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Stress and neuroinflammation. 压力和神经炎症。
Pub Date : 2013-01-01 Epub Date: 2013-02-27 DOI: 10.1159/000343965
Angela J Grippo, Melissa-Ann L Scotti

It has been well established that there is bidirectional communication between the immune and central nervous systems. One context in which this interaction has been extensively studied is that of the stress response. Stress, whether physical or psychological, induces alterations in immune function. Often exposure to a stressor results in pro-inflammatory responses in the brain and periphery. These responses are mediated by a variety of inflammatory molecules including neuropeptides, cytokines, and stress hormones among others. Here, we will discuss several of the more comprehensively studied of these inflammatory mediators and their role(s) in stress-induced neurogenic inflammation.

免疫系统和中枢神经系统之间存在着双向交流,这一点已经得到了很好的证实。这种相互作用被广泛研究的一个背景是应激反应。压力,无论是生理上的还是心理上的,都会引起免疫功能的改变。通常暴露于压力源会导致大脑和周围的促炎症反应。这些反应是由多种炎症分子介导的,包括神经肽、细胞因子和应激激素等。在这里,我们将讨论几个更全面研究的这些炎症介质及其在应激性神经源性炎症中的作用。
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引用次数: 32
Virus infection as a cause of inflammation in psychiatric disorders. 病毒感染是精神疾病炎症的一个原因。
Pub Date : 2013-01-01 Epub Date: 2013-02-27 DOI: 10.1159/000343967
Karl Bechter

Many neurotropic viruses exist and may cause classical inflammation but also low-level neuroinflammation. However, viruses may be dormant within the CNS and become active later. The role of neurotropic virus infections in the causation of psychiatric disorders may be underestimated, because the diagnostic approach to the CNS is difficult and to dormant infections in general, but especially within the CNS. Evidence is increasing that infections increase the risk of psychiatric disorders, not only prenatal infections but also infections during the lifetime. The question how low level neuroinflammation may be involved in severe psychiatric disorders like affective and schizophrenic spectrum disorders is intriguing but remains to be studied. Experimental data clearly show that low-level neuroinflammation can be induced by viruses, but the definitions of inflammation and low level neuroinflammation appear to be blurred and apparently the previous classical definition of inflammation has to be widened. Virus infection itself or virus-related products or virus-induced autoimmunity may play a role in disease pathogenesis. More sensitive diagnostic approaches from neuroimaging and CSF investigations may hold the key to a better understanding and definition of CNS viral infections as an etiopathogenetic subgroup of severe psychiatric disorders.

存在许多嗜神经病毒,可引起经典炎症,也可引起低水平的神经炎症。然而,病毒可能在中枢神经系统内处于休眠状态,随后变得活跃。嗜神经病毒感染在精神疾病病因中的作用可能被低估,因为对中枢神经系统的诊断方法是困难的,对一般的潜伏感染,尤其是中枢神经系统内的感染。越来越多的证据表明,感染增加了精神疾病的风险,不仅是产前感染,而且是终生感染。低水平的神经炎症如何可能涉及严重的精神疾病,如情感和精神分裂症谱系障碍,这个问题很有趣,但仍有待研究。实验数据清楚地表明,低水平的神经炎症可以由病毒诱导,但炎症和低水平神经炎症的定义似乎是模糊的,显然,以前的经典定义炎症必须扩大。病毒感染本身或病毒相关产物或病毒诱导的自身免疫可能在疾病发病机制中起作用。来自神经影像学和脑脊液检查的更敏感的诊断方法可能是更好地理解和定义中枢神经系统病毒感染作为严重精神疾病的致病亚群的关键。
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引用次数: 16
Anxiety and cardiovascular disease. 焦虑和心血管疾病。
Pub Date : 2013-01-01 Epub Date: 2013-09-20 DOI: 10.1159/000351945
Simon J C Davies, Christer Allgulander

This chapter examines the association of anxiety disorders and anxiety symptoms with cardiovascular disease, focussing on hypertension (an independent risk factor for myocardial infarction and stroke) and coronary heart disease. In both cases, epidemiological data linking the cardiovascular disorder with specific anxiety disorders and anxiety symptoms are examined first, and evidence relating to putative mechanisms that may underlie these associations is explored. For hypertension, an association with panic attacks and panic disorder has been reported most consistently, but the literature relating to other forms of anxiety is inconsistent, especially as some studies have reported an association of anxiety with low blood pressure. Recent work which has attempted to elucidate this confusing situation is presented. Mechanisms which may be responsible for the link between hypertension and panic include autonomic nervous system dysfunction (which may be under serotonergic control), respiratory mechanisms, cytokines, platelet dysfunction and behavioural factors. While an association of depression with coronary heart disease has been studied extensively, the association with anxiety disorders has been slower to emerge. Studies contributing to this evidence base are examined, and as for hypertension putative mechanisms are discussed.

