The Neurobiology of the Dissociative Defense
In severe attachment pathologies the developing infant/toddler is repeatedly exposed to the ambient cumulative trauma that emanates from an interactive dysregulating context with a misattuning caregiver. Since this growth-inhibiting context generates dense and prolonged levels of negative affect in the infant, for self-protective purposes it severely restricts it’s overt expressions of an attachment need for dyadic regulation. The child thus significantly reduces the output of its emotion-processing, limbic-centered attachment system. And so for defensive functions it shifts from interactive regulatory modes into long-enduring, less complex autoregulatory modes. These subcortical-limbic organizational patterns are primitive strategies for survival, and therefore they become self-organizing attractor states. This sets the stage for primitive autoregulation, for the habitual use of dissociation. Indeed the type D attachment classification utilizes dissociative behaviors in later life (van Ijzendoorn et al., 1999).
The principle that severe attachment psychopathologies frequently access more primitive modes of autoregulation can be translated into the clinical tenet that more severe psychiatric disorders use dissociation as a characterological defense. In the parasympathetic-dominant state of dissociation, the individual is cut off (dis-associated) from both the external and the internal environment. This clearly implies a dysfunction of the orbitofrontal cortex, a site at which cortically processed exteroceptive information concerning the external environment is integrated with subcortically processed interoceptive information regarding the internal visceral environment.
The orbitofrontal system directly connects into the body via its direct connections into the ANS (Neafsey, 1990), and its modulation of the ANS is achieved via descending axons that synapse on dendritic fields of the hypothalamus, the head ganglion of the ANS, and vagal areas of the medulla. An extensive parcellation or thinning of these synaptic connections would lead to an inefficient regulation of the ANS by higher centers in the CNS. This loss means that under stress there would be not be a counterbalancing mechanism between the sympathetic-excitatory and parasympathetic-inhibitory components of the ANS, a loss of a coupled reciprocal mode of autonomic control, in which increases in activity in one ANS division are associated with a decrease in the other (Berntson, Cacioppo, and Quigley, 1991).
Under stress a developmentally immature orbitofrontal regulatory system would give way to a coupled nonreciprocal mode of autonomic control (Berntson et al., 1991). The result is an intensely high state of sympathetic ergotropic plus parasympathetic trophotropic arousal, the same pattern of Perry’s infant trauma response. Although right vagal and sympathetic innervation of the heart elicits, respectively, decreased and increased cardiac activity, simultaneous stimulation produces an even greater cardiac output and aortic blood flow (Koizumi et al, 1982). Behaviorally this is like "riding the gas and the brake at the same time," and the simultaneous activation of hyperexcitation and hyperinhibition results in the "freeze response".
In classic neurological primate research, Ruch and Shenkin (1943) lesioned the orbitofrontal cortex (area 13) and observed a "definite reduction in emotional expression," and an elimination of "fear" and aggressive" behaviors that were replaced by "gazing into the distance with a blank expression." Such behavior was interpreted as an "over-reactive" response to the presence of the experimenter-observer. This is identical to the blank, dazed behavior of the "freeze" or "surrender" reaction of "type D" infants, to the "frozen watchfulness" observed in the abused child who waits warily for parental demands, responds quickly and compliantly, and then returns to her previous vigilant state, and to the "frozen state" of speechless terror seen in adult PTSD patients. Primate studies by Kalin et al. (1998) show that freezing in infants, which is elicited by eye contact, correlates with extreme right frontal EEG activity and high basal cortisol levels. This pattern, first measured in late infancy, endures for the rest of the lifespan as a fearful temperament. Extremely inhibited fearful children show heightened sympathetic activity as well as increased cortisol levels (Kagan, Reznick, & Snidman, 1987).
