草酸艾司西酞普兰治疗卒中后抑郁的疗效及其对患者MMSE评分、ADL评分的影响

目的探讨草酸艾司西酞普兰治疗卒中后抑郁(PSD)的疗效及其对患者MMSE评分、ADL评分的影响。方法将120例PSD患者随机分为对照组(60例)与观察组(60例),对照组在常规治疗基础上加用疏肝解郁胶囊,观察组在常规治疗基础上加用草酸艾司西酞普兰,采用美国国立卫生研究院卒中量表(NIHSS)、汉密尔顿抑郁量表(HAMD)、经简易智力状态检查量表(MMSE)、日常生活能力量表(ADL)进行疗效评价。结果治疗前,两组患者NIHSS评分、HAMD评分、MMSE评分、ADL评分比较差异无统计学意义(P0.05);治疗4周后,观察组HAMD评分显著低于对照组(P0.05),两组患者其余量表评分比较差异无统计学意义(P0.05);治疗24周后,观察组NIHSS评分、HAMD评分显著低于对照组,MMSE评分、ADL评分显著高于对照组(P0.05)。结论草酸艾司西酞普兰能够缓解PSD的抑郁症状,改善神经功能和认知功能,提高日常生活能力。     

西酞普兰对急性脑卒中后抑郁患者神经功能恢复的影响

目的研究西酞普兰对急性卒中后患者抑郁状态、日常生活活动能力和神经功能缺损程度的影响。方法根据汉密顿抑郁量表(HAMD)将卒中后抑郁患者86例随机分为治疗组和对照组,全部病例均进行常规药物治疗和康复训练,治疗组加用西酞普兰20mg口服,1次/d。所有患者在治疗前和治疗后4周用HAMD、Barthel指数(BI)、神经功能缺损程度量表(CSS)进行评分。结果治疗组治疗后HAMD评分、CSS评分均较治疗前显著下降(P<0.05),且明显低于对照组治疗后(P<0.05)。治疗组治疗后BI较治疗前显著升高(P<0.05),且明显高于对照组治疗后(P<0.05)。结论PSD脑卒中患者早期恢复有明显负面影响。西酞普兰能明显改善PSD患者抑郁状态,促进日常生活活动能力和神经功能的恢复。     

草酸艾司西酞普兰联合黛力新对脑卒中后抑郁障碍患者的疗效及对血清指标的影响

目的探讨草酸艾司西酞普兰联合黛力新对脑卒中后抑郁障碍(PSD)的疗效及对一些血清指标的影响。方法将92例PSD患者随机分为两组:观察组(n=46)应用草酸艾司西酞普兰联合黛力新治疗,对照组(n=46)应用黛力新治疗。治疗前后评估美国国立卫生研究院卒中量表(NIHSS)、日常生活活动能力Barthel指数(BI)、汉密尔顿抑郁量表(HAMD)和简易智力状态检查量表(MMSE)评分,测定血清5-羟色胺(5-HT)、多巴胺(DA)、去甲肾上腺素(NE)、神经生长因子(NGF)和脑源性神经营养因子(BDNF)水平。结果治疗前两组患者的上述指标结果,组间无明显差异(P0.05);治疗后观察组的NIHSS、HAMD评分显著低于对照组,BI、MMSE评分显著高于对照组(P0.05);治疗后观察组血清5-HT、NGF和BDNF水平均显著高于对照组(P0.05),两组血清NE、DA无明显差异(P0.05)。结论草酸艾司西酞普兰联合黛力新治疗PSD能够促进保护性神经递质与神经细胞因子的合成与释放,有效减轻抑郁状态,促进神经功能和认知功能的改善。     

