Neurofeedback as a Treatment for Adhd a Methodological Review With Implications for Future Research
Curr Psychiatry Rep. 2019; 21(6): 46.
Neurofeedback as a Treatment Intervention in ADHD: Electric current Show and Practice
Stefanie Enriquez-Geppert
1Department of Clinical and Developmental Neuropsychology, Faculty of Behavioural and Social Sciences, University of Groningen, Grote Kruisstraat 2/ane, 9712 TS Groningen, The Netherlands
2Section of Biomedical Sciences of Cells & Systems, Section of Cognitive Neuropsychiatry, University of Groningen, Groningen, The netherlands
Diede Smit
aneDepartment of Clinical and Developmental Neuropsychology, Faculty of Behavioural and Social Sciences, University of Groningen, Grote Kruisstraat 2/1, 9712 TS Groningen, The Netherlands
Miguel Garcia Pimenta
1Department of Clinical and Developmental Neuropsychology, Faculty of Behavioural and Social Sciences, University of Groningen, Grote Kruisstraat 2/1, 9712 TS Groningen, The netherlands
Martijn Arns
iiiSection of Experimental Psychology, Utrecht University, Utrecht, The netherlands
fourneuroCare Group, Munich, Frg
5Inquiry Institute Brainclinics, Nijmegen, The Netherlands
Abstract
Purpose of Review
Electric current traditional treatments for ADHD present serious limitations in terms of long-term maintenance of symptom remission and side effects. Here, nosotros provide an overview of the rationale and scientific evidence of the efficacy of neurofeedback in regulating the encephalon functions in ADHD. We also review the institutional and professional person regulation of clinical neurofeedback implementations.
Recent Findings
Based on meta-analyses and (large multicenter) randomized controlled trials, three standard neurofeedback training protocols, namely theta/beta (TBR), sensori-motor rhythm (SMR), and slow cortical potential (SCP), turn out to be efficacious and specific. Nevertheless, the applied implementation of neurofeedback as a clinical handling is currently not regulated.
Summary
Nosotros conclude that neurofeedback based on standard protocols in ADHD should be considered as a viable treatment alternative and suggest that further research is needed to understand how specific neurofeedback protocols work. Eventually, we emphasize the need for standard neurofeedback training for practitioners and binding standards for use in clinical practice.
Keywords: Neurofeedback, ADHD, Current status, Brain computer interface, Clinical practise
Introduction
Similar to many of his ix-year-old school peers, Brian was put on psychostimulants after complaints of poor concentration and impulsivity that met ADHD diagnostic criteria. Despite a remarkable comeback in his academic performance, parent and teachers noticed a reduction in ambition and weight loss later on the onset of the medication. Moreover, when not under the effects of medication, inattention and impulsivity rebounded creating innumerous embarrassments to him and his family unit. His parents are now considering neurofeedback—a non-pharmacological and not-invasive intervention that has shown promising results in managing the ADHD symptoms in the long run and without side effects [one].
Despite being the most often practical and accustomed treatments for ADHD, recent large-scale studies and meta-analyses have demonstrated limitations of psychostimulants and behavioral therapy. Thus, enquiry and the evolution of non-pharmacological treatments such as neurofeedback have been recommended. To date, however, the clinical value of neurofeedback is still debated, with evaluations ranging from "efficacious and specific" [2, iii] to "fails to back up neurofeedback as an constructive handling for ADHD". [four•] In this contribution, nosotros will introduce neurofeedback and review the awarding of neurofeedback to ADHD also as its past and current evidence in the treatment of ADHD. Nosotros will also attempt to reconcile these seemingly discrepant research findings.
Current Treatment Approaches in ADHD
Several guidelines exist for the diagnosis and treatment of children who take or are suspected of having ADHD. Among these are international, national, and various regional guidelines for general practitioners. Additionally, in that location are guidelines for youth assistance and youth protective services.
Traditionally, the handling of ADHD consists of pharmacotherapy, often complemented by behavioral therapy based on parent management training and arbitration training for parents and teachers [five]. Additionally, classroom interventions, academic interventions, and peer-related interventions are being used equally psychosocial therapeutic approaches [half dozen]. Regarding pharmacotherapy, the administration of methylphenidate is often the method of choice (e.g., Ritalin, Concerta, Equasym, Medikinet); however, D-amphetamine, equally well as non-psychostimulants, such every bit atomoxetine and guanfacine, are prescribed also [7]. Over the past years, the Multimodal Treatment Study of Children with ADHD and follow-upwards studies (the so-chosen MTA studies) accept provided ample research regarding stimulant medication, behavioral treatments, their combination, and self-chosen community care. Results demonstrate that both stimulant medication and a combined handling had a clear clinical do good in the short term, only on the long-term group differences benumb, every bit assessed after 24 months, too equally after half dozen and 8 years [8]. These findings, in combination with studies indicating the potential side effects of pharmacotherapy [9•, x], partial drug response [7], and the time and price intensiveness of combining treatments due to the involvement of multiple professionals [6], have resulted in a growing involvement into the evolution of alternative non-pharmacological treatments in ADHD.
