Neurofeedback for Children

Anxiety is one of the most common mental disorders affecting children, adolescents, and adults. Anxiety can express as feelings of intense fear, inadequacy, or reduced coping ability in social interactions and functions of daily living. It may start early in life and persist over time, or it may rise suddenly in middle age without provocation. It may begin during a period of extreme stress, or arise as a subtle symptom of irregular sleep patterns. Anxiety can be sufficiently crippling to keep someone from leaving their home, and so subtle, that it goes undetected in close friends.

Traditional medicine has offered counseling and prescription medication with great benefit to some, mild benefit to others, and no relief for too many. Neurofeedback has successfully treated anxiety in all age groups and across all forms. Successful treatment leads to better sleep quality, improved relationships, and greater ease and comfort while engaging with others.

NEUROFEEDBACK RESEARCH SUPPORTING TREATMENT of ANXIETY

A neurofeedback protocol to improve mild anxiety and sleep quality.

Rev Bras Psiquiatr. 2016 Jul-Sep;38(3):264-5. doi: 10.1590/1516-4446-2015-1811.

As most psychiatric disorders, anxiety, and depression are conditions whose severity can be represented over continuums that range from subclinical manifestations (expectancy/fear without proper justification and low mood, respectively) to full-blown biosocial disabilities. From an endophenotypic perspective, alpha band (8-12 Hz) asymmetry in the left frontal cortex has emerged as the most prominent electroencephalographic (EEG) correlate of both anxiety and depression in right-handed people, followed by excessive band power in beta 1 (12-20 Hz) and beta 2 waves (20-30 Hz) in the right parietal lobe.¹ Shared features also extend to the genetic level, where the presence of copies of the short variation of the 5-HTTLPR polymorphism increases the risk of both anxiety and depression.

EEG neurofeedback is an operant conditioning technique in which subjects learn to self-regulate and modify their brain activity through a feedback loop. In the recent past, induction of healthy alpha asymmetry²,³ and regulation of alpha power bands⁴ have been successfully used to treat anxiety and depression, whereas increasing the power of sensorimotor rhythm (SMR) bands – a sort of EEG activity ranging from 12-15 Hz over the sensorimotor cortex – has been used successfully to improve memory and sleep quality.⁵

We report the case of a 29-year-old woman, with no previous psychiatric history, who presented with anxiety symptoms, sleep problems, and mild cognitive impairments which she associated to a contingent situation she was facing. We assessed pre- and post-EEG data using a protocol reported elsewhere.³ Anxiety and depression symptoms were assessed using Beck scales (Beck Anxiety Inventory [BAI] and Beck Depression Inventory [BDI]) and sleep quality, with the Pittsburgh Sleep Quality Index (PSQI). Cognitive measures were also administered. A summary of results is presented in Table 1.

Table 1 Pre- and post-treatment evaluations

Construct or domain	Task or inventory	Score or time
		Pre	Post
Anxiety	Beck Anxiety Inventory*	14 (mild)	5 (minimum)
Depression	Beck Depression Inventory*	11 (minimum)	3 (minimum)
Sleep quality	Pittsburgh Sleep Quality Index	9 (poor)	4 (good)
Cognitive flexibility	Trail Making B	65 s	43 s
	Stroop (task switching)	53 s	43 s
Selective attention	Stroop (response inhibition)	48 s	46 s
Attention	CPT total score	2.0890	2.4812
Planning	Tower of Hanoi (accuracy ratio)	1.78	1.27

CPT = Continuous Performance Test.

The training protocol lasted 20 sessions, during which the subject was trained to increase beta 1 (12-15 Hz) at C4 with eyes open, followed by closed-eyes training designed to increase the alpha/beta 3 ratio (9.5-12 Hz/23-38 Hz) at P4. There was a marked improvement of anxiety, depression, and sleep quality, as well as some improvement in executive functions (Table 1). From an endophenotypic viewpoint, there was an overall increase in beta 1, low alpha (8-10 Hz), and high alpha (10-12 Hz) powers and a decrease in beta 2 (a stress biomarker). Low and high alpha changes from the pre-treatment baseline were particularly prominent at P4, increasing from 8.9 to 14% and from 12.2 to 26.2% respectively. These results are encouraging and suggest that neurofeedback can be used as an adjunct in the treatment of subclinical anxiety and, perhaps, other psychiatric conditions, with minimal risk and low technology costs.

The use of an alpha/beta 3 ratio neurofeedback protocol is not well documented in the literature and seems to have potential efficacy in reducing anxiety and associated symptoms. In this case, the combination of two protocols – SMR followed by alpha/beta 3 ratio – led to an overall improvement in the symptoms reported by the patient. To the best of our knowledge, this is the first time such a combination has been used. Although our initial findings are promising, caution is needed in their interpretation, and these results should be replicated in larger, controlled clinical trial settings. Moreover, the specific effects of SMR and of alpha/beta 3 training for anxiety should be investigated separately.

Effects of neurofeedback on adult patients with psychiatric disorders in a naturalistic setting.

Appl Psychophysiol Biofeedback. 2015 Mar;40(1):17-24. doi: 10.1007/s10484-015-9269-x.

Few well-controlled studies have considered neurofeedback treatment in adult psychiatric patients. In this regard, the present study investigates the characteristics and effects of neurofeedback on adult psychiatric patients in a naturalistic setting. A total of 77 adult patients with psychiatric disorders participated in this study. Demographic data and neurofeedback states were retrospectively analyzed, and the effects of neurofeedback were evaluated using clinical global impression (CGI) and subjective self-rating scales. Depressive disorders were the most common psychiatric disorders (19; 24.7 %), followed by anxiety disorders (18; 23.4 %). A total of 69 patients (89.6 %) took medicine, and the average frequency of neurofeedback was 17.39 ± 16.64. Neurofeedback was applied to a total of 39 patients (50.6 %) more than 10 times, and 48 patients (62.3 %) received both β/SMR and α/θ training. The discontinuation rate was 33.8 % (26 patients). There was a significant difference between pretreatment and posttreatment CGI scores (<.001), and the self-rating scale also showed significant differences in depressive symptoms, anxiety, and inattention (<.001). This is a naturalistic study in a clinical setting and has several limitations, including the absence of a control group and a heterogeneous sample. Despite these limitations, the study demonstrates the potential of neurofeedback as an effective complementary treatment for adult patients with psychiatric disorders.

Effects of Increase in Amplitude of Occipital Alpha & Theta Brain Waves on Global Functioning Level of Patients with GAD.

Basic Clin Neurosci. 2015 Jan;6(1):14-20.

The basic objective of this study is to investigate the effects of alpha and theta brain waves amplitude increase in occipital area on reducing the severity of symptoms of generalized anxiety disorder and to increase the global functioning level in patients with GAD.

METHODS: This study is a quasi-experimental study with pretest and posttest with two groups. For this purpose, 28 patients who had been referred to Sohrawardi psychiatric and clinical psychology center in Zanjan were studied based on the interview with the psychiatrist, clinical psychologist and using clinical diagnostic criteria for the Diagnostic and Statistical Manual of Mental Disorders text revision – the DSM-IV-TR Fourth Edition diagnosis of GAD, 14 subjects were studied in neurofeedback treatment group and 14 subjects in the waiting list group. Patients in both groups were evaluated at pretest and posttest with General Anxiety Disorder Scale (GAD-7) and Global Assessment Functioning Scale (GAFs). The treatment group received fifteen 30-minute alpha training sessions and fifteen 30-minute theta brain training sessions in the occipital area by neurofeedback training (treatment group). This evaluation was performed according to the treatment protocol to increase the alpha and theta waves. And no intervention was done in the waiting list group. But due to ethical issues after the completion of the study all the subjects in the waiting list group were treated.

RESULTS: The results showed that increase of alpha and theta brain waves amplitude in the occipital area in people with GAD can increase the global functioning level and can reduce symptoms of generalized anxiety disorder in a treatment group, but no such change was observed in the waiting list group.

DISCUSSION: Increase of alpha and theta brain waves amplitude in the occipital area can be useful in the treatment of people with GAD.

Neurofeedback and Biofeedback for Mood and Anxiety Disorders: A Review of the Clinical Evidence and Guidelines – An Update [Internet].

Ottawa (ON): Canadian Agency for Drugs and Technologies in Health; 2014 Aug.

Patients with mental health disorders usually require pharmacological and/or psychological interventions such as cognitive-behavioral therapy. However, patients may not have easy access to such treatments, especially for those living in rural areas, or may not respond well to them. For example, approximately two-thirds of patients with major depressive disorder do not have adequate responses to pharmacological and/or psychological interventions. Biofeedback therapies are non-pharmacological treatments that use non-invasive electrical devices with bio-monitoring system and sensors to measure, amplify and feedback information primarily from nervous system processes such as respiration, heart rate, muscle tension, skin temperature, blood flow and blood pressure, to the individual being monitored, thus promoting awareness of these processes in an individual to assist with gaining voluntary control over body and mind. Neurofeedback is a specific form of biofeedback that monitors central nervous system activity via the measurement and regulation of brainwave activity from electrodes placed on the scalp. Training with neurofeedback aims to enable the individual to modify patterns of cortical activity and normalize brain activity. In general, biofeedback and neurofeedback are designed to increase patients’ coping skills for their current situations, and usually, multiple sessions of treatment are required. This report was undertaken to update a previous summary of the evidence on the clinical effectiveness and safety of neurofeedback and biofeedback which was completed in 2012. In that report, findings from preliminary analyses raised the possibility that biofeedback and neurofeedback may have a potential for the treatment of post-traumatic stress disorder (PTSD), generalized anxiety disorder (GAD) or depression.

