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9 Sep 2018

Franke B et al. Eur Neuropsychopharmacol 2018; 28: 1059-1088

Presentation of ADHD in childhood and adulthood is highly dynamic, and the development of preventative measures as well as age-related diagnoses and interventions require knowledge of these changes. In this review article, the authors summarised published literature and current knowledge on ADHD from a developmental and lifespan perspective.

The phenotype of ADHD

The characteristic profile of ADHD changes through development, with hyperactive/impulsive symptoms highly present in very young children and inattentive symptoms becoming more apparent in adolescence and persisting into adulthood. However, overt hyperactivity and impulsivity are still observed in some adults with ADHD, and particularly those with comorbid problems such as substance abuse and antisocial behaviour. There are also gender differences in ADHD throughout development, as typically more males than females present with symptoms in child and adolescent clinics, whereas in adult clinics, males and females are equally present. This could be attributed to the observation that in childhood, males are more likely to display greater hyperactivity and impulsivity, and therefore more disruptive behaviour, than females. However, in adulthood, it is known that females are more likely to seek support for mental health problems, which could explain why rates of ADHD are similar in adults.

Age of onset of ADHD

Individuals can present with symptoms of ADHD at any age; however, according to the Diagnostic and Statistical Manual of Mental Disorders – 5th Edition (DSM-5TM), the age of onset criterion for childhood-onset ADHD is 12 years. There is evidence to suggest that ADHD in adulthood can be secondary to traumatic brain injury, which is distinct from childhood-onset ADHD. However, the concept of adult-onset idiopathic ADHD is more controversial, and although population studies estimate high rates of adult-onset ADHD, the authors highlighted that each of these studies had serious limitations. Therefore, it has been suggested that apparent adult-onset ADHD is instead due to undiagnosed or subthreshold ADHD in adolescence.

Psychiatric comorbidities associated with ADHD

In addition to the phenotype of ADHD changing through a lifespan, the associated psychiatric comorbidities also change. In childhood, individuals may exhibit oppositional defiant disorder and conduct disorder, whereas in adolescence and adulthood, antisocial personality, anxiety, mood, sleep and substance-use disorders become more apparent.

Response to pharmacological and non-pharmacological treatment

Regardless of age, it is recommended that treatment of ADHD should be multimodal and should include psychoeducation, pharmacotherapy and disorder-orientated psychotherapy, encompassing cognitive behavioural therapy (CBT) and family or couple therapy if required. In most European countries, only methylphenidate, lisdexamfetamine and atomoxetine are officially approved for both childhood and adulthood ADHD, and the National Institute for Health and Care Excellence guidelines recommend methylphenidate as the first-choice treatment for adult ADHD. The effect size of pharmacotherapy can differ throughout the lifespan, and may differ due to the presence of comorbid psychiatric disorders. More research is needed to compare the effects of different ADHD treatments in adults, as well as the efficacy and safety of these treatments in adults with ADHD and psychiatric comorbidities.

Non-pharmacological treatments to manage ADHD are also available to individuals throughout the lifespan. In many countries, children and adolescents with mild ADHD are often recommended non-pharmacological interventions as first-line therapy; however, these approaches demonstrate less efficacy compared with pharmacological treatments, but may be very useful in reducing psychiatric comorbidities or behavioural problems. Moreover, CBT has demonstrated efficacy in adolescents and adults with ADHD, and both mindfulness-based interventions and neurofeedback are other non-pharmacological options being explored as treatments for ADHD.

Outcome of ADHD with and without treatment

It has been reported that ADHD is associated with poor academic outcomes, unemployment, financial difficulties, poor social outcomes and increased mortality. Evidence from systematic reviews has suggested that individuals with untreated ADHD in both childhood and adulthood have poorer long-term outcomes compared with treated individuals in relation to academic outcomes, antisocial behaviour, driving, non-medicinal drug use/addictive behaviour, obesity, occupation, services used, self-esteem and social function. However, pharmacoepidemiological analyses indicated that individuals with ADHD who are treated with medication have a reduced risk for criminality and serious traffic accidents, as well as substance-use disorders and depression.

Cognitive and neuroimaging profiles of ADHD

Cognitive differences and brain abnormalities have been observed between children and adults with ADHD in cross-sectional studies. Meta-analyses of cognitive studies indicate that ADHD may be linked with poor performance in inhibition-, working memory-, planning- and vigilance-related tasks during childhood, adolescence and adulthood. Moreover, using magnetic resonance imaging, meta-analyses have shown that individuals with ADHD have reduced brain volumes, most robustly across studies in the basal ganglia area linked to reward and processing. Large-scale neuroanatomical studies have also shown that there are differences in brain volume and connectivity between those who have persistent ADHD and those who have remitted ADHD.

Genetics and environmental factors affecting ADHD

ADHD has a strong genetic component and its heritability is stable across the lifespan. Linkage studies have demonstrated converging evidence for common biological pathways which underlie ADHD, thereby emphasising that both common and rare genetic polymorphisms account for a large proportion of the genetic susceptibility of ADHD. Different genetic loci and a few positional candidate genes have also been identified for ADHD, and genome-wide association studies have shown an enrichment of genes related to neurobiological functions, which may be relevant to ADHD. However, these studies have also highlighted that the genetic background of ADHD is similar to that of other disorders, such as major depressive disorder, migraine and obesity. The authors indicated that although it is clear that ADHD exhibits high heritability and has complex genetics, more research is needed to find specific genes which underlie ADHD and also what causes it to persist into adulthood.

In addition to the genetic risk factors associated with ADHD, pre- and perinatal risk factors such as maternal stress, smoking or alcohol consumption during pregnancy, low birth weight, unfavourable psychosocial conditions and nutritional factors may also be associated with the development of ADHD. Moreover, many studies have reported that environmental risk factors for ADHD can be influenced by genetic polymorphisms.

The authors concluded that the lifelong trajectory of ADHD is highly variable, and that although it may be a burden to many individuals, some people with ADHD may remit or funnel the associated deficits into adaptive behaviours to lead very successful lives. This suggests that recognising the signs of ADHD early and providing optimal treatment could improve the lives of individuals with ADHD. The authors admit that although challenging, more longitudinal, granular and multimodal studies are necessary in order to clarify the course of ADHD and identify those at risk of unfavourable outcomes, and to provide a tailored treatment programme.

Read more about how ADHD changes throughout a lifespan here

Franke B, Michelini G, Asherson P, et al. Live fast, die young? A review on the developmental trajectories of ADHD across the lifespan. Eur Neuropsychopharmacol 2018; 28: 1059-1088.

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