For case, computerized cerebral–based training approaches (e.grand., working-retention and attention training) aim to reduce ADHD core symptoms and tackle neuropsychological performance. Inquiry into this topic is still in the early stages and more controlled studies regarding the effects on ADHD core symptoms are required [eleven]. Another alternative treatment method for ADHD which is already more extensively studied in the past is neurofeedback. In the following paragraphs, we will (i) introduce neurofeedback, (2) present standard protocols for ADHD, (iii) review the by and current evidence in the treatment of ADHD, and (4) draw the electric current condition of institutional and professional person regulation of the clinical implementation of neurofeedback.
Definition, History, and Mechanism of Action of Neurofeedback
Despite the recent popularity of neuromodulation techniques, neurofeedback is for the most part withal an unknown territory. Neurofeedback is based on a brain-computer interface (BCI) and is implemented by a software system and a processing pipeline, birthday consisting of v elements (Fig.1) [12•]. Neurofeedback measures the participant's own encephalon activeness, which is pre-processed (steps ane and 2). Pre-selected brain parameters (a specific frequency ring or a encephalon potential) are calculated online (step 3) and translated to signals that are fed back to the user in real fourth dimension (step 4). Thus, selected features of brain activity are made perceivable for the participant. Through this feedback, the participant (step 5) can learn to self-regulate his own brain activeness to directly alter the underlying neural mechanism of cognition and behavior.
Overview neurofeedback: neurofeedback pipeline and iii areas of neurofeedback application. The pipeline includes the five most important processing steps and parts of a neurofeedback arrangement
Information technology has been proposed that neurofeedback is based on principles of operant conditioning and procedural skills learning. Due to these learning mechanisms, neuroplasticity is expected to take place during neurofeedback preparation either via Hebbian plasticity or anti-Hebbian/homeostatic plasticity. Such intrinsic regulatory mechanisms are believed to prevent extreme states of brain action, such equally pathologically high or low synaptic strengths or oscillatory states; for farther reading, see [13•].
Nowadays, neurofeedback is used in 3 ways: (i) as a therapeutic tool to normalize deviating brain action and treat neurocognitive disorders, (ii) as a then-called peak performance preparation to heighten cognitive operation in good for you participants, and (three) as an experimental method to investigate the causal role of neural oscillations in cognition and behavior. More precisely, the neurofeedback research is dominated by two streams: clinical research and neuroscientific inspired inquiry, which is mainly based on recent methodological and technical innovations, besides every bit on an increasing knowledge about the neural correlates of beliefs and knowledge. Some examples of recently developed EEG neurofeedback protocols are the upregulation or downregulation of loftier alpha [14, 15], the upregulation of frontal beta [16], and frontal midline theta [17], but also neurofeedback protocols using fMRI neurofeedback [18•].
Historically, neurofeedback dates back to the initial discovery of the man electroencephalogram (EEG) by Hans Berger. But half-dozen years later on this breakthrough, two French researchers—Gustave Durup and Alfred Fessard—kickoff reported that the EEG alpha rhythm could be subject to classical conditioning [xix], which is thought to be ane of the basic premises of neurofeedback. This initial observation was followed upwards past more systematic studies in the early on 1940s that further demonstrated all of the Pavlovian types of conditioned responses could exist demonstrated on the "EEG alpha blocking response". [20] In a follow-up written report, Jasper and Shagass [21] investigated farther whether participants could likewise exert voluntary control over this alpha blocking response. In this study, they had participants press a push, which would switch the lights on and off, and use subvocal verbal commands when pressing the push, (eastward.chiliad., "Block" when pressing the push button and "Terminate" when releasing the button). After 5 sessions, the subject was able to voluntarily suppress alpha action, while the lights were off (a condition where normally synchronous alpha would be present). Despite these early developments, it was only in the 1970s that these aforementioned principles were practical more systematically, and the get-go clinical implications were described in the literature. These developments were motivated by the discovery of the anticonvulsant furnishings of sensori-motor rhythm (SMR) neurofeedback in cats [22] and later humans [23]. The presumed role of SMR modulation on motor behavior was followed by the outset demonstrations of the positive effects of SMR neurofeedback in hyperkinetic disorder [24]. Effectually the same 1960–1970 menstruum, the starting time report of voluntary control over a slow encephalon potential called the contingent negative variation (CNV) or "bereitschaftspotential" (readiness potential, due to the property of this potential to sally when preparing for activeness, eastward.1000., when waiting in front of a traffic light) was reported [25], which laid the foundation of another well-known neurofeedback approach, namely of dull cortical potential (SCP) neurofeedback. The kickoff application of SCP neurofeedback in ADHD was reported in 2004 [26]. The initial findings described higher up as SMR and TBR neurofeedback resulted into what we currently known as "frequency band neurofeedback."
