儿童注意缺陷与多动障碍的病因与发病机理

儿童注意缺陷与多动障碍(attention deficit and hyperactive disorder, ADHD)主要临床特征是:明显的注意定向障碍和注意持续时间短暂,活动过度,行为冲动,并伴有学习困难和30%～58%有品行障碍[1].ADHD发病率较高,国内报道为1.5%～10%,国外报道为3%～5%,男多于女为9:4.1[1].     

青少年行为问题与遗传、环境因素关系的双生子研究

目的:探讨青少年行为问题与遗传、环境因素的相关性。方法:选择重庆市12~18岁66对青少年双生子,采用Achenbach青少年自评量表(Youth Self-Report,YSR)测查行为问题,采集双生子静脉血标本,提取DNA进行卵型鉴定。根据同卵双生子间表型相关系数(rMZ)和异卵双生子间表型相关系数(rDZ)的比较,进行遗传效应的粗约估计,构建结构方程模型(SEM),定量分析加性遗传因素(A)、共享环境因素(C)、特殊环境因素(E)与青少年行为问题的关系。结果:社交问题及违纪行为rMZrDZ,提示数据不适合进行遗传分析;其余各因子rMZ、rDZ比较:退缩行为、躯体主诉、焦虑/抑郁情绪、攻击行为、思维问题、注意问题因子rMZ2rDZ,均拟合ACE模型。其最优模型均为AE模型。在遗传效应(A)及个体特异性环境(E)总变异方差中,焦虑/抑郁情绪、攻击行为因子遗传效应在0.52~0.57之间,个体特异性环境在0.43~0.48之间;退缩行为、躯体主诉、思维问题及注意问题遗传效应在0.17~0.45之间,个体特异性环境在0.55~0.83之间。结论:青少年社交问题及违纪行为与遗传效应关系不明显;退缩行为、躯体主诉、焦虑/抑郁情绪、思维问题、注意问题、攻击行为与加性遗传因素及个体特异性环境因素均有相关性;焦虑/抑郁、攻击行为与遗传因素相关程度大,其余因子均与个体特异性环境因素相关度大。     

10—16岁儿童少年行为问题的双生子研究

目的:调查遗传因素和环境因素对10-16岁儿童少年行为问题的影响程度,为儿童少年行为问题的防治提供依据.方法:采用多级随机抽样的方法选取64对双生子,使用Achenbach儿童行为量表评定行为问题,估算遗传因素及环境因素对儿童少年行为问题的影响程度.结果:10-16岁儿童少年总的行为问题的遗传度为0.33,共享环境的影响程度为0.57,非共享环境的影响程度为0.10.其中退缩行为、躯体主诉、注意缺陷及违纪行为的遗传度超过0.6,共享环境对焦虑/抑郁、社交问题及攻击行为的影响程度在0.41～0.64之间.结论:遗传因素和环境因素对儿童少年的行为问题均有影响,但环境因素影响程度更大,尤其是共享环境因素.     

注意缺陷多动障碍诊断量表父母版构想效度的验证性因素分析

目的：考察注意缺陷多动障碍诊断量表父母版的构想效度。方法：根据DSM-IV和ICD-10建立理论模型，用结构方程模型对1616名中国城市儿童的注意缺陷多动障碍诊断量表父母版测试结果做验证性因素分析。结果：二因素模型和三因素模型均是可以接受的模型，三因素模型拟合优于二因素模型，项目的第12条归属于冲动因子比归属于多动因子更符合数学模型。结论：注意缺陷多动障碍诊断量表父母版具有较好的结构效度。     

