Concordance of actigraphy with polysomnography in children with and without attention‐deficit/hyperactivity disorder

This study sought to: (1) compare actigraphy‐derived estimated sleep variables to the same variables based on the gold‐standard of sleep assessment, polysomnography; (2) examine whether the correlations between the measures differ between children with attention‐deficit/hyperactivity disorder and typically developing children; and (3) determine whether these correlations are altered when children with attention‐deficit/hyperactivity disorder are treated with medication. Participants (24 attention‐deficit/hyperactivity disorder; 24 typically developing), aged 6–12 years, completed a 1‐week baseline assessment of typical sleep and daytime functioning. Following the baseline week, participants in the attention‐deficit/hyperactivity disorder group completed a 4‐week blinded randomized control trial of methylphenidate hydrochloride, including a 2‐week placebo and 2‐week methylphenidate hydrochloride treatment period. At the end of each observation (typically developing: baseline; attention‐deficit/hyperactivity disorder: baseline, placebo and methylphenidate hydrochloride treatment), all participants were invited to a sleep research laboratory, where overnight polysomnography and actigraphy were recorded concurrently. Findings from intra‐class correlations and Bland–Altman plots were consistent. Actigraphy was found to provide good estimates (e.g. intra‐class correlations >0.61) of polysomnography results for sleep duration for all groups and conditions, as well as for sleep‐onset latency and sleep efficiency for the typically developing group and attention‐deficit/hyperactivity disorder group while on medication, but not for the attention‐deficit/hyperactivity disorder group during baseline or placebo. Based on the Bland–Altman plots, actigraphy tended to underestimate for sleep duration (8.6–18.5 min), sleep efficiency (5.6–9.3%) and sleep‐onset latency, except for attention‐deficit/hyperactivity disorder during placebo in which actigraphy overestimated (?2.1 to 6.3 min). The results of the current study highlight the importance of utilizing a multimodal approach to sleep assessment in children with attention‐deficit/hyperactivity disorder.     

Circadian motor activity affected by stimulant medication in children with attention‐deficit/hyperactivity disorder

Attention‐deficit/hyperactivity disorder (ADHD) is a highly prevalent disorder occurring in approximately 3–5% of school‐aged children. The core symptoms of ADHD are effectively treated with stimulant medications such as methylphenidate; however, there are also negative side effects, including insomnia. It has been suggested that administration of stimulant medication may alter the timing or regularity of circadian motor activity levels. This study aimed to investigate the impact of stimulant medication on the strength and timing of circadian rhythms in 16 stimulant medication‐naïve children with ADHD. Participants were monitored for changes in motor activity during a 3‐week blinded placebo‐controlled medication trial to examine the impact of immediate‐release methylphenidate hydrochloride. Motor activity was measured by actigraphy, and 24‐h activity profiles were analysed using cosinor analyses to identify measurable changes in circadian rhythms. The children in this sample demonstrated significant increases in motor activity during the sleep‐onset latency period. They also showed a significant reduction in relative circadian amplitude and a phase‐delay in the timing of the daily rhythm. Clinicians and parents of children being treated with stimulant medication for ADHD should be aware that stimulant medication may cause disruption of sleep/circadian rhythms. Behavioural strategies to improve sleep may be useful for children experiencing these negative effects from medication.     

Disturbed sleep in attention‐deficit hyperactivity disorder (ADHD) is not a question of psychiatric comorbidity or ADHD presentation

