A neurophysiological marker of impaired preparation in an 11‐year follow‐up study of attention‐deficit/hyperactivity disorder (ADHD)

Child and Adolescent Psychiatric Clinics of North America

Sonuga‐Barke

Cortese

et al. 2014

Self Cite

109

KEYWORDS ADHD Treatment Neurofeedback Slow cortical potentials Frequency bands Reward KEY POINTSAmong alternative treatment approaches for attention-deficit/hyperactivity disorder (ADHD), neurofeedback has gained empirical support in recent years.Via neurofeedback, children with ADHD are trained to regulate their neurophysiologic profile or to bring it closer to that of nonaffected children; learning of self-regulation is thus a key mechanism.According to recent meta-analytic evidence, neurofeedback leads to significant decreases of ADHD core symptoms; however, if only probably blinded ratings are applied, these effects were reduced to a statistical trend. The evidence remains inconclusive because subsequent studies could demonstrate neither learning of self-regulation nor significant effects for the best blinded assessments.There is a strong need for more evidence from well-blinded, methodologically sound, and sensitive trials demonstrating also learning of self-regulation, before neurofeedback can be assigned the highest level of evidence as a front-line treatment of ADHD. ContinuedChild Adolesc Psychiatric Clin N Am -(2014) ---http://dx

Section: Eeg Frequency Band Studiesmentioning

confidence: 83%

Neurofeedback for ADHD

Child and Adolescent Psychiatric Clinics of North America

Sonuga‐Barke

Cortese

et al. 2014

Self Cite

109

“…The latter aims to regulate cortical excitation thresholds by focusing on activity generated by external cues (similar to event-related potentials), focusing primarily on EEG components registered in the late latency range, i.e., several seconds after the cue. For instance, this form of training has been used to target the contingent negative variation (CNV) which occurs during this time window and is involved in effective preparation, decision-making and time estimation, which have all been found to be deficient in individuals with ADHD, or at least in subgroups of them 12,13 .…”

Section: Introductionmentioning

confidence: 99%

The European ADHD Guidelines Group replies:

Cortese

Brandeis

Journal of the American Academy of Child & Adolescent Psych

et al. 2016

Self Cite

“…Although these studies provide invaluable insights into common mechanisms underlying clinical symptoms and neurocognitive deficits in general, the heterogeneity of ADHD requires further steps. The aetiology, clinical picture and course of the behavioural phenotype called ADHD is most probably related to a variety of pathophysiological pathways, a multitude of genes and various environmental influences.Doehnert and colleagues' article in this issue (Doehnert et al, 2013) illustrates the value of longitudinal electrophysiological and experimental approaches to disentangle different pathways underlying the phenotype of ADHD. Their contribution is a unique first electrophysiological follow-up of ADHD children as young adults.…”

mentioning

confidence: 99%

“…Doehnert and colleagues' article in this issue (Doehnert et al, 2013) illustrates the value of longitudinal electrophysiological and experimental approaches to disentangle different pathways underlying the phenotype of ADHD. Their contribution is a unique first electrophysiological follow-up of ADHD children as young adults.…”

mentioning

confidence: 99%

Commentary: Persistent time estimation deficits in ADHD? From developmental trajectories to individual targets for intervention – reflections on Doehnert et al. (2013)

Child Psychology Psychiatry

2012

EEG research dating back 70 years has established the presence of various degrees of EEG abnormalities in children with ADHD (named 'behaviour problem children' in those times). These early cross-sectional studies used visual evaluation of paper recordings of the EEG; the most common finding with this methodology was an increase in slow wave activity in ADHD children, often frontal, which is largely consistent with modern data. Although these studies provide invaluable insights into common mechanisms underlying clinical symptoms and neurocognitive deficits in general, the heterogeneity of ADHD requires further steps. The aetiology, clinical picture and course of the behavioural phenotype called ADHD is most probably related to a variety of pathophysiological pathways, a multitude of genes and various environmental influences.Doehnert and colleagues' article in this issue (Doehnert et al., 2013) illustrates the value of longitudinal electrophysiological and experimental approaches to disentangle different pathways underlying the phenotype of ADHD. Their contribution is a unique first electrophysiological follow-up of ADHD children as young adults. The article gives an initial idea in which direction research might proceed. It has inspiring implications for both clinicians and researchers.The authors carried out a longitudinal study of neuropsychological and electrophysiological markers of attention, inhibitory control and time processing in a sample of subjects with ADHD and normal controls diagnosed in childhood to analyse trajectories of developmental delay versus developmental deviation.Data from a 3-year follow-up of this sample have been published before, and revealed both aspects of developmental lag (for markers of response inhibition) and developmental deviation (for time estimation and attentional functions) during adolescence. The present additional follow-up of the same sample is critical as it covers a substantial time window from mean age 13 to mean age 22 with major developmental changes. Despite the attrition and the small samples surprisingly clear results emerged. The exciting message becomes apparent only by the concomitant presentation of the results for various ERP components relating to preparation and time processing (CNV) and inhibition and attention (NoGo P300, Cue P300), and the splitted analysis for ADHD remitters and non-remitters. By doing so, different developmental trajectories become apparent.The Cue P300, NoGo P300 and perceptual sensitivity in older ADHD subjects resembled those of younger controls; these group differences diminished in early adulthood. In contrast, abnormalities of the CNV and reaction time variability remained detectable in young adult ADHD subjects, even in ADHD remitters, compared to controls. Both CNV and reaction time variability have been proposed to be related to impaired timing. The results seem to indicate residual timing deficits even in young adults with remitted ADHD.An increasing amount of scientific evidence mirrors the clinical knowledge that tempo...