Neurofeedback Research

People with ADD can have a variety of symptoms. They can be easily distracted, impulsive, and inattentive However, ADD is not laziness or a psychological problem – it’s a brain problem. Doctors know ADD is not laziness; that’s why they prescribe medications. Unlike medication, neurofeedback trains the brain, resulting in significant improvement in ADHD/ADD symptoms, With neurofeedback, people can increase self-control and attention. According to health professionals who use neurofeedback in their practices, many clients with ADD/ADHD learn to increase focus, reduce impulsivity, and manage their behavior when they train with neurofeedback on a consistent basis.

Evidence-Based Information on the Clinical Use of Neurofeedback for ADHD [pdf]
Tais S. Moriyama, Guilherme Polanczyk, and Luis A. Rohde www.ncbi.nlm.nih.gov/pmc/articles/PMC3441929/ 
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.

Many people think addiction is due to a lack of self-discipline, but addiction is physiological, not psychological. People with addiction are often called “weak” by their family and friends, but addiction is a disease, and it is very hard to change. Addicts struggle with emotions such as guilt and shame, anger and frustration. Addiction is a brain disease, a mental health disorder that severely debilitates a person in all aspects of his or her life. In addition, people with addiction frequently suffer from other mental health disorders such as depression, bipolar disorder, and anxiety. Neurofeedback targets the brain disorder of addiction. Through neurofeedback, a person’s brain is retrained. Teaching the brain how to be calm, focused, and relaxed helps a person think more clearly. Neurofeedback training provides a solid base on which to build recovery and prevent relapses. It helps teach the tools one needs to cope long term.

Neurofeedback Training for Opiate Addiction: Improvement of Mental Health and Craving [pdf]
Fateme Dehghani-Arani, Reza Rostami, and Hosein Nadali 
Published online: 20 April 2013.

This article is published with open access at Springerlink.com ABSTRACT 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.

Anxiety sufferers are often overwhelmed, exhausted, and stressed out. Some can’t concentrate due to their intense internal focus. Others obsess about specific things. Anxiety is easily detected if someone appears outwardly nervous. At other times, anxious people can appear calm but their brain seems to never quiet down. They can’t stop thinking. The constant internal chatter can get so bad that it interrupts their sleeping and steals their quality of life. They don’t live in the present, they constantly worry about the future or live in the past. Helping people learn to calm or quiet themselves is by far the best and most effective solution for anxiety. Learning to decrease anxiety gives sufferers hope as they take control of their lives. Biofeedback and EEG neurofeedback are two of the quickest and fastest ways to teach people to learn to help themselves, and it’s easy to learn. These technologies have been used for many years with solid, proven results. It’s true, one can learn how to decrease anxiety and remain calmer with neurofeedback.

Orbitofrontal Cortex Neurofeedback Produces Lasting Changes in Contamination Anxiety and Resting-state Connectivity [pdf]
D Scheinost, T Stoica, J Saksa, X Papademetris, RT Constable, C Pittenger and M Hampson From Translational Psychiatry (2013)
Abstract
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.

Neurofeedback training has been used with several thousand autistic spectrum children over the last 15 years, by hundreds of clinicians. There have been several research studies published to support these efforts. What’s the first thing parents consistently report as their children start training? They usually notice their child is more calm, manages emotions better, and doesn’t get overwhelmed as easily. There are many other changes, as noted below, but these are typically the first.

QEEG Characteristics and Spectrum Weighted Frequency for Children Diagnosed as Autistic Spectrum Disorder [pdf]
Nada Pop-Jordanova, Tatjana Zorcec, Aneta Demerdzieva, Zoran Gucev Pop-Jordanova et al. Nonlinear Biomedical Physics 2010 
Background: Autistic spectrum disorders are a group of neurological and developmental disorders associated with social, communication, sensory, behavioral and cognitive impairments, as well as restricted, repetitive patterns of behavior, activities, or interests. The aim of this study was a) to analyze QEEG findings of autistic patients and to compare the results with data base; and b) to introduce the calculation of spectrum weighted frequency (brain rate) as an indicator of general mental arousal in these patients. Results: Results for Q-EEG shows generally increased delta-theta activity in frontal region of the brain. Changes in QEEG pattern appeared to be in a non-linear correlation with maturational processes. Brain rate measured in CZ shows slow brain activity (5. 86) which is significantly lower than normal and corresponds to low general mental arousal. Recent research has shown that autistic disorders have as their basis disturbances of neural connectivity. Neurofeedback seems capable of remediating such disturbances when these data are considered as part of treatment planning. Conclusions: 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.

