伴轻度抑郁症状的双相障碍患者执行和注意功能对照研究

目的:探讨伴轻度抑郁症状的双相障碍患者执行功能、注意功能与健康对照者的差异。方法:40例伴轻度抑郁症状的双相障碍患者(研究组)和40名年龄、性别、受教育年限与研究组匹配的健康者(健康对照组)均采用威斯康星卡片分类测验(WCST)及持续操作测验(CPT)测试两组执行功能和注意功能。结果:两组WCST测试成绩除完成第1个分类所需应答数、非持续性错误数差异无统计学意义(P0.05)外,完成分类数、总应答数、正确应答数、错误应答数、持续性错误数、持续性错误率组间差异有统计学意义(t=-6.10~5.96,P均=0.000);CPT测验中正确数研究组明显低于健康对照组(t=-3.87,P=0.000);错误数明显高于健康对照组(t=5.21,P=0.000)。结论:伴轻度抑郁症状的双相障碍患者存在执行功能损害和注意功能损害。     

注意缺陷多动障碍儿童反应抑制功能的磁共振成像研究

目的 探讨注意缺陷多动障碍(ADHD)儿童执行高级反应抑制脑激活的模式和功能状态.方法 对12例注意缺陷多动障碍儿童(ADHD组)和12名正常对照者(对照组)检测执行持续性操作测试任务(CPT)时的功能磁共振成像(fMRT)和行为学,并采集全脑血氧水平依赖对比的fMRI扫描数据.结果 (1)行为学检测,ADHD组的击中数[(18.6±4.1)个]少于对照组[(22.8±1.8)个],反应时间[(579±56)ms]长于正常对照组[(510±35)ms;均P＜0.01],漏击数[(6.3±4.1)个]和错击数[(3.9±2.4)个]均多于对照组[(2.2±1.9)个和(1.9±1.0)个;P＜0.01～0.05].(2)fMRI检测,ADHD组扣带前回、前额叶腹外侧、尾状核和小脑激活弱于对照组(P＜0.05,未校正,体素值＞20).结论 ADHD儿童反应抑制功能存在缺陷,其扣带前回、前额叶、基底节及小脑的功能低下.     

小脑损伤患者28例注意网络功能受损的特点

目的 研究小脑损伤患者注意网络功能受损的特点.方法 应用注意网络测验,对28例小脑损伤患者和31名健康对照进行注意网络功能的测试.结果 与对照组相比,小脑损伤患者定向效率减低[病例组、对照组分别为(36.32±30.58)、(54.39±22.17)ms],差异有统计学意义(Z=-2.309,P＜0.05);执行控制受到损害[(160.05±83.25)、(93.42±37.41)ms],差异有统计学意义(Z=-3.500,P＜0.01);警觉效率[(35.14±45.59)、(28.81±26.09)ms]与总平均反应时[(797.14±94.11)、(739.90±97.90)ms]的差异无统计学意义.病例组的总平均错误率(6.57%±9.84%)明显高于对照组(3.38%±5.42%,Z=-2.119,P＜0.05).结论 小脑参与了注意网络的认知功能;小脑病变可选择性损害注意网络的定向和执行控制功能,而警觉功能相对保持正常.     

