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Attention deficit hyperactivity disorder (ADHD) and autism spectrum disorder (ASD) in adults are often undiagnosed and overlap in psychopathology. Here we investigated the transdiagnostic traits of emotion recognition and mind wandering in a sample of 103 adults (43 with ADHD and 14 with ASD). The ability to correctly identify a facial expression of anger, fear, disgust or surprise was no different between the adults with ADHD or ASD and neurotypical (NT) adults. However, adults with ADHD or ASD were on average almost 200 ms slower in making a correct decision, suggesting a larger speed-accuracy trade-off in facial emotion recognition compared to NT adults. General processing speed was associated with excessive mind wandering in adults with ADHD, but not with ASD. The deficits in emotional processing were independent from mind wandering in both adults with ADHD or ASD. Emotional dysregulation and functional impairment scales separated adults with ADHD and ASD from the NT adults, but not from each other. When controlling for self-reported ADHD and ASD symptom severity, mind wandering in ADHD was independent from both ADHD and ASD symptom severity. In ASD, mind wandering was related to ASD but not ADHD symptom severity. Our results suggest that ASD and ADHD share a slower ability to recognize emotions, which is exacerbated by excessive mind wandering in ADHD, and by decreased processing speed in ASD.

Background. Adults with attention deficit hyperactivity disorder (ADHD) frequently suffer from sleep problems and report high levels of daytime sleepiness compared to neurotypical controls, which has detrimental effect on quality of life. Methods. We evaluated daytime sleepiness in adults with ADHD compared to neurotypical controls using an observer-rated sleepiness protocol during the Sustained Attention Response Task as well as electroencephalogram (EEG) slowing, a quantitative electroencephalographic measure collected during a short period of wakeful rest. Results. We found that adults with ADHD were significantly sleepier than neurotypical controls during the cognitive task and that this on-task sleepiness contributed to cognitive performance deficits usually attributed to symptoms of ADHD. EEG slowing predicted severity of ADHD symptoms and diagnostic status, and was also related to daytime sleepiness. Frontal EEG slowing as well as increased frontal delta were especially prominent in adults with ADHD. We have validated and adapted an objective observer-rated measure for assessing on-task sleepiness that will contribute to future sleep research in psychology and psychiatry. Conclusions. These findings indicate that the cognitive performance deficits routinely attributed to ADHD and often conceptualized as cognitive endophenotypes of ADHD are largely due to on-task sleepiness and not exclusively due to ADHD symptom severity. Daytime sleepiness plays a major role in cognitive functioning of adults with ADHD.

Background. We investigated whether adults with attention-deficit/hyperactivity disorder (ADHD) show pseudoneglect—preferential allocation of attention to the left visual field (LVF) and a resulting slowing of mean reaction times (MRTs) in the right visual field (RVF), characteristic of neurotypical (NT) individuals —and whether lateralization of attention is modulated by presentation speed and incentives. Method. Fast Task, a four-choice reaction-time task where stimuli were presented in LVF or RVF, was used to investigate differences in MRT and reaction time variability (RTV) in adults with ADHD (n = 43) and NT adults (n = 46) between a slow/no-incentive and fast/incentive condition. In the lateralization analyses, pseudoneglect was assessed based on MRT, which was calculated separately for the LVF and RVF for each condition and each study participant. Results. Adults with ADHD had overall slower MRT and increased RTV relative to NT. MRT and RTV improved under the fast/incentive condition. Both groups showed RVF-slowing with no between-group or between-conditions differences in RVF-slowing. Conclusion. Adults with ADHD exhibited pseudoneglect, a NT pattern of lateralization of attention, which was not attenuated by presentation speed and incentives.

