正念冥想在ADHD儿童干预中的应用

正念冥想是有意识、非评判地将注意集中于当下经验的方法。近年来,正念冥想作为一种潜在的方法被引进到ADHD儿童干预领域。因为ADHD儿童的特异性,为了增加正念冥想方案对ADHD儿童的适切性,研究者从练习设置、奖励系统、解释方式和家长纳入几个方面对标准的正念减压训练方案做了改编。越来越多的研究证据表明,正念冥想训练能有效地减轻ADHD儿童的核心缺陷、改善其内外化症状和亲子关系。本文通过对已有相关实证研究的分析认为这些积极的影响可能与ADHD儿童的执行功能与去中心化等心理功能的改善有关,而大脑相关区域激活模式的变化和结构的积极改变可能是正念冥想影响ADHD儿童的神经基础。文章也提出已有研究在内容和方法学上的不足及其以后的探究方向。     

正念冥想训练水平对情绪加工的影响

越来越多的研究表明,正念冥想训练影响情绪加工。本文从正念冥想训练水平（包括临时训练、短时训练和长期训练）角度出发,系统回顾了不同水平的正念冥想训练对情绪加工的调节效应。综述发现,不同水平正念冥想训练都能够提高个体情绪调节能力,临时正念冥想训练作为一种有效的情绪调节方法影响情绪加工,而短期正念冥想训练和长期禅修训练通过增加个体正念意识,增强个体情绪接受力影响情绪加工。未来的研究需进一步在区分正念冥想训练时间和正念冥想训练类别基础上,探讨正念冥想训练影响情绪加工的认知神经机制。     

正念认知疗法用于抑郁症复发预防的研究现状

正念指对当下的体验(包括个人的感觉、想法、身体状态和环境)不加评判地觉知,同时又抱着开放、好奇和接纳的心态.正念认知疗法(MBCT)主要用于抑郁症复发的预防,帮助患者从反刍思维、体验逃避等适应不良的应对模式中摆脱出来.本文对近几年正念及相关疗法的内涵,MBCT在预防抑郁症复发上的优势,以及MBCT的作用机制和疗效等研究状况进行了综述.     

不同冥想类型对创造性思维的影响及作用机制

冥想与创造性的关系正逐渐被关注,澄清冥想练习对创造性思维的影响效果和作用机制对个体创新潜能的培养与提升具有重要意义。不同冥想类型对创造性思维的影响具有特异性,专注冥想主要通过注意聚焦和提升自上而下的执行控制能力来对聚合思维产生积极影响;正念冥想引起的离焦的注意状态,以及对认知灵活性和积极情绪的促进,有助于发散思维。未来应加强不同冥想类型与创造性思维的整合研究,探讨冥想影响创造性思维的脑机制,以及冥想与其他干预训练对创造性思维的不同作用机制等。     

初中生校园排斥对抑郁的影响：反刍思维与特质正念的作用

研究采用问卷法对955名初中生进行问卷调查,探讨校园排斥对抑郁的影响,以及反刍思维和特质正念的作用。结果表明：（1）校园排斥正向预测初中生抑郁,反刍思维在校园排斥与抑郁间具有中介作用;（2）校园排斥对抑郁的直接效应受到特质正念的调节,直接效应对低特质正念初中生更为显著;（3）特质正念还调节了反刍思维对校园排斥与初中生抑郁中介过程的后半段路径,高特质正念初中生的抑郁水平更低。研究以校园排斥、反刍思维和特质正念为切入点构建了青少年抑郁的影响机制模型,为预防和干预青少年抑郁提供了新的视角和数据支持。      

正念冥想对情绪的调节作用:理论与神经机制

正念冥想可调节个体的负性情绪、促进个体正性情绪,对于心身疾病具有显著的干预效用.正念冥想的再感知模型、正念应对模型、推动性上升螺旋模型以及正念情绪调节模型都强调了正念冥想对情绪的调节作用.认知神经科学的研究发现,正念冥想可促进左侧前额叶脑区激活增强,涉及的脑区主要包括背外侧前额叶皮层(DLPFC)和背内侧前额叶皮层(DMPFC).研究者进一步发现,正念特质是通过改善前额叶对边缘系统反应的调节来实现对情绪的调节作用.而且,这种调节作用还有可能体现为通过冥想训练分离联结在一起的两种自我参照神经机制,从而加强体验性神经机制.另外,研究者还发现,正念冥想训练还可以改变与情绪加工相关的大脑结构.进一步澄清冥想训练与大脑偏侧化的关系和不同类型被试之间的比较研究将成为该领域日后研究的重点.     