中文版注意缺陷多动障碍SNAP-Ⅳ评定量表-父母版的信效度

目的:引进中文版注意缺陷多动障碍SNAP-Ⅳ评定量表-父母版(Chinese version of Swanson Nolan and Pelham,VersionⅣScale-parent form,SNAP-Ⅳ)并检验其信效度.方法:对31名符合美国精神障碍诊断与统计手册第4版诊断标准的注意缺陷多动障碍(ADHD)门诊患儿和231名正常儿童进行中文版注意缺陷多动障碍SNAP-Ⅳ评定量表父母版、中文版Conners父母用症状问卷(PSQ)及中文版Achenbach儿童行为量表(CBCL)评估,以检验校标效度.对27名受试者(ADHD组3人,正常组24人)1周内再次进行中文版注意缺陷多动障碍SNAP-Ⅳ评定量表父母版评估,以检验重测信度.结果:中文版注意缺陷多动障碍SNAP-Ⅳ评定量表父母版全量表内部一致性信度Cronbachα系数为0.95,注意力不集中、多动冲动、对立违抗3个分量表Cronbach α系数分别为0.90、0.89、0.88.重测信度组内相关系数(ICC)为0.68,3个分量表的重测信度ICC分别为0.75、0.76、0.24.中文版注意缺陷多动障碍SNAP-Ⅳ评定量表父母版与PSQ及CBCL对应各因子得分之间相关系数分别介于0.29～0.73、0.30～0.74,验证性因子分析显示中文版注意缺陷多动障碍SNAP-Ⅳ评定量表父母版的3因子及4因子模型均合理.中文版注意缺陷多动障碍SNAP-Ⅳ评定量表父母版诊断ADHD敏感度为0.87,特异度为0.79.结论:中文版注意缺陷多动障碍SNAP-Ⅳ评定量表父母版具有良好的信度与效度.     

伴有品行问题注意缺陷多动障碍儿童家庭环境与家长压力的关系

目的:探讨伴有品行问题的注意缺陷多动障碍(ADHD)儿童的家庭环境与父母压力的关系。方法:根据DSM-5诊断标准纳入175例ADHD儿童,采用Conners儿童行为问卷评估品行问题,根据Conners行为量表品行因子是否超过该年龄组正常范围定义为ADHD伴品行问题(n=124)或不伴品行问题(n=51)。采用家庭环境量表中文版(FES-CV)、家长压力问卷(PSQ)评估家庭环境及家长压力。结果:ADHD伴品行问题儿童的家庭环境量表中文版中的亲密度、情感表达、娱乐性、组织性、知识性得分低于ADHD不伴品行问题儿童(P 0. 05)。Logistic回归分析显示FES-CV的娱乐性得分与ADHD儿童发生品行问题呈负向关联(OR=0. 89,95%CI:0. 80～1. 00)。ADHD伴品行问题儿童的父母PSQ得分高于ADHD不伴品行问题儿童的父母[(77. 6±23. 5) vs.(56. 6±13. 5),P 0. 05]。结论:伴有品行问题的注意缺陷多动障碍儿童的家庭环境常存在功能缺陷,家庭环境中的娱乐性可能是注意缺陷多动障碍儿童发生品行问题的保护因素,伴有品行问题的注意缺陷多动障碍儿童父母常可能有更大客观压力。     

儿童注意缺陷多动障碍反应抑制、厌恶延迟和时间感觉的研究进展

儿童注意缺陷多动障碍(attention deficit hyperactivity disorder，ADHD)是儿童期常见精神障碍，在学龄期儿童中患病率约为3．0～7．5％，有统计显示在儿童青少年中患病率达17％。多在3～7岁起病。主要表现为注意缺陷、多动／冲动，大部分儿童伴随焦虑障碍、学习困难、品行障碍、违法犯罪行为以及反社会人格等。一般病情常常持续到青春期，部分病例一直持续到成年．给个人、家庭和社会造成负担。     

注意缺陷多动障碍患儿的脑电图与临床特点

目的:分析注意缺陷多动障碍(attention deficit hyperactivity disorder,ADHD)患儿脑电图改变,探讨注意缺陷多动障碍患儿临床与脑电图改变的关系。方法:将在本院儿童神经专科确诊的116例注意缺陷多动障碍患儿的脑电与临床特点进行分析总结。结果:116例ADHD脑电图中正常24例(20%),正常范围29例(25%),异常63例(54.3%)异常脑电图均表现为枕区α波的频率慢于该年龄组正常标准2Hz以上。基本波不规则,间有大量多形性θ波或中高幅θ活动阵发性出现。结论:注意缺陷多动障碍(ADHD)患儿脑电图检查显示脑电的非特异性改变。可为临床诊断和鉴别诊断提供一定的辅助诊断参考价值。     

注意缺陷多动障碍与青少年犯罪(综述)

注意缺陷多动障碍(Attention Deficit Hyperactivity Disorder,ADHD )是儿童期常见的早期发生的认知行为发展性的精神障碍,其主要特征为与年龄不相称的注意力不集中、多动和冲动行为.学龄期儿童患病率为4 % ～12 %,男女比例为(3～9)∶ 1,其中50 %～80 %可持续至青年,30%～50%持续到成年.美国精神疾病诊断和统计手册第四版(Diagnostic and Statistical Manual of Mental Disorders,Fourth Edition,DSM-IV)将其分为注意缺陷、多动-冲动和混合型三种亚型[1].     

