Cognitive and behavioral performance in children with epilepsy with myoclonic-atonic seizures.

Background Attention-Deficit/Hyperactivity Disorder (ADHD) is the most common neurodevelopmental disorder in children (Polanczyk, Willcutt, Salum, Kieling, & Rohde, 2014) and is highly comorbid with Autism Spectrum Disorder (ASD) (Green et al., 2015; Kotte et al., 2013). Although it is well established that children with ADHD or ASD and their families experience poorer functioning including child and parent mental health problems, child peer problems, poorer family quality of life (FQoL) and parenting difficulties, it is unknown how comorbid ASD symptoms contribute to child and family functioning in children with ADHD. It is important to understand which comorbidities contribute to poorer child and family functioning to guide treatment planning. Aims This study aimed to examine the prevalence of ASD symptoms in children with ADHD and the association between ASD symptoms and child and family functioning across three connected studies. The specific aims of each study are outlined below. Study 1. To examine the prevalence and type of ASD symptoms (social interaction, communication and stereotyped behaviour) in children with ADHD and non-ADHD controls. Within the ADHD group only, we also examined the relationship between ADHD subtype, hyperactive/impulsive and inattentive symptoms, ADHD symptom severity and child gender and ASD symptom severity. Study 2. To examine the association between ASD symptoms and (a) social functioning; (b) mental health; (c) quality of life and (d) sleep, in children with and without ADHD. Study 3. To examine the association between ASD symptoms (measured dimensionally) in children with and without ADHD and a broad range of family functioning variables and to examine differences between ADHD+ASD, ADHD and control groups on family functioning variables. Methods Participants were 6-10 year old children (164 ADHD; 198 non-ADHD control) attending 43 schools in Melbourne, Australia, who were participating in the Children’s Attention Project. ADHD was assessed in two stages using the parent and teacher Conners’ 3 ADHD index and the Diagnostic Interview Schedule for Children IV (DISC-IV). ASD symptoms were identified using the Social Communication Questionnaire (SCQ). Child functioning measures were social functioning (Strengths and Difficulties Questionnaire (SDQ), mental health (DISC-IV, SDQ), quality of life (QoL: Pediatric Quality of Life Inventory 4.0) and sleep problem severity. Family functioning outcome variables were parent mental health, family quality of life (FQoL), and scales assessing couple conflict, couple support and parenting behaviours. Unadjusted and adjusted linear and logistic regression examined continuous and categorical outcomes, respectively. Results Study 1. Children with ADHD had more ASD symptoms than non-ADHD controls (adjusted mean difference = 4.0, 95% confidence interval (CI) 2.8; 5.3, p < 0.001, effect size = 0.7). Boys with ADHD had greater ASD symptom severity than girls with ADHD (adjusted mean difference = 2.9, 95% CI 0.8; 5.2, p = 0.01, effect size = 0.4). Greater ADHD symptom severity was associated with greater ASD symptom severity (regression co-efficient = 1.6, 95% CI 1.2; 2.0, p < 0.001). No differences were observed by ADHD subtype. Greater hyperactive/impulsive