Neurofeedback: A Treatment for Reactive Attachment Disorder
Sebern F. Fisher, M.A.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.
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.
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.
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.
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.
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 care takers. 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.
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, disregulating. He willneed 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.
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 disregulation 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 disregulation model of certain neuropsychiatric syndromes with magnetoencephalography (Llinas, 1999). And McCormick proposed that certain neuropsychological disorders may be traceable to disregulations 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.
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.
Davidson, Richard J.; Putnam, Katherine M.; Larson, Christine L., Dysfunction in the Neural Circuitry of Emotion Regulation—A Possible Prelude to Violence. Science, 289, pp591-594, 28 July, 2000
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