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Pharmacological and Nonpharmacological Interventions to Arrest Neuroprogression in Psychiatric Disorders. 阻止精神疾病神经进展的药物和非药物干预。
Pub Date : 2017-01-01 Epub Date: 2017-07-24 DOI: 10.1159/000470814
Fotini Boufidou, Angelos Halaris

The concept of neuroprogression describes the progressive course of the disorder and stresses the progressive, recurrent, and chronic course of the disease entity under consideration. It subsumes clinical manifestations of the disease process and may also entail morphological, biochemical, neurochemical, immunological, physiological, and genetic aspects that contribute to the progressive course of the disease in question. In an attempt to identify the appropriate agent or method that could arrest neuroprogression in psychiatric patients, we conducted an evaluation of the use of anti-inflammatory drugs under the perspective of current pharmacological and neurophysiological data. This evaluation included the use of nonsteroidal anti-inflammatory drugs (NSAIDs) as adjunctive treatment to conventional pharmacotherapy as well as the use of natural products exerting anti-inflammatory properties (i.e., ω-3 fatty acids) given as adjunctive or monotherapeutic treatments in less severe cases. The therapeutic significance of nonpharmacological methods, such as psychotherapy, physical exercise, and body-mind therapies, was also considered and will be discussed in this chapter. In conclusion, the role of psychotropic and select anti-inflammatory drugs in arresting neuroprogression is a very promising new frontier in psychiatric research and clinical practice. Modulators of a specific prostanoid synthase or receptor across the cyclooxygenase (COX)-2 downstream pathway along with new multitarget NSAIDs are expected to be tested by the pharmaceutical industry as potential agents to antagonize neuroprogression. Meanwhile, salicylates and selective COX-2 inhibitors could still be used in carefully selected subgroups of patients. Psychotherapy and nonpharmacological, stress-relieving methods should be considered as adjunctive tools to aid in arresting neuroprogression.

神经进展的概念描述了疾病的进展过程,并强调了所考虑的疾病实体的进展性、复发性和慢性过程。它包括疾病过程的临床表现,也可能涉及形态学、生化、神经化学、免疫学、生理学和遗传方面,这些方面有助于疾病的进展过程。为了寻找合适的药物或方法来阻止精神病患者的神经进展,我们从目前的药理学和神经生理学数据的角度对消炎药的使用进行了评估。该评估包括使用非甾体抗炎药(NSAIDs)作为常规药物治疗的辅助治疗,以及在较轻的病例中使用具有抗炎特性的天然产物(即ω-3脂肪酸)作为辅助治疗或单药治疗。非药物方法的治疗意义,如心理治疗、体育锻炼和身心疗法,也被考虑并将在本章中讨论。综上所述,精神药物和选择性抗炎药物在抑制神经进展中的作用是精神病学研究和临床实践中一个非常有前途的新领域。通过环氧化酶(COX)-2下游通路的特定前列腺素合成酶或受体调节剂以及新的多靶点非甾体抗炎药有望被制药行业作为对抗神经进展的潜在药物进行测试。同时,水杨酸盐和选择性COX-2抑制剂仍可用于精心挑选的患者亚组。心理治疗和非药物缓解压力的方法应被视为辅助工具,以帮助阻止神经进展。
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引用次数: 9
Major Depression as a Neuroprogressive Prelude to Dementia: What Is the Evidence? 重度抑郁症是痴呆的神经进行性前奏:证据是什么?
Pub Date : 2017-01-01 Epub Date: 2017-07-24 DOI: 10.1159/000470807
Brian E Leonard

Epidemiological studies implicate chronic depression as a predisposing factor for dementia in later life. However, the link is incompletely understood and controversial. The aim of this review is to consider some of the biological factors that contribute to neuroprogressive brain dysfunction in late life as a consequence of prolonged, low-grade inflammation in the course of depressive episodes. As chronic inflammation is known to precipitate increased apoptosis of neurons and astrocytes, this could be a contributing factor to brain dysfunction. In addition, certain proinflammatory cytokines activate the neurotoxic derivatives of the tryptophan-kynurenine pathway. This results in the synthesis of the NMDA glutamate agonist, quinolinic acid, and kynurenine metabolites which initiate oxidative stress and insulin receptor resistance. As a consequence of these changes, combined with a structural and functional defect in brain mitochondria, glucose transport into the brain is affected. Due to the ensuing reduction in the metabolic energy needed to sustain brain function, brain cells die prematurely. These changes could provide a link between chronic inflammation and dementia, at least in some patients with recurrent and chronic depression. This outcome may be particularly true in poor responders and treatment-resistant depression.

