百忧解治疗脑卒中后抑郁及神经功能缺损的疗效观察

目的　观察百忧解治疗脑卒中后抑郁状态的疗效。方法　对 5 6例脑卒中后抑郁状态患者 ,随机分为治疗组 (加用百忧解 )和对照组 (常规治疗 )各 2 8例 ,进行对照观察。治疗前后行汉密尔顿抑郁量表 (HAMD)、日常生活能力 Barthel指数(BI)量表及神经功能缺损评分 (SSS)量表进行评定其疗效。结果　治疗组 HAMD评分治疗后 (4.8± 1.6 )较治疗前 (2 1.4±4 .1)显著下降 (P <0 .0 1) ,对照组治疗后 (15 .1± 2 .3)与治疗前 (2 0 .4± 3.6 )比较无显著差异 (P >0 .0 5 )。治疗组治疗后 SSS评分显著降低 ,BI评分明显提高 ,与对照组比较也有显著差异 (均 P <0 .0 1)。结论　百忧解治疗脑卒中后抑郁状态不仅对抑郁有明显效果 ,且可促进脑卒中后神经功能的恢复     

抗抑郁治疗对卒中后抑郁康复的影响

目的 探讨和研究选择性5-羟色胺再摄取抑制剂(SSRI)类药物百优解对卒中后抑郁的疗效,及其对肢体功能康复的影响.方法 选择86例卒中后抑郁的患者作为研究对象,随机分为治疗组和对照组,治疗组给予百优解口服,对照组给予安慰剂口服,其他治疗相同.分别于治疗后2、4、6周末进行HAMD抑郁量表评分和神经功能缺损、生活能力状态评定.结果 治疗组和对照组比较,抑郁改善程度、神经功能缺损及生活能力状态改善程度均有显著性差异.结论 对脑卒中后抑郁的抗抑郁治疗不但能有效改善抑郁症状,而且有利于患者神经功能缺损的康复和生活能力的提高.     

盐酸帕罗西汀治疗老年脑卒中后抑郁症32例观察

目的　观察盐酸帕罗西汀对老年脑卒中后抑郁状态的疗效。方法　对 64例老年脑卒中合并抑郁的患者随机分为治疗组 (加用盐酸帕罗西汀 )和对照组 (常规治疗 )各 3 2例。治疗前后行汉密尔顿抑郁量表 (HAMD)、日常生活能力Barthel指数(BI)量表及神经功能缺损计分 (SSS)量表进行评定 ,对照观察其疗效。结果　治疗组HAMD评分治疗后 ( 9 0 8± 1 5 8)较治疗前 ( 17 5 0± 3 3 7)显著下降。治疗组治疗后SSS评分显著降低 ,BI评分明显提高 ,与对照组比较有显著性差异 (均P <0 0 1)。结论　盐酸帕罗西汀治疗老年脑卒中后抑郁状态疗效显著 ,并有效提高脑卒中后神经功能的恢复     

帕罗西汀与阿米替林治疗脑卒中后抑郁症的对照研究

目的对比帕罗西汀与阿米替林治疗脑卒中后抑郁、神经功能康复的疗效。方法 59例脑卒中后抑郁患者随机分为2组,抑郁评分采用汉密尔顿抑郁量表(HAMD)在2组治疗前及治疗后2、4、8周末评分,神经功能康复采用斯堪的纳维亚卒中量表(SSS)及日常生活能力Barthel指数(BI)在2组治疗前后评分。结果治疗2、4、8周末帕罗西汀组HAMD评分与对照组比较有显著性差异(P0.01);治疗后帕罗西汀组SSS、BI评分均明显增加,与对照组相比有显著性差异(P0.01)。结论帕罗西汀对脑卒中后抑郁、神经功能康复的疗效优于阿米替林。     

抗抑郁治疗对老年脑卒中后抑郁及康复的影响

目的:观察抗抑郁治疗对老年缺血性脑卒中后抑郁症状及神经功能康复的作用.方法:将老年脑卒中后抑郁患者356例分为文拉法辛组128例、阿米替林组116例及对照组112例,于治疗前后进行汉密尔顿抑郁量表(HAMD)和神经功能缺损量表(CSS)、日常生活能力量表(ADL)评定.结果:文拉法辛组和阿米替林组治疗第2周HAMD评分和第12周CSS评分较治疗前和对照组均明显降低;文拉法辛组和阿米替林组3个月后ADL亦明显改善(P均＜0.05),但阿米替林组不良反应明显高于文拉法辛组.结论:抗抑郁治疗有利于老年脑卒中后抑郁患者神经功能康复,提高生活能力,减少并发症.     

