AdamC
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Posts posted by AdamC
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I find it most telling that all of this evasion doesn't raise any red flags to you.
I'm going to stop our exchange here to consider what I can learn about myself from having engaged in this discussion with you.
If it means anything to you, I promise to watch out for any evidence you might post of these other factors you keep suggesting.
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The discussion here is about whether it's accurate at this point to claim there aren't other things that also lead to violence/aggression and, if there are, what those might be.
Do you believe childhood trauma is the ONLY thing that can lead to violence/aggression? If so, please state that as your belief. If not, please name some of the other factors you sincerely think might contribute and deserve some attention along with childhood trauma. I mean this as a serious inquiry, so please be sincere in your response.
I'm withholding evidence of other factors??
I would willfully ignore evidence of other factors??
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Why do you suppose you won't directly reply, for example, to Godwin's well-articulated questions about Stefan's BIB logic?
I don't consider them to be well articulated or well timed, and I prefer to spend my time reading and sharing actionable research rather than debating a body of knowledge that most seem to accept as still evolving and far from settled.
Also, I accept the non-aggression principle, and peaceful parenting logically/morally follows for all children, sufferers of diabetes included.
My best guess is that it is because this board
attracts people who, for various reasons, have a bias for believing
strongly in the nurture side of this argument and who are not
comfortable with that being challenged. They have bought into an entire
philosophy built upon that stone and do not want that stone prodded at.
So better, when it is being prodded at, to try to sidetrack discussion
over and over.And you've lowered your expectations accordingly?
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Perhaps you can summarize what you're getting across?
Oh, something like: Abuse and neglect seriously messes children up. And if children get messed up, they can't grow up to become researchers to figure out how to prevent children from getting messed up.
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So, I'm curious if, at any point, you plan to ask Stefan to clarify the questions being put to him in this thread? Or do you only plan to keep asking questions of the questioners while their actual questions go unanswered?
Why do you suppose you're not receiving the response you're hoping for?
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Some neuropsychobiological perspective on nature/nurture and psychopathology:
Allan Schore in "The Neurobiology of a Secure Attachment"
https://www.youtube.com/watch?v=MD5MI-EACI0Joseph Burgo: Attachment Theory and the Origins of Shame
“One of the great fallacies that many scientists have is that everything that is before birth is genetic and that everything that is after birth is learned. This is not the case.” [schore] goes on to explain that there is much more genetic material in the brain at ten months than at birth. Only the brain stem or “primitive brain” is “well advanced” at birth; the rest of brain continues to unfold and develop for the next two years as neurons become myelinated and interconnect. This development does not occur in an automatic and predetermined way in all people; it is powerfully affected by the environment, in particular by interactions and relationships with the primary caretakers.
It’s a more nuanced view of the nature vs nurture debate. Not only is it nature AND nurture, as most of us already believe; an individual’s particular genetic makeup (nature) also continues to evolve during the first two years of life under the influence of the environment (nurture). In other words, what happens to you, emotionally and psychologically, during those first two years, and especially in the first nine months of life, will powerfully influence your neurological development, determining how your brain takes shape in lasting ways. Most important among the brain parts that develop during these early months are those that involve the “emotional and social functioning of the child.” And if those parts of the brain are to develop appropriately, “certain experiences are needed. Those experiences are embedded in the relationship between the caretaker and the infant.”
So what is Schore telling us? If an infant doesn’t receive the kind of emotional interactions it needs from its caretakers during the early months of life, its brain won’t develop optimally. Certain neurons that should have interconnected will instead die. “Use or lose it” — if you don’t get what you need during those first two years, that experience will alter you for life. As my own client translates it, this means “brain damage.” You might be able to modify that damage to a degree, with a lot of hard work, but you will never be the person you might have been if you’d gotten what you needed during that critical period of emotional development.
A deeply sobering thought. You can call it what you like — bad parenting, failure of attunement, insecure attachment — but when things go wrong between parent and child in the first two years of life, you are permanently damaged by it in ways that cannot be erased. The awareness that you are damaged, the felt knowledge that you didn’t get what you needed and that as a result, your emotional development has been warped and stunted in profound ways — this is what I refer to as basic shame.Allan N. Schore: Attachment and the Regulation of the Right Brain
Attachment theory, as first propounded in Bowlby’s (1969) definitional volume, is fundamentally a regulatory theory. Attachment can thus be conceptualized as the interactive regulation of synchrony between psychobiologically attuned organisms.
Critical Period Gene–Environment Interactions and the Development of a Vulnerability to Psychopathology
The development, in the first 2 years of life, of a right hemispheric dynamic system that adaptively regulates psychobiological states is a product of the interaction of genetic systems and early experience. Current models of the genetic analysis of complex diseases prescribe an interaction between a susceptibility gene with a predisposing environmental agent. In these studies, “environmental” usually refers to factors in the physical environment, but I propose that in the case of the transmission of psychiatric diseases stressors in the social environment interact with genetic mechanisms to amplify a genetic predisposition and create a vulnerability to later forming mental illness.
