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Involvement of Neuroactive Steroids in Pain, Depression and Anxiety. 神经活性类固醇在疼痛、抑郁和焦虑中的作用。
Pub Date : 2015-01-01 Epub Date: 2015-09-18 DOI: 10.1159/000435935
Katherine Mifflin, Curtis Benson, Bradley Kerr, Feyza Aricioglu, Mesut Cetin, Serdar Dursun, Glen Baker

Comorbidity between major depressive disorder (MDD), anxiety (generalized anxiety, panic disorder, social anxiety disorder) and pain is a major complicating factor in the diagnosis and treatment of psychiatric and neurological disorders. Although numerous neurotransmitters and/or neuromodulators may be involved, abnormalities in the GABAergic and glutamatergic systems seem to be a common factor in all these disorders. Neuroactive steroids (NASs) have been the object of considerable interest in this area in recent years since they appear to act predominantly on GABA-A and glutamate NMDA receptors. An overview of the possible involvement of NASs in MDD, anxiety and pain is provided in this chapter.

重度抑郁障碍(MDD)、焦虑(广泛性焦虑、惊恐障碍、社交焦虑障碍)和疼痛之间的共病是精神和神经疾病诊断和治疗的一个主要复杂因素。虽然可能涉及许多神经递质和/或神经调节剂,但氨基丁酸能和谷氨酸能系统的异常似乎是所有这些疾病的共同因素。近年来,神经活性类固醇(NASs)主要作用于GABA-A和谷氨酸NMDA受体,因此在这一领域受到广泛关注。本章概述了NASs在重度抑郁症、焦虑和疼痛中的可能参与。
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引用次数: 14
Biogenic Amines and the Amino Acids GABA and Glutamate: Relationships with Pain and Depression. 生物胺和氨基酸GABA和谷氨酸:与疼痛和抑郁的关系。
Pub Date : 2015-01-01 Epub Date: 2015-09-18 DOI: 10.1159/000435933
Curtis Benson, Katherine Mifflin, Bradley Kerr, Sam J B Jesudasan, Serdar Dursun, Glen Baker

Although it is well known that there is a high degree of comorbidity between chronic pain and mood and anxiety disorders, the mechanisms involved in these co-occurrences are not clear. It appears that numerous neurotransmitters and neuromodulators are involved, and this chapter focuses on the monoamine neurotransmitters noradrenaline, 5-hydroxytryptamine (5-HT, serotonin), and dopamine and the amino acid neurotransmitters GABA (γ-aminobutyric acid) and glutamate in chronic pain and depression. Numerous preclinical and clinical neurochemical, neuroanatomical, pharmacological and molecular biological studies as well as clinical pharmacological treatment investigations implicate noradrenaline, 5-HT and, to a lesser extent, dopamine in the etiology of pain and depression. Similarly, preclinical and clinical studies on GABAergic and glutamatergic mechanisms as well as reports on the actions of neuroactive steroids suggest that GABA and glutamate play an important role in the etiology of pain and depression and may contribute to comorbidity.

虽然众所周知,慢性疼痛与情绪和焦虑障碍之间存在高度的共病,但这些共病的机制尚不清楚。似乎有许多神经递质和神经调节剂参与其中,本章主要讨论单胺类神经递质去甲肾上腺素、5-羟色胺(5-HT、5-羟色胺)和多巴胺以及氨基酸类神经递质GABA (γ-氨基丁酸)和谷氨酸在慢性疼痛和抑郁中的作用。大量的临床前和临床神经化学、神经解剖学、药理学和分子生物学研究以及临床药理学治疗调查表明,去甲肾上腺素、5-羟色胺和多巴胺在疼痛和抑郁的病因学中有一定的作用。同样,关于GABA能和谷氨酸能机制的临床前和临床研究以及关于神经活性类固醇作用的报道表明,GABA和谷氨酸在疼痛和抑郁的病因中起着重要作用,并可能导致合并症。
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引用次数: 41
Pain in Borderline Personality Disorder. 边缘型人格障碍中的疼痛。
Pub Date : 2015-01-01 Epub Date: 2015-09-18 DOI: 10.1159/000435940
Christian Schmahl, Ulf Baumgärtner

