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Neurofeedback (NF) is a training to enhance self-regulatory capacity over brain activity patterns and consequently over brain mental states. Recent findings suggest that NF is a promising alternative for the treatment of attention-deficit/hyperactivity disorder (ADHD). We comprehensively reviewed literature searching for studies on the effectiveness and specificity of NF for the treatment of ADHD. In addition, clinically informative evidence-based data are discussed. We found 3 systematic review on the use of NF for ADHD and 6 randomized controlled trials that have not been included in these reviews. Most nonrandomized controlled trials found positive results with medium-to-large effect sizes, but the evidence for effectiveness are less robust when only randomized controlled studies are considered. The direct comparison of NF and sham-NF in 3 published studies have found no group differences, nevertheless methodological caveats, such as the quality of the training protocol used, sample size, and sample selection may have contributed to the negative results. Further data on specificity comes from electrophysiological studies reporting that NF effectively changes brain activity patterns. No safety issues have emerged from clinical trials and NF seems to be well tolerated and accepted. Follow-up studies support long-term effects of NF. Currently there is no available data to guide clinicians on the predictors of response to NF and on optimal treatment protocol. In conclusion, NF is a valid option for the treatment for ADHD, but further evidence is required to guide its use.


Since the first reports of neurofeedback treatment in Attention Deficit Hyperactivity Disorder (ADHD) in 1976, many studies have investigated the effects of neurofeedback on different symptoms of ADHD such as inattention, impulsivity and hyperactivity. This technique is also used by many practitioners, but the question as to the evidence-based level of this treatment is still unclear. In this study selected research on neurofeedback treatment for ADHD was collected and a meta-analysis was performed.

Both prospective controlled studies and studies employing a pre- and post-design found large effect sizes (ES) for neurofeedback on impulsivity and inattention and a medium ES for hyperactivity. Randomized studies demonstrated a lower ES for hyperactivity suggesting that hyperactivity is probably most sensitive to nonspecific treatment factors.

Due to the inclusion of some very recent and sound methodological studies in this meta-analysis, potential confounding factors such as small studies, lack of randomization in previous studies and a lack of adequate control groups have been addressed, and the clinical effects of neurofeedback in the treatment of ADHD can be regarded as clinically meaningful. Three randomized studies have employed a semi-active control group which can be regarded as a credible sham control providing an equal level of cognitive training and client-therapist interaction. Therefore, in line with the AAPB and ISNR guidelines for rating clinical efficacy, we conclude that neurofeedback treatment for ADHD can be considered “Efficacious and Specific” (Level 5) with a large ES for inattention and impulsivity and a medium ES for hyperactivity.


Although methodological weaknesses limited early research into electroencephalograpic (EEG) biofeedback (EBF) for treatment of attention-deficit/hyperacticity disorder (ADHD), recent stronger randomized controlled trials have provided substantial, but not yet conclusive, empirical support. Additional support is found in research on functional magnetic resonance imaging (fMRI) feedback and brain-computer interface (BCI) models which involve feedback-guided learning to achieve control over neural activation.

Orbitofrontal cortex neurofeedback produces lasting changes in contamination anxiety and resting-state connectivity

Anxiety is a core human emotion but can become pathologically dysregulated. We used functional magnetic resonance imaging (fMRI) neurofeedback (NF) to noninvasively alter patterns of brain connectivity, as measured by resting-state fMRI, and to reduce contamination anxiety. Activity of a region of the orbitofrontal cortex associated with contamination anxiety was measured in real time and provided to subjects with significant but subclinical anxiety as a NF signal, permitting them to learn to modulate the target brain region. NF altered network connectivity of brain regions involved in anxiety regulation: subjects exhibited reduced resting-state connectivity in limbic circuitry and increased connectivity in the dorsolateral prefrontal cortex. NF has been shown to alter brain connectivity in other contexts, but it has been unclear whether these changes persist; critically, we observed changes in connectivity several days after the completion of NF training, demonstrating that such training can lead to lasting modifications of brain functional architecture. Training also increased subjects’ control over contamination anxiety several days after the completion of NF training. Changes in resting-state connectivity in the target orbitofrontal region correlated with these improvements in anxiety. Matched subjects undergoing a sham feedback control task showed neither a reorganization of resting-state functional connectivity nor an improvement in anxiety. These data suggest that NF can enable enhanced control over anxiety by persistently reorganizing relevant brain networks and thus support the potential of NF as a clinically useful therapy.


Alpha, theta and alpha-theta enhancements are effective treatments of the anxiety disorders (Table 1). Alpha suppression is also effective, but less so (Table 2). Perceived success in carrying out the task plays an important role in clinical improvement.


In the short term, Alfa EEG biofeedback therapy is almost as efficacious as pharmacological intervention in the management of anxiety symptoms, and relatively more useful in females.

Prognosis of this pervasive disorder depends on the intellectual abilities: the better intellectual functioning, the possibilities for life adaptation are higher QEEG shows generally increased delta-theta activity in frontal region of the brain which is related to poor cognitive abilities.
Brain rate measured in CZ shows slow brain activity related to under arousal. Pharmacotherapy combined with behavior therapy, social support and especially neurofeedback technique promise slight improvements.


Neurofeedback for the Autism Spectrum

Neurofeedback is a highly promising emerging therapy for the autism spectrum. At issue here is a tool for the direct training of brain function, one that has already shown itself highly effective in addressing a wide range of “mental health” concerns. As has been the case for other therapies, its application to the autism spectrum has been complicated by the inherent complexity of the condition we confront. In the following, we recapitulate the development of neurofeedback for the autism spectrum and give some guidance to both therapists and parents with regard to the choices open to them.