流行病学研究表明,慢性抑郁症是晚年痴呆的易感因素。然而,人们对这种联系的理解并不完全,而且存在争议。这篇综述的目的是考虑一些生物学因素,这些因素导致抑郁发作过程中长期、低度炎症导致晚年神经进行性脑功能障碍。众所周知,慢性炎症会导致神经元和星形胶质细胞凋亡增加,这可能是导致脑功能障碍的一个因素。此外,某些促炎细胞因子可激活色氨酸-犬尿氨酸途径的神经毒性衍生物。这导致NMDA谷氨酸激动剂、喹啉酸和犬尿氨酸代谢产物的合成,这些代谢产物会引发氧化应激和胰岛素受体抵抗。由于这些变化,再加上脑线粒体的结构和功能缺陷,葡萄糖进入大脑的运输受到影响。由于随后维持大脑功能所需的代谢能量减少,脑细胞过早死亡。这些变化可能提供了慢性炎症和痴呆之间的联系,至少在一些复发性和慢性抑郁症患者中是这样。这一结果可能在不良反应和治疗难治性抑郁症中尤其真实。
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引用次数: 24
Cytokines in Neuropathic Pain and Associated Depression. 细胞因子在神经性疼痛和相关抑郁中的作用。
Pub Date : 2015-01-01 Epub Date: 2015-09-18 DOI: 10.1159/000435932
Justin G Lees, Brett Fivelman, Samuel S Duffy, Preet G S Makker, Chamini J Perera, Gila Moalem-Taylor

Neuropathic pain occurs as a result of lesion or disease affecting the somatosensory nervous system and is present in a diverse set of peripheral and central pathologies such as nerve trauma, diabetic neuropathy, post-herpetic neuralgia, chemotherapy-induced peripheral neuropathy, spinal cord injury and multiple sclerosis. Debilitating symptoms including allodynia, hyperalgesia and spontaneous pain have a substantial negative impact on patients' quality of life. The currently available therapeutic treatments are generally ineffective and characterised by poor response rates. Accumulating evidence suggests that neuroinflammation and cytokine signalling play a critical role in neuropathic pain. Numerous experimental studies have demonstrated that certain pro-inflammatory cytokines are elevated in neuropathic pain conditions, and administration of these cytokines can elicit pain hypersensitivity in the absence of injury or disease. This phenomenon is also apparent in the 'sickness response', which encompasses a broad inflammatory response to disease and injury and involves a series of physiological and behavioural changes including pain hypersensitivity. Interestingly, the 'sickness response' is also similar in nature to some of the defining characteristics of the depressed state of affective disorder. In this review, we explore links that may relate the co-existence of depression in neuropathic pain patients with the activity of cytokines and discuss the role of several key pro-inflammatory and anti-inflammatory cytokines in neuropathic pain.

神经性疼痛是影响体感觉神经系统的病变或疾病的结果,存在于多种周围和中枢病变中,如神经创伤、糖尿病神经病变、疱疹后神经痛、化疗引起的周围神经病变、脊髓损伤和多发性硬化症。异常性痛觉、痛觉过敏和自发性疼痛等衰弱症状对患者的生活质量有实质性的负面影响。目前可用的治疗方法通常是无效的,其特点是反应率差。越来越多的证据表明,神经炎症和细胞因子信号在神经性疼痛中起着关键作用。大量实验研究表明,某些促炎细胞因子在神经性疼痛条件下升高,这些细胞因子的施用可以在没有损伤或疾病的情况下引起疼痛超敏反应。这种现象在“疾病反应”中也很明显,它包括对疾病和损伤的广泛炎症反应,并涉及一系列生理和行为变化,包括疼痛过敏。有趣的是,“疾病反应”在本质上也与情感障碍中抑郁状态的一些定义特征相似。在这篇综述中,我们探讨了神经性疼痛患者抑郁共存与细胞因子活性的联系,并讨论了几种关键的促炎和抗炎细胞因子在神经性疼痛中的作用。
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引用次数: 35
Emotional and Cognitive Influences on Pain Experience. 情绪和认知对疼痛体验的影响。
Pub Date : 2015-01-01 Epub Date: 2015-09-18 DOI: 10.1159/000435938
Madelon L Peters

Multiple emotional and cognitive factors impact on the experience of pain. This chapter will review some of the most important emotional and cognitive determinants of the pain experience as found in experimental and clinical studies with human participants. Emotional factors that may increase pain perception are anxiety, depression and anger. Positive emotions usually decrease perceived pain. The cognitive factors attention, expectancy and appraisal can either increase or decrease pain experiences depending on their specific focus and content. Many brain regions are involved in nociceptive processing and bringing pain into awareness. There are profound interconnections between areas processing sensory, emotional and cognitive information. Descending pathways from cortical areas to the midbrain and spinal levels can facilitate or inhibit spinal nociceptive information and thereby afferent nociceptive input to the brain. The underlying mechanisms of the various emotional and cognitive modulatory influences may partly overlap, but also have some unique aspects. What becomes clear is that pain is not merely a reflection of the nociceptive input, but should be considered as a complex experience shaped by psychological factors that may be unique for each individual.