Standard Protocols with ADHD
Theta/beta (4–7 Hz/12–21 Hz) ratio (TBR) neurofeedback strives to decrease theta and/or increase beta power in fundamental and frontal locations. This protocol straight targets important electrophysiological characteristics such as high theta/beta ratios, high theta power, and/or low beta power commonly observed in children (for a review, see [27]) and adults with ADHD [28–30]. Contempo randomized controlled trials suggest that xxx to xl sessions of TBR neurofeedback were as effective as methylphenidate in reducing inattentive and hyperactivity symptoms and were fifty-fifty associated with superior post-treatment academic performance [31, 32]. It has been proposed that the effects of TBR neurofeedback on ADHD might be explained past the learned self-regulation of attention [33] equally evidenced by enhanced aamplitude of endogenous evoked-related potentials such as the P300 [34]. However, more neuroscientific evidence is needed to determine the specific mechanisms past which TBR neurofeedback might bear upon cognitive functioning in ADHD.
SMR neurofeedback preparation over the sensori-motor strip (predominantly in the cardinal correct hemispheric region) was first practical to ADHD children by Lubar and colleagues [24, 35], based on the functional clan of the sensori-motor rhythm with behavioral inhibition and the promising results in reducing cortical excitability in epileptics obtained by Sterman, MacDonald, and Stone [36]. Lubar'due south seminal studies revealed that the beneficial hyperactivity-reducing furnishings of a combined SMR/theta neurofeedback training were maintained after psychostimulants was withdrawn in hyperactive children.
Studies suggest that SMR neurofeedback training reduces inattentive and hyperactive/impulsive symptoms in ADHD children to the same extent equally TBR training and comparable number of treatment sessions. Nonetheless, the two protocols might attain the aforementioned results through distinct mechanisms. Arns, Feddema, and Kenemans [37] provided evidence that ADHD patients trained with the SMR protocol showed decreased slumber onset latency (SOL) and improved sleep quality in comparison to those administered with TBR, midway treatment. A arbitration assay revealed that this normalized sleep mid-treatment was responsible for the improved inattention post-handling. The improvements in ADHD symptoms following SMR training might hence be the result of the vigilance stabilization mediated past the regulation of the locus coeruleus noradrenergic system of which activation has been shown to affect the sleep spindle circuitry [38]. This caption seems to be in line with previous indications that patients with ADHD nowadays delays in SOL [39] and that SMR training increases slumber spindle density and improves sleep quality in good for you adults [xl].
Another standard protocol is the cocky-regulation of SCP [41, 42••] subsequently around 35 sessions. SCP neurofeedback is based on the learned self-regulation of cortical activation and inhibition which are associated with the electrical negativation and positivation of slow cortical electrical deflections respectively. These periodical shifts from electrical positivity to negativity take been described as a phasic tuning mechanism in the regulation of attention [43] as shown by the enhanced reaction fourth dimension, stimulus detection, and brusk-term memory during the negative shift phase [44]. Since SCP, of which the CNV is an example, are closely associated with preparatory motor responses with a maximal topographic representation in the motor areas, the vertex is usually the site of choice for training. Differently from TBR and SMR protocols which are typically unidirectional (i.east., instructions either require the participant to increase or decrease the power of the EEG parameter), the self-regulation of SCP ordinarily involves the preparation in generating both cortical activation and inhibition. In the case of ADHD, the therapeutic focus is on promoting an increase in the firing probabilities of the underlying cortical areas (i.east., negativation). Another difference relative to frequency neurofeedback is that in SCP neurofeedback the learning trials are higher in number and considerably shorter in duration. Interestingly, it has been hypothesized that SCP might besides be associated with improvements in slumber. The generation of tiresome oscillations, in particular negative slow direct current, shifts training during SCP neurofeedback, might exert command over the sleep spindle circuit and therefore facilitate the transition from wakefulness to sleep [45].
Electric current Condition of Efficacy of Standard Protocols for Neurofeedback in ADHD
As with whatever emerging new treatments, noesis of technical aspects of the treatment, proper standards, and educational activity are crucial for accordingly evaluating the merits and pitfalls of neurofeedback. Unfortunately, the unfounded assumption that "neurofeedback = neurofeedback" is ofttimes made. Neurofeedback can differentially impact brain functioning depending on the kind protocol and implementation the same mode as different pharmacological treatments exercise (e.g., antidepressants and analgesic drugs). Every bit an analogy, neurofeedback treatments such as the earlier mentioned SMR, TBR, and SCP neurofeedback are well-investigated and effective in the treatment of ADHD while other approaches such as posterior alpha enhancement have been found to be not effective (for a review, see [iii].