Neurofeedback with anxiety and affective disorders.

Child Adolesc Psychiatr Clin N Am. 2005 Jan;14(1):105-23, vii.

A robust body of neurophysiologic research is reviewed on functional brain abnormalities associated with depression, anxiety, and obsessive-compulsive disorder. A review of more recent research finds that pharmacologic treatment may not be as effective as previously believed. A more recent neuroscience technology, electroencephalographic (EEG) biofeedback (neurofeedback), seems to hold promise as a methodology for retraining abnormal brain wave patterns. It has been associated with minimal side effects and is less invasive than other methods for addressing biologic brain disorders. Literature is reviewed on the use of neurofeedback with anxiety disorders, including posttraumatic stress disorder and obsessive-compulsive disorder, and with depression.

Brain mapping allows trained individuals to view electrical activity in multiple regions of the brain. Ranges of brain wave activity within the regions predict mood and resilience. Treatment of depression with neurofeedback has resulted in more positive thinking patterns and a reduction in ways of thinking that have been associated with depression.

Standard treatment protocols frequently prescribe medications before assessing neurotransmitter levels or brain wave activity. This approach is effective only 33% of the time. The majority of patients prescribed anti-depressants will have no effect at all or side effects that force patients to stop medications and seek alternative therapies.

The proper treatment of depression requires a comprehensive assessment of metabolic, endocrine, and immune disorders along with brain wave activity or quantitative encephalography (qEEG). Neurofeedback treatment begins to tap at the root of depressive symptoms. When neurofeedback is combined with genetic, neurotransmitter, and hormone testing, a more complete and whole treatment plan will produce positive outcomes without the risk of side effects.

Neurofeedback Research Supporting Treatment of Depression

The Efficacy of Neurofeedback in Patients with Major Depressive Disorder: An Open Labeled Prospective Study.

Appl Psychophysiol Biofeedback. 2016 Mar;41(1):103-10. doi: 10.1007/s10484-015-9315-8.

The purpose of this study was to evaluate the effect of neurofeedback on depressive symptoms and electrophysiological disturbances in patients with major depressive disorder. We recruited participants suffering from depression to evaluate efficacy of left prefrontal beta with alpha/theta training. An 8-week, prospective, open-label study was undertaken. Twenty participants were recruited. The treatment protocol was twice or three times a week training of beta at F3 with alpha/theta at Pz for 8 weeks. When every visit, patients were received beta training for 30 min, and then alpha/theta training for 30 min. Baseline, 4 and 8 week scores of; the Hamilton rating scale for Depression (HAM-D), the Hamilton rating scale for Anxiety (HAM-A), the Beck Depression Inventory (BDI)-II, the Beck Anxiety Inventory (BAI), Clinical global impression-severity (CGI-S), and pre- and post-treatment resting state EEGs were compared. Interhemispheric alpha power asymmetry (A score) was computed for homologous sites F3-F4. Pre- and post-training clinical assessments revealed significant improvements in HAM-D, HAM-A, BDI, and CGI-S scores. Cumulative response rates by HAM-D were 35.0 and 75.0 % at 4 and 8 weeks, respectively, corresponding cumulative remission rates by HAM-D were 15.0 and 55.0 %, respectively. No significant differences were found between pre- and post-treatment A score. Neurofeedback treatment could improve depressive symptoms significantly. In addition, anxiety symptoms and clinical illness severity decreased significantly after neurofeedback treatment. Despite its several limitations, such as, small sample size and lack of a control group, this study suggested neurofeedback has significant effects in patients with major depressive disorder.

Neurofeedback and networks of depression

Dialogues Clin Neurosci. 2014 Mar; 16(1): 103–112.

Recent advances in imaging technology and in the understanding of neural circuits relevant to emotion, motivation, and depression have boosted interest and experimental work in neuromodulation for affective disorders. Real-time functional magnetic resonance imaging (fMRI) can be used to train patients in the self regulation of these circuits, and thus complement existing neurofeedback technologies based on electroencephalography (EEG). EEG neurofeedback for depression has mainly been based on models of altered hemispheric asymmetry. fMRI-based neurofeedback (fMRI-NF) can utilize functional localizer scans that allow the dynamic adjustment of the target areas or networks for self-regulation training to individual patterns of emotion processing. An initial application of fMRI-NF in depression has produced promising clinical results, and further clinical trials are under way. Challenges lie in the design of appropriate control conditions for rigorous clinical trials, and in the transfer of neurofeedback protocols from the laboratory to mobile devices to enhance the sustainability of any clinical benefits.

Neurofeedback Treatment of Depression and Anxiety

Journal of Adult Development, Vol. 12, Nos. 2/3, August 2005 (C 2005)

A robust body of research documents that there are biological predispositions that often exist for depression, anxiety, and obsessive–compulsive disorder. However, new research has shown that medication is only mildly more effective than placebo in the treatment of these problems. In treating these conditions, neurofeedback (EEG biofeedback) may offer an alternative to invasive treatments such as medication, ECT, and intense levels of transcranial magnetic stimulation. This paper reviews the neurofeedback literature with these problems, finding particularly positive research support for the treatment of anxiety disorders. New findings on the neurofeedback treatment of depression are presented.

Behavioral disorders in children are extremely disruptive to optimal learning and interactions within families and community life. Behavioral disorders include Reactive Attachment Disorder (RAD), Obsessive Compulsive Disorder(OCD), Oppositional Defiant Disorder(ODD), generalized anger, and hyper-emotional states.

Forceful actions to regulate behavior, even when well intended, often intensify the mis-behavior. Some are under a false illusion that the child has control over their reactions. This may not be the case. Often, for varying reasons, children’s brains can become temporarily hijacked by emotions such as fear, anger, shame. These emotions have very little to do with the reality of the present moment, but the brain in a mal-functioning state may lead to misinterpretations and intense behavioral reactions.

Neurofeedback can been applied with children of any age. Some children have behavioral disorders which may accompany other learning or social engaging disorders such as attention deficit or autism. Behavioral conditions are rarely just the only problem but go hand in hand with other difficulties in engaging within a normal or routine structure.

Neurofeedback has been shown to have a very positive response in varying behavioral disorders. Even though each child can present very different from other children, even with the same diagnosis, neurofeedback optimizes neural networks and connections. These changes within the brain lead to improved ability in learning, flexibility with others needs and requests, and being more receptive toward structure and correction in the child’s interest.

Neurofeedback Research Supporting Treatment of Reactive Attachment Disorder and Other Behavioral Disorders

Dysfunction in the Neural Circuitry of Emotion Regulation—A Possible Prelude to Violence.

Science. 2000 Jul 28:289(5479):591-4

Emotion is normally regulated in the human brain by a complex circuit consisting of the orbital frontal cortex, amygdala, anterior cingulate cortex, and several other interconnected regions. There are both genetic and environmental contributions to the structure and function of this circuitry. We posit that impulsive aggression and violence arise as a consequence of faulty emotion regulation. Indeed, the prefrontal cortex receives a major serotonergic projection, which is dysfunctional in individuals who show impulsive violence. Individuals vulnerable to faulty regulation of negative emotion are at risk for violence and aggression. Research on the neural circuitry of emotion regulation suggests new avenues of intervention for such at-risk populations.

The psychology of powerlessness. Disorders of self-regulation and interactional regulation as a new paradigm for psychopathology.

Psychoanalytic Inquiry, 6, 93-118.

Proceedings of the National Academy of Sciences.

NAS 96, #26, pp. 15222-15227, December 21, 1999.

Are thalamocortical rhythms the rosetta stone of a subset of neurological disorders?

Nature Medicine, 5, #12, pp1349-1351, December 1999.

EEG Biofeedback: An Emerging Model for its Global Efficacy.

In Introduction to Quantitative EEG and Neurofeedback, Evans and Abarbanel, editors, Academic Press, 1999, pp. 243-309.

Affect Regulation and the Origin of Self.

Lawrence Erlbaum Associates, Publishers, 1994.

Webinars on developmental trauma by Psychiatrist and trauma expert Dr. Bessel van der Kolk, MD

5 min intro: http://neurofeedback2015.kajabi.com/fe/79711-rewiring-the-brain-free-ce-seminar .

72 min seminar: http://neurofeedback2015.kajabi.com/fe/80095-support-neurofeedback-research-2015]

For a more detailed and comprehensive discussion of Reactive Attachment Disorder and the possible benefits with Neurofeedback consider the following excellent article by Sebern F. Fisher, M.A.