Pain processing in patients with borderline personality disorder (BPD) is abnormal primarily with respect to pain thresholds which are typically elevated or perception of phasic nociceptive stimuli which is reduced. In spite of this common finding, nonsuicidal self-injury (NSSI), often expressed as cutting, is a hallmark sign of the disease and serves to release aversive inner tension. The question thus arises, how does a painful stimulus release inner tension when these patients feel less pain than healthy people? However, intensity discrimination is normal in these patients. Imaging data have provided evidence that inhibitory top-down modulation is increased in BPD patients, and that processing of the affective-emotional pain component is altered. Recent studies have focused on the role of pain, tissue injury and seeing blood in the context of NSSI. Preliminary findings suggest a significant role of pain irrespective of concomitant tissue injury, and of seeing blood expressed as a stronger immediate stress release. Taken together, BPD patients exhibit altered pain processing that can be assigned to altered processing of nociceptive stimuli in prefrontal and limbic brain areas, which may help to mechanistically explain the clinical behavior.

边缘型人格障碍(BPD)患者的疼痛处理异常主要表现为疼痛阈值升高或阶段性伤害性刺激的感知降低。尽管有这种普遍的发现,非自杀性自伤(NSSI),通常表现为割伤,是该疾病的一个标志性标志,用于释放厌恶的内心紧张。那么问题来了,当这些病人比健康人感到更少的疼痛时,痛苦的刺激是如何释放内心的紧张的?然而,在这些患者中,强度区分是正常的。成像数据提供了证据,表明BPD患者抑制性自上而下的调节增加,并且情感-情绪疼痛成分的处理发生了改变。最近的研究集中在疼痛、组织损伤和看到血在自伤中的作用。初步研究结果表明,疼痛与伴随的组织损伤无关,并将血液表达为一种更强的即时压力释放。综上所述,BPD患者表现出疼痛处理的改变,这可以归因于前额叶和边缘脑区域伤害性刺激的改变,这可能有助于从机制上解释临床行为。
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引用次数: 29
Generalized Anxiety Disorder and Pain. 广泛性焦虑障碍和疼痛。
Pub Date : 2015-01-01 Epub Date: 2015-09-18 DOI: 10.1159/000435939
Borwin Bandelow

In this article, the co-occurrence of anxiety disorders (in particular generalized anxiety disorder) and pain conditions is described, characteristics of chronic pain are explained, and data on the prevalence of co-comorbidity of both conditions are reviewed. Further, hypotheses on the possible psychosocial and neurobiological backgrounds of the high rate of co-occurrence are discussed. This review will also focus on the role of 'unexplained' pain syndromes (e.g. somatic symptom disorder and fibromyalgia) and anxiety. Finally, we address possible treatment strategies for patients with both conditions. There is a need for a rigorous assessment of pain syndromes in generalized anxiety disorder and anxiety in chronic pain conditions in order to prevent subsequent mortality by early treatment of both conditions.

在这篇文章中,焦虑症(特别是广泛性焦虑症)和疼痛的共同发生被描述,慢性疼痛的特征被解释,并对两种情况的共病患病率的数据进行了回顾。此外,假设可能的社会心理和神经生物学背景的高发生率的讨论。本综述还将重点关注“不明原因”疼痛综合征(如躯体症状障碍和纤维肌痛)和焦虑的作用。最后,我们提出可能的治疗策略,为患者的这两种情况。有必要对广泛性焦虑障碍的疼痛综合征和慢性疼痛条件下的焦虑进行严格的评估,以便通过早期治疗这两种情况来预防随后的死亡。
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引用次数: 18
The origin of anxiety disorders - an evolutionary approach. 焦虑症的起源——一种进化的方法。
Pub Date : 2013-01-01 Epub Date: 2013-09-20 DOI: 10.1159/000351919
Lisette E W G Willers, Nienke C Vulink, Damiaan Denys, Dan J Stein

There is growing interest in the application of evolutionary theory to medicine. In this review, we outline an evolutionary approach to the anxiety disorders. We begin by considering the nature of fear and anxiety, and their evolutionary benefits. We emphasize that fear and anxiety exist in multiple organisms, and note the implications of brain complexity in Homo sapiens for the anxiety disorders. This account emphasizes the importance of distance from a threat; in H. sapiens, it is possible to experience fear and anxiety even when threats are temporally and spatially distant.

