脑卒中后抑郁的研究进展

脑卒中后抑郁(poststroke depression,PSD)是脑卒中后最常见的情绪障碍。PSD会影响患者日常生活能力和神经功能缺损的恢复,造成脑卒中病程迁延,是影响脑卒中后患者生活质量的因素之一。PSD的病理生理机制尚未完全阐明,可能涉及生物学、行为和社会等多项因素。本文对脑卒中后抑郁的发病机制以及诊断和治疗的最新进展进行综述。     

脑卒中后抑郁的研究进展

随着全球经济的发展,人民生活水平的提高,生活节奏的加快,竞争的日趋激烈,脑血管病（cerebral vascular disease CVD）发病率呈现明显上升趋势,并成为当今世界严重危害人类健康的三大疾病之一。CVD不但发病率、死亡率高,而且有很高的致残率,不仅导致患的生理性残疾,同时也给患带来精神上的压力从而造成心理障碍。脑卒中后抑郁（poststroke depression PSD）则是脑卒中后情绪障碍的主要表现形式,它不仅使CVD康复时间延长,而且降低了患的生活质量,增加了死亡率。有学对脑卒中患进行了为期10年的随访,发现有539／6的患死于PSD,其死亡率比无抑郁组高3～4倍。这表明PSD对CVD的病程、康复和预后都将产生重大的影响。近年来国内外学PSD进行了广泛的研究,而其发生机制目前尚无一致的结论。本就近年来PSD的研究进展综述如下。     

脑卒中后抑郁发病机制的研究进展

脑卒中是造成第三位全球人类死亡的原因,多数研究者更关注脑卒中后运动功能障碍,但脑卒中后患者的认知和情绪等方面也受到不同程度的损害,主要表现为精力不足、睡眠障碍、兴趣降低、被动、悲观甚至自杀.大约20％的脑卒中幸存者在12个月的随访中发展为抑郁症[1] ,并且脑卒中后抑郁( post-stroke depression,...     

脑卒中后焦虑抑郁共病研究进展

脑卒中患者除偏瘫外,还可出现一系列情感行为的变化,其中抑郁和焦虑是脑卒中后常见的心理障碍.有研究表明只有39.5%的情感障碍和59.3%的焦虑障碍是以单独的形式出现的,而焦虑抑郁共病（comorbid anxiety and depression,CAD）则是最常见的共病模式[1].这种情绪变化不仅影响患者的生存质量,也妨碍其神经功能的恢复,不仅给患者带来躯体上和精神上痛苦,而且增加了家庭和社会的负担,为此,越来越多的学者意识到脑卒中后抑郁焦虑共病早期诊断和积极干预的重要性.现将脑卒中后焦虑抑郁共病的研究情况作一介绍.     

脑卒中后抑郁的相关因素

脑卒中后抑郁(post-stroke depression,PSD)是脑卒中后急性期至2-3年内常见的并发症。目前对PSD的研究发现,PSD的发生不但与卒中损伤部位和卒中后神经功能缺损程度等生物学因素有关,还与病人本身的人格特征、认知功能损害程度以及社会支持等心理社会因素有关。     

脑卒中后抑郁对神经功能的影响

目的探讨脑卒中后抑郁对神经功能的影响。方法根据Hamilton抑郁量表(21项评分标准)评定结果,将208例急性脑卒中患者分成抑郁组及非抑郁组(对照组),比较2组患者12周后的神经功能恢复情况。结果 208例急性脑卒中患者中发生抑郁症53例,发生率25.48%。12周后神经功能恢复总有效率:抑郁组67.92%,对照组79.35%,差异有统计学意义(P<0.05)。抑郁组比对照组神经功能缺损评分高,差异有统计学意义(P<0.05)。抑郁组不同程度抑郁患者神经功能缺损程度不同,两者呈正相关。结论脑卒中后抑郁严重影响患者神经功能恢复,抑郁程度与神经功能缺损呈正相关。     

脑卒中后抑郁的研究进展

抑郁(depression)是脑卒中后的常见并发症,脑卒中后重度抑郁者占10%～25%,轻度抑郁者占10%～40%[1].症状在脑卒中后第3个月最为常见,且在随后1年中患病率无下降.有研究表明,脑卒中后抑郁对日常生活能力(activity of daily living,ADL)有不利影响,易损害注意力、学习能力及记忆功能.脑卒中后抑郁症的严重程度与脑卒中的愈后有密切关系,如不给予及时治疗,抑郁症状至少持续7～8月,给患者的康复训练带来困难.目前,脑卒中后抑郁(post-stroke depression,PSD)作为治疗学单位受到越来越多学者的重视.     

