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Objective Children with epilepsy experience cognitive deficits and well-being issues that have detrimental effects on their development. Pharmacotherapy is the standard of care in epilepsy; however, few interventions exist to promote cognitive development and to mitigate disease burden. We aimed to examine the impact of two different modalities of neurofeedback (NFB) on cognitive functioning and quality-of-life (QOL) measurements in children and adolescents with controlled focal epilepsy. The study also explored the effects of NFB on clinical outcomes and electroencephalography (EEG) quantitative analysis. Methods Participants (n = 44) with controlled focal epilepsy were randomized to one of three arms: sensorimotor rhythm (SMR) NFB (n = 15), slow cortical potentials (SCP) NFB (n = 16), or sham NFB (n = 13). All participants received 25 sessions of intervention. The attention switching task (AST), Liverpool Seizure Severity Scale (LSSS), seizure frequency (SF), EEG power spectrum, and coherence were measured at baseline, postintervention, and at 3-month follow-up. Results In children and adolescents with controlled focal epilepsy, SMR training significantly reduced reaction time in the AST (p = 0.006), and this was correlated with the difference of change for theta power on EEG (p = 0.03); only the SMR group showed a significant decrease in beta coherence (p = 0.03). All groups exhibited improvement in QOL (p = Conclusions This study provides the first data on two NFB modalities (SMR and SCP) including cognitive, neurophysiological, and clinical outcomes in pediatric epilepsy. Sensorimotor rhythm NFB improved cognitive functioning, while all the interventions showed improvements in QOL, demonstrating a powerful placebo effect in the sham group.

Recently several new tests have received US Federal Drug Administration (FDA) marketing approval as aids in the diagnostic process for attention deficit hyperactivity disorder (ADHD), including the Neuropsychiatric electroencephalogram (EEG)-Based ADHD Assessment Aid (NEBA) Health test. The NEBA test relies upon an EEG-based measure, called the theta to beta ratio (TBR). Although this measure has yielded large differences between ADHD and non-ADHD groups in studies prior to 2009, recent studies and a meta-analysis could not replicate these findings. In this article, we have used the NEBA device as an exemplar for a discussion that distinguishes between FDA de novo marketing approval for a device and any claims that that device is empirically supported, scientifically validated with replicated findings. It is understood that the aims of each differ; however, for many, including the lay public as well as some mental health professionals, these terms may be confused and treated as though they are synonymous. With regard to the TBR measure, there is no reliable association or replication for its clinical usage in the ADHD diagnostic process. The recommendation for potential consumers of the NEBA Health test (as well as perhaps for other existing FDA-approved diagnostic tests) is caveat emptor (let the buyer beware!).

Brain activity assessed by electroencephalography (EEG) has been demonstrated to respond to conditioning techniques. The concept of modulating this activity has been called EEG biofeedback, more recently neurofeedback, and is based on operant learning principles. Technological advancements have significantly enhanced the ease and affordability of recording and analyzing brain activity. Thus, properly trained practitioners can implement these conditioning strategies in their practice. Recent research indicating evidenced-based efficacy has made this technique a more viable option for clinical intervention. The objective of this article is to highlight the learning principles that have provided the fundamentals of this neuromodulatory approach. In addition, it is recommended that future applications in clinical work, research, and development adhere to these principles.

The treatment of epilepsy through operant conditioning of the sensorimotor rhythm electroencephalogram has a 35-year history. Neurophysiological studies have shown that this phasic oscillation reflects an inhibitory state of the sensorimotor system. Operant learning of sensory motor rhythm production results in an upregulation of excitation thresholds within the thalamocortical sensory and motor circuitry, which in turn is associated with reduced susceptibility to seizures. The clinical benefits derived from this neurofeedback training protocol, particularly in patients that are nonresponsive to pharmacotherapy, have been documented in many independent laboratories. Recent advances in computer technology have resulted in the availability of relatively inexpensive high-quality equipment for the application of neurofeedback therapy, thus presenting a viable and promising treatment alternative to the interested clinician.