本章探讨了焦虑障碍和焦虑症状与心血管疾病的关系,重点是高血压(心肌梗死和中风的独立危险因素)和冠心病。在这两种情况下,首先检查将心血管疾病与特定焦虑障碍和焦虑症状联系起来的流行病学数据,并探索与可能构成这些关联的假定机制有关的证据。对于高血压来说,与惊恐发作和惊恐障碍的联系是最一致的报道,但与其他形式的焦虑有关的文献是不一致的,特别是一些研究报道了焦虑与低血压的联系。最近的工作,试图阐明这一令人困惑的情况提出。可能导致高血压和恐慌之间联系的机制包括自主神经系统功能障碍(可能受血清素能控制)、呼吸机制、细胞因子、血小板功能障碍和行为因素。虽然抑郁症与冠心病之间的关系已被广泛研究,但抑郁症与焦虑症之间的关系却迟迟没有出现。研究有助于这一证据基础进行审查,并讨论了高血压的假定机制。
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引用次数: 21
Essential fatty acids as potential anti-inflammatory agents in the treatment of affective disorders. 必需脂肪酸在情感性疾病治疗中的潜在抗炎作用。
Pub Date : 2013-01-01 Epub Date: 2013-02-27 DOI: 10.1159/000343970
Cai Song

In the last two decades, many studies have demonstrated that increased inflammatory responses occur in patients with affective disorders, which could contribute to the dysfunction of neuroendocrine and neurotransmission in these diseases. The evidence consequently suggests that drugs or natural products with anti-inflammatory properties should be developed to treat the illness. Among several candidates that modulate the neuro-immune network, omega-(n)-3 essential unsaturated fatty acids have emerged as effective treatments for affective disorders. Because these fatty acids can influence membrane structure, reduce inflammation and regulate protein and gene expressions, their effects seem promising. In this chapter, the newest findings that support the inflammatory theory of affective disorders have been first selected and reviewed. Secondly, the role of n-3 fatty acids in the immune system and brain has been introduced and then the possible mechanisms by which n-3 fatty acids attenuated symptoms of depression are discussed by the insight of the results from the animal studies. Finally, the clinical effects of n-3 fatty acids on major, bipolar and postpartum depression are summarized. Furthermore, the chapter points out the limitations and future research in this area.

近二十年来,许多研究表明,情感性疾病患者的炎症反应增加,可能导致这些疾病的神经内分泌和神经传递功能障碍。因此,证据表明,应该开发具有抗炎特性的药物或天然产品来治疗这种疾病。在调节神经免疫网络的几种候选物质中,omega-(n)-3必需不饱和脂肪酸已成为情感障碍的有效治疗方法。因为这些脂肪酸可以影响膜结构,减少炎症,调节蛋白质和基因表达,它们的效果似乎很有希望。在本章中,我们首先对支持情感障碍炎症理论的最新发现进行了选择和综述。其次,介绍了n-3脂肪酸在免疫系统和大脑中的作用,并结合动物实验结果探讨了n-3脂肪酸减轻抑郁症状的可能机制。最后总结了n-3脂肪酸治疗重度抑郁症、双相抑郁症和产后抑郁症的临床效果。此外,本章还指出了该领域的局限性和未来的研究方向。
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引用次数: 12
The question of pro-inflammatory immune activity in schizophrenia and the potential importance of anti-inflammatory drugs. 精神分裂症的促炎免疫活性问题和抗炎药物的潜在重要性。
Pub Date : 2013-01-01 Epub Date: 2013-02-27 DOI: 10.1159/000343972
Volker Arolt, Oliver Ambrée

Throughout the last 20 years, numerous studies have indicated pro-inflammatory activity in patients with an acute schizophrenic episode. In this report, the most relevant findings concerning the cytokine systems in schizophrenia are demonstrated, together with recent studies on gene expression. Findings in humans are supplemented by observations from rodent models of schizophrenia. Furthermore, the current state of both neuroleptic and anti-inflammatory compounds on the immune system is reported, together with clinical data on the effects of anti-inflammatory medications on the course of the acute illness in patients with schizophrenia.