禅修对创造性思维的影响

禅修是一种能够对人类心理有广泛影响的训练工具。作为两种重要、相似但又不同的禅修方式, 冥想和正念对创造性思维中的发散思维和聚合思维产生了不同影响。在发散思维方面, 冥想主要通过对注意调控和无意识激活影响以及对解题动机和情绪的有效调控两方面显著增强了发散思维, 尤其是认知灵活性; 在聚合思维方面, 正念和冥想的影响相当复杂, 主要是通过聚合思维所需的执行功能和可能涉及表征重构来促进定势转移或功能固着的消除。就机制而言, 禅修对创造性思维的影响总体上不仅得益于走神时的无意识关联加工, 而且受禅修中诱发的情绪效应的调节。基于这些, 对未来研究的趋势进行了展望。     

正念冥想对走神的影响及其作用机制

走神是普遍存在的一种心理现象,这种普遍存在会为人们带来许多的妨碍。正念冥想是减轻或避免走神的重要干预方式之一。为此,在系统回顾以往研究基础上,首先通过不同时长、不同形式、对照组的设置以及不同群体等多个方面,梳理正念冥想对走神的改善作用;其次,结合神经机制及相关理论模型两方面内容阐述其作用机制;最后,围绕走神类型以及不同形式正念冥想直接对比等角度提出未来研究建议,探讨正念冥想对走神的改善,构建完善的理论模型。     

慈悲冥想对利他行为的影响及其认知神经机制

慈悲冥想是一类旨在培养对自己和他人无条件的善意与同情的冥想练习方法, 主要包括慈心禅和怜悯禅修。诸多研究表明, 慈悲冥想可以促进练习者的利他行为。就影响机制而言, 慈悲冥想可能是通过增强对他人不幸的共情反应, 促进情绪的有效调控和提高亲社会动机来影响练习者的利他行为。未来的研究需选择更具生态效度的利他行为测量方法, 深入挖掘慈悲冥想影响利他行为的动态神经加工过程, 并尝试将慈悲冥想应用于临床群体。     

坐忘、正念、冥想治疗焦虑的心理与脑电变化研究

采用不同压力管理策略(坐忘、正念、冥想)考察其对焦虑的干预效用,并用脑电探究其脑机制差异。首先用焦虑量表筛选出高焦虑被试60名,随机分入坐忘、正念、冥想和对照组,并对被试实施持续4周的干预,用焦虑量表进行后测,再采用EEG比较脑电波差异。研究发现:坐忘、正念与冥想都能降低个体的状态焦虑,坐忘对降低特质焦虑作用更大(t_(TAI)=-3.14,P0.01);坐忘在额叶激活了更高的α波,正念在顶叶激活了更高的θ波,冥想组α波的均值高于对照组。因此,不同的压力管理策略对焦虑的干预效用显著,而且三者的脑电存在差异。     

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     

Depression and motivation

Among the characteristic features of depression is a diminishment in or lack of action and motivation. In this paper, I consider a dominant philosophical account which purports to explain this lack of action or motivation. This approach comes in different versions but a common theme is, I argue, an over reliance on psychologistic assumptions about action–explanation and the nature of motivation. As a corrective I consider an alternative view that gives a prominent place to the body in motivation. Central to the experience of depression are changes to how a person is motivated to act and, also as central, are changes to bodily feelings and capacities. I argue that broadly characterizing motivation in terms of bodily capacities can, in particular, provide a more compelling account of depressive motivational pathology.     

Codependency and Depression

SUMMARY

The focus of this study was to investigate a correlation between codependency and depression. The instruments that were used for the study were the Beck Depression Inventory (BDI) and The Awareness Activity: How Codependent Are You? Results of this study were based on 149 paired inventories. The individuals who volunteered to complete the inventories were selected from three clinical settings in the New Orleans area; Subjects utilized were adults of both sexes and all ages. There was a strong, positive correlation between the two variables, codependency and depression, of .5966 (p < .00001). When the relationship between codependency and depression was assessed for each of the separate groups, the same trend prevailed across all three groups.