帕罗西汀联合心理干预治疗卒中后抑郁/焦虑的前瞻性对照研究

目的　探讨卒中后抑郁/焦虑对卒中患者日常生活能力和神经功能康复的影响,以及帕罗西汀联合早期心理干预的临床疗效。方法　采用抑郁自评量表(SDS)、焦虑自评量表(SAS)对272例脑卒中患者进行抑郁/焦虑状态评定,其中患有卒中后抑郁并发焦虑的81名患者随机分成3组,分别接受单用帕罗西汀治疗、帕罗西汀联合心理治疗以及不干预。采用斯堪的那维亚脑卒中量表(SSS)、Barthel指数(BI)、汉密尔顿抑郁量表(HAMD)、汉密尔顿焦虑量表(HAMA)评测治疗前后的疗效。结果　急性脑卒中患者卒中后抑郁并焦虑患病率为29.78%,抑郁与焦虑共病率为65.85%,额叶、左侧大脑半球、基底节病灶与卒中后抑郁/焦虑的发生相关(额叶P <0.05、左侧大脑半球P <0.0001、基底节P <0.0001);治疗组I和治疗组II HAMD、HAMA、SSS评分减少和BI评分增加与对照组比较均有显著性差异(P均<0.01),治疗组II HAMD、HAMA、SSS评分减少和BI评分增加较治疗组I有显著性差异(P均<0.05)。结论　卒中后抑郁/焦虑的发生与脑卒中部位相关;卒中后抑郁/焦虑障碍明显降低患者神经功能康复程度和生活能力恢复;对卒中后抑郁/焦虑患者单用药物帕罗西汀或给予帕罗西汀联合心理干预治疗均能提高患者神经功能康复程度和生活能力恢复,而且帕罗西汀联合心理干预治疗疗效更满意     

脑卒中后伴发抑郁状态的临床分析

目的 通过对脑卒中后抑郁状态(post-stroke depression, PSD)发病率及抗精神病药物治疗的对比分析,探讨其发病机制及药物干预的可行性.方法 对230例脑卒中患者用抑郁自评量表(SDS)及汉密尔顿抑郁量表(HAMD)进行评定,并把HAMD17项版总分>20分的84例患者随机分为2组,治疗组给予5-羟色胺再摄取抑制剂类药物帕罗西汀治疗4周,并分别于治疗后2、4周以HAMD减分率作为判断疗效指标,同时进行神经功能缺损评定.结果 脑卒中后PSD发病率为36.52%,2组HAMD评分4周后较2周后显著减少(P<0.01),但4周后2组有效率无显著差异(P>0.05);2组神经功能缺损评分4周后较2周后有显著改善(P<0.05),但4周后有效率2组无明显差别.     

舍曲林治疗青年脑卒中后抑郁疗效观察

目的 探讨舍曲林对青年脑卒中后抑郁（post-stroke depression PSD）的治疗效果.方法 青年脑卒中患者在入院时采用Hamiliton 抑郁量表（HAMD）、Spitzer生存质量指数量表（QLI）、神经功能缺损量表进行筛选评分,对符合抑郁状态诊断的47例患者随机分为治疗组和常规组,常规组采用常规的药物治疗和护理,治疗组同时给予舍曲林治疗,治疗8周后采用Hamiliton 抑郁量表（HAMD）、Spitzer生存质量指数量表（QLI）、神经功能缺损量表对2组进行评定.结果 治疗组活动能力、日常生活评分、健康感觉、家庭和社会的支持以及对前景的认识方面明显优于常规组,抑郁情况与常规组比较明显改善（P＜0.01）.结论 舍曲林可明显改善青年脑卒中后抑郁患者的抑郁症状,加快神经功能恢复,提高生活质量.     