symptoms were associated with greater ASD symptoms (regression coefficient = 1.0; 95% CI 0.0; 2.0, p = 0.04) however, this finding attenuated in adjusted analyses, which accounted for parent educational attainment, socioeconomic status, child internalising and externalising comorbidities (p = 0.45). Study 2. Each standard deviation (SD) increase in SCQ scores was associated with a 6.7 unit reduction in QoL (p < 0.001) and greater parent and teacher-reported peer problems, emotional and conduct problems. For every SD increase in SCQ scores, internalising (OR = 1.8, 95% CI 1.3, 2.6, p = 0.001) and externalising disorders (OR = 1.5, 95% CI 1.1, 2.1, p = 0.02) increased, as did moderate/severe sleep problems (OR = 1.5, 95% CI 1.0, 2.2, p = 0.04). Most findings held in analyses adjusting for socio-demographic factors, ADHD symptom severity, and comorbidities (when not the outcome), with the exception of externalising disorders and sleep problems. Study 3. In unadjusted dimensional analyses, higher ASD symptoms were associated with more couple conflict (p = 0.04) and poorer FQoL for all subscales (p ≤ 0.001), with non-significant trends for less couple support (R2 = 0.10, p = 0.06), more hostile parenting (R2 = 0.02, p = 0.06) and poorer parent mental health (R2 = 0.02, p = 0.07). In adjusted dimensional analyses, higher ASD symptoms were only associated with poorer FQoL, across all subscales only (p ≤ 0.01). The trend association between ASD symptoms and parent mental health attenuated due to meaningful associations with comorbid internalising disorder (p = 0.003) and ADHD symptom severity (p = 0.05). The trend association between ASD symptoms and hostile parenting attenuated due to significant associations with comorbid externalising disorders (p = 0.002), lower parent education attainment (p = 0.03) and greater ADHD symptom severity (p = 0.04). Less couple support attenuated due to a significant association with socioeconomic status (p = 0.004). In unadjusted categorical analyses, parents of children with ADHD+ASD reported more couple conflict (p = 0.04), less couple support (p = 0.001), poorer FQoL (p <0.001) and a non-significant trend for greater mental health difficulties (p = 0.07), compared to the ADHD group. In adjusted categorical analyses, parents of children with ADHD+ASD had poorer parent self-efficacy (p = 0.02), poorer FQoL (p < 0.05) (p < 0.05) and a non-significant trend for less couple support (p = 0.06), compared to parents of children with ADHD. In unadjusted categorical analyses, family functioning was significantly poorer for the ADHD and ADHD+ASD groups, compared to controls for most outcomes (p <0.001). In adjusted categorical analyses, all findings attenuated except FQoL was significantly poorer for the ADHD and ADHD+ASD groups, compared to controls. Conclusion ASD symptoms are common, and associated with poorer functioning in children with ADHD. It is important for clinicians working with children with ADHD to identify and manage ASD symptoms, given that they exacerbate functional impairments in this already vulnerable group. The relationship between ASD symptoms and broader family functioning appears to be largely driven by internalising and externalising disorders, ADHD severity, and socioeconomic status. Poorer FQoL appears to be independently associated with ASD symptoms in children with ADHD.