人们对将进化论应用于医学的兴趣越来越大。在这篇综述中,我们概述了一种进化的方法来治疗焦虑症。我们首先考虑恐惧和焦虑的本质,以及它们对进化的好处。我们强调恐惧和焦虑存在于多种生物中,并注意到智人大脑复杂性对焦虑障碍的影响。这种说法强调了与威胁保持距离的重要性;在智人中,即使威胁在时间和空间上都很遥远,也有可能经历恐惧和焦虑。
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引用次数: 6
Role of inflammation in depression: implications for phenomenology, pathophysiology and treatment. 炎症在抑郁症中的作用:现象学、病理生理学和治疗的意义。
Pub Date : 2013-01-01 Epub Date: 2013-02-27 DOI: 10.1159/000343966
Charles L Raison, Andrew H Miller

Like all psychiatric conditions, depression is a complex phenomenon that is unlikely to yield to simple monolithic explanatory paradigms. Nonetheless, increasing evidence suggests that the immune system in general and inflammatory processes in particular, may contribute to depressive pathogenesis in a significant proportion of otherwise medically healthy individuals struggling with the disorder. In this chapter, we review the best current evidence suggesting that inflammatory processes contribute to the development of depression, both via direct actions on the brain as well as by effects on secondary pathways that marry brain to body. We review epidemiological evidence linking inflammation to depression before reviewing findings that exposure to inflammatory stimuli produce depressive symptoms in concert with brain-body changes known to be common in depression. Following this review of the role of inflammation in depressive causation, we consider emerging evidence that immunomodulatory interventions may hold promise as antidepressants, especially in individuals with elevations in peripheral inflammatory biomarkers. Interventions discussed include cytokine and cyclo-oxygenase antagonists, as well as agents that impact inflammatory transcription factors/signaling cascades. We conclude with a brief discussion of the potential role of various behavioral strategies in reducing inflammation and thereby enhancing emotional well-being.

像所有精神疾病一样,抑郁症是一种复杂的现象,不太可能屈从于单一的解释范式。尽管如此,越来越多的证据表明,免疫系统,特别是炎症过程,可能在很大一部分医学上健康的个体中与抑郁症作斗争。在本章中,我们回顾了目前最好的证据,表明炎症过程有助于抑郁症的发展,既通过对大脑的直接作用,也通过对大脑与身体结合的次要途径的影响。我们回顾了将炎症与抑郁症联系起来的流行病学证据,然后回顾了暴露于炎症刺激下产生抑郁症状与已知抑郁症中常见的脑-体变化相一致的发现。在回顾炎症在抑郁病因中的作用后,我们考虑了新的证据,即免疫调节干预可能作为抗抑郁药有希望,特别是在外周炎症生物标志物升高的个体中。讨论的干预措施包括细胞因子和环加氧酶拮抗剂,以及影响炎症转录因子/信号级联的药物。最后,我们简要讨论了各种行为策略在减少炎症从而增强情绪健康方面的潜在作用。
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引用次数: 79
Pharmacological treatment of social anxiety disorder. 社交焦虑障碍的药物治疗。
Pub Date : 2013-01-01 Epub Date: 2013-09-20 DOI: 10.1159/000351960
Vasilios G Masdrakis, Darko Turic, David S Baldwin

Social anxiety disorder (social phobia) is a common and typically long-standing medical condition, characterized by an excessive fear of being observed or evaluated negatively in social or performance situations. Efficacious interventions in acute treatment include cognitive behavioural therapy and a range of medications including many antidepressants, some benzodiazepines and anticonvulsants, and the antipsychotic olanzapine. Most studies report no significant differences in overall efficacy or tolerability between active compounds. Responders to previous acute treatment benefit from continuing active medication for 6 months. Evidence of a dose-response relationship with antidepressant drugs is inconsistent, though only higher doses of pregabalin are efficacious. Switching between treatments with proven efficacy may be helpful. Augmentation of a selective serotonin reuptake inhibitor with buspirone or clonazepam can be beneficial. It is unlikely that combining pharmacotherapy with psychotherapy results in greater overall efficacy compared to either treatment given alone. Proof-of-concept and other preliminary studies suggest the efficacy of psychotherapy can be enhanced through prior administration of D-cycloserine, cannabidiol, or oxytocin.