Neurofeedback: A Treatment for Reactive Attachment Disorder

In 1939, John Bowlby began what amounted to a campaign for the recognition of the primacy of attachment in the development of the human infant. Near the end of his life, in 1991, he reportedly expressed some measure of satisfaction that his ideas were gaining acceptance. It has only been within the last decade that attachment paradigms have become widely enough accepted to encourage widespread research and an increasing body of literature on theories of attachment and disordered attachment. Attachment research is still under-funded. Findings remain controversial in the field of psychotherapy, and in the arena of public policy, their implications go unheeded. Reactive Attachment Disorder, although having gained some recognition in the DSM IV, is still a misunderstood and underutilized diagnosis. Neurofeedback has met something of the same fate. Traditional biofeedback practitioners, already feeling their work trivialized by mainstream medicine, have been slow to embrace this new modality. The psychotherapy community is, at best, wary and in many instances, hostile to the neurofeedback interloper. In the January 2000 issue of The Journal of Clinical EEG, Frank Duffy, MD of Harvard Medical School said, “The literature, which lacks any negative study of substance, suggests that [neurofeedback] should play a major role in many difficult areas. In my opinion, if any medication had demonstrated such a wide spectrum of efficacy it would be universally accepted and widely used.” None-the-less, for reasons he goes on to explore, this has not yet become the case. As neurofeedback is increasingly understood and accepted, it may well be those in the field of attachment and attachment disorder that embrace it most readily.

The widespread failure to recognize Reactive Attachment Disorder (to be referred to as RAD) and the lack of understanding of neurofeedback make writing about RAD and neurofeedback a somewhat daunting prospect. It is, however, timely. Allan Schore has written a detailed study of the interaction between not only the psyche of mother and infant but between the brain of mother and infant. [Throughout this paper I will use mother instead of primary caretaker. Although I believe that attachment can and does occur between an infant and a primary caretaker other than the mother, it is the mother-infant dyad that is central in human attachment. Although these effects can differ widely, there are, none-the-less, effects on every child who has lost his mother.] In his exhaustive work on the mother-infant relationship, Affect Regulation and the Origin of Self, Schore argues that the mother’s affective attunement is not only the path to emotional regulation but to the regulation of its infrastructure, the brain, and further that it is from within this regulation that the infant develops her sense of self and other.

The DSM IV describes the essential feature of RAD as “markedly disturbed and developmentally inappropriate social relatedness in most contexts that begins before age 5 years and is associated with grossly pathological care”. It goes on to further classify: “There are two types of presentations. In the Inhibited Type, the child persistently fails to initiate and to respond to most social interactions in a developmentally appropriate way. The child shows a pattern of excessively inhibited, hypervigilant, or highly ambivalent responses (e.g. frozen watchfulness, resistance to comfort, or a mixture of approach and avoidance). In the Disinhibited Type, there is a pattern of diffuse attachments. The child exhibits indiscriminate sociability or a lack of selectivity in the choice of attachment figures. By definition, the condition is associated with grossly pathological care that may take the form of persistent disregard of the child’s basic emotional needs for comfort, stimulation, and affection; the persistent disregard of the child’s basic physical needs; or repeated changes of primary caretaker that prevent formation of stable attachments (e.g. frequent changes in foster care). The pathological care is presumed to be responsible for the disturbed social relatedness.” The DSM IV describes the course of RAD: “The onset is usually in the first several years of life and, by definition, begins before age five years. The course seems to vary depending on individual factors in the child and caregivers, the severity and duration of associated psychosocial deprivation, and the nature of intervention. Considerable remission may occur if an appropriately supportive environment is provided. Otherwise the disorder follows a continuous course”. And on prevalence, it says, ô Epidemiological data are limited, but Reactive Attachment Disorder appears to be very uncommon.” Attachment therapists, most of whom would sadly disagree with the rarity of this condition, would add the following symptoms: lack of cause and effect thinking; lack of empathy; poor social cueing; lack of remorse; pre-occupation with blood and gore; fascination with knives; ‘primary process lying’ (lying about something that the other has witnessed); gaze aversion; tactile defensiveness; controlling behaviors; cruelty; explosive rages; impulsivity; instrumental relationships; insensitivity to pain; and co-morbidity with speech pathology, learning disability and Attention Deficit Disorder with Hyperactivity (ADHD).

Therapists also describe routine failure in treating these patients. The initial endeavor of psychotherapy does not necessarily require that a patient care about their treatment or about themselves. If these were requirements, then most therapies would fail. Therapy to succeed does require that the patient, in some way, care about the therapist. In this, RAD is self-defining as a disorder that cannot be treated. The RAD patient by definition lacks the capacity to care about the therapist. The therapist barely exists, and when she does, it is as a needs gratifying object or as a thin cognitive trace against a stark, usually unrecognized, backdrop of absence. He cannot care about the other because there is no other; in the absence of self there is absence of other. He lives as a child or adult within the mirrored reflection of the original infant state, one in which he had no experience of mother and, as a result, no experience of the reality of other or of self. Therapy with the unattached is a game of ghosts.

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As suggested in the DSM IV description, RAD is a disorder of relational neglect, initially and profoundly, the mother’s relational neglect of the child. Although many people with RAD have histories of trauma as well, the etiology of attachment disorder is not the trauma per se, but the trauma primarily as a further indicator of an environment of neglect. It is a disorder born from the significant failure of emotional and neurological attunement between mother and baby. Maternal depression can result in attachment disorders that are as profound as those that result from the mother’s physical abandonment. The “passive” aspect of disorganized attachment is maternal non-presence. The “active” element is the installation of the mother’s psychic state of abandonment. She is not psychically present and this evacuation of self becomes the object reality of the infant. Her state of absence becomes the state that the baby internalizes, the state of no one there. This mother is unable to recognize the reality of the “otherness” of her baby and in this lacks the capacity to protect or even wish to protect the infant whose survival depends on her. This psychic reality can and does exist even when the infant’s basic physical needs are met, a fact that can make some situations of severe relational neglect difficult to discern.

Although maternal neglect and “pathological care” are the focus of this paper, it is not the only path to disordered attachment. The disruption to attachment that is inherent in adoption makes it a significant risk factor for attachment disorder, even when the baby is adopted at birth. There is growing evidence that the baby hears the mother’s voice in utero, knows intimately the rhythms of her body and recognizes her smell and her voice immediately after birth. This sensorium of experience and expectation are the beginning of bonding and it is reasonable to consider that when this infant is put in different arms, and hears a different voice he feels an attachment shock. Like all shocks that children suffer, the good enough mother can soothe and mediate its power and she will be much more able to do so if she knows that a shock has occurred. “One gets the impression that children get over even severe shocks without amnesia or neurotic consequences, if the mother is at hand with understanding and tenderness and (with what is most rare) complete sincerity” (Ferenczi, 1931, p.138).

There is also the phenomenon of “bad fit”. There are situations in which the temperament of the baby and that of the mother seem like magnetic poles, they cannot attract each other. “Bad fit”, however, may have maternal or infant pathology hidden within it. The infant’s contribution to bad fit is neurologically not psychologically determined. Some babies are born with severe tactile defensiveness, other cannot be soothed or cannot sleep and some are born autistic. These babies can profoundly discourage or even occlude the most devoted mother and the level to which they do this predicts the level of attachment disorder. Asperger’s Syndrome and other more clinically demonstrative autistic disorders, which are all disorders of extreme overarousal, make it neurologically impossible for the child to emotionally comprehend the existence of the mother even in her adoring presence.

Although it is very important to understand problems that arise within the infant that can contribute to attachment dilemmas, I will be focusing on how attachment breaks affect the unimpaired infant. Further, there is growing clinical evidence, much of it from the practice of neurofeedback,that even in these extreme situations, beneath the press of the highly aroused nervous system there is the desire for attachment. Attachment is the fundamental drive in human beings. It is a drive that brings aggression and sexuality to its defense and to its enhancement, and it is the precursor to human love. It is gained through the delicate interplay of vocal tone and facial expression, through body to body communication, through the dyadic system of care that develops when the mother attunes to her baby. When attachment fails through the significant interruption or destruction of this system, the infant suffers not only what appears to be irreparable emotional harm but significant brain damage.

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PET Scan studies reveal that men in the prison population who meet criteria for anti-social personality disorder have smaller right hemispheres than those of “normals”. The right hemisphere is the part of the brain that is responsible for the regulation of affect and it is the hemisphere that develops most rapidly in the first 18 months. Schore argues that it is this part of the brain that most requires appropriate entrainment by the mother’s brain to permit the development of affect regulation in the infant. Bonding involves the mother’s modulation of her baby’s affect through attunement to his needs for stimulation or arousal alternating with soothing and lowering of arousal. This process rides the waves of sympathetic and parasympathetic systems in both infant and mother and begins to encode the possibility of future self-regulation of state.