Excessive Developmental Parcellation and the Pathomorphogenesis of Frontolimbic Circuits
As opposed to an adaptive stable dynamic system that can flexibly transition between states, a pathological system lacks variability in the face of environmental challenge. What early factors could produce such an organization? According to the classical diathesis–stress model, psychiatric disorders are caused by the interaction of genetic–constitutional vulnerability and environmental psychosocial stressors. The interface of nature and nurture is now thought to occur in the psychobiological interaction between mother and infant, “the first encounter between heredity and the psychological environment” (Lehtonen, 1994, p. 28). In such transactions the primary care-giver is providing experiences which shape genetic potential by acting as a psychobiological regulator (or dysregulator) of hormones that directly influence gene transcription. This mechanism mediates a process by which psychoneuroendocrinological changes during critical periods initiate permanent effects at the genomic level. The final developmental outcome of early endocrine–gene interactions is expressed in the imprinting of evolving brain circuitry.
Of particular importance to the creation of a brain system which is “invulnerable” or “vulnerable” to future psychopathology are steroid hormones associated with stress responses. These bioagents regulate gene expression, and, depending upon the cell type, induce or repress sets of genes, and in this manner they act as an essential link between “nature and nurture.”
Early abuse experiences of neglect and/or trauma thus create abnormal critical period microenvironments for the development of corticolimbic areas. Critical period cell death of orbitofrontal and/or temporal cortical neurons that respond to emotional facial displays would lead to permanent deficits in reading the facially expressed emotional states of others. Deficits in emotion decoding ability are seen in abused children (Camras, Grow, & Ri-
bordy, 1983). Since the orbitofrontal areas are tied into both limbic circuits and both branches of the autonomic nervous system, an extensive developmental parcellation of both circuits would result in a poorly evolved fronto-limbic cortex, one in which sympathetic and parasympathetic components could not operate reciprocally (Berntson, Cacioppo, & Quigley, 1991). This organization of autonomic control prevents the integration of lower more primitive autonomic states that allows for the elaboration of new higher states. Because of its fragile regulatory capacities, under even of moderate stress, it is vulnerable to disorganization and to affect shifts that are extremely discontinuous and labile.
Early Forming Structural Pathology of Nonlinear Right Hemisphere and Origins of Predisposition to Psychiatric Disorders
Early attachment experiences represent psychobiological transactions between the mother’s and infant’s right hemispheres. The child’s growing brain imprints the output of the mother’s right cortex which contains the mechanism for the maternal capacity to comfort the infant (Horton, 1995). Structural limitations in the mother’s emotion processing right brain are reflected in a poor ability to comfort and regulate the infant’s negative affective states, and these experiences are stamped into the infant’s right orbitofrontal system and its cortical and subcortical connections. Exposure to such conditions throughout a critical period of corticolimbic marturation results in inefficient coping systems that cannot adaptively switch internal states in response to stressful external environmental challenges. The functional indicators of this intergenerationally transmitted adaptive limitation are specifically manifest in recovery deficits of internal reparative coping mechanisms, a poor capacity for the state regulation involved in self-comforting in times of stress.
Such deficits are most obvious under highly emotional and challenging conditions that call for behavioral flexibility and affect regulation. The adaptive limitation of all psychopathologies is manifest in more intense and longer lasting emotional responses and the amplification of negative states.
Systems that exhibit good primitive organization become more complex (Schwalbe, 1991), but those with a compromised early ontogeny are inefficient at state regulation and therefore exhibit an abnormality in the dimensionality of state transitions, specifically an overreliance on an oversimplified set of transition paths among attractors which constrains the individual’s flexibility to adapt to challenging situations with new strategies.
The fact that a broad spectrum of psychiatric disorders show disturbances of the right hemisphere, the hemisphere that is centrally influenced by attachment experiences, accounts for the principle that all early forming psychopathology constitutes disorders of attachment and manifests itself as failures of interactional and/or self-regulation.A large body of evidence supports the principle that cortical and subcortical networks are generated by a genetically programmed initial overabundant production of synaptic connections, which is then followed by an environmentally driven process of competitive interaction to select those connections that are most effectively entrained to environmental information. This parcellation, the activity-dependent fine tuning of connections and pruning of surplus circuitry, is a central mechanism of the self-organization of the developing brain (Chechik, Meilijson, & Ruppin, 1999; Schore, 1994). It is important to emphasize, however, that environmental experience can either enable or constrain the structure and function of the developing brain. In other words, early interpersonal events positively or negatively impact the structural organization of the brain and its expanding adaptive functional capacities. This clearly implies, in the broadest of terms, a direct relationship between an enabling socioemotional environment, an optimally developing brain, and adaptive infant mental health.
A major conclusion of the last decade of developmental neuroscience research is that there is now agreement that the infant brain “is designed to be molded by the environment it encounters” (Thomas et al., 1997, p. 209). The brain is thus considered to be a bioenvironmental or biosocial organ (Gibson, 1996), and investigators are now exploring the unique domains of the “social brain” (Brothers, 1990) and the central role of emotions in social communication (Adolphus, 2000). In applying this principle to social-emotional development, the connections between the neurobiological concept of “enriched environment” and the psychological concept of “optimal development” can now be more closely coupled in the psychoneurobiological construct of a “growth-facilitating” (as opposed to “growth-inhibiting”) interpersonal environment (Greenspan, 1981; Schore, 1994) that positively (or negatively) effects the experience-dependent maturation of the brain.