丁苯酞软胶囊联合艾司西酞普兰治疗卒中后抑郁的临床研究

分析丁苯酞软胶囊联合艾司西酞普兰对卒中后抑郁患者的临床疗效。方法根据PSD诊断标准,共纳入102例PSD患者。随机将PSD患者分为研究组(丁苯酞软胶囊联合艾司西酞普兰治疗组)和对照组(艾司西酞普兰治疗组)各51例,共治疗8周。治疗前及治疗后第8周末采用美国国立卫生院脑卒中量表(NIHSS)、Barthel指数、汉密尔顿抑郁量表(Hamilton depression scale,HAMD)和汉密尔顿焦虑量表(Hamilton anxiety scale,HAMA)对患者神经功能缺损、日常生活能力、抑郁及焦虑程度进行评定,并观察治疗期间出现的不良反应。结果研究组临床有效率明显高于对照组(P<0.05);2组治疗后NIHSS评分、Barthel指数、HAMD和HAMA评分均明显改善(P<0.001),且研究组各评分明显优于对照组。2组不良反应均为轻中度,且发生率无明显差异(P>0.05)。结论丁苯酞软胶囊联合艾司西酞普兰可显著改善卒中后抑郁患者的神经功能缺损及焦虑、抑郁情绪,提高患者生活质量,且安全性良好。     

舒必利联合西酞普兰治疗老年抑郁症伴躯体症状疗效分析

目的探讨舒必利联合西酞普兰治疗老年抑郁症伴躯体症状的疗效。方法老年抑郁症患者随机数字表法分为2组,观察组:西酞普兰+舒必利组;对照组:西酞普兰组,评估比较2组疗效。结果经治疗8周后,观察组汉密顿抑郁量表(HAMD)、临床疗效总评量表(CGI)及老年抑郁量表(GDS)评分均显著低于对照组(P0.05);而2组TESS量表评分比较差异无统计学意义(t=0.323;P=0.748)。治疗8周后,观察组躯体症状发生率显著低于对照组,差异有统计学意义(11.63%.5/43vs 28.89,13/45;χ2=4.026,P=0.045)。结论舒必利联合西酞普兰治疗老年抑郁症伴躯体症状临床疗效佳,改善躯体症状明显,值得临床应用。     

西酞普兰治疗卒中后抑郁障碍的临床观察

目的 观察西酞普兰对卒中后抑郁障碍的疗效及神经功能康复的影响.方法 67例患者随机分为观察组33例,西酞普兰 常规脑血管病治疗;对照组34例.常规脑血管病治疗,治疗前及治疗2、4、8周时行汉密尔顿抑郁量表(HAMD)、日常生活能力(ADL)及神经功能缺损评分.结果 治疗2周时,观察组的抑郁评分显著下降(P＜0.01);8周结束时,观察组的抑郁分、神经功能缺陷分显著低于对照组(P＜0.01),ADL分显著高于对照组(P＜0.01).结论 西酞普兰不仅能改善早期卒中后抑郁患者的抑郁情绪,且对神经功能的恢复、日常生活能力的提高都有显著促进作用.     

草酸艾司西酞普兰联合经颅磁刺激对青壮年卒中后抑郁的治疗研究

目的 探讨经颅磁刺激(rTMS)联合草酸艾司西酞普兰治疗青壮年卒中后抑郁(PSD)的治疗效果。方法 选取2021年6月至2023年7月就诊于保定市第一中心医院与河北省第六人民医院的的青壮年PSD患者共106例,随机分为草酸艾司西酞普兰治疗组(38例)、草酸艾司西酞普兰联合高频rTMS治疗组(32例)及草酸艾司西酞普兰联合低频rTMS治疗组(36例),经过4 w治疗后采用汉密尔顿抑郁量表17 (HAMD-17)及患者健康问卷-9 (PHQ-9)观察各组治疗效果及抑郁症状改善情况。结果经治疗后,各组HAMD-17量表评分较治疗前均有降低;除单纯草酸艾司西酞普兰治疗组外,其余两组PHQ9量表抑郁评分较治疗前均有降低。总体来说,草酸艾司西酞普兰联合rTMS治疗组评分均低于非联合治疗组,差异有统计学意义(P<0.05),但高频rTMS治疗组与低频rTMS治疗组之间差异不明显(P>0.05)。结论 草酸艾司西酞普兰联合rTMS能够降低青壮年PSD患者HAMD-17评分及PHQ-9评分,改善抑郁症状。     

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.     

