抑郁与焦虑共病障碍临床研究

目的:调查抑郁与焦虑共病障碍的发生率,探讨其特点及预后.方法:对150例抑郁障碍患者用汉密尔顿抑郁量表(HAMD)、汉密尔顿焦虑量表(HAMA)、社会功能缺陷筛选量表(SDSS)和临床疗效总评量表(CGI)评定,3个月后进行随访.结果:45.3%的抑郁障碍患者共病焦虑障碍,共病以广泛焦虑障碍与惊恐障碍为最多(分别为22.0%、13.3%);入组时及3个月末,共病组HAMD、HAMA、CGI及SDSS总分均显著高于抑郁组(P＜0.05),3个月末共病组HAMA减分率显著低于抑郁组(P＜0.05),HAMD减分率两组差异无显著性.结论:抑郁与焦虑共病障碍发生率高,具有抑郁及焦虑症状重、社会功能损害重,焦虑症状不易缓解等特征.     

小学生焦虑抑郁障碍共病调查

目的：探讨小学生焦虑抑郁障碍共病情况。方法：用儿童焦虑障碍筛查量表（SCRED）对县城2900名及农村1800名8～14岁小学生进行筛查,对筛查出的焦虑障碍儿童进行抑郁障碍诊断,对焦虑与抑郁障碍共病儿童实施相关量表及问卷测量。结果：儿童焦虑抑郁障碍共病率为12.7%,其中县城12.9%,农村12.3%,两地差异无统计学意义（χ2=0.011,P=0.915）。焦虑抑郁障碍共病儿童与仅有焦虑障碍儿童在焦虑量表及家庭功能评定量表上得分差异均无显著性（P均〉0.05）,抑郁量表分与焦虑量表的躯体焦虑、广泛焦虑及焦虑总分呈显著相关（P〈0.001）。结论：小学生焦虑与抑郁障碍共病率较高。     

单相与双相抑郁障碍患者临床特征的对照研究

目的比较单相与双相抑郁障碍患者的临床特征,为单相和双相抑郁障碍的鉴别诊断提供参考。方法连续入组2012年6月-2013年11月在广州医科大学附属脑科医院住院、符合《国际疾病分类(第10版)》(ICD-10)诊断标准的单相抑郁障碍(单相组,n=72)和双相抑郁障碍(双相组,n=64)患者,收集并分析两组一般人口学资料和临床特征,采用汉密尔顿抑郁量表17项版(HAMD-17)评定抑郁症状。结果单相组女性及已婚患者比例均高于双相组(χ2=18.74、4.68,P0.05或0.01);双相组平均起病年龄小于单相组(t=-2.13,P=0.035);双相组性格外向者比例高于单相组(χ2=9.74,P=0.002);单相组有病前诱因者比例高于双相组(χ2=18.96,P0.01);双相组伴不典型抑郁症状者比例高于单相组(χ2=24.60,P0.01);双相组既往抑郁发作次数多于单相组(Z=-5.37,P0.01);单相组HAMD-17总评分及躯体化焦虑和食欲减退因子评分均高于双相组,差异均有统计学意义(t=-2.78~-2.06,P0.05或0.01)。结论单相与双相抑郁障碍患者在性别、婚姻状况、发病年龄、是否有病前诱因、是否伴不典型抑郁症状、既往发作次数及HAMD-17评分方面存在差异。     

综合医院与精神专科医院双相障碍识别率及相关因素分析

目的:比较综合医院和精神专科医院抑郁障碍门诊中未识别出的双相障碍患者的临床特征及相关影响因素。方法:使用一般情况调查表和简明国际神经精神访谈(MINI)对综合医院和精神专科医院抑郁障碍门诊患者各50例进行调查,检出其中未被识别出的双相障碍患者,对其临床特征进行初步分析。结果:双相障碍的总检出率综合医院和精神专科医院之间差异无统计学意义(χ2=2.38,P=0.123);但在41~50岁年龄段精神专科医院的检出率高于综合医院(Z=2.11,P=0.035)。精神专科医院双相障碍的检出率与年龄(r=-0.46,P=0.001)和首发年龄(r=-0.37,P=0.008)的相关性具有统计学意义。综合医院和精神专科医院未识别出的双相障碍患者在年龄(t=2.43,P=0.020)和首发年龄(t=3.67,P=0.001)上的差异具有统计学意义。精神专科医院中未识别出的双相障碍更多的伴有精神病性症状(χ2=3.99,P=0.046)。综合医院中未识别出的轻躁狂症状"目前发作"比率更高(χ2=8.15,P=0.017)。结论:综合医院和精神专科医院抑郁障碍门诊患者中双相障碍的漏诊和误诊因素不同。     