P03-30 Do ADHD and autism symptoms predict specific OC symptom dimensions or OC symptom severity in OCD?

Attention deficit hyperactivity disorder (ADHD) symptoms persist significantly into adulthood; however, only a few studies have examined the overlap between ADHD and autism spectrum disorder (ASD) symptoms in adults. This study compared ASD symptoms in adults with ASD, ADHD, and neurotypical controls using the Autism Diagnostic Observation Schedule, Second Edition (ADOS-2). In total, 150 adults (69 with ADHD [mean age, 34.5 years; 43 men], 50 with ASD [mean age, 33.8 years; 35 men], and 31 controls [mean age, 38.7 years; 17 men]) completed Module 4 of the ADOS-2, the Autism Spectrum Quotient, Conners' Adult ADHD Rating Scale, and the Wechsler Adult Intelligence Scale. Consistent with juvenile studies, adults with ADHD exhibited significant ASD symptoms, which were between those with ASD and neurotypical individuals. Item-level analysis suggested more similarities than differences between the two disorders; the differences may be of degree rather than quality. This study shows the importance of assessing full ASD symptoms in adults with ADHD.

BackgroundAutism spectrum disorder (ASD) traits are continuously distributed throughout the population, and ASD symptoms are also frequently observed in patients with attention-deficit/hyperactivity disorder (ADHD). Both ASD and ADHD have been linked to alterations in reward-related neural processing. However, whether both symptom domains interact and/or have distinct effects on reward processing in healthy and ADHD populations is currently unknown.MethodsWe examined how variance in ASD and ADHD symptoms in individuals with ADHD and healthy participants was related to the behavioural and neural response to reward during a monetary incentive delay (MID) task. Participants (mean age: 17.7 years, range: 10–28 years) from the NeuroIMAGE study with a confirmed diagnosis of ADHD (n = 136), their unaffected siblings (n = 83), as well as healthy controls (n = 105) performed an MID task in a magnetic resonance imaging (MRI) scanner. ASD and ADHD symptom scores were used as predictors of the neural response to reward anticipation and reward receipt. Behavioural responses were modeled using linear mixed models; neural responses were analysed using FMRIB’s Software Library (FSL) proprietary mixed effects analysis (FLAMEO).ResultsASD and ADHD symptoms were associated with alterations in BOLD activity during reward anticipation, but not reward receipt. Specifically, ASD scores were related to increased insular activity during reward anticipation across the sample. No interaction was found between this effect and the presence of ADHD, suggesting that ASD symptoms had no differential effect in ADHD and healthy populations. ADHD symptom scores were associated with reduced dorsolateral prefrontal activity during reward anticipation. No interactions were found between the effects of ASD and ADHD symptoms on reward processing.ConclusionsVariance in ASD and ADHD symptoms separately influence neural processing during reward anticipation in both individuals with (an increased risk of) ADHD and healthy participants. Our findings therefore suggest that both symptom domains affect reward processing through distinct mechanisms, underscoring the importance of multidimensional and multimodal assessment in psychiatry.Electronic supplementary materialThe online version of this article (doi:10.1186/s13229-015-0043-y) contains supplementary material, which is available to authorized users.

Dementia is characterized by a progressive cognitive decline that could be caused by several disorders. Autism spectrum disorder (ASD) and attention deficit hyperactivity disorder (ADHD) are two prevalent neurodevelopmental disorders that might overlap with dementia symptoms. Hence, this study aimed to evaluate the ASD and ADHD symptoms in dementia patients referred to a memory clinic in Iran. We recruited 65 dementia patients and instructed them to fill out the autism quotient (AQ) and the Conners’ Adult ADHD Rating Scales (CAARS) questionnaires. Considering the cutoff points of AQ and CAARS questionnaires, 18.5% of participants were at higher risk of ASD, and 35.4% were at higher risk of ADHD. The results indicated that ADHD and ASD symptoms might be common comorbidities in patients with dementia which can increase the disease burden. Specialized ADHD and ASD screening tools in the elderly population with dementia are needed to prevent misdiagnoses due to symptom overlaps.

Autism spectrum disorder (ASD) symptoms frequently occur in subjects with attention deficit/hyperactivity disorder (ADHD). While there is evidence that both ADHD and ASD have differential structural correlates, no study to date has investigated these structural correlates within a framework that robustly accounts for the phenotypic overlap between the two disorders. The presence of ASD symptoms was measured by the parent-reported Children’s Social and Behavioural Questionnaire (CSBQ) in ADHD subjects (n = 180), their unaffected siblings (n = 118) and healthy controls (n = 146). ADHD symptoms were assessed by a structured interview (K-SADS-PL) and the Conners’ ADHD questionnaires. Whole brain T1-weighted MPRAGE images were acquired and the structural MRI correlates of ASD symptom scores were analysed by modelling ASD symptom scores against white matter (WM) and grey matter (GM) volumes using mixed effects models which controlled for ADHD symptom levels. ASD symptoms were significantly elevated in ADHD subjects relative to both controls and unaffected siblings. ASD scores were predicted by the interaction between WM and GM volumes. Increasing ASD score was associated with greater GM volume. Equivocal results from previous structural studies in ADHD and ASD may be due to the fact that comorbidity has not been taken into account in studies to date. The current findings stress the need to account for issues of ASD comorbidity in ADHD.

