观察

目的探讨舍曲林联合小剂量舒必利治疗抑郁症的临床疗效及安全性。方法将60例抑郁症患者随机分为两组各30例,研究组给予舍曲林联合小剂量舒必利治疗,对照组单用舍曲林治疗,观察6w;采用汉密尔顿抑郁量表和副作用量表评定临床疗效和不良反应。结果研究组起效快,显效率高于对照组（P〈0．05）,不良反应发生率明显低于对照组。结论舍曲林联合小剂量舒必利治疗抑郁症起效快,疗效好,不良反应发生率低,依从性好,值得推广应用。     

文拉法辛合并舒必利治疗抑郁症的随机对照研究

目的观察文拉法辛合并舒必利治疗抑郁症的疗效和不良反应。方法对64例住院的抑郁症患者随机分为两组,研究组给予文拉法辛合并舒必利治疗,对照组单用文拉法辛治疗,采用汉密尔顿抑郁量表（HAMD）及副反应量表（TESS）评定疗效和不良反应。结果研究组第一周HAMD减分率33．08％显著高于对照组10．64％,四周后研究组显效率87．5％优于对照组68．8％,两组均无严重不良反应。结论文拉法辛合并舒必利能快速缓解抑郁症状,疗效优于单用文拉法辛,不良反应不增加,患者依从性好。     

氯丙嗪、氯氮平和舒必利所致体重增加的对照研究

目的　比较氯丙嗪、氯氮平与舒必利治疗对精神分裂症患者体重的影响。方法　对 90例住院男性精神分裂症患者单独服用氯丙嗪、氯氮平或舒必利的体重采用自身对照及组间对照前瞻性研究方法 ,进行为期 12w的观察 ,并对其相关因素进行分析。结果　治疗 12w末平均体重与治疗前比 ,氯丙嗪和氯氮平组均有显著性差异 (P <0 .0 5 ) ,舒必利组有极显著性差异 (P <0 .0 1) ,平均增加体重舒必利组大于其他两组。体重增加与精神症状改善有关 ,与药物剂量及睡眠时间无明显关系。结论　氯丙嗪、氯氮平和舒必利均能导致体重增加 ,尤以舒必利为甚     

Modulation of ovarian LH receptor and serum hormone levels in rats with hyperprolactinemia induced by administration of ovine prolactin or sulpiride

Hyperprolactinemia was experimentally produced in rats by administration of ovine prolactin (oPRL) and sulpiride, and tried to evaluate the effect of hyperprolactinemia on ovarian receptor for luteinizing hormone (LH) as well as that on serum gonadotropin and steroid hormone levels. Wistar-Imamichi strain mature female rats showing 4-day estrous cycles were treated with various doses of oPRL or sulpiride twice a day for 4 days from diestrus. They were killed on the fifth day. Binding of ovarian LH receptors was reduced by a small dose of oPRL (0.1 IU) or sulpiride (0.25 mg) and restored to normal by larger doses of oPRL. However, larger doses of sulpiride (50 or 100 mg) increased the receptor bindings beyond the control level (4.39 +/- 0.40 ng/mg homogenate protein). Serum prolactin levels decreased in rats treated with larger doses of oPRL, but increased with larger doses of sulpiride. Serum LH levels increased with both agents. Although the ovaries treated with either oPRL or sulpiride suggested the lack of ovulation, there were no significant changes of steroid hormones in oPRL groups. In contrast, sulpiride treatment resulted in a reduction of estradiol and an increase of progesterone secretion, suggesting the prolonged effect of the drug. Thus, prolactin appeared to act on the rat ovarian LH receptors in two different manners in hyperprolactinemia, depending on the amount of this hormone or a ratio of prolactin to LH.     