汶川地震所致创伤后应激障碍患者的共病分析

目的:了解汶川地震部分极重灾区所致创伤后应激障碍(PTSD)患者共病其他精神障碍的情况,以及影响共病的因素。方法:采用方便取样,对四川省绵阳市所辖的安县、平武县及北川县部分受灾群众进行调查,以DSM-Ⅳ-TR轴Ⅰ障碍定式临床检查(SCID-I/P)为诊断工具。结果:共138例诊断PTSD,其中90例共病其他精神障碍,共病率65.2%;42.8%患者共病重性抑郁障碍,12.3%共病特殊恐怖症,10.9%共病惊恐发作;40～59岁共病率最高为70.4%(χ2=5.94,P=0.05),有亲人死亡者共病抑郁症35例,明显高于无亲人死亡者24例,两者差异有统计学意义(χ2=4.16;P=0.04)。结论:65.2%PTSD患者共病其他精神障碍,以共病重性抑郁障碍、特殊恐怖症、惊恐发作最多见,共病率与年龄相关,地震中有亲人死亡将增加PTSD共病抑郁症风险。     

首发精神分裂症与双相障碍及抑郁障碍认知功能比较

目的探讨首发精神分裂症、双相障碍及抑郁障碍患者认知功能差异。方法纳入首发精神分裂症患者61例,双相障碍患者57例,抑郁障碍患者48例,另设正常对照59名。所有研究对象采用重复性神经心理测查系统(Repeatable Battery for the Assessment of Neuropsychological Status,RBANS)评估认知功能,首发精神分裂症组采用阳性和阴性症状量表(positive and negative syndrome scale,PANSS)评定精神病性症状,双相障碍组、抑郁障碍组采用汉密尔顿抑郁量表(Hamilton depression scale,HAMD)、汉密尔顿焦虑量表(Hamilton anxiety scale,HAMA)评估抑郁和焦虑症状,贝克—拉范森躁狂(Bech-Rafaelsen mania scale,BRMS)量表评估躁狂症状。结果 4组对象的RBANS总分(F=5.18,P0.01)、即刻记忆(F=4.09,P0.01)、言语功能(F=9.53,P0.01)、注意(F=3.87,P=0.01)、延时记忆(F=9.86,P0.01)因子得分差异具有统计学意义,其中首发精神分裂症、双相障碍组RBANS总分低于对照组(P0.01),首发精神分裂症、双相障碍、抑郁障碍组即刻记忆、言语功能、延时记忆得分低于对照组(P0.05),双相障碍组言语功能得分低于首发精神分裂症组(P0.01),首发精神分裂症组注意得分低于抑郁障碍及对照组(P0.01)。结论首发精神分裂症、双相障碍、抑郁障碍患者均存在认知功能损伤,首发精神分裂症认知功能缺陷重于抑郁障碍,轻于双相障碍。     

抑郁障碍患者非自杀性自伤行为及其风险因素分析

目的:探讨抑郁障碍患者非自杀性自伤(NSSI)行为及其风险因素。方法:采用自编的一般情况调查表收集153例抑郁障碍患者一般资料(性别、年龄、受教育年限、病程等);应用NSSI行为问卷对入组者进行评估并将其分为伴与不伴NSSI两组,应用简明国际神经精神访谈中文版(MINI)评估患者是否共病焦虑障碍;分析NSSI行为的风险因素。结果:59例(38. 6%)患者有NSSI行为,归为伴NSSI组;不伴NSSI组(94例)。伴NSSI组女性患者的比率及共病焦虑障碍的比率明显高于不伴NSSI组(P均0. 01),年龄明显低于不伴NSSI组(P 0. 05)。伴NSSI组中,女性患者NSSI行为方式依次为割伤、阻止伤口愈合、刺伤,男性患者依次为割伤、灼烧伤、过度摩擦皮肤;性别间NSSI行为分布比较差异有统计学意义(P 0. 05);共病焦虑障碍患者NSSI方式及频率与非共病焦虑障碍者比较差异具有统计学意义(P均0. 05)。二分类Logistic回归分析显示共病焦虑障碍是抑郁障碍患者NSSI危险因素。结论:抑郁障碍患者中NSSI行为发生率较高,尤其是女性患者;共病焦虑障碍抑郁障碍患者更容易发生NSSI。     