Attention‐deficit hyperactivity disorder (ADHD) is a heterogeneous psychiatric disorder with three different presentations and high levels of psychiatric comorbidity. Serious sleep complaints are also common, but the role of the presentations and comorbidity in sleep is under‐investigated in ADHD. Consequently, the goal of the study was to investigate sleep problems in medicine‐naive school‐aged children (mean age = 9.6 years) with ADHD compared to controls using objective methods and to examine the role of comorbidity and presentations. Ambulatory polysomnography results suggested that children with ADHD (n = 76) had significantly more sleep disturbances than controls (n = 25), including a larger percentage of rapid eye movement (REM) sleep and more sleep cycles, as well as lower mean sleep efficiency, mean non‐REM (NREM) sleep stage 1 and mean NREM sleep stage 3. No significant between‐group differences were found on the multiple sleep latency test. Stratifying for comorbidity in the ADHD group did not reveal major differences between groups, but mean sleep latency was significantly longer in children with ADHD and no comorbidity compared to controls (36.1 min; SD = 30.1 versus 22.6 min; SD = 15.2). No differences were found between ADHD presentations. Our results support the presence of night‐time sleep disturbances in children with ADHD. Poor sleep does not appear to be attributable to comorbidity alone, nor do sleep disturbances differ within ADHD presentations.     

Association between symptoms and subtypes of attention‐deficit hyperactivity disorder and sleep problems/disorders

This study aimed to investigate the association between attention‐deficit hyperactivity disorder (ADHD) symptoms and subtypes, and sleep schedules, daytime inadvertent napping, and sleep problems/disorders in children and adolescents with and without ADHD. The sample included 325 patients with ADHD, aged 10–17 years [male: 81.5%; combined type (ADHD‐C): 174; predominantly inattentive type (ADHD‐I): 130; predominantly hyperactive‐impulsive type (ADHD‐HI): 21], and 257 children and adolescents without lifetime ADHD (non‐ADHD). We conducted psychiatric interviews with the participants and their mothers before making the diagnoses of ADHD, other psychiatric disorders, and sleep problems or disorders. We also collected the medication treatment data and parent and teacher reports of ADHD symptoms. Multi‐level models were used for data analyses controlling for sex, age, psychiatric comorbidities, and treatment with methylphenidate. The ADHD‐C and ADHD‐I groups had more daytime inadvertent napping. In general, the three subtypes were associated with increased rates of sleep problems/disorders. Specifically, ADHD‐C rather than ADHD‐I was associated with circadian rhythm problems, sleep‐talking, nightmares (also ADHD‐HI), and ADHD‐I was associated with hypersomnia. The most‐related sleep schedules and problems for inattention and hyperactivity‐impulsivity were earlier bedtime, later rise time, longer nocturnal sleep, more frequent daytime napping, insomnia, sleep terrors, sleep‐talking, snoring, and bruxism across informants. The findings imply that in addition to the dichotomous approach of ADHD and considering the psychiatric comorbid conditions, ADHD subtypes and symptom dimensions need to be considered in clinical practice and in the research regarding the association between ADHD and sleep problems/disorders.     

No association between CHRNA7 microsatellite markers and attention‐deficit hyperactivity disorder

Attention‐deficit hyperactivity disorder (ADHD) is a highly heritable, common psychiatric disorder of childhood that probably involves several genes. There are several lines of evidence suggesting that the nicotinic system may be functionally significant in ADHD. First, nicotine promotes the release of dopamine and has been shown to improve attention in adults with ADHD, smokers, and nonsmokers. Second, ADHD is a significant risk factor for early initiation of cigarette smoking in children and maternal cigarette smoking appears to be a risk factor for ADHD. Finally, animal studies in rats and monkeys also suggest that nicotine may be involved in attentional systems and locomotor activity. The nicotinic system has previously been studied in schizophrenia where the neuronal nicotinic acetylcholine receptor α7 subunit gene (CHRNA7) has been implicated in decreased P50 inhibition and attentional disturbances in patients with schizophrenia and in many of their nonschizophrenic relatives. Three known microsatellite markers (D15S165, D15S1043, and D15S1360) near the nicotinic acetylcholine α7 receptor gene, CHRNA7, were studied in 206 ADHD parent‐proband trios of children aged 5–16 with ADHD according to DSM‐IV criteria. Children with known major medical or psychiatric conditions or mental retardation (IQ < 70) were excluded from the study. Markers D15S165 and D15S1360 were in linkage disequilibrium. The extended Transmission Disequilibrium Test analyses demonstrated no evidence that variation at the microsatellite markers D15S1360, D15S1043, and D15S165 influences susceptibility to ADHD. However, it remains possible that the CHRNA7 gene and other nicotinic system genes may be involved in conferring susceptibility to ADHD. © 2001 Wiley‐Liss, Inc.     

