Distinct effects of different neurofeedback protocols on the neural mechanisms of response inhibition in ADHD.

OBJECTIVE: In attention deficit/hyperactivity disorder (ADHD), impaired response inhibition is frequently observed. A promising non-pharmacological treatment is electroencephalography (EEG)-neurofeedback (NF) training. However, the widely used theta-down/beta-up regulation (↓θ↑ß) NF protocol may not be optimal for targeting these deficits. We examined how neurofeedback protocols training the upregulation of theta and/or beta power affect inhibitory control in children and adolescents with ADHD. METHODS: 64 patients with ADHD took part in the three NF trainings. Aside from parent-reported ADHD symptoms and behavioural performance data, neurophysiological parameters collected via a Go/Nogo task and corrected to account for intraindividual variability were compared in a pre-post design and to an ADHD (n = 20) as well as a typically developing control group (n = 24). RESULTS: The examined NF protocols resulted in similar improvements in response inhibition with the neurophysiological mechanisms differing substantially. The upregulation of theta led to a specific Nogo-P3 increase, while training beta upregulation as well as the combined protocol resulted in less specific effects. CONCLUSIONS: This study shows distinct effects of different theta/beta-neurofeedback protocols on the neural mechanisms underlying improvements in response inhibition in patients with ADHD. SIGNIFICANCE: These effects shed further light on the oscillatory dynamics underlying cognitive control in ADHD and how these may be targeted in neurofeedback treatments.

Neurofeedback trains a superordinate system relevant for seemingly opposing behavioral control deficits depending on ADHD subtype.

ADHD is one of the most prevalent neuropsychiatric disorders of childhood, but symptoms vary considerably between individuals. Therefore, different ADHD subtypes can be distinguished. Yet, it is widely elusive whether the specific subtype is critical to consider when examining treatment effects. Based on theoretical considerations, this could be the case for EEG theta/beta neurofeedback. We examine the effects of such an intervention on rapid response execution and inhibition processes using a Go/Nogo task in the inattentive (ADD) and the combined (ADHD-C) subtype. We show that a single neurofeedback protocol affects opposing deficits depending on the ADHD subtype - namely the execution (in ADD) and inhibition of action (in ADHD-C). No changes occurred in the healthy controls. These findings are discussed in relation to overarching principles of neural oscillations, particularly in the beta frequency band. The data suggest that theta/beta neurofeedback trains a superordinate system strongly related to the function of neural beta frequency oscillations to tune neural networks important for the sampling of sensory information used for behavioral control.

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.

The neuronal mechanisms underlying improvement of impulsivity in ADHD by theta/beta neurofeedback.

Neurofeedback is increasingly recognized as an intervention to treat core symptoms of attention deficit hyperactivity disorder (ADHD). Despite the large number of studies having been carried out to evaluate its effectiveness, it is widely elusive what neuronal mechanisms related to the core symptoms of ADHD are modulated by neurofeedback. 19 children with ADHD undergoing 8 weeks of theta/beta neurofeedback and 17 waiting list controls performed a Go/Nogo task in a pre-post design. We used neurophysiological measures combining high-density EEG recording with source localization analyses using sLORETA. Compared to the waiting list ADHD control group, impulsive behaviour measured was reduced after neurofeedback treatment. The effects of neurofeedback were very specific for situations requiring inhibitory control over responses. The neurophysiological data shows that processes of perceptual gating, attentional selection and resource allocation processes were not affected by neurofeedback. Rather, neurofeedback effects seem to be based on the modulation of response inhibition processes in medial frontal cortices. The study shows that specific neuronal mechanisms underlying impulsivity are modulated by theta/beta neurofeedback in ADHD. The applied neurofeedback protocol could be particularly suitable to address inhibitory control. The study validates assumed functional neuroanatomical target regions of an established neurofeedback protocol on a neurophysiological level.

Editorial Perspective: How to optimise frequency band neurofeedback for ADHD.

Attention deficit/hyperactivity disorder (ADHD) is one of the most prevalent paediatric neuropsychiatric disorders and is characterised by hyperactivity, inattention and increased impulsivity. Children with ADHD are often also characterised by deficits in a variety of cognitive domains, including problems in working memory, a generally slower and more variable style of information processing and deficits in temporal processing, inhibitory functions and delay processing. Overarching executive functions like information updating, response inhibition and mental set shifting are also impaired in many, but not all, children with ADHD, demonstrating the neuropsychological heterogeneity characterising this disorder. Deficits in executive functions can persist into adulthood and have a substantial negative impact on everyday life. A variety of approaches are commonly considered for the treatment of ADHD (including pharmacological interventions, patient-centred cognitive-behavioural therapy approaches and specific teacher/parent training programmes). More recently, adding to this multimodal treatment approach, neurofeedback has grown in popularity as an intervention option for patients with ADHD. This article considers this intervention approach and the opportunities for optimising treatment for executive control dysfunctions in ADHD using theta/beta neurofeedback.

Neurofeedback and its possible relevance for the treatment of Tourette syndrome.

Neurofeedback is an increasingly recognized therapeutic option in various neuropsychiatric disorders to treat dysfunctions in cognitive control as well as disorder-specific symptoms. In this review we propose that neurofeedback may also reflect a valuable therapeutic option to treat executive control functions in Gilles-de-la-Tourette syndrome (GTS). Deficits in executive control functions when ADHD symptoms appear in GTS likely reflect pathophysiological processes in cortico-thalamic-striatal circuits and may also underlie the motor symptoms in GTS. Such executive control deficits evident in comorbid GTS/ADHD depend on neurophysiological processes well-known to be modifiable by neurofeedback. However, so far efforts to use neurofeedback to treat cognitive dysfunctions are scarce. We outline why neurofeedback should be considered a promising treatment option, what forms of neurofeedback may prove to be most effective and how neurofeedback may be implemented in existing intervention strategies to treat comorbid GTS/ADHD and associated dysfunctions in cognitive control. As cognitive control deficits in GTS mostly appear in comorbid GTS/ADHD, neurofeedback may be most useful in this frequent combination of disorders.

Cortical post-movement and sensory processing disentangled by temporary deafferentation.

Motor system calibration depends crucially on the adjustment to the consequences of a movement, which often occur when the movement itself is already completed. The mechanisms by which reafferent feedback information is compared to the programmed movement remain unclear. In the current study, the hypothesis of a short term memory trace in the motor cortex which outlasts quick movements and is generated independently from reafferent feedback was challenged by temporal deafferentation. Post-movement cortical potentials were recorded by high-resolution EEG during a reaction time task which required speeded unilateral right-hand or left-hand button presses. We analysed lateralized motor N700 (motor post-imperative negative variation), a post-movement component, under temporary deafferentation achieved through application of a blood pressure tourniquet in ten healthy adult subjects. Motor N700 persisted under deafferentation in the absence of reafferent tactile and proprioceptive feedback input into the sensorimotor cortex, which was abolished under deafferentation. Source analysis pointed towards continuing activation in the pre-/primary motor cortex. Thus, motor post-processing can be dissociated from reafferent sensory feedback. Motor cortex activation outlasts quick movements for about a second also in the absence of a reafferent signal. Continuing motor cortex activation could act as an internal motor model in motor learning and allow better adjustment of movements according to the evaluation of their consequences.