抑郁症患者工作记忆内情绪刺激加工的特点及其机制

抑郁症患者在工作记忆内情绪刺激加工的特点为倾向于加工与负性心境一致的材料, 被认为是抑郁症认知易感性的核心特征。目前研究者们围绕抑郁症工作记忆中央执行系统三个子功能的情绪刺激加工特点及其作用机制进行了大量研究, 发现在更新功能上, 患者难以移除负性情绪信息, 且在正性信息的加工上存在缺损; 在抑制功能上, 患者难以抑制无关负性情绪信息进入工作记忆; 在转换功能上, 患者情绪材料转换困难的研究证据尚不充分。神经生理与脑成像的研究初步表明, 工作记忆中的情绪刺激加工与抑郁症患者背外侧前额叶和前扣带回的功能激活水平异常有关。未来研究需评估工作记忆三个子功能对抑郁症状的差异性贡献及在情绪刺激加工上的统一性, 并探究其随疾病发生发展变化的轨迹, 谨慎选取并评估不同情绪刺激材料指标的诱发效应及其对工作记忆功能的独特影响。在此基础上, 深入探究工作记忆内情绪刺激加工的神经机制, 为工作记忆偏向矫正干预的临床应用及其预期效果提供理论依据和方向。     

细胞因子和抑郁症

在心理神经免疫学领域,越来越多的证据表明神经和免疫之间存在双向交流通路,免疫系统可能在一些心理精神障碍中具有重要作用。“抑郁症的细胞因子假说”认为细胞因子作为神经调质,可能在抑郁症的病因和病理过程中具有重要作用。这个假说得到了很多证据的支持。而在动物身上应用前炎性细胞因子也能够引起与人类抑郁症行为症状非常类似的“病态行为”。研究认为外周细胞因子通过信号传导进入脑内与中枢产生的细胞因子共同作用于下丘脑－垂体－肾上腺轴和5－羟色胺系统,从而导致抑郁症。细胞因子的中枢效应可以解释很多抑郁症状,“抑郁症的细胞因子假说”为探讨抑郁症状的机制和治疗抑郁症提供了一个新的视角     

抑郁症的脑结构与功能异常:来自静息态下多模态脑影像的研究证据

传统单一模态、单一分析方法在揭示抑郁症脑机制上存在较多局限;而新近多种模态、多种分析方法的结合可在一定程度上较好地促进对抑郁症脑功能和结构的全面探索、挖掘,可以更加有效地运用和实施于早期辅助诊断、干预治疗当中。因此,本文首先简要介绍了多种模态下的脑影像指标及其分析技术,而后分别从结构及功能神经影像数据融合等方面,概述了抑郁症脑结构和功能的研究现状,发现抑郁症患者存在诸多脑区及相关环路结构及功能的异常。同时,通过对抑郁症多模态研究现状的梳理和总结,结合我们已有的相关前期研究工作,对未来抑郁症等情感障碍的进一步研究工作提出了一些思考和展望。     

女性绝经进程与抑郁易感性

采用系统论观点对女性围绝经期的生物学改变进行分析,并在此基础上对该时期抑郁症易感性增加的原因进行探讨,指出绝经进程的系统性特征,对大脑皮层、下丘脑、垂体等中枢神经系统结构和卵巢等外周器官的功能改变和失调进行多层次、关联性、动态性分析,对围绝经期抑郁症病因的进一步研究具有重要意义。     

抑郁症的脑网络失调:来自图论分析的证据

以脑成像数据为支撑,基于图论的复杂脑网络分析实现了在大尺度上对于大脑的整体定量分析,克服了传统抑郁症病理改变研究仅关注少数几个脑区的缺点。本文主要总结了:(1)基于图论的脑网络分析的概念;(2)基于图论的抑郁症研究现状;(3)以往传统研究的不足,抑郁症脑网络研究的当前总结和未来展望。总体来说:抑郁症病人脑网络的小世界属性依旧存在,但在节点指标上存在明显的异常,且随疾病发展呈线性变化,整个网络趋向于随机化。区域性的异常主要存在于默认网络和前额叶?边缘系统环路。未来研究中,任务状态下的脑网络构建和"最小生长树"技术的应用可能会为抑郁症病人的脑网络异常提供更多的信息。     

