简述焦虑障碍治疗循证研究现状

焦虑障碍是常见的精神疾病,根据DSM-IV主要分为六种:惊恐障碍(PD)伴或不伴有广场恐惧症(agoraphobia),强迫症(OCD),社交恐惧症(SAD),广泛性焦虑障碍(GAD),特定类型的恐惧症(specific phobia),创伤后应激障碍(PTSD).大部分焦虑障碍患者自身有强烈的求治愿望.如果不适当治疗,长此以往将损害患者社会功能,严重可导致自杀、物质滥用等.     

惊恐障碍时的心理生理反应

在急性应激状态下焦虑与自主神经活动有关。但在非应激状态下,慢性焦虑者是否也表现过高的自主神经活动以及他们对日常应激事件的反应是否有别于非焦虑者尚不清楚。新近研究发现,广泛性焦虑障碍(GAD)病人并不表现出普遍的自主神经活动过度,而且自主神经对刺激事件的反应比非焦虑对照者可适应性更小。惊恐障碍(PD)病人的     

不同疗效广泛性焦虑障碍患者大脑半球间功能连接差异的功能磁共振研究

目的:探讨广泛性焦虑障碍(GAD)患者大脑半球间功能连接变化特征,以及这些变化与疗效之间的相关性。方法:使用1.5 T磁共振扫描仪,比较38例经艾司西酞普兰治疗8周后的GAD患者(GAD组)及30名性别、年龄、教育程度相匹配的健康对照者(正常对照组)的基于体素镜像同伦连接(VMHC)值;同时比较痊愈患者(n=13)及非痊愈患者(n=25)VMHC值;运用DEPASF 4.3 Advanced Edition软件处理数据进行全脑VMHC比较,并分析相关因素。结果:GAD患者的双侧颞中回、双侧中央前回、双侧枕中叶VMHC降低(P0.05,Alphasim校正);GAD患者双侧小脑6区,双侧前扣带和旁扣带脑回VMHC值与基线汉密尔顿焦虑量表(HAMA)评分负相关,双侧眶内额上回VMHC值与病程负相关(P0.05,Alphasim校正);痊愈组的双侧颞下回VMHC值显著高于非痊愈组(P0.05,Alphasim校正)。结论:GAD患者在颞叶、额叶、部分枕叶存在双侧大脑半球间功能连接异常,两侧颞下回大脑半球间高功能连接预示艾司西酞普兰有较好的8周末疗效。     

焦虑障碍的核心特征与治疗

焦虑障碍的代表疾病主要包括广泛性焦虑障碍、惊恐障碍、场所恐怖症、社交焦虑障碍(社交恐怖症)等,该组障碍的共同特征是过度害怕和焦虑的心境,以及相关的行为紊乱。广泛性焦虑障碍表现为对多种主题、事件或任务感到严重的焦虑与担心。惊恐障碍是指在没有预警的情况下反复出现惊恐发作并担心再次发作。场所恐怖症是指个体对某些场合的强烈恐惧、焦虑与回避,患者常担心无法逃离、得不到帮助或健康受到威胁。社交焦虑障碍表现为回避社交环境,过分担心他人的负性评价。焦虑障碍的治疗方法包括药物治疗、心理咨询等。     

惊恐障碍患者的儿童期虐待与认知功能研究

目的:研究惊恐障碍(PD)患者儿童期虐待经历与其认知功能水平的特征,并探讨儿童期虐待对PD认知功能的影响。方法:选取33例PD患者为病例组;采用儿童期虐待问卷对正常对照组筛选出伴儿童期虐待对照组31名和不伴儿童期虐待对照组38名。采用惊恐障碍严重度量表评定患者症状,威斯康星卡片分类测验(WCST)和韦氏记忆量表(WMS)评估3组的认知功能。结果:PD组与伴儿童期虐待对照组和不伴儿童期虐待对照组在儿童期情感虐待上差异均有统计学意义(P均0.05)。在认知功能得分上,PD组与不伴儿童期虐待对照组在WCST持续错误数得分(P0.05)、WMS视觉再生和理解记忆得分上差异有统计学意义(P均0.01);PD组与伴儿童期虐待对照组在WMS理解记忆分量表上差异有统计学意义(P0.05);伴与不伴儿童期虐待的两对照组在WMS4个分量表上差异均有统计学意义(P均0.05)。相关分析显示PD的症状得分与儿童期情感虐待存在较强的正相关(P均0.01);PD的WMS理解记忆得分与儿童期情感虐待呈负相关(P0.01),偏相关分析也显示两者呈负相关(P0.05)。结论:PD患者可能会具有更多的儿童期虐待,尤其是情感虐待。儿童期虐待不仅可能会影响PD患者的惊恐症状严重程度,还可能对工作记忆等认知功能产生损害。     