This interdisciplinary model is compatible with very recent conceptions that emphasize that developmental processes can best be understood in terms of a context in which evolving biological systems are interacting with the social realm. As Cairns and Stoff describe:
It is necessary to go beyond the conventional notion that biological variables not only influence behavior and environment to the more modern notion that behavioral and environmental variables also impact on biology. Maturation and developmental processes may provide the common ground for understanding the process of biological social integration. On the one hand, it is virtually impossible to conceptualize developmental changes without recognition of the inevitable internal modifications that occur within the organism over time. On the other hand, it is misleading to focus on the individual’s biology in the absence of detailed information about the interaction and social circumstances in which the behavior occurs. (1996, p. 349)
This integration of biology and psychology to understand development has a rich tradition in science. In The Expression of Emotions in Man and Animals, Darwin (1872) established the scientific study of emotions and proposed that movements of expression in the face and body serve as the first means of communication between the mother and her infant (Schore, 2000a, 2000b, 2000c). And in The Project for a Scientific Psychology, Freud (1895), in an attempt to link neurology and psychology, first presented both his models of early development and ideas on how early traumatic events could heighten the risk of later forming psychopathology (Schore, 1995, 1997a, 1997c). Although others have followed this line of integrating the biological and psychological realms, perhaps the most important scientist of the late twentieth century to apply an interdisciplinary perspective to the understanding of how early developmental processes influence later mental health was John Bowlby. Over two decades ago he asserted that attachment theory can frame specific hypotheses that relate early family experiences to different forms of psychiatric disorders, including the neurophysiological changes that accompany these disturbances of mental health. It is thus no coincidence that attachment theory, the dominant theoretical model of development in contemporary psychology, psychoanalysis, and psychiatry, is the most powerful current source of hypotheses about infant mental health.
If attachment is interactive synchrony, stress is defined as an asynchrony in an interactional sequence, but a period of synchrony following this allows for stress recovery (Chapple, 1970).
It is now thought that the process of reexperiencing positive affect following negative experience may teach a child that negativity can be endured and conquered. Infant resilience emerges from an interactive context in which the child and parent transition from positive to negative and back to positive affect, and resilience in the face of stress is an ultimate indicator of attachment capacity and therefore adaptive mental health.
The continuing ontogeny of this self-regulating and self-correcting dynamic system allows for an expansion of the boundaries of the emotion communicating self. The early right brain capacities of processing socioemotional information and bodily states are not only central to the origin of the self, they are required for the ongoing development of the self over the lifespan.
This evolution of the developmental trajectory allows for an elaboration and increased complexity of the known functions of the right brain: the storage of internal working models of the attachment relationship (Schore, 1994), the processing of socioemotional information that is meaningful to the individual (Schore, 1998a), the ability to empathize with the emotional states of other humans beings (Schore, 1996), the mediation of emotional-imagistic processes in moral development (Vitz, 1990), the appreciation of humor, a mechanism for coping with daily stress (Shammi & Stuss, 1999), the cerebral representation of one’s own past and the activation of autobiographical memory (Fink et al., 1996), the establishment of a “personally relevant universe” (Van Lancker, 1991), and “the capacity to mentally represent and become aware of subjective experiences in the past, present, and future” (Wheeler, Stuss, & Tulving, 1997, p. 331).
On the most fundamental level, however, the emotion processing right hemisphere is dominant for the control of vital functions that support survival and enable the organism to cope with stressors (Wittling & Schweiger, 1993).Allan N. Schore: The Effects of Relational Trauma on Right Brain Development Affect Regulation
...from the beginning, attachment theory has also had a parallel interest in the etiology of abnormal development. In applying the theory to the links between stress coping failures and psychopathology, Bowlby (1978) proposed:
In the fields of etiology and psychopathology [attachment theory] can be used to frame specific hypotheses which relate different family experiences to different forms of psychiatric disorder and also, possibly, to the neurophysiological changes that accompany them. These germinal ideas have lead to the field of developmental psychopathology, an interdisciplinary approach that conceptualizes normal and aberrant development in terms of common underlying mechanisms (Cicchetti, 1994).
This field is also now incorporating current data from neuroscience into more complex models of psychopathogensis.
This is because contemporary neuroscience is now producing more studies of not just the pathology of the mature brain, but the early developmental failures of the brain. And so neurobiology is currently exploring “early beginnings for adult brain pathology” (Altman, 1994, 1997) and describing “alteration in the functional organization of the human brain which can be correlated with the absence of early learning experiences” (Castro-Caldas, Petersson, Reis, Stone-Elander, & Ingvar, 1998).
These trends indicate that an integration of current attachment theory, neuroscience, and infant psychiatry can offer more complex models of psychopathogenesis (Schore, 1997d, 1998d). Toward that end, in this second part of this sequential work, I will offer interdisciplinary data to strengthen the theoretical connections between attachment failures, impairments of the early development of the brain’s stress coping systems, and maladaptive infant mental health. And so I will present ideas on the effects of traumatic attachment experiences on the maturation of brain regulatory systems, the neurobiology of relational trauma, the neuropsychology of a disorganized/disoriented attachment pattern, the inhibitory effects of early trauma on the development of control systems involved in affect regulation, the links between early relational trauma and a predisposition to postraumatic stress disorder, a neurobiological model of dissociation, the connections between traumatic attachment and enduring right hemisphere dysfunction, and implications for early intervention.