Peculiarly when restricted to standard protocols such as TBR, SMR, and SCP protocols [3], neurofeedback is a well-investigated treatment for ADHD. This has become evident from several meta-analyses [2, 46••, 47], including a critical meta-analysis from the European ADHD Guidelines Group (EAGG) that also conducted a sensitivity analysis focused on then called "blinded" ratings (i.e., instructor reports only) [4•]. Blinded ratings accept usually lower furnishings sizes than ratings by people most-proximal to the kid and therefore least blinded (east.g., parents) and both rating types are only modestly correlated [48]. 1 explanation for this may be that the rating types focus on different aspects of ADHD symptoms. This is reflected in studies showing different rating-ADHD attribute associations, as for example parent ratings of hyperactive-impulsive behaviors were found to be correlated with genetics [49], whereas teacher ratings accept been shown to be associated to medication furnishings [50], about probable due to the fast onset of action of psychostimulants. To come back to the latter meta-analysis [iv•], the researchers did not find an consequence of neurofeedback in general on instructor-rated ADHD symptoms, but there was an consequence when the analysis was restricted to the above mentioned "standard protocols." Finally, a recent meta-assay that included 10 RCTs and specifically looked at long-term effects of neurofeedback, compared to active treatments (including psychostimulants) and semi-agile treatments (eastward.g., cognitive training), institute that afterward on average half dozen months follow-upwardly, the effects of neurofeedback were superior to semi-active control groups and no dissimilar from agile treatments including methylphenidate [46••]. Interestingly, this meta-analysis confirmed the tendency for medication effects to diminish with time, and the effects of neurofeedback—without additional sessions being conducted—to increase with time. These data suggest the promising aspect, namely of long-term efficacy, of neurofeedback. Currently, i of the largest and well-nigh comprehensive double-bullheaded multisite RCT is carried out: the International Collaborative ADHD Neurofeedback report (ICAN). This study consists of a cross-site investigation team with different background of ADHD treatment approaches assessing 140 participants in full (see the report design in [51]), and results are foreseen to be published in 2019.
Current Condition of Institutional and Professional Regulation of Clinical Neurofeedback Implementations
Although standard protocols turn out to be efficacious and specific, the practical implementation of neurofeedback as a clinical therapy is currently not regulated. This applies to the educational standards, medical security, and the usage of standard protocols indicated for specific disorders such as ADHD. The lack of regulation and agreed upon standards comes with the danger of patients being treated with ineffective neurofeedback protocols applied by unlicensed personal (or even worse by people without whatsoever health-related background). For instance, although practitioners should stick to standard protocols with functional specificity of the frequency and topographic locations, clinical practice often deviates from what is recommended by research. The lack of regulation and missing standards have furthermore caused a surge in commercial driven applications and proclaimed "innovations" of neurofeedback protocols and implementations. Several studies have now demonstrated that some of those "innovations" and implementations do not work. Ane example of such ineffective technique is the SmartBrain neurofeedback approach using the "NASA patented engagement index" with Sony PlayStation feedback [51, 52]. Additionally, there is no evidence in favor of the efficacy of unconventional neurofeedback protocols used in some neurofeedback clinics [53] and frequently advertised applications such as Z score and LORETA neurofeedback [54]. Unfortunately, these proclaimed innovations and commercial-driven applications just add noise to the ongoing contend of neurofeedback efficacy and hazard "throwing the infant out with the bathwater." However, above all this demonstrates the demand for further research into the effectiveness of already bachelor and newly developed neurofeedback protocols (i.due east., the number of sessions, targeted brain expanse, selected brain parameter, working mechanism) in addition to proper "agreed-upon standards" and training within the field of neurofeedback.
Neurofeedback researchers and practitioners can affiliate to scientific and professional organizations at the international and national level. On an international level, there are mainly two societies. The Society of Applied Neuroscience (SAN) (http://www.applied-neuroscience.org/) is an EU-based nonprofit membership organization for the advancement of neuroscientific knowledge and development of innovative applications for optimizing brain functioning (such as neurofeedback with EEG, fMRI, NIRS). The International Society for Neurofeedback & Inquiry (ISNR (https://www.isnr.org) is a membership organisation aimed at supporting scientific research in practical neurosciences, promoting didactics in the field of neurofeedback, admitting not always clearly separating commercial and objective interests. Other neurofeedback societies or organizations are oft connected to certain neurofeedback equipment manufacturers and have (seemingly) conflicting interests. Furthermore, the Biofeedback Certification International Alliance (BCIA) is a broader international licensure as well including biofeedback (www.BCIA.org).