Common obesity risk alleles in childhood attention‐deficit/hyperactivity disorder

Children with attention‐deficit/hyperactivity disorder (ADHD) have a higher rate of obesity than children without ADHD. Obesity risk alleles may overlap with those relevant for ADHD. We examined whether risk alleles for an increased body mass index (BMI) are associated with ADHD and related quantitative traits (inattention and hyperactivity/impulsivity). We screened 32 obesity risk alleles of single nucleotide polymorphisms (SNPs) in a genome‐wide association study (GWAS) for ADHD based on 495 patients and 1,300 population‐based controls and performed in silico analyses of the SNPs in an ADHD meta‐analysis comprising 2,064 trios, 896 independent cases, and 2,455 controls. In the German sample rs206936 in the NUDT3 gene (nudix; nucleoside diphosphate linked moiety X‐type motif 3) was associated with ADHD risk (OR: 1.39; P = 3.4 × 10^?4; P_corr = 0.01). In the meta‐analysis data we found rs6497416 in the intronic region of the GPRC5B gene (G protein‐coupled receptor, family C, group 5, member B; P = 7.2 × 10^?4; P_corr = 0.02) as a risk allele for ADHD. GPRC5B belongs to the metabotropic glutamate receptor family, which has been implicated in the etiology of ADHD. In the German sample rs206936 (NUDT3) and rs10938397 in the glucosamine‐6‐phosphate deaminase 2 gene (GNPDA2) were associated with inattention, whereas markers in the mitogen‐activated protein kinase 5 gene (MAP2K5) and in the cell adhesion molecule 2 gene (CADM2) were associated with hyperactivity. In the meta‐analysis data, MAP2K5 was associated with inattention, GPRC5B with hyperactivity/impulsivity and inattention and CADM2 with hyperactivity/impulsivity. Our results justify further research on the elucidation of the common genetic background of ADHD and obesity. © 2013 Wiley Periodicals, Inc.     

Body temperature,activity and melatonin profiles in adults with attention‐deficit/hyperactivity disorder and delayed sleep: a case–control study

Irregular sleep–wake patterns and delayed sleep times are common in adults with attention‐deficit/hyperactivity disorder, but mechanisms underlying these problems are unknown. The present case–control study examined whether circadian abnormalities underlie these sleep problems in a naturalistic home setting. We included 12 medication‐naïve patients with attention‐deficit/hyperactivity disorder and delayed sleep phase syndrome, and 12 matched healthy controls. We examined associations between sleep/wake rhythm in attention‐deficit/hyperactivity disorder and circadian parameters (i.e. salivary melatonin concentrations, core and skin temperatures, and activity patterns) of the patients and controls during five consecutive days and nights. Daily bedtimes were more variable within patients compared with controls (F = 8.19, P < 0.001), but melatonin profiles were equally stable within individuals. Dim‐light melatonin onset was about 1.5 h later in the patient group (U = 771, Z = ?4.63, P < 0.001). Patients slept about 1 h less on nights before work days compared with controls (F = 11.21, P = 0.002). The interval between dim‐light melatonin onset and sleep onset was on average 1 h longer in patients compared with controls (U = 1117, Z = ?2.62, P = 0.009). This interval was even longer in patients with extremely late chronotype. Melatonin, activity and body temperatures were delayed to comparable degrees in patients. Overall temperatures were lower in patients than controls. Sleep‐onset difficulties correlated with greater distal–proximal temperature gradient (DPG; i.e. colder hands, r² = ?0.32, P = 0.028) in patients. Observed day‐to‐day bedtime variability of individuals with attention‐deficit/hyperactivity disorder and delayed sleep phase syndrome were not reflected in their melatonin profiles. Irregular sleep–wake patterns and delayed sleep in individuals with attention‐deficit/hyperactivity disorder and delayed sleep phase syndrome are associated with delays and dysregulations of the core and skin temperatures.     

