Early onset neurodevelopmental disorders, including autism spectrum disorder (ASD), attention-deficit hyperactivity disorder (ADHD), learning and language disorders and other cognitive impairments are each common and together affect 10–15% of all children. Many children have more than one of these conditions. This overall prevalence amounts to 50 to 75 million individuals in Europe. Some diagnoses, specifically ASD, seem to be increasing in frequency over the past decades. (1)

Early onset neurodevelopmental disorders carry a huge burden to the patients and their families as well as bringing enormous costs to society.(2)  The burden is strongly linked to their onset early in life and persistence during the entire lifespan, their high morbidity, their substantial risk for developing secondary complications as well as the absence of curative treatments. Ultimately, these disorders have a profound negative impact on the welfare and productivity of entire societies. 

These neurodevelopmental disorders are thought to result from the disruption of normal brain development and related neurobiological mechanisms during the prenatal and early postnatal period. The vast majority of research on neurodevelopmental disorders however takes place in patients at childhood age or later in life, after the diagnosis has been established. It is clear that ASD and ADHD are associated with a range of different genetic and environmental risk factors that predominately act in the prenatal period. For example, recent genetic evidence indicates that most genes associated with autism have patterns of peak expression during very early development.(3) Similarly, a range of prenatal environmental factors have been linked to later ASD or ADHD; for example, prenatal exposure to valproate is a recognized risk factor for ASD, especially in the first trimester of pregnancy. (4) 

Initial findings from prospective longitudinal studies of infants who later develop ASD have confirmed that perturbations to brain function can be detected in the first year of life. (5) Behavioural and cognitive signs become clear in the second year (6), with clinical diagnosis becoming possible by age 2 to 3 years for many children. These early difficulties disrupt the child’s immediate environment, for example influencing the dyadic mutuality of interactions with their primary caregiver. (7) Thus, symptoms of ASD or ADHD likely emerge from a combination of genetic or environmental risk factors, and compensatory processes or secondary ‘cascading’ effects. (8)

Symptoms of ASD and ADHD frequently co-occur in the same individuals. For example about 20% of UK 7- year-old children with ASD meet criteria for ADHD, and vice versa. (9) Research on infant markers of later ADHD however is currently less developed than for ASD. ASD and ADHD may share developmental pathways and endophenotypes, as well as genetic and environmental risk factors (10) , and it has even been suggested that the two conditions represent different manifestations of a common underlying disorder. (11) Differential expression of common genes in different neural systems or at different time points in development could potentially lead to a combination of overlapping and distinct clinical symptoms.

References

  1. Lai et al. (2014) Lancet.383(9920):896-910.
  2. Knapp et al. (2009) Autism 13(3):317-36; Doshi et al. (2012) J Am Acad Child Adolesc Psychiatry 51(10):990-1002.
  3. Parikshak et al. (2013) Cell 155(5):1008-21; Willsey et al. (2013) Cell 155(5):997-1007
  4. Rasalam et al, (2005). Dev Medicine Child Neurology, 7(8):551-555
  5. Elsabbagh et al. (2012). Current Biology, 22(4):338-42.
  6. Elsabbagh et al. (2013 ). Biol Psychiatry, 74(3):189-94
  7. Wan et al. (2013). J Child Psychol Psychiatry 54(7):763-71
  8. Dennis &Thompson (2013). Neuropsychology Review 15(3):359-84; Johnson, Jones & Gliga (2014), in press.
  9. Russell et al. (2014). J Autism Dev Disord 44(1):31-40
  10. Rommelse et al. (2010). Eur Child Adolesc Psychiatry 19(3):281-95; Rommelse et al. (2011). Neurosci Biobehav Rev. 35(6):1363-96; Ronald et al. (2011). Front Psychol 19;1:223.
  11. van der Meer (2012) J Am Acad Child Adolesc Psychiatry 51(11):1160-1172