焦虑症的生化病理机制探讨

目的：从神经递质与神经内分泌角度探讨焦虑症的生化病理机制。方法：采用高效液相色谱法及放射免疫测定法，分别测定25例焦虑症患者和28例正常对照者血小板5—羟色胺(5—HT)含量及血浆催乳素(PRL)含量、地塞米松抑制实验(DST)皮质醇含量。结果：广泛性焦虑(GAD)组血小板5—HT水平高于正常对照组，惊恐障碍(PD)组与正常对照组无显著差异；GAD组与对照组血浆PRL均极显著低于PD组；GAD组与PD组血浆基础皮质醇含量均显著高于正常对照组，两组DST阳性率均为20％，正常对照组为14．3％，3组阳性率无显著性差异；汉密尔顿焦虑量表(HAMA)评分与血浆皮质醇浓度呈显著正相关。结论：焦虑症患者存在神经递质和神经内分泌功能的紊乱，但不同亚型间可能存在不同的病理机制，皮质醇浓度可能是焦虑水平的标志因子。     

焦虑障碍的脑电生理学研究进展

焦虑障碍(anxiety disorder,AD)是中国精神科门诊最常见的神经症之一[1],按照中国精神疾病诊断标准 (CCMD-3),可根据其临床表现主要分为广泛性焦虑和惊恐发作两类.但在DSM-Ⅳ中,焦虑障碍则包括广泛性焦虑(generalized anxiety disorder, GAD)、惊恐障碍(panic disorder, PD)、社交焦虑(social anxiety disorder, SAD)、强迫症(obsessive-compulsive disorder, OCD)和创伤后应激障碍(posttraumatic stress disorder, PTSD),其终身患病率3.5%～13.3%.本文结合DSM-Ⅳ诊断标准,以中国临床上常见的4种神经症(广泛性焦虑、惊恐障碍、社交焦虑和强迫症)为例,复习其脑电生理学领域的最新热点.     

重复经颅磁刺激对惊恐障碍及广泛性焦虑障碍治疗机制的研究进展

惊恐障碍和广泛性焦虑障碍（GAD）是焦虑障碍的两种主要类型,两种疾病的发病机制复 杂且常共病。研究表明脑部特定区位异常活化或代谢作用对两者发病有重要影响。目前对于两者的 治疗手段主要为药物治疗和心理干预,以上疗法虽有一定疗效但不够明显。近年来,重复经颅磁刺激 （rTMS）作为新型的神经调控技术,其有效性、安全性等特性显著,被推荐用于焦虑障碍治疗中。rTMS 对 于上述两种疾病的治疗机制复杂且存在差异。现总结并分析关于rTMS 治疗惊恐障碍和GAD 的相关机 制,明确两者之间的异同,为精准地治疗惊恐障碍和GAD 提供相关线索。     

广泛性焦虑障碍患者认知监控网络异常的功能磁共振研究

目的:通过任务态功能磁共振(f MRI)扫描,分析广泛性焦虑障碍(GAD)患者与正常人在不同情绪图片刺激下的脑功能变化,探讨GAD患者认知监控网络(CCN)的功能异常。方法:对20例GAD患者(实验组)和14名健康对照者(健康对照组)在不同的情绪图片刺激下进行f MRI扫描,比较两组被试CCN脑区的差异。结果:以中性情绪为基线对照,在观察高兴情绪图片时,实验组被试左岛盖部额下回(MNI:-51,15,21;t=-5.178;P0.05)、左顶下小叶(MNI:-42,-42,48;t=-4.055;P0.05)、左侧补充运动区(MNI:-9,12,54;t=-4.778;P0.05)激活减弱;在观察恐惧情绪图片时,实验组被试右背外侧额上回(MNI:24,24,51;t=5.375;P0.05)激活增加。结论:CCN的功能异常可能与GAD的发病机制有关。     

广泛焦虑障碍的下丘脑-垂体-肾上腺轴及PRL研究

目的　研究广泛焦虑障碍 (GAD)的下丘脑 垂体 肾上腺轴 (HPA轴 )功能及催乳素 (PRL)改变。方法　研究组分别为 3 0例GAD患者 ,对照组为 2 5例抑郁性神经症 (DN)患者及 1 5例健康人。测基础状态时皮质醇及PRL浓度 ,行地塞米松抑制试验 (DST)后再检测皮质醇浓度。比较GAD与DN及正常对照组 (NC)的差别。结果　 3组基础皮质醇、PRL水平无显著差异。GAD组DST阳性率显著小于DN组而大于正常组。DST阳性率与基础皮质醇呈正相关。 3组PRL浓度均无差异。结论　GAD可能有HPA轴功能异常 ,PRL未见异常     