The norepinephrine transporter gene and attention‐deficit hyperactivity disorder

The adrenergic system plays a known role in attentional systems and a suspected causal role in attention‐deficit hyperactivity disorder (ADHD), based on evidence from pharmacological interventions and animal models. The efficacy of the highly selective noradrenergic reuptake inhibitor, tomoxetine, in treating ADHD symptoms supports the system's role in ADHD and points to the norephinephrine transporter as a candidate gene. This study tested the gene for the norepinephrine transporter (NET1) as a susceptibility factor in ADHD using three polymorphisms located in exon 9, intron 9, and intron 13. We examined the inheritance of these polymorphisms in a sample of 122 families with a total of 155 children with ADHD identified through an ADHD proband. Use of the transmission disequilibrium test failed to show significant evidence for biased transmission of any of the alleles or the haplotypes of these polymorphisms. We further investigated this gene by screening the probands for five known amino acid variants to determine if they contributed to the ADHD phenotype but observed only one (Thr99Ile) in our sample. Since the frequency of this variant (1.8%) was similar to that previously reported in a control sample (2.2%), it is unlikely that this variant is related to the ADHD phenotype. Our results do not support the NET1 gene as a major genetic susceptibility factor in ADHD. © 2002 Wiley‐Liss, Inc.     

The sleep of children with attention deficit hyperactivity disorder on and off methylphenidate: a matched case–control study

In the present study, we assessed the effects of regular use of methylphenidate medication in children diagnosed with attention deficit hyperactivity disorder (ADHD) on sleep timing, duration and sleep architecture. Twenty‐seven children aged 6–12 years meeting diagnostic criteria for Diagnostic and Statistical Manual version IV ADHD and 27 control children matched for age (±3 months) and gender. Two nights of standard polysomnographic (PSG) recordings were conducted. ADHD children were allocated randomly to an on‐ or 48 h off‐methylphenidate protocol for first or second recordings. Control children’s recordings were matched for night, but no medication was used. Mixed modelling was employed in the analyses so that the full data set was used to determine the degree of medication effects. Methylphenidate in ADHD children prolonged sleep onset by an average of 29 min [confidence interval (CI) 11.6, 46.7], reduced sleep efficiency by 6.5% (CI 2.6, 10.3) and shortened sleep by 1.2 h (CI 0.65, 1.9). Arousal indices were preserved. Relative amounts of stages 1, 2 and slow wave sleep were unchanged by medication. Rapid eye movement sleep was reduced (?2.4%) on the medication night, an effect that became non‐significant when control data were incorporated in the analyses. PSG data from ADHD children off‐medication were similar to control data. Our findings suggest that methylphenidate reduces sleep quantity but does not alter sleep architecture in children diagnosed with ADHD. An adequate amount of sleep is integral to good daytime functioning, thus the sleep side effects of methylphenidate may affect adversely the daytime symptoms the drug is targeted to control.     

Glutamatergic copy number variants and their role in attention‐deficit/hyperactivity disorder

Attention‐Deficit/Hyperactivity Disorder (ADHD) is a common neurodevelopmental disorder with a strong genetic component. The glutamate metabotropic receptor genes (GRMs) have been considered potential candidates for ADHD susceptibility. The aim of the present study was to investigate if copy number variants (CNVs) in GRM1, GRM5, and GRM8 genes are overrepresented in ADHD subjects. A total of 1038 individuals with ADHD and 1057 subjects without this disorder were investigated. No significant difference in the total number of CNVs was found comparing the entire ADHD sample and the population sample without ADHD (P = 0.326, OR = 1.112, 95% CI = 0.762–1.624). The presence of CNVs was associated with lower intelligence quotient (IQ) scores in ADHD samples (P = 0.026, OR = 1.824, 95% CI = 1.066–3.121) but not in the sample of individuals without ADHD. CNVs in GRM5 were associated with presence of anxiety disorders in ADHD cases (P = 0.002, OR = 3.915, 95% CI = 1.631–9.402), but not in individuals without ADHD. Taken together, our results suggest a role for glutamate in ADHD as CNVs in the glutamatergic genes investigated herein were associated with cognitive and clinical characteristics of ADHD individuals. © 2014 The Authors. American Journal of Medical Genetics Part B: Neuropsychiatric Genetics Published by Wiley Periodicals, Inc.     