But in addition due to a loss of a counterbalancing functions of the ANS, severe attachment pathologies also show an inefficient orbitofrontal capacity in coordinating the two branches of the ANS and therefore in regulating affective shifts. Henry et al. (1992) point out that a simultaneous activation of the sympathetic-adrenal medullary and hypothalamic-pituitary adrenal axes typically occurs in the initial phases of overwhelming stress, but these systems can operate also independently. In PTSD, they note, these two systems can undergo an "increasing separation," and this "dissociation" is the basis for the emotional psychopathology of this disorder. This represents what Berntson et al. (1991) call an uncoupled nonreciprocal mode of autonomic control, in which responses in one division of the ANS occur in absence of change in the other.
A resultant rapid uncoupling of the two frontolimbic circuits would occur in response to even low levels of interactive stress, and be expressed in emotional lability and rapid state shifts. Putnam (1997) describes pathological "dissociative switches" between states, which occur rapidly, and are manifest in "Inexpliable shifts in affect", changes in facial appearance, mannerisms and speech, and discontinuities in train of thought. Recall, in trauma sympathetic hyperarousal is suddenly followed by hyperparasympathetic dissociation. Meares also concludes that "dissociation, at its first occurrence, is a consequence of a ‘psychological shock’ or high arousal" (1999, p. 1853).
A habitual tendency to shift into primitive parasympathetic states is a characterstic of a developmentally immature regulatory system with weak connections between the highest level of the limbic system and the ANS. Of particular importance is the experience-dependent maturation of orbital areas that regulate the parasympathetic system, a development that is slower and later than the sympathetic (Schore, 1994). The orbitofrontal areas, like the amygdala, have direct inputs into the medulla (Mizuno, Sauerland, & Clemente, 1968; Yasui et al., 1991), including the medullary reticular formation (Travers, Dinardo, & Karimnamazi, 1997) and medullary noradrenergic neurons in the nucleus of the solitary tract (see Figure 2).
These are the sites of the medullary vagal system, but it is now known that there are two parasympathetic vagal systems, a late developing "mammalian" or "smart" system in the nucleus ambiguus which allows for the ability to communicate via facial expressions, vocalizations, and gestures via contingent social interactions, and a more primitive early developing "reptillian" or "vegetative" system in the dorsal motor nucleus of the vagus that acts to shutdown metabolic activity during immobilization, death feigning, and hiding behaviors (Porges, 1997). Both of these vagal systems are right laterlized (Porges, Doussard-Roosevelt, & Mati, 1994). The central nucleus of the amygdala has extensive connections into the dorsal motor vagal nucleus (Schwaber et al., 1982) and is involved in passive coping, immobile behavior, and parasympathetic activity (Roozendaal et al., 1997).
In an earlier discussion of traumatic brain injury I referred to this same dorsal medullary region that functions as an energy conservation system. I posit that in growth-facilitating socioemotional environments, the orbitofrontal system enhances its inputs into the nucleus ambiguus vagal system and therefore expands its affect regulatory capacities, but in traumatic growth inhibiting environments, this "smart" system never optimally develops, and the "vegetative" system dominates. I suggest that the longer enduring "developmental vegetative state" (Multi-Society Task Force on Persistent Vegetative State, 1994) of trauma-induced widespread hypometabolism would interfere with the growth of the developing brain, which requires massive amounts of energy for the biosynthetic processes of the brain growth spurt (Schore, 1994; Schore, 1997a; 2000c).
In neurological patients the vegetative state is characterized as a "complete loss of attention to the external world" (Laureys et al., 2000), a description that echoes the psychiatric concept of dissociation. I propose that the massive inhibition of the dorsal motor vegetative vagal system mediates dissociation, a primitive defensive mechanism which has long been implicated in trauma-induced psychopathogenesis (Janet, 1889; Chu & Dill, 1990). Porges states that the dorsal motor nucleus of the vagus "contributes to severe emotional states and may be related to emotional states of ‘immobilization’ such as extreme terror" (1997, p. 75). Perry’s description of the traumatized infant’s sudden state switch from sympathetic hyperarousal into parasympathetic dissociation is reflected in Porges’ characterization of
the sudden and rapid transition from an unsuccessful strategy of struggling requiring massive sympathetic activation to the metabolically conservative immobilized state mimicking death associated with the dorsal vagal complex (1997, p. 75).
