西酞普兰治疗脑卒中后抑郁对照研究

目的：比较西酞普兰与阿米替林治疗脑卒中后抑郁的疗效和安全性。方法：72例脑卒中后抑郁患者，随机分成两组，分别用西酞普兰和阿米替林治疗8周。采用汉密顿抑郁量表(HAMD)、Montgomerg-Asberg抑郁量表(MADS)和副反应量表(TESS)于治疗前和治疗后1、2、4、8周末分别评定疗效和不良反应。结果：西酞普兰组与阿米替林组间的HAMD、MADS评分差异均无显著性，西酞普兰组不良反应较阿米替林组少而轻。结论：西酞普兰治疗脑卒中后抑郁疗效好，安全性高，不良反应轻微。     

西酞普兰和阿米替林治疗脑卒中后抑郁临床对照观察

目的:比较西酞普兰与阿米替林治疗脑卒中后抑郁的疗效和安全性。方法:41例脑卒中后抑郁患者,随机分两组,分别用西酞普兰和阿米替林治疗6周。采用汉密尔顿抑郁量表(HAMD)、抑郁自评量表(SDS)和副反应量表(TESS)于治疗前和治疗1、2、4、6周末分别评定疗效和不良反应。结果:两组治疗后各周HAMD和SDS评分均较治疗前下降(P均<0.05);其中治疗后1周末,西酞普兰组评分下降较阿米替林组更明显,两组比较差异有显著性(P<0.05),但治疗2~6周末比较,差异均无显著性(P均>0.05);西酞普兰组不良反应较阿米替林组少而轻。结论:西酞普兰治疗脑卒中后抑郁疗效与阿米替林相当,但起效较快,安全性高,不良反应轻微。     

西酞普兰治疗脑卒中后抑郁临床分析

目的探讨西酞普兰治疗脑卒中后抑郁的疗效和安全性。方法将符合脑卒中诊断标准同时符合CCMD-3抑郁症诊断标准的66例患者随机分为2组,分别给予西酞普兰和阿米替林治疗。治疗时间为6周,采用汉密顿抑郁量表(HAMD)、副反应量表(TESS)于治疗前和治疗1、2、4、6周分别评定疗效和不良反应。结果 2组治疗各周末评分HAMD均较前下降(P<0.05),但治疗1周末,西酞普兰组HAMD评分下降较阿米替林组显著(P<0.01),治疗6周末2组HAMD分值下降差异无统计学意义(P>0.05)。西酞普兰组不良反应较阿米替林组少而轻。结论西酞普兰治疗脑卒中后抑郁疗效与阿米替林相当,但起效快,不良反应少,安全性高。     

西酞普兰治疗老年脑卒中后抑郁临床对照研究

目的探讨西酞普兰治疗老年抑郁症的临床疗效和安全性。方法将40例老年脑卒中后抑郁患者随机分为两组,分别给予西酞普兰和阿米替林治疗,共6周,采用汉密顿抑郁量表(HAMD)、副反应量表(TESS)于治疗前和治疗1、2、4、6周末分别评定疗效及不良反应。结果西酞普兰和阿米替林治疗老年脑卒中后抑郁的疗效相似,但西酞普兰比阿米替林起效快,不良反应轻,疗效指数优于阿米替林(P<0.05)。结论西酞普兰可作为治疗老年脑卒中后抑郁的首选药物。     

西酞普兰治疗脑卒中后抑郁临床观察

目的：评价西酞普兰治疗脑卒中后抑郁的疗效和不良反应。方法：采用西酞普兰与阿米替林对42例脑卒中后抑郁患者进行8周双盲对照治疗。用汉密尔顿抑郁量表(HAMD)、临床疗效总评量表病情严重程度(CGI-SI)、副反应量表(TESS)评定疗效及不良反应。结果：西酞普兰与阿米替林疗效相近，但西酞普兰起效快，不良反应少。结论：西酞普兰治疗脑卒中后抑郁安全有效。     