Psychoanalytic and dynamic theories have posited that babies internalize their mothers or their perceptions of their mothers. What is being suggested here is that babies not only internalize their mothers, they build their brains around them; that good enough mothers provide their babies with good enough brains. We may, in time, discover that unimpaired babies learn to fire their brains the way their mothers’ brains fire and that without the organizing template of mother there can be no organization of firing patterns of higher order than limbic survival. (Interestingly, Gary Schwartz at the University of Arizona has been able to identify the EEG of the mother encoded in the EEG of the child and vice versa and speculates that the more bonded the pair the more pronounced the signal within a signal.)

One of Schore’s core conclusions is that “the prefrontal lobe of the mother becomes the pre-frontal lobe of the baby”. The prefrontal lobe sits behind the forehead and in the right hemisphere it is the part of the brain that organizes emotional agency. I am reminded of a film I saw in graduate school titled “Ben”. In it, for purposes of the experiment, an emotionally attuned mother agrees not to respond to the smile of her well bonded six month old son. When he smiled, she made no expression. He looked momentarily bewildered and smiled again. She still did not respond. His face clouded and he began to look agitated but he tried again. This time when his mother failed to smile in return he looked alarmed and anxious and began to cry. His mother, who has been valiantly cooperative with the researchers up to that point, could stand it no longer. She picked him up and comforted him, holding and rocking him, cooing and mirroring his facial expressions. His equilibrium was rapidly restored. This entire interaction, as I recall, unfolded in less than two minutes.

Imagine, then, what it must be like for the child of a depressed or addicted or narcissistically absent mother who cannot provide this attunement and emotional repair. This child, too, will attempt to engage her mother; it is her nature. These attempts to recruit the mother could go on intermittently for weeks, months or even years. I am suggesting that, as was true for Ben, each failure heightens negative affect. The child experiences increasing levels of distress that, without predictable maternal intervention escalate into disorganizing anxiety until, finally, the baby gives up, affectively “burning out” and collapsing into a state of deep characterological despair. Her initial distress becomes fear that mounts into terror and then implodes into nothingness, a state beyond hopelessness, a state of no other and no self, a state too diffuse, too cellular, too absolute and too horrifying to any longer be recognized as fear.

Although she lives in this baseline state, the person with RAD rarely experiences either fear or grief. Just as empathy requires the recognition of self and other, learning to feel requires self and other. The baby develops her emotional repertoire in response to the responses of her mother. Joy, sadness, yearning, shame, and grief are dyadic emotions; they require the presence of the other. Fear and its second-level manifestations, anger and rage, are hardwired within the organism; they are affects of survival. In good enough mothering they are mediated by the soothing presence of the mother who teaches the baby that arousal can be mediated, and moment by moment and over time, how to mediate his own arousal. He internalizes her soothing presence. For those without this internalization, those with RAD, the only genuine affective state that survives is anger, an anger that readily escalates into rage. When the anger is cold, when even this aspect of the person is no longer warm, this is sociopathy, the unspecified “continuing course” of attachment disorder as described in the DSM IV.

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These are the Romanian orphans, who need be neither Romanian nor orphans, the children whose faces look like bombed out buildings. They survive through instrumentality, often in the form of a superficial charm, but they fundamentally do not recognize the fact of the existence of the other, much less the needs of the other. Empathic failure is a significant manifestation of the state of ‘no other’ but it understates the extent of the damage. These are children and adults who live in barren, unpopulated internal landscapes. One adult patient of mine said, “I know this isn’t possible but I live in a place without landmarks and without horizons. I don’t know how I see it, but I do.” She was describing the territory of motherlessness. Another described a dream in which she walked past her mother and saw that she, who looked at first three dimensional, was in fact only a cardboard cut out.

RAD then is the result of unmitigated affective arousal that obliterates the possibility of psyche. It occurs in the absence of the mother and in the installation of her state of absence. It is a disorder of stark overarousal, (in affective terms, unrelenting terror), and it is a disorder of the right hemisphere. It is a disorder of damage to the brain as well as to the psyche. The human being survives, but only as an instrument for survival. She is not harbored within the presence of the other or within a self.

Once we can begin to recognize RAD as a disorder in brain development in all realms, structure, chemistry and timing, we can also begin to see the possibilities for treatment through training the brain. This is vitally important. Attachment disorder in children predicts conduct disorder in adolescence and anti-social personality disorder in adulthood. To date, there has been no effective treatment developed to remediate RAD, particularly in its most severe forms. Traditional talk, play and behavioral therapies have failed this population because they do not and cannot address extreme emotional and neurological arousal. To date, there are no reliable psychopharmacalogical interventions. Even when a therapist recognizes the attachment issues before him, which is rare enough, there is little that he can do about the neurology of the disorder. Those RAD patients who regain awareness of sensation in their bodies describe feeling that they lack a sense of containment. It is as if their nerve endings do not stop at their skin but continue, unbearably, forever into space. There is no constraint on their nervous systems. In this light, it is not surprising that the controversial use of holding a child through the rage has claimed the most therapeutic success. Holding therapy has not, however, met with acceptance, as it is widely misunderstood as coercive and it triggers the current cultural fears around touching children.

To compound the problem of treatment, most young children with attachment disorders elude this diagnosis (unless they are in the small percentage who actually fail to thrive), often being diagnosed as ADHD or ODD. This means that most RAD kids are discovered in adolescence and often during the course of a criminal career. Their “treatment programs” are juvenile detention centers and then the prison system. Even if holding therapy demonstrated more efficacy than it has, this would not be a population that could use it. (It must be said here that although RAD is overly represented in the criminal justice system, not all people in prison are attachment disordered and not all RAD people are in jail. They are, sadly, well distributed through corporate boardrooms.)

Holding therapy, however, gives us a way to think about the neurological substrata of the attachment dilemma. Barry Sterman had successfully used neurofeedback to control seizures in cats. When he sought to replicate this work with monkeys, he ran into a predictable problem. His new subjects would pull the electrodes off their heads. This meant that they had to be restrained. After an initial struggle, at the point when they succumbed to the restraints, they produced a predominance of 12-15 Hertz, the very brain waves Sterman wanted them to make. Like the cats, they too learned to become seizure-resistant, and when they did, they also became calmer, more sociable and less aggressive. One has to wonder if this is also the mechanism, neurologically, that accounts for the successes of holding therapy. In the process of release into the hold, the child’s brain begins to shift into a dominant 12-15 Hertz pattern, a pattern that is often described as the relaxation response. In this state shift, the child can begin to recognize the holding for what it is, rather than as a threat to her survival. She can begin to see her mother’s face and may even begin to feel the yearning and grief that are the frozen feelings in RAD. It suggests that the key in successful holding is the induction of a change in brain wave activity that may mimic the brain activity of a relaxed infant, bonded to and held by her mother. It follows then that we can significantly impact people who suffer the ravages of brain disorganization that we call RAD if we can teach them how to produce these brain wave patterns. This is the potential of neurofeedback.

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Neurofeedback is increasingly available as a clinical tool. It is a system through which people can learn to alter the timing and communication patterns in their brains through operant conditioning. Sensors are placed on the patient’s scalp to record the real time EEG and then, as determined by assessment and protocol, they are provided feedback when they produce the desired brainwaves. People meeting criteria for RAD are often rewarded for increasing the amplitude of lower frequency brain waves from SMR (12-15 Hertz) to alpha (8-12 Hertz) in the right hemisphere of their brains. In this process, the RAD patient learns to change the timing of the right hemisphere and to reduce the arousal of the entire system. With the lowering of arousal come decreases in aggression and impulsivity. The individual not only begins to behave more pro-socially but to feel more pro-social. As the threshold of terror is reduced, he warms up, and he begins to feel a greater array of affective states. Over time this resetting of the brain’s rhythms can translate into significant changes in state, and the state change translates into the person’s perception of himself and others.

Several case histories will help to illustrate the effects of neurofeedback. T. is a thirty-two year-old man who was abandoned at birth and raised in orphanages and residential treatment centers. At age ten, he was adopted by a family ill-prepared to parent an attachment disordered boy. The adoption was terminated after a series of assaults on the adoptive mother, the last of which was a blow across her head with a two by four, provoked when she withheld a snack. He was returned to residential care until age 18 when he entered the correctional system. It was during this tenure in residential care, ages 13-18, that I was his therapist. It was T. who introduced me to attachment disorder. Nothing we did, including a course of holding therapy, affected him. He was unable to inhibit his aggressive impulsivity, he lacked cause and effect thinking, a fact that essentially made it impossible for him to learn emotionally, he could not generalize, and he felt no empathy or remorse. He was also unable to recruit empathy from others. Although he demonstrated some dependency on me, he never developed a real attachment to me or any other person in his network of care. He assaulted a female staff member, nearly choking her when he perceived her as taunting him; and on a camping trip to Maine with the program, he struck up a conversation with a family at a nearby site and left with them. This was more an act of indiscriminant attachment than running away. It never occurred to him (nor, evidently, to the others) that this might be a problem. He was in constant petty squabbles and unable, even with constant reminders, to understand the consequences of his actions.