Conclusions
Recent years witness a renewed interest in neurofeedback in response to the lack of long-term effects for both medication and behavioral therapy and the side effects of medication. Herein, we provide evidence for the efficacy and specificity of standard neurofeedback protocols, namely theta/beta, sensori-motor rhythm, and boring cortical potential. In line with the guidelines for rating evidence developed by the APA, "standard" neurofeedback protocols have been considered to be "Efficacious and Specific, Level V" in the treatment of ADHD (AAPB Guidelines: [57]).
Even so, currently there are no uniform standards regarding training courses for neurofeedback that are accepted past expert associations, neither national-wide, nor in the Eu or USA. While performing neurofeedback in a therapeutic context, a thorough basic training, a distinct technical understanding of the medical devices, the software, and the EEG caps, as well as continuing education, are imperative. Regarding the medical security performing neurofeedback in a clinical context, neurofeedback devices (hardware: amplifier and EEG caps, neurofeedback software) are neither regulated in a strict way. Even so, it is essential that too the absolute minimum technical requirements after the Medical Device Regulation (MDR) EU 2017/745), neurofeedback devices should be regulated by both the CE (that confirms a medical device meets the essential MDR requirements) and a European equivalent of the Food and Drug Administration (FDA). The FDA enforces laws to protect the consumer's health, prophylactic, and bag. Such potential regulating mechanisms could exist implemented past the European medicine regulatory network. In curt, tasks ahead concern regulating neurofeedback as therapy, developing internationally accepted binding standards for education and NF implementation and the qualification of neurofeedback trainers.
Final merely not to the lowest degree, Brian—now 4 years later on—discontinued his medication successfully under medical supervision. Due to neurofeedback, his impulsivity symptoms strongly reduced and he gained control over his concentration, doing well in high school performance.
Compliance with Upstanding Standards
Conflict of Interest
Stefanie Enriquez-Geppert and Diede Smit each declare that they accept no conflict of involvement. Miguel Thou Pimenta declares that he is a lecturer in neurofeedback for the neuroCare Grouping (Munich, Frg). Martijn Arns (MAr) reports research grants and options from Brain Resource (Sydney, Commonwealth of australia); owns stock in and serves as Master Scientific Adviser of the neuroCare Group (Munich, Germany) and Director and Researcher of Research Constitute Brainclinics (Nijmegen, Netherlands); is a consultant on a National Institute of Mental Health, The states-funded iCAN report (CNG 2013); and is a co-inventor on four patent applications (A61B5/0402; US2007/0299323, A1; WO2010/139361 A1; 1 pending) related to EEG, neuromodulation, and psychophysiology (not related to neurofeedback). MAr declares no buying or financial gains for these patents - just authorship.
Human and Fauna Rights and Informed Consent
This commodity does not contain any studies with man or animal subjects performed by any of the authors.
Footnotes
This article is role of the Topical Collection on Attention-Deficit Disorder
Publisher'southward Note
Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.
References
Papers of particular interest, published recently, have been highlighted as: • Of importance •• Of major importance
one. Hammond DC, Kirk 50. Negative effects and the need for standards of practise in neurofeedback. Biofeedback. 1982;35(iv):139–145. [Google Scholar]
2. Arns M, de Ridder S, Strehl U, Breteler Thousand, Coenen A. Efficacy of neurofeedback treatment in ADHD: the effects on inattention, impulsivity and hyperactivity: a meta-analysis. Clin EEG Neurosci. 2009;twoscore(3):180–189. [PubMed] [Google Scholar]
3. Arns Grand, Heinrich H, Strehl U. Evaluation of neurofeedback in ADHD: the long and winding road. Biol Psychol. 2014;95:108–115. [PubMed] [Google Scholar]