BackgroundChildren with autism spectrum disorder (ASD) often have co‐occurring symptoms of attention‐deficit/hyperactivity disorder (ADHD) and/or anxiety. It is unclear whether these disorders arise from shared or distinct developmental pathways. We explored this question by testing the specificity of early‐life (infant and toddler) predictors of mid‐childhood ADHD and anxiety symptoms compared to ASD symptoms.MethodsInfants (n = 104) at high and low familial risk for ASD took part in research assessments at 7, 14, 24 and 38 months, and 7 years of age. Symptoms of ASD, ADHD and anxiety were measured by parent report at age 7. Activity levels and inhibitory control, also measured by parent report, in infancy and toddlerhood were used as early‐life predictors of ADHD symptoms. Fearfulness and shyness measured in infancy and toddlerhood were used as early‐life predictors of anxiety symptoms. Correlations and path analysis models tested associations between early‐life predictors and mid‐childhood ADHD and anxiety symptoms compared to mid‐childhood ASD symptoms, and the influence of controlling for ASD symptoms on those associations.ResultsIncreased activity levels and poor inhibitory control were correlated with ADHD symptoms and not ASD or anxiety; these associations were unchanged in path models controlling for risk‐group and ASD symptoms. Increased fearfulness and shyness were correlated with anxiety symptoms, but also ASD symptoms. When controlling for risk‐group in path analysis, the association between shyness and anxiety became nonsignificant, and when further controlling for ASD symptoms the association between fearfulness and anxiety became marginal.ConclusionsThe specificity of early‐life predictors to ADHD symptoms suggests early developmental pathways to ADHD might be distinct from ASD. The overlap in early‐life predictors of anxiety and ASD suggests that these disorders are difficult to differentiate early in life, which could reflect the presence of common developmental pathways or convergence in early behavioural manifestations of these disorders.

Autism spectrum disorder symptoms in children with ADHD: A community-based study

Difficulties in neurocognition and social interaction are the most prominent causes of morbidity and long-term disability in children with neurofibromatosis type 1 (NF1). Symptoms of attention-deficit-hyperactivity disorder (ADHD) have also been extensively recognized in NF1. However, systematic evaluation of symptoms of autism spectrum disorder (ASD) in children with NF1 has been limited. We present a retrospective, cross-sectional study of the prevalence of symptoms of ASD and ADHD and their relationship in a consecutive series of 66 patients from our NF1 clinic. The Social Responsiveness Scale and the Vanderbilt ADHD Diagnostic Parent Rating Scale were used to assess symptoms of ASD and ADHD. Sixty-six participants (42 males, 24 females) were included in this study. Mean age at assessment was 10 years 11 months (SD 5 y 4 mo). Forty percent of our NF1 sample had raised symptom levels reaching clinical significance on the Social Responsiveness Scale (T ≥ 60), and 14% reached levels consistent with those seen in children with ASDs (T ≥ 75). These raised levels were not explained by NF1 disease severity or externalizing/internalizing behavioral disorders. There was a statistically significant relationship between symptoms of ADHD and ASD (χ(2) =9.11, df=1, p=0.003, φ=0.56). Particularly salient were the relationships between attention and hyperactivity deficits, with impairments in social awareness and social motivation. We found that symptoms of ASD in our NF1 population were raised, consistent with previous reports. Further characterization of the specific ASD symptoms and their impact on daily function is fundamental to the development and implementation of effective interventions in this population, which will probably include a combination of medical and behavioral approaches.