Sleep disorders in Taiwanese children with attention deficit/hyperactivity disorder

To assess obstructive sleep apnea syndrome (OSAS) and periodic limb movement disorder (PLMD) in children with attention deficit/hyperactivity disorder (ADHD) compared with a control group. The ADHD was diagnosed based on Diagnostic and Statistical Manual, version IV (DSM-IV) criteria on successively seen elementary school children aged 6-12 years referred to a psychiatric clinic for suspected ADHD. A standardized interview (Kiddie-SADS-E), parents and teacher questionnaires, neuropsychological testing, and nocturnal polysomnography were completed for each child. Eighty-eight children (77 boys) with ADHD and 27 controls were involved in the study. Fifty children with ADHD (56.8%) had an apnea-hypopnea index (AHI) >1 event h(-1) and 17 (19.3%) had an AHI >5 event h(-1). Nine children (10.2%) had a periodic limb movement index (PLMI) >5 events h(-1). There is one child with AHI >1 and none with a PLMI > 5 in the control group. In the test of variables of attention (TOVA), the response time was significantly worse in ADHD with sleep disorders than those without them. The child behavior checklist (CBCL) showed a significant difference between groups in the hyperactivity subscale. The diagnostic criteria for ADHD based on DSM-IV do not differentiate between children with or without sleep disorders. Evaluation of sleep disorders should be considered before starting drug treatment for ADHD.     

Clinically significant symptom change in children with attention‐deficit/hyperactivity disorder: does it correspond with reliable improvement in functioning?

This study examined the relation between clinically significant (CS) change in symptoms of attention‐deficit/hyperactivity disorder (ADHD) and of oppositional defiant disorder (ODD), and reliable change in multiple domains of functioning in children who participated in the Multimodal Treatment Study of Children with ADHD. Children with CS change in symptoms were significantly more likely than children without CS change to have reliable change across five domains of functioning. Interestingly, however, depending on the measure of functioning, 14 to 52% of children who did not achieve CS change in symptoms showed reliable improvement in functional domains. The results have implications for the definition and measurement of CS change in child treatment‐outcome studies. © 2008 Wiley Periodicals, Inc. J Clin Psychol 65:1–18, 2009.     

Sleep in adults with attention deficit hyperactivity disorder (ADHD) before and during treatment with methylphenidate: a controlled polysomnographic study

STUDY OBJECTIVES: Sleep problems are frequently associated with childhood ADHD, as indicated by numerous polysomnographic investigations showing increased nocturnal movements, reduced sleep efficiency, and decreased percentage of REM sleep (although findings are not consistent over all studies). Data on objective and subjective sleep parameters in adults with ADHD are sparse, and to date the impact of stimulants, the most widely used pharmacological treatment for ADHD, on sleep in adults with ADHD has not been examined. Thus the objectives of our study were to assess objective and subjective sleep parameters in adults with ADHD and the impact of stimulant medication on sleep. DESIGN: Two-group comparison and open-label therapy study. PARTICIPANTS: We enrolled 34 nonmedicated patients with ADHD, of whom 24 were without current comorbid psychiatric disorders, and 34 sex- and gender-matched control subjects without current psychiatric disorders or psychotropic medication. INTERVENTIONS: Ten patients were treated with methylphenidate over > or =26 days with a mean daily dose of 36.7 +/- 11.2 mg. MEASUREMENTS: Polysomnographic recording over 2 consecutive nights as well as assessments of subjective sleep parameters were performed in all patients and controls before treatment and reassessed in those patients receiving methylphenidate. RESULTS: Compared to controls untreated patients showed increased nocturnal activity, reduced sleep efficiency, more nocturnal awakenings and reduced percentage of REM sleep. Treatment with methylphenidate resulted in increased sleep efficiency as well as a subjective feeling of improved restorative value of sleep. CONCLUSIONS: Sleep problems in patients with ADHD continue from childhood to adulthood, with similar objective sleep characteristics in adults and children with ADHD. Medication with methylphenidate appears to have beneficial effects on sleep parameters in adults with ADHD.     