During his most recent probation, at age 31, T. had a course of sixty neurofeedback training sessions. He felt it was the first thing that helped him. He never missed a session. Most importantly, he began to show the first stirrings of empathy and regret. After forty sessions, he called me to tell me he was worried about how he had treated a staff member. In all the time I’d known him, I had never heard him acknowledge the existence of another person (except as a tormentor) or any awareness that he had an impact on that person. He went on to say, “I still get angry, but it used to just keep going and going. Now, a half an hour later I am calling the person, apologizing and trying to make it right.” Unfortunately, the training came too late as he had committed a second crime within two days of his release and was returned to jail. It is important to note, that I am the treatment control in this situation. For five years, I struggled with him in all known treatment modalities to little effect. He made significant progress in three months of neurofeedback, and he was able to recognize that this was the case.

The people in the system surrounding him expected the worst and felt burned out both by him and by their expectations of him. They were unable to discern the subtle changes in behavior and affect that were apparent to his therapist and to me. As T’s arousal dropped, he began to feel an intense yearning that was difficult for him to articulate and which his psychodynamic therapist failed to recognize. Because he had re-offended, he was kept isolated, making this yearning even more unbearable to feel. His long-standing inability to recruit empathy and the lack of recognition of the awakening of yearning in him by his care providers undermined his recovery. From jail, he reports that he is better able to walk away from the taunts and provocations of other inmates and he may, for the first time, be truly suffering his incarceration. He is maintaining contact with me and with his neurofeedback therapist.

E. came to me after leaving a private psychiatric facility against medical advice. She was diagnosed with bipolar disorder, attention deficit disorder with hyperactivity, post-traumatic stress disorder, alcoholism, learning disability and borderline personality disorder. When I asked her mother whether she thought she was truly bipolar she responded, “If you think if you drive a car fast enough you can make it fly, would that qualify?” Although she had spent her first year in an orphanage, no one had considered the diagnosis of attachment disorder. She had multiple physical complaints including lack of co-ordination, clumsiness, chronic pain, irritable bowel, headache, constipation and asthma. She was unable to sit still during our first sessions together, reporting that she felt like she was coming out of her skin.

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She reported that it was routine for her to drink to black out and wake up in the bed of an unknown man. She did not believe that she was an alcoholic but that she used alcohol to self-medicate, and she came to realize that she drank to allow herself to be held. In any other situation, she was touch aversive. She was unable to sleep, maintain relationships or work. She could not read, and not surprisingly, she was unable to concentrate. She had been in special education classes since she began schooling. In our initial sessions she talked of nothing but what man she was interested in, who was cheating on whom and complaints about the neglect of her parents, and all of this in a superficial and perseverative way. There was no room in this girl’s state of chronic agitation and arousal for reflection or thoughtfulness, much less insight or connection with me. I was the vessel for her complaint. She was trying to manage a severely over-aroused nervous system in every way that she could, including men, alcohol and hospitalization. She was also prescribed, and was intermittently taking lithium and Paxil and Trazadone, but she felt they were of little use.

Within two months of beginning neurofeedback, E. had stopped drinking, and within three, no longer needed case management. She had stopped both the lithium and the Paxil with no ill effect. She established a relationship with a young man that has endured for three years. She was increasingly able to work regular hours, and she finished her college degree program. At one point during the therapy of 2 1/2 years and with over 150 neurofeedback sessions, she announced that she could now see what she was reading. I was astounded. I had no idea that she had been trying to read without the capacity to visualize. Neither, of course, did she. She also reported that one evening, while waiting for a movie she went into a batting cage with her boyfriend. She amazed herself (and him) by hitting 95% of the balls. She gradually became less explosive, and she warmed up, making it increasingly possible for her to engage in a sustained and emotionally deepened psychotherapeutic relationship.

E.’s therapy, however, was rocky. Neurofeedback presented us both with new clinical dilemmas. Most symptomatic behavior abated rapidly as she became neurologically, emotionally and physically more regulated. What emerged in its place were profound questions of identity. She said at one point, “I have never been more myself and never known less who I am.’ E was beginning to experience affect regulation and it was, in fact, giving birth to a sense of self that was organizing so quickly that it took us both by surprise. She was familiar with the whirl of reactivity that had served her as a sense of self, but not with the core self that was emerging. As she began to wonder who she was, she also wondered who I was. I, too, was suddenly brand new to her, and she could not tolerate the transferential yearnings that were stirring in her. She turned the nearly intolerable yearning away from me and into her relationship with her boyfriend, with predictable complications.

She also felt critically disappointed that life was like it was. She had imagined a Hollywood version, and the new dailiness of life and her ability to cope with it felt, in some ways, more disheartening than welcomed. As she grew bored with drinking and drugs and with this crowd, she also felt unbearably lonely. At the same time, she grew calmer, more mature, warmer and better able to both advocate and care for herself. Her interpersonal judgment improved and she became less impulsive in all areas of her life. Although in some ways left bewildered by all that has changed, E. reports that she feels smarter, more resilient, more understanding and more competent. Her self-esteem has improved dramatically.

I met S. when my young tenants took him in for foster care, and I have been a consultant to them on his treatment. S. is a five year-old boy with a history of profound neglect and abuse. He was the first child of two kids who were themselves foster children, and he came to the attention of the Department of Social services when he was hospitalized after a fall from a third-floor window. It was revealed that he had been hospitalized at 18 months for failure to thrive following an apparent seizure. One of his parents also had a seizure disorder. Investigators further discovered that S. was left for days in a crib alone. He was placed with his grandmother, who apparently sexually molested him, and when he was returned to his parents there was a new baby, a sister whom he tried to kill. Both children were removed to foster care when S. was three and he once again tried to kill his sibling. He had to be removed from the home. He was further physically abused in the next foster home, and he may have attempted to set it on fire. His placement across the driveway came as an emergency response to this situation.

S., as one could predict, was severely attachment disordered and traumatized. He did not fall asleep until after midnight. Once he did, he lapsed into night terrors, during which he crawled on his hands and knees screaming “no, no, no.” He would come awake at five to begin a day that was hallmarked by non-stop and entirely disorganized activity, high risk behaviors like climbing a tree to the top, pinching the cats, hoarding food, throwing tantrums, breaking objects, defecating on the floor and showing no capacity to take direction or obey his new caretakers. He expected sexual abuse and engaged in sexual reenactments. He had no language and grunted and gestured to make his needs known. He made no eye contact. When you did see his eyes, they were vacant and momentarily flecked with terror. He resisted physical comfort, and he was terrified to be held. As it grew dark each night, he screamed without let up until he fell into the half conscious terror of night.

S.’s treatment began immediately. It included allowing him to eat all that he wanted from a diet of no sugar, no wheat and no dairy. He ate constantly. The foster parents gave him a bottle whenever he wanted it. He loved the bottle but he had to learn how to suck. They did hours of holding therapy daily. His foster father describes the style they developed as “Nazi parenting”. They did not allow him to move without their permission. And they started daily neurofeedback training.

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Within a week, his sleep was normalizing. When he was finally able to sleep, he slept for twelve hours a night without night terrors. It seemed as if he was making up for a lifelong sleep deficit. He still had numerous nightmares, but he could be comforted. If his sleep had not changed and had not changed rapidly, the placement would not have survived. Over the succeeding weeks his appetite normalized, and he began to share food. He began to use words and to better tolerate the holding sessions. Eventually, he even began to request them. He stopped the screaming that greeted the dark almost immediately after beginning neurofeedback. Through a combination of all of these interventions, S. has emerged as a loving and emotionally compelling human being. Eight months into his treatment and new family life, he greeted me when I arrived home. He ran across the driveway and jumped into my embrace. I was wearing dark sunglasses and he leaned away, still cradled in my arms, looked at me and with real dismay said, “Seboin, I can’t see your eyes”.

His parents remained alarmed over his indiscriminate attachment. He seemed to seek comfort from strangers as readily as from his mother. This disturbed her and left her feeling unrecognized and, at times, hurt. Although those familiar with attachment disorder would not find this problem unusual, I mention it here because the solution to it was as simple as it was profound. His mother sat down with him and taught him that they were his parents and this meant that they were the ones that he was to come to when he needed things. This fact had entirely eluded him. She described a light going on in his awareness, and with that one instruction he seemed to immediately organize his sense of primary attachment. It all fell into place for him and the parents reported no further episodes of inappropriate reliance on strangers.

This compelling case underscores not only the parenting needs of children like S. but also the neurological substrata of RAD. Every successful intervention has been one that moved this little boy toward regulation. He was held, fed, nursed, directed, redirected, and disciplined, all to enhance the possibility of regulation that was so drastically absent in his infancy. It is unlikely that neurofeedback would have been as dramatically helpful were it not for this gifted parenting and by demands for regulation in every quarter. It is equally clear, however, that without neurofeedback S. would be untreatable. No parents, regardless of their devotion could have sustained this onslaught. He has now had 180 neurofeedback sessions, and he is beginning kindergarten. The transition into school has evoked separation anxiety and renewed fear of losing his mother. This means, of course, that S. has, in his psychic reality, a mother to lose. Further, we know that he is experiencing this fear because he is able to articulate it to his parents. The classroom is chaotic and, for him, dysregulating. He will need help to make it through this transition. Some of this help will come from a one-to-one aide and some through increasing the frequency of his neurofeedback training sessions. His foster parents have finalized S.’s adoption.

