The opposite end of the attention deficit hyperactivity disorder continuum: genetic and environmental aetiologies of extremely low ADHD traits.

BACKGROUND: Although attention deficit hyperactivity disorder (ADHD) is thought to reflect a continuously distributed quantitative trait, it is assessed through binary diagnosis or skewed measures biased towards its high, symptomatic extreme. A growing trend is to study the positive tail of normally distributed traits, a promising avenue, for example, to study high intelligence to increase power for gene-hunting for intelligence. However, the emergence of such a 'positive genetics' model has been tempered for ADHD due to poor phenotypic resolution at the low extreme. Overcoming this methodological limitation, we conduct the first study to assess the aetiologies of low extreme ADHD traits. METHODS: In a population-representative sample of 2,143 twins, the Strength and Weaknesses of ADHD Symptoms and Normal behaviour (SWAN) questionnaire was used to assess ADHD traits on a continuum from low to high. Aetiological influences on extreme ADHD traits were estimated using DeFries-Fulker extremes analysis. ADHD traits were related to behavioural, cognitive and home environmental outcomes using regression. RESULTS: Low extreme ADHD traits were significantly influenced by shared environmental factors (23-35%) but were not significantly heritable. In contrast, high-extreme ADHD traits showed significant heritability (39-51%) but no shared environmental influences. Compared to individuals with high extreme or with average levels of ADHD traits, individuals with low extreme ADHD traits showed fewer internalizing and externalizing behaviour problems, better cognitive performance and more positive behaviours and positive home environmental outcomes. CONCLUSIONS: Shared environmental influences on low extreme ADHD traits may reflect passive gene-environment correlation, which arises because parents provide environments as well as passing on genes. Studying the low extreme opens new avenues to study mechanisms underlying previously neglected positive behaviours. This is different from the current deficit-based model of intervention, but congruent with a population-level approach to improving youth wellbeing.

How 'core' are motor timing difficulties in ADHD? A latent class comparison of pure and comorbid ADHD classes.

Children with attention-deficit/hyperactivity disorder (ADHD) have motor timing difficulties. This study examined whether affected motor timing accuracy and variability are specific for ADHD, or that comorbidity with autism spectrum disorders (ASD) contributes to these motor timing difficulties. An 80-trial motor timing task measuring accuracy (µ), variability (σ) and infrequent long response times (τ) in estimating a 1-s interval was administered to 283 children and adolescents (8-17 years) from both a clinic and population based sample. They were divided into four latent classes based on the SCQ and CPRS-R: L data. These classes were: without behavioral problems 'Normal-class' (n = 154), with only ADHD symptoms 'ADHD-class' (n = 49), and two classes with both ASD and ADHD symptoms; ADHD(+ASD)-class (n = 39) and ASD(+ADHD)-class (n = 41). The pure ADHD-class did not deviate from the Normal class on any of the motor timing measures (mean RTs 916 and 925 ms, respectively). The comorbid ADHD(+ASD) and ASD(+ADHD) classes were significantly less accurate (more time underestimations) compared to the Normal class (mean RTs 847 and 870 ms, respectively). Variability in motor timing was reduced in the younger children in the ADHD(+ASD) class, which may reflect a tendency to rush the tedious task. Only patients with more severe behavioral symptoms show motor timing deficiencies. This cannot merely be explained by high ADHD severity with ASD playing no role, as ADHD symptom severity in the pure ADHD-class and the ASD(+ADHD) class was highly similar, with the former class showing no motor timing deficits.

Recognition of facial emotion and affective prosody in children with ASD (+ADHD) and their unaffected siblings.

Autism is a highly heritable and clinically heterogeneous neuropsychiatric disorder that frequently co-occurs with other psychopathologies, such as attention-deficit/hyperactivity disorder (ADHD). An approach to parse heterogeneity is by forming more homogeneous subgroups of autism spectrum disorder (ASD) patients based on their underlying, heritable cognitive vulnerabilities (endophenotypes). Emotion recognition is a likely endophenotypic candidate for ASD and possibly for ADHD. Therefore, this study aimed to examine whether emotion recognition is a viable endophenotypic candidate for ASD and to assess the impact of comorbid ADHD in this context. A total of 90 children with ASD (43 with and 47 without ADHD), 79 ASD unaffected siblings, and 139 controls aged 6-13 years, were included to test recognition of facial emotion and affective prosody. Our results revealed that the recognition of both facial emotion and affective prosody was impaired in children with ASD and aggravated by the presence of ADHD. The latter could only be partly explained by typical ADHD cognitive deficits, such as inhibitory and attentional problems. The performance of unaffected siblings could overall be considered at an intermediate level, performing somewhat worse than the controls and better than the ASD probands. Our findings suggest that emotion recognition might be a viable endophenotype in ASD and a fruitful target in future family studies of the genetic contribution to ASD and comorbid ADHD. Furthermore, our results suggest that children with comorbid ASD and ADHD are at highest risk for emotion recognition problems.