山东滨州市6～16岁少儿注意缺陷多动障碍现况调查

目的:比较少年(12～16岁)与学龄儿童(6～11岁)注意缺陷多动障碍(attention deficit hyperactivity disorder,ADHD)患病情况及临床特点,为儿童ADHD的全面干预提供依据.方法:用分层整群抽样的方式,以学校为单位从鲁北4县市抽取4263名6～16岁儿童,采用问卷调查和专科访谈相结合的方法,按DSM-Ⅳ的ADHD诊断标准进行诊断,根据症状维度分布进一步区分为3种亚型:注意缺陷型(ADHD-I)、多动冲动型(ADHD-HI)和混合型(ADHD-C).结果:(1)6～16岁少儿ADHD的总患病率为6.4%,ADHD-I型是主要类型,占63.7%;男童患病率高于女童(8.9%vs 4.1%,P＜0.001);少年患病率低于学龄儿童(5.3% vs.7.7%, P=0.002).(2)不同年龄少儿ADHD亚型分布有差别,与学龄儿童组相比,少年组ADHD-HI和ADHD-C明显减少(9.5% vs.18.4%,9.5% vs.32.7%),ADHD-I明显增多(81.0% vs.49.0%)(P＜0.001);少年ADHD患者的3项注意缺陷症状因子和6项多动-冲动症状因子患病率降低(P＜0.001或0.01或0.05).结论:注意力缺陷是少儿注意缺陷多动障碍的核心症状;注意缺陷多动障碍在较高年龄组的少年中患病率有降低趋势,多动-冲动症状改善更明显.     

Common genetic liability to major depression and posttraumatic stress disorder in men

BACKGROUND: Major depression (MD) and posttraumatic stress disorder (PTSD) are highly comorbid. The degree to which a common genetic liability explains the etiology of the MD-PTSD association has not been quantified and has important implications for research and prevention. METHODS: This paper presents an analysis of data from 6744 members of the Vietnam Era Twin Registry. MD and PTSD were assessed using the Diagnostic Interview Schedule-III-R in 1991-92. Bivariate twin modeling was conducted to determine the genetic and environmental etiology of the MD-PTSD association. RESULTS: The best-fitting model for the MD-PTSD association included a substantial genetic correlation (r=.77; 95% CI, .50-1.00) and a modest individual-specific environmental correlation (r=.34; 95% CI, .19-.48). Common genetic liability explained 62.5% of MD-PTSD comorbidity. Genetic influences common to MD explained 15% of the total variance in risk for PTSD and 58% of the genetic variance in PTSD. Individual-specific environmental influences common to MD explained only 11% of the individual-specific environmental variance in PTSD. LIMITATIONS: Our participants were male Vietnam era veterans and our findings may not generalize to civilians, females or other cohorts. CONCLUSIONS: MD-PTSD comorbidity is largely explained by common genetic influences. Substantial genetic overlap between MD and PTSD implies that genes implicated in the etiology of MD are strong candidates for PTSD and vice versa. Environmental influences on MD and PTSD explain less of their covariation and appear to be largely disorder-specific. Research is needed to identify environmental factors that influence the development of MD versus PTSD in the context of common genetic liability.     

