卒中后焦虑和抑郁障碍的心理干预

<正>卒中(stroke)是突发性的脑部疾病,患者可因脑内动脉狭窄、闭塞甚至破裂导致脑部血液供应障碍和一过性/永久性脑功能损伤[1]。卒中后情感障碍是卒中的常见并发症之一,而焦虑和抑郁又是卒中后情感障碍最常见的类型。急性卒中常并发焦虑障碍,发生率为40%~50%[2],而有1/3卒中后患者发生卒中后抑郁(post-stroke depression,PSD)[3],国外Paolucci等[4]对卒中患者长期追踪观察发现,PSD的发生率为36%,轻度抑郁占80%。目前,     

重视卒中后情感障碍

卒中后可出现各种情感障碍,如抑郁、焦虑、淡漠、情感失禁和躁狂。卒中后情感障碍会加重认知功能的损害和阻碍神经功能的恢复,影响患者的预后和生活质量。虽然卒中后情感障碍发病率高,但在临床实践中其诊断率却很低,其主要原因是医师及家属一般只重视患者的躯体功能康复情况,忽视了患者情感方面的变化。1卒中后抑郁卒中后抑郁(post-stroke depression,PSD)是最常见的卒中后情感障碍之一,文献报道的PSD发病率为18%～78%,综合估计值     

卒中后抑郁临床实践的中国专家共识

<正>卒中后抑郁(post-stroke depre s sion,PSD)是指发生于卒中后,表现为一系列抑郁症状和相应躯体症状的综合征,是卒中后常见且可治疗的并发症之一,如未及时发现和治疗,将影响卒中后患者神经功能的恢复和回归社会的能力。最近的流行病学资料显示,PSD在卒中后5年内的综合发生率为31%~([1])。PSD可以发生在卒中后急性期(1个月),中期(1~6个月)和恢复期(6个月),发生率分别为33%、33%和34%~([2])。大量研究发现,PSD与卒中的不良预后密切相关,不仅可以导致住院时间延长,神经     

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。     

卒中后抑郁的前瞻性随访调查

目的 研究卒中后抑郁(PSD)2周及3个月的患病率与相关因素.方法 对257例急性卒中患者进行2周及3个月前瞻性随访,调查卒中2周及3个月PSD患病率及相关因素.结果 卒中2周PSD患病率为32.59％,其中轻型抑郁20.92％,重型抑郁11.67％.卒中3个月PSD患病率为42.68％,其中轻型抑郁19.87％,重型抑郁22.81％.卒中2周PSD相关因素是人格特质中的内向特质(P=0.000)、是否合并有糖尿病(P=0.000)及神经功能缺损评分(P=0.000).卒中3个月PSD相关因素是急性期已经诊断PSD(P =0.000)及前循环卒中(P=0.04).结论 PSD患病率较高.卒中2周PSD发生与内向人格特质、合并糖尿病及神经缺损有关,3个月发生与急性期PSD及前循环卒中有关.     

卒中后抑郁促发因素研究进展

卒中后抑郁(post stroke depression,PSD)是脑血管病后常见并发症之一,它属于继发性抑郁.是指卒中发生后,以情绪低落、兴趣减退为主要表现的心境障碍或情感障碍,它不仅影响患者的生活质量,导致患者出现不良的心境体验和躯体功能障碍,同时还影响患者神经功能和肢体活动功能的康复.其发生与病灶部位、病人的年龄、性别、个性、社会、家庭、卒中后神经功能缺陷等因素有关.PSD发病机制尚不完全清楚,临床分轻、重两型,本文就卒中后抑郁的相关促发因素作一概述.     

卒中后抑郁的流行病学及临床特点

卒中后抑郁(poststroke depression,PSD)是卒中常见的并发症之一,是在有明显临床症状的卒中后出现的以情绪低落、兴趣减退、睡眠障碍等为特征的情感障碍性疾病,是继发性     

卒中后抑郁的发生与识别

抑郁是卒中后最常见的精神障碍,而卒中后是并发抑郁障碍的高危期.卒中后抑郁(Post-stroke Depression,PSD)不仅影响患者神经功能的恢复和生活质量,还增加卒中的病死率.一项随访10年的研究发现,在控制了人口学因素、共患躯体疾病、用药、躯体及认知损害、病灶部位等因素后,PSD患者的死亡率是卒中后非抑郁者的3.5倍.然而,PSD症状常常被临床医生及家属忽视,约75%的患者因种种原因被漏诊.因此,神经科医生有必要对PSD的发生、危险因素、诊断标准等深入了解,在临床工作中早期筛选与识别PSD患者.……     

