The Diagnostic and Statistical Manual of Mental Disorders – 5th edition (DSM-5™) has grouped ADHD with other neurodevelopmental disorders such as autism spectrum disorder, intellectual disability, communication disorders, specific learning disorders and motor disorders. Neurodevelopmental disorders are generally considered to result from deviations in normal brain development, and are characterised by onset during childhood, usually accompanied by neurocognitive deficits, and a steady course over time.
This notion has been supported by a large number of studies, and recent studies published in European Child & Adolescent Psychiatry point to ADHD being a neurobiological disorder. Some studies indicate preterm birth and low birth weight as potential risk factors for onset of ADHD symptoms in later years.
However, despite this general consensus, three independent longitudinal studies involving samples from Brazil, New Zealand and the UK have consistently refuted the theory of ADHD as a neurodevelopmental disorder. These cohorts highlighted that most cases of adults with ADHD did not result from childhood ADHD. Could this be the result of emergence of subthreshold childhood ADHD in adulthood due to inability to meet life’s demands? Or is it that ADHD is not, in fact, always a neurodevelopmental disorder?
Evidence of distinct genetic factors responsible for distinct ADHD disorders is emerging: the ‘polygenetic risk score’ predicts childhood- but not adult-onset forms of ADHD; there is no increased risk of a monozygotic twin developing adult-onset ADHD if the co-twin is diagnosed with childhood ADHD; and there has been an increase in evidence indicating that the genetic factors influencing onset of ADHD are discrete from genes implicated in determining its course.
A male preponderance has been highlighted in cases of childhood ADHD; however, this has not been observed for adult-onset ADHD. Does this mean that adult-onset ADHD is associated with changes in areas of the brain linked to sexual dimorphism? Additionally, children with ADHD typically have a lower intelligence quotient when compared with children with no such diagnosis. This indicator is not as prevalent in adults with ADHD. Does this indicate that the neurobiology of adult-onset ADHD occurs via divergence from ‘normal’ brain development typically characterised in children?
It is possible to keep the concept of ADHD as a multifactorial entity; environmental factors which limit symptom expression through neurogenetic protection in childhood may explain the onset of previously unseen symptoms in adults.
Further epidemiological studies are necessary to determine whether adult-onset ADHD, the existence of which is supported by strong evidence, is the result of the late expression of early-onset neurogenetic factors, or a separate entity.
Shaw P, Polanczyk GV. Combining epidemiological and neurobiological perspectives to characterize the lifetime trajectories of ADHD. Eur Child Adolesc Psychiatry 2017; 26: 139-141.