Neurofeedback is an intervention that is showing a lot of promise for people diagnosed with Autistic Spectrum Disorder (ASD). While other childhood behaviour disorders such as Attention Deficit Hyperactivity Disorder (ADHD) have been in the neurofeedback limelight for some years, it would appear that ASD is about to have its day in the sun. Recent research is showing that children with ASD are responding very well to both electroencephalographic (EEG) and haemoencephalographic (HEG) neurofeedback. Furthermore, our own research indicates that neurofeedback can be an effective schoolbased intervention for children in the autistic spectrum.

A new diagnostic category is emerging: Childhood bipolar disorder. It was traditionally thought that as few as one in 200 cases of bipolar disorder had an onset which could be traced to childhood. Biederman’s recent research shows that perhaps on the other of 20% of children identified as ADHD could be on the way to developing full-blown bipolar disorder. To make this identification, however, the markers of childhood bipolar disorder are destructive rage and irritation rather than the euphoria and elation that characterizes the adult form. The proof that the childhood form of the disorder metamorphoses into the adult form eventually must still be outstanding. The model is still too new.

The Bipolar Disorder model is the latest attempt to give diagnostic order and specificity to the most extreme end of the disruptive behavior spectrum. It is of course not the first. Years ago, George Murray of Harvard suggested that temporal lobe epilepsy was under-recognized by mental health professionals by a factor of 25. Clearly he was not referring to overt seizures here, which tend to attract clinical attention, but rather to the subclinical seizure activity that can manifest in erratic behavior, severe mood swings, rages and explosive behavior – but goes unrecognized as such. Partly based on Murray’s model, we have emphasized as well the continuity between overt seizures and extreme behavioral disregulation. Both are effectively treated with anti-convulsants, and both respond to the same Neurofeedback protocols. The developments in Neurofeedback therapy neatly parallel developments in psychopharmacology. But seizures have remained in the domain of neurology, and other mental health professionals have been reluctant to build on that model.


Over the years we have talked about our own son Brian in terms of his temporal lobe epilepsy, and we generalized from there to severe behavioral disorders. That always had limited appeal as a model for both practitioners attending our classes and for parents of difficult children. Most professionals don’t relate readily to “subclinical seizure phenomena,” nor are parents thrilled to see the term seizure disorder used in connection with their children unless the diagnosis is obligatory. Talking about seizure disorder in larger terms was a non-starter.

Pain is one of several sensory systems that keep us apprised of the status of our bodies. As we hurry through our daily lives, we usually view pain at the very least as an inconvenience, if not a major disruption. It’s fortunate that we have our pain sensors – they provide a valuable warning to us that we need to stop and take care of ourselves. Pain has considerable survival value, but when an injury has healed and the pain continues unabated, or when pain seems to have no obvious connection to any injury, it no longer serves a useful purpose. Pain of this type is referred to as chronic pain, and once you have fallen under its sway, it may be very difficult to escape.

The Challenge of Pain Management The management of chronic pain has always been a medical challenge. Treatment often involves increasing doses of a variety of medications in an effort to gain a measure of relief. In some instances, the pain is significantly reduced with the use of medication, but when the drugs are removed the pain returns, and so the meds become a more or less permanent fixture of life, often resulting in drug dependence or even addiction. In other cases even heavy use of medication provides the sufferer little or no relief; the brain simply adjusts to the presence of the medications and demands more, while the pain continues


Modern views conceptualize pain as a brain-based phenomenon. Advances in neuroscience have allowed us to explore how the varieties of pain experience we observe are mediated by the complex relationships between the mind, brain, and body. We have learned that far from activating a single “pain” center in the brain, pain results in widespread activation of multiple cortical and subcortical regions involved in many functions including primary and secondary somatosensory areas (SI, SII), primary motor (MI) and premotor cortices (PMC), supplementary motor area (SMA), basal ganglia, parietal and insular cortices, periaqueductal gray (PAG), rostral ventromedial medulla, hippocampus, amygdala, parahippocampus, anterior cingulate cortex (ACC), and prefrontal cortex (PFC).

Pain experience can be influenced by many cognitive, emotional, and other factors affecting brain function. Indeed, evidence suggests that many of these areas participate in a pain modulatory pathway and can have a significant effect on pain experience. The brain’s central role in pain experience is underscored by the growing appreciation that chronic pain involves dysregulation of central pain modulatory systems. A number of studies have revealed that the brains of patients with chronic pain are functionally and structurally altered compared to healthy controls. Alterations in functional connectivity between brain regions have been found in various chronic pain conditions


If an individual can learn to directly control activation of localized regions within the brain, this approach might provide control over the neurophysiological mechanisms that mediate behavior and cognition and could potentially provide a different route for treating disease. Control over the endogenous pain modulatory system is a particularly important target because it could enable a unique mechanism for clinical control over pain. Here, we found that by using real-time functional MRI (rtfMRI) to guide training, subjects were able to learn to control activation in the rostral anterior cingulate cortex (rACC), a region putatively involved in pain perception and regulation. When subjects deliberately induced increases or decreases in rACC fMRI activation, there was a corresponding change in the perception of pain caused by an applied noxious thermal stimulus. Control experiments demonstrated that this effect was not observed after similar training conducted without rtfMRI information, or using rtfMRI information derived from a different brain region, or sham rtfMRI information derived previously from a different subject. Chronic pain patients were also trained to control activation in rACC and reported decreases in the ongoing level of chronic pain after training. These findings show that individuals can gain voluntary control over activation in a specific brain region given appropriate training, that voluntary control over activation in rACC leads to control over pain perception, and that these effects were powerful enough to impact severe, chronic clinical pain.

