A comparative study on the neurophysiological mechanisms underlying effects of methylphenidate and neurofeedback on inhibitory control in attention deficit hyperactivity disorder.

In Attention Deficit Hyperactivity Disorder (AD(H)D), treatments using methylphenidate (MPH) and behavioral interventions like neurofeedback (NF) reflect major therapeutic options. These treatments also ameliorate executive dysfunctions in AD(H)D. However, the mechanisms underlying effects of MPH and NF on executive functions in AD(H)D (e.g. the ability to inhibit prepotent responses) are far from understood. It is particularly unclear whether these interventions affect similar or dissociable neural mechanisms and associated functional neuroanatomical structures. This, however, is important when aiming to further improve these treatments. We compared the neurophysiological mechanisms of MPH and theta/beta NF treatments on inhibitory control on the basis of EEG recordings and source localization analyses. The data show that MPH and theta/beta NF both increase the ability to inhibit pre-potent responses to a similar extent. However, the data suggest that MPH and NF target different neurophysiological mechanisms, especially when it comes to functional neuroanatomical structures associated with these effects. Both treatments seem to affect neurophysiological correlates of a 'braking function' in medial frontal areas. However, in case of the NF intervention, inferior parietal areas are also involved. This likely reflects the updating and stabilisation of efficient internal representations in order to initiate appropriate actions. No effects were seen in correlates of perceptual and attentional selection processes. Notably, reliable effects were only obtained after accounting for intra-individual variability in the neurophysiological data, which may also explain the diversity of findings in studies on treatment effects in AD(H)D, especially concerning neurofeedback.