脑卒中后抑郁与认识功能的关系研究

目的 研究脑卒中后抑郁与脑卒中后认知功能的关系。方法 选取2014年6月～2014年12月西安交通大学第二附属医院住院的首发脑卒中患者,简短照料者问卷得分≤56分,脑卒中发病2周之内,无意识障碍及失语,至少一侧上肢肌力≥3级,能够完成量表测查者,于脑卒中急性期、脑卒中后3月应用MMSE和MOCA评定认知功能,应用流调用自评抑郁量表(CES-D)评定抑郁情况。结果 脑卒中后急性期共入组患者128例,完成脑卒中后3月随访患者106例; 脑卒中后3月MMSE、MOCA评分较脑卒中急性期升高(P<0.05)。脑卒中后3月CES-D得分≥16分(存在抑郁)者22例,脑卒中后抑郁发生率为20.7%。脑卒中后急性期抑郁组与非抑郁组MMSE、MOCA评分差异不明显(P>0.05),脑卒中后3月抑郁组MMSE得分、MOCA得分明显低于非抑郁组,抑郁组与非抑郁组比较MMSE、MOCA评分增加值差异明显(P<0.05)。结论 脑卒中后3月认知功能较脑卒中急性期改善,脑卒中后抑郁加重了脑卒中后认知功能障碍,影响了脑卒中后认知功能的改善。     

288例脑卒中后抑郁的临床分析

目的探讨脑卒中后抑郁（PSD）的发生率及其主要相关因素。方法选择在本院住院确诊为脑卒中患者769例,采用汉密尔顿抑郁量表（HAMD）17项评分≥18分及卒中患者神经功能缺损程度进行评估。结果 PSD288例,发生率为37.45%,且与卒中性质、部位、程度、生化指标异常等密切相关。动态观察卒中患者CRP水平有助于早期发现PSP。结论预防性抗抑郁剂应用和抗抑郁剂治疗PSD,不仅减低PSD发生率,且有助于PSD和卒中患者神经功能的恢复。     

脑卒中后抑郁相关因素的研究进展

脑卒中是发病率、死亡率高、敛残率高的疾病。近年来其发病率呈现明显上升趋势,已成为当今世界严重危害人类健康的三大疾病之一。它不仅导致患者的运动功能障碍,同时也给患者带来精神上的压力而造成心理障碍。脑卒中后抑郁（post stroke depression PSD）则是脑卒中后情绪障碍的主要表现形式,它不仅使脑卒中康复时间延长,降低患者的生活质量,延长住院时间,增加医疗费用,而且增加死亡率。有学者对脑卒中患者进行了为期10年的随访,发现有53％的患者死于PSD,其死亡率比无抑郁组高3～4倍。这表明PSD对脑卒巾的病程、康复和预后都将产生重大的影响。然而有关PSD发生的相关因素的研究结果尚不一致,目前PSD相关因素研究已由神经生物学因素的研究转为对生物心理社会因素相互作用模式的探讨,本文对PSD相关因素的研究进展综述如下。     

男性卒中后焦虑/抑郁症患者血清性激素水平变化研究

目的 探讨男性性激素水平(雌二醇、睾酮、孕酮)与卒中后焦虑、抑郁症的关系.方法 检测和比较30例男性卒中后焦虑、抑郁症患者和30例非卒中后焦虑、抑郁症患者的血清雌二醇、睾酮、孕酮的水平,并应用汉密尔顿焦虑量表(HAMA)和汉密尔顿抑郁量表(HAMD)对卒中后焦虑、抑郁症患者进行临床评分,同时作相关分析.结果 男性卒中后焦虑、抑郁症患者血清雌二醇水平均显著低于对照组(P<0.05),雌二醇水平与HAMA分和HAMD分呈负相关(r=-0.540,P<0.05;r=-0.503,P<0.05).睾酮水平显著低于对照组(P<0.05),睾酮水平与HAMA分和HAMD分呈负相关(r=-0.535,P<0.05;r=-0.602,P<0.05).两组的孕酮水平无显著变化(P>0.05).结论 卒中后焦虑、抑郁症存在明显的性激素水平的紊乱,与脑卒中的发病发展有着密切的关系.血清雌二醇、睾酮可能成为卒中后焦虑、抑郁症的生物学标记.     