Many patients show no or incomplete responses to current pharmacological or psychological therapies for depression. Here we explored the feasibility of a new brain self-regulation technique that integrates psychological and neurobiological approaches through neurofeedback with functional magnetic resonance imaging (fMRI). In a proof-of-concept study, eight patients with depression learned to upregulate brain areas involved in the generation of positive emotions (such as the ventrolateral prefrontal cortex (VLPFC) and insula) during four neurofeedback sessions. Their clinical symptoms, as assessed with the 17-item Hamilton Rating Scale for Depression (HDRS), improved significantly. A control group that underwent a training procedure with the same cognitive strategies but without neurofeedback did not improve clinically. Randomized blinded clinical trials are now needed to exclude possible placebo effects and to determine whether fMRI-based neurofeedback might become a useful adjunct to current therapies for depression.


Two experiments were done with subjects from a paid pool of undergraduates. In each study, there were five 1-hour sessions on each of 5 days: (1) Baseline: Rewards given for randomly selected 20% of the 700-ms sequential epochs; mean and SD of baseline power differences determined. 2) Exploration: Subjects were rewarded when right minus left alpha differences in an epoch were greater than the baseline mean plus about .85 SD (p = .20); subjects told to discover how to generate rewards. (3)-(5). Training: Subjects were paid (over and above the $8/h flat rate) in proportion to their hit rates. In the first study (in which active filters passed 8-12 Hz activity, and the rectified, integrated amplitude was utilized), 6 of 8 subjects met learning criteria (a significant difference between baseline and training scores). In the second study (in which on-line FFTs were used to extract alpha power), 3 of 5 subjects met learning criteria.


This was an experimental study of 14 alcoholic outpatients using the Peniston and Kulkosky (1989, 1991) brainwave treatment protocol for alcohol abuse. After temperature biofeedback pretraining, experimental subjects completed 20 40-minute sessions of alpha-theta brainwave neurofeedback training (BWNT). Experimentally treated alcoholics with depressive syndrome showed sharp reductions in self-assessed depression (Beck’s Depression Inventory). On the Millon Clinical Multiaxial Inventory-I, the experimental subjects showed significant decreases on the BR scores: schizoid, avoidant, dependent, histrionic, passive-aggression, schizotypal, borderline, anxiety, somatoform, hypomanic, dysthmic, alcohol abuse, drug abuse, psychotic thinking, and psychotic depression. Twenty-one-month follow-up data indicated sustained prevention of relapse in alcoholics who completed BWNT.

Phonological theories of dyslexia assume a specific deficit in representation, storage and recall of phonemes. Various brain imaging techniques, including qEEG, point to the importance of a range of areas, predominantly the left hemispheric temporal areas. This study attempted to reduce reading and spelling deficits in children who are dyslexic by means of neurofeedback training based on neurophysiological differences between the participants and gender and age matched controls. Nineteen children were randomized into an experimental group receiving qEEG based neurofeedback (n = 10) and a control group (n = 9). Both groups also received remedial teaching. The experimental group improved considerably in spelling (Cohen’s d = 3). No improvement was found in reading. An indepth study of the changes in the qEEG power and coherence protocols evidenced no fronto-central changes, which is in line with the absence of reading improvements. A significant increase of alpha coherence was found, which may be an indication that attentional processes account for the improvement in spelling. Consideration of subtypes of dyslexia may refine the results of future studies.

Here we present several refinements to a model of feedback control for the suppression of epileptic seizures. We utilize a stochastic partial differential equation (SPDE) model of the human cortex. First, we verify the strong convergence of numerical solutions to this model, paying special attention to the sharp spatial changes that occur at electrode edges. This allows us to choose appropriate step sizes for our simulations; because the spatial step size must be small relative to the size of an electrode in order to resolve its electrical behavior, we are able to include a more detailed electrode profile in the simulation. Then, based on evidence that the mean soma potential is not the variable most closely related to the measurement of a cortical surface electrode, we develop a new model for this. The model is based on the currents flowing in the cortex and is used for a simulation of feedback control. The simulation utilizes a new control algorithm incorporating the total integral of the applied electrical potential. Not only does this succeed in suppressing the seizure-like oscillations, but it guarantees that the applied signal will be charge-balanced and therefore unlikely to cause cortical damage.