A new quantitative EEG metric is described here that examines the temporal correspondence of magnitude modulation between cortical recording sites. It is termed “comodulation,” and is applied as a cross-correlation analysis either within-subject or statistically between subject and a control database. Analysis can be performed for any selected frequency band between 1 and 23 Hz and for each of four basic functional states, including eyes closed, eyes open, and two task engagement conditions. The metric is tested here by application to clinical cases where structural alterations and functional disturbances of the brain are documented.

Two issues concerning sensorimotor EEG operant conditioning, or biofeedback, as a therapeutic modality for the treatment of seizure disorders are the focus of this review. The first relates to the question of whether relevant physiological changes are associated with this procedure. This question is addressed through review of an extensive neurophysiological literature that is likely unfamiliar to many clinicians but that documents both immediate and sustained functional changes that are consistent with elevation of seizure thresholds. The second focuses on the clinical efficacy of this method and whether it should carry the designation of "experimental". This designation is challenged through an assessment of over 25 years of peer-reviewed research demonstrating impressive EEG and clinical results achieved with the most difficult subset of seizure patients.

Averaged event-related EEG frequency response profiles were generated from normalized spectral analysis data obtained in 2 studies of short-term memory. A continuous performance task was used requiring a keyboard response to targeted letter sequences presented on a video screen at 2 sec. intervals. Seven 2 Hz frequency bands between 5–15 Hz were evaluated. In the first study (n=14) response profiles from control and target stimuli were compared. This analysis disclosed 1) a short latency increase at 5–7 and 7–9 Hz in posterior cortex that was identical in both conditions and was attributed to frequency manifestations of the extrinsic visual evoked response (VEP), 2) a separate long-latency increase of uncertain origin at 5–7 Hz in anterior cortex only in the task condition, and 3) a generalized mid-latency alpha frequency suppression and recovery pattern (event-related desynchronization, or ERD) in all bands during both conditions. The ERD in bands between 9–13 Hz was significantly increased at left central and bilateral parietal cortex during target recall. The second study (n=26) compared good vs. poor performance in the target recall task. Findings disclosed significant differences at 7–9 Hz localized to posterior temporal cortex bilaterally. These differences included reduced magnitude in the VEP component and increased suppression in the ERD component among good performers.

This review traces the application of electroencephalographic (EEG) operant conditioning, or biofeedback, from animal research to its emergence as an alternative treatment for the major types of seizure disorder. Initial animal studies focusing on brain mechanisms that mediate learned behavioral inhibition revealed a uniquely correlated 12- to 15-Hz EEG rhythm localized to sensorimotor cortex. We labeled this the sensorimotor rhythm, or SMR. The similarity of the SMR to the known EEG spindle pattern during quiet sleep led to the novel idea of attempting to increase the SMR using EEG operant conditioning. The hypothesis was that this might produce a corresponding increase in sleep spindle activity, thus establishing a common EEG marker for the state of motor inhibition. Results supported this hypothesis but led also to the accidental discovery of an anticonvulsant effect on drug-induced seizures in cats and monkeys. Continuing animal studies identified a pattern of neurophysiologic responses correlated with the SMR in primary motor pathways. These and other findings were indicative of reduced motor excitability. Simultaneously, we undertook studies in human epileptic subjects that documented a significant reduction in seizure incidence and severity, together with EEG pattern normalization. This work expanded internationally, resulting in numerous well-controlled group and single-case studies summarized in recent meta-analyses. Exciting new findings in functional neuroimaging/EEG correlation studies provide a rational model for the basis of these clinical effects. In recognition of the diversity of clinical applications of EEG biofeedback and the complexity of seizure disorders, this review also details specific methods used in our EEG biofeedback program.

This review provides an updated overview of the neurophysiological rationale, basic and clinical research literature, and current methods of practice pertaining to clinical neurofeedback. It is based on documented findings, rational theory, and the research and clinical experience of the authors. While considering general issues of physiology, learning principles, and methodology, it focuses on the treatment of epilepsy with sensorimotor rhythm (SMR) training, arguably the best established clinical application of EEG operant conditioning. The basic research literature provides ample data to support a very detailed model of the neural generation of SMR, as well as the most likely candidate mechanism underlying its efficacy in clinical treatment. Further, while more controlled clinical trials would be desirable, a respectable literature supports the clinical utility of this alternative treatment for epilepsy. However, the skilled practice of clinical neurofeedback requires a solid understanding of the neurophysiology underlying EEG oscillation, operant learning principles and mechanisms, as well as an in-depth appreciation of the ins and outs of the various hardware/software equipment options open to the practitioner. It is suggested that the best clinical practice includes the systematic mapping of quantitative multi-electrode EEG measures against a normative database before and after treatment to guide the choice of treatment strategy and document progress towards EEG normalization. We conclude that the research literature reviewed in this article justifies the assertion that neurofeedback treatment of epilepsy/seizure disorders constitutes a well-founded and viable alternative to anticonvulsant pharmacotherapy.