Brain training via neurofeedback teaches the brain to maintain a consistent state. Learning self-regulation allows a person to achieve mood stabilization. After beginning neurofeedback, clients commonly comment that they can once again “trust their brain.” What does this mean? Bipolar clients undergoing neurofeedback training report less susceptibility to mood swings, increased ability to focus, and reduced anger. Their ability to function increases as they find themselves less reactive and increasingly able to respond and act appropriately.

The Bipolar Child
by Demitri and Janice Papolos Book review by Siegfried Othmer, Ph.D
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.

With a traumatic brain injury (TBI), the brain itself needs to be targeted. With neurofeedback, the brain is exercised. The specific areas of the brain affected by the TBI are targeted during neurofeedback therapy. Often in the case of TBI, a neurofeedback practitioner will utilize a qEEG brain map to determine which areas should be targeted. A variety of symptoms can be improved through neurofeedback training, such as speech, movement, regulating moods, controlling behavior, and reducing headaches. Neurofeedback works because the brain regulates each of those issues. For people recovering from TBI, neurofeedback training can be particularly helpful in improving speech. During neurofeedback training, the specific areas of the brain related to speech can be targeted. In this way, the areas associated with speech can be strengthened and improved. In fact, some neuropsychologists believe that neurofeedback is actually rehabilitating the damaged speech areas of the brain rather than just dealing with compensation.

Evaluation of Differentiated Neurotherapy Programs for a Patient After Severe TBI and Long Term Coma Using Event-related Potentials
Maria Pachalska1, Małgorzata Łukowicz, Juri D. Kropotov, Izabela Herman-Sucharska, Jan Talar The Medical Science Monitor, 2011 
Background This article examines the effectiveness of differentiated rehabilitation programs for a patient with frontal syndrome after severe TBI and long-term coma. We hypothesized that there would be a small response to relative beta training, and a good response to rTMS, applied to regulate the dynamics of brain function. Case Report M. L-S, age 26, suffered from anosognosia, executive dysfunction, and behavioral changes, after a skiing accident and prolonged coma, rendering him unable to function independently in many situations of everyday life. Only slight progress was made after traditional rehabilitation. The patient took part in 20 sessions of relative beta training (program A) and later in 20 sessions of rTMS (program B); both programs were combined with behavioral training. We used standardized neuropsychological testing, as well as ERPs before the experiment, after the completion of program A, and again after the completion of program B. As hypothesized, patient M.L-S showed small improvements in executive dysfunction and behavioral disorders after the conclusion of program A, and major improvement after program B. Similarly, in physiological changes the patient showed small improvement after relative beta training and a significant improvement of the P300 NOGO component after the rTMS program. Conclusions 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.

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. For chronic pain, neurofeedback can help reduce pain or perhaps how the brain manages pain, even in severe cases.

New Hope for Sufferers of Chronic Pain [pdf]
by Siegfried Othmer, Ph.D.
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.

Feeling down or depressed from time to time happens to most people. Usually such feelings pass, and a person can improve his or her mood naturally. However, some people cannot break out of a depressed state over an extended period of time. In those cases, a person is considered to have clinical depression. However, there is much research that shows that depression is neurological, not psychological. Certain brain patterns are frequently linked to depression. Therefore, training the brain through neurofeedback has a powerful ability to treat depression. With neurofeedback training, the brain practices a healthy pattern of mood regulation. Sometimes people with depression notice improvement after only a few sessions. However, for the brain to fully learn, more training is required. In time, the brain learns to regulate mood on its own.

Real-Time Self-Regulation of Emotion Networks in Patients with Depression [pdf]
David E. J. Linden, Isabelle Habes, Stephen J. Johnston, Stefanie Linden, Ranjit Tatineni, Leena Subramanian, Bettina Sorger, David Healy1, Rainer Goebe 
Abstract 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.

A seizure disorder can be explained as a brain that has lost stability. People with seizures can regulate and stabilize their brains through neurofeedback training. Eighteen well-run research studies show how effective neurofeedback training can be in the reduction of seizures. Interestingly, this research began with studies performed on cats. In an experiment to determine neurofeedback’s effectiveness to combat seizures, it was found that cats with neurofeedback training, when exposed to a chemical, experienced far fewer seizures than those without the training.