About one third of patients with epilepsy do not benefit from medical treatment. For these patients electroencephalographic (EEG) biofeedback is a viable alternative. EEG biofeedback, or neurofeedback, normalizes or enhances EEG activity by means of operant conditioning. While dozens of scientific reports have been published on neurofeedback for seizure disorder, most have been case series with too few subjects to establish efficacy. The purpose of this paper is to meta-analyze existing research on neurofeedback and epilepsy. We analyzed every EEG biofeedback study indexed in MedLine, PsychInfo, and PsychLit databases between 1970 and 2005 on epilepsy that provided seizure frequency change in response to feedback. Sixty-three studies have been published, 10 of which provided enough outcome information to be included in a meta-analysis. All studies consisted of patients whose seizures were not controlled by medical therapies, which is a very important factor to keep in mind when interpreting the results. Nine of 10 studies reinforced sensorimotor rhythms (SMR) while 1 study trained slow cortical potentials (SCP). All studies reported an overall mean decreased seizure incidence following treatment and 64 out of 87 patients (74%) reported fewer weekly seizures in response to EEG biofeedback. Treatment effect was mean log (post/pre) where pre and post represent number of seizures per week prior to treatment and at final evaluation, respectively. Due to prevalence of small groups, Hedges's g was computed for effect size. As sample heterogeneity was possible (Q test, p=.18), random effects were assumed and the effect of intervention was -0.233, SE = 0.057, z = -4.11, p<.001. Based on this meta-analysis, EEG operant conditioning was found to produce a significant reduction on seizure frequency. This finding is especially noteworthy given the patient group, individuals who had been unable to control their seizures with medical treatment.


With electroencephalographic (EEG) biofeedback (or neurofeedback), it is possible to train the brain to de-emphasize rhythms that lead to generation and propagation of seizure and emphasize rhythms that make seizures less likely to occur. With recent improvements in quantitative EEG measurement and improved neurofeedback protocols, it has become possible in clinical practice to eliminate seizures or reduce the amount of medication required to control them. In this article, the history of neurofeedback for epilepsy is presented followed by discussions of the relevant neurophysiology of epilepsy. A model of how neurofeedback might raise the seizure threshold is then presented. Clinical experience using a quantitative EEG-guided approach is described, including a representative case study.

Biofeedback (BFB) is an established intervention in the rehabilitation of headache and other pain disorders. Little is known about this treatment option for fibromyalgia syndrome (FMS). The aim of the present review is to integrate and critically evaluate the evidence regarding the efficacy of biofeedback for FMS. Methods. We conducted a literature search using Pubmed, clinicaltrials.gov (National Institute of Health), Cochrane Central Register of Controlled Trials, PsycINFO, SCOPUS, and manual searches. The effect size estimates were calculated using a random-effects model. Results. The literature search produced 123 unique citations. One hundred sixteen records were excluded. The meta-analysis included seven studies (321 patients) on EEG-Biofeedback and EMG-Biofeedback. In comparison to control groups, biofeedback (BFB) significantly reduced pain intensity with a large effect size (g = 0.79; 95% CI: 0.22–1.36). Subgroup analyses revealed that only EMG-BFB and not EEG-BFB significantly reduced pain intensity in comparison to control groups (g = 0.86; 95% CI: 0.11–1.62). BFB did not reduce sleep problems, depression, fatigue, or health-related quality of life in comparison to a control group. Discussion. The interpretation of the results is limited because of a lack of studies on the long-term effects of EMG-BFB in FMS. Further research should focus on the long-term efficacy of BFB in fibromyalgia and on the identification of predictors of treatment response.


Contrary to the belief that schizophrenic patients will be unable to learn self control of electrocortical activity due to attentional and motivational deficits, the two studies which have investigated this, both involving operant conditioning of slow cortical potentials, have demonstrated that self regulation can take place. This was particularly true of a study of interhemispheric control. Learning difficulties were found to be more to do with sustaining motivation towards the end of sessions or training programs, rather than in initial learning. Schizotypical features in the normal population have in the case of anhedonia been associated with slower learning, while withdrawn introversion has been associated with faster learning. In view of the affirmative evidence and advances in understanding the functional significance of electroencephalographic (EEG) rhythms, the undertaking of therepeutic regimens with electrocortical operant conditioning is warranted in the schizophrenia spectrum.


We designed a randomized, rater blind study to assess the efficacy of EEG Biofeedback (Neurofeedback-NFB) in patients with fibromyalgia syndrome (FMS). Eighteen patients received twenty sessions of NFB-sensory motor rhythm (SMR) treatment (NFB group) during 4 weeks, and eighteen patients were given 10 mg per day escitalopram treatment (control group) for 8 weeks. Visual Analog Scales for pain and fatigue, Hamilton and Beck Depression and Anxiety Inventory Scales, Fibromyalgia Impact Questionnaire and Short Form 36 were used as outcome measures which were applied at baseline and 2nd, 4th, 8th, 16th, 24th weeks. Mean amplitudes of EEG rhythms (delta, theta, alpha, SMR, beta1 and beta2) and theta/SMR ratio were also measured in NFB group. All post-treatment measurements showed significant improvements in both of the groups (for all parameters p < 0.05). NFB group displayed greater benefits than controls (for all parameters p < 0.05). Therapeutic efficacy of NFB was found to begin at 2nd week and reached to a maximum effect at 4th week. On the other hand, the improvements in SSRI treatment were also detected to begin at 2nd week but reached to a maximum effect at 8th week. No statistically significant changes were noted regarding mean amplitudes of EEG rhythms (p > 0.05 for all). However, theta/SMR ratio showed a significant decrease at 4th week compared to baseline in the NFB group (p < 0.05). These data support the efficacy of NFB as a treatment for pain, psychological symptoms and impaired quality of life associated with fibromyalgia.Neurofeedback Intervention in Fibromyalgia Syndrome;
A Randomized, Controlled, Rater Blind Clinical Trial [link]

