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Background: Neurodevelopmental conditions frequently co-occur. The aim of this paper was to determine whether there is a cumulative association between (1) the number of neurodevelopmental conditions, specifically hyperkinetic disorder (hereafter referred to as attention deficit hyperactivity disorder), autism spectrum disorder (hereafter referred to as autism) and intellectual disability, and (2) behavioural and socio-emotional problems and the level of clinician-rated functioning for young males and females., Methods: In this cross-sectional study, diagnostic information, caregiver-rated behavioural and socio-emotional data (as conceptualised by the Strengths and Difficulties Questionnaire) and clinician-rated functioning scores (as conceptualised by the Children's Global Assessment Scale) were extracted from electronic patient records for 2768 young people aged 3-17 years (mean = 11.55, SD = 3.46). All data were extracted at baseline, that is, at the time the young person was diagnosed with attention deficit hyperactivity disorder, autism and/or an intellectual disability. Ordinal regression analyses tested associations between the number of neurodevelopmental conditions met (i.e. 1, 2 or 3) and behavioural and socio-emotional outcomes and functioning., Results: After controlling for age and biological sex, the number of neurodevelopmental conditions was associated with higher levels of inattention/hyperactivity and peer problems, lower levels of prosocial behaviour and poorer clinician-rated functioning. Although these findings were consistent for males, a cumulative association was not identified for females, except for clinician-rated functioning., Conclusions: For young people, the presence of multiple neurodevelopmental conditions may have a cumulative impact across domains, but this may differ between males and females., (© 2024 The Author(s). Journal of Intellectual Disability Research published by John Wiley & Sons and MENCAP.)

Aim: To investigate the interdependence between risk factors associated with long-term intellectual development in individuals with tuberous sclerosis complex (TSC)., Method: The Tuberous Sclerosis 2000 Study is a prospective longitudinal study of individuals with TSC. In phase 1 of the study, baseline measures of intellectual ability, epilepsy, cortical tuber load, and mutation were obtained for 125 children (63 females, 62 males; median age=39mo). In phase 2, at an average of 8 years later, intellectual abilities were estimated for 88 participants with TSC and 35 unaffected siblings. Structural equation modelling was used to determine the risk pathways from genetic mutation through to IQ at phase 2., Results: Intellectual disability was present in 57% of individuals with TSC. Individuals without intellectual disability had significantly lower mean IQ compared to unaffected siblings, supporting specific genetic factors associated with intellectual impairment. Individuals with TSC who had a slower gain in IQ from infancy to middle childhood were younger at seizure onset and had increased infant seizure severity. Structural equation modelling indicated indirect pathways from genetic mutation, to tuber count, to seizure severity in infancy, through to IQ in middle childhood and adolescence., Interpretation: Early-onset and severe epilepsy in the first 2 years of life are associated with increased risk of long-term intellectual disability in individuals with TSC, emphasizing the importance of early and effective treatment or prevention of epilepsy., What This Paper Adds: Intellectual disability was present in 57% of individuals with tuberous sclerosis complex (TSC). Those with TSC without intellectual disability had significantly lower mean IQ compared to unaffected siblings. Earlier onset and greater severity of seizures in the first 2 years were observed in individuals with a slower gain in intellectual ability. Risk pathways through seizures in the first 2 years predict long-term cognitive outcomes in individuals with TSC., (© 2019 The Authors. Developmental Medicine & Child Neurology published by John Wiley & Sons Ltd on behalf of Mac Keith Press.)