在过去的20年中,许多研究表明急性精神分裂症发作患者具有促炎活性。在本报告中,最相关的发现有关细胞因子系统在精神分裂症被证明,连同最近的研究基因表达。精神分裂症啮齿动物模型的观察补充了对人类的研究结果。此外,本文还报道了抗精神病药物和抗炎药物对免疫系统的影响现状,以及抗炎药物对精神分裂症患者急性病程的影响的临床数据。
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引用次数: 6
Inflammation in suicidality: implications for novel treatment options. 自杀中的炎症:对新治疗方案的启示。
Pub Date : 2013-01-01 Epub Date: 2013-02-27 DOI: 10.1159/000346085
Shorena Janelidze, Lena Brundin

Suicide is an increasing health problem worldwide and the most severe complication of multiple psychiatric disorders. It is also prevalent in several somatic conditions. In recent years, significant advances have been made in understanding the neurobiology of suicidal behaviors. Several lines of evidence have emerged suggesting that inflammation may contribute to the pathophysiology of suicide. Basic and clinical data indicate that the effects of inflammation on mood and behavior are likely to be mediated by the kynurenine pathway metabolites and glutamatergic neurotransmission. At the same time, the triggers of inflammatory changes observed in suicidal patients are largely unknown but may include stress, infectious agents and autoimmune diseases. As available treatment options against suicidality are only moderately effective, targeting the inflammatory system may provide novel therapeutic opportunities. For this goal to be achieved, however, we need to gain better insight into the origin, mechanisms and outcomes of inflammation in suicidal behavior.

自杀是世界范围内日益严重的健康问题,也是多种精神疾病最严重的并发症。它也普遍存在于几种躯体疾病中。近年来,在了解自杀行为的神经生物学方面取得了重大进展。几条线索的证据表明,炎症可能有助于自杀的病理生理。基础和临床数据表明,炎症对情绪和行为的影响可能是由犬尿氨酸途径代谢物和谷氨酸神经传递介导的。与此同时,在自杀患者中观察到的炎症变化的触发因素在很大程度上是未知的,但可能包括压力、感染因子和自身免疫性疾病。由于针对自杀的现有治疗方案只有中等效果,针对炎症系统可能提供新的治疗机会。然而,为了实现这一目标,我们需要更好地了解自杀行为中炎症的起源、机制和结果。
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引用次数: 6
Inflammation, neurotoxins and psychiatric disorders. 炎症,神经毒素和精神疾病。
Pub Date : 2013-01-01 Epub Date: 2013-02-27 DOI: 10.1159/000343968
Aye-Mu Myint

Although immune reactions are necessary to defend against danger signals, the mediator molecules such as cytokines can be detrimental to the organism if the exposure is longer than necessary or in certain abnormal concentrations. The neuroprotection and neurotoxicity induced by the interaction between certain cytokines and the metabolites from tryptophan catabolism, the neuroactive kynurenines, which is partly influenced by corticosteroid action plays an important role in several neurotransmissions such as serotonergic, dopaminergic and glutamatergic transmissions and receptor functions such as N-methyl-D-aspartate receptor or α7-nicotinic-acetylcholine receptor. While the molecules in normal concentrations are essential to the normal glial-neuronal interaction, any changes that induce imbalance in the network between those molecules could disturb the interaction. The role of this network in major psychiatric disorders such as depression, bipolar disorder and schizophrenia and future therapeutic roles are discussed in this manuscript.

尽管免疫反应是防御危险信号所必需的,但如果暴露时间超过必要时间或处于某些异常浓度,细胞因子等中介分子可能对生物体有害。某些细胞因子与色氨酸分解代谢产物、神经活性犬尿氨酸(部分受皮质类固醇作用影响)相互作用所诱导的神经保护和神经毒性,在5 -羟色胺能、多巴胺能和谷氨酸能等神经传递和n -甲基- d -天冬氨酸受体或α - 7-烟碱-乙酰胆碱受体等受体功能中起重要作用。虽然正常浓度的分子对正常的胶质-神经元相互作用至关重要,但任何导致这些分子之间网络失衡的变化都可能干扰这种相互作用。该网络在抑郁症、双相情感障碍和精神分裂症等主要精神疾病中的作用以及未来的治疗作用在本文中进行了讨论。
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引用次数: 14
Duration of untreated illness and duration of illness in anxiety disorders: assessment and influence on outcome. 焦虑症中未治疗的疾病持续时间和疾病持续时间:评估及其对结果的影响。
Pub Date : 2013-01-01 Epub Date: 2013-09-20 DOI: 10.1159/000351950
A Carlo Altamura, Giulia Camuri, Bernardo Dell'Osso

Anxiety disorders are disabling and generally chronic conditions, with a lifetime prevalence of 15-20% in the general population. These disorders are usually associated with early onset and often remain untreated for several years with important consequences on patients' functioning and quality of life. From this perspective, recent literature has considered duration of illness (DI) and duration of untreated illness (DUI), two important variables influencing outcome in many psychiatric conditions including anxiety disorders. The DUI has been defined as the interval between the onset of a specific psychiatric disorder and the subsequent administration of the first adequate pharmacological treatment given at standard dosages and for an adequate period of time in compliant subjects. The DI can be defined as the time elapsing between the onset of a psychiatric disorder and the recovery from the illness. The two variables are likely interrelated, with a longer DUI being a major contributor to a longer DI. A significant body of evidence has shown that prolonged DI and DUI are associated with structural and functional brain abnormalities as well as with poor treatment response, particularly in schizophrenia. More recently, an increasing number of studies have been pointing toward a similar conclusion in affective disorders. As a consequence, the assessment of the latency to treatment (DUI) may represent one of the first steps in order to plan early interventions and reduce the overall DI. The present chapter highlights the role of the DI and latency to treatment in anxiety disorders, focusing on epidemiologic, neuropathological, clinical and prognostic issues.