黛力新对脑卒中后抑郁患者预后的影响

目的观察氟哌噻吨美利曲辛(黛力新)对脑卒中后抑郁症患者预后的影响。方法将122例脑卒中后抑郁患者按随机数字表法分为治疗组(61例)和对照组(61例),2组均给予常规治疗,治疗组加用黛力新治疗4周。于治疗前和治疗2、4周末采用汉密尔顿抑郁量表(HAMD)评定疗效,同时采用中国卒中量表(CSS)评价患者神经功能缺损程度,蒙特利尔认知评估量表(MoCA)评估患者认知功能。结果治疗组总有效率明显高于对照组[91.8%(56/61)vs.70.5%(43/61),P<0.05]。治疗组治疗4周末HAMD评分、CSS评分、MoCA评分均明显优于对照组,且治疗组未发现明显不良反应。结论黛力新可显著改善脑卒中后抑郁症患者的抑郁症状,且对神经功能和认知功能的恢复也有一定的促进作用。     

心理干预联合早期康复对脑卒中后抑郁及神经功能缺损的影响

目的探讨心理干预联合早期康复对脑卒中后抑郁及其神经功能缺损症状和日常生活能力的影响。方法将90例脑卒中后抑郁患者随机分为治疗组45例,对照组45例。治疗组在神经内科常规治疗的基础上进行心理干预及早期康复训练;对照组进行神经内科常规治疗。两组患者入院第3 d及治疗后第2、4、6周均进行汉密尔顿抑郁量表（HAMD）、美国国立卫生研究院卒中量表（NIHSS）和日常生活能力量表（ADL）评分。结果治疗组HAMD评分和NIHSS评分明显减少,ADL评分明显增高（p〈0.05）。结论心理干预联合早期康复对改善脑卒中后抑郁及神经功能缺损症状和日常生活能力效果明显。     

氢溴酸西酞普兰对缺血性脑卒中后抑郁患者的情绪、认知功能和神经功能的影响

目的探讨氢溴酸西酞普兰联合奥扎格雷钠对缺血性脑卒中后抑郁患者的情绪、认知功能和神经功能的影响。方法选取我科2017年7月~2019年7月期间收治的119例缺血性脑卒中后抑郁患者作为研究对象,采用随机数字表法分为2组,均给予奥扎格雷钠作为基础治疗,对照组59例增加氟西汀治疗,观察组60例增加氢溴酸西酞普兰治疗,16周后,对比两组患者临床疗效、抑郁状态、认知功能、神经功能和药物安全性。结果观察组治疗后有效率91.67%(55/60)高于对照组76.27%(45/59)(P<0.05);两组治疗方案均可降低患者治疗后汉密尔顿抑郁量表(HAMD-17)评分和提高简易精神状态量表(MMSE)评分,但观察组降低HAMD-17评分和提高MMSE评分幅度高于对照组(P<0.05);两组治疗方案均可降低患者治疗后的美国国立卫生研究院卒中量表(NIHSS)评分和提高巴氏量表(Barthel指数),但观察组降低NIHSS评分和提高Barthel指数高于对照组(P<0.05);观察组在治疗期间西酞普兰平均用药量(23.68±3.49)mg略低于对照组氟西汀平均用药量(27.73±3.56)mg(t=6.2667,P<0.05)。结论氢溴酸西酞普兰联合奥扎格雷钠治疗缺血性脑卒中后抑郁患者效果确切,能够更好改善患者的抑郁状态,提高认知功能,促进神经功能的恢复,提高日常生活活动能力。     