Biofeedback (BFB) is an established intervention in the rehabilitation of headache and other pain disorders. Little is known about this treatment option for fibromyalgia syndrome (FMS). The aim of the present review is to integrate and critically evaluate the evidence regarding the efficacy of biofeedback for FMS. Methods. We conducted a literature search using Pubmed, clinicaltrials.gov (National Institute of Health), Cochrane Central Register of Controlled Trials, PsycINFO, SCOPUS, and manual searches. The effect size estimates were calculated using a random-effects model. Results. The literature search produced 123 unique citations. One hundred sixteen records were excluded. The meta-analysis included seven studies (321 patients) on EEG-Biofeedback and EMG-Biofeedback. In comparison to control groups, biofeedback (BFB) significantly reduced pain intensity with a large effect size (g = 0.79; 95% CI: 0.22–1.36). Subgroup analyses revealed that only EMG-BFB and not EEG-BFB significantly reduced pain intensity in comparison to control groups (g = 0.86; 95% CI: 0.11–1.62). BFB did not reduce sleep problems, depression, fatigue, or health-related quality of life in comparison to a control group. Discussion. The interpretation of the results is limited because of a lack of studies on the long-term effects of EMG-BFB in FMS. Further research should focus on the long-term efficacy of BFB in fibromyalgia and on the identification of predictors of treatment response.


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We designed a randomized, rater blind study to assess the efficacy of EEG Biofeedback (Neurofeedback-NFB) in patients with fibromyalgia syndrome (FMS). Eighteen patients received twenty sessions of NFB-sensory motor rhythm (SMR) treatment (NFB group) during 4 weeks, and eighteen patients were given 10 mg per day escitalopram treatment (control group) for 8 weeks. Visual Analog Scales for pain and fatigue, Hamilton and Beck Depression and Anxiety Inventory Scales, Fibromyalgia Impact Questionnaire and Short Form 36 were used as outcome measures which were applied at baseline and 2nd, 4th, 8th, 16th, 24th weeks. Mean amplitudes of EEG rhythms (delta, theta, alpha, SMR, beta1 and beta2) and theta/SMR ratio were also measured in NFB group. All post-treatment measurements showed significant improvements in both of the groups (for all parameters p < 0.05). NFB group displayed greater benefits than controls (for all parameters p < 0.05). Therapeutic efficacy of NFB was found to begin at 2nd week and reached to a maximum effect at 4th week. On the other hand, the improvements in SSRI treatment were also detected to begin at 2nd week but reached to a maximum effect at 8th week. No statistically significant changes were noted regarding mean amplitudes of EEG rhythms (p > 0.05 for all). However, theta/SMR ratio showed a significant decrease at 4th week compared to baseline in the NFB group (p < 0.05). These data support the efficacy of NFB as a treatment for pain, psychological symptoms and impaired quality of life associated with fibromyalgia.

37 migraine patients underwent an average of 40 neurofeedback sessions combined with thermal biofeedback in an outpatient biofeedback clinic. All patients were on at least one type of medication for migraine; preventive, abortive or rescue. Patients kept daily headache diaries a minimum of two weeks prior to treatment and throughout treatment showing symptom frequency, severity, duration and medications used. Treatments were conducted an average of three times weekly over an average span of 6 months. Headache diaries were examined after treatment and a formal interview was conducted. After an average of 14.5 months following treatment, a formal interview was conducted in order to ascertain duration of treatment effects.


Seventy-one patients with recurrent migraine headaches, aged 17-62, from one neurological practice, completed a quantitative electroencephalogram (QEEG) procedure. All QEEG results indicated an excess of high-frequency beta activity (21-30 Hz) in 1-4 cortical areas. Forty-six of the 71 patients selected neurofeedback training while the remaining 25 chose to continue on drug therapy. Neurofeedback protocols consisted of reducing 21-30 Hz activity and increasing 10 Hz activity (5 sessions for each affected site). All the patients were classified as migraine without aura.

While neurofeedback has been extensively studied in the treatment of many disorders, there have been only three published reports, by D.C. Hammond, on its clinical effects in the treatment of obsessive compulsive disorder (OCD). In this paper the efficacy of QEEG-guided neurofeedback for subjects with OCD was studied as a case series. The goal was to examine the clinical course of the OCD symptoms and assess the efficacy of QEEG guided neurofeedback training on clinical outcome measures. Thirty-six drug resistant subjects with OCD were assigned to 9-84sessions of QEEG-guided neurofeedback treatment. Daily sessions lasted 60minutes where 2 sessions with half-hour applications with a 30 minute rest given between sessions were conducted per day. Thirty-three outof36 subjects who received neurofeedback training showed clinical improvement according to the Yale-Brown obsessive-compulsive scale (Y-BOCS). The Minnesota multiphasic inventory(MMPI) was ad-ministered before and after treatment to 17 of the subjects. The MMPI results showed significant improvements not only in OCD measures, but all of the MMP1 scores showed a general decrease. Finally ,according to the physicians’ evaluation of the subjects using the clinical global impression scale (CGI), 33 of the 36 subjects were rated as improved. Thirty-six of the subjects were followed for an average of 26months after completing the study. According to follow-up interviews conducted with them and/or their family members 19of the subjects maintained the improvements in their OCD symptoms. This study provides good evidence for the efficacy of neurofeedback treatment in OCD. The results of this study encourage further controlled research in this area.


Two patients with OCD were screened with the Padua Inventory, the Yale-Brown ObsessiveCompulsive Scale, qEEG, and in one case, the MMPI. Each patient displayed different qEEG patterns associated with OCD. Neurofeedback individualized to qEEG findings was used.