Linkage studies between attention‐deficit hyperactivity disorder and the monoamine oxidase genes

Attention‐deficit hyperactivity disorder (ADHD) is a prevalent behavioral disorder in children and the etiology of this disorder is not clear. Molecular genetic and pharmacological studies suggest the involvement of dopaminergic and noradrenergic neurotransmitter systems in ADHD, e.g., several reports have found association between ADHD and the dopamine receptor gene DRD‐4, the dopamine transporter gene DAT1, and the catecholamine clearance enzyme catechol‐O‐methyltransferase. Monoamine oxidase (MAO) A and B genes encode enzymes that participate in the metabolism of neurotransmitters of the dopaminergic and noradrenergic systems. MAO inhibitors have been shown to be effective in the treatment of ADHD. Our previous studies showed an association between ADHD and the DXS7 locus, which is located in close vicinity to the MAO genes on chromosome X. These findings suggest that there might be linkage between ADHD and MAO genes. To test this hypothesis, we used the transmission/disequilibrium test (TDT) to test for linkage between a VNTR polymorphism at the MAOA(CA)_n or MAOB(GT)_n locus and DSM‐III‐R–diagnosed ADHD in 82 nuclear families of the Chinese population. The TDT analysis revealed linkage between ADHD and the MAOA(CA)_n locus (chi‐square = 15.25, df = 7, P < 0.05), but not the MAOB(GT)_n locus (chi‐square = 11.18, df = 7, P > 0.05). The data showed that ADHD was in linkage with the MAOA gene and suggested that MAOA might be a susceptibility factor for ADHD. © 2001 Wiley‐Liss, Inc.     

Methylphenidate enhances prepulse inhibition during processing of task‐relevant stimuli in attention‐deficit/hyperactivity disorder

ADHD is characterized by inattention, hyperactivity, and disinhibition, including the inability to screen out distracting stimuli. Prepulse inhibition (PPI) of startle indexes a related gating process and is enhanced during attended compared to ignored stimuli. We predicted that PPI during attended stimuli would be enhanced by the stimulant methylphenidate (MPH) and that this effect would be moderated by baseline PPI. Children with ADHD (n=36) completed a baseline day and a randomized, double‐blind medication trial (placebo vs. sustained release MPH). Bilateral startle eyeblink EMG was measured during a tone discrimination task. MPH enhanced PPI during attended, but not during ignored stimuli. Extending findings that pretreatment functioning moderates stimulant effects on PPI, this effect tended to be inversely related to baseline PPI. These data fit with the clinical literature on ADHD and the hypothesis that MPH enhances interference control for important environmental stimuli.     

The dopaminergic system in attention deficit/hyperactivity disorder

ABSTRACT  Numerous studies have shown the importance of the mesocorticolimbic dopamine system in the pathophysiology of attention deficit/hyperactivity disorder. However, there has been inconsistency in the findings of those studies. Varied and sometimes contradictory interpretation has been made on the basis of similar results. It is, therefore, still unclear whether the dopaminergic system is hypo- or hyperfunctioning in attention deficit/hyperactivity disorder. The majority of the functional brain imaging studies in both clinical and experimental settings support hypofunction of the basal ganglia which receive abundant dopaminergic afferent. The experimental studies, using dopamine-depleted animals, also support the hypodopaminergic hypothesis, whereas recent studies with the dopamine transporter knockout/knockdown mouse suggest hyperdopaminergic function as the underlying abnormality. In this review we attempt to clarify the issues raised by previous neuroimaging and functional neuroimaging studies. Research involving animal models with genetic traits, genetic manipulation or with brain lesions is analysed, concentrating on the significance of the dopaminergic system in the abnormal behavior of attention deficit/hyperactivity disorder. In addition, the functional state of the dopaminergic system is considered through the speculated mechanism of psychostimulant therapy of the disorder. No final conclusions have been reached regarding the pathological, biochemical and physiological mechanisms responsible for various symptoms. Inconsistency in the findings and their interpretations may indicate the heterogeneity of the pathogenesis of this syndrome.     