Cohort differences in genetic and environmental influences on retrospective reports of conduct disorder among adult male twins

BACKGROUND: Rates of child and adolescent conduct disorder (CD) have increased steadily over the past several decades. What is not known is whether the underlying genetic and environmental influences on individual differences in CD have also changed. METHODS: Retrospective reports of antisocial behaviour prior to age 18 were obtained from a population-based sample of 2769 adult males from male-male twin pairs born between 1940 and 1974. Using a summary score of number of CD symptoms, structural equation modelling was used to investigate whether mean level and variation in CD increased with more recent cohorts, and whether any increase in variance could be explained by familial or non-familial factors. RESULTS: Both mean level CD symptoms and variation were increased in more recent cohorts. Model fitting indicated that the primary increase in variance was due to familial factors, most notably, an increase in the shared environmental influences on CD, from 0.01 (95 % CI = 0.00; 0.27) to 0.30 (95 % Cl = 0.01; 0-44). Heritability estimates remained largely unchanged, although an increase in genetic factors could not be ruled out. CONCLUSIONS: Secular changes in sociodemographic factors responsible for increasing rates of CD may also account for the greater magnitude of shared environmental influences on variation in CD found among more recent cohorts.     

Interrelationship of genetic and environmental influences on conduct disorder and alcohol and marijuana dependence symptoms

Data from the Vietnam Era Twin (VET) Registry were analyzed to explore the degree to which the same genetic and environmental factors contribute to childhood conduct disorder symptoms and to alcohol and marijuana dependence symptoms. Data on conduct disorder and alcohol and marijuana dependence were obtained from administration of the Diagnostic Interview Schedule to 1,856 monozygotic and 1,479 dizygotic male-male twin pair members of the VET Registry. Multivariate genetic models were compared to determine the genetic and environmental influences common and or specific to all three phenotypes. A full model that allowed for common genetic and environmental influences to all three phenotypes gave a good fit to the data, but the best fitting reduced model did not allow for a genetic influence on conduct disorder symptoms. Under the best fitting reduced model, genes explained 44.7% of the variance in risk for alcohol dependence symptoms. The genetic liability for symptoms of marijuana dependence was due to a 36.3% specific contribution and a 7.6% contribution from genes common with alcohol dependence symptoms. Family environmental contributions common to all three phenotypes explained 46.7%, 11.9%, and 21.3% of variance in risk for symptoms of conduct disorder, alcohol dependence, and marijuana dependence, respectively. Common family environmental factors contribute to risk of conduct disorder symptoms and alcohol and marijuana dependence symptoms. Common genetic influences contribute to risk of symptoms of alcohol dependence and marijuana dependence. While our findings suggest genes do not contribute to co-morbid conduct disorder symptoms, comparisons with other twin studies suggest that the role of genes in risk for conduct disorder remains uncertain. Am. J. Med. Genet. (Neuropsychiatr. Genet.) 88:391–397, 1999. © 1999 Wiley-Liss, Inc.     

Interrelationship of genetic and environmental influences on conduct disorder and alcohol and marijuana dependence symptoms.

Data from the Vietnam Era Twin (VET) Registry were analyzed to explore the degree to which the same genetic and environmental factors contribute to childhood conduct disorder symptoms and to alcohol and marijuana dependence symptoms. Data on conduct disorder and alcohol and marijuana dependence were obtained from administration of the Diagnostic Interview Schedule to 1,856 monozygotic and 1,479 dizygotic male-male twin pair members of the VET Registry. Multivariate genetic models were compared to determine the genetic and environmental influences common and or specific to all three phenotypes. A full model that allowed for common genetic and environmental influences to all three phenotypes gave a good fit to the data, but the best fitting reduced model did not allow for a genetic influence on conduct disorder symptoms. Under the best fitting reduced model, genes explained 44.7% of the variance in risk for alcohol dependence symptoms. The genetic liability for symptoms of marijuana dependence was due to a 36.3% specific contribution and a 7.6% contribution from genes common with alcohol dependence symptoms. Family environmental contributions common to all three phenotypes explained 46.7%, 11.9%, and 21.3% of variance in risk for symptoms of conduct disorder, alcohol dependence, and marijuana dependence, respectively. Common family environmental factors contribute to risk of conduct disorder symptoms and alcohol and marijuana dependence symptoms. Common genetic influences contribute to risk of symptoms of alcohol dependence and marijuana dependence. While our findings suggest genes do not contribute to co-morbid conduct disorder symptoms, comparisons with other twin studies suggest that the role of genes in risk for conduct disorder remains uncertain.     