Clinically, dissociation is described as "a submission and resignation to the inevitability of overwhelming, even psychically deadening danger" (Davies & Frawley, 1994, p. 65).
Dissociation is a primitive defense, and in early traumatized developmental psychopathologies more complex defenses never organize. The inhibitory vagal brake in such systems is predominantly provided by the rigid, fixed "vegetative" dorsal motor vagus, and not the more evolved and flexible "smart" nucleus ambiguus that allows for social communication. The vagal brake must be withdrawn when the individual shifts from a state of low to high metabolic demand, an operation that is adaptive for engaging and disengaging with the dynamically changing environment (Porges, 1997). This precludes involvement in dyadic play states and loss of a context for interactively creating high levels of arousal and metabolic energy for brain biosynthesis (see earlier section on developmental instability). The lack of the ability to engage in interactive play is an indicator of maladaptive infant health.
Dissociation and Body-Mind Psychopathology
Dissociation is a common symptom of a spectrum of severe psychopathologies, from reactive attachment disorder of infants (Hinshaw-Fuselier et al., 1999), to dissociative identity disorders (Putnam, 1989), psychotic experiences (Allen & Coyne, 1995), borderline personality disorders (Golynkina & Ryle, 1999), and posttraumatic stress disorders of adults (van der kolk, McFarlane, & Weisaeth, 1996). The DSM-IV lists five dissociative disorders: dissociative amnesia, dissociative fugue, depersonaliztion disorder, dissociative identity disorder, and dissociative disorder not otherwise identified (American Psychiatric Association, 1994).
Since dissociation appears in the earliest life stage, a developmental psychopathology perspective is being utilized to understand its etiology (Putnam, 1997), and disorganization of attachment is now proposed as a model system to understand dissociative psychopathology (Liotti, 1992, 1999). However, these models are purely psychological, and do not refer to the neurobiological mechanisms that underlie the phenomena. An integration of neuroscience and clinical data can offer such a model.
It is important to emphasize that in traumatic abuse the individual dissociates not only from the external world, from processing external stimuli associated with terror, but also from the internal world, that is painful stimuli originating within the body. It is sometimes difficult to keep in mind the fact that the body of an abused infant is physically assaulted, and therefore in pain. Darwin, in the work that began the scientific study of emotion, asserted that "Pain, if severe, soon induces extreme depression or prostration but it is first a stimulant and excites to action...Fear again is the most depressing of all emotions, and it soon induces utter helpless prostration" (1872, p. 31). Krystal, in a classic text on trauma, also describes the state switch from sympathetic hyperaroused-terror into parasympathetic hypoaroused conservation-withdrawal hopelessness and helplessness:
The switch from anxiety to the catatonoid response is the subjective evaluation of the impending danger as one that cannot be avoided or modified. With the perception of fatal helplessness in the face of destructive danger, one surrenders to it (1988, p. 114-115).
Using interdisciplinary data, Krystal further explains how the catatonoid reaction is the affective response to unavoidable danger, a pattern of surrender, and equates it with the "freeze" response and state of cataleptic immobility. "[I]n the state of surrender and catatonoid reaction, all pain is stilled and a soothing numbness ensues" (Krystal, 1988, p. 117). As previously described, this numbness is due to a sudden massive elevation of endogenous opioids in stress-induced catalepsy or immobility (Fanselow, 1986). A clinical description of the traumatized child state is offered by Nijenhuis et al.:
[I]ndividuals tend to hide in dark places, freeze there, and prefer to physically disappear when they feel threatened. Adopting a fetal position, they seem to be unresponsive to external stimuli (1998, p. 114-115).