This study presents a clinical treatment regime for the treatment of tic manifestation, both simple and complex. The response of a case of simple tic and a case of complex tic (Gilles de la Tourette’s syndrome) to EEG sensorimotor rhythm biofeedback training are presented. Specifically, the simple and the complex tic, both of long duration, were eliminated via this EEG biofeedback training procedure. It is hypothesized that this exercising of the sensorimotor cortex resulted in increased activation of this cerebrocortical subsystem and was reflected in increased voluntary muscle control and a heightened threshold for random motor discharge, resulting in the elimination of both tics as in the response of cases of epilepsy with motor involvement to EEG sensorimotor rhythm biofeedback training. The additional psychophysiologic sequelae of the complex tic–attention deficit disorder–remediated in the manner of the response of learning-disabled to EEG sensorimotor rhythm biofeedback training.

The gradual emergence of symptoms following exposure to traumatic events has presented a major conceptual challenge to psychiatry. The mechanism that causes the progressive escalation of symptoms with the passage of time leading to delayed onset post-traumatic stress disorder (PTSD) involves the process of sensitization and kindling. The development of traumatic memories at the time of stress exposure represents a major vulnerability through repeated environmental triggering of the increasing dysregulation of an individual’s neurobiology. An increasing body of evidence demonstrates how the increased allostatic load associated with PTSD is associated with a significant body of physical morbidity in the form of chronic musculoskeletal pain, hypertension, hyperlipidaemia, obesity and cardiovascular disease. This increasing body of literature suggests that the effects of traumatic stress need to be considered as a major environmental challenge that places individual’s physical and psychological health equally at risk. This broader perspective has important implications for developing treatments that address the underlying dysregulation of cortical arousal and neurohormonal abnormalities following exposure to traumatic stress.


The application of neurofeedback to post traumatic stress disorder (PTSD) in returning veterans is described
herein and is illustrated with two case histories. Initially, frequency-based electroencephalogram training was employed to promote functional recovery, in the manner of the traditional sensorimotor rhythm/beta approach. An optimization procedure was employed in which the reinforcement frequency is tailored to the client on the basis of symptom response, with particular regard for the regulation of arousal. Low frequencies, down to .01 Hz, have been found especially useful in the remediation of post traumatic stress disorder. This training was complemented with traditional alpha-theta work as pioneered at the
Menninger Foundation and by Peniston. The objective here is experiential, because prior traumas typically are revisited in a nonforced, nontraumatic manner. The benign witnessing of traumas consolidates the experience of safety for which the prior training laid the groundwork. Collectively, this approach has been found to be much better tolerated than traditional exposure therapies. In addition, it is helpful in the shedding of substance dependencies that are common in treatment-resistant PTSD


Electroencephalographic (EEG) biofeedback has been in use since the early 1970’s for treatment of anxiety disorders and a variety of psychosomatic disorders. Early work conducted by researchers such as Kamiya and Kliterman focused on alpha wave biofeedback (Kamyi & Noles, 1970). Much of this initial research associated changes in EEG state with different states of consciousness (Basmajian, 1989). Researchers learned that certain tasks, such as mental arithmetic, reduce or suppress alpha wave production. Furthermore, researchers found that these changes in brain activity were positively correlated with changes in electromyographic (EMG) activity and skin temperature. This finding was significant in that it suggested that brainwave activity could be operantly conditioned in the same manner as EMG or temperature. Alpha waves are smooth, high amplitude waves in frequency range of 9-13 Hertz (Hz). Alpha wave biofeedback was explored by some researchers, as a treatment adjunct for alcohol abuse (Passini, Watson, and Dehnel, 1977). There were two theoretical rationales: first, investigators had reported that EEGs of alcoholics were “deficient in alpha rhythms and alcohol use induced more alpha wave activity (Pollock, Volavka, Goodwin, et al., 1983). Clinicians speculated that alcoholics might drink less if they could be taught to produce more alpha waves (Jones & Holmes, 1976). Secondly, many alcoholics and other drug abusers reported using alcohol or other drugs to relax. Thus, biofeedback training was proposed as a way teach alcoholics an alternative to using alcohol to relax. Alpha training did not, however, appear to be of benefit to most alcohol abusers because they were unable to learn to increase their production of alpha waves.

Progress in identifying the neural correlates of auditory verbal hallucinations (AVHs) experienced by patients with schizophrenia has not fulfilled its promise to lead to new methods of treatments. Given the existence of a large number of such patients who have AVHs that are refractory to traditional treatments, there is the urgent need for the development of new effective interventions. This article proposes that the technique of neurofeedback may be an appropriate method to allow the translation of pure research findings from AVH-research into a clinical intervention. Neurofeedback is a method through which individuals can self-regulate their neural activity in specific neural regions/frequencies, following operant conditioning of their intentional manipulation of visually presented real-time feedback of their neural activity. Four empirically testable hypotheses are proposed as to how neurofeedback may be employed to therapeutic effect in patients with AVHs.


Contrary to the belief that schizophrenic patients will be unable to learn self control of electrocortical activity due to attentional and motivational deficits, the two studies which have investigated this, both involving operant conditioning of slow cortical potentials, have demonstrated that self regulation can take place. This was particularly true of a study of interhemispheric control. Learning difficulties were found to be more to do with sustaining motivation towards the end of sessions or training programs, rather than in initial learning. Schizotypical features in the normal population have in the case of anhedonia been associated with slower learning, while withdrawn introversion has been associated with faster learning. In view of the affirmative evidence and advances in understanding the functional significance of electroencephalographic (EEG) rhythms, the undertaking of therepeutic regimens with electrocortical operant conditioning is warranted in the schizophrenia spectrum.


