注意缺陷多动障碍低觉醒模型的新证据

注意缺陷多动障碍(Attention Deficit Hyperactivity Disorder,ADHD)是儿童期常见的一种发展性的异常,其病因及发生机理至今未明。低觉醒模型是ADHD成因的一种假设。本文从睡眠障碍导致的低觉醒探讨ADHD发生机理。通过对ADHD儿童的睡眠障碍进行分析以及将ADHD外在表现与睡眠剥夺后的表现进行对比分析,得出ADHD儿童存在的低觉醒是由于外显的或内隐的睡眠障碍引起的,一方面间接证明了低觉醒模型,另一方面为ADHD的成因研究开拓了新的思路。     

注意缺陷多动障碍儿童睡眠障碍与铁缺乏关系的临床研究

目的:探讨注意缺陷多动障碍(ADHD)患儿睡眠障碍与血清铁蛋白水平的关系。方法:符合美国精神疾病诊断与统计手册第4版(DSM-Ⅳ)中ADHD诊断标准的62例6-14岁ADHD患儿,由ADHD患儿的父母填写睡眠障碍量表(SDSC),检测ADHD患儿的血清铁蛋白水平。结果:与血清铁蛋白水平高于45μg/L的ADHD患儿相比较,血清铁蛋白水平低于45μg/L的ADHD患儿的SDSC\"睡眠醒觉转换障碍\"项评分和总分明显高于前者(P<0.05)。2组间其他项评分比较无显著性差异(P>0.05)。SDSC\"睡眠醒觉转换障碍\"项评分与血清铁蛋白水平成负相关(P<0.05)。结论:血清铁蛋白水平低于45μg/LADHD患儿SDSC\"睡眠醒觉转换障碍\"(睡眠中的异常运动)的危险性显著增加。     

注意缺陷多动障碍儿童睡眠障碍与铁缺乏关系的临床研究

目的：探讨注意缺陷多动障碍（ADHD）患儿睡眠障碍与血清铁蛋白水平的关系。方法：符合美国精神疾病诊断与统计手册第4版（DSM-Ⅳ）中ADHD诊断标准的62例6．14岁ADHD患儿,由ADHD患儿的父母填写睡眠障碍量表（SDSC）,检测ADH-D患儿的血清铁蛋白水平。结果：与血清铁蛋白水平高于45／μg／L的ADHD患儿相比较,血清铁蛋白水平低于45／μg／L的ADHD患儿的SDSC“睡眠醒觉转换障碍”项评分和总分明显高于前者（P〈0．05）。2组间其他项评分比较无显著性差异（P〉0．05）。SDSC“睡眠醒觉转换障碍”项评分与血清铁蛋白水平成负相关（P〈0．05）。结论：血清铁蛋白水平低于451μg／LADHD患儿SDSC“睡眠醒觉转换障碍”（睡眠中的异常运动）的危险性显著增加。     

注意缺陷损多动障碍关联于DXS7位点

采用单体型相对风险和传递／不平衡检验方法,在中国人群中对注意中对注意缺陷损多动障碍（ＡＤＰＤ）与ＤＸＳ７位点进行了遗传关联分析。     

注意缺陷多动障碍儿童肠道菌群特点及与行为问题的相关性研究

分析注意缺陷多动障碍（ADHD）儿童肠道菌群特点与行为问题的相关性。

选取2022年1月到2023年5月我院收治的96例ADHD患儿和健康体检的96例儿童,分别作为研究组和对照组。对所有儿童粪便样本进行宏基因组测序并分析肠道菌群特点。采用Conners儿童行为问卷－家长版（PSQ）评估两组儿童的行为。采用Pearson相关性分析肠道菌群分布与行为问题的相关性。

研究组患儿肠道菌群α−多样性低于对照组,肠杆菌属、气味杆菌属和枸橼酸杆菌属相对丰度均高于对照组,韦荣球菌属、拟杆菌属、双歧杆菌属和普氏栖粪杆菌相对丰度均低于对照组,差异均具有统计学意义（P＜0.05）。研究组患儿Conners PSQ问卷评分高于对照组（P＜0.05）。研究组患儿Conners PSQ问卷各因子评分与肠道肠杆菌属、气味杆菌属和枸橼酸杆菌属均呈正相关（P＜0.05）,与韦荣球菌属、拟杆菌属、双歧杆菌属和普氏栖粪杆菌均呈负相关（P＜0.05）。

ADHD儿童肠道菌群构成与健康儿童不同,不同肠道菌群与患儿行为问题有相关性。

     