Within the biopsychosocial model of infant psychiatry, the diathesis-stress concept prescribes that psychiatric disorders are caused by a combination of a genetic-constitutional predisposition and environmental or psychosocial stressors that activate the inborn neurophysiological vulnerability. In light of the fact that the brain growth spurt begins in the third trimester in utero (Dobbing & Smart, 1974), genetic-constitutional factors can be negatively impacted during this period by adverse conditions within the uterine maternal – infant environment. For example, very recent research shows that maternal hormones regulate the expression of genes in the fetal brain, and that acute changes in maternal hormone induce changes in gene expression in the fetal brain that are retained when it reaches adulthood (Dowling, Martz, Leonard, & Zoeller, 2000). Other studies reveal that high levels of maternal corticotropin-releasing hormone during pregnancy negatively affects fetal brain development (Glynn, Wadhwa, & Sandman, 2000) and reduces later postnatal capacities to respond to stressful challenge (Williams, Hennessey, & Davis, 1995).
These and other data indicate that certain maternal stimuli that impinge upon the fetus negatively impact the hypothalamo – pituitary – adrenocortical (HPA) axis (Glover, 1997; Sandman et al., 1994; Weinstock, 1997) and thereby produce an enduring neurophysiological vulnerability. There is now convincing evidence of the enduring detrimental effects of maternal alcohol (Streissguth et al., 1994), drug (Espy, Kaufman, & Glisky, 1999; Jacobson et al., 1996), and tobacco (Fergusson, Woodward, & Horwood, 1998) use during pregnancy on the child’s development. These risk factors, in part, reflect a delay in postnatal brain development (Huppi et al., 1996) that is expressed not only in prematurity and low birth weight, but also in poor infant interactive capacities (Aitken & Trevarthen, 1997). These limitations in social responsiveness may be aligned with parental avoidance or rejection (Field, 1977), and even physical abuse of the premature infant (Hunter, Kilstom, Kraybill, & Loda, 1978).
Various maternal behaviors may severely dysregulate the homeostasis and even future development of the developing fetus, yet these are not usually considered to be instances of trauma. On the other hand, caregiver abuse and neglect of the postnatal infant are viewed as clear examples of relational trauma. Again, in neonatal phases, both genetic factors that influence stress responsivity and detrimental environmental effects interact to contribute to a behavioral outcome, that is stress exaggerates the effects of a developmental lesion (Lipska & Weinberger, 1995). This biopsychosocial model suggests that high-risk infants born with delayed brain development and poor interactive capacites, and thereby a vulnerable predisposition, would experience even low levels of relational stress as traumatic, while an infant with a more durable constitution would tolerate higher levels of dyadic misattunement before shifting into dysregulation. There is no one objective threshhold at which all infants initiate a stress response; rather, this is subjectively determined and created within a unique organismic-environmental history. Even so, the severe levels of stress associated with infant abuse and neglect base of text are pathogenic to all immature human brains, and the latter maybe even more detrimental to development than the former.
These principles suggest that caregiver-induced trauma is qualitatively and quantitatively more potentially psychopathogenic than any other social or physical stressor (aside from those that directly target the developing brain). In an immature organism with undeveloped and restricted coping capacities, the primary caregiver is the source of the infant’s stress regulation, and therefore, sense of safety. When not safety but danger emanates from the attachment relationship, the homeostatic assaults have significant short- and long-term consequences on the maturing psyche and soma. The stress regulating systems that integrate mind and body are a product of developing limbic – autonomic circuits (Rinaman, Levitt, & Card, 2000), and because their maturation is experience dependent, during their critical period of organization they are vulnerable to relational trauma. Very recent basic research is revealing that perinatal distress leads to a blunting of the stress response in the right (and not left) prefrontal cortex that is manifest in adulthood (Brake, Sullivan, & Gratton, 2000), and that interruptions of early cortical development specifically affect limbic association areas and social behavior (Talamini, Koch, Luiten, Koolhaas, & Korf, 1999).
In human infancy, relational trauma, like exposure to inadequate nutrition during the brain growth spurt (Levitsky & Strupp, 1995; Mendez & Adair, 1999), to biological pathogens or chemical agents that target developing brain tissue (Connally & Kvalsvig, 1993), and to physical trauma to the baby’s brain (Anderson, Bechara, Damasio, Tranel, & Damasio, 1999), interferes with the experience-dependent maturation of the brain’s coping systems, and therefore, have a long-enduring negative impact on the trajectory of developmental processes.
NEGATIVE IMPACT OF RELATIONAL TRAUMA ON INFANT MENTAL HEALTH
The neuropsychobiological literature underscores a central finding of developmental science — that the maturation of the infant’s brain is experience dependent, and that these experiences are embedded in the attachment relationship (Schore, 1994, 2000b; Siegel, 1999). If there is truth to the dictum that security of the attachment bond is a primary defense against trauma-induced psychopathology, then what about the infant who does not have such an experience but its antithesis? And because attachment transactions occur in a period in which the brain is massively developing, what is the future course of the brain/mind/body of an infant who does not have the good fortune of engaging with a caregiver who cocreates the child’s internal sense of emotional security? What if the brain is evolving in an environment of not interpersonal security, but danger? Is this a context for the intergenerational transmission of psychopathology, and the origins of maladaptive infant mental health? Will early trauma have lasting consequences for future mental health, in that the trajectory of the developmental process will be altered?
A number of scientific and clinical disciplines are now focusing on not only the interactional aspects of early trauma, but also on the untoward effects of abuse and deprivational neglect on the development of the infant brain. In a major advance of our knowledge, discoveries in the developmental sciences now clearly show that the primary caregiver acts as an external psychobiological regulator of the “experience-dependent” growth of the infant’s nervous system (Schore, 1994, 1996, 1997a, 2000c). These early social events are imprinted into the neurobiological structures that are maturing during the brain growth spurt of the first two years of life, and therefore have far-reaching effects. Eisenberg (1995) refers to “the social construction of the human brain,” and argues that the cytoarchitectonics of the cerebral cortex are sculpted by input from the social environment. The social environment can positively or negatively modulate the developing brain.