卒中伴失语患者抑郁障碍诊断方法的研究进展

卒中后抑郁（post-stroke depression,PSD）是卒中后常见的情感障碍,严重影响患者的生活质量及预后。约有1/3的卒中患者由于失语导致交流障碍,对其是否伴有PSD及其程度无法准确评估。评价失语患者是否伴有抑郁情绪及其程度,评价工具和手段是关键。对PSD患者进行抑郁评估的手段有很多,但是尚缺乏公认的统一标准。失语患者抑郁障碍的诊断和评价工具亟待深入研究。     

色氨酸代谢对卒中后抑郁影响的研究

卒中后抑郁(PSD)是脑卒中患者常见的并发症,是一种以抑郁、情绪低落、认知功能障碍和兴趣下降为特征的精神疾病。PSD是由多种因素引起的,包括生物、心理和社会因素,但其发病机制尚不清楚。近年来,色氨酸代谢异常与PSD的相关性引起了广泛关注,卒中后在促炎细胞因子介导下调节色氨酸代谢被认为对PSD的发生中起着重要作用。本文就卒中后炎症反应对色氨酸分解代谢中的酶表达和活性及代谢产物的影响进而导致PSD的病理机制的研究进行综述。     

新型冠状病毒肺炎疫情时期急性缺血性卒中的急诊取栓治疗

目的 探讨总结新型冠状病毒（coronavirus disease-19，COVI D-19）肺炎疫情时期急性缺血性卒中 （acute ischemic stroke，AIS）的急诊取栓治疗经验。 方法 回顾性分析2020年1月20日-3月20日疫情期间，首都医科大学附属北京天坛医院神经介入中 心进行急诊取栓治疗的AIS病例资料，包括患者的一般资料、NIHSS评分、ASPECTS评分（DWI）、病变部 位、手术策略、恢复情况，以及COVID-19筛查、预防标准与流程。并与2019年1月20日-3月20日同期取栓 病例进行对照分析。 结果 共纳入33例颅内大血管闭塞致AIS进行急诊取栓的患者，其中2020年18例，2019年15例。2020 年疫情期间与2019年同期相比，入院到手术开始时间稍长[4.0（2.9～4.1）h vs 3.0（2.0～4.0）h， P =0.103]，更少采用全身麻醉（55.6% vs 100.0%，P =0.003），更倾向采取直接导管抽吸取栓（27.8% vs 13.3%，P =0.32）。出院时死亡率低于2019年同期取栓患者（0 vs 20.0%，P =0.050）。2020年疫情期 间纳入的患者及参与救治的医护人员无COVID-19可疑病例，无COVI D-19疑似或确诊病例。 结论 COVID-19疫情期间，入院到手术开始时间受到疫情筛查的影响而有所延长，取栓策略倾向于 采取局部麻醉、抽吸取栓策略，作为疫情期间的特殊考虑是合理的。     

Brain-derived neurotrophic factor and post-stroke depression

Brain-derived neurotrophic factor (BDNF) is well known to play a critical role in cognition. Its role in mood disorders, including post stroke depression (PSD), is also recognized with more evidence surfacing. In patients with PSD, their serum BNDF level is lower than in those without depression. Furthermore, antidepressants could enhance BDNF expression in the brain, resulting in an alleviation of depression symptoms. Such therapeutic effect can be abolished in animals with the BDNF gene deleted. In PSD patients, the presence of stroke may contribute to the development of depression, including affecting the expression of BDNF. However, the mechanisms of BDNF in the development of PSD remain largely unknown. Lower BDNF levels may have existed in some patients before stroke onset, making them vulnerable to develop depressive symptoms. Meanwhile, the hypoxic environment induced by stroke could possibly downregulate BDNF expression in the brain. Current antidepressant treatments are not specific for PSD and there is a lack of treatments to address the linkage between stroke and PSD. This review summarizes the current knowledge of BDNF in PSD. By regulating BDNF expression, a synergistic effect may be achieved when such treatments are applied together with existing antidepressants.     