注意缺陷多动障碍共患阅读障碍：认知-脑-基因的多维度研究进展

注意缺陷多动障碍(attention-deficit/hyperactivity disorder,ADHD)和发展性阅读障碍(developmental dyslexia,DD)是两种常见的神经发育性障碍,二者共患的比率高达25%～48%.本文拟从认知-脑-基因等多个维度对ADHD共患DD的研究进展进行综述. ADHD和DD共患的共同认知损害可能是加工速度缺陷,其作为内表型能够很好地帮助解释遗传因素如何通过影响认知功能进而导致出现ADHD共患DD的临床表型.而国内对ADHD共患DD的研究较少,已有的多项研究仅关注ADHD伴学习障碍,但缺乏标准的DD临床诊断标准.本文指出了统一诊断标准、结合多学科研究以及未来个体化训练的必要性.     

多巴胺D1受体基因多态性与注意缺陷多动障碍的相关性研究

目的:探讨多巴胺D1受体(Dopamine D1 receptor, DRD1)基因启动子区G-48A、外显子区T1403C两个SNP位点与注意缺陷多动障碍(attention deficit hyperactivity disorder,ADHD)的关联性.方法:选取87名ADHD患者和103名正常对照,提取基因组DNA,采用聚合酶链反应-限制性片段长度多态性(PCR-RFLP)技术检测G-48A和T1403C两个多态性位点的基因型,SPSS13.0软件分析各位点的等位基因及基因型频率.结果:DRD1的G-48A基因型及等位基因频率分布在ADHD和对照组之间有统计学差异(p<0.05),ADHD组中等位基因A频率显著高于正常组(p<0.05).T1403C位点基因型及等位基因频率在ADHD组与健康对照组无统计学差异.结论:DRD1基因G-48A多态性可能与ADHD的发病有关,携带有等位基因A的个体可能更容易患ADHD.T1403C多态性与ADHD的发病无明显相关性.     

营养性缺铁性贫血与注意缺陷多动障碍的临床关系研究——258例病例分析

目的:通过对营养性缺铁性贫血与注意缺陷多动障碍的病例研究,探讨两者之间的关系。方法:对258例NIDA的病因、临床表现和治疗进行临床分析,包括其中的31例中重度ADHD。结果:本组NIDA患儿病因主要为未及时添加富铁辅食、饮食结构不合理、消化道疾病、鼻衄等,临床主要表现为头晕、乏力、注意力不集中、记忆力减退等,对患者进行病因治疗以及服用生血宁片;ADHD的病因不明,临床表现为注意力不集中、活动过度、行为冲动等,通过综合治疗可以改善症状。NIDA的患儿ADHD的发病率较正常儿童为高。结论:NIDA与ADHD的关系密切。     

脑源性神经营养因子基因多态性与注意缺陷多动障碍的关联性研究

目的：探讨脑源性神经营养因子（Brain-derivedneurotrophicfactor,BDNF）G196A、C270T及Val66Met3个单核苷酸多态性（SNP）位点与注意缺陷多动障碍（ADHD）的关系。方法：选取无亲缘关系的ADHD患者共114例,健康对照共96例。采用聚合酶链反应-限制性片段长度多态性（PCR-RFLP）技术检测G196A、C270T和Val66Met3个多态性位点的多态性,采用HaploView4.0及SPSS13.0软件进行连锁不平衡分析并比较两组基因型分布和等位基因频率。结果：BDNF三个多态性位点基因型及等位基因频率分布均符合Hardy-Weinberg定律。ADHD组G196A和C270T多态性位点分布与正常对照组比较差异无统计学意义,而BDNF基因Val66Met位点的基因型及等位基因频率分布在ADHD组与对照组存在显著性差异（p〈0.05）,ADHD组Val66Met位点的等位基因G（Val）频率显著高于正常对照组。结论：BDNF基因Val66Met多态性可能与ADHD发病有关,携带有Val66Met多态性位点G等位基因的个体可能更容易产生ADHD。     