We report on the feasibility of teaching 16 (DSM-IV) schizophrenic patients, subdivided by syndrome, self-regulation of interhemispheric asymmetry having demonstrated efficient learning of interhemispheric control in normal subjects. Reversal of asymmetry may be important to treatment and recovery in schizophrenia for following improvement on neuroleptic drugs functional hemispheric asymmetries have reversed, with directions of reversal and pre-existing asymmetry dependent on syndrome. Asymmetry reversal in animals, manifested by spatial turning tendencies, has been used as a marker of neuroleptic action and involves striatal dopamine under reciprocal hemispheric control. We gave as feedback the left right asymmetry in slow potential negativity recorded from the sensory motor strip (C3,4). Feedback took the form of a rocket on a screen which rose or fell with leftward or rightward shifts in negativity. Patients were able to learn control (P < 0.01). In those patients with lesser ability this was due to inability to sustain concentration throughout the session rather than slow initial learning. Active syndrome patients were better able to shift negativity rightward and withdrawn patients leftward, directions associated with drug reversal of functional asymmetry and symptom recovery for each syndrome. Accordingly our demonstration that many symptomatic schizophrenic patients are capable of learning control opens the door to electrocortical operant conditioning training in schizophrenia with therapeutic regimens.

In this review article an overview of the history and current status of neurofeedback for the treatment of ADHD and insomnia is provided. Recent insights suggest a central role of circadian phase delay, resulting in sleep onset insomnia (SOI) in a sub-group of ADHD patients. Chronobiological treatments, such as melatonin and early morning bright light, affect the suprachiasmatic nucleus. This nucleus has been shown to project to the noradrenergic locus coeruleus (LC) thereby explaining the vigilance stabilizing effects of such treatments in ADHD. It is hypothesized that both Sensori-Motor Rhythm (SMR) and Slow-Cortical Potential (SCP) neurofeedback impact on the sleep spindle circuitry resulting in increased sleep spindle density, normalization of SOI and thereby affect the noradrenergic LC, resulting in vigilance stabilization. After SOI is normalized, improvements on ADHD symptoms will occur with a delayed onset of effect. Therefore, clinical trials investigating new treatments in ADHD should include assessments at follow-up as their primary endpoint rather than assessments at outtake. Furthermore, an implication requiring further study is that neurofeedback could be stopped when SOI is normalized, which might result in fewer sessions.


To replicate a previous study, 16 psychophysiological insomniacs were randomly assigned to either Theta feedback or sensorimotor rhythm (SMR) feedback. Evaluations by home sleep logs and by 3 nights in the laboratory were done before biofeedback, immediately after biofeedback, and 9 months later. Results from this study replicate previous findings. Both Theta and SMR feedback seemed effective treatments of insomnia according to home sleep logs. According to evaluations at the sleep laboratory, tense and anxious insomniacs benefited only from Theta feedback but not from SMR feedback, while those who were relaxed at intake but still could not sleep benefited only from SMR but not from Theta feedback.


Intracellular studies reveal that, during slow wave sleep (SWS), the entire cortical network can swing rhythmically between extremely different microstates, ranging from wakefulness-like network activation to functional disconnection in the space of a few hundred milliseconds. This alternation of states also involves the thalamic neurons and is reflected in the EEG by a slow (<1 Hz) oscillation. These rhythmic changes, occurring in the thalamo-cortical circuits during SWS, may have relevant, phasic effects on the transmission and processing of sensory information. However, brain reactivity to sensory stimuli, during SWS, has traditionally been studied by means of sequential averaging, a procedure that necessarily masks any short-term fluctuation of responsiveness. The aim of this study was to provide a dynamic evaluation of brain reactivity to sensory stimuli in naturally sleeping humans. To this aim, single-trial somatosensory evoked potentials (SEPs) were grouped and averaged as a function of the phase of the ongoing sleep slow (<1 Hz) oscillation. This procedure revealed a dynamic profile of responsiveness, which was conditioned by the phase of the spontaneous sleep EEG. Overall, the amplitude of the evoked potential changed sistematically, increasing and approaching wakefulness levels along the negative slope of the EEG oscillation and decaying below SWS average levels along the positive drift. These marked and fast changes of stimulus-correlated electrical activity involved both short (N20) and long latency (P60 and P100) components of SEPs. In addition, the observed short-term response variability appeared to be centrally generated and specifically related to the evolution of the spontaneous oscillatory pattern. The present findings demonstrate that thalamo-cortical processing of sensory information is not stationary in the very short period (approximately 500 ms) during natural SWS.

This single case concerns the treatment of a 71- year-old female stroke patient. The patient’s MRI revealed that the location of the stroke was in the right side basal ganglia with damage extending into the anterior limb of the internal capsule. She presented with a virtual paralysis of the left side of her body (hemiplegia with immobilized left arm, contracted fist, minimal motor control over left leg, absence of muscle tonus in left side of face and slurred, monotonic speech).