Early fluoxetine treatment of post-stroke depression

Objective: Poststroke depression is a frequent psychiatric complication after stroke that may have strong negative impact on rehabilitation therapy and functional recovery. This study was conducted to show the efficacy and safety of early treatment with the selective serotonin reuptake inhibitor fluoxetine in post-stroke depressed patients. Methods: This double-blind, randomized placebo-controlled study was of patients within two weeks after stroke. Moderate to severe depressed patients (determined by Hamilton Depression Scale (HDS) > 15, the Beck Depression Inventory (BDI) and the Clinical Global Impression (CGI) Scale) were randomized to receive either 20 mg/d fluoxetine or placebo for 3 months. Beside the psychiatric assessment, patients were evaluated by use of the Scandinavian Stroke Scale (SSS), the Mini-Mental-State-Examination (MMSE) and the Barthel-Index (BI). An open-label long-term follow up was done 18 months after the initial assessment. Results: 54 depressed patients of an inpatient population of 242 consecutive stroke patients aged 25 to 85 years entered the trial within the first two weeks post-stroke. 50 patients completed the trial per-protocol. The initial severity of depression was comparable in the two groups (mean baseline HDS score 32.8 in the fluoxetine vs. 30.3 in the placebo group), as were neurological symptom severity and demographic parameters. Significant improvement was seen in both groups within 4 weeks of treatment, whereas no advantages of fluoxetine could be observed at this time. This indicates a high degree of spontaneous recovery during early rehabilitation therapy. BDI scores of patients treated with fluoxetine further decreased until the follow-up at 12 weeks, whereas the scores increased again in the placebo group. This depressive relapse of the placebo patients after the end of most rehabilitation efforts was evident at a long-term follow-up 18 months after inclusion, when patients who had been treated with fluoxetine were significantly less depressed. No side effects of fluoxetine treatment were detected. Conclusions: The advantages of fluoxetine were obvious at the follow-up 18 months after inclusion, but could not be demonstrated within the first three months of controlled treatment. The multitude of therapeutic efforts that take place in the early phase of rehabilitation might have facilitated spontaneous recovery from depression and might have hindered benefits of antidepressant treatment to become obvious. Fluoxetine treatment was well tolerated and safe. Received: 5 February 2002, Received in revised form: 8 October 2002, Accepted: 28 October 2002 Correspondence to Stefan Fruehwald, MD     

文拉法辛对脑卒中后抑郁患者的神经功能缺损及生活自理能力的影响

目的研究文拉法辛治疗脑卒中后抑郁患者时对神经功能缺损及生活自理能力的影响。方法选取2013-04—2014-12我科60例脑卒中后抑郁患者,随机分为对照组及研究组,对照组采用黛力新0.5mg/d治疗,研究组给予文拉法辛75mg/d治疗,此外,所有入选患者均接受相同的康复治疗和常规药物治疗,疗程共6周。在治疗前及治疗后第2、4、6周末,用汉密尔顿抑郁评定量表(HAMD)、焦虑量表(HAMA)和巴氏指数(BI)及美国国立卫生院卒中评分(NIHSS)评估疗效。结果 2组治疗后HAMD、HAMA得分较治疗前明显下降(P0.05)。治疗前BI及NIHSS评分差异均无统计学意义(P0.05),治疗第2周后NIHSS评分,治疗组较对照组明显降低(P0.05),而BI 2组无明显差异(P0.05);起病后6周,研究组BI较对照组升高(P0.01)。结论文拉法辛治疗脑卒中后抑郁的疗效可靠,并能改善患者神经功能及日常生活能力,促进肢体神经功能的康复,从而提高患者的生活质量。     

疏肝解郁胶囊治疗脑卒中后抑郁患者疗效及日常生活活动能力研究

目的探讨疏肝解郁胶囊治疗脑卒中后抑郁的疗效、日常生活能力、安全性的研究。方法未服用过抗抑郁药物的脑卒中后抑郁患者40例做为对照组,实验组为40例服用疏肝解郁胶囊治疗前、治疗6 w末及12 w末脑卒中后抑郁的患者,采用汉密尔顿抑郁量表(HAMD)评分,日常生活活动能力量表(Barthel指数)评分。结果实验组未治疗前与对照组HAMD评分及Barthel指数评分比较无明显统计学差异(P0.05),服用疏肝解郁胶囊治疗6 w末与对照组HAMD评分及Barthel指数评分有统计学差异(P0.05),并且治疗12 w末与对照组HAMD评分及Barthel指数评分有明显的统计学差异(P0.01)。同时HAMD评分有效率结果表明,对照组未服用疏肝解郁胶囊6 w及12 w末有效率为0%,治疗组服用疏肝解郁胶囊6 w及12 w末有效率分别为75%及85%。结论疏肝解郁胶囊能有效治疗脑卒后抑郁,并且能改善脑卒中后抑郁患者日常生活活动能力,不良反应较少,安全性高。     

Effect of chronic antidepressant treatment with adinazolam and desipramine on melatonin output.