脑源性神经营养因子基因多态性与注意缺陷多动障碍的关联性研究

目的:探讨脑源性神经营养因子(Brain-derivedneurotrophicfactor,BDNF)G196A、C270T及Val66Met3个单核苷酸多态性(SNP)位点与注意缺陷多动障碍(ADHD)的关系。方法:选取无亲缘关系的ADHD患者共114例,健康对照共96例。采用聚合酶链反应-限制性片段长度多态性(PCR-RFLP)技术检测G196A、C270T和Val66Met3个多态性位点的多态性,采用HaploView4.0及SPSS13.0软件进行连锁不平衡分析并比较两组基因型分布和等位基因频率。结果:BDNF三个多态性位点基因型及等位基因频率分布均符合Hardy-Weinberg定律。ADHD组G196A和C270T多态性位点分布与正常对照组比较差异无统计学意义,而BDNF基因Val66Met位点的基因型及等位基因频率分布在ADHD组与对照组存在显著性差异(p<0.05),ADHD组Val66Met位点的等位基因G(Val)频率显著高于正常对照组。结论:BDNF基因Val66Met多态性可能与ADHD发病有关,携带有Val66Met多态性位点G等位基因的个体可能更容易产生ADHD。     

Neurofeedback: An Alternative and Efficacious Treatment for Attention Deficit Hyperactivity Disorder

Current research has shown that neurofeedback, or EEG biofeedback as it is sometimes called, is a viable alternative treatment for Attention Deficit Hyperactivity Disorder (ADHD). The aim of this article is to illustrate current treatment modalities(s), compare them to neurofeedback, and present the benefits of utilizing this method of treatment to control and potentially alleviate the symptoms of ADHD. In addition, this article examines the prevalence rates and possible etiology of ADHD, the factors associated with ADHD and brain dysfunction, the current pharmacological treatments of ADHD, Ritalin, and the potential risks and side effects. Behavior modification and cognitive behavioral treatment for ADHD is discussed as well. Lastly, a brief history of the study of neurofeedback, treatment successes and clinical benefits, comparisons to medication, and limitations are presented.     

Inhibition in Adults with Attention Deficit/Hyperactivity Disorder: Event-Related Potentials in the Stop Task

The core deficit in Attention Deficit/Hyperactivity Disorder (ADHD) may be a deficiency in executive functions, particularly the processes that are associated with the inhibition of predominant responses. To test this notion in the adult population, healthy undergraduate volunteers and students with ADHD symptoms performed a visual Stop Signal Task (Logan et al. J Exp Psychol: Hum Percept Perform 10:276–291, 1984) while Event-Related brain Potentials were recorded. The two groups did not differ on behavioral measures of performance, but there was a significant difference in the N2–P3 component. These results underline the robustness of an N2–P3 difference between healthy adults and people with ADHD symptoms that have persisted into young adulthood.     

Delayed Sleep Timing and Symptoms in Adults With Attention-Deficit/Hyperactivity Disorder: A Controlled Actigraphy Study

Patients with attention-deficit/hyperactivity disorder (ADHD) often exhibit disrupted sleep and circadian rhythms. Determination of whether sleep disturbance and/or circadian disruption are differentially associated with symptom severity is necessary to guide development of future treatment strategies. Therefore, we measured sleep and ADHD symptoms in participants aged 19–65 who met the DSM-IV-TR (Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision) criteria for ADHD and insomnia without psychiatric comorbidities by monitoring actigraphy and daily sleep logs for 2 wks, as well as the Pittsburgh Sleep Quality Index (PSQI), Epworth Sleepiness Scale (ESS), the ADHD Rating Scale (ADHD-RS), and a clinic-designed sleep behavior questionnaire. Principal components analysis identified correlated circadian- and sleep-related variables in all participants with ADHD who completed the study (n?=?24). The identified components were entered into a backwards stepwise linear regression analysis, which indicated that delayed sleep timing and increased sleepiness (ESS) (but not sleep duration or sleep efficiency) significantly predicted greater severity of both hyperactive-impulsive and inattentive ADHD symptoms (p <?.05 for partial regression coefficients). In addition, combined subtypes had the most impaired age-adjusted sleep quality (PSQI scores; p?<?.05 compared with healthy controls; n?=?13), and 91.7% of them reported going to bed late due to being “not tired/too keyed up to sleep” compared with 57.2% and 50% of inattentive and symptom-controlled participants, respectively (p?<?.05). In conclusion, the results of this study suggest that ADHD symptom severity correlates with delayed sleep timing and daytime sleepiness, suggesting that treatment interventions aimed at advancing circadian phase may improve daytime sleepiness. In addition, ADHD adults with combined hyperactive-impulsive and inattentive symptoms have decreased sleep quality as well as the delayed sleep timing of predominately inattentive subtypes. (Author correspondence: rfargason@uab.edu)     

Electroencephalographic Biofeedback in the Treatment of Attention-Deficit/Hyperactivity Disorder