抗抑郁剂联合心境稳定剂治疗双相障碍患者:1年随访

目的:观察抗抑郁剂联合心境稳定剂治疗双相障碍1年的结局,并评价不同疗效对双相抑郁结局的影响。方法:选择符合ICD-10双相障碍诊断标准患者,急性期进行8周抗抑郁剂和心境稳定剂联合治疗,痊愈和有效者进入1年维持治疗期。用24项汉密顿抑郁量表(HAMD)、Bech-Rafaelsen躁狂量表(BRMS)和临床疗效总评量表(CGI)评定疾病严重程度和疗效。结果:76例患者急性期治疗痊愈者53例,有效者23例。随访1年后,共43例(56.57%)维持痊愈,17例症状复发,总复发率22.36%。痊愈组36例(67.92%)仍保持痊愈,有效组7例(30.43%)达痊愈,两组差异有显著性(χ2=9.176,P=0.002)。痊愈组抑郁复发率低于有效组(3.77%vs.17.39%,χ2=4.091,P=0.045),两组转躁率差异无统计学意义(11.32%vs.21.74%;χ2=1.406,P=0.236)。生存分析显示痊愈组平均复发时间显著长于有效组[(10.06±2.14)个月vs.(9.00±3.67)个月;u=9.327,P=0.002]。结论:抗抑郁剂联合心境稳定剂治疗双相障碍抑郁发作患者1年后复发率低,急性期治疗痊愈者优于非痊愈者。     

酒依赖共病双相情感障碍患者冲动攻击行为与5-HTR1B基因多态性关联分析

目的探讨酒依赖共病双相情感障碍患者的冲动攻击行为与5-HTR1B rs6296基因多态性的关联,为酒依赖共病双相情感障碍患者冲动攻击行为导致病理生理改变机制的潜在遗传学差异的研究提供参考。方法采用病例对照研究,纳入符合《精神障碍诊断与统计手册(第4版)》(DSM-IV)酒依赖共病双相情感障碍诊断标准的患者230例,依据修订版外显攻击行为量表(MOAS)评分分为有冲动攻击行为组(n=128)和无冲动攻击性行为组(n=102)。通过PCR直接测序法对rs6296基因多态性进行测定,并分析5-HTR1B rs6296基因多态性与酒依赖共病双相情感障碍患者冲动攻击行为的关联性。结果酒依赖共病双相情感障碍患者有冲动攻击行为组与无冲动攻击行为组rs6296位点的等位基因频率分布差异无统计学意义(χ~2=2.135,P0.05);两组rs6296位点基因型分布差异无统计学意义(χ~2=2.771,P0.05)。结论酒依赖共病双相情感障碍患者冲动攻击行为与5-HTR1B rs6296基因多态性无关联。     

单双相抑郁障碍患者应对方式的比较

目的 比较双相抑郁障碍与复发性抑郁障碍患者的应对方式,并评估应对方式与两种疾病的关联.方法 采用横断面的病例对照设计,共入组双相抑郁障碍患者144例,复发性抑郁障碍患者189例,健康对照123例,应用特质应对方式问卷(TCSQ)评估被试的应对方式.结果 与对照组比较,两患者组消极应对方式得分较高,积极应对方式得分较低,差异均有统计学意义(P<0.01);与复发抑郁障碍患者相比,双相抑郁障碍组积极应对方式较高(P<0.01).同种疾病中,非缓解期的患者较缓解期患者消极应对方式得分更高,积极应对方式得分更低.Logistic回归分析结果显示,在控制了年龄和疾病状态的影响后,积极应对方式仍是患双相障碍的危险因素(OR=1.064,95%CI=1.026~1.102),该模型对双相障碍的预测准确率为64.3%.结论 与复发抑郁障碍患者相比,双相抑郁障碍患者多采用较为积极的应对方式;采用较为积极的应对方式的抑郁障碍患者,发展成双相障碍的可能性较大.     

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。     

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.     

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.     

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.     

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.