抑郁症的脑功能异常:来自静息态功能磁共振成像的证据

静息态功能磁共振成像是指在静息状态下测量的BOLD信号,即受试者安静地躺在扫描仪中,不给受试者任何特定的任务,受试者也不用做任何反应,此时受试者的大脑活动处于自发状态。通过使用该技术可以为抑郁症发作的临床现象提供神经影像学依据,以期为将来抑郁症的治疗提供生物标记。因此,本文综述了大量抑郁症患者在静息态脑功能方面的差异研究,发现了单、双相抑郁症,首、复发抑郁症,早发性、晚发性抑郁症,难治、非难治性抑郁症等不同类型的抑郁症在包括局部一致性(Re Ho)和低频振幅(ALFF)在内的功能分化以及包括功能连接密度(FCD)、功能同伦(VMHC)、复杂网络(Complex Network)和ROI功能连接在内的功能整合两大指标的改变。     

基于“心理痛苦”理论的眶额皮质介导抑郁症自杀机制

近年来,自杀的心理痛苦三因素模型(包括痛苦唤醒、痛苦体验和痛苦逃避)在临床抑郁症患者群体得到验证。痛苦逃避是该模型的核心成分。行为学研究证据显示,痛苦逃避维度得分对抑郁症患者自杀意念和自杀行为的预测力远高于Beck抑郁问卷得分和痛苦体验得分。由于眶额皮质是介导情绪反应和控制复杂行为的关键界面,主要参与负性情绪引发回避惩罚(痛苦)的动机控制,与动机、决策和行为监控密切相关。眶额皮质及其与前额叶、皮层下结构(扣带前回、杏仁核和下丘脑等)的异常激活模式可能是痛苦体验引发高逃避动机、进而产生自杀行为(风险决策)的重要神经基础。本文在综述以往研究的基础上,提出通过改编和发展情感激励延迟和金钱激励延迟的认知任务,对痛苦体验和痛苦逃避动机阶段进行时间上的分离,建立眶额皮质介导抑郁症自杀的脑功能病理模型的研究思路。     

情绪通路异常与认知情绪偏差:慢性痛与抑郁症共病的神经心理机制

慢性疼痛与抑郁症具有高度共病性,但迄今尚无成熟理论能够阐释二者共病的神经心理机制。对慢性痛与抑郁的脑机制研究提示,慢性痛和抑郁常常涉及到相似的情绪脑区活动的异常改变;与此相对应的是,行为学研究发现,疼痛患者与抑郁患者在加工疼痛或抑郁相关信息时表现出了模式相似的认知情绪偏差(CAB)。近年来,越来越多证据趋于一致,指出慢性痛和抑郁共有的情绪通路异常变化可能导致了相似的信息加工异常,是二者共病的神经心理基础,而认知情绪偏差则在行为上反映了这种变化,并且很可能是共病发生、发展及维持的重要因素。     

反馈相关负波：一种抑郁症的生物标记物

反馈相关负波(feedback-related negativity, FRN)是一种反映个体奖赏敏感性的脑电成分; 而抑郁症患者的特征之一是奖赏敏感性的减弱。大量横向研究发现了重度抑郁症患者(major depressive disorder, MDD)及有患抑郁症风险群体的FRN异常; 另外, 纵向研究发现FRN的异常能够预测青春期抑郁发作及抑郁症状发展, 压力、睡眠等因素在其中起调节作用。这提示FRN可能在对抑郁症的诊断及分型、抑郁高危群体的筛查及干预等方面具有潜在价值。目前关于FRN的心理功能依然存在一些争议, 在未来的研究中应该进一步明确FRN的功能和测量方法, 并探明抑郁症的异质性和共病对FRN的作用, 也应关注老年人群体中FRN与抑郁症的关系。     

强迫症的脑功能障碍

近期,对强迫症(OCD)的现象学解释强调了病人在特定情境下错误识别和情绪与动机功能的异常加工。来自神经解剖、神经生理以及近期神经心理和功能成像等的相关研究证据显示：OCD病人眶额皮层（OFC）、前扣带回皮层（ACC）的过度激活可能会导致错误识别功能和对行为结果预期的情绪与动机评价增高;背外侧前额皮层(DLPC)的活动减弱损害了对信息加工的认知整合能力。以上这些皮层信号在控制行为活动程序的尾状核进行整合。OCD病人的强迫性观念和行为可能由这些结构相关的神经网络中一个或多个环节的功能障碍所致     