Genetic and environmental contributions to depressive personality disorder in a population-based sample of Norwegian twins

BACKGROUND: Depressive personality disorder (DPD) was introduced in DSM-IV as a new category requiring further study. The aim of this study was to estimate genetic and environmental contributions to DPD in a population-based twin sample, and include data on criteria performance, prevalence and diagnostic overlap. METHODS: Axis I and Axis II diagnoses were obtained by structured interviews in a population-based sample of 2794 young adult twins. Statistical analyses included correlation and factor analysis based on polychoric correlation coefficients, and diagnostic overlap applying adjusted odds ratios. Contributions from additive genetic and common and unique environmental influences to the liability to DPD were computed using structural equation modelling, applying a multiple threshold variable. RESULTS: Liability to DPD could best be explained by additive genetic and unique environmental factors, with heritability estimates of 49% (95% CI 0.41-0.57) in females and 25% (95% CI 0.12-0.40) in males. The best-fitting model indicated that some of the genes contributing to DPD differ between men and women. Chronbach's alpha was 0.87. 2.0% of participants fulfilled the criteria for DPD, and overlap was most pronounced for dysthymic disorder and avoidant personality disorder. LIMITATIONS: Low prevalence rates and subsequent inclusion of subthreshold criteria could have influenced parameter estimates, especially in males. CONCLUSIONS: DPD was almost twice as heritable in females as in males, comparable to previous studies on major depression. The proposed criteria showed good measurement properties, and DPD was not completely subsumed within any other disorder.     

Genetic and environmental contributions to retrospectively reported DSM-IV childhood attention deficit hyperactivity disorder

BACKGROUND: A variety of methodologies and techniques converge on the notion that adults and children with attention deficit hyperactivity disorder (ADHD) have similar deficits, but there is limited knowledge about whether adult retrospective reports reflect similar genetic and environmental influences implicated in childhood ADHD. METHOD: DSM-IV ADHD symptoms were collected retrospectively from 3896 young adults participating in the National Longitudinal Study of Adolescent Health. Responses from this genetically informative sample of same- and opposite-sex twins and siblings were used to determine the magnitude of genetic and environmental influences. Possible gender differences in these effects were also examined. The degree of familial specificity of the genetic and environmental influences on the Inattentive and Hyperactive-Impulsive symptom dimensions was also determined. RESULTS: Additive genetic effects contributed moderately to DSM-IV Inattentive, Hyperactive-Impulsive and Combined ADHD subtypes (heritability estimates of 0.30-0.38). Individual-specific influences accounted for the remaining proportion of the variance. Both genetic and individual-specific environmental effects contributed to the covariation of Inattentive and Hyperactive-Impulsive symptomologies. CONCLUSIONS: Results from our genetic analyses agree with previous findings based on self-assessment of current and retrospectively reported ADHD symptoms in adolescents and adults. Large individual-specific environmental influences as identified here suggest that current questionnaires used for retrospective diagnoses may not provide the most accurate reconstruction of the etiological influences on childhood ADHD in general population samples.     

Genetic and environmental influences on behavioral disinhibition

Comorbidity among childhood disruptive behavioral disorders is commonly reported in both epidemiologic and clinical studies. These problems are also associated with early substance use and other markers of behavioral disinhibition. Previous twin research has suggested that much of the covariation between antisocial behavior and alcohol dependence is due to common genetic influences. Similar results have been reported for conduct problems and hyperactivity. For the present study, an adolescent sample consisting of 172 MZ and 162 DZ twin pairs, recruited through the Colorado Twin Registry and the Colorado Longitudinal Twin Study were assessed using standardized psychiatric interviews and personality assessments. DSM-IV symptom counts for conduct disorder and attention deficit hyperactivity disorder, along with a measure of substance experimentation and novelty seeking, were used as indices of a latent behavioral disinhibition trait. A confirmatory factor model fit to individual-level data showed a strong common factor accounting for 16-42% of the observed variance in each measure. A common pathway model evaluating the genetic and environmental architecture of the latent phenotype suggested that behavioral disinhibition is highly heritable (a(2) = 0.84), and is not influenced significantly by shared environmental factors. A residual correlation between conduct disorder and substance experimentation was explained by shared environmental effects, and a residual correlation between attention deficit hyperactivity disorder and novelty seeking was accounted for by genetic dominance. These results suggest that a variety of adolescent problem behaviors may share a common underlying genetic risk.     