Bodily stiffening frequently accompanies these incidents, and the passive defense of dissociation increases with the severity of abuse.
The long-term effect of infantile psychic trauma is the arrest of affect development and the process of desomatization (Krystal, 1997). The ultimate endpoint of experiencing catastrophic states of relational-induced trauma in early life is a progressive impairment of the ability to adjust, take defensive action, or act on one’s own behalf, and, most importantly, a blocking of the capacity to register affect and pain. Lane et al. assert that "traumatic stress in childhood could lead to self-modulation of painful affect by directing attention away from internal emotional states" (1997, p. 840), a principle consonant with the well-documented association between traumatic childhood events and proneness to dissociation (Irwin, 1994; Ogawa et al., 1997).
In an earlier section of this paper I offered a psychoneurobiological model of the developmental events that lead to such maladaptive coping strategies. The pattern of cataleptic immobility described by Krystal is normally seen in the first two months of life of human infants: "[In] dangerous situations a sudden behavioral change in the infant may occur...the infant lies motionless with non-converging, staring eyes and sleep-like respiration" (Papousek & Papousek, 1975, p. 251). The right lateralized dorsal motor "vegetative vagus" is involved with respiration (Porges et al., 1994). Recall traumatized infants are observed to be staring off into space with a glazed look, and the child’s dissociation and immobility in the midst of terror result from elevated levels of cortisol and vagal tone, while opiates induce pain numbing and blunting. The state of conservation-withdrawal occurs in hopeless and helpless contexts, and is behaviorally manifest as feigning death (Powles, 1992). Krystal (1988) notes that in German catalepsy is called Totstell-reflex, or "death-posturereflex."
The purpose of this primitive defensive reaction is to protect the developing organism against the overwhelming psychobiological pain of the attachment disruptions induced by early relational trauma. MacLean points out that "nature appears to have ensured that maternal-offspring separation in mammals results in distress comparable to pain" (1987, p. 136). This implies that maternal regulation of pain-distress occurs as a normal attachment function. But what if the caregiver is a source of intense noxious and painful stimulation? There is now an increasing consensus that both the child’s reactivity and the parenting context contribute to changes in the infant’s pain response (Sweet, McGrath, & Symons, 1999). According to Grunau et al:
[N]on-optimal parenting may contribute to the development of inappropriate strategies for coping with common pains in childhood, or of chronic pain patterns, in some children who have experienced prolonged or repeated pain as neonates (1994, p. 353).
Since these are attachment experiences occurring in a critical period of limbic ontogeny, they alter the organization of the brain circuits that process pain. What do we know of these circuits?
Recent basic research reveals that persistent pain experiences during the early neonatal period, a critical period for the organization of nociceptive neuronal circuits, rewires immature pain circuits, and leads to lasting and potentially detrimental alterations in the individual’s response to pain in adulthood (Ruda et al., 2000). These studies track the long term effects of physical pain, but the effects of pain associated with relational trauma may lead to even more adverse consequences. It is now established that a traumatic painful event, in contrast to nontraumatic pain, triggers an intense emotional experience with concomitant autonomic / somatic outflow, and activates increased sympathetic activity and prominent responses in the limbic system, i.e., hypothalamus, periaqueductal gray, anterior cingulate, insula, posterior parietal and prefrontal cortex (Hsieh et al., 1995a; Hutchison, Harfa, & Dostrovsky, 1996). Positron emission tomography (PET) studies show that the right anterior cingulate plays a central role in the sensorial / affective aspect of pain (Hsieh et al., 1995b; Price, 2000) and that the orbitofrontal regions modulate distant processing of pain and therefore coping with a painful stimulus (Petrovic et al., 2000).