Post‐stroke depression and apathy: Interactions between functional recovery,lesion location,and emotional response

Depression and apathy are often observed after stroke and are often confused with one another. In the present review, we argue that the current concept of ‘post‐stroke depression’ (PSD) in fact consists of two core symptoms or syndromes: (i) affective (depressive) PSD; and (ii) apathetic PSD. We argue that these two core symptoms are each associated with a different underlying neuroanatomical mechanism, a pattern that influences functional recovery. Post‐stroke disabilities can provoke several distinct emotional responses, some of which are associated with severe depression. We examined one of these emotional responses previously, namely ‘insistence on recovery’, which was believed to be a negative indicator of functional improvement in disabled stroke patients. However, an appropriate level of insistence on recovery may, in fact, be associated with reduced depression and apathy, resulting in enhanced recovery from stroke‐related disabilities. Improvements in physical disabilities (trunk stability or activities of daily living, such as walking) also reduce depression and apathy. Therefore, the experience of PSD/apathy may be intertwined with various initial emotional responses and improvements in physical functioning. Effective treatment of PSD/apathy requires a multidisciplinary approach, such that neuroanatomical/neurobiological, emotional, and physical (rehabilitation) domains are all addressed.     

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。     

The Post-Stroke depression rating scale: A test specifically devised to investigate affective disorders of stroke patients

Abstract

Owing to the lack of instruments specifically constructed to study emotional and affective disorders of stroke patients, the nature of post-stroke depression (PSD) remains controversial. With this in mind, the authors constructed a new scale, the Post-Stroke Depression Rating Scale (PSDS) which takes into account a series of symptoms and problems commonly observed in depressed stroke patients. The PSDS and the Hamilton Depression Rating Scale (HDS) were administered to a group of 124 stroke patients, who had been classified, on the basis of DSM III-R diagnostic criteria, in the following categories: No depression (n =32); Minor PSD (n =47); Major PSD (n =45). Scores obtained by these stroke patients on the PSDS and on the HDS were compared to those obtained on the same scales by 17 psychiatric patients also classified as major depression on the basis of DSM III-R diagnostic criteria. An analysis of the symptomatological profiles clearly showed that: (1) a continuum exists between the so-called “major” and “minor” forms of PSD; (2) in both groups of depressed stroke patients the depressive symptomatology seems due to the psychological reaction to the devastating consequences of stroke, since the motivated aspects of depression prevailed in depressed stroke patients, whereas the (biologically determined) unmotivated aspects prevailed in patients with a functional form of major depression; and (3) in stroke patients a DSM Ill-based diagnosis of major PSD could be in part inflated by symptoms (such as apathy and vegetative disorders) that are typical of major depression in a patient free from brain damage, but that could be due to the brain lesion per se in a stroke patient.     

Post-stroke affective or apathetic depression and lesion location: left frontal lobe and bilateral basal ganglia

This study was designed to examine the correlation between damage to the basal ganglia or frontal lobe and depression status (both affective and apathetic dimensions) in 243 stroke patients. We assessed the affective dimension in post-stroke depression (PSD) using the Zung Self-rating Depression Scale (SDS) and the apathetic dimension in PSD using the apathy scale (AS). We classified basal ganglia or frontal lobe damage into four groups: no damage, damage to the left side only, damage to the right side only, and damage to both sides. Affective and/or apathetic PSD was found in 126 patients (51.9%). The severity of affective depression (SDS score) was associated with left frontal lobe (but not basal ganglia) damage, and that of apathetic depression (AS score) was related to damage to the bilateral basal ganglia (but not to the frontal lobe). The anatomical correlates of PSD differ depending on the PSD dimension (affective or apathetic) and may explain interstudy differences regarding the association between lesion location and type of PSD.     

Frequency-specific alterations in functional connectivity in treatment-resistant and -sensitive major depressive disorder

Major depressive disorder (MDD) may involve alterations in brain functional connectivity in multiple neural circuits and present large-scale network dysfunction. Patients with treatment-resistant depression (TRD) and treatment-sensitive depression (TSD) show different responses to antidepressants and aberrant brain functions. This study aims to investigate functional connectivity patterns of TRD and TSD at the whole brain resting state. Seventeen patients with TRD, 17 patients with TSD, and 17 healthy controls matched with age, gender, and years of education were recruited in this study. The brain was divided using an automated anatomical labeling atlas into 90 regions of interest, which were used to construct the entire brain functional networks. An analysis method called network-based statistic was used to explore the dysconnected subnetworks of TRD and TSD at different frequency bands. At resting state, TSD and TRD present characteristic patterns of network dysfunction at special frequency bands. The dysconnected subnetwork of TSD mainly lies in the fronto-parietal top-down control network. Moreover, the abnormal neural circuits of TRD are extensive and complex. These circuits not only depend on the abnormal affective network but also involve other networks, including salience network, auditory network, visual network, and language processing cortex. Our findings reflect that the pathological mechanism of TSD may refer to impairment in cognitive control, whereas TRD mainly triggers the dysfunction of emotion processing and affective cognition. This study reveals that differences in brain functional connectivity at resting state reflect distinct pathophysiological mechanisms in TSD and TRD. These findings may be helpful in differentiating two types of MDD and predicting treatment responses.     