西酞普兰治疗抑郁症临床观察

目的：评价西酞普兰治疗抑郁症的疗效和不良反应。方法：84例抑郁症患者，随机平分为两组，分别给予西酞普兰和阿米替林治疗，疗程8周。用汉密顿抑郁量表(HAMD)、临床疗效总评量表病情严重程度(CGI—SI)和副反应量表(TESS)评定疗效和不良反应结果：西酞普兰与阿米替林对抑郁症疗效相仿，但前者起效快，不良反应少于后者。结论：西酞普兰是一种安全有效的抗抑郁药。     

西酞普兰与舍曲林治疗老年抑郁症对照研究

目的:探讨西酞普兰与舍曲林治疗首发老年抑郁症的疗效及安全性. 方法:56例首发老年抑郁症患者,分别用西酞普兰和舍曲林治疗,疗程8周.采用汉密尔顿抑郁量表(HAMD)和治疗中出现的症状量表(TESS)评定疗效及不良反应. 结果:西酞普兰和舍曲林疗效与不良反应相近,以西酞普兰组起效较快;治疗2周,两组HAMD评分比较,以西酞普兰组降分较多(P<0.05). 结论:西酞普兰和舍曲林可作为老年抑郁症的首选药物.     

西酞普兰与阿米替林治疗老年抑郁症的临床对照研究

目的探讨西酞普兰治疗老年抑郁症的临床疗效和安全性。方法将79例老年抑郁症患者随机分配至西酞普兰组和阿米替林组。西酞普兰治疗剂量为20mg～60mg/d,阿米替林治疗剂量为100mg～300mg/d,疗程均为6周。采用汉米顿抑郁量表（HAMD）评定疗效,采用副反应症状量表（TESS）、体格检查、实验室检查评定其安全性。结果西酞普兰组有效率为92%,与阿米替林的87%相当（P〉0.05）,西酞普兰组不良反应少且轻微,患者耐受性好。结论西酞普兰治疗老年抑郁症疗效好且安全。     

西酞普兰与阿米替林治疗老年抑郁症对照研究

目的评价西酞普兰治疗老年抑郁症的疗效及安全性。方法收集各类抑郁发作老年患者82例,随机分为两组,分别给予西酞普兰和阿米替林治疗,疗程8周。采用17项汉密尔顿抑郁量表(HAMD)和副反应量表(TESS)评定疗效及安全性。结果两组总体疗效差异无显著性,但西酞普兰起效快,平均(6.3±3.5)天,口干、便秘、排尿困难及心血管的副反应较小。结论西酞普兰可作为治疗老年抑郁症的一线抗抑郁药。     

西酞普兰治疗抑郁症的疗效对照研究

目的 探讨选择性五羟色胺再摄取抑制剂西酞普兰治疗抑郁症的疗效及安全性.方法 将60例符合CCMD-3诊断标准的抑郁症病人随机分为两组,分别给予西酞普兰和阿米替林治疗.疗程6周.采用汉密尔顿抑郁量表（HAMD）、汉密尔顿焦虑量表（HAMA）评定疗效,并以不良反应量表（TESS）评定不良反应.结果 西酞普兰组显效率为83.33%,阿米替林组为76.67%,差异无显著性.西酞普兰不良反应少而轻微,主要有恶心、口干、头痛.结论 西酞普兰是一见效快、疗效肯定及不良反应少而轻微的抗抑郁药.     