four. Cortese S, Ferrin One thousand, Brandeis D, Holtmann M, Aggensteiner P, Daley D, et al. Neurofeedback for attending-deficit/hyperactivity disorder: meta-Analysis of clinical and neuropsychological outcomes from randomized controlled trials. J Am Acad Child Adolesc Psychiatry. 2016;55(half dozen):444–455. [PubMed] [Google Scholar]
5. Taylor Eastward, Dopfner M, Sergeant J. European clinical guidelines for hyperkinetic disorder – first upgrade. Eur Child Adolesc Psychiatry. 2004;13(Suppl 1):i7–i30. [PubMed] [Google Scholar]
vi. Daly BP, Creed T, Xanthopoulos M, Brownish RT. Psychosocial treatments for children with attention deficit/hyperactivity disorder. Neuropsychol Rev. 2007;17(1):73–89. [PubMed] [Google Scholar]
7. Faraone SV, Buitelaar J. Comparing the efficacy of stimulants for ADHD in children and adolescents using meta-analysis. Eur Child Adolesc Psychiatry. 2010;nineteen(four):353–364. [PubMed] [Google Scholar]
eight. Molina BSG, Hinshaw SP, Swanson JM, Arnold LE, Vitiello B, Jensen PS, Epstein JN, Hoza B, Hechtman L, Abikoff HB, Elliott GR, Greenhill LL, Newcorn JH, Wells KC, Wigal T, Gibbons RD, Hur K, Houck PR, MTA Cooperative Group The MTA at 8 years: prospective follow-up of children treated for combined-blazon ADHD in a multisite study. J Am Acad Kid Adolesc Psychiatry. 2009;48(five):484–500. [PMC gratis article] [PubMed] [Google Scholar]
9. Storebø OJ, Ramstad E, Krogh HB, Nilausen TD, Skoog M, Holmskov M, et al. Methylphenidate for children and adolescents with attention arrears hyperactivity disorder (ADHD) Cochrane Database Syst Rev. 2015;11:CD009885. [PMC free commodity] [PubMed] [Google Scholar]
x. Charach A, Figueroa Yard, Chen S, Ickowicz A, Schachar R. Stimulant handling over 5 years: effects on growth. J Am Acad Child Adolesc Psychiatry. 2006;45(iv):415–421. [PubMed] [Google Scholar]
11. Sonuga-Barke EJ, Brandeis D, Holtmann M, Cortese S. Computer-based cognitive training for attending-deficit/hyperactivity disorder: a review of electric current testify. Child Adolesc Psychiatr Clin N Am. 2014;23(4):807–824. [PubMed] [Google Scholar]
12. Enriquez-Geppert S, Huster RJ, Herrmann CS. EEG-neurofeedback as a tool to attune cognition and behavior: a review tutorial. Front end Hum Neurosci. 2017;11:51. [PMC complimentary commodity] [PubMed] [Google Scholar]
13. Ros T, Baars BJ, Lanius RA, Vuilleumier P. Tuning pathological brain oscillations with neurofeedback: a systems neuroscience framework. Front Hum Neurosci. 2014;eight:1008. [PMC free article] [PubMed] [Google Scholar]
xiv. Escolano C, Aquilar M, Minguey J. EEG-based upper alpha neurofeedback training improves working memory performance. Conf Proc IEEE Eng Med Biol Soc. 2011:2327–thirty. [PubMed]
15. Ros T, Munneke M, Ruge D, Gruzelier J, Rothwell J. Endogenous command of waking brain rhythms induces neuroplasticity in humans. Eur J Neurosci. 2010;31(four):770–778. [PubMed] [Google Scholar]
16. Engelbregt HJ, Keeser D, Van Eijk Fifty, Suiker EM, Eichhorn D, Karch Due south, et al. Short and long-term furnishings of sham-controlled prefrontal EEG-neurofeedback training in healthy subjects. Clin Neurophysiol. 2016;127(4):1931–1937. [PubMed] [Google Scholar]
17. Enriquez-Geppert S, Huster RJ, Figge C, Herrmann CS. Self-regulation of frontal-midline theta facilitates memory updating and mental set shifting. Front end Behav Neurosci. 2014;viii:420. [PMC free article] [PubMed] [Google Scholar]
18. Alegria AA, Wulff M, Brinson H, Barker GJ, Norman LJ, Brandeis D, et al. Real-time fMRI neurofeedback in adolescents with attention deficit hyperactivity disorder. Hum Encephalon Mapp. 2017;38(6):3190–3209. [PMC free article] [PubMed] [Google Scholar]
19. Durup G, Fessard A. I. L'électrencéphalogramme de l'homme. Observations psycho-physiologiques relatives à l'action des stimuli visuels et auditifs. Ann Psychol. 1935;36(i):1–32. [Google Scholar]
20. Jasper H, Shagass C. Conditioning the occipital alpha rhythm in man. J Exp Psychol. 1941;28(5):373–388. [Google Scholar]
21. Jasper H, Shagass C. Conscious time judgments related to conditioned time intervals and voluntary control of the blastoff rhythm. J Exp Psychol. 1941;28(6):503–508. [Google Scholar]