Mind wandering, emotional lability and sleep quality are currently mostly independently investigated but are all interlinked and play a major role is adult attention-deficit/ hyperactivity disorder (ADHD). Emotional lability is a core feature of the disorder, excessive mind wandering has recently been linked to symptoms and impairments of ADHD and poor sleep quality is experienced by a clear majority of adults with ADHD. All three phenomena lead to functional impairment in ADHD, however their relationship to each other and to ADHD symptom severity is not well understood. Here we used serial multiple mediation models to examine the influence of mind wandering, sleep quality and emotional lability on ADHD symptom severity. 81 adults diagnosed with ADHD participated in this study. We found that mind wandering and emotional lability predicted ADHD symptom severity and that mind wandering, emotional lability and sleep quality were all linked and significantly contributed to the symptomatology of adult ADHD. Mind wandering was found to lead to emotional lability which in turn lead to ADHD symptom severity; and poor sleep quality was found to exacerbate mind wandering leading to ADHD symptoms. Future research should employ objective on-task measures of mind wandering, sleepiness and emotional lability to investigate the neural basis of these impairing deficits in ADHD.

BackgroundRecent studies point to overlap between neuropsychiatric disorders in symptomatology and genetic aetiology.AimsTo systematically investigate genomics overlap between childhood and adult attention-deficit hyperactivity disorder (ADHD), autism spectrum disorder (ASD) and major depressive disorder (MDD).MethodAnalysis of whole-genome blood gene expression and genetic risk scores of 318 individuals. Participants included individuals affected with adult ADHD (n = 93), childhood ADHD (n = 17), MDD (n = 63), ASD (n = 51), childhood dual diagnosis of ADHD–ASD (n = 16) and healthy controls (n = 78).ResultsWeighted gene co-expression analysis results reveal disorder-specific signatures for childhood ADHD and MDD, and also highlight two immune-related gene co-expression modules correlating inversely with MDD and adult ADHD disease status. We find no significant relationship between polygenic risk scores and gene expression signatures.ConclusionsOur results reveal disorder overlap and specificity at the genetic and gene expression level. They suggest new pathways contributing to distinct pathophysiology in psychiatric disorders and shed light on potential shared genomic risk factors.

Autism spectrum disorder (ASD) is a neurodevelopmental condition with multiple causes, comorbid conditions, and a wide range in the type and severity of symptoms expressed by different individuals. This makes the neuroanatomy of autism inherently difficult to describe. Here, we demonstrate how a multiparameter classification approach can be used to characterize the complex and subtle structural pattern of gray matter anatomy implicated in adults with ASD, and to reveal spatially distributed patterns of discriminating regions for a variety of parameters describing brain anatomy. A set of five morphological parameters including volumetric and geometric features at each spatial location on the cortical surface was used to discriminate between people with ASD and controls using a support vector machine (SVM) analytic approach, and to find a spatially distributed pattern of regions with maximal classification weights. On the basis of these patterns, SVM was able to identify individuals with ASD at a sensitivity and specificity of up to 90% and 80%, respectively. However, the ability of individual cortical features to discriminate between groups was highly variable, and the discriminating patterns of regions varied across parameters. The classification was specific to ASD rather than neurodevelopmental conditions in general (e.g., attention deficit hyperactivity disorder). Our results confirm the hypothesis that the neuroanatomy of autism is truly multidimensional, and affects multiple and most likely independent cortical features. The spatial patterns detected using SVM may help further exploration of the specific genetic and neuropathological underpinnings of ASD, and provide new insights into the most likely multifactorial etiology of the condition.