Conclusion:

Neurofeedback training offers a remedy not previously available for reactive attachment disorder. It appears to address the core symptoms of sense of self and other, of emotional bonding, and of empathy,setting the stage for meaningful psychotherapy and reparenting. Reactive attachment disorder is, at its foundation, a disorder of brain regulation. Neurofeedback challenges the brain to regulate itself more competently in the emotional realm.

J.S. Grotstein, a psychoanalyst speaking from a psychodynamic perspective, was the first to propose a dysregulation model for psychopathology. (Grotstein, 1986). His speculations raised the question about how the brain organizes itself in the domain of affect, a question that Davidson further elaborated (Davidson, 2000). Rodolfo Llinas found evidence for the dysregulation model of certain neuropsychiatric syndromes with magnetoencephalography (Llinas, 1999). And McCormick proposed that certain neuropsychological disorders may be traceable to dysregulations in thalamic rhythms (McCormick, 1999). Finally, Othmer and Kaiser describe how EEG neurofeedback can effectively normalize thalamic rhythmic activity and in doing so remediate certain psychopathologies, including autism, Asperger’s, and RAD (Othmer, 1999). Jointly, these studies lay the theoretical basis for the results presented in this paper.

Neurofeedback is a technique of operant conditioning which directly changes brain function, in particular the timing of specific regulatory networks in the brain. It most dramatically affects arousal regulation. In so doing, this ‘brain training’ can normalize the propensity to high arousal seen as the hallmark of Reactive Attachment Disorder. More specifically, it can exercise the cortical-subcortical circuitry involved in emotional regulation and fear response. Theories that the brain organizes itself through regulation of timing supports clinical experience that neurofeedback addresses even the stark baseline fear which is the affective underpinning of RAD, as well as its multiple manifestations or co-morbidities: sleep disorder, hyperactivity, learning disabilities, explosive disorder, oppositional defiant disorder and conduct disorder. Clinical experience with neurofeedback further suggests that despite Schore’s observation of a specific time window for the learning of emotional regulation, we are not dealing with a “critical period” in which such learning has to occur or it remains forever unlearned. The “wiring” for attachment (the drive) is in place before or at birth, and under the right set of conditions it can be activated. Neurofeedback has proven itself one of these conditions.

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In RAD, the most devastating reality is the absence of the other, the internal experience of no other. In every case I have seen to date in which neurofeedback has been used, the person with RAD begins to recognize the existence of an other. Their internal landscapes develop horizons, and they find three-dimensional people there. As their arousal set point comes down, and they begin to recognize the existence of the other, they begin to experience a new organization of self in relation to the other. As I have suggested above, this is not without its hazards, but it makes treatment of these hazards possible through more traditional interpersonal psychotherapies. My experience and that of many others suggests that the introduction of neurofeedback makes Reactive Attachment Disorder a condition that can be, finally, successfully treated.

Learning disabilities are estimated to affect 15% of the student population. Approximately 63% of these children have specific learning disabilities or speech and language problems without any physical disability. A diverse number of studies have found irregular patterns of neuron development and activity in specific regions of the brain in dyslexic children. Current interventions have largely have been unsuccessful in obtaining significant and meaningful results. Many researchers have concluded that ‘‘despite the widespread inclusion of multisensory techniques in remedial programs for dyslexic students… there was little empirical evidence to support the “theoretical premises” or show significant response rates.

Although research on the effectiveness of neurofeedback for learning disabilities is in its early stages, the few studies completed show that neurofeedback can be useful in several types of learning disabilities including reading and math. Instead of helping a person compensate for, or work around, their learning difficulties, neurofeedback actually improves the ability to learn by training the areas of the brain relevant to math, reading, auditory and visual processing and execution. Neurofeedback should not replace essential or beneficial support in overcoming learning disorders because it will speed progress in learning objectives when applied at the same time.

Neurofeedback for learning disabilities is often especially helpful with a history of head injuries and when other difficulties including frustration, irritability, anger, anxiety, and mood are also present. In addition we find that children with sensory, autism, or behavioral problems often have undiagnosed learning disorders. Learning cannot occur optimally until these initial layers of brain dysregulation are cleared. Neurofeedback has demonstrated great ability to clear these lower layers with eventual  improvement in symptoms and disabilities of higher functioning.

Neurofeedback Research Supporting Treatment of Reading and Learning Disorders

Self-regulation of inter-hemispheric visual cortex balance through real-time fMRI neurofeedback training.

Neuroimage. 2014 Oct 15;100:1-14. doi: 10.1016/j.neuroimage.2014.05.072. Epub 2014 Jun 4.

Recent advances in neurofeedback based on real-time functional magnetic resonance imaging (fMRI) allow for learning to control spatially localized brain activity in the range of millimeters across the entire brain. Real-time fMRI neurofeedback studies have demonstrated the feasibility of self-regulating activation in specific areas that are involved in a variety of functions, such as perception, motor control, language, and emotional processing. In most of these previous studies, participants trained to control activity within one region of interest (ROI). In the present study, we extended the neurofeedback approach by now training healthy participants to control the interhemispheric balance between their left and right visual cortices. This was accomplished by providing feedback based on the difference in activity between a target visual ROI and the corresponding homologue region in the opposite hemisphere. Eight out of 14 participants learned to control the differential feedback signal over the course of 3 neurofeedback training sessions spread over 3 days, i.e., they produced consistent increases in the visual target ROI relative to the opposite visual cortex. Those who learned to control the differential feedback signal were subsequently also able to exert that control in the absence of neurofeedback. Such learning to voluntarily control the balance between cortical areas of the two hemispheres might offer promising rehabilitation approaches for neurological or psychiatric conditions associated with pathological asymmetries in brain activity patterns, such as hemispatial neglect, dyslexia, or mood disorders.

Intracerebral functional connectivity-guided neurofeedback as a putative rehabilitative intervention for ameliorating auditory-related dysfunctions.

Front Psychol. 2014 Oct 29;5:1227. doi: 10.3389/fpsyg.2014.01227. eCollection 2014.

Electroencephalography (EEG) constitutes one of the most eligible candidates for neurofeedback applications, principally due to its excellent temporal resolution best reflecting the natural dynamics of brain processes. In addition, EEG is easy to use and provides the opportunity for mobile applications. In the present opinion article, we pinpoint the advantages of using intracerebral functional connectivity (IFC) instead of quantitative scalp EEG for interventional applications. In fact, due to the convergence of multiple signals originating from different spatial locations and electrophysiological interactions, miscellaneous scalp signals are too unspecific for therapeutic neurofeedback applications. Otherwise, IFC opens novel perspectives for influencing brain activity in specific dysfunctional small- and large-scale neuronal networks with a reasonable spatial resolution. In the present article, we propose concrete interventional IFC applications that may be used to ameliorate auditory-related dysfunctions such as developmental dyslexia.

The effectiveness of neurofeedback training on EEG coherence and neuropsychological functions in children with reading disability.

Clin EEG Neurosci. 2012 Oct;43(4):315-22. doi: 10.1177/1550059412451880.

Neurofeedback training (NFT) is an effective intervention in regulating electroencephalogram (EEG) abnormalities leading to improvements in behavioral deficits, which exist in children with reading disabilities. This single-subject study explores our evaluation of the improvements in the reading ability and phonological awareness deficit, as well as the changes in the EEG in children with reading disabilities as a result of NFT. Participants were 6 children, aged between 8 and 10 years, who completed twenty 30-minute sessions of NFT and follow-up measurement sessions 2 months subsequent to the completion of the training sessions. The results showed significant improvement in reading and phonological awareness skills. Furthermore, EEG analysis did not show notable changes in the power of the targeted bands (delta, theta, and beta), rather there was normalization of coherence of the theta band at T3-T4, delta band at Cz-Fz, and beta band at Cz-Fz, Cz-Pz, and Cz-C4. These significant changes in coherence possibly indicate integration of sensory and motor areas that explains the improvements in reading skills and phonological awareness.

Post WISC-R and TOVA improvement with QEEG guided neurofeedback training in mentally retarded: a clinical case series of behavioral problems.

Clin EEG Neurosci. 2010 Jan;41(1):32-41.