Genetic and environmental contributions to cannabis dependence in a national young adult twin sample

BACKGROUND: This paper examines genetic and environmental contributions to risk of cannabis dependence. METHOD: Symptoms of cannabis dependence and measures of social, family and individual risk factors were assessed in a sample of 6265 young adult male and female Australian twins born 1964-1971. RESULTS: Symptoms of cannabis dependence were common: 11.0% of sample (15.1% of men and 7.8% of women) reported two or more symptoms of dependence. Correlates of cannabis dependence included educational attainment, exposure to parental conflict, sexual abuse, major depression, social anxiety and childhood conduct disorder. However, even after control for the effects of these factors, there was evidence of significant genetic effects on risk of cannabis dependence. Standard genetic modelling indicated that 44.7% (95% CI = 15-72.2) of the variance in liability to cannabis dependence could be accounted for by genetic factors, 20.1% (95% CI = 0-43.6) could be attributed to shared environment factors and 35.3% (95% CI = 26.4-45.7) could be attributed to non-shared environmental factors. However, while there was no evidence of significant gender differences in the magnitude of genetic and environmental influences, a model which assumed both genetic and shared environmental influences on risks of cannabis dependence among men and shared environmental but no genetic influences among women provided an equally good fit to the data. CONCLUSIONS: There was consistent evidence that genetic risk factors are important determinants of risk of cannabis dependence among men. However, it remains uncertain whether there are genetic influences on liability to cannabis dependence among women.     

No objectively measured sleep disturbances in children with attention‐deficit/hyperactivity disorder

The main goal of this study was to gain more insight into sleep disturbances in children with attention‐deficit/hyperactivity disorder, using objective measures of sleep quality and quantity. The evidence for sleep problems in children with attention‐deficit/hyperactivity disorder thus far is inconsistent, which might be explained by confounding influences of comorbid internalizing and externalizing problems and low socio‐economic status. We therefore investigated the mediating and moderating role of these factors in the association between attention‐deficit/hyperactivity disorder and sleep problems. To control for the effects of stimulant medication use, all participants were tested free of medication. Sixty‐three children with attention‐deficit/hyperactivity disorder and 61 typically developing children, aged 6–13 years, participated. Sleep was monitored for one to three school nights using actigraphy. Parent and teacher questionnaires assessed symptoms of attention‐deficit/hyperactivity disorder, internalizing behaviour, oppositional defiant disorder and conduct disorder. Results showed no differences between the attention‐deficit/hyperactivity disorder and typically developing group in any sleep parameter. Within the attention‐deficit/hyperactivity disorder group, severity of attention‐deficit/hyperactivity disorder symptoms was not related to sleep quality or quantity. Moderation analyses in the attention‐deficit/hyperactivity disorder group showed an interaction effect between attention‐deficit/hyperactivity disorder symptoms and internalizing and externalizing behaviour on total sleep time, time in bed and average sleep bout duration. The results of our study suggest that having attention‐deficit/hyperactivity disorder is not a risk factor for sleep problems. Internalizing and externalizing behaviour moderate the association between attention‐deficit/hyperactivity disorder and sleep, indicating a complex interplay between psychiatric symptoms and sleep.     

Genetic Effects on ADHD Symptomatology in 7- to 13-Year-Old Twins: Results from a Telephone Survey

The magnitude of genetic and environmental factors and the influence of contrast effects on attention-deficit hyperactivity disorder (ADHD) symptomatology were examined on a sample of 900 twin pairs, aged 7–13, participating in the Virginia Twin Study of Adolescent Behavioral Development (VTSABD). In addition, the genetic and environmental correlations between ADHD and oppositional-defiant disorder/conduct disorder (ODD/CD) symptomatology were estimated. A series of structural models was applied to maternal ratings from a telephone survey, designed to screen for the three dimensions of ADHD symptomatology (hyperactivity, impulsivity, and inattention) and ODD/CD symptomatology. Model-fitting results suggested that ADHD symptomatology is highly heritable and influenced mostly by additive genetic, specific environmental, and contrast effects. However, this analysis could not exclude with statistical significance additional effects from dominance. The results of the best-fitting bivariate model suggested that the genetic correlation between the two traits is 50% and replicated previous findings of a common genetic factor influencing the comorbidity of ADHD and ODD/CD symptomatologies.