BACKGROUND Attention-deficit hyperactivity disorder (ADHD) is increasingly recognised as occurring in people with intellectual disability (ID), although treatment of ADHD in this population has not been tested widely. Amfetamine has been used to treat ADHD in people with and without ID, although the evidence for its efficacy in people with ID is unclear. OBJECTIVES To examine the effectiveness of amfetamine for the treatment of attention deficit hyperactivity disorder in people with intellectual disabilities. SEARCH STRATEGY MEDLINE, PsycINFO, EMBASE, AMED, ISI Web of Science and WorldCat Dissertations were searched using an extensive list of synonyms for ADHD and ID. CENTRAL, Current Controlled Trials meta-register (mRCT), CenterWatch, NHS National Research Register, clinicaltrials.gov were searched in August 2007. Pharmaceutical companies and experts in the field were contacted. Reference lists of review articles were examined and citation searches were performed in ISI Web of Knowledge. SELECTION CRITERIA All randomised controlled studies, both published and unpublished, in any language, in which children or adults with ADHD and ID were treated with amfetamine. DATA COLLECTION AND ANALYSIS Data were extracted independently by two reviewers using a standardised extraction sheet. Risk of bias was assessed by two authors using a standardised framework. Meta-analyses were planned but were not performed due to a lack of suitable studies. MAIN RESULTS Only one study was suitable for inclusion. This was a cross-over study in 15 children with ADHD, ID and Fragile X syndrome. Duration of treatment was only one week. No significant difference was reported between amfetamine and placebo for any of the ADHD measures, but significantly more side effects were reported while taking amfetamine, mainly mood lability and irritability. AUTHORS' CONCLUSIONS There is very little evidence for the effectiveness of amfetamine for ADHD in people with ID . Prescribing in this population is based on extrapolation of research in people without ID. More research into effectiveness and tolerability is urgently needed.

BACKGROUND: Attention‐deficit hyperactivity disorder (ADHD) is increasingly recognised as occurring in people with intellectual disability (ID), although treatment of ADHD in this population has not been tested widely. Amfetamine has been used to treat ADHD in people with and without ID, although the evidence for its efficacy in people with ID is unclear. OBJECTIVES: To examine the effectiveness of amfetamine for the treatment of attention deficit hyperactivity disorder in people with intellectual disabilities. SEARCH METHODS: MEDLINE, PsycINFO, EMBASE, AMED, ISI Web of Science and WorldCat Dissertations were searched using an extensive list of synonyms for ADHD and ID. CENTRAL, Current Controlled Trials meta‐register (mRCT), CenterWatch, NHS National Research Register, clinicaltrials.gov were searched in August 2007. Pharmaceutical companies and experts in the field were contacted. Reference lists of review articles were examined and citation searches were performed in ISI Web of Knowledge. SELECTION CRITERIA: All randomised controlled studies, both published and unpublished, in any language, in which children or adults with ADHD and ID were treated with amfetamine. DATA COLLECTION AND ANALYSIS: Data were extracted independently by two reviewers using a standardised extraction sheet. Risk of bias was assessed by two authors using a standardised framework. Meta‐analyses were planned but were not performed due to a lack of suitable studies. MAIN RESULTS: Only one study was suitable for inclusion. This was a cross‐over study in 15 children with ADHD, ID and Fragile X syndrome. Duration of treatment was only one week. No significant difference was reported between amfetamine and placebo for any of the ADHD measures, but significantly more side effects were reported while taking amfetamine, mainly mood lability and irritability. AUTHORS' CONCLUSIONS: There is very little evidence for the effectiveness of amfetamine for ADHD in people with ID . Prescribing in this population is based on extrapolation of research in people without ID. More research into effectiveness and tolerability is urgently needed.

Background ADHD is a common childhood onset mental health disorder that persists into adulthood in two-thirds of cases. One of the most prevalent and impairing comorbidities of ADHD in adults are substance use disorders. We estimate rates of ADHD in patients with substance abuse disorders and delineate impairment in the co-morbid group. Method Screening for ADHD followed by a research diagnostic interview in people attending in-patient drug and alcohol detoxification units. Results We estimated prevalence of undiagnosed ADHD within substance use disorder in-patients in South London around 12%. Those individuals with substance use disorders and ADHD had significantly higher self-rated impairments across several domains of daily life; and higher rates of substance abuse and alcohol consumption, suicide attempts, and depression recorded in their case records. Conclusions This study demonstrates the high rates of untreated ADHD within substance use disorder populations and the association of ADHD in such patients with greater levels of impairment. These are likely to be a source of additional impairment to patients and represent an increased burden on clinical services.