参松养心胶囊联合黛力新对卒中后抑郁及神经功能恢复的影响

目的观察参松养心胶囊联合黛力新治疗卒中后抑郁的疗效。方法64例卒中后抑郁患者随机分组后分剐接受参松养心胶囊和黛力新联合治疗（治疗组）及单纯黛力新治疗（对照组）,疗程为6周;采用汉密尔顿抑郁量表（HAMD）和Barthel指数（BI）及生活质量指数量表进行评定。结果在治疗6周后,治疗组的总有效率为87．5％,对照组为65．6％,两者相比有显著差异（P〈0．05）;两组分别于治疗前和治疗后2、4、6周末汉密顿抑郁量表（HAMD）和Barthel指数（BI）及生活质量指数量表评分均有显著差异（P〈0．05或P〈0．01）。结论参松齐心胶囊联合黛力新治疗可改善卒中后抑郁的症状,优于单用黛力新。     

卒中后抑郁的相关因素分析

目的探讨卒中后抑郁(PSD)的相关因素。方法采用汉密尔顿抑郁量表(HAMD)在卒中后14 d及90 d对300例脑卒中患者进行评分,并据此分为PSD组及非PSD组,对两组间的卒中部位、美国国立卫生研究院卒中量表(NIHSS)评分、改良Rankin量表评分(mRS)及简易精神状态检查表(MMSE)评分进行比较。结果 140例(46.7%)患者发生PSD;卒中灶多发或位于左侧半球、额颞叶及基底节的患者PSD发生率明显高于卒中灶单发、位于右侧半球、顶枕叶及皮质的患者(均P<0.05);PSD组发病14 d时NIHSS评分、发病14 d及90 d时mRS评分明显高于非PSD组(P<0.05～0.01)。结论 PSD发生与多灶性卒中及卒中灶位于左侧半球、额颞叶、基底节区有关;且与卒中后神经功能缺损程度及残疾程度有关。     

Epidemiology and treatment of post-stroke depression

Mood depression is a common and serious complication after stroke. According to epidemiological studies, nearly 30% of stroke patients develop depression, either in the early or in the late stages after stroke. Although depression may affect functional recovery and quality of life after stroke, such condition is often ignored. In fact, only a minority of patients is diagnosed and even fewer are treated in the common clinical practice. Moreover, the real benefits of antidepressant (AD) therapy in post-stroke depression have not been fully clarified. In fact, controlled studies on the effectiveness of ADs in post stroke depression (PSD) are relatively few. Today, data available suggest that ADs may be generally effective in improving mood, but guidelines for the optimal treatment and its length are still lacking.     

Platelet 5-HT uptake in post-stroke depression

Serotonin (5-HT) uptake into platelets is reduced in functionally depressed patients. Depression following stroke (cerebrovascular accident; CVA) is common and severe. Sixteen patients who had suffered a CVA within 6 to 12 months and who were medication-free had blood taken for measurement of platelet 5-HT uptake. Seven of these patients were depressed. These were compared with age- and sex-matched hospital controls. No difference in platelet 5-HT uptake was found across these groups.     

Risk factors for post-stroke depression

An unselected cohort of 285 stroke patients, median age 69 years, were studied for correlation between potential risk factors and the 1-year incidence of post-stroke depression (PSD). The following factors correlated significantly with PSD: a history of previous stroke, a history of previous depression, female gender, living alone and social distress prestroke. Further, social inactivity, decrease in social activity, pathological crying and intellectual impairment at 1 month but not functional outcome correlated to PSD. A multivariate regression analysis showed that intellectual impairment explained 42% of variance of mood score. Major depression was unrelated to lesion location. We conclude that etiology to PSD is a complex mixture of prestroke personal and social factors, and stroke induced social, emotional and intellectual handicap.     

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     

卒中后抑郁的研究进展

卒中后抑郁(post-stroke depression，PSD)是常见的脑血管病并发症之一。目前国内外学者对PSD进行了许多研究．对于PSD的认识有了很大提高，但是这些研究都有一定的局限性，存这一领域的研究仍有许多问题有待进一步探讨。本文对PSD的研究现状及治疗进展进行了综述。     

脑卒中后抑郁的相关因素分析

目的:探讨脑卒中后抑郁的相关因素。方法:采用汉密尔顿抑郁量表(HAMD)对198例脑卒中患者进行现状调查。结果:73例脑卒中患者有抑郁表现,发生率为36.9%,经Logistic多元回归分析,脑卒中后抑郁的相关因素有负性生活事件、心血管病史、抑郁症史、病灶数目、病灶部位以及脑卒中史。结论:脑卒中后抑郁的相关因素有负性生活事件,心血管病史,抑郁症史、病灶数目,病灶部位以及脑卒中史。脑卒中后抑郁的发生可能是神经生物学因素和社会心理学因素共同作用的结果。