多种情绪和认知因素影响疼痛的体验。本章将回顾在实验和临床研究中发现的一些最重要的疼痛体验的情感和认知决定因素。可能增加痛觉的情绪因素有焦虑、抑郁和愤怒。积极的情绪通常会减少感知到的痛苦。认知因素注意、期望和评价可以增加或减少疼痛体验,这取决于它们的特定焦点和内容。大脑的许多区域都参与了伤害处理,并将疼痛转化为意识。在处理感觉、情感和认知信息的区域之间存在着深刻的相互联系。从皮质区到中脑和脊髓水平的下行通路可以促进或抑制脊髓伤害性信息,从而传入伤害性信息到大脑。各种情绪和认知调节影响的潜在机制可能部分重叠,但也有一些独特的方面。越来越清楚的是,疼痛不仅仅是伤害性输入的反映,而应该被视为一种由心理因素形成的复杂体验,这种心理因素可能对每个人来说都是独特的。
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引用次数: 46
Neuroinflammatory Mechanisms Linking Pain and Depression. 疼痛和抑郁之间的神经炎症机制。
Pub Date : 2015-01-01 Epub Date: 2015-09-18 DOI: 10.1159/000435931
Nikita N Burke, David P Finn, Michelle Roche

Depression and chronic pain have been estimated to co-occur in up to 80% of patients suffering from these disorders, with this co-morbidity being more disabling and more expensive to both patients and society than either disorder alone. A number of neural substrates have been proposed to underlie this association; however, there has been increased interest and support for a role of neuroimmune and neuroinflammatory mechanisms as key players in this dyad. This chapter will provide an overview of the clinical and preclinical data supporting a role for neuroimmune alterations in depression-pain co-morbidity. We propose that such changes may impact on the functioning of key brain regions modulating emotional and nociceptive processing, thus resulting in the behavioural, psychological and physical symptoms observed in patients exhibiting depression and co-morbid pain.

据估计,多达80%患有这些疾病的患者同时患有抑郁症和慢性疼痛,与单独患有任何一种疾病相比,这种合并症对患者和社会造成的致残性更大,成本更高。已经提出了一些神经基质来支持这种关联;然而,越来越多的人对神经免疫和神经炎症机制在这两种机制中的关键作用感兴趣和支持。本章将概述支持神经免疫改变在抑郁-疼痛合并症中的作用的临床和临床前数据。我们认为,这些变化可能会影响调节情绪和伤害性处理的关键大脑区域的功能,从而导致在表现出抑郁和共病疼痛的患者中观察到的行为、心理和身体症状。
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引用次数: 49
Animal Models for the Study of Comorbid Pain and Psychiatric Disorders. 共病疼痛和精神疾病研究的动物模型。
Pub Date : 2015-01-01 Epub Date: 2015-09-18 DOI: 10.1159/000435929
Hugo Leite-Almeida, Filipa Pinto-Ribeiro, Armando Almeida

Animal models of chronic pain have provided valuable information on the mechanisms of initiation and maintenance of the disease. Much of the research effort has targeted sensory abnormalities like hyperalgesia and allodynia. However, in the past 15 years a significant number of research groups have focused their attention on comorbid anxiety, depression and cognitive impairments that frequently emerge in chronic pain conditions. A myriad of paradigms have since then been introduced in the field to tackle multiple dimensions of rodents' behavior. Concerning emotional behavior, these include the elevated plus (and zero) maze and dark/light box for anxiety, the forced swimming and tail suspension tests for depression, and the spontaneous burrowing behavior for general well-being. Regarding the cognitive dimension, several water mazes (spatial-reference memory), attentional set-shifting test (attention and reversal learning), novel object recognition (memory), 5-choice serial reaction time task (sustained attention) and variable delay-to-signal task (impulsivity) are among the most commonly employed paradigms. The construct of some of these paradigms in the context of chronic pain will be reviewed in this chapter, with special emphasis on mood and cognitive alterations that are associated with the development of neuropathic and arthritic pain.