While one cannot conclude from this study that codependency and depression are equal, one may suggest that a relationship exists between them. These findings indicate that if a person reports himself/herself to be highly codependent, he/she is likely to experience an elevated level of depression.     

Depression

Abstract— The theory of clinical depression presented here integrates etiological factors, changes in specific structural and cellular substrates, ensuing symptomatology, and treatment and prevention. According to this theory, important etiological factors, such as stress, can suppress the production of new neurons in the adult human brain, thereby precipitating or maintaining a depressive episode. Most current treatments for depression are known to elevate brain serotonin neurotransmission, and such increases in serotonin have been shown to significantly augment the ongoing rate of neurogenesis, providing the neural substrate for new cognitions to be formed, and thereby facilitating recovery from the depressive episode. This theory also points to treatments that augment neurogenesis as new therapeutic opportunities.     

Depression

Beck initially set out to test the Freudian notion that depression is a consequence of “anger turned inward” (rage directed the introjected parent for not gratifying infantile desires) but soon came to conclude that no such unconscious motivation existed and that instead depressed patients actually believe that they were unlovable or inadequate. He developed a treatment that he named cognitive therapy that is as efficacious as and more enduring than antidepressant medications. It stands as the most often tested and most widely practiced treatment for depression.     

Defense Mechanisms in Mania,Bipolar Depression and Unipolar Depression

The present study compared the use of defense mechanisms in ten bipolar manic, ten bipolar depressed and ten unipolar depressed patients. The defense mechanisms were assessed by two methods: TAT stories scored by Defense Mechanism Manual and Defense Mechanism Rating Scale ratings of psychodynamic interviews. The severity of symptoms was assessed by Beck Depression Inventory for depressed patients and Young’s Manic Rating Scale for manic patients. Both bipolar manic and depressed groups used the defense mechanism of denial, borderline level defenses and immature defenses significantly more than the unipolar depression group. The manic group showed greater dependence on narcissistic level defenses as compared to the other two groups. Positive relationships were found between severity of manic symptoms and the defense mechanisms of denial as well as the narcissistic level defenses. The bipolar depression group also used more action level defenses as compared to the unipolar depression group. The unipolar depression group scored higher on the defense mechanism of identification and adaptive level defenses as compared to the manic group. A negative correlation was found between the severity of depressive symptoms for unipolar depression group and the defense mechanism of identification. The neurotic level defenses were used most frequently by unipolar depression group, followed by the bipolar depression group and manic group. Some of these findings are in consonance with the psychoanalytic understanding of mania and depression.     

Depression

Patients with myocardial infarction who suffer from a depression are at increased risk of dying of a subsequent heart attack or some other complication of coronary artery disease (CAD). A considerable body of research has provided evidence that a major depression, which is found in 16 to 23 percent of patients with CAD, but also subliminal depressive symptoms are independent risk factors for an unfavourable outcome of CAD. However, it is not yet clear whether depression is a causal risk factor having impact on the course of the heart disease or merely a prognostic marker that allows predicting the outcomes of interest, without any causal influence on them. Several pathways between depression and CAD have been discussed. These include behavioral mechanisms such as low compliance with both medical treatment and life style recommendations as well as neurobiological links. Much attention has been paid to the hypothalamic-pituitary-adrenocortical and sympathomedullary hyperactivity found in depression. Other possible links include diminished heart rate variability, stress-induced ischemia, platelet activation, and immunological dysregulation. To resolve the issue whether depression is a causal risk factor or only a prognostic marker, experimental studies are needed to evaluate interventions aimed at improving depression and test whether mortality is subsequently reduced. Such studies brought in the past mixed results. Whereas comprehensive intervention programs including risk factor management have produced a reduction in both coronary morbidity and mortality, a recent multicenter study providing either cognitive-behavioral therapy or usual care to depressed patients with CAD could not demonstrate a survival benefit among the participants of the intervention. Finally, results of evaluation studies regarding integrated disease management programs for patients with comorbid depression are presented.