Early relational trauma, which is usually not a singular event but “ambient” and “cumulative,” is of course a prime example of the latter. These events may not be so uncommon. In 1995, over 3 million children in this country were reported to have been abused or neglected (Barnet & Barnet, 1998), and the Los Angeles Times reported that in California, in 1997, there were 81,583 reported cases of neglect and 54,491 reported cases of physical abuse. Although these sources did not specify how many infants were in these categories, other evidence indicates that in the United States the most serious maltreatment occurs to infants under two years of age (National Center of Child Abuse and Neglect, 1981). Homicide (Karr-Morse & Wiley, 1997) and traumatic head injury (Colombani, Buck, Dudgeon, Miller & Hiller, 1985) are the leading causes of death for children under four. A 1997 issue of Pediatrics contains a study of covert video recordings of infants hospitalized for life-threatening events, and it documents, in a most careful and disturbing manner, the various forms of child abuse that are inflicted by caregivers on infants as young as three months while they are in the hospital (Southall, Plunkett, Banks, Falkov, & Samuels, 1997). These experiences are recorded and stored in the infant. Terr (1988, p. 103) has written that “literal mirroring of traumatic events by behavioral memory [can be] established at any age, including infancy.” According to Luu and Tucker, “To understand neuropsychological development is to confront the fact that the brain is mutable, such that its structural organization reflects the history of the organism” (1996, p. 297). Because early abuse negatively impacts the developing brain of these infants, it has enduring effects. There is extensive evidence that trauma in early life impairs the development of the capacities of maintaining interpersonal relationships, coping with stressful stimuli, and regulating emotion. A body of interdisciplinary research demonstrates that the essential experiences that shape the individual’s patterns of coping responses are forged in the emotion-transacting caregiver – infant relationship (Schore, 1994, 2000b). We are now beginning to understand, at a psychobiological level, specifically how beneficial early experiences enhance and detrimental early histories inhibit the development of the brain’s active and passive stress coping mechanisms.
There is now agreement that, in general, the enduring effects of traumatic abuse are due to deviations in the development of patterns of social information processing. I suggest that, in particular, early trauma alters the development of the right brain, the hemisphere that is specialized for the processing of socioemotional information and bodily states. The early maturing right cerebral cortex is dominant for attachment functions (Henry, 1993; Schore, 1994, 2000b, 2000c; Siegel, 1999) and stores an internal working model of the attachment relationship. An enduring developmental impairment of this system would be expressed as a severe limitation of the essential activity of the right hemisphere — the control of vital functions supporting survival and enabling the organism to cope actively and passively with stressors (Wittling & Schweiger, 1993).
Davies and Frawley (1994) describe the immediate effects of parent-inflicted trauma on attachment:
The continued survival of the child is felt to be at risk, because the actuality of the abuse jeopardizes (the) primary object bond and challenges the child’s capacity to trust and, therefore, to securely depend. (p. 62)
In contexts of relational trauma the caregiver, in addition to dysregulating the infant, withdraws any repair functions, leaving the infant for long periods in an intensely disruptive psychobiological state that is beyond her immature coping strategies. In studies of a neglect paradigm, Tronick and Weinberg describe:
When infants are not in homeostatic balance or are emotionally dysregulated (e.g., they are distressed), they are at the mercy of these states. Until these states are brought under control, infants must devote all their regulatory resources to reorganizing them. While infants are doing that, they can do nothing else. (1997, p. 56)
In other words, infants who experience chronic relational trauma too frequently forfeit potential opportunities for socio-emotional learning during critical periods of right brain development. But there is also a pernicious long-term consequence of relational trauma — an enduring deficit at later points of the life span in the individual’s capacity to assimilate novel (and thus stressful) emotional experiences. At the end of the nineteenth century Janet (1889) speculated:
All [traumatized] patients seem to have the evolution of their lives checked; they are attached to an unsurmountable object. Unable to integrate traumatic memories, they seem to have lost their capacity to assimilate new experiences as well. It is . . . as if their personality development has stopped at a certain point, and cannot enlarge any more by the addition of new elements.
The functional limitations of such a system are described by Hopkins and Butterworth (1990): “Undifferentiated levels of development show relatively rigid but unstable modes of organization in which the organism cannot adapt responses to marked changes coming from within or without” (p. 9). From a psychoanalytic perspective, Emde (1988) defines pathology as a lack of adaptive capacity, an incapacity to shift strategies in the face of environmental demands.
THE NEUROBIOLOGY OF INFANT TRAUMA
...intense relational stress alters calcium metabolism in the infant’s brain, a critical mechanism of cell death (Farber, 1981). Dopamine (Filloux & Townsend, 1993; McLaughlin, Nelson, Erecinska, & Chesselet, 1998) and glutamate (Tan, Sagara, Liu, Maher, & Schubert, 1998) can be neurotoxic, by generating superoxide free radicals associated with oxidative stress (Lafon-Cazal, Pietri, Culcas, & Bockaert, 1993), especially hydroxyl radicals that destroy cell membranes (Lohr, 1991). These events greatly enhance “apoptotic” or “programmed cell death” (Margolis et al., 1994; Schore, 1997a). During a critical period of growth of a particular brain region, DNA production is highly increased, and so excitotoxic stress, which is known to cause oxidative damage to DNA, lipid membrane, and protein (Liu, Wang, Shigenaga, Yeo, Mori, & Ames, 1996), also negatively impacts the genetic systems within evolving limbic areas.
