Timing deficits in attention-deficit/hyperactivity disorder (ADHD):evidence from neurocognitive and neuroimaging studies

Relatively recently, neurocognitive and neuroimaging studies have indicated that individuals with attention-deficit/hyperactivity disorder (ADHD) may have deficits in a range of timing functions and their underlying neural networks. Despite this evidence, timing deficits in ADHD are still somewhat neglected in the literature and mostly omitted from reviews on ADHD. There is therefore a lack of integrative reviews on the up-to-date evidence on neurocognitive and neurofunctional deficits of timing in ADHD and their significance with respect to other behavioural and cognitive deficits. The present review provides a synthetic overview of the evidence for neurocognitive and neurofunctional deficits in ADHD in timing functions, and integrates this evidence with the cognitive neuroscience literature of the neural substrates of timing. The review demonstrates that ADHD patients are consistently impaired in three major timing domains, in motor timing, perceptual timing and temporal foresight, comprising several timeframes spanning milliseconds, seconds, minutes and longer intervals up to years. The most consistent impairments in ADHD are found in sensorimotor synchronisation, duration discrimination, reproduction and delay discounting. These neurocognitive findings of timing deficits in ADHD are furthermore supported by functional neuroimaging studies that show dysfunctions in the key inferior fronto-striato-cerebellar and fronto-parietal networks that mediate the timing functions. Although there is evidence that these timing functions are inter-correlated with other executive functions that are well established to be impaired in the disorder, in particular working memory, attention, and to a lesser degree inhibitory control, the key timing deficits appear to survive when these functions are controlled for, suggesting independent cognitive deficits in the temporal domain. There is furthermore strong evidence for an association between timing deficits and behavioural measures of impulsiveness and inattention, suggesting that timing problems are key to the clinical behavioural profile of ADHD. Emerging evidence shows that the most common treatment of ADHD with the dopamine agonist and psychostimulant Methylphenidate attenuates most timing deficits in ADHD and normalises the abnormally blunted recruitment of the underlying fronto-striato-cerebellar networks. Timing function deficits in ADHD, therefore, next to executive function deficits, form an independent impairment domain, and should receive more attention in neuropsychological, neuroimaging, and pharmacological basic research as well as in translational research aimed to develop pharmacological or non-pharmacological treatment of abnormal timing behaviour and cognition in ADHD