According to the DSM-IV, Mental Retardation is significantly sub-average general intellectual functioning accompanied by significant limitations in adaptive functioning in at least two of the following skill areas: communication, self-care, home living, social/interpersonal skills, use of community resources, self-direction, functional academic skills, work, leisure, health and safety. In pilot work, we have seen positive clinical effects of Neurofeedback (NF) applied to children with Trisomy 21 (Down Syndrome) and other forms of mental retardation. Given that many clinicians use NF in Attention Deficit Hyperactivity Disorder and Generalized Learning Disability cases, we studied the outcomes of a clinical case series using Quantitative EEG (QEEG) guided NF in the treatment of mental retardation. All 23 subjects received NF training. The QEEG data for most subjects had increased theta, alpha, and coherence abnormalities. A few showed increased delta over the cortex. Some of the subjects were very poor in reading and some had illegible handwriting, and most subjects had academic failures, impulsive behavior, and very poor attention, concentration, memory problems, and social skills. This case series shows the impact of QEEG-guided NF training on these clients’ clinical outcomes. Fourteen out of 23 subjects formerly took medications without any improvement. Twenty-three subjects ranging from 7-16 years old attending private learning centers were previously diagnosed with mental retardation (severity of degree: from moderate to mild) at various university hospitals. Evaluation measures included QEEG analysis, WISC-R (Wechsler Intelligence Scale for Children-Revised) IQ test, TOVA (Test of Variables of Attention) test, and DPC-P (Developmental Behaviour Checklist) were filled out by the parents. NF trainings were performed by Lexicor Biolex software. NX-Link was the commercial software reference database used to target the treatment protocols, along with the clinical judgment of the first author. QEEG signals were sampled at 128 samples per second per channel and electrodes were placed according to the International 10-20 system. Between 80 and 160 NF training sessions were completed, depending on the case. None of the subjects received any special education during NF treatment. Two subjects with the etiology of epilepsy were taking medication, and the other 21 subjects were medication-free at the baseline. Twenty-two out of 23 patients who received NF training showed clinical improvement according to the DPC-P with QEEG reports. Nineteen out of 23 patients showed significant improvement on the WISC-R, and the TOVA. For the WISC-R test, 2 showed decline on total IQ due to the decline on some of the subtests, 2 showed no improvement on total IQ although improvement was seen on some of the subtests, however even these cases showed improvement on QEEG and DPC-P. This study provides the first evidence for positive effects of NF treatment in mental retardation. The results of this study encourage further research.

[Neurofeedback and personal development].

Przegl Lek. 2010;67(9):716-20.

BACKGROUND: Development of neurofeedback was preceded by development of classical and quantitative EEG, construction of computer devices, programmes and individual medical protocols.

METHODS: The basic rule of this method is to achieve effective change of rhythm and power of brain bioelectric activity based on knowledge of normal activity and identification of abnormalities of present activity. Various types of disturbed activity occur in many syndromes and brain development disorders. Training process is characterized by repetitive local activation of chosen brain structures as well as by general activation. Moreover, this method enables monitoring of emotional and social development. In accordance with disorders pathogenesis consecutive technical modules of this method are being introduced.

RESULTS: Neurofeedback has been used in the treatment of post traumatic stress disorder, sequels of stroke and head trauma, emotional, anxiety disorders and depression. Good results of this neurotherapy have been also found in children with ADHD/ ADD, developmental dyslexia, tics and Tourette syndrome, learning difficulties and developmental disturbances and acquired speech disorders. It has been also used with a success in treatment of headaches, epilepsy and chosen disturbances in cerebral palsy.

SUMMARY: Neurofeedback as a method of instrumental therapy of CSN is now undergoing thorough evaluation. New requirements that place further demands on the quantitative bioelectric activity estimation when qualification for the treatment is performed and on the elaboration of therapy results as a material for future meta analysis.

Improvements in spelling after QEEG-based neurofeedback in dyslexia: a randomized controlled treatment study.

Appl Psychophysiol Biofeedback. 2010 Mar;35(1):5-11. Epub 2009 Aug 27.

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.

Autism spectrum disorder (ASD) presents with core deficits in human social behaviors among children and adults. Increasing in frequency, children and adults with ASD show deficits in social and communicative skills, including imitation, empathy, shared attention, as well as restricted interests and repetitive patterns of behaviors. Many of the symptoms may coincide with other obvious or masked symptoms including sensory processing disorders(SPD), anxiety, attention disorders, behavioral disorders(i.e. Reactive Attachment Disorder(RAD), Obsessive Compulsive Disorder(OCD), Oppositional Defiant Disorder(ODD), and learning disorders(i.e. Dyslexia). These deficits substantially impair satisfactory social interactions and prevent children and adults from establishing adequate relations with families and friends and reaching educational goals.

Sensory processing disorders(SPD) are caused by a block or “traffic jam” in the processing of external stimuli such as touch, taste, sight, sounds, and smells. Signals are either intensified or diluted as they are processed through our nervous system such that an appropriate response fails to be organized. Even simple everyday tasks become a significant challenge.

Brain mapping studies of people with ASD and SPD have revealed distinctive patterns of neural dysregulation. As with many brain-based disorders, autism and sensory processing disorders are distinguished by abnormalities in the brain’s electrical activity patterns, a factor that neurofeedback therapy has been clinically proven to help correct.

Neurofeedback reduces symptoms by improving self-regulation in children with ASD and SPD through balancing brain rhythms or electrical patterns. Neurofeedback is able to reduce sensory “overload”, improve behavioral dysregulation and communication and enhanced learning. Neurofeedback therapy can be used on its own, or in conjunction with other treatments such as occupational therapy. Improvements reported include increase in verbal and social engaging, reduced self stimulatory behavior(i.e. hand flapping), improvement in following through with verbal requests, increase in empathy, better sleep onset and duration, less anxiety, improved behavior, and improved sensory response. For children with ASD and SPD, neurofeedback therapy presents an incredibly safe and side-effect-free option for managing and reducing problems with autism and sensory processing.

Neurofeedback Research Supporting Treatment of ASD and SPD

An Effective Neurofeedback Intervention to Improve Social Interactions in Children with Autism Spectrum Disorder.

J Autism Dev Disord. 2015 Dec;45(12):4084-100. doi: 10.1007/s10803-015-2523-5

Neurofeedback training (NFT) approaches were investigated to improve behavior, cognition and emotion regulation in children with autism spectrum disorder (ASD). Thirteen children with ASD completed pre-/post-assessments and 16 NFT-sessions. The NFT was based on a game that encouraged social interactions and provided feedback based on imitation and emotional responsiveness. Bidirectional training of EEG mu suppression and enhancement (8-12 Hz over somatosensory cortex) was compared to the standard method of enhancing mu. Children learned to control mu rhythm with both methods and showed improvements in (1) electrophysiology: increased mu suppression, (2) emotional responsiveness: improved emotion recognition and spontaneous imitation, and (3) behavior: significantly better behavior in every-day life. Thus, these NFT paradigms improve aspects of behavior necessary for successful social interactions.

Neurofeedback application in the treatment of autistic spectrum disorders (ASD).

Psychiatr Danub. 2015 Sep;27 Suppl 1:S391-4.

The aim of this paper is to describe neurofeedback (NFB) treatment in Autistic spectrum disorder (ASD) children. There is no specific cure for autism and therapeutic guidelines are directed to improve the quality of life of people with autism by reducing the symptoms and by increasing their functioning. Neurofeedback is a computerized method based on tracking electrical activity of the brain (EEG) and giving a feedback about it. The method has been developed in neurophysiological labs of scientific institutes in USA and has been used very successfully for over last 20 years. It has proven its efficacy in practise, but also in scientific and clinical research. During 2010 and 2011 neurofeedback treatment was administered to 10 children (N=10, 7 males and 3 females) age range 4 to 7 years which have been diagnosed as autistic spectrum disorder (highly functional) with an unspecific impairment of speech development and trouble communicating. An evaluation of treatment was done according to estimation of changes in functioning (parents, teachers and therapists’ ratings and all other experts that were monitoring the child before, during and after the treatment) and tracking of changes in electrophysiology. The results have shown most changes in behaviour (less aggressive, more cooperation, better communication), attention span and sensory motor skills. According to the assessment of parents, teachers, therapists and other experts all children have accomplished a certain degree of improvement in the level of daily functioning. Our experiences in usage of neurofeedback in Autistic spectrum disorder (ASD) children confirmed previous data that this method can be applied to this category of patients.

A pilot feasibility study of neurofeedback for children with autism.

Appl Psychophysiol Biofeedback. 2014 Jun;39(2):99-107. doi: 10.1007/s10484-014-9241-1.

Neurofeedback (NFB) is an emerging treatment for children with autism spectrum disorder (ASD). This pilot study examined the feasibility of NFB for children with ASD. Ten children ages 7-12 with high functioning ASD and attention difficulties received a NFB attention training intervention. A standardized checklist captured feasibility, including focus during exercises and academic tasks, as well as off-task behaviors. Active behaviors and vocalizations were the most frequent off-task behaviors. Positive reinforcement and breaks including calm breathing exercises were the most common supports. Low motivation was associated with higher feasibility challenges, yet parental involvement and accommodations were helpful. This pilot study shows that it is feasible to conduct NFB sessions with children with high functioning autism and attention difficulties.

Neurofeedback training produces normalization in behavioural and electrophysiological measures of high-functioning autism.

Philos Trans R Soc Lond B Biol Sci. 2014 Apr 28;369(1644):20130183. doi: 10.1098/rstb.2013.0183. Print 2014.