Indeed, there is now evidence to show that adverse social experiences during early critical periods result in permanent alterations in opiate, corticosteroid, corticotropin releasing factor, dopamine, noradrenaline, and serotonin receptors (Coplan, Andrews, Rosenblum, Owens, Gorman, & Nemeroff, 1996; Ladd, Owens, & Nemeroff, 1996; Lewis, Gluck, Beauchamp, Keresztury, & Mailman, 1990; Martin, Spicer, Lewis, Gluck, & Cork, 1991; Rosenblum, Coplan, Fridman, Basoff, Gorman, & Andrews, 1994; van der Kolk, 1987). Such receptor alterations are a central mechanism by which “early adverse developmental experiences may leave behind a permanent physiological reactivity in limbic areas of the brain” (Post, Weiss, & Leverich, 1994, p. 800).
It is now established that “dissociation at the time of exposure to extreme stress appears to signal the invocation of neural mechanisms that result in long-term alterations in brain functioning” (Chambers et al., 1999, p. 274). In other words, infants who experience states of terror and dissociation and little interactive repair, especially those with a genetic-constitutional predisposition and an inborn neurophysiological vulnerability, are high risk for developing severe psychopathologies at later stages of life. Bowlby asserted,
RELATIONAL TRAUMA, ORBITOFRONTAL DYSFUNCTION, AND A PREDISPOSITION TO POSTTRAUMATIC STRESS DISORDERS
The connections between the orbitofrontal areas and the amygdala form postnatally, and are negatively impacted by the adverse environmental events of relational trauma (see Figure 4). A severe experientially driven pruning of these interconnections would allow for amygdala-driven states, such as fear-flight states to be later expressed without cortical inhibition. It is now established that a pathological response to stress reflects the functions of a hyperexcitable amygdala (Halgren, 1992), and that the memory processes of the amygdala are amplified by extreme stress (Corodimas, LeDoux, Gold, & Schulkin, 1994). Even subliminally processed low-intensity interpersonal stressors could activate unmodulated terrifying and painful emotional experiences of the individual’s early history that are imprinted into amygdalar – hypothalamic circuits. These fear-freeze responses would be intense, because they are totally unregulated by the orbitofrontal areas that are unavailable for the correction and adjustment of emotional responses.
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A substantial body of neurological studies also indicate that aggression dysregulation is associated with specifically altered orbitofrontal function (Fornazzari et al., 1992; Grafman, Schwab, Warden, Pridgen, Brown, & Salazar, 1996; Miller, Darby, Benson, Cummings, & Miller, 1997; Raine, Stoddard, Bihrle, & Buschbaum, 1998a; Starkstein & Robinson, 1997). Davidson, Putnam, and Larson (2000) implicate a dysregulation of an orbitofrontal – anterior cingulate – amygdala circuit of emotion regulation in a risk for violence and aggression. Right orbitofrontal impairment is associated with difficulties in emotional recognition of angry and disgusted facial expressions, autonomic responding, and social cognition, as well as with high levels of aggression (Blair & Cipolotti, 2000).
There is now evidence that there are two types of aggression: predatory or “stalking” attack, and defensive or “affective” rage (Panksepp, 1998; Siegel, Roeling, Gregg, & Kruk, 1999). Positron emission tomography (PET) studies reveal that both predatory and affective murderers show reduced prefrontal and increased subcortical activity (Raine et al., 1998b). Increased metabolic rate in the right hemisphere is also seen in affective, impulsive muderers. Affective rage is mediated by the hypothalamic ventromedial nucleus, a structure associated with elevated sympatho-adrenal and cardiovascular activity (Stoddard-Apter, Levin, & Siegel, 1983), increases in anxiety (Adamec & McKay, 1993), and parasympathetic vagal suppression (Colpaert, 1975). This system is also involved in maternal rage that is part of maternal protectiveness, and so, in line with the finding that maternal aggression shares similarities with hypothalamic attack (Siegel et al., 1999), it is tempting to speculate that a functional dysregulation of this system occurs in maternal abuse.
Sympathetic ventromedial hypothalamic neurons continue to develop in a postnatal critical period (Almli & Fisher, 1985), a time when their dendrites receive frontolimbic axonal projections. These neurons also receive input from the amygdala (Adamec, 1998), and thus an excessive developmental parcellation of the orbitofrontal (and cingulate-insular) inhibitory pathway to the sympathetic ventromedial hypothalamic nucleus (Ohta & Oomura, 1979) would seriously interfere with the ability of higher limbic inputs to regulate amygdala-driven affective rage. This deficit represents the outcome of early relational trauma, and it mediates the intermittent states of relationally triggered uncontrolled aggression seen in certain traumatized populations.