Citalopram for agitation in Alzheimer's disease: design and methods

BackgroundAgitation is one of the most common neuropsychiatric symptoms of Alzheimer’s disease (AD), and is associated with serious adverse consequences for patients and caregivers. Evidence-supported treatment options for agitation are limited. The citalopram for agitation in Alzheimer’s disease (CitAD) study was designed to evaluate the potential of citalopram to ameliorate these symptoms.MethodsCitAD is a randomized, double-masked, placebo-controlled multicenter clinical trial, with two parallel treatment groups assigned in a 1:1 ratio and randomization stratified by clinical center. The study included eight recruiting clinical centers, a chair’s office, and a coordinating center located in university settings in the United States and Canada. A total of 200 individuals having probable AD with clinically significant agitation and without major depression were recruited for this study. Patients were randomized to receive citalopram (target dose of 30 mg/d) or matching placebo. Caregivers of patients in both treatment groups received a structured psychosocial therapy. Agitation was compared between treatment groups using the NeuroBehavioral Rating Scale and the AD Cooperative Study- Clinical Global Impression of Change, which are the primary outcomes. Functional performance, cognition, caregiver distress, and rates of adverse and serious adverse events were also measured.ConclusionThe authors believe the design elements in CitAD are important features to be included in trials assessing the safety and efficacy of psychotropic medications for clinically significant agitation in AD.     

帕罗西汀治疗阿尔茨海默病的抑郁对照研究

目的：比较帕罗西汀与氯米帕明在阿尔茨海默病(AD)抑郁症状治疗中的疗效和不良反应。方法：帕罗西汀组51例，氯米帕明组44例，均诊断为AD，汉密顿抑郁量表(HAMD，17项)≥18分。比较两组患者治疗后的HAMD减分率，采用副反应量表(TESS)评定不良反应。结果：帕罗西汀组与氯米帕明组总体疗效相当，但帕罗西汀组起效较快，不良反应发生率低。结论：帕罗西汀在AD抑郁症状治疗中具有一定优势，值得临床推广应用。     

西酞普兰与米安色林治疗老年抑郁症对照研究

目的:比较西酞普兰与米安色林治疗老年抑郁症的疗效及安全性。方法:将106例老年抑郁症患者随机分为西酞普兰组和米安色林组,疗程6周。采用汉密尔顿抑郁量表(HAMD)评定临床疗效,副反应量表(TESS)评定不良反应。结果:西酞普兰组与米安色林组疗效相仿;疗后HAMD总分均有显著减少。西酞普兰显效快,不良反应小。结论:西酞普兰是治疗老年抑郁症较好的药物。     

西酞普兰与氟西汀治疗抑郁症对照研究

目的 :比较西酞普兰与氟西汀治疗抑郁症的疗效及不良反应。　方法 :5 7例抑郁症患者被随机分为西酞普兰组 (2 9例 )和氟西汀组 (2 8例 )进行为期 6周的治疗。以汉密尔顿抑郁量表 (HAMD)、副反应量表 (TESS)于治疗前及治疗 1、2、4、6周末分别评定疗效和不良反应。　结果 :西酞普兰组显效率为 72 .4 % ,氟西汀组为 71.4 % ,两组间比较差异无显著性。两组HAMD评分于治疗 1、2周末差异有显著性 ,提示西酞普兰起效较早。治疗后各周两组间TESS评分比较差异均无显著性。　结论 :西酞普兰和氟西汀均有良好的抗抑郁效果。西酞普兰具有起效早、不良反应小的优点     

西酞普兰与文拉法辛治疗抑郁症的对照研究

目的:比较西酞普兰与文拉法辛治疗抑郁症的疗效及安全性.方法:将50例抑郁症患者随机分入两组分别用西酞普兰和文拉法辛治疗,疗程6周,用汉密尔顿抑郁量表(HAMD)评定临床疗效,副反应量表(TESS)评定不良反应.结果:西酞普兰组显效率64.0%,有效率88.0%,文拉法辛组为60.0%,80.0%,两组疗效相仿.在治疗2周末时,文拉法辛组减分多于西酞普兰组,差异有显著性.两组不良反应均轻微.结论:西酞普兰和文拉法辛抗抑郁疗效肯定,不良反应轻.     