A model of feedback control for the charge-balanced suppression of epileptic seizures [link]
Beth A. Lopour and Andrew J. Szericorresponding Journal of Computational Neuroscience, (2010) 
Abstract 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.

Fibromyalgia is “A common syndrome of chronic widespread soft-tissue pain accompanied by weakness, fatigue, and sleep disturbances; the cause is unknown.” The word fibromyalgia comes from the Greek myos meaning “muscle”, Greek algos meaning “pain”, and New Latin fibro meaning “fibrous tissue”. Fibromyalgia is a common and chronic disorder. When a health illness or condition is chronic it means it is long-lasting. Even though fibromyalgia is frequently referred to as an arthritis-related condition, it does not cause joint damage or inflammation, as arthritis does. Neither does fibromyalgia cause damage to muscle and other tissues. However, it is similar to arthritis because it causes severe pain. Fibromyalgia is seen as a rheumatic condition. A rheumatic condition is one that causes joint and soft tissue pain.

Efficacy of EMG- and EEG-Biofeedback in Fibromyalgia Syndrome: A Meta-Analysis and a Systematic Review of Randomized Controlled Trials [link]
Julia Anna Glombiewski, Kathrin Bernardy and Winfried Häuser www.ncbi.nlm.nih.gov/pmc/articles/PMC3776543/ 
Abstract 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.

Many of the methods used and promoted to help people with learning disabilities are intended to help a person compensate for, or work around, their learning difficulties. Neurofeedback actually improves learning skills by training the areas of the brain relevant to learning or executing skills such as math, reading, and auditory and visual processing. Research studies show that several areas of the brain coordinate in the learning process. These separate parts of the brain communicate with each other at extremely fast speeds. If the timing of the communication is even slightly off, there can be impairment in the ability to learn. New research shows that this “connectivity training” seems to consistently improve learning difficulties. Neurofeedback training can improve the coordination and communication between different areas of the brain. Improved timing in the brain has a significant impact on one’s ability to learn. Neurofeedback directly targets the coordination and communication between areas of the brain to improve timing, and therefore learning. pain and tiredness, and can undermine the patient’s ability to go about his daily activities.

Research Review: Emanuel Miller Memorial Lecture 2012 – Neuroscientific studies of intervention for language impairment in children: interpretive and methodological problems [link]
D V M Bishop www.ncbi.nlm.nih.gov/pmc/articles/PMC3593170/ 
Background Our ability to look at structure and function of a living brain has increased exponentially since the early 1970s. Many studies of developmental disorders now routinely include a brain imaging or electrophysiological component. Amid current enthusiasm for applications of neuroscience to educational interventions, we need to pause to consider what neuroimaging data can tell us. Images of brain activity are seductive, and have been used to give credibility to commercial interventions, yet we have only a limited idea of what the brain bases of language disorders are, let alone how to alter them. Scope and findings A review of six studies of neuroimaging correlates of language intervention found recurring methodological problems: lack of an adequate control group, inadequate power, incomplete reporting of data, no correction for multiple comparisons, data dredging and failure to analyse treatment effects appropriately. In addition, there is a tendency to regard neuroimaging data as more meaningful than behavioural data, even though it is behaviour that interventions aim to alter. Conclusion In our current state of knowledge, it would be better to spend research funds doing well-designed trials of behavioural treatment to establish which methods are effective, rather than rushing headlong into functional imaging studies of unproven treatments.

Although neurofeedback training can stop a migraine while it is occurring, stopping individual migraines is not the main goal. Training with neurofeedback can be very effective in reducing the intensity and frequency of migraines over the long term providing real relief for people suffering from migraines. Deborah Stokes, Ph.D, a neurofeedback clinician in Alexandria, VA. recently published a study that showed significant improvement in migraines using neurofeedback. The study was co-authored with Martha S. Lappin and entitled “Neurofeedback and biofeedback with 37 migraineurs: a clinical outcome study”. The study found that, with neurofeedback, 70% of migraine sufferers have a significant reduction in the frequency of their migraines.

Neurofeedback and biofeedback with 37 migraineurs: a clinical outcome study [pdf]
Deborah A Stokes, Martha S Lappin Behavioral and Brain Functions 2010, 6:9 
Background: Traditional peripheral biofeedback has grade A evidence for effectively treating migraines. Two newer forms of neurobiofeedback, EEG biofeedback and hemoencephalography biofeedback were combined with thermal handwarming biofeedback to treat 37 migraineurs in a clinical outpatient setting. Methods: 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.