Effects of apomorphine on heart rate during simultaneous administration of sulpiride: a challenge of the composed concentration-effect model

Apomorphine elicits opposite concentration-dependent effects on the heart rate in rat bradycardia at low concentrations and tachycardia at higher ones. This has been modeled with a composed sigmoid Emax equation. To challenge this model, a selective antagonist, sulpiride, was administered simultaneously with apomorphine. Four short intravenous infusions of apomorphine, at different rates, were administered to rats, while a steady state concentration of sulpiride was maintained by intravenous infusion. Another group of rats was infused with apomorphine at the same rates of infusion as in the above groups, together with saline. In this latter group a biphasic concentration-response relationship was observed, while in the group receiving sulpiride and apomorphine no bradycardia was detected. A sigmoid Emax model with one term describing bradycardia and one tachycardia was used for the saline plus apomorphine data. For the sulpiride plus apomorphine data a single-term sigmoid Emax model was used. The maximal induced tachycardia was found to be the same in both groups. The tachycardia occurred at lower concentrations in the sulpiride group, probably as a result of an antagonist-induced shift of the bradycardia towards higher concentrations. The obtained results show that a composite concentration-effect curve of apomorphine has experimental validity and that it is possible to separate its pharmacodynamic characteristics on heart rate into its components, bradycardia and tachycardia, by sulpiride.     

Systemic sulpiride modulates striatal blood flow: relationships to spatial working memory and planning

The dopamine D2 receptor antagonist sulpiride can produce a range of cognitive deficits in normal volunteers, consistent with those seen in Parkinson's disease (PD). This, together with studies in experimental animals, implies sulpiride might be acting in the striatum. However, subtle changes in prefrontal cortex (PFC) activity are seen following L-Dopa withdrawal in PD during working memory tasks, suggesting that this may be a further site of action for dopamine D2 receptor antagonists. We have investigated the effects of sulpiride within the PFC and striatum in normal male volunteers. In two separate experiments, using identical PET regional cerebral blood flow (rCBF) methods, a combined drug and psychological challenge was performed, utilising working memory and planning tasks, and oral sulpiride 400 mg and placebo. Data were analysed using SPM99. Sulpiride increased striatal rCBF bilaterally and the working memory and planning tasks activated discrete frontoparietal networks in keeping with previous studies. However, for the working memory tasks, no changes in performance or task-induced rCBF were observed after sulpiride. For the planning task, improved performance was seen on sulpiride. Also, sulpiride attenuated striatal activity during planning (as assessed using a small volume correction, P<0.05 corrected), and this attenuation was related to performance changes. These findings suggest that (1) sulpiride produces clear increases in striatal rCBF, (2) in contrast to previous studies no effects of sulpiride on performance of the working memory tasks or the associated neural networks were observed, and (3) sulpiride may modulate performance of more complex cognitive tasks via alterations in striatal neural activity.     

Sulpiride and Paroxetine in the Treatment of Chronic Tension-Type Headache. An Explanatory Double-Blind Trial

SYNOPSIS
Drugs influencing monoaminergic pathways are of potential use in the treatment of pain.
A serotonin re-uptake inhibitor, paroxetine (20-30 mg daily), and a dopamine antagonist, sulpiride (200-400 mg daily) were compared in a randomized, double-blind, response-conditional cross-over pilot study in 50 non-depressed patients with chronic tension-type headache.
Headache was scored daily on a 5-point verbal scale during 4-weeks baseline and during 8 weeks of treatment for each drug. A 5-point 'Global' assessment was obtained for each drug, In both treatment groups headache score decreased compared to baseline.
Group comparison of 24 patients first treated with paroxetine and 24 patients first treated with sulpiride showed a non-significant trend in favor of sulpiride by 'Global' evaluation and by evaluation of the available diary records (18 paroxetine-treated and 19 sulpiride-treated).
Cross-over analysis of 'Global' records from 20 patients treated with paroxetine followed by sulpiride and 17 patients treated in the reverse order showed better relief from sulpiride compared to paroxetine in patients having tested both drugs (P=.03). A similar difference was reflected in available headache scores (13 and 10 patients respectively; P=.03). Predominant side effects were sedation and depression, for paroxetine also nausea and head pain. None of the drugs improved headache more than one score-point on average. A placebo controlled trial of sulpiride may be warranted.     

Patterns of depressive symptom response in duloxetine-treated outpatients with mild, moderate or more severe depression

AIMS: This was a post hoc analysis to determine whether baseline severity of depression influenced the efficacy of duloxetine in treating major depressive disorder (MDD) and to better characterise the symptom response profile for duloxetine in patients with mild, moderate or more severe depression. METHODS: Data were pooled from four double-blind, placebo-controlled studies in which outpatients with MDD were randomised to duloxetine (60 mg/day) or placebo for 8-9 weeks. Patients were retrospectively stratified according to baseline 17-item Hamilton Depression Rating scale (HAMD17) total scores: mild=total score相似文献