Rates of depression in individuals with pathologic but not clinical Alzheimer disease are lower than those in individuals without the disease: findings from the Baltimore Longitudinal Study on Aging (BLSA)

The prevalence of major depression is increased in Alzheimer disease (AD), but currently the basis of this association remains unclear. The present study examined rates of depression in 4 groups of participants with postmortem examination from the Baltimore Longitudinal Study of Aging: (1) cognitively normal controls with no Alzheimer pathology, (2) cognitively normal individuals with Alzheimer pathology, (3) individuals with mild cognitive impairment plus Alzheimer pathology, (4) individuals with clinical diagnoses of dementia plus Alzheimer pathology. Depressive symptoms were assessed using the Center for Epidemiologic Studies Depression Scale. Individuals with Alzheimer pathology but no cognitive decline before death had significantly lower rates of depression than cognitively normal controls with no Alzheimer pathology and individuals with Alzheimer pathology plus clinical diagnoses of dementia. These findings suggest that depression is a risk factor for AD in the presence of AD pathology, but depression is not a risk factor for AD pathology.     

西酞普兰与氟西汀治疗恶劣心境对照研究

目的：探讨西酞普兰与氟西汀治疗恶劣心境的疗效和安全性。方法：将116例恶劣心境患者随机分为西酞普兰组和氟西汀组，治疗6周，用汉密尔顿抑郁量表（HAMD）和治疗中出现的症状量表（TESS）评定疗效和不良反应。结果：西酞普兰组和氟西汀组总体疗效相当，西酞普兰起效较快，不良反应较轻。结论：西酞普兰治疗恶劣心境既有效又安全。     

Selegiline-citalopram combination in patients with Parkinson's disease and major depression

INTRODUCTION: We evaluated the efficacy and safety of the selegiline citalopram combination in the treatment of major depression in patients with Parkinson's disease. METHOD: Eight consecutive depressed outpatients who had received previously selegiline monotherapy or (one patient) selegiline-levodopa combination (the dose of selegiline was 5-10 mg/day in each case) for mild to severe Parkinson's disease were treated with 20 mg citalopram/day. The severity of depression was evaluated on the Hamilton Depression Rating Scale before and 8 weeks after citalopram treatment. RESULTS: The majority of the patients (six) responded well to citalopram treatment and no adverse events occurred. CONCLUSION: The combination of a low dose of selegiline (5-10 mg daily) and citalopram (20 mg daily) may be an effective and safe method in the treatment of major depression in patients with Parkinson's disease. (Int J Psych Clin Pract 2000; 4:123-125)     

Pharmacologic management of neuropsychiatric symptoms of Alzheimer disease.

OBJECTIVE: To systematically review published clinical trials of the pharmacotherapy of neuropsychiatric symptoms of Alzheimer disease (AD). METHOD: We searched MEDLINE and EMBASE for published English-language medical literature. Our review focused on randomized controlled trials (RCTs) and corresponding metaanalyses. RESULTS: The pharmacotherapy of neuropsychiatric symptoms of AD has been studied with numerous RCTs. The largest number of studies has focused on antipsychotics. Data are of reasonably high quality and indicate that risperidone and olanzapine are more effective than placebo for institutionalized patients with severe agitation, aggression, and psychosis. The efficacy of antipsychotics is counterbalanced by safety concerns that include cerebrovascular adverse events and mortality. Cholinesterase inhibitors and memantine appear to have modest benefits for patients with mildly to moderately severe symptoms. Antidepressants are effective for treating depression in AD, but more data are required to determine the efficacy of trazodone and citalopram for agitation and aggression. Carbamazepine appears to be efficacious, although side effects and concerns about drug-drug interactions limit its use. The data do not support the use of valproate. Benzodiazepines should only be used for short-term, as-needed use. There are insufficient data on other pharmacologic interventions, such as beta blockers, buspirone, and estrogen preparations. CONCLUSIONS: Although there have been numerous well-designed studies of the pharmacotherapy of neuropsychiatric symptoms in AD, safer and more effective treatments are urgently needed.