22. Sterman B, LoPresti RW, Fairchild Physician. Electroencephalographic and behavioral studies of monomethylhydrazine toxicity in the cat. J Neurother. 2010;14(4):293–300. [Google Scholar]
23. Sterman MB, Friar L. Suppression of seizures in an epileptic post-obit sensorimotor EEG feedback training. Electroencephalogr Clin Neurophysiol. 1972;33(1):89–95. [PubMed] [Google Scholar]
24. Lubar JF, Shouse MN. EEG and behavioral changes in a hyperkinetic child concurrent with training of the sensorimotor rhythm (SMR) Biofeedback Self Regul. 1976;1(3):293–306. [PubMed] [Google Scholar]
25. McAdam DW, Irwin DA, Rebert CS, Knott JR. Conative control of the contingent negative variation. Electroencephalogr Clin Neurophysiol. 1966;21(2):194–195. [PubMed] [Google Scholar]
26. Heinrich H, Gevensleben H, Freisleder FJ, Moll GH, Rothenberger A. Grooming of boring cortical potentials in attending-arrears/hyperactivity disorder: evidence for positive behavioral and neurophysiological furnishings. Biol Psychiatry. 2004;55(7):772–775. [PubMed] [Google Scholar]
27. Barry RJ, Clarke AR, Johnstone SJ. A review of electrophysiology in attending-deficit/hyperactivity disorder: I. Qualitative and quantitative electroencephalography. Clin Neurophysiol. 2003;114(ii):171–183. [PubMed] [Google Scholar]
28. Bresnahan SM, Barry RJ. Specificity of quantitative EEG analysis in adults with attention deficit hyperactivity disorder. Psychiatry Res. 2002;112(ii):133–144. [PubMed] [Google Scholar]
29. Bresnahan SM, Anderson JW, Barry RJ. Age-related changes in quantitative EEG in attention-deficit/hyperactivity disorder. Biol Psychiatry. 1999;46(12):1690–1697. [PubMed] [Google Scholar]
xxx. Clarke AR, Barry RJ, Heaven PCL, McCarthy R, Selikowitz M, Byrne MK. EEG in adults with attention-deficit/hyperactivity disorder. Int J Psychophysiol. 2008;70(three):176–183. [PubMed] [Google Scholar]
31. Duric NS, Assmus J, Gundersen D, Elgen IB. Neurofeedback for the handling of children and adolescents with ADHD: a randomized and controlled clinical trial using parental reports. BMC Psychiatry. 2012;12:107. [PMC free article] [PubMed] [Google Scholar]
32. Meisel Five, Servera M, Garcia-Banda G, Cardo E, Moreno I. Neurofeedback and standard pharmacological intervention in ADHD: a randomized controlled trial with 6-month follow-up. Biol Psychol. 2013;94(1):12–21. [PubMed] [Google Scholar]
33. Gevensleben H, Rothenberger A, Moll GH, Heinrich H. Neurofeedback in children with ADHD: validation and challenges. Skillful Rev Neurother. 2012;12(four):447–460. [PubMed] [Google Scholar]
34. Egner T, Gruzelier JH. EEG biofeedback of low beta ring components: frequency-specific effects on variables of attending and outcome-related brain potentials. Clin Neurophysiol. 2004;115(1):131–139. [PubMed] [Google Scholar]
35. Shouse MN, Lubar JF. Operant workout of EEG rhythms and Ritalin in the treatment of hyperkinesis. Biofeedback Self Regul. 1979;4(4):299–312. [PubMed] [Google Scholar]
36. Sterman MB, Macdonald LR, Rock RK. Biofeedback training of the sensorimotor electroencephalogram rhythm in man: effects on epilepsy. Epilepsia. 1974;15(iii):395–416. [PubMed] [Google Scholar]
37. Arns M, Feddema I, Kenemans JL. Differential effects of theta/beta and SMR neurofeedback in ADHD on sleep onset latency. Forepart Hum Neurosci. 2014;8:1019. [PMC gratuitous commodity] [PubMed] [Google Scholar]
38. Sinha SR. Basic mechanisms of sleep and epilepsy. J Clin Neurophysiol. 2011;28(two):103–110. [PubMed] [Google Scholar]
39. Van Veen MM, Kooij JJS, Boonstra AM, Gordijn MCM, Van Someren EJW. Delayed circadian rhythm in adults with attention-arrears/hyperactivity disorder and chronic slumber-onset insomnia. Biol Psychiatry. 2010;67(11):1091–1096. [PubMed] [Google Scholar]
40. Schabus One thousand, Heib DPJ, Lechinger J, Griessenberger H, Klimesch W, Pawlizki A, Kunz AB, Sterman BM, Hoedlmoser Grand. Enhancing sleep quality and retentivity in insomnia using instrumental sensorimotor rhythm workout. Biol Psychol. 2014;95:126–134. [PubMed] [Google Scholar]