Background:Young people living with 22q11.2 Deletion Syndrome (22q11.2DS) are at increased risk of schizophrenia, intellectual disability, attention-deficit hyperactivity disorder (ADHD) and autism spectrum disorder (ASD). In common with these conditions, 22q11.2DS is also associated with sleep problems. We investigated whether abnormal sleep or sleep-dependent network activity in 22q11.2DS reflects convergent, early signatures of neural circuit disruption also evident in associated neurodevelopmental conditions.Methods:In a cross-sectional design, we recorded high-density sleep EEG in young people (6–20 years) with 22q11.2DS (n=28) and their unaffected siblings (n=17), quantifying associations between sleep architecture, EEG oscillations (spindles and slow waves) and psychiatric symptoms. We also measured performance on a memory task before and after sleep.Results:22q11.2DS was associated with significant alterations in sleep architecture, including a greater proportion of N3 sleep and lower proportions of N1 and REM sleep than in siblings. During sleep, deletion carriers showed broadband increases in EEG power with increased slow-wave and spindle amplitudes, increased spindle frequency and density, and stronger coupling between spindles and slow-waves. Spindle and slow-wave amplitudes correlated positively with overnight memory in controls, but negatively in 22q11.2DS. Mediation analyses indicated that genotype effects on anxiety, ADHD and ASD were partially mediated by sleep EEG measures.Conclusions:This study provides a detailed description of sleep neurophysiology in 22q11.2DS, highlighting alterations in EEG signatures of sleep which have been previously linked to neurodevelopment, some of which were associated with psychiatric symptoms. Sleep EEG features may therefore reflect delayed or compromised neurodevelopmental processes in 22q11.2DS, which could inform our understanding of the neurobiology of this condition and be biomarkers for neuropsychiatric disorders.Funding:This research was funded by a Lilly Innovation Fellowship Award (UB), the National Institute of Mental Health (NIMH 5UO1MH101724; MvdB), a Wellcome Trust Institutional Strategic Support Fund (ISSF) award (MvdB), the Waterloo Foundation (918-1234; MvdB), the Baily Thomas Charitable Fund (2315/1; MvdB), MRC grant Intellectual Disability and Mental Health: Assessing Genomic Impact on Neurodevelopment (IMAGINE) (MR/L011166/1; JH, MvdB and MO), MRC grant Intellectual Disability and Mental Health: Assessing Genomic Impact on Neurodevelopment 2 (IMAGINE-2) (MR/T033045/1; MvdB, JH and MO); Wellcome Trust Strategic Award ‘Defining Endophenotypes From Integrated Neurosciences’ Wellcome Trust (100202/Z/12/Z MO, JH). NAD was supported by a National Institute for Health Research Academic Clinical Fellowship in Mental Health and MWJ by a Wellcome Trust Senior Research Fellowship in Basic Biomedical Science (202810/Z/16/Z). CE and HAM were supported by Medical Research Council Doctoral Training Grants (C.B.E. 1644194, H.A.M MR/K501347/1). HMM and UB were employed by Eli Lilly & Co during the study; HMM is currently an employee of Boehringer Ingelheim Pharma GmbH & Co KG. The views and opinions expressed are those of the author(s), and not necessarily those of the NHS, the NIHR or the Department of Health funders.

Links Between Autism Spectrum Disorder and ADHD Symptom Trajectories: Important Findings and Unanswered Questions

Functional Connectivity of Frontoparietal and Salience/Ventral Attention Networks Have Independent Associations With Co-occurring Attention-Deficit/Hyperactivity Disorder Symptoms in Children With Autism

Children with attention deficit/hyperactivity disorder (ADHD) combined with autism spectrum disorder (ASD) symptoms (ADHD + ASD) have poorer social and emotional functioning than those with ADHD alone. However, no studies have specifically examined the associations between ASD symptoms, measures of social and emotional functioning and limbic system white matter microstructure. Tractography on the cingulum, uncinate fasciculus and fornix were performed for 151 children with (N = 78) and without (N = 73) ADHD. Participants in the ADHD group who scored 11 or above on the Social Communication Questionnaire were classified as the ADHD + ASD group (N = 16). Significant differences in mean cingulum FA were present between the control group and the ADHD (all) group, however, no significant differences were seen between the ADHD and ADHD + ASD groups. Despite this, significant associations were seen between mean FA of the left cingulum and emotional problems for the ADHD + ASD group. Results give greater insights into the specific biological basis of emotional problems in the ADHD + ASD group, indicating that the cingulum may play a role.