脑卒中后早期抑郁障碍患者磁共振波谱分析研究

目的应用磁共振波谱分析(MRS)技术探讨卒中后早期抑郁障碍的神经生化改变。方法选择住院连续病例223例,入院72h内均经头颅CT或磁共振成像(MRI)检查确诊为急性脑卒中,于卒中后72h给予汉密顿抑郁量表(HAMD 24项版)评分,44例评分≥8分,界定为卒中后早期抑郁。根据病例编号,采用随机数字表法,分为对照组(23例)、抗抑郁药物治疗组(21例)。对照组中男性14例,年龄47～75岁,平均年龄62.40±3.17岁;女性9例,年龄54～75岁,平均年龄63.00±4.12岁。有1例于1-2M间失访。对照组分别于发病72h、1M、2M及3M进行HAMD量表评分,得出1M时HAMD评分≥8分组(1组)、<8分组(2组);2M时评分≥8分组(3组)、<8分组(4组);3M时评分≥8分组(5组)、<8分组(6组)。对以上各组患者发病72h的MRS检测结果进行分析。结果在NAA/CR中,第1组各VOI的比值均低于第2组,差异有统计学意义;第3组左侧颞叶、双侧丘脑各比值明显低于第4组(P<0.01);第5组与第6组相比,差异均无统计学意义。在Cho/Cr中,第1组各VOI的比值高于第2组,差异有统计学意义;第3组各VOI的比值明显高于第4组(P<0.01);第5组与第6组相比,差异均无统计学意义。结论 MRS可在一定程度上反映卒中后脑的细微结构及功能的改变,卒中后早期抑郁障碍患者MRS显著异常对病程1M、2M时PSD的真正发生有一定的预示意义,并推测针对这一人群早期药物干预治疗在改善脑代谢方面具有积极意义。     

卒中后抑郁与脑损伤部位相关性的临床研究

目的探讨不同的脑损伤部位与脑卒中后抑郁病变的关系,探讨PSD的现况以及对结局的影响。方法收集2010年09月～2011年09月期间河北联合大学附属医院神经内科脑卒中患者300例,通过颅脑CT或MRI进行卒中病灶定位,采用Hamilton抑郁量表对卒中患者在发病14±2d及90±7d进行抑郁及程度的评价。对收集患者的相关临床指标如美国国立卫生院神经功能缺损评分(NIHSS)、改良Rankin量表评分(MRS)、简易精神状态检查表(MMSE)评分等相关因素进行统计分析。结果 140例脑卒中患者合并PSD,总发生率为46.67%,其中轻中度抑郁占46.00%,重度抑郁占0.67%;多发性、左侧半球、额颞叶、基底节区脑卒中患者PSD发生率高。结论脑卒中患者神经功能缺损程度评分越高,其患抑郁的程度也就越高。PSD发生与卒中类型无关,而与卒中部位、卒中残疾程度等因素有关。     

Distinct functional networks associated with improvement of affective symptoms and cognitive function during citalopram treatment in geriatric depression

Variability in the affective and cognitive symptom response to antidepressant treatment has been observed in geriatric depression. The underlying neural circuitry is poorly understood. This study evaluated the cerebral glucose metabolic effects of citalopram treatment and applied multivariate, functional connectivity analyses to identify brain networks associated with improvements in affective symptoms and cognitive function. Sixteen geriatric depressed patients underwent resting positron emission tomography (PET) studies of cerebral glucose metabolism and assessment of affective symptoms and cognitive function before and after 8 weeks of selective serotonin reuptake inhibitor treatment (citalopram). Voxel-wise analyses of the normalized glucose metabolic data showed decreased cerebral metabolism during citalopram treatment in the anterior cingulate gyrus, middle temporal gyrus, precuneus, amygdala, and parahippocampal gyrus. Increased metabolism was observed in the putamen, occipital cortex, and cerebellum. Functional connectivity analyses revealed two networks which were uniquely associated with improvement of affective symptoms and cognitive function during treatment. A subcortical-limbic-frontal network was associated with improvement in affect (depression and anxiety), while a medial temporal-parietal-frontal network was associated with improvement in cognition (immediate verbal learning/memory and verbal fluency). The regions that comprise the cognitive network overlap with the regions that are affected in Alzheimer's dementia. Thus, alterations in specific brain networks associated with improvement of affective symptoms and cognitive function are observed during citalopram treatment in geriatric depression.