焦虑症是致残的,通常是慢性疾病,在一般人群中终生患病率为15-20%。这些疾病通常与早期发病有关,并且往往在数年内得不到治疗,对患者的功能和生活质量产生重要影响。从这个角度来看,最近的文献考虑了疾病持续时间(DI)和未治疗疾病持续时间(DUI),这是影响包括焦虑症在内的许多精神疾病结局的两个重要变量。DUI被定义为一种特定精神障碍的发作和随后在依从性受试者中给予标准剂量和适当时间的第一次适当药物治疗之间的间隔。残障期可以定义为从精神疾病发病到从疾病恢复之间的时间。这两个变量可能是相互关联的,较长的DUI是较长的DI的主要贡献者。大量证据表明,长期酒后饮酒和酒后驾车与大脑结构和功能异常以及治疗效果差有关,尤其是精神分裂症。最近,越来越多的研究在情感障碍方面也得出了类似的结论。因此,评估治疗潜伏期(DUI)可能是计划早期干预和减少总体DI的第一步。本章重点介绍了焦虑障碍治疗中DI和潜伏期的作用,重点介绍了流行病学、神经病理学、临床和预后问题。
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引用次数: 15
On the nature of obsessions and compulsions. 关于强迫和强迫的本质。
Pub Date : 2013-01-01 Epub Date: 2013-09-20 DOI: 10.1159/000351929
Sanneke de Haan, Erik Rietveld, Damiaan Denys

In this chapter, we give an overview of current and historical conceptions of the nature of obsessions and compulsions. We discuss some open questions pertaining to the primacy of the affective, volitional or affective nature of obsessive-compulsive disorder. Furthermore, we add some phenomenological suggestions of our own. In particular, we point to the patients' need for absolute certainty and the lack of trust underlying this need. Building on insights from Wittgenstein, we argue that the kind of certainty the patients strive for is unattainable in principle via the acquisition of factual knowledge. Moreover, we suggest that the patients' attempts to attain certainty are counter-productive as their excessive conscious control in fact undermines the trust they need.

在本章中,我们概述了当前和历史上关于强迫和强迫本质的概念。我们讨论了一些关于强迫症的情感,意志或情感性质的首要问题。此外,我们还补充了一些我们自己的现象学建议。我们特别指出,患者需要绝对的确定性,而这种需求背后缺乏信任。基于维特根斯坦(Wittgenstein)的见解,我们认为,患者所追求的那种确定性,原则上是无法通过获得事实性知识来实现的。此外,我们认为患者试图获得确定性是适得其反的,因为他们过度的有意识控制实际上破坏了他们所需要的信任。
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引用次数: 20
Pharmacological treatment of panic disorder. 惊恐障碍的药物治疗。
Pub Date : 2013-01-01 Epub Date: 2013-09-20 DOI: 10.1159/000351953
Borwin Bandelow, David S Baldwin, Peter Zwanzger

A comprehensive database has developed and precise recommendations can be provided for treating patients with panic disorder. Selective serotonin reuptake inhibitors and serotonin-norepinephrine reuptake inhibitors are standard treatments for panic disorder. Tricyclic antidepressants are as effective as modern antidepressants, but less well tolerated. For short-term treatment and in non-responsive cases, benzodiazepines such as alprazolam may be used when the patient does not have a history of dependency and tolerance. Combining drug treatment with cognitive behaviour therapy is the most successful treatment strategy for panic disorder. This chapter also includes treatment recommendations for pregnant or lactating women, children, adolescents, elderly patients, and patients who are non-responsive to standard treatments.

已经建立了一个全面的数据库,可以为治疗恐慌症患者提供精确的建议。选择性5 -羟色胺再摄取抑制剂和5 -羟色胺-去甲肾上腺素再摄取抑制剂是惊恐障碍的标准治疗方法。三环类抗抑郁药与现代抗抑郁药一样有效,但耐受性较差。对于短期治疗和无反应的病例,当患者没有依赖史和耐受性时,可以使用苯二氮卓类药物,如阿普唑仑。药物治疗与认知行为治疗相结合是治疗恐慌症最成功的策略。本章还包括对孕妇或哺乳期妇女、儿童、青少年、老年患者和对标准治疗无反应的患者的治疗建议。
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引用次数: 11
期刊
Modern trends in pharmacopsychiatry
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