Socio-emotional and communication difficulties might be present as secondary symptoms in people with ADHD, deriving from primary inattention, hyperactive and impulsive behaviours which tend to cause difficulties in social relationships and peer rejection, limiting the exposure to social situations and development of social skills (Leitner, 2014; Rommelse et al., 2011). However, social functioning is distinctly impaired in people with ADHD and with ASD, with ADHD more associated with externalising negative behaviours and less severe difficulties in experimental lab-based situations, and ASD more characterised by the absence of positive behaviours and difficulties in social cognition, as it is usually observed in laboratory settings (Mikami et al., 2019).
ASD symptomatology has been found positively associated with inattention and hyperactivity/impulsivity symptoms (Reiersen et al., 2007), even at subclinical level in the general population (Ronald et al., 2008). Moreover, first-degree relatives of patients with ADHD are at higher risk of having ASD, compared to individuals from the general population (Ronald et al., 2008). The commonalities between ADHD and ASD made some authors speculate that the two conditions might therefore be different phenotypical expressions of one overarching disorder, so that ADHD could be a milder expression of ASD-symptomatology (Rommelse et al., 2016). If this would be the case, individuals at elevated risk of developing either ADHD or ASD would be more likely
to also display clinically relevant symptoms of the other condition, while people with mild but clinically significant symptoms of ADHD or ASD might just have a single primary diagnosis and only subclinical traits of the other condition, if any.
Research on the aetiology of the comorbidity between ADHD and ASD has showed that the two conditions are likely to emerge from shared genetic and environmental factors, which are likely to interact and increase the susceptibility risk for the onset of behavioural traits of these conditions from early development (Cross- Disorder Group of the Psychiatric Genomics Consortium, 2019; Ghirardi et al., 2017; Rommelse et al., 2010). More specifically, inattention and reduced joint attention, high negative affect and emotionality, and deficits in effortful control, in early infancy, seem to be common pathways to both ADHD and ASD (Johnson et al., 2015; Visser et al., 2014).
While shared genetic and familial risk factors might influence early post-natal development and give rise to non-specific precursors of ADHD and ASD, the phenotypical expression of ADHD- and ASD-symptomatology is likely to diverge already during the second year of age. Around this time, ASD-specific symptoms seem in fact more associated with increased interest for non-social objects, high persistence, and increased perceptual sensitivity, distress, shyness, fear and sadness (see Visser et al., 2014 for a review). On the opposite, ADHD-specific symptoms have been found more associated with increased positive affect and extraversion, high anger and emotional reactivity, high distractibility, low attentional and inhibitory control (Visser et al., 2014). Different atypicalities in brain volume and cortical matter growth have also been reported (Dougherty et al., 2016). More specifically, brain overgrowth and increased volume (especially during childhood and adolescence) have been found in people with ASD, while decreased brain volume and cortical thinning is more prevalent
in individuals with ADHD. Moreover, deficits in executive functions are different in the two conditions, with ASD more associated with deficits in task shifting, while inhibition deficits are more likely to characterise ADHD (Visser et al., 2014).
The additive model of ADHD/ASD comorbidity suggests that while ADHD and ASD might emerge from shared or similar risk factors, the phenotypical expression of the conditions in the same individual would be an additive combination of the symptomatology and atypicalities reported in the two conditions, e.g., different executive functioning deficits (Banaschewski et al., 2007; Craig et al., 2016; Leitner, 2014; Tye et al., 2014). While this might be true for some domains, for other domains an interactive model of comorbidity would be more appropriate. According to the interactive model, in fact, people with ADHD+ASD are more likely to display an independent profile of impairments, resembling the atypicalities found in each disorder but at a greater severity than what found in the single conditions (Berenguer-Forner et al., 2015; Craig et al., 2015). The interactive model has been supported by studies showing that the simultaneous presence of clinical diagnoses of ADHD and ASD negatively affects patients’ quality of life, impacting social, cognitive and adaptive functioning to a greater extent than a single diagnosis of ADHD (Leitner, 2014; van der Meer et al., 2012). Delayed language development (Berenguer-Forner et al., 2015) and lower IQ (Craig et al., 2015) have also been reported in children with co-occurring ADHD+ASD, when compared with children with ASD- or ADHD-only, leading to delayed diagnoses (up to 2 years later than children with a single condition), and direct or indirect negative effects on interventional outcomes (Kentrou et al., 2019). This may also be the case when non-clinical sub-threshold symptoms of ASD are present in a child with ADHD (Ronald et al., 2014). The co-occurring presence of ADHD and ASD seems to impact the outcome effects of medical treatments as well. For example, a
review by Davis and Kollins (2012) pointed out that traditionally used stimulant treatments for ADHD might have increased negative side effects (such as increased stereotypies and RRBs) and reduced positive outcomes in individuals with co-occurring ADHD+ASD, who might benefit more from different medications, such as non- stimulants.
Since ADHD and ASD are likely to be characterised by similarities in genetic and familial risk factors, investigating both convergences and differences in their behavioural, neuro-cognitive and physiological phenotypes, might prove helpful in clarifying the etiological pathways of these conditions, both when they emerge separately and when they co-occur (Kandel, 1998). Identifying transdiagnostic and condition-specific atypicalities associated with ADHD and ASD, and understanding at what level they are present in individuals with co-occurring ADHD+ASD, seems an important step towards improving the diagnostic classification of the most clinically complex cases, which might benefit from quicker and more specific diagnoses, and personalised interventions. Moreover, investigating if specific phenotypes are mainly associated with ADHD or ASD, in patients with comorbid ADHD+ASD, might help clinicians to identify the core areas of impairment which should be given priority for interventions. For example, if those with a comorbid diagnosis of ADHD+ASD showed a pattern of atypicalities separately associated with ADHD and ASD (additive model of comorbidity), using combined interventions separately designed for ADHD and ASD might be beneficial. Conversely, if more severe deficits are present in those with ADHD+ASD (in support of the interactive model of ADHD/ASD comorbidity), commonly used medications for ADHD, such as stimulants, might have negative consequences on the population of patients with comorbid ADHD+ASD.