The AAN/ACNS report is misleadingly negative regarding the current status of quantitative EEG and tends to discourage its development and use with other related clinical problems. There have been many excellent studies showing that QEEG can be useful for the evaluation and understanding of mild traumatic brain injury, learning disabilities, attention deficit disorders, alcoholism, depression, and other types of substance abuse. In fact, Hughes and John recently provided in this Journal an extensive and detailed review of the use of QEEG in psychiatric disorders. The bias of the AAN/ACNS report is also evident when contrasted to the outstanding review of the clinical utility of QEEG by the American Medical EEG Association, which clearly articulates the opposite points in many cases and concludes that QEEG has reached maturity. At present, the most one can say is that there are legitimate scientific debate and differences of opinion concerning the utility of QEEG, as there are in many other areas of medicine. The AAN/ACNS article should not be considered the definitive opinion. Too many implications for health care are at stake. The debate and research may continue without withholding valuable help from the public. We hope that revised guidelines will be drafted in such a way as to encourage the development of quantitative EEG and brain mapping rather than discourage future research support and use of QEEG with patients. Furthermore, we strongly feel that this technology should be available to, and be explored and used by, nonphysicians who are properly trained and certified.

Amygdala kindling stimulation produced significant changes in plasma zinc levels in cats otherwise unaffected by zinc loading or deprivation. While a normal diet had no effect, moderate zinc loading was accompanied by a marked increase in plasma zinc during kindling. Conversely, plasma zinc sharply declined in animals fed a zinc-deficient diet. Corresponding differences were obtained in the development of generalized seizures with kindling such that loading delayed and deprivation accelerated this process.

Since our initial reports of successful seizure reduction in drug-refractory epileptics through the application of EEG biofeedback techniques developed in cat research (Sterman & Friar, 1972; Sterman, Macdonald, & Stone, 1974), there have been abundant confirmations of this therapeutic effect in man (Finley, Smith, & Etherton, 1975; Seifert & Lubar, 1975; Ellertsen & Klove, 1976; Lubar & Bahler, 1976; Wyler, Lockard, Ward, & Finch, 1976; Wyler, Robbins, & Dodrill, 1979; Sterman & Macdonald, 1978; Kuhlman, 1978; Cott, Pavloski, & Black, 1979; Sterman & Shouse, 1981; Lubar, Shabsin, Natelson, Holder, Whitsett, Pamplin, & Krulikowski, 1981). Moreover, the questions immediately raised concerning the incorporation of adequate control procedures and the specificity of this effect have now been put to rest. What remains at issue, however, is an understanding of the mechanism responsible for the elevated seizure thresholds produced by this technique (see, for example, Wyler, Chapter 6). Also in question is the appropriate clinical utilization of EEG biofeedback therapy as an alternative to extended drug trials or neurosurgery for poorly controlled patients. This discussion will address both of these issues.

Recent advances in the diagnosis of epilepsy include the development of a clinically useful classification of epileptic seizures and the recognition of specific epileptic disorders. These advances have been aided by the advent of x-ray computed tomography, long-term electroencephalographic telemetry, and video monitoring. Techniques for functional imaging of the human brain promise even greater diagnostic capabilities. New antiepileptic drugs have improved medical management, and technical and theoretical advances in pharmacokinetics have permitted physicians to design balanced dosing for individual patients. Although currently underused, surgical treatment of partial complex epilepsy can be safe and effective when used appropriately. Operant conditioning of electroencephalography may become another practical alternative therapy. Contributions of basic research to understanding the complications of status epilepticus have influenced treatment protocols and greatly improved the prognosis of this potentially lethal condition.