Autism spectrum disorder (ASD) symptoms are elevated in populations of children with attention-deficit/hyperactivity disorder (ADHD). This study examined cross-sectional associations between ASD symptoms and family functioning in children with and without ADHD. Participants were recruited to a longitudinal cohort study, aged 6-10years (164 ADHD; 198 controls). ADHD cases were ascertained using community-based screening and diagnostic confirmation from a diagnostic interview. ASD symptoms were measured using the Social Communication Questionnaire. Outcome variables were parent mental health, family quality of life (FQoL), couple conflict and support, and parenting behaviours. After adjustment for a range of child and family factors (including other mental health comorbidities), higher ASD symptoms were associated with poorer FQoL across all three domains; emotional impact (p=0.008), family impact (p=0.001) and time impact (p=0.003). In adjusted analyses by subgroup, parents of children with ADHD+ASD had poorer parent self-efficacy (p=0.01), poorer FQoL (p≤0.05), with weak evidence of an association for less couple support (p=0.06), compared to parents of children with ADHD only. Inspection of covariates in the adjusted analyses indicated that the association between ASD symptoms and most family functioning measures was accounted forby child internalising and externalising disorders, ADHD severity, and socioeconomic status; however, ASD symptoms appear to be independently associated with poorer FQoL in children with ADHD. The presence of ASD symptoms in children with ADHD may signal the need for enhanced family support.

BackgroundPartially driven by public concerns about modern food production practices, organic food has gained popularity among consumers. However, the impact of organic food consumption during pregnancy on offspring health is scarcely studied. We aimed to investigate the association between maternal intake of organic food during pregnancy and symptoms of attention deficit/hyperactivity disorder (ADHD) and autism spectrum disorder (ASD) in offspring at 8 years of age.MethodsThis study was based on the Norwegian Mother, Father and Child Cohort Study (MoBa) and the Medical Birth Registry of Norway (MBRN). The total study sample included 40,707 mother–child pairs (children born 2002–2009). Organic food consumption during pregnancy was assessed by six questions from a food frequency questionnaire in mid-pregnancy (sum score 0–18). Symptoms of ADHD and ASD in the offspring aged 8 years were measured by ADHD (0–54) and ASD (0–39) symptom scores based on the Parent/Teacher Rating Scale for Disruptive Behaviour disorders and the Social Communication Questionnaire. Associations between maternal intake of organic food during pregnancy and symptoms of ADHD and ASD in the offspring were analyzed using regression models with adjustment for covariates such as maternal anxiety and depression, including sibling analysis.ResultsMean ADHD and ASD symptom scores in the offspring differed only slightly by maternal intake of organic food. The covariate-adjusted unstandardized regression coefficient (adjusted(Adj)beta) with 95% confidence interval for the ADHD symptom score with one unit increase in organic food sum score was 0.03 (0.01, 0.05). Similarly, Adjbeta for autism symptom score was 0.07 (0.04, 0.10). For ADHD, the adjusted estimates weakened when adjusting for maternal symptoms of ADHD. The sibling analyses showed no significant results with Adjbeta − 0.07 (− 0.15, 0.01) and − 0.001 (− 0.12, 0.12) for ADHD and ASD outcomes, respectively.ConclusionsWe observed weak positive associations between frequent maternal organic food consumption during pregnancy and offspring ADHD and ASD symptom levels at 8 years of age. This trend weakened or disappeared after adjusting for maternal symptoms of ADHD, and in sibling analyses, suggesting that the associations mainly reflect genetic confounding. Our study indicates that consumption of organic food during pregnancy should neither be considered a risk factor nor protective against symptoms of ADHD and ASD in offspring.