Background: Adult ADHD has been assumed to be a continuation of childhood-onset ADHD. However, recent studies have identified individuals with ADHD in adulthood who have not had ADHD in childhood. Whether or not these individuals have a 'typical' neurodevelopmental profile is not clear.
Methods: We tested two explanations for the emergence of apparent late-onset ADHD symptomatology using the ALSPAC epidemiological cohort, by grouping individuals according to their scores on the Strengths and Difficulties Questionnaire (SDQ) hyperactivity subscale at ages 12 and 17 years. First, we tested whether some of those with apparent late-onset ADHD symptoms had been potentially misclassified on the basis of earlier SDQ hyperactivity scores (ages 7, 8 and 9 years) or of subthreshold symptoms at age 12 years. Second, we investigated the possibility that those with 'genuine' late-onset ADHD symptoms had a delayed manifestation of the same liability that underlies childhood-onset symptoms, by investigating whether they had a similar profile of neurodevelopmental impairments (in the domains of autistic symptomatology, language, reading, spelling, executive functioning and IQ) as those with typical childhood-onset ADHD.
Results: N = 56/75 (75%) of those with apparent late-onset ADHD had had high ADHD scores at least one point in childhood, suggesting that they may have been misclassified on the basis of their score at age 12 years. The remaining 19 individuals (25%) with genuine late-onset ADHD symptoms did not show a profile of neurodevelopmental impairment typically seen in ADHD, instead showing similar levels of autistic symptoms, language skills, executive functioning ability and IQ to those without ADHD symptoms. The only exceptions were that this group showed reading and spelling problems at age 9 years.
Conclusions: Our work suggests that this small number of individuals with genuine late-onset symptoms may not be most appropriately considered as having a typical neurodevelopmental disorder.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6175329 | PMC |
| http://dx.doi.org/10.1111/jcpp.12911 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Late adolescent outcomes of different developmental trajectories of ADHD symptoms in a large longitudinal study.
Eur Child Adolesc Psychiatry
July 2024
Department of Psychology, University of Edinburgh, 7 George Square, Edinburgh, EH8 9JZ, UK.
There exists substantial heterogeneity in the developmental trajectories of ADHD symptoms, with distinctions often made between persistent versus remittent, and early- versus late-onset. However, how these trajectories relate to late adolescent functioning and whether, in particular, later onset trajectories mark a milder subtype remains unclear. Building on earlier work that has examined early life predictors of ADHD symptom trajectories up to age 14, we applied latent class growth analysis to data from the UK Millennium Cohort Study (N = 10,262) to evaluate whether developmental trajectories of ADHD symptoms up to age 17 (from age 3) were similar to those identified up to age 14 and associated with differing levels of impairment in peer victimisation, mental health, substance use, and delinquency outcomes at age 17.
View Article and Find Full Text PDFThe neural and genetic underpinnings of different developmental trajectories of Attention-Deficit/Hyperactivity Symptoms in children and adolescents.
BMC Med
June 2024
State Key Laboratory of Cognitive Neuroscience and Learning, Beijing Normal University, Beijing, 100875, China.
Background: The trajectory of attention-deficit hyperactivity disorder (ADHD) symptoms in children and adolescents, encompassing descending, stable, and ascending patterns, delineates their ADHD status as remission, persistence or late onset. However, the neural and genetic underpinnings governing the trajectory of ADHD remain inadequately elucidated.
Methods: In this study, we employed neuroimaging techniques, behavioral assessments, and genetic analyses on a cohort of 487 children aged 6-15 from the Children School Functions and Brain Development project at baseline and two follow-up tests for 1 year each (interval 1: 1.
Late onset psychosis in a case of 15q11.2 BP1-BP2 microdeletion () syndrome: A case report and literature review.
SAGE Open Med Case Rep
January 2024
Northern Health, Victoria, Australia.
Burnside-Butler syndrome is an inheritable genetic condition characterized by the partial deletion of specific genetic material located on chromosome 15q11. Individuals diagnosed with this particular medical condition display a variety of neuropsychiatric disorders, including psychosis, aggression, mood disorders, anxiety disorders, developmental disorders involving learning difficulties, language delays, autism spectrum disorders, and attention-deficit/hyperactivity disorder. The authors discuss the case of a 51-year-old Caucasian female diagnosed with Burnside-Butler syndrome at 8 years.
View Article and Find Full Text PDFExternalizing Behaviors and Alzheimer's Disease and Any Dementia: A Multigeneration Cohort Study in Sweden.
Innov Aging
October 2023
Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
Article Synopsis
- Research investigated the link between externalizing behaviors (like violent/nonviolent crime and substance use disorders) in individuals born between 1973 and 1997 and the risk of Alzheimer's disease (AD) or dementia in their family members.
- A nationwide study with over 2.4 million people showed that parents of those with such behaviors had a significantly higher risk of developing AD compared to parents without those behaviors.
- Findings suggest that shared genetic and environmental factors may underlie both externalizing behaviors and the development of AD or dementia, prompting the need for further studies in this area.
Want AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!