慢性疼痛的动物模型为疾病的发生和维持机制提供了有价值的信息。大部分研究都针对感觉异常,如痛觉过敏和异常性疼痛。然而,在过去的15年里,大量的研究小组把注意力集中在慢性疼痛条件下经常出现的共病焦虑、抑郁和认知障碍上。从那时起,无数的范式被引入该领域,以解决啮齿动物行为的多个维度。关于情绪行为,这些包括焦虑的升高的正(零)迷宫和暗/光盒,抑郁的强迫游泳和悬尾测试,以及一般幸福感的自发挖洞行为。在认知维度上,几个水迷宫(空间参照记忆)、注意集合转移测试(注意和反转学习)、新物体识别(记忆)、5选择连续反应时间任务(持续注意)和可变延迟信号任务(冲动性)是最常用的范式。本章将回顾慢性疼痛背景下的一些范式的构建,特别强调与神经性疼痛和关节炎疼痛发展相关的情绪和认知改变。
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引用次数: 35
Genetic and Epigenetic Mechanisms Linking Pain and Psychiatric Disorders. 疼痛与精神疾病相关的遗传和表观遗传机制。
Pub Date : 2015-01-01 Epub Date: 2015-09-18 DOI: 10.1159/000435937
Artur H Swiergiel, Grzegorz R Juszczak, Adrian M Stankiewicz

The neurophysiological link between neuropathic pain and depression remains unknown despite evident high comorbidity of these two disorders. However, there is convincing evidence that genotype plays a role in both pain and depression. Using various types of genetic analysis - population genetics, cytogenetics and molecular technologies - specific genes have been implicated in mediating almost all aspects of nociception and mood disorders. The current review attempts to identify specific genes and epigenetic mechanisms common to both disorders. It is concluded that external and internal factors (inflammation, stress, gender, etc.) that contribute to the pathologies may do so through epigenetic mechanisms that may affect expression of these particular genes. The possible involvement of epigenetic regulation in pain and psychiatric disorders suggests that treatments targeting epigenetic mechanisms that mediate adverse life events should be considered.

神经性疼痛和抑郁症之间的神经生理学联系仍然未知,尽管这两种疾病明显高合并症。然而,有令人信服的证据表明,基因型在疼痛和抑郁中都起着作用。使用各种类型的遗传分析-群体遗传学,细胞遗传学和分子技术-特定基因已涉及介导几乎所有方面的伤害和情绪障碍。目前的综述试图确定两种疾病共同的特定基因和表观遗传机制。由此得出结论,外部和内部因素(炎症、压力、性别等)可能通过影响这些特定基因表达的表观遗传机制导致这些疾病。表观遗传调控在疼痛和精神疾病中的可能参与表明,应该考虑针对介导不良生活事件的表观遗传机制进行治疗。
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引用次数: 6
Pain, Depression and Inflammation: Are Interconnected Causative Factors Involved? 疼痛、抑郁和炎症:是否有相互关联的致病因素?
Pub Date : 2015-01-01 Epub Date: 2015-09-18 DOI: 10.1159/000435930
Brian E Leonard

Co-morbid depression and chronic pain are highly prevalent. The purpose of this review is to examine the role of chronic inflammation as a common mediator of these co-morbidities. Dysfunctional bidirectional pathways between the brain and the immune, endocrine and neurotransmitter systems have been extensively described and implicated in pain and psychiatric disorders. This short review therefore accesses the evidence in favour of the psychoneuroendocrine hypothesis of psychiatric disorders under three main headings: (1) by illustrating how different types of stress play a crucial role in initiating chronic inflammation in major depression, (2) by accessing the evidence that pain is frequently an important component of, and an initiator of, depression, and (3) considering the evidence that chronic inflammation provides an important link between chronic pain and depression, and the possible cellular mechanisms involved in this process. By understanding the critical role that chronic inflammation plays in pain and depression, novel approaches to the development of drugs may emerge that offer improvements in treatment.