通窍活血胶囊联合草酸艾司西酞普兰对脑卒中后抑郁患者神经功能、认知功能及脑血流量的影响

目的观察通窍活血胶囊联合草酸艾司西酞普兰对脑卒中后抑郁(PSD)患者神经功能、认知功能及脑血流量的影响。方法将84例PSD患者分为对照组与观察组各42例,对照组采用草酸艾司西酞普兰治疗,观察组在此基础上加用通窍活血胶囊,均治疗8周,治疗前后采用美国国立卫生研究院卒中量表(NIHSS)评定患者神经功能,采用简易精神状态量表(MMSE)及汉密尔顿抑郁量表(HAMD)评定患者认知功能及抑郁状况的改善情况,并作脑CT灌注检查,测定患者脑血流量的变化,统计治疗不良反应。结果 (1)治疗8周,两组NIHSS、HAMD评分降低,MESS评分上升,与同组治疗前对比差异有统计学意义(P0.05),观察组NIHSS、HAMD评分降低及MESS评分上升幅度均高于对照组(P0.05);(2)治疗8周,两组CBV增加,MTT缩短,CBF上升,与同组治疗前对比差异有统计学意义(P0.05),观察组CBV、CBF上升幅度及MTT降低幅度均高于对照组(P0.05);(3)两组不良反应发生率对比差异无统计学意义(P0.05)。结论在PSD患者的临床治疗中,采用通窍活血胶囊联合草酸艾司西酞普兰方案,可优化患者神经功能、认知功能,改善其抑郁状态及血脑灌注水平,且安全性良好。     

西酞普兰联合认知行为治疗老年抑郁症的疗效及对生活质量的影响

目的探讨西酞普兰联合认知行为治疗老年抑郁症患者的临床疗效及对生活质量的影响。方法将116例老年抑郁症患者随机分为对照组与观察组,对照组单纯接受西酞普兰治疗,观察组接受西酞普兰联合认知行为治疗,疗程8周。采用汉密尔顿抑郁量表(HAMD)及健康状况问卷(SF-36)评估临床疗效及生活质量。结果治疗后4周及8周,观察组HAMD评分显著低于对照组,HAMD减分率显著高于对照组(P<0.05);观察组SF-36各项评分均显著优于对照组,差异具有统计学意义(P<0.05)。结论西酞普兰联合认知行为治疗老年抑郁症临床疗效更为理想,可显著提高患者生活质量。     

Depression after minor stroke: prevalence and predictors

Background and purpose: Post‐stroke depression (PSD) is one of the most frequent complications of stroke, with a prevalence ranging 20–60%. As PSD seems to be related to stroke severity, we hypothesized that the prevalence of PSD would be lower in patients with minor stroke. Methods: We investigated the prevalence and predictors of PSD over a 30‐month follow‐up period in a cohort of patients with minor ischaemic stroke (NIHSS ≤ 5). Results: We enrolled 105 patients (mean age 64.38 ± 11.2 years, M/F 69/36). PSD was diagnosed in 43 (41%) patients, 40 (93%) of whom had dysthymia; 22% of patients were already depressed at 1 month. The most frequent depressive symptoms (DSs) were working inhibition, indecisiveness, and fatigability. Patients who developed PSD were less educated (P = 0.044) and diabetic (P = 0.006). After excluding patients that were already depressed at 1 month, we performed a logistic regression model to detect predictors of PSD. Crying (P = 0.012, OR 1.067, CI 0.269–4.553) and guilt (P = 0.007, OR 0.037, CI 0.02ì03–0.401) at baseline were two DSs found to be significantly correlated with PSD. Higher educational level (P = 0.022, OR 0.084, CI 0.010–0.698) and diabetes (P = 0.007, OR 14.361, CI 2.040–101.108) were the risk factors significantly correlated with PSD. Conclusion: Post‐stroke depression is frequent even in patients with minor stroke. Early detection of DSs might help to predict long‐term development of PSD. No correlation was observed between lesion site or side and the development of PSD.     