抑郁症还是双相障碍？

1 病史简介 患者,男,34岁,工人,已婚。因反复烦躁不安、情绪低落发作19年,于2011年5月26日第1次住我院。患者于1992年读初中二年级时与同学打架后,对老师的处理方式不满,渐出现不愿意读书,眠差,情绪不稳定,烦躁,之后出现情绪低落,注意力不易集中,记忆力下降,兴趣减退,自1992年起休学。     

Posttraumatic stress disorder and substance use disorder in adolescent bipolar disorder

Objective: Anxiety disorders such as posttraumatic stress disorder (PTSD) and substance use disorders (SUD) are increasingly recognized as comorbid disorders in children with bipolar disorder (BPD). This study explores the relationship between BPD, PTSD, and SUD in a cohort of BPD and non‐BPD adolescents. Methods: We studied 105 adolescents with BPD and 98 non‐mood‐disordered adolescent controls. Psychiatric assessments were made using the Kiddie Schedule for Affective Disorders and Schizophrenia–Epidemiologic Version (KSADS‐E), or Structured Clinical Interview for DSM‐IV (SCID) if 18 years or older. SUD was assessed by KSADS Substance Use module for subjects under 18 years, or SCID module for SUD if age 18 or older. Results: Nine (8%) BPD subjects endorsed PTSD and nine (8%) BPD subjects endorsed subthreshold PTSD compared to one (1%) control subject endorsing full PTSD and two (2%) controls endorsing subthreshold PTSD. Within BPD subjects endorsing PTSD, seven (39%) met criteria for SUD. Significantly more SUD was reported with full PTSD than with subthreshold PTSD (χ² = 5.58, p = 0.02) or no PTSD (χ² = 6.45, p = 0.01). Within SUD, the order of onset was BPD, PTSD, and SUD in three cases, while in two cases the order was PTSD, BPD, SUD. The remaining two cases experienced coincident onset of BPD and SUD, which then led to trauma, after which they developed PTSD and worsening SUD. Conclusion: An increased rate of PTSD was found in adolescents with BPD. Subjects with both PTSD and BPD developed significantly more subsequent SUD, with BPD, PTSD, then SUD being the most common order of onset. Follow‐up studies need to be conducted to elucidate the course and causal relationship of BPD, PTSD and SUD.     

双相障碍与强迫症的共病

概述

在双相障碍患者中强迫症状是常见的。因为双相障碍和强迫症的共病状态会令这两种障碍的临床治疗复杂化，所以确定这些共病的患者是很重要的。我们讨论了强迫症和双相障碍的共病，介绍了可能导致这种常见共病状态的发病机制，也讨论了该领域最新的研究进展，并提出一些管理这些患者的临床原则。