社交焦虑障碍(社交恐惧症)是一种常见且典型的长期医疗状况,其特征是过度害怕在社交或表演场合被消极地观察或评价。在急性治疗中,有效的干预措施包括认知行为疗法和一系列药物,包括许多抗抑郁药、一些苯二氮卓类药物和抗惊厥药,以及抗精神病药奥氮平。大多数研究报告在活性化合物之间的总体疗效或耐受性没有显着差异。对先前急性治疗有反应者可继续积极用药6个月。抗抑郁药物的剂量-反应关系的证据是不一致的,尽管只有高剂量的普瑞巴林有效。在已证实有效的治疗方法之间转换可能会有所帮助。丁螺环酮或氯硝西泮增加选择性血清素再摄取抑制剂可能是有益的。与单独给予任何一种治疗相比,药物治疗与心理治疗相结合不太可能产生更大的总体疗效。概念验证和其他初步研究表明,心理治疗的效果可以通过事先服用d -环丝氨酸、大麻二酚或催产素来增强。
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引用次数: 7
Neuroimaging in anxiety disorders. 焦虑症的神经影像学。
Pub Date : 2013-01-01 Epub Date: 2013-09-20 DOI: 10.1159/000351938
Mats Fredrikson, Vanda Faria

Neuroimaging studies using functional magnetic resonance imaging (fMRI), positron emission tomography (PET) and single-photon emission computed tomography (SPECT) to evaluate neurofunctional and neurochemical alterations related to the generation and control of affect in patients with anxiety disorders are reviewed. We performed a meta-analysis of symptom provocation studies, where neural activity was measured using fMRI, PET or SPECT to test the hypothesis that prefrontal regions modulate amygdala activity. Data revealed that reactivity in the amygdala was enhanced in patients with phobia as well as posttraumatic stress disorder (PTSD). The dorsal anterior cingulate cortex was activated in concert with the amygdala, both in PTSD and in phobic states, suggesting a role in fear expression, rather than emotional control. Activity in emotion-regulating areas in the ventromedial prefrontal cortex including the subgenual anterior cingulate cortex and the medial orbitofrontal cortex was compromised in the symptomatic state in PTSD and phobic disorders, respectively. Increased amygdala reactivity was restored with psychological treatment. Treatment effects across different modalities including pharmacological and psychological interventions as well as with placebo regimens support that reduction of neural activity in the amygdala may be a final common pathway for successful therapeutic interventions irrespective of method, thereby linking neurotransmission to plasticity in a pivotal node of the core fear network of the brain.

本文综述了使用功能磁共振成像(fMRI)、正电子发射断层扫描(PET)和单光子发射计算机断层扫描(SPECT)来评估焦虑障碍患者与情感产生和控制相关的神经功能和神经化学改变的神经影像学研究。我们对症状激发研究进行了荟萃分析,使用功能磁共振成像(fMRI)、PET或SPECT测量神经活动,以验证前额叶区域调节杏仁核活动的假设。数据显示,患有恐惧症和创伤后应激障碍(PTSD)的患者的杏仁核反应性增强。在创伤后应激障碍和恐惧状态下,背前扣带皮层与杏仁核一起被激活,这表明它在恐惧表达中起作用,而不是情绪控制。PTSD和恐惧症患者在症状状态下,腹内侧前额叶皮层包括亚属前扣带皮层和内侧眶额叶皮层的情绪调节区域的活动分别受到抑制。经心理治疗后,杏仁核反应性恢复。包括药理学和心理干预以及安慰剂方案在内的不同治疗方式的治疗效果支持,杏仁核神经活动的减少可能是成功治疗干预的最终共同途径,无论采用何种方法,从而将神经传递与大脑核心恐惧网络关键节点的可塑性联系起来。
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引用次数: 0
Co-morbidity between cardiovascular pathology and depression: role of inflammation. 心血管病理与抑郁的共发病:炎症的作用。
Pub Date : 2013-01-01 Epub Date: 2013-02-27 DOI: 10.1159/000343981
Angelos Halaris