卒中后抑郁与脑卒中患者载脂蛋白E水平对照研究

目的:探讨卒中后抑郁(PSD)患者载脂蛋白E(ApoE)水平特点,为PSD的诊断提供新的客观依据。方法:采用实时荧光定量PCR技术和酶联免疫吸附法(ELISA)检测PSD患者及卒中后非抑郁患者ApoE水平。结果:PSD组ApoE基因mRNA表达量低于卒中组,差异具有统计学意义(P<0.01);PSD组血清ApoE水平高于卒中组,差异具有统计学意义(P<0.05)。结论:PSD患者外周血ApoE基因mRNA表达和血清ApoE水平与卒中非抑郁患者不同。     

卒中亚急性期抑郁与急性期血浆同型半胱氨酸水平的相关性研究

目的 研究卒中亚急性期发生的卒中后抑郁（post-stroke depression,PSD）与卒中急性期血浆同型半胱氨酸（homocysteine,Hcy）水平的相关性。
方法 连续收集2010年4月～2011年7月北京航天总医院神经内科住院的198例缺血性卒中患者,根据《中国精神疾病分类方案与诊断标准》第3版（Chinese Classification and Diagnostic Criteria of Mental Disorders-3,CCMD-3）进行PSD的诊断,根据诊断结果分为PSD组102例和卒中后无抑郁组（对照组）96例。由固定的、经过培训的心理咨询师对PSD患者进行汉密尔顿抑郁量表17项（Hamilton Rating Scale for Depression-17,HRSD-17）评定,根据评定结果分为轻度、中度、重度抑郁组。采用微量荧光偏振免疫分析法于入院次日对所有患者进行血浆Hcy水平测定,比较两组患者血浆Hcy水平,并与PSD进行相关分析。
结果 PSD组102例患者有高同型半胱氨酸血症（hyperhomocysteinemia,HHcy）68例（66.7%）,对照组有12例（12.5%）,PSD组HHcy阳性检出率较对照组差异具有显著性（χ2=17.29,P＜0.001）。经非条件Logistic回归分析PSD的危险因素,显示血浆Hcy水平与PSD有相关性[优势比（odds ratio,OR）=1.946,P<0.001,95%可信区间（confidence interval,CI）1.10～1.22]。
结论 卒中急性期血浆Hcy水平与卒中亚急性期抑郁有相关性。     

Methylphenidate-enhanced antidepressant response to citalopram in the elderly: a double-blind, placebo-controlled pilot trial.

OBJECTIVE: The authors evaluated the potential of methylphenidate to accelerate and enhance antidepressant response to citalopram in elderly depressed patients. METHODS: Sixteen outpatients with major depression were treated in a 10-week double-blind trial. Response was defined as a score on the Hamilton Depression Rating Scale (24-item) of less than 10. RESULTS: An accelerated response was observed by week 3 in five subjects receiving citalopram (CIT)+methylphenidate (MPH) and in none of those receiving CIT+placebo (PBO). Subjects receiving citalopram and methylphenidate showed a significant improvement in depressive symptoms compared with those on citalopram and placebo. CONCLUSION: Combined treatment with citalopram and methylphenidate appears to be a viable strategy for accelerating and enhancing antidepressant response in elderly depressed patients limited by tolerability and safety.     

Association of post stroke depression with social factors,insomnia, and neurological status in Chinese elderly population

The purpose of this study was to investigate the association of post stroke depression (PSD) with social factors, insomnia, and neurological status among elderly Chinese patients with ischemic stroke. Six hundred and eight patients over 60 years of age, who had suffered from a first episode of ischemic stroke within 7 days, were enrolled into the study. They were divided into PSD and non-PSD groups according to the Self-rating Depression Scale (SDS) scores. The association of PSD with social factors, insomnia, and neurological status was analyzed using multivariable logistic regression analysis. Compared with the patients who did not develop PSD, those with PSD reported adverse life events more frequently, and more subjects with PSD lived alone, had left carotid artery infarction and cortical infarction (P < 0.05), history of insomnia, and high National Institute of Health Stroke Scale (NIHSS) scores and low Barthel Index (BI) scores (P < 0.01). The multivariable logistic regression analysis showed that the occurrence of PSD was associated with a history of insomnia (HR = 1.59, 95 % CI 1.12–2.36, P < 0.01), NIHSS scores (HR = 2.45, 95 % CI 1.42–3.91, P < 0.01) and BI scores (HR = 2.56, 95 % CI 1.39–4.25, P < 0.01). Insomnia and the degree of neurological deficit were associated with PSD in an elderly population of Chinese people.     