冠心病患者的抑郁和焦虑

许多临床研究表明,冠心病患者常发生抑郁及焦虑。而在严重精神症状（如抑郁或/和焦虑）者中有较高的冠心病发生率。抑郁增加冠心病患者的不良心血管事件发生率,影响预后。其机制有如下几个方面：对医疗措施及生活方式改变的依从性差、血小板功能异常、血管内皮功能紊乱以及心率变异性降低。选择性5-羟色胺再摄取抑制剂由于其较好的耐受性且无明显的心血管副作用而应用于冠心病合并抑郁及焦虑的药物治疗并改善患者的生活质量。但仍需要更大规模的临床研究以确定抑郁及焦虑对冠心病预后的影响。临床上应更加关注焦虑对冠心病的影响,进一步探讨焦虑能否作为冠心病的危险因素。     

Individual and Family Contributions to Depressive Symptoms in African American Children with Sickle Cell Disease

Depressive disorders in children with chronic illnesses have received little attention despite some evidence suggesting that these children experience increased psychological difficulties as a result of their medical condition. Most of the research on depressive disorders among children has been conducted primarily with Caucasian youth, limiting generalizability to ethnically diverse populations. Further, even less research exists on depressive disorders among African American children with Sickle Cell Disease (SCD) and for African American youth from lower socioeconomic status who are at greater risk for depressive disorders. This paper is an extensive review of the major studies conducted on depression and psychosocial aspects of SCD in African American children. The Transactional Stress and Coping model is provided as a conceptual framework. Following the review, clinical and research implications are provided, as well as an illustration of a psychoeducational family intervention with an African American child who has SCD and internalizing behaviors.     

Frontal Brain Asymmetry and Depression: A Self-regulatory Perspective

Recent findings indicate that frontal brain asymmetry may be a marker of for depression. However, the psychological predispositions that account linkage between frontal brain asymmetry and depression are unclear. approach-withdrawal hypothesis is the primary framework that has been to account for the linkages between frontal brain asymmetry and or emotional disorders. We review evidence consistent with this and suggest several directions for its extension. One such direction is to constrain the approach-withdrawal hypothesis by linking frontal asymmetry to the known functions of the prefrontal cortex. On this we propose that frontal brain asymmetry may be preferentially linked processes that promote the temporal continuity and shifting of or emotional priorities and the suppression of interference by sources of motivation or emotion. We review evidence from and neurobiological studies of depression that is broadly consistent with these predictions. We emphasise the need for future studies testing our hypotheses.     

Using an Emotion Regulation Framework to Understand the Role of Temperament and Family Processes in Risk for Adolescent Depressive Disorders

Although recent evidence implicates the importance of the family for understanding depressive disorders during adolescence, we still lack a coherent framework for understanding the way in which the myriad of developmental changes occurring within early adolescents and their family environments actually operate to increase adolescents’ vulnerability to, or to protect them from, the development of depressive disorders. In this review we propose a framework that places the mechanisms and processes of emotion regulation at the centre of these questions. We argue that emotion regulation can provide an organising rubric under which the role of various factors, such as adolescent and parent temperament and emotion regulation, and parental socialization of child emotion, as well as the interaction amongst these factors, can be understood to account for the role of the family in adolescents’ risk for depression. In particular, we posit that adolescent emotion regulation functions as a mechanism through which temperament and family processes interact to increase vulnerability to developing depression.     

Cognitive specificity in emotional distress

Cognitive approaches to emotional distress posit that specific cognitive factors are critically linked to the etiology, course, or treatment of dysfunction. Although a number of empirical studies have assessed cognitive factors in emotional disorders such as depression and anxiety, research has yet to assess these variables simultaneously and with identical cognitive measures. Using depression and test anxiety as models of dysfunctional affective states, we examined cognitive specificity on measures of information processing, attributions, automatic thinking, and cognitive interference. Results indicated a pattern of specificity showing several differences and similarities in depression and anxiety. Specifically, "purely" depressed individuals showed evidence of selectively processing depressive information, making dysfunctional attributions, and engaging in more negative automatic thinking. "Purely" anxious individuals, on the other hand, showed evidence of selective anxious information processing and increased cognitive interference. Results are discussed in terms of a taxonomy for classifying depressive and anxious cognition.     

