Individuals with autistic spectrum disorder (ASD) and attention deficit hyperactivity disorder (ADHD) share behavioural and cognitive deficits in sustained attention. It is unclear, however, whether these deficits are related to shared underlying neuro-functional deficits or arise from a different underlying pathophysiology.
Objectives:
We used functional magnetic resonance imaging (fMRI) to compare brain activation in boys with ASD, ADHD and healthy controls to investigate disorder-specific brain dysfunctions during a parametrically modulated sustained attention/vigilance task where the load on sustained attention was progressively increased.
Methods:
29 boys (11-18 years old) with ASD, 24 age and IQ matched healthy boys and 28 age-matched ADHD boys completed an event-related parametric vigilance task on a 3T magnetic resonance imaging scanner. All participants were right-handed, with an IQ >70. All ASD children met ADI and ADOS cut-offs for autism and had no ADHD diagnosis. All ADHD children met DSM-IV ADHD criteria, but had no ASD diagnosis. The 12 min vigilance task requires subjects to respond as quickly as possible to a visual stimulus (timer counting ms) that appears under two different delay conditions: 1) short, frequent, predictable delays of 500ms (synchronisation) 2) randomly interspersed long, unpredictable delays of 2s, 5s, or 8s. Long unpredictable delays place a higher load on sustained attention (parametrically modulated with increasing delays), while short predictable delays place a higher load on sensorimotor timing. Data analysis used non-parametric image analysis (XBAM).
Results:
Performance: All children had slower reaction times (RT) with increasing delays. ASD and ADHD boys relative to controls both had slower RT to all delays. ADHD children had significantly enhanced response variability relative to boys with ASD and Controls.
fMRI analysis: Several brain regions differed between groups; post-hoc analyses showed significant delay and group by delay interaction effects in these regions. Activation in right inferior parietal lobe, right midcingulate and bilateral supplementary motor area (SMA) increased with increasing delay in all subjects, with activation more pronounced in controls relative to both patient groups. In midbrain, bilateral ventrolateral prefrontal cortices, thalamus and basal ganglia, controls showed enhanced activation with increasing delays during sustained attention, but both ASD and ADHD boys showed progressively more activation during synchronisation. Disorder-specific dysfunctions were not observed for ASD boys, but only for ADHD, in 3 brain regions: cerebellum and left inferior/dorsolateral prefrontal activation was increased in controls and in ASD with increasing delays, while ADHD showed progressively more activation during synchronisation. In anterior cingulate, however, ADHD boys showed progressively enhanced activation with increasing delays, while ASD boys and controls activated this region progressively more during synchronisation.
Conclusions:
Children with ASD and ADHD share poorer performance and reduced activation compared to controls in a sustained attention network comprising bilateral inferior fronto-striato-thalamic, SMA, parietal and cerebellar regions. ADHD boys, however, showed more severe and disorder-specific underactivation in L inferior fronto-cerebellar regions that correlated with increased response variability. Findings show that children with ASD and ADHD share neurofunctional abnormalities during sustained attention, but ADHD boys have additional disorder-specific inferior fronto-cerebellar dysfunctions in ADHD, presumably reflecting greater attention-related dysfunctions.