哌甲酯控释剂治疗对注意缺陷多动障碍儿童父母压力的影响

目的:探讨哌甲酯控释剂(OROS-MPH)治疗对注意缺陷多动障碍(attention deficit hyper-activity disorder,ADHD)患者临床症状和父母压力的影响。方法:采用自身对照研究设计,对符合美国精神障碍诊断与统计手册第四版(Diagnostic and Statistical Manual of Mental Disorders-Fourth Edition,DSM-IV)诊断标准的73名ADHD患者(年龄6~15岁),使用哌甲酯控释剂(18~54mg/d)治疗8周。以父母填写的IOWA Conners量表及研究者填写的ADHD症状评定问卷评估患者的临床症状,并作为主要临床疗效评价指标,以父母填写的父母压力指数量表(Parenting Stress Index,PSI)来评估父母的压力,分别在基线、治疗4周末和8周末用以上问卷进行评估。结果:66名ADHD患儿完成了8周的治疗。经哌甲酯控释剂治疗后,ADHD患者IOWA Conners量表中的注意缺陷/多动因子分、对立/违抗因子分和总分随治疗时间下降(均P<0.001);ADHD症状评定问卷的注意缺陷因子分、多动冲动因子分和总分较服药前下降(均P<0.001);PSI量表的压力总分随时间明显下降(P<0.01),PSI量表中儿童方面分量表中,适应性、父母的接受度、要求、心境、注意不能/多动、父母的强制性6个因子得分均随着时间下降(均P<0.01);在父母方面分量表中,抑郁、角色的限制、配偶关系、孤独、健康状况5个因子得分均随着时间显著下降(均P<0.01)。基线时PSI总分与IOWA Conners量表总分、ADHD症状评定问卷总分呈正相关(r=0.346~0.902,均P<0.01)。结论:哌甲酯控释剂治疗能有效改善ADHD患者的临床症状和改善患者及其父母的压力,提高社会功能。     

The role of glutamate receptors in attention‐deficit/hyperactivity disorder: From physiology to disease

Attention‐deficit hyperactivity disorder (ADHD) is the most common psychiatric disorder in children and adolescents, which is characterized by behavioral problems such as attention deficit, hyperactivity, and impulsivity. As the receptors of the major excitatory neurotransmitter in the mammalian central nervous system (CNS), glutamate receptors (GluRs) are strongly linked to normal brain functioning and pathological processes. Extensive investigations have been made about the structure, function, and regulation of GluR family, describing evidences that support the disruption of these mechanisms in mental disorders, including ADHD. In this review, we briefly described the family and function of GluRs in the CNS, and discussed what is recently known about the role of GluRs in ADHD, that including GluR genes, animal models, and the treatment, which would help us further elucidate the etiology of ADHD.     

Parent reports of sleep disturbances in stimulant-medicated children with attention-deficit hyperactivity disorder

In a study of the severity of sleep disturbances in children with attention-deficit hyperactivity disorder (ADHD) who are taking stimulant medication, parents of 20 children diagnosed as having ADHD and on medication, 20 unmedicated children with some other psychiatric diagnosis (OPD), and 20 nonclinical control children responded to a 40-question structured interview to report the frequency of their children's sleep disturbances occurring during a 1-month interval. Parents of children in the ADHD group reported significantly more problems than parents of children in the other groups on variables within all three categories of behaviors: (a) settling and going to sleep, (b) disruptions during sleep, and (c) morning activities. From 25% to 50% of these parents reported very frequent difficulties in their children settling and going to sleep. These findings indicate that monitoring sleep-related behaviors and providing adjunctive therapies for sleep-related disturbances would be beneficial for many families with ADHD children who are taking stimulant medication. © 1998 John Wiley & Sons, Inc. J Clin Psychol 54: 701–716, 1998.