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Neurofeedback: A Treatment for Reactive Attachment Disorder
Posted on Sunday November 4, 2007Sebern 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.
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.