With Obsessive Compulsive Disorder (OCD), a person can’t stop repeating specific behaviors or stop his or her brain from repeating particular thoughts. A substantial body of research shows that problems with OCD are related to the functioning of areas in the front of the brain. If that part of the brain is working too slowly or quickly, a person is unable to stop repeating certain thoughts or behaviors. Many therapists and other health professionals using neurofeedback to treat OCD note marked reductions in OCD symptoms in their clients after neurofeedback training. People with OCD relate that, after neurofeedback training, they do not really need to make an effort to stop unwanted repetitive thoughts and behaviors. They say that their minds are much quieter. With neurofeedback training, the brain learns to respond to situations in a more conventional and healthy manner.

Obsessive Compulsive Disorder and the Efficacy of qEEG-Guided Neurofeedback Treatment: A Case Series [pdf]
Tanju Siirmeli and Ayben Exrteme Clinical EEG & Neuroscience, Volume 42 No 3 
ABSTRACT 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.

Post Traumatic Stress Disorder (PTSD) is a serious type of anxiety caused by an extremely stressful event or series of events. People who suffer from PTSD are looking for a method to treat their symptoms, and unfortunately, many people experience only limited benefit after trying various therapies and medication. Neurofeedback trains the brain to produce a calm state as well as regulate stress response. In addition, the specific areas of the brain affected by PTSD can be targeted. Frequently, the first sign of improvement is that a client sleeps better. Then other symptoms begin to improve. After sufficient training, someone with PTSD can maintain a calm state on his or her own. When a person has reached this stable state, neurofeedback treatments can be decreased until no further trainings are necessary.

The long-term costs of traumatic stress: intertwined physical and psychological consequences [pdf]
Alexander C. McFarlane 
ABSTRACT 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.

Schizophrenia is a mental disorder that generally appears in late adolescence or early adulthood – however, it can emerge at any time in life. It is one of many brain diseases that may include delusions, loss of personality (flat affect), confusion, agitation, social withdrawal, psychosis, and bizarre behavior. It may be hard to make sense of what a person with schizophrenia is talking about. In some cases, the individual may spend hours completely still, without talking. On other occasions he or she may seem fine, until they start explaining what they are truly thinking. According to the National Institute of Mental Health (NIMN), treatment can help relieve many of the symptoms of schizophrenia.

Taking Back the Brain: Could Neurofeedback Training Be Effective for Relieving Distressing Auditory Verbal Hallucinations in Patients With Schizophrenia? [link]
Simon McCarthy-Jones www.ncbi.nlm.nih.gov/pmc/articles/PMC3406539/ 
ABSTRACT 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.

At least 40 million Americans each year suffer from chronic, long-term, sleep disorders. An additional 20 million experience occasional sleep problems. Neurofeedback is a powerful tool for helping people fall asleep and stay asleep. Over 3,000 licensed health professionals such as psychologists, therapists, and doctors now use this new technology daily with patients. As a group, they report significant and consistent improvements for client sleep problems. Many brain training options can help as well as making lifestyle changes and changes in sleep “hygiene”. A skilled neurofeedback clinician can review many different options with clients to help them assess what’s most appropriate for their problem, including several brain regulating technologies such as Alpha-Stim and Brain Music.

Neurofeedback in ADHD and insomnia: Vigilance stabilization through sleep spindles and circadian networks. [link]
Arns M, Kenemans JL. www.ncbi.nlm.nih.gov/pubmed/23099283 
Abstract 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.

A stroke is a condition in which the brain cells suddenly die because of a lack of oxygen. A stroke can be caused by an obstruction in the blood flow, or the rupture of an artery that feeds the brain. The patient may suddenly lose the ability to speak, there may be memory problems, or one side of the body can become paralyzed.

Parietofrontal integrity determines neural modulation associated with grasping imagery after stroke [pdf]
Ethan R. Buch,Amirali Modir Shanechi, Alissa D. Fourkas, Cornelia Weber, Niels Birbaumer, and Leonardo G. Cohen Brain: A Journal Of Neurology 2012 
ABSTRACT 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.

Neurofeedback in ADHD and insomnia: Vigilance stabilization through sleep spindles and circadian networks. [link]
Arns M, Kenemans JL. www.ncbi.nlm.nih.gov/pubmed/23099283 
Abstract 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.