Output of melatonin or its main metabolite, 6-sulphatoxy melatonin, provides an index of noradrenergic activity in the pineal gland, which is of interest in major depression and during its treatment with antidepressants. Fifteen female depressed outpatients did not differ in levels of 24-hour urinary 6-sulphatoxy melatonin compared with 13 female control subjects. However, a subgroup of the depressed patients (n = 9) who were treated with desipramine showed a significant elevation of 6-sulphatoxy melatonin levels after 1 week of treatment and a return to baseline levels after 6 weeks. There was also a significant negative correlation between 6-sulphatoxy melatonin levels and symptom severity as measured by the Hamilton Rating Scale for Depression after 3 weeks of treatment with desipramine. The other subgroup of depressed patients (n = 6) were treated with adinazolam, a benzodiazepine with antidepressant properties. Despite comparable antidepressant effects to those achieved with desipramine, adinazolam was not associated with any apparent change in 6-sulphatoxy melatonin output during 6 weeks of treatment. There was also no correlation between 6-sulphatoxy melatonin levels and symptom severity.     

Using a self-report depression scale to identify remission in depressed outpatients

OBJECTIVE: Some have suggested that standardized rating scales be used in clinical practice to monitor the course of treatment; however, the time demands of clinical practice make it difficult to use such measures. This study derived a cutoff on a self-report depression questionnaire corresponding to the most widely used definition of remission (a score < or =7 on the 17-item Hamilton Depression Rating Scale). METHOD: Two hundred sixty-seven depressed outpatients were rated on the Hamilton depression scale and completed the Clinically Useful Depression Outcome Scale (CUDOS). The authors used receiver operating curve analysis to examine the ability of the CUDOS to identify remission on the Hamilton depression scale. RESULTS: A high level of agreement was found between the self-report and Hamilton depression scale assessments of remission. CONCLUSIONS: Self-report questionnaires represent a practical option for thoroughly and objectively evaluating the course of treatment and determining remission in depressed patients.     

A study of post-stroke depression in a rehabilitative center

This was a prospective study of 52 stroke patients. The incidence of post-stroke depression was 55%. A past history of depression was significantly associated with the clinical assessment of depression. There was no association between the clinical assessment of depression and type and site of lesion and intellectual impairment. The clinical assessment of depression was significantly associated with the degree of functional impairment. The clinical assessment of depression also correlated well with Hamilton Depression Rating Scale score. We conclude that post-stroke depression is unlikely to be caused by neuronal injury due to the cerebrovascular accident. There is also a significant reactive component to it. The Hamilton Depression Rating Scale is suitable for assessing the severity of depression in stroke patients.     

Cognitive function,thyroid status and postpartum depression

Impairment of cognitive function can occur with thyroid disorder and also with depression. Since depression occurs in conjunction with postpartum autoimmune thyroiditis, the question arises as to whether any impairment of cognitive function in postpartum women is related to change in thyroid status or to depressed mood. A total of 242 women (110 thyroid antibody-positive and 132 antibody-negative) were assessed at 8, 12, 20 and 28 weeks postpartum in the outpatients of a district general hospital. Thyroid antibody levels (antimicrosomal and antithyroglobulin) were monitored at monthly intervals, together with plasma T3, T4 and thyroid-stimulating hormone. The main outcome measures were Research Diagnostic Criteria for depression, the 17-item Hamilton Depression Rating Scale and the Edinburgh Postnatal Depression Scale, together with reaction time and digit span. Subjects with postnatal depression showed detectable cognitive impairment independent of thyroid antibody status and actual thyroid dysfunction.     