Furthermore,a large body of studies indicates disrupted early attachments and early trauma and abuse in the histories of children and adults diagnosed as borderline personality disorder (Lyons-Ruth & Jacobvitz, 1999), and thus there is a high correlation of PTSD and borderline diagnoses (Famularo et al., 1992; Herman, Perry, & van der Kolk, 1989; van der Kolk, Hostetler, Heron, & Fisler, 1994). Zanarini et al. (1997) report that 91% of borderline patients report childhood abuse, and 92% report some type of childhood neglect. In an overview of the literature Paris summarizes the developmetal data and asserts “the weight of the research evidence supports the hypothesis that abuse during childhood is an important risk factor for borderline personality disorder” (1995, p. 15). Herman and van der Kolk (1987) assert that PTSD and borderline personality disorders both share massive disturbances in affect regulation, impulse control, interpersonal difficulties, self-integration, and a bias to use dissociation when under stress. Neurobiological studies reveal altered amygdala (Carrigan, Davidson, & Heard, 2000) and orbitofrontal (Goyer, Konicki, & Schulz, 1994) function in borderline personality disorders.
Brain imaging research also demonstrates decreased orbitofrontal metabolism in another class of psychiatric patients with a history of violent behavior (Raine et al., 1998a), that is, sociopathic personality disorder. These authors implicate a defective orbitofrontal system in a “predisposition to violence,” a finding of numerous studies (see previous references). These personalities show the second type of aggression, predatory or “stalking” attack (Panksepp, 1998; Siegel et al., 1999). This type of aggression is also associated with hypothalamic activity, but from different areas in the parasympathetic lateral hypothalamus, an area also innervated by amygdala inputs. In natural settings, predatory attacks are released when modulatory brain mechanisms, such as those in the amygdala and prefrontal cortex, are suppressed (Siegel et al., 1999). These authors report that stimulation of the medial prefrontal cortex blocks predatory attack elicited from the lateral hypothalamus.
The orbital prefrontal cortex has direct connections with lateral hypothalamus, and thereby regulates its activity (Kita & Oomura, 1981). Because this hypothalamic system also continues to develop in a postnatal critical period (Fisher & Almli, 1984), an excessive experience-dependent parcellation of prefrontal-lateral hypothalamic connections would result in an inefficient higher cortical regulation of not just the immobility response, but under extremely intense stressful levels, predatory attack. This predisposition to relational violence, which may result from a toxic growth-inhibiting combination of early maternal neglect and later paternal abuse, is expressed in “type D” attachments (Lyons-Ruth et al., 1993; Lyons-Ruth & Jacobvitz, 1999). This model clearly suggests that a sociopathic personality organization is frequently another manifestation of developmental posttraumatic stress disorder.
In an earlier work I presented ideas on the regulation of infantile rage reactions and on how structural impairments associated with attachment failures can be incorporated into models of primitive personality disorders (Schore, 1994). Continuing this, in an upcoming publication (Schore, work in progress) I offer data to show that “type D” disorganized/disoriented attachments and severe orbitofrontal pruning and apoptotic programmed cell death represent the developmental origins of both the affective aggression of various levels of borderline personality disorders and the predatory or stalking type of aggression of sociopathic personality disorders.
IMPLICATIONS FOR MODELS OF EARLY INTERVENTION
The promotion of affect regulation is now seen as a common mechanism in all forms of psychotherapy (Bradley, 2000). Furthermore, current developmental models clearly suggest that psychotherapeutic treatment for severe attachment disorders should begin as early in the lifespan as possible. Osofsky and her colleagues demonstrate that effective therapeutic interventions can be made in traumatized two year olds. They conclude, “Helping young children acquire self-regulation through reciprocal management of affects with an emotionally available therapist” can allow for a “return to a healthy developmental pathway” (1995, p. 605). The interactive regulation embedded in the therapeutic relationship functions as a “growth facilitating environment,” specifically for the experience-dependent maturation of right orbitofrontal systems (Schore, 1994, 1997a, in press a, in press b, in press c). This context can alter attachment patterns from “insecurity” to “earned security” (Phelps, Belsky, & Crnic, 1998).
A logical outcome of psychological, psychoanalytic, and psychiatric theories that emphasize the centrality of early development to later functioning is that early prevention is an essential goal. In accord with clinical findings (e.g., Eckenrode et al., 2000), the latest psychoneurobiological developmental models that focus on the effects of early environmental interactions on evolving brain – behavior relationships also emphatically stress the fundamental importance of early intervention. A core postulate of classical developmental biology and now of developmental neurobiology is the concept of critical periods. This construct emphasizes that certain detrimental early influences lead to particular irreversible or only partially reversible enduring effects, highlighting the fact that limitations of biological organization set into place once systems differentiate.
It is important to remember, however, that the flip side of the critical period concept emphasizes the extraordinary sensitivity of developing dynamic systems to their environment, and asserts that these systems are most plastic in periods when they are in the process of differentiating. The right hemisphere, which is centrally involved in both the capacity to perceive the emotional states of other human beings and the control of vital functions supporting survival and enabling the individual to cope actively and passively with stress, is in a growth spurt in the first year-and-a-half of life, and is dominant for the first three. Its maturation is “experience-dependent,” and this “experience” is embedded in the attachment relationship between caregiver and infant. Developmentally focused clinicians are familiar with the various patterns of emotional transactions of securely and insecurely attached dyads. But they also have extensive clinical knowledge of how the relationship between the patient and therapist cocreates a safe environment that facilitates what Emde (1990) calls a mobilization of the patient’s “biologically prepared positive developmental thrust.” These same interpersonal skills and intersubjective sensitivities are valuable assets in preventive programs.