认知行为疗法合并艾司西酞普兰治疗惊恐障碍的对照研究

目的比较认知行为治疗合并艾司西酞普兰与单用药物治疗惊恐障碍的临床效果、安全性、依从性及复发率的情况。方法将2012年1月-2013年6月湖北省孝感市康复医院60例符合《国际疾病分类(第10版)》(ICD-10)惊恐障碍诊断标准的患者采用随机数字表法分为研究组和对照组各30例。研究组采用认知行为治疗合并艾司西酞普兰治疗,对照组单用艾司西酞普兰治疗。在治疗前及治疗2、4、6周进行汉密尔顿焦虑量表(HAMA)、临床总体印象量表-病情严重程度量表(CGI-SI)及副反应量表(TESS)评分,随访1年。结果研究组显效率为75.9%,对照组显效率为51.7%,差异有统计学意义(χ2=4.51,P0.05)。治疗后2、4、6周,研究组患者HAMA评分低于对照组,差异有统计学意义[(20.9±6.2)vs.(23.4±3.5)、(15.1±5.1)vs.(19.3±7.8)、(8.5±3.1)vs.(14.6±3.5)(P均0.05)]。CGI-SI评分低于对照组,差异有统计学意义[(3.21±0.56)vs.(3.65±0.82)、(2.32±0.64)vs.(2.85±0.35)、(1.51±0.52)vs.(2.28±0.31)(P均0.05)]。两组TESS评分各期差异均无统计学意义(P均0.05)。第6个月、12个月随访依从性比较,研究组均高于对照组(89.7%vs.72.4%,75.9%vs.62.1%),研究组复发率低于对照组[(20.7%)vs.(41.4%)]。结论认知行为治疗合并艾司西酞普兰治疗惊恐障碍可能有助于改善惊恐障碍,提高远期服药依从性,减少复发率,提高患者社会功能。     

惊恐障碍与心绞痛患者血清一氧化氮水平对照研究

目的:探讨惊恐障碍与心绞痛之间的关系.方法:检测并比较17例惊恐障碍(惊恐障碍组)与27例心绞痛(心绞痛组)及39名健康者(对照组)血清一氧化氮(NO)和一氧化氮合酶(NOS).结果:两患者组血清NO水平均显著低于对照组,惊恐障碍组与心绞痛组比较血清NO水平无显著差异;惊恐障碍组血清NOS水平与对照组比较无显著差异,心绞痛组血清NOS水平显著低于对照组,两患者组血清NOS水平无显著差异.结论:惊恐障碍与心绞痛症状相似可能与NO的下降有关.惊恐障碍成为心绞痛的危险因素由NO下降得到解释.     

艾司西酞普兰与氯丙咪嗪治疗惊恐障碍的临床对照研究

目的比较艾司西酞普兰和氯丙咪嗪治疗惊恐障碍的临床疗效和安全性。方法采用随机数字表将68例惊恐障碍患者分为艾司西酞普兰组(n=34)和氯丙咪嗪组(n=34),分别给予艾司西酞普兰和氯丙咪嗪治疗,疗程均为10周,分别于治疗前及治疗后1、2、4、6、8、10周末采用惊恐相关症状量表(PASS)、汉密尔顿焦虑量表(HAMA)及副反应量表(TESS)分别评定疗效及安全性。结果治疗后,两组PASS和HAMA评分均较治疗前下降,差异有统计学意义(P均0.01)。艾司西酞普兰组和氯丙咪嗪组有效率分别为87.5%和81.3%,差异无统计学意义(P0.05)。艾司西酞普兰组和氯丙咪嗪组TESS评分[(2.78±1.03)vs.(4.07±2.89)],差异有统计学意义(P0.05)。结论艾司西酞普兰治疗惊恐障碍疗效与氯丙咪嗪相当,但艾司西酞普兰组不良反应少,安全性好。     

双相情感障碍血清尿酸水平研究

目的探讨双相情感障碍患者血清尿酸(uric acid,UA)水平变化及其临床意义。方法纳入双相情感障碍患者126例(躁狂发作77例,抑郁发作49例)、首发精神分裂症患者69例和正常对照126名,测定其血清UA水平,并采用杨氏躁狂量表(Young mania rating scale,YMRS)和汉密尔顿抑郁量表(Hamilton depressionscale,HAMD)评定双相情感障碍患者症状。结果双相情感障碍组血清UA水平[(349.34±107.21)μmol/L]高于精神分裂症组[(319.71±84.48)μmol/L]和对照组[(280.94±71.90)μmol/L],差异有统计学意义(P0.01);躁狂发作患者UA水平高于抑郁发作患者[(366.45±104.01)μmol/L vs.(322.45±107.69)μmol/L],且二者均高于对照组(P0.01);双相情感障碍患者中是否使用精神科药物的亚组间UA水平无统计学差异(P0.05)。双相情感障碍患者血清UA水平与YMRS、HAMD分数线性相关均无统计学意义(P0.05)。结论双相情感障碍患者血清UA水平升高,血清UA水平升高可能是双相情感障碍的一个生物标记物。     