Morbidity and mortality of cardiovascular disease is exceedingly high worldwide. Depressive illness is a serious psychiatric illness that afflicts a significant portion of the population worldwide. Epidemiological studies have confirmed the high co-morbidity between these two entities and the co-morbidity is bidirectional. Systems that are involved in and accountable for this co-morbidity in a major, complex and interactive way include the central and autonomic nervous systems, the neuroendocrine system, the immune system, and the vascular and hematologic systems. Specific pathophysiologic factors across these systems include homeostatic imbalance between the sympathetic and the parasympathetic systems with loss of heart rate variability in depression, sympathoadrenal activation, hypothalamic-pituitary-adrenal axis activation resulting in hypercortisolemia, immune system dysregulation with release of pro-inflammatory cytokines and chemokines, platelet activation and hypercoagulability. All of these abnormalities have been demonstrated in most individuals diagnosed with major depressive disorder. This chapter will focus on inflammatory processes. Inflammation occurs in cardiac and cardiovascular pathology independent of the presence or absence of depression. A chronic pro-inflammatory status has been documented in numerous studies of depression. Inflammation is closely associated with endothelial dysfunction which is a preamble to atherosclerosis and atherothrombosis. Endothelial dysfunction has been detected in depression and may prove to be a trait marker for this illness. Thus, understanding vascular biology in conjunction with psychiatric co-morbidity will be of critical importance. A likely common instigator underlying the co-morbidity between cardiovascular pathology and depression is mental stress. Chronic stress shifts the homeostatic balance in the autonomic nervous system with sustained sympathetic overdrive and diminished vagal tone. Diminished vagal tone contributes to a pro-inflammatory status which affects neurotransmitter regulation, specifically serotonergic transmission. Antidepressant drug therapy is of definite benefit to patients with medical and psychiatric co-morbidity and may reverse the pro-inflammatory status associated with depression.

全世界心血管疾病的发病率和死亡率都非常高。抑郁症是一种严重的精神疾病,折磨着世界上很大一部分人。流行病学研究证实了这两种疾病之间的高合并症,并且合并症是双向的。以一种主要的、复杂的和相互作用的方式参与并负责这种合并症的系统包括中枢和自主神经系统、神经内分泌系统、免疫系统、血管和血液系统。这些系统中的特定病理生理因素包括交感神经和副交感神经系统之间的稳态失衡,导致抑郁时心率变异性丧失,交感肾上腺活化,下丘脑-垂体-肾上腺轴活化导致高皮质醇血症,免疫系统失调,释放促炎细胞因子和趋化因子,血小板活化和高凝性。所有这些异常在大多数被诊断为重度抑郁症的个体中都得到了证实。本章将集中讨论炎症过程。炎症发生在心脏和心血管病理中,与抑郁的存在与否无关。许多关于抑郁症的研究都证实了慢性促炎状态。炎症与内皮功能障碍密切相关,内皮功能障碍是动脉粥样硬化和动脉粥样硬化血栓形成的前兆。内皮功能障碍已经在抑郁症中被发现,并且可能被证明是这种疾病的一个特征标记。因此,了解血管生物学与精神病学合并症将是至关重要的。心血管疾病和抑郁症共同发病的一个可能的共同诱因是精神压力。慢性压力改变自主神经系统的内稳态平衡,持续交感神经过度驱动和迷走神经张力减弱。迷走神经张力减弱导致促炎状态,影响神经递质调节,特别是血清素能传递。抗抑郁药物治疗对患有医学和精神疾病的患者确实有益,并可能逆转与抑郁症相关的促炎状态。
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引用次数: 24
Concerted efforts to improve the understanding and treatment of anxiety disorders. Preface. 共同努力提高对焦虑症的认识和治疗。前言。
Pub Date : 2013-01-01
Jules Angst, David S Baldwin
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引用次数: 0
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Modern trends in pharmacopsychiatry
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