Peer-reviewed article

Annual Research Review: Does late‐onset attention‐deficit/hyperactivity disorder exist?

Philip J. Asherson, Jessica C. Agnew‐Blais · 7 Mar 2019

Abstract

Attention-deficit/hyperactivity disorder (ADHD) is conceptualized as an early onset childhood neurodevelopmental disorder. Prevalence in adults is around two-thirds that in childhood, yet longitudinal outcome studies of children with ADHD found a minority continue to meet full criteria in adulthood. This suggests that not all adult cases meet ADHD criteria as children, a conclusion supported by earlier studies relying on retrospective recall in adolescent and adult samples. More recently prospective follow-up of population and control samples suggest that adolescent and young adult ADHD is not always a continuation of childhood ADHD. Here, we review the literature on age of onset, to explore whether late-onset ADHD exists, and if so, examine the evidence for whether this should be considered the same or a different disorder as childhood onset ADHD. We conclude that current evidence supports the view that a significant proportion of young adults meeting criteria for ADHD would not have met full diagnostic criteria for ADHD as children. However, many in the late-onset group show some ADHD symptoms in childhood, or an externalizing disorder such as oppositional defiant disorder. Furthermore, the current studies suggest that most (but not all) cases of late-onset ADHD develop the disorder between the ages of 12-16 and can therefore be considered adolescent or early adult onset ADHD. There is a relative lack of data spanning young to older adulthood to address the question of adult-onset. Currently, there is insufficient data to clarify the extent to which early and late onset ADHD reflect a different balance of genetic and environmental risks or share the same underlying neural mechanisms. Clinicians should be aware that significantly impairing forms of ADHD can emerge beyond the age of 12 years, although perhaps rarely in the context of a complete absence of precursors. The current evidence on treatment responses is limited.