Do High and Low Extremes of ADHD and ASD Trait Continua Represent Maladaptive Behavioral and Cognitive Outcomes? A Population-Based Study.

OBJECTIVE: Attention deficit hyperactivity disorder (ADHD) and autism spectrum disorders (ASD) are thought to reflect the high, symptomatic extreme of quantitative trait continua. However, extreme deviations in either direction on disorder continua, high and low, may both represent maladaptive behavioral and cognitive outcomes. We aimed to test this hypothesis. METHOD: In a population sample of 378 children, ADHD and ASD traits were rated by parents on questionnaires that provide resolution at high and low extremes of the ADHD and ASD trait continua. ADHD and ASD traits were related to parent-ratings of internalizing and externalizing behavior problems and tests of cognitive functioning using polynomial regression. RESULTS: The low ends of the ADHD and ASD trait continua were related to fewer behavior problems and better cognitive functioning than symptomatic ends. CONCLUSION: Studying the correlates of the low continuum ends may deepen our understanding of the mechanisms underlying adaptive behavioral and cognitive outcomes.

Homogeneous Combinations of ASD-ADHD Traits and Their Cognitive and Behavioral Correlates in a Population-Based Sample.

OBJECTIVE: Autism Spectrum Disorders (ASD) and ADHD are assumed to be the extreme manifestations of continuous heterogeneous traits that frequently co-occur. This study aims to identify subgroups of children with distinct ASD-ADHD trait profiles in the general population, using measures sensitive across both trait continua, and show how these subgroups differ in cognitive functioning. METHOD: We examined 378 children (6-13 years) from a population-based sample. RESULTS: Latent class analyses (LCA) detected three concordant classes with low (10.1%), medium (54.2%), or high (13.2%) scores on both traits, and two discordant classes with more ADHD than ASD characteristics (ADHD > ASD, 18.3%) and vice versa (ASD > ADHD, 4.2%). Findings suggest that ASD and ADHD traits usually are strongly related in the unaffected population, and that a minority of children displays atypical discordant trait profiles characterized by differential visual-spatial functioning. CONCLUSION: This dissociation suggests that heterogeneity in ASD and ADHD is rooted in heterogeneity in the lower unaffected end of the distribution.

Are autism spectrum disorder and attention-deficit/hyperactivity disorder different manifestations of one overarching disorder? Cognitive and symptom evidence from a clinical and population-based sample.

OBJECTIVE: Autism spectrum disorders (ASD) and attention-deficit/hyperactivity disorder (ADHD) frequently co-occur. Given the heterogeneity of both disorders, several more homogeneous ASD-ADHD comorbidity subgroups may exist. The current study examined whether such subgroups exist, and whether their overlap or distinctiveness in associated comorbid symptoms and cognitive profiles gives support for a gradient overarching disorder hypothesis or a separate disorders hypothesis. METHOD: Latent class analysis was performed on Social Communication Questionnaire (SCQ) and Conners' Parent Rating Scale (CPRS-R:L) data for 644 children and adolescents (5 through 17 years of age). Classes were compared for comorbid symptoms and cognitive profiles of motor speed and variability, executive functioning, attention, emotion recognition, and detail-focused processing style. RESULTS: Latent class analysis revealed five classes: two without behavioral problems, one with only ADHD behavior, and two with both clinical symptom levels of ASD and ADHD but with one domain more prominent than the other (ADHD[+ASD] and ASD[+ADHD]). In accordance with the gradient overarching disorder hypothesis were the presence of an ADHD class without ASD symptoms and the absence of an ASD class without ADHD symptoms, as well as cognitive functioning of the simple ADHD class being less impaired than that of both comorbid classes. In conflict with this hypothesis was that there was some specificity of cognitive deficits across classes. CONCLUSIONS: The overlapping cognitive deficits may be used to further unravel the shared etiological underpinnings of ASD and ADHD, and the nonoverlapping deficits may indicate why some children develop ADHD despite their enhanced risk for ASD. The two subtypes of children with both ASD and ADHD behavior will most likely benefit from different clinical approaches.