注意缺陷多动障碍患儿事件相关电位N400研究

目的:探讨注意缺陷多动障碍(ADHD)患儿汉语句子结尾词匹配和非匹配语言时相关电位(ERP)N400的变化。方法:应用ERP仪,采用汉语正常句子结尾词匹配与非匹配的范式,对35例ADHD患儿(ADHD组)和41名正常儿童(正常对照组)进行视觉诱发电位N400检测。结果:在Cz脑区匹配及非匹配条件下,ADHD组N400潜伏期[(384±45)ms,(436±35)ms]比正常对照组[(348±32)ms,(399±29)ms]显著延迟(P均0.01);波幅ADHD组[(4.2±4.5)μV,(7.5±5.1)μV]显著低于正常对照组[(7.6±5.0)μV,(12.4±6.5)μV](P均0.01)。结论:ADHD患儿N400异常,N400检测可能成为判断注意缺陷多动障碍的客观指标。     

西酞普兰治疗惊恐障碍对照研究

目的探讨西酞普兰对惊恐障碍患者的疗效及副作用。方法对46例惊恐障碍患者随机分成西酞普兰治疗组、帕罗西汀对照组,并用HAMA、GAS、SERS对患者治疗前后进行评估。结果除了在治疗第1周末,西酞普兰治疗组的HAMA分值高于对照组外,在第2、4、6周末,两组患者的HAMA、GAS分值差异均无显著性意义。西酞普兰组患者在治疗6周末,治愈率及有效率分别为63.2%、84.2%,而帕罗西汀组分别为68.2%、90.9%,与帕罗西汀组相比差异无显著性意义。西酞普兰组平均剂量(41.87±15.36)mg/d;帕罗西汀组平均剂量(40.91±14.44)mg/d。在副作用方面,两组患者差异也无统计学意义。结论西酞普兰治疗惊恐障碍患者疗效及副作用与帕罗西汀相当。     

惊恐障碍在综合性医院识别现状和艾司西酞普兰治疗效果

目的:探讨目前综合性医院临床各科室对惊恐障碍识别的临床分析和艾司西酞普兰在综合医院治疗惊恐障碍的有效性和安全性。方法:以胸闷、心慌、濒死感等不适主诉至我院就诊排除躯体疾病后转诊至医学心理科就诊268例患者,分析其中确诊为惊恐障碍的179例患者在临床各科室的首诊诊断构成,以及对其中168例惊恐障碍患者随机分为艾司西酞普兰组和帕罗西汀组,疗程8周,并用惊恐相关症状量表(PASS)、汉密尔顿焦虑量表(HAMA)、不良反应评定量表(SERS)对患者治疗前后进行评估。结果:确诊为惊恐障碍的179例患者在临床各科室的首诊诊断包括惊恐障碍、广泛性焦虑、抑郁症、心脏神经官能症、癔症、其他疾病等,首诊时诊断为惊恐障碍的患者仅占9.5%。患者在治疗1周、治疗2周艾司西酞普兰组的HAMA、PASS分值均低于对照组,而在治疗4、6、8周,两组患者的HA-MA、PASS分值差异无统计学意义(P>0.05)。在治疗8周时,艾司西酞普兰组治愈率为65.4%,有效率为91.4%,帕罗西汀组分别为63.7%,91.3%。两组差异无统计学意义。在不良反应方面,两组差异无统计学意义。结论:综合医院临床各科室对惊恐障碍患者首诊时的识别率较低。艾司西酞普兰治疗惊恐障碍疗效肯定,安全性较高。     

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.     

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.     

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.