What causes increased stroke mortality in patients with prestroke dementia?

BACKGROUND AND PURPOSE: In patients with dementia, the incidence of stroke is higher and strokes are more severe and lethal. The purpose of this population-based study was to describe in what way previous dementia affects mortality in stroke patients. METHODS: Subjects were all persons > or =65 years old who had a first-ever stroke during 1 year (n = 327). The prestroke dementia (PSD) diagnosis was made at the time of the stroke diagnosis using data from next of kin and from patient records. Patients were followed prospectively and causes of death were evaluated. RESULTS: The 28-day case fatality was 44% for PSD patients and 15% for non-PSD patients. Corresponding ratios at 1 year were 71 and 36%, respectively. Twenty-eight percent of the PSD patients had a new stroke during the first year, compared to 8% of the non-PSD patients. More patients in the PSD group died as a direct or indirect consequence of their stroke. Multivariate analysis showed that PSD, in addition to age, atrial fibrillation and stroke severity, was an independent predictor of mortality. CONCLUSIONS: The PSD patients more often had a stroke-related death, even when we adjusted for a number of other factors. The cause for this is most likely multifactorial, including an increased tendency to contract complications in the acute phase, and iatrogenic causes. The brain of the PSD patients may also be frailer and more susceptible to ischemic or hemorrhagic damage than the nondemented brain.     

Post-stroke depression: different characteristics based on follow-up stage and gender–a cohort perspective study from Mainland China

Background: Post-stroke depression (PSD) is a common and important comorbidity in patients after stroke. It negatively impacts stroke survivors’ outcomes. Plenty of studies have investigated risk factors for PSD, especially sex differences. However, the results remain inconsistent. In this study, we explored the prevalence and risk factors for PSD both in the acute phase and the chronic phase of stroke, emphasizing on the impact of gender in PSD.

Methods: About 1094 patients with first-ever ischemic stroke were included in the study. Patients were followed up, respectively, 2 weeks, 3 months, and 12 months after stroke. Data collected included demographic and stroke-related factors, and whether patients still suffer from PSD at each time points. T-test, chi-square test, and Wilcoxon rank-sum test were used to explore the group differences between patients with PSD and without PSD, and between female and male patients. Logistic regression was performed to investigate the risk factors for PSD both in the acute and the chronic stage of stroke.

Results: The prevalence of PSD was 25.4, 17.6, and 12.4%, respectively 2 weeks, 3 months, and 12 months after stroke. Female patients had higher prevalence of PSD compared with male patients (31.4 vs. 22.4% 2 weeks after stroke; 20.05 vs. 16.22% 3 months after stroke; 15.04 vs. 11.05% 12 months after stroke). In the acute stage of stroke, female gender (OR 1.686 95%CI 1.155–2.462) and National Institutes of Health Stroke Scale (NIHSS) score (OR 1.118 95%CI 1.076–1.162) were independent risk factors for PSD. However, in the chronic stage of stroke, risk factors for PSD were different. At 3 months, NIHSS score (OR 1.082 95%CI 1.037–1.128), smoking (OR 1.772 95%CI 1.163–2.701), and frontal lobe lesion (OR 2.331 95%CI 1.472–3.692) were independent risk factors for PSD. On the other hand, education level (OR 0.693 95%CI 0.486–0.998) was a protective factor. About 12 months after stroke onset, NIHSS score (OR 1.113 95%CI 1.062–1.167) and living alone (OR 3.608 95%CI 1.538–8.466) were risk factors for PSD.