Autism spectrum disorder (ASD) is a neurodevelopmental condition exhibiting impairments in behaviour, social and communication skills. These deficits may arise from aberrant functional connections that impact synchronization and effective neural communication. Neurofeedback training (NFT), based on operant conditioning of the electroencephalogram (EEG), has shown promise in addressing abnormalities in functional and structural connectivity. We tested the efficacy of NFT in reducing symptoms in children with ASD by targeting training to the mirror neuron system (MNS) via modulation of EEG mu rhythms. The human MNS has provided a neurobiological substrate for understanding concepts in social cognition relevant to behavioural and cognitive deficits observed in ASD. Furthermore, mu rhythms resemble MNS phenomenology supporting the argument that they are linked to perception and action. Thirty hours of NFT on ASD and typically developing (TD) children were assessed. Both groups completed an eyes-open/-closed EEG session as well as a mu suppression index assessment before and after training. Parents filled out pre- and post-behavioural questionnaires. The results showed improvements in ASD subjects but not in TDs. This suggests that induction of neuroplastic changes via NFT can normalize dysfunctional mirroring networks in children with autism, but the benefits are different for TD brains.

Neurofeedback outcomes in clients with Asperger’s syndrome.

Appl Psychophysiol Biofeedback. 2010 Mar;35(1):63-81. doi: 10.1007/s10484-009-9120-3.

This paper summarizes data from a review of neurofeedback (NFB) training with 150 clients with Asperger’s Syndrome (AS) and 9 clients with Autistic Spectrum Disorder (ASD) seen over a 15 year period (1993-2008) in a clinical setting. The main objective was to investigate whether electroencephalographic (EEG) biofeedback, also called neurofeedback (NFB), made a significant difference in clients diagnosed with AS. An earlier paper (Thompson et al. 2009) reviews the symptoms of AS, highlights research findings and theories concerning this disorder, discusses QEEG patterns in AS (both single and 19-channel), and details a hypothesis, based on functional neuroanatomy, concerning how NFB, often paired with biofeedback (BFB), might produce a change in symptoms. A further aim of the current report is to provide practitioners with a detailed description of the method used to address some of the key symptoms of AS in order to encourage further research and clinical work to refine the use of NFB plus BFB in the treatment of AS. All charts were included for review where there was a diagnosis of AS or ASD and pre- and post-training testing results were available for one or more of the standardized tests used. Clients received 40-60 sessions of NFB, which was combined with training in metacognitive strategies and, for most older adolescent and adult clients, with BFB of respiration, electrodermal response, and, more recently, heart rate variability. For the majority of clients, feedback was contingent on decreasing slow wave activity (usually 3-7 Hz), decreasing beta spindling if it was present (usually between 23 and 35 Hz), and increasing fast wave activity termed sensorimotor rhythm (SMR) (12-15 or 13-15 Hz depending on assessment findings). The most common initial montage was referential placement at the vertex (CZ) for children and at FCz (midway between FZ and CZ) for adults, referenced to the right ear. Metacognitive strategies relevant to social understanding, spatial reasoning, reading comprehension, and math were taught when the feedback indicated that the client was relaxed, calm, and focused. Significant improvements were found on measures of attention (T.O.V.A. and IVA), core symptoms (Australian Scale for Asperger’s Syndrome, Conners’ Global Index, SNAP version of the DSM-IV criteria for ADHD, and the ADD-Q), achievement (Wide Range Achievement Test), and intelligence (Wechsler Intelligence Scales). The average gain for the Full Scale IQ score was 9 points. A decrease in relevant EEG ratios was also observed. The ratios measured were (4-8 Hz)(2)/(13-21 Hz)(2), (4-8 Hz)/(16-20 Hz), and (3-7 Hz)/(12-15 Hz). The positive outcomes of decreased symptoms of Asperger’s and ADHD (including a decrease in difficulties with attention, anxiety, aprosodias, and social functioning) plus improved academic and intellectual functioning, provide preliminary support for the use of neurofeedback as a helpful component of effective intervention in people with AS.

Neurofeedback for autistic spectrum disorder: a review of the literature.

Appl Psychophysiol Biofeedback. 2010 Mar;35(1):83-105. doi: 10.1007/s10484-009-9117-y.
There is a need for effective interventions to address the core symptoms and problems associated with autistic spectrum disorder (ASD). Behavior therapy improves communication and behavioral functioning. Additional treatment options include psychopharmacological and biomedical interventions. Although these approaches help children with autistic problems, they may be associated with side effects, risks or require ongoing or long-term treatment. Neurofeedback is a noninvasive approach shown to enhance neuroregulation and metabolic function in ASD. We present a review of the literature on the application of Neurofeedback to the multiple problems associated with ASD. Directions for future research are discussed.

The relative efficacy of connectivity guided and symptom based EEG biofeedback for autistic disorders.

Appl Psychophysiol Biofeedback. 2010 Mar;35(1):13-23. doi: 10.1007/s10484-009-9102-5. Epub 2009 Aug 1.

Autism is a neurodevelopmental disorder characterized by deficits in communication, social interaction, and a limited range of interests with repetitive stereotypical behavior. Various abnormalities have been documented in the brains of individuals with autism, both anatomically and functionally. The connectivity theory of autism is a recently developed theory of the neurobiological cause of autisic symptoms. Different patterns of hyper- and hypo-connectivity have been identified with the use of quantitative electroencephalogray (QEEG), which may be amenable to neurofeedback. In this study, we compared the results of two published controlled studies examining the efficacy of neurofeedback in the treatment of autism. Specifically, we examined whether a symptom based approach or an assessment/connectivity guided based approach was more effective. Although both methods demonstrated significant improvement in symptoms of autism, connectivity guided neurofeedback demonstrated greater reduction on various subscales of the Autism Treatment Evaluation Checklist (ATEC). Furthermore, when individuals were matched for severity of symptoms, the amount of change per session was significantly higher in the Coben and Padolsky (J Neurother 11:5-23, 2007) study for all five measures of the ATEC. Our findings suggest that an approach guided by QEEG based connectivity assessment may be more efficacious in the treatment of autism. This permits the targeting and amelioration of abnormal connectivity patterns in the brains of people who are autistic.

Neurofeedback is a clinically proven, non-drug method for reducing ADD/ADHD symptoms. In November 2012 the American Academy of Pediatrics approved neurofeedback as a Level 1 or “best support” treatment option for children suffering from attention deficit/hyperactivity disorder. It is estimated that over two million children in the United States are struggling with this disorder.

Neurofeedback creates positive, lasting changes in adults and children by encouraging the brain to reorganize itself toward more optimal function. For decades, the widely accepted practice for treating patients with ADD/ADHD has been to prescribe medication. Many people who take medications still struggle with symptoms or side effects that range from mild to severe. Further, it is common to take medications for a very long time, which is concerning as dependence can develop; there are also growing concerns about the long-term use of medications. The pills don’t TEACH one how to change one’s brain. They manage symptoms.

Neurofeedback as part of a treatment strategy can be incredibly powerful. Children and adults who suffer from ADD/ADHD typically have slower brain wave activity in the brain’s frontal lobe, or executive functioning center. Neurofeedback restores the strength of the frontal region of the brain, and builds better connections/communication between the mid-brain and forebrain, allowing focus, attention, impulses and emotional reactions to become manageable. With neurofeedback, changes in concentration/attention, academic performance, mood stability, impulsivity, hyperactivity, sleep, and even IQ have been reported.

This change is not instant; however, brain science has shown that repetitive exercise of the brain’s networks reshapes the brain. Neurofeedback has been proven to change the brain – to teach the brain to return to, and maintain, its optimum function. When the brain works better there is less need for medication.

Baseline testing and treatment of ADD/ADHD begins with baseline neurotransmitter levels, food allergies, genetic defects, nutritional deficiencies, and immune distractions or infections including chronic strep, candida, and Epstein Barr Virus (EBV). When Neurofeedback is utilized while addressing all possible factors associated with learning, mood, and behavior, improvements are noticed quickly

C.L.’s story
13-year-old C.L. came to us after being diagnosed with Generalized Anxiety Disorder (GAD), ADD, and complaints of being unable to pay attention in school, of racing thoughts and inability to sleep, and feeling overwhelmed by simple tasks. Once an avid wrestler, he quit, expressing, “I am just a loser.” C.L’s parents were searching for a non-chemical treatment for their son that would allow him to be more successful academically and to reach his full potential.

After the first session of neurofeedback, both Lars and his mother began reporting positive effects: increased energy and motivation, “he ran to the carpool vehicle this morning without being prompted; this was the first time he has ever done that.” “He has also been running every night – he wants new running shoes and decided to prove to us that he needs them.”

By the fourth treatment, C.L. reported the following: “I used to hate loading the dishwasher.” “Now I like doing the dishes.” “I do them every day and I like not having to do anything else.” Lars’ mother stated that pt was doing the dishes without being asked to do so and that one year ago, the task seemed overwhelming to him. “He could not pick up a glass without being told how and he did not know what to do with one after he picked it up.” “Now things that seemed stressful to him seem easier for him to process.” ” He seems to have more motivation to do things and is showing more excitement about activities he enjoys.” Lars continues to express feeling more relaxed and increasingly able to focus and maintain attention in school, expressing excitement about entering his freshman year in high school, and about the future in general.