n-3系多元不饱和脂肪酸对抑郁症的影响及其机制

越来越多的实验证据表明,n-3系多元不饱和脂肪酸(n-3PUFA)与抑郁症之间存在联系,二十二碳六烯酸(DHA)和二十碳五烯酸(EPA)可能具有预防和治疗抑郁症的作用.回顾国内外关于n-3PUFA与抑郁症之间存在的负性关系的研究并介绍其主要的研究结果和现状,解释n-3PUFA引起的抗抑郁效果可能涉及的神经机制,包括神经传递、葡萄糖的新陈代谢、促炎细胞因子的分泌、5-羟色胺(5-HT)以及脑源性神经营养因子(BDNF)的水平、还有神经元的凋亡等的变化.并且总结现有研究中存在的一些问题,例如使用的n-3PUFA种类和剂量问题,DHA或EPA是否对于不同种类的抑郁症均有效,单独作用还是共同作用才能引起抗抑郁效果等等,n-3PUFA对抑郁症病理机制的具体影响可能是未来的研究方向.     

Informing the continuity controversy: a taxometric analysis of depression

Researchers and practitioners have long debated the structural nature of mental disorders. Until recently, arguments favoring categorical or dimensional conceptualizations have been based primarily on theoretical speculation and indirect empirical evidence. Within the depression literature, methodological limitations of past studies have hindered their capacity to inform this important controversy. Two studies were conducted using MAXCOV and MAMBAC, taxometric procedures expressly designed to assess the underlying structure of a psychological construct. Analyses were performed in large clinical samples with high base rates of major depression and a broad range of depressive symptom severity. Results of both studies, drawing on 3 widely used measures of depression, corroborated the dimensionality of depression. Implications for the conceptualization, investigation, and assessment of depression are discussed.     

Facial affect processing and depression susceptibility: cognitive biases and cognitive neuroscience

Facial affect processing is essential to social development and functioning and is particularly relevant to models of depression. Although cognitive and interpersonal theories have long described different pathways to depression, cognitive-interpersonal and evolutionary social risk models of depression focus on the interrelation of interpersonal experience, cognition, and social behavior. We therefore review the burgeoning depressive facial affect processing literature and examine its potential for integrating disciplines, theories, and research. In particular, we evaluate studies in which information processing or cognitive neuroscience paradigms were used to assess facial affect processing in depressed and depression-susceptible populations. Most studies have assessed and supported cognitive models. This research suggests that depressed and depression-vulnerable groups show abnormal facial affect interpretation, attention, and memory, although findings vary based on depression severity, comorbid anxiety, or length of time faces are viewed. Facial affect processing biases appear to correspond with distinct neural activity patterns and increased depressive emotion and thought. Biases typically emerge in depressed moods but are occasionally found in the absence of such moods. Indirect evidence suggests that childhood neglect might cultivate abnormal facial affect processing, which can impede social functioning in ways consistent with cognitive-interpersonal and interpersonal models. However, reviewed studies provide mixed support for the social risk model prediction that depressive states prompt cognitive hypervigilance to social threat information. We recommend prospective interdisciplinary research examining whether facial affect processing abnormalities promote-or are promoted by-depressogenic attachment experiences, negative thinking, and social dysfunction.     

A taxometric analysis of the MMPI-2 Depression scales

The MMPI (Hathaway & McKinley, 1943) and MMPI-2 (Butcher et al., 2001) have long been used as measures of psychopathology. Both clinicians and researchers have noted the widespread existence of negative affectivity on the MMPI and MMPI-2 that may elevate scale scores and eclipse the tests' ability to differentiate depression from other clinical disorders. Using taxometric analyses, in this study we sought to test directly whether the MMPI-2 depression scales could differentiate patients with depressive symptoms from patients with other disorders. A large psychiatric sample (N = 2,000) was utilized and analyses were run separately for men and women. Taxometric analyses did not find a MMPI-2 Depression scale cut point that categorizes patients with depressive symptoms from other patients. Rather, these findings support previous studies finding an underlying dimensionality of depression. We discuss implications for MMPI-2 scale use and depression nosology in light of these findings.