41. Gevensleben H, Holl B, Albrecht B, Schlamp D, Kratz O, Studer P, Wangler Due south, Rothenberger A, Moll GH, Heinrich H. Distinct EEG effects related to neurofeedback training in children with ADHD: a randomized controlled trial. Int J Psychophysiol. 2009;74(two):149–157. [PubMed] [Google Scholar]
42. Strehl U, Aggensteiner P, Wachtlin D, Brandeis D, Albrecht B, Arana M, et al. Neurofeedback of deadening cortical potentials in children with attending-deficit/hyperactivity disorder: a multicenter randomized trial decision-making for unspecific effects. Front Hum Neurosci. 2017;11:135. [PMC gratuitous commodity] [PubMed] [Google Scholar]
43. Rockstroh B, Elbert T, Birbaumer N, Lutzenberger W. Biofeedback-produced hemispheric asymmetry of slow cortical potentials and its behavioural effects. Int J Psychophysiol. 1990;nine(two):151–165. [PubMed] [Google Scholar]
44. Birbaumer N, Elbert T, Canavan AG, Rockstroh B. Slow potentials of the cerebral cortex and behavior. Physiol Rev. 1990;70(1):1–41. [PubMed] [Google Scholar]
45. Marshall Fifty, Mölle M, Born J. Spindle and slow wave rhythms at slow wave sleep transitions are linked to strong shifts in the cortical direct current potential. Neuroscience. 2003;121(4):1047–1053. [PubMed] [Google Scholar]
46. •• Van Doren J, Arns M, Heinrich H, Vollebregt MA, Strehl U, Loo SK. Sustained effects of neurofeedback in ADHD: A systematic review and meta-analysis. Eur Child Adolesc Psychiatry. 2018:1–xiii. This contempo meta-analysis with ten RCTs shows that the effects of neurofeedback increase in fourth dimension, other than medication effects that diminish with time, and suggest of long-term efficacy of neurofeedback.
47. Micoulaud-Franchi JA, Geoffroy PA, Fond M, Lopez R, Bioulac S, Philip P. EEG neurofeedback treatments in children with ADHD: an updated meta-assay of randomized controlled trials. Front Hum Neurosci. 2014;eight:906. [PMC free article] [PubMed] [Google Scholar]
48. Sollie H, Larsson B, Morch WT. Comparison of mother, father, and teacher reports of ADHD core symptoms in a sample of child psychiatric outpatients. J Atten Disord. 2013;17(viii):699–710. [PubMed] [Google Scholar]
49. Bralten J, Franke B, Waldman I, Rommelse North, Hartman C, Asherson P, Banaschewski T, Ebstein RP, Gill M, Miranda A, Oades RD, Roeyers H, Rothenberger A, Sergeant JA, Oosterlaan J, Sonuga-Barke East, Steinhausen HC, Faraone SV, Buitelaar JK, Arias-Vásquez A. Candidate genetic pathways for attention arrears/hyperactivity disorder (ADHD) show association to hyperactive/impulsive symptoms in children with ADHD. J Am Acad Child Adolesc Psychiatry. 2013;52(11):1204–1212. [PubMed] [Google Scholar]
50. Wang LJ, Chen C-K, Huang YS. Changes in behaviour symptoms of patients with attention arrears/hyperactivity disorder during treatment: observation from different informants. Psychiatry Investig. 2013;10(ane):1–7. [PMC free article] [PubMed] [Google Scholar]
51. Arnold LE, Lofthouse N, Hersch S, Pan X, Hurt E, Bates B, Kassouf Thou, Moone Southward, Grantier C. EEG neurofeedback for ADHD: double-bullheaded sham-controlled randomized pilot feasibility trial. J Atten Disord. 2013;17(5):410–419. [PMC free commodity] [PubMed] [Google Scholar]
52. DeBeus R, Kaiser D. Neurofeedback with children with attention arrears hyperactivity disorder: a randomized double-blind placebo-controlled study. In: Coben R, Evans J, editors. Neurofeedback and neuromodulation: techniques and applications. San Diego: Elsevier; 2011. pp. 127–152. [Google Scholar]
53. Van Dongen-Boomsma M, Vollebregt MA, Slaats-Willemse D, Buitelaar J. A randomized placebo-controlled trial of electroencephalographic (EEG) neurofeedback in children with attention-deficit/hyperactivity disorder. J Clin Psychiatry. 2013;74(8):821–827. [PubMed] [Google Scholar]
54. Coben Robert, Hammond D. Corydon, Arns Martijn. nineteen Channel Z-Score and LORETA Neurofeedback: Does the Evidence Support the Hype? Applied Psychophysiology and Biofeedback. 2018;44(1):1–8. [PMC gratuitous article] [PubMed] [Google Scholar]
Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6538574/
0 Response to "Neurofeedback as a Treatment for Adhd a Methodological Review With Implications for Future Research"
Post a Comment