中文全文

本文全文中文版从2015年10月26日起在http://dx.doi.org/10.11919/j.issn.1002-0829.215009可供免费阅览下载 Previous studies have documented high rates of comorbidity of other psychiatric conditions among individuals with bipolar disorders (BD).[1] One study estimated that obsessive-compulsive disorders (OCD) accounted for 21% of all comorbidities in BD.[2] There is continuing debate about whether (a) these are two independent conditions that can co-occur or (b) OCD is a specific subtype of BD. Regardless of the interrelationship of the two conditions, the comorbid occurrence of these two types of symptoms can cause a clinical dilemma because selective serotonin reuptake inhibitors (SSRIs)-which are quite commonly used to treat OCD-increases the risk of precipitating manic symptoms.[3,4,5,6] The OCD symptoms that occur in individuals with BD often occur during the depressive episodes or during the intervals between episodes of depressive or manic symptoms.[7,8] This timing of OCD symptoms during BD is consistent with the cyclic nature of BD and suggests shared biological mechanisms between the two disorders. In support of this hypothesis, a study using Positron Emission Tomography (PET) found that in untreated persons with BD the serotonin-transporter binding potential in the insular and dorsal cingulate cortex was higher among BD patients with pathological obsessions and compulsions than among BD patients without such symptoms.[9] Moreover, a linkage study found that compared to OCD patients without comorbid BD, patients with comorbid OCD and BD were more likely to have a family history of mood disorders but less likely to have a family history of OCD.[10] However, another study found no significant difference in the rates of a positive family history of OCD between patients with OCD alone and those with comorbid OCD and BD.[11] Further support for the hypothesized common etiology comes from a preliminary molecular genetic study which found that hyperpolarization activated cyclic nucleotide-gated channel 4 (HCN4) is a common susceptible locus for both mood disorders and OCD, but further studies with larger sample sizes are needed to replicate this finding.[12] The presence of OCD in BD complicates the clinical presentation. Compared to patients with BD without comorbid OCD, those that have comorbid BD and OCD often have a more severe form of BD, have more prolonged episodes, are less adherent to medication, and are less responsive to medication. Recent studies about comorbid BD and OCD have reported the following: (a) Temporal relationship. Some studies suggest that OCD is an antecedent of BD,[10] but others report concurrent onset of OCD and BD.[13,14] (b) Course of disease. In 44% of patients with comorbid BD and OCD the episodes are cyclic.[15] The course of disease is more chronic among BD patients with OCD compared to those without comorbid OCD.[16,17] OCD is more commonly observed in patients with Type II BD, among whom the prevalence of OCD has been reported to be as high as 75%.[18] (c) Compulsive behaviors. The most commonly reported compulsions among patients with comorbid OCD and BD are compulsive sorting,[14,19,20,21] controlling or checking, [20] repeating behaviors,[13,22] excessive washing,[20] and counting.[19] Obsessive reassurance-seeking is also commonly reported in these patients.[23] In children and adolescents with BD, compulsive hoarding, impulsiveness,[24] and sorting[25] are more common. (d) Substance and alcohol abuse. A study found a higher prevalence of sedative, nicotine, alcohol, and caffeine use among individuals with comorbid OCD and BD compared to those with BD without OCD.[14] Similarly, compared to OCD patients without comorbid mood disorders, those with a comorbid mood disorder were more likely to have a substance abuse diagnosis (OR=3.18, 95%CI=1.81-5.58) or alcohol abuse diagnosis (OR=2.21, 95%CI=1.34-3.65).[11,13,26,27,28] (e) Suicidal behaviors. Compared to BD patients without OCD, a greater proportion of patients with both disorders had a lifetime history of suicidal ideation and suicide attempts.[2,11,13,29,30] The clinical management of comorbid OCD and BD requires first focusing on stabilizing the patient’s mood, which requires the combined use of multiple medications such as the use of lithium with anticonvulsants or atypical antipsychotic medications such as quetiapine;[31,32,33] adjunctive treatment with aripiprazole may be effective for the comorbid OCD symptoms.[4] In the case of OCD comorbid with type II BD, after full treatment of the mood symptoms with mood stabilizers the clinician can, while monitoring for potential drug interactions, cautiously try adjunctive treatment with antidepressants that are effective for both depressive symptoms and OCD symptoms and that have a low risk of inducing a full manic episode, including the selective serotonin reuptake inhibitors (SSRIs): fluoxetine, fluvoxamine, paroxetine, and sertraline.[32,35] In summary, BD comorbid with OCD may be etiologically distinct from either of the disorders. Clinicians should pay attention to its complex clinical manifestations and carefully consider the treatment principles outlined above.     

Substance use disorder and personality disorder

Personality disorders (PDs) and substance use disorders (SUDs) frequently co-occur in both the general population and in clinical settings. Literature is reviewed documenting high comorbidity between these two classes of disorders, possible mechanisms of comorbidity, and the clinical implications of this comorbidity. Special emphasis is given to antisocial personality disorder (ASPD) and borderline personality disorder (BPD) as these disorders not only co-occur frequently with SUDs in the clinical populations and present clinical challenges, but also because recent research points to etiologic processes that are common to these specific PDs and SUDs. Although most attention on comorbidity between PDs and SUDs has focused on ASPD and BPD, it is also clear that other PDs (in particular, avoidant PD and paranoid PD) are prevalent among those suffering from SUDs.     

Thought disorder in attention-deficit hyperactivity disorder

OBJECTIVE: This study compared thought disorder and associated cognitive variables in attention-deficit hyperactivity disorder (ADHD) and schizophrenia. METHOD: Speech samples of 115 ADHD, 88 schizophrenic, and 190 normal children, aged 8 to 15 years, were coded for thought disorder. A structured psychiatric interview, the WISC-R, the Continuous Performance Test, and the Span of Apprehension task were administered to each child. RESULTS: The ADHD and schizophrenic groups had thought disorder compared with the normal children. However, the subjects with ADHD had a narrower range of less severe thought disorder than did the schizophrenic subjects. The younger children with ADHD and schizophrenia had significantly more thought disorder than did the older children with these diagnoses. IQ, attention, and working memory were associated with thought disorder in the ADHD but not the schizophrenic group. CONCLUSIONS: Thought disorder in childhood is not specific to schizophrenia and reflects impaired development of children's communication skills.