Chronic stroke patients with heterogeneous lesions, but no direct damage to the primary sensorimotor cortex, are capable of longitudinally acquiring the ability to modulate sensorimotor rhythms using grasping imagery of the affected hand. Volitional modulation of neural activity can be used to drive grasping functions of the paralyzed hand through a brain–computer interface. The neural substrates underlying this skill are not known. Here, we investigated the impact of individual patient’s lesion pathology on functional and structural network integrity related to this volitional skill. Magnetoencephalography data acquired throughout training was used to derive functional networks. Structural network models and local estimates of extralesional white matter microstructure were constructed using T1-weighted and diffusion-weighted magnetic resonance imaging data. We employed a graph theoretical approach to characterize emergent properties of distributed interactions between nodal brain regions of these networks.

We report that inter-individual variability in patients’ lesions led to differential impairment of functional and structural network characteristics related to successful post-training sensorimotor rhythm modulation skill. Patients displaying greater magnetoencephalography global cost-efficiency, a measure of information integration within the distributed functional network, achieved greater levels of skill. Analysis of lesion damage to structural network connectivity revealed that the impact on nodal betweenness centrality of the ipsilesional primary motor cortex, a measure that characterizes the importance of a brain region for integrating visuomotor information between frontal and parietal cortical regions and related thalamic nuclei, correlated with skill. Edge betweenness centrality, an analogous measure, which assesses the role of specific white matter fibre pathways in network integration, showed a similar relationship between skill and a portion of the ipsilesional superior longitudinal fascicle connecting premotor and posterior parietal visuomotor regions known to be crucially involved in normal grasping behaviour. Finally, estimated white matter microstructure integrity in regions of the contralesional superior longitudinal fascicle adjacent to primary sensorimotor and posterior parietal cortex, as well as grey matter volume co-localized to these specific regions, positively correlated with sensorimotor rhythm modulation leading to successful brain–computer interface control. Thus, volitional modulation of ipsilesional neural activity leading to control of paralyzed hand grasping function through a brain–computer interface after longitudinal training relies on structural and functional connectivity in both ipsilesional and contralesional parietofrontal pathways involved in visuomotor information processing. Extant integrity of this structural network may serve as a future predictor of response to longitudinal therapeutic interventions geared towards training sensorimotor rhythms in the lesioned brain, secondarily improving grasping function through brain–computer interface applications.

Psychological improvements in patients with substance use disorders have been reported after neurofeedback treatment. However, neurofeedback has not been commonly accepted as a treatment for substance dependence. This study was carried out to examine the effectiveness of this therapeutic method for opiate dependence disorder. The specific aim was to investigate whether treatment leads to any changes in mental health and substance craving. In this experimental study with a pre-post test design, 20 opiate dependent patients undergoing Methadone or Buprenorphine maintenance treatment were examined and matched and randomized into two groups. While both experimental and control groups received their usual maintenance treatment, the experimental group received 30 sessions of neurofeedback treatment in addition. The neurofeedback treatment consisted of sensory motor rhythm training on Cz, followed by an alpha-theta protocol on Pz. Data from the general health questionnaire and a heroin craving questionnaire were collected before and after treatment. Multivariate analysis of covariance showed that the experimental group achieved improvement in somatic symptoms, depression, and total score in general mental health; and in anticipation of positive outcome, desire to use opioid, and relief from withdrawal of craving in comparison with the control group. The study supports the effectiveness of neurofeedback training as a therapeutic method in opiate dependence disorder, in supplement to pharmacotherapy.

 


A behavioral research team announced today that it has doubled the recovery rate for drug addicts in a study that gave patients feedback on their brain’s electrical activity in conjunction with conventional treatment for drug abuse. William C. Scott, principal investigator of the study, said that across the country, drug rehab programs have generally achieved a success rate of 20 to 30 percent in relapse prevention one to two years following treatment. In the current study, in excess of 50% of experimental subjects remained drug-free a year later. The study used neurofeedback, a technique that trains patients to alter their brainwave patterns as they receive information about those patterns. The researchers placed electrodes on patient’s scalps and displayed the brain’s electrical activity on a computer monitor in the form of an audiovisual exercise. The feedback process informed patients about their success in making changes.


Electroencephalographic (EEG) biofeedback has been employed in substance use disorder (SUD) over the last three decades. The SUD is a complex series of disorders with frequent comorbidities and EEG abnormalities of several types. EEG biofeedback has been employed in conjunction with other therapies and may be useful in enhancing certain outcomes of therapy. Based on published clinical studies and employing efficacy criteria adapted by the Association for Applied Psychophysiology and Biofeedback and the International Society for Neurofeedback and Research, alpha theta training-either alone for alcoholism or in combination with beta training for stimulant and mixed substance abuse and combined with residential treatment programs, is probably efficacious. Considerations of further research design taking these factors into account are discussed and descriptions of contemporary research are given.

The rTMS program produced larger physiological and behavioral changes than did relative beta training. A combination of different neurotherapeutical approaches (such as neurofeedback, rTMS, tDCS) can be suggested for similar severe cases of TBI. ERPs can be used to assess functional brain changes induced by neurotherapeutical programs.


The author discloses a personal history of undiagnosed mild traumatic brain injury (MBTI) and identifies a typical course and progression of this condition. He advocates a careful inquiry for possible head injury whenever the clinical history shows an original period of normal functioning, a progression of disturbance over time, multiple diagnoses, and poor response to treatment with medication. He discusses the use of quantitative electroencephalography (QEEG) in assessing possible mild traumatic brain injury, describes typical features of quantitative electroencephalography in mild traumatic brain injury, and cautions about the frequency of false negatives. He provides two case histories showing the progression of disturbing cognitive, personality, and impulse control problems following early head injuries.