As a number of issues of this journal document, attachment researchers in association with infant mental health workers are now devising interventions that effectively alter the affect-communicating capacities of mother – infant systems, and thereby the attachment experiences of high risk dyads. By providing an optimal context for the cocreation of a system of interactive regulation that is timed to critical periods of socioemotional development, such interventions can facilitate the maturation of neurobiologically adaptive regulatory systems. Early interventions thus have life-long effects on the adaptive capacities of a developing self. These efforts, if expanded onto a larger scale, could make deep inroads into not only altering the intergenerational transmission of psychiatric disorders but improving the quality of a life throughout the lifespan. A deepening social and political commitment to early treatment and prevention programs would thus be a major contribution to the problems our societies are now facing. -
...I completely support working to reduce childhood
trauma. It is a worthy goal for its own sake. I simply don't think it's
responsible to claim that doing so will lead to the grand scale things
that people on this board often claim...Irresponsible compared to what?
It's pretty hard to imagine how you could read my posts and still have to ask that question.
If I recall correctly, in an earlier thread you suggested that peaceful parenting techniques might harm a hypothetical purely-genetically-determined sociopath.
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None of us is even saying childhood violence isn't a problem or we shouldn't work to stop it. All we've said is that the science does not show in any conclusive way at this time that nurture is primary and nature secondary in causing the overall problems of violence and aggression on the larger scale as Stefan seems to claim.
I claim to be agnostic on the roots of larger scale violence and
aggression and I back that up by promoting more research rather than
claiming that reducing environmental factors is primary. Stefan, on the
other hand, appears to claim to be agnostic but at the same time claim
that reducing childhood trauma will bring about a peaceful world on a
larger scale.I repeat for the umpteenth time: I completely favor reducing childhood
trauma. I simply do not agree that at this time it is responsible to
claim that doing so will also bring about some larger scale anarchist
peaceful paradise because a world of non-traumatized children will grow
into rational adults that agree with FDR's philosophy. I think that is a
stretch that cannot be backed up by anything empirical.Is it your position that all current efforts to prevent violence against children should stop until the nurture/nature debate is settled?
How much do you think those children currently suffering inflictions of violence care about a future "anarchist
peaceful paradise"? -
i feel the podcasts have not worked for me or my life, i feel massively rejected by the community here, and also feel massively let down by my own agressive, needy behaviour on here as well, i know im not innocent in all this, all i know is that this website brings out the worst in me and makes me feel bad about myself.
I sympathize with your frustration.
It may be worth considering that forum posts are only words, and podcasts only sounds – and that you just can't get the full spectrum of real-time relational/biological resonance and reassurance you need from such impersonal means.
Some perspective from Stan Tatkin's couples therapy that seems to confirm much of what you are experiencing:
The anticipation of relationship failure is as
psychobiologically wired for the angry resistant individual, as
autoregulation and indifference are for the avoidant individual. The strategy of the angry resistant individual is to
offset anticipatory disappointment and failure through negativistic
conduct, a personality feature influenced by early childhood
development... Driven by hope that is dashed instantly by the
anticipation of failure, the angry resistant individual employs
negativism as a control mechanism against dependency. The angry
resistant individual ‘knows’, with certainty from within his or her
body, what is to come from hope, and it is bad. This becomes what is, in
essence, an allergy to hope. While the avoidant individual is allergic to dependency, the angry resistant is allergic to hope.As a result of their negative early life experiences with preoccupied
caregiver(s), angry resistant partners often present with problems with
self-regulation. Easily overtaxed by
responsibilities (e.g., school, work, marriage, children), angry
resistant individuals often view themselves not only as overwhelmed, but
as envious of and threatened by their partner’s ability to do whatever
he or she wants. Feeling the underdog, angry resistant individuals complain about not getting the help they need or deserve.The meta complaints of angry resistant individuals
may appear situational, but really are global and not so easily managed.
Their complaints include worries about a partner’s unreliability or
recalcitrance, rejection, being neglected or punished, being wrong,
being deprived (usually of love and affection), unfair treatment,
injustice, confusion, ambivalence, and being hurt or wounded. They
are unable to remember ever feeling this way before, yet such
sensitivities originate very early in childhood as relational trauma
involving caregivers. Inwardly, they believe something is wrong with
them, that they are a burden to their partner, that they are too needy,
and that they don’t deserve to be loved in the way they long to be.People are hurt by people, and only people can repair those injuries. No
one is better positioned to repair injuries than the primary
relationship partner, and the couple therapist can promote this. The
angry resistant’s negativism both engages and pushes away, as we have
seen. The angry resistant’s partner, regardless of his or her own
attachment orientation, likely will be faced with an ongoing challenge
to remain undaunted by the waxing and waning of this negativism. The
partner must come to understand in therapy that the corrective
counter-movement is to move forward on the angry resistant (in
friendliness) and not away. Angry resistant
individuals expect their partner to move away, pull back, or otherwise
rebuke their cloaked wish for the angry resistant partner to override
his or her negativism. The true hope of angry resistant individuals
is that their most important other, their partner will see beyond their
negativism and recognise it for what it is: a real bid for patience
and understanding; kindness and compassion; and ultimate reassurance
that the angry resistant is not a burden, overly needy, or destined for
rejection. In other words:- She: [approach and reunion] “You are so handsome. I love you.”
- He: [angry resistant reaction to approach and reunion] “Yeah, right. Tell that to someone who’ll believe you.”
- She: [typical but wrong response] “Forget it. You’re impossible.”
- She: [corrective response] “You are my handsome man and I – LOVE – YOU.” [she kisses him]
Narcissist's Psychological Defense Mechanisms [Sam Vaknin]
in Self Knowledge
Posted
Heinz Kohut
Basic Shame, Toxic Shame