抑郁症首次发病患者认知功能的研究

目的探讨抑郁症首次发病(以下简称首发)患者的认知功能特点及其影响因素。方法采用韦氏成人智力量表、韦氏记忆量表、威斯康星卡片分类测验(WCST)分别评定116例首发抑郁症患者(抑郁症组)和41名健康人(对照组)的认知状况,采用汉密尔顿抑郁量表(24项,HAMD)评定病情严重程度。对影响神经心理学测验成绩的临床症状进行逐步多元回归分析。结果(1)抑郁症组的长时记忆[(35.28±7.27)分]、短时记忆[(51.32±13.41)分]、记忆商数[(89.46±17.84)]、语言智商数[(110.96±13.72)]、操作智商数[101.90±15.98)]、智商数[(107.41±15.78)]均明显低于对照组[长时记忆(44.05±5.06)分,短时记忆(71.41±8.51)分,记忆商数(121.90±11.26),语言智商数(117.49±10.99),操作智商数(117.24±10.54),智商数[(118.98±10.95)],差异均有统计学意义(均P<0.01)。抑郁症组的WCST总测验数[(74.70±27.96)个]、持续错误数[(26.07±15.31)个]、随机错误数[(24.46±17.54)个]均明显高于对照组[WCST总测验数(60.15±23.05)个,持续错误数(17.56±11.44)个,随机错误数(17.73±14.27)个],差异有统计学意义(P<0.01或<0.05)。抑郁症组长时记忆成绩、短时记忆成绩和记忆商数低于对照组2个标准差。(2)逐步多元回归分析显示,抑郁症患者的长时记忆成绩及记忆商数与绝望感因子分均呈负相关(均P=0.00),短时记忆成绩和即刻记忆成绩与阻滞因子分均呈负相关(均P=0.00),语言智商与焦虑/躯体化因子分呈负相关(P=0.01),操作智商及智商与HAMD总分均呈负相关(均P=0.01),WCST总测验数和持续错误数与HAMD总分均呈正相关(P=0.01,P=0.02),随机错误数与阻滞因子分呈正相关(P=0.02)。结论首发抑郁症患者急性期的记忆、语言智商、操作智商和执行功能明显减退,临床症状严重程度影响认知功能的改变。     

生物反馈治疗卒中后焦虑抑郁状态伴失眠的研究

目的 研究生物反馈治疗卒中恢复期焦虑抑郁状态伴失眠的疗效及安全性。 方法 纳入卒中恢复期焦虑抑郁伴失眠患者,均给予生物反馈训练,训练方法为每周五次,每次 30 min的自主神经系统放松康复训练。所有患者在训练前后评定汉密尔顿焦虑量表（Hamilton Anxiety Scale,HAMA）、汉密尔顿抑郁量表（Hamilton Depression Scale,HAMD）、匹兹堡睡眠质量指数量表 （Pittsburgh Sleep Quality Index,PSQI）、患者健康问卷-9（Patient Health Questionnaire-9,PHQ-9）、简 易精神状态检查表（Mi ni -mental State Examination,MMSE）、Fugle-Meyer肢体功能评分（Fugl e-Meyer Scale,FMS）、美国国立卫生研究院卒中量表（National Institutes of Health Stroke Scale,NIHSS）以及 Barthel指数（Barthel Index,BI）,并采集患者的睡眠时间,对比分析训练前后这些量表评分及睡眠时 间的变化。 结果 研究共纳入并完成3 0例患者的数据统计。治疗后患者睡眠时间较治疗前显著增 加[（4.81±1.58）h vs（7.30±1.34）h,P＜0.001]。HA M A[（17.50±8.41）vs（9.00±7.01）]和 HAMD（[ 19.53±7.82）vs（9.23±4.42）]评分均有显著改善（均P＜0.001）。训练4周后患者的MMSE评 分有提高,Fugl e-Meyer分数增加,Barthel指数增加,但无统计学意义,NIHSS评分降低,差异有显著性 （P =0.033）。 结论 生物反馈疗法有利于卒中后焦虑抑郁伴失眠患者的睡眠和情绪改善,提高康复效果。