Conclusion: PSD is common in stroke survivors, and female patients have higher prevalence of PSD. Risk factors for PSD in the acute phase are different from that in the chronic phase of stroke. Female gender is an independent risk factor for PSD in the acute stage of stroke. Smoking, frontal lobe lesion, and living alone are predictive factors for PSD in the chronic stage of stroke. NIHSS score is a risk factor for PSD both in the acute and in the chronic stage of stroke. Further studies are needed to understand the mechanisms underlying the elevated prevalence of PSD in female.     

Mild depression in young adults with cerebral infarction at long-term follow-up: A population-based study

We sought to evaluate the prevalence of and risk factors for post-stroke depression (PSD) at long-term follow-up in young adults aged 15-49 years with first-ever cerebral infarction in a population-based study. Scores on Montgomery-Asberg Depression Rating Scale (MADRS) were obtained at follow-up (mean time 6.0 years after the stroke) and analysed in subgroups. MADRS scores were obtained in 196 of 209 surviving patients. PSD (MADRS>or=7) was detected in 56 patients (28.6%). None had severe PSD. Alcoholism (P=0.006), depressive symptoms any time before the index stroke (P=0.016), and severe neurological deficits on admission for the index stroke (P=0.043) were independently associated with PSD. PSD seems milder in young ischaemic stroke patients compared with older patients. Alcoholism, depression any time before the index stroke, and severity of neurological deficits on admission for the stroke increased the risk of developing PSD in the long run.     

RISK FACTORS FOR POST-STROKE DEPRESSION

Objective. To examine possible risk factors in post-stroke depression (PSD) other than site of lesion in the brain. Data sources. 191 first-ever stroke patients were examined physically shortly after their stroke and examined psychiatrically and physically 4 months post-stroke. Setting. A geographically defined segment of the metropolitan area of Perth, Western Australia, from which all strokes over a course of 18 months were examined (the Perth Community Stroke Study). Measures. Psychiatric Assessment Schedule, Mini Mental State Examination, Barthel Index, Frenchay Activities Index, physical illness and sociodemographic data were collected. Post-stroke depression (PSD) included both major depression and minor depression (dysthymia without the 2-year time stipulation) according to DSM-III (American Psychiatric Association) criteria. Patients depressed at the time of the stroke were excluded. Patients. 191 first-ever stroke patients, 111M, 80F, 28% had PSD, 17% major and 11% minor depression. Results. Significant associations with PSD at 4 months were major functional impairment, living in a nursing home, being divorced and having a high pre-stroke alcohol intake (M only). There was no significant association with age, sex, social class, cognitive impairment or pre-stroke physical illness. Conclusion. Results favoured the hypothesis that depression in an unselected group of stroke patients is no more common, and of no more specific aetiology, than it is among elderly patients with other physical illness. © 1997 John Wiley & Sons, Ltd.     

Post-stroke dementia is associated with alpha(1)-antichymotrypsin polymorphism

BACKGROUND AND PURPOSE: Alpha-1-antichymotrypsin (ACT) is an acute phase protein involved in inflammatory reaction, promoting the assembly of beta amyloid protein into filaments and contributing to its resistance to proteolytic digestion. The aim of our study was to determine ACT signal peptide polymorphism (A/T) as a possible risk factor for post-stroke dementia (PSD). METHODS: 142 consecutive ischemic stroke patients and 188 controls were included in this study. Pre-stroke dementia (PRESD) was evaluated using the Informant Questionnaire on Cognitive Decline in the Elderly (IQCODE). The diagnosis of the post-stroke dementia (PSD) was established according to DSM-IV criteria. The ACT gene (A/T) polymorphism was determined by PCR-RFLR. RESULTS: Both ACT-TT genotype and T-allele were significantly more prevalent in patients with PSD than in non-demented stroke patients, controls or patients with PRESD. After adjustment for age, gender, and vascular risk factors, both the ACT-TT genotype and T-allele remained independently associated with PSD. CONCLUSION: Our findings suggest that ACT polymorphism (A/T) is a risk factor for PSD.