Historically, pharmacological treatments for attention-deficit/hyperactivity disorder (ADHD) have been considered to be the only type of interventions effective for reducing the core symptoms of this condition. However, during the past three decades, a series of case and controlled group studies examining the effects of EEG biofeedback have reported improved attention and behavioral control, increased cortical activation on quantitative electroencephalographic examination, and gains on tests of intelligence and academic achievement in response to this type of treatment. This review paper critically examines the empirical evidence, applying the efficacy guidelines jointly established by the Association for Applied Psychophysiology and Biofeedback (AAPB) and the International Society for Neuronal Regulation (ISNR). On the basis of these scientific principles, EEG biofeedback was determined to be “probably efficacious” for the treatment of ADHD. Although significant clinical improvement was reported in approximately 75% of the patients in each of the published research studies, additional randomized, controlled group studies are needed in order to provide a better estimate of the percentage of patients with ADHD who will demonstrate such gains in clinical practice.     

Salivary Melatonin Rhythm as a Marker of the Circadian System in Healthy Children and Those With Attention-Deficit/Hyperactivity Disorder

Attention-deficit/hyperactivity disorder (ADHD) is the most common neurobehavioral disorder of childhood. Problems with sleep structure, efficiency, and timing have been reported in some, but not all, studies on ADHD children. As the sleep-wake cycle belongs to circadian rhythms, the timekeeping circadian system might be involved in ADHD. To assess whether the circadian system of ADHD children differs from that of controls, the rhythm of the pineal hormone melatonin was used as a reliable marker of the system. Saliva from 34 ADHD and 43 control 6- to 12-yr-old children was sampled at 2-h intervals throughout the entire 24-h cycle, and the melatonin profiles of the ADHD and control children were compared. The nocturnal melatonin peaks of the ADHD and control group did not differ significantly. The high nocturnal interindividual variability of the peaks seen in adulthood was present already in the studied children. The 24-h melatonin profiles of all the ADHD subjects did not differ significantly from those of the control subjects. Categorization of subjects according to age, into groups of 6- to 7-yr-old (9 ADHD, 5 control), 8- to 9-yr-old (16 ADHD, 26 control), and 10- to 12-yr-old (9 ADHD, 12 control) children, revealed significant differences between the ADHD and control group in the melatonin rhythm waveform, but not in nocturnal melatonin peaks; the peaks were about the same in both groups and did not change significantly with increasing age. In the oldest, but not in the younger, children, the melatonin signal duration in the ADHD group was shorter than in the control group. The difference might be due to the fact that whereas in the control group both the evening melatonin onset and the morning offset phase delayed in the oldest children relative to those in the youngest children, in the ADHD group only the onset, but not the offset, phase delayed with increasing age. The data may indicate subtle differences between the circadian system of ADHD and control children during development. (Author correspondence: sumova@biomed.cas.cz)     

Effect of EEG Biofeedback on Cognitive Flexibility in Children with Attention Deficit Hyperactivity Disorder With and Without Epilepsy

Attention deficit hyperactivity disorder (ADHD) is one of the most common developmental disorders in school-aged children. Symptoms consistent with ADHD have been observed in 8–77 % of children with epilepsy. Researchers have been motivated to search for alternative forms of treatment because 30 % of patients with ADHD cannot be treated by psychostimulants. Several studies support the use of a multimodal treatment approach that includes neurofeedback (NF) for the long-term management of ADHD. These studies have shown that NF provides a sustained effect, even without concurrent treatment with stimulants. We aimed to assess cognitive flexibility in ADHD children with and without temporal lobe epilepsy (TLE), and to evaluate the effects of NF on cognitive flexibility in these groups of children. We prospectively evaluated 69 patients with ADHD aged 9–12 years. The control group was 26 ADHD children without TLE who received no treatment. The first experimental group comprised 18 children with ADHD. The second experimental group comprised 25 age-matched ADHD children with TLE. This group was further divided in two subgroups. One subgroup comprised those with mesial temporal lobe epilepsy (16 patients, 9 with hippocampal sclerosis and 7 with hippocampal atrophy), and the other with lateral temporal lobe epilepsy (9 patients, 5 with temporal lobe dysplasia, 3 with temporal lobe cysts, and 1 with a temporal lobe cavernoma). We treated their ADHD by conducting 30 sessions of EEG NF. Reaction time and error rates on the Trail Making Test Part B were compared before and after treatment, and significant differences were found for all groups of patients except those who had mesial temporal lobe epilepsy with hippocampal atrophy. Our results demonstrate that in most cases, NF can be considered an alternative treatment option for ADHD children even if they have TLE. Additional studies are needed to confirm our results.