并存的抑郁症和慢性疼痛非常普遍。本综述的目的是研究慢性炎症作为这些合并症的共同媒介的作用。大脑与免疫、内分泌和神经递质系统之间的双向通路功能失调已被广泛描述,并与疼痛和精神疾病有关。因此,这篇简短的综述在三个主要标题下获得了支持精神疾病的精神神经内分泌假说的证据:(1)阐明不同类型的压力如何在引发重度抑郁症的慢性炎症中发挥关键作用;(2)通过获取疼痛通常是抑郁症的重要组成部分和发起者的证据;(3)考虑慢性炎症在慢性疼痛和抑郁症之间提供重要联系的证据,以及可能参与这一过程的细胞机制。通过了解慢性炎症在疼痛和抑郁中所起的关键作用,开发药物的新方法可能会出现,从而改善治疗。
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引用次数: 23
Supraspinal Transient Receptor Potential Subfamily V Member 1 (TRPV1) in Pain and Psychiatric Disorders. 疼痛和精神疾病中的棘上瞬时受体电位亚家族V成员1 (TRPV1)。
Pub Date : 2015-01-01 Epub Date: 2015-09-18 DOI: 10.1159/000435934
Manish K Madasu, Michelle Roche, David P Finn

The transient receptor potential subfamily V member 1 (TRPV1) belongs to the diverse transient receptor potential (TRP) family of cation channels. It was first characterized in primary afferent fibres as a receptor for capsaicin. Peripheral TRPV1 has a very well-described role in nociception. However, TRPV1 is now recognized to have a broader distribution and function, with supraspinal/brain TRPV1 known to modulate pain processing. Recently, studies employing histological, genetic and pharmacological approaches have provided evidence that supraspinal TRPV1 also modulates brain neurobiology and behaviours related to anxiety, depression and schizophrenia. Key brain regions involved in TRPV1-mediated modulation of pain and affect include the periaqueductal grey, hippocampus and medial prefrontal cortex. Thus, TRPV1 in the brain is emerging as an important molecular substrate which is dually implicated in both pain and psychiatric disorders, and represents a novel therapeutic target for these conditions and their comorbidity.

瞬时受体电位亚家族V成员1 (TRPV1)属于多种瞬时受体电位(TRP)阳离子通道家族。它首先在初级传入纤维中被表征为辣椒素的受体。外周TRPV1在伤害感觉中有很好的作用。然而,TRPV1现在被认为具有更广泛的分布和功能,已知脊柱上/脑TRPV1调节疼痛加工。最近,采用组织学、遗传学和药理学方法的研究提供了证据,表明棘上TRPV1也调节与焦虑、抑郁和精神分裂症相关的脑神经生物学和行为。参与trpv1介导的疼痛和情绪调节的关键脑区包括导水管周围灰质、海马和内侧前额皮质。因此,大脑中的TRPV1正在成为一个重要的分子底物,它在疼痛和精神疾病中都有双重作用,并且代表了这些疾病及其合并症的新治疗靶点。
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引用次数: 25
Visceral Pain and Psychiatric Disorders. 内脏疼痛和精神疾病。
Pub Date : 2015-01-01 Epub Date: 2015-09-18 DOI: 10.1159/000435936
Valeria D Felice, Rachel D Moloney, John F Cryan, Timothy G Dinan, Siobhain M O'Mahony

The high comorbidity existing between visceral pain and psychiatric disorders such as depression and anxiety is well documented and it is gaining increasing interest among scientists. When visceral pain and psychiatric disorders are comorbid, they present a more debilitating condition than each disorder alone, impacting significantly on the quality of life of these patients. Despite several groups having shown that an overlapping pathophysiology exists between visceral pain and stress-related disorders the link between them is not clear yet. Moreover, it still remains to be elucidated if psychiatric conditions predispose the individual to develop visceral hypersensitivity or vice versa. The brain-gut-microbiome axis is the bidirectional communication between the CNS and the gastrointestinal tract. Alterations at different levels of this axis have been implicated in both visceral hypersensitivity and psychiatric disorders. Here we give an overview of what it is known about comorbid visceral pain and psychiatric disorders and provide evidence of potential overlapping pathophysiological mechanisms involved. Preclinical models of comorbid visceral pain and stress-related disorders are also discussed.

内脏疼痛与精神疾病(如抑郁和焦虑)之间的高共病性已经得到了充分的证明,科学家们对此越来越感兴趣。当内脏疼痛和精神疾病合并症时,它们比单独的疾病更使人衰弱,严重影响这些患者的生活质量。尽管一些研究小组已经表明,内脏疼痛和压力相关疾病之间存在重叠的病理生理学,但它们之间的联系尚不清楚。此外,它仍然有待阐明,如果精神状况倾向于个人发展内脏过敏或反之亦然。脑-肠-微生物轴是中枢神经系统和胃肠道之间的双向通信。该轴不同水平的改变与内脏过敏和精神疾病都有关系。在这里,我们给出了什么是已知的共病内脏疼痛和精神疾病,并提供证据的潜在重叠的病理生理机制参与。还讨论了共病内脏疼痛和应激相关疾病的临床前模型。
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引用次数: 17
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Modern trends in pharmacopsychiatry
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