Medication versus Neurofeedback: Effects on impulsivity
Comparing Effects of Medication and Neurofeedback on Inhibitory Control (impulsivity)
In ADHD, a key executive functionthat is typically impaired is that of inhibitory control. This refers to the ability to ignore stimuli that are irrelevant to completing current tasks and inhibit prepotent reactions to those stimuli. A large body of evidence suggests that psychostimulatory medication which has become a first-line treatment option for ADHD, is effective at improving inhibitory control through the increase of dopamine receptor activation in the mid-frontal brain. However, associated side-effects (especially sleep issues, anxiety, decreased appetite, and headaches) and a lack of long-term efficacy (measured at two-years post-treatment) have driven research in ADHD treatment toward non-pharmacological means. The most common of this is neurofeedback, a form of self-regulation training which influences brain functioning without using direct stimulatory input, and thus circumvents many of the problems associated with medication. A 2016 neuroimaging studyfound that just 20 sessions of neurofeedback were able to increase activation in several brain regions associated with inhibitory control, providing the basis of a mechanistic explanation of how neurofeedback improves behavioural ADHD symptoms. As this is a promising alternative to medication, Bluschke and colleagues directly compared the neurophysiological mechanisms underlying the effects of neurofeedback and medication on inhibitory control in 2018.
The authors recruited 61 patients who were clinically diagnosed to have ADHD, and were assigned to receive either medication (MP), theta/beta neurofeedback therapy, or continue their usual treatment over an 8-week period. All participants performed a classic inhibitory control task before and after their treatment, while undergoing EEG monitoring. This monitoring technique can be used to identify brainwave responses to specific stimuli and compile the average waveform amplitudes of these responses (called ‘event-related potentials’ (ERPs)), which therefore index some cognitive function.
As expected, both the medication and neurofeedback groups significantly improved in their performance on the inhibitory control task (measured by number of successfully inhibited reactions), while no difference was found in the treatment-as-usual group. The degree of improvement for the methylphenidate and neurofeedback groups were not significantly different. The ERP analysis also revealed that both treatments elicited some similar activation patterns*, which, together with the task performance data, likely reveals the strengthening of a common ‘braking’ function. However, source localisation analysis of the ERP data also highlighted differences between the treatments: while the dopamine-promoting effects of methylphenidate improved activation in mid-frontal brain regions, neurofeedback also improved activation in the temporal parietal junction, in which there are few dopaminergic connections and is thus inaccessible to methylphenidate. One proposed function of the temporal-parietal junction is the processing of task-relevant information and initiation of appropriate reactions. The neurofeedback protocol used was also aimed at increasing beta brainwave oscillations, which have been suggested to be involved in stabilising mental processes recruited by current tasks against interfering events. Hence, the authors suggest that the benefit of neurofeedback over medication is that neurofeedback also helps to support representations of current tasks, allowing the initiation of appropriate reactions.
Ultimately, the authors found that the beneficial effects of neurofeedback on inhibitory control among individuals with ADHD are more widespread than that medication, covering more brain areas and possibly supporting more functions. This may be because medication is restricted to brain regions which have dopaminergic connections, whereas neurofeedback, which requires the participant to actively train a skill, can influence any brain regions involved in supporting that skill. Since these treatments work through different mechanisms, a combined treatment approach may be optimal for some individuals with ADHD – otherwise, among those who are unable to take methylphenidate, neurofeedback is a robust alternative.
*modulations in C-clusters for successful inhibition trials.
Bluschke, A., Friedrich, J., Schreiter, M. L., Roessner, V., & Beste, C. (2018). A comparative study on the neurophysiological mechanisms underlying effects of Methyl and neurofeedback on inhibitory control in attention deficit hyperactivity disorder. NeuroImage: Clinical, 20, 1191-1203. doi: 10.1016/j.nicl.2018.10.027