Neurobiological studies indicate that through its hierarchical connections with the pain processing areas in the periaqueductal gray, hypothalamus, anterior cingulate, and insula, the orbitofrontal areas are involved in both the perception (Zhang et al., 1997) and the regulation (Gyulai et al., 1997) and therefore coping with pain, especially the affective-motivational aspects of pain (Petrovic et al., 2000). The latter authors conclude that increased orbitofrontal activation is necessary for coping "during pain with a relevant threat to the organism" (p. 28). Such a context occurs in relational traumatic abuse.
An efficient mature orbitofrontal system can adaptively regulate both sympathoadrenomedullary catecholamine (Euler & Folkow, 1958) and corticosteroid levels (Hall & Marr, 1975), and therefore hyper- and hypoarousal. It can also facilitate or inhibit the defense reactions of the amygdala (Timms, 1977). But stress may also take the prefrontal areas "off-line", allowing the "more habitual" responses mediated by the subcortical structures to regulate behavior (Arnsten, & Goldman-Rakic, 1998). This occurs all-to-frequently in a severely developmentally compromised immature frontolimbic system, especially one with an inefficient medial orbitofrontal area involved in processing and regulating negative emotional states (Northoff et al., 2000).
When optimally functioning, the orbitofrontal cortex is "one of the few brain regions that is "privy to signals about virtually any activity taking place in our beings’ mind or body at any given time" (Damasio, 1994, p. 181). This implies that an inefficient frontolimbic system will not process pain signals that come from the body, an adaptive loss. Indeed, inactivation of the medial orbitofrontal cortex produces an analgesic effect (Cooper, 1975), and its removal elicits a suppression of pain-related behaviors and an increased threshold of pain associated with affect (Reshetniak & Kukushkin, 1989). Patients with neurological damage in this cortex report that they know a stimulus is pain-producing, but that the pain does not feel very bad (Melzack & Wall, 1996).
These studies suggest that an inefficient orbitofrontal-cingulate higher limbic circuit (Dostrovsky et al., 1995) would be unable to adaptively sense and regulate pain, and a lower amygdala limbic level-driven dissociation would dominate. Cutting, a common form of self-destructive behavior associated with early trauma (van der Kolk et al., 1991; Russ et al., 1992), may be an attempt to autoregulate out of the altered pain sensitivity associated with the elevated opioid activity of the dissociative state.
Dissociation is a common symptom in PTSD patients, and its occurrence at the time of a trauma is a strong predictor of this disorder (Koopman, Classen, & Spiegel, 1994; Shalev et al., 1996). At the moment of feeling threatened, individuals who characterlogically dissociate switch into a trance-like state, freeze, become analgesic, and later report out-of-body experiences and dissociative amnesia. Total amnesia for traumatic events is now increasingly documented (van der Hart & Nijjenhuis, 1995; Elliott, 1997).
In very recent work Markowitsch et al. (2000) report a case of "dissociative amnesia" triggered by re-exposure to a traumatic scene, a fire in the patient’s house. For the next two months he exhibited a severe memory impairment, barely recognized his partner, and failed to remember any friends. He showed flat affect and lack of interest, and his mood was sad and helpless. After 3 weeks of psychotherapy he recalled an early memory of childhood, a car crash in which he witnessed the driver’s screams and death in flames. PET studies at 2 months after the trauma showed an "unusually drastic" hypometabolism in memory-sensitive regions, which improved upon recovery at 12 months. The authors conclude that early emotionally negative childhood events and prolonged stress lead to a dissociative (functional) amnesia, that acute stress can trigger posttraumatic stress disorder, and that "even sporadic environmental stress can apparently induce long-lasting brain dysfunction with subsequent cognitive deterioration" (p. 65).
In considering possible factors for generating the hypometabolic state these authors point to the memory-influencing role of dopamine under stress conditions and alterations within the hypothalamo-hypophysal-adrenocortical axis, specifically excessive release of glucocorticoids. I suggest the finding of these researchers that psychic trauma can grossly reduce brain metabolism and thereby cognitive deterioration describes the hypometabolic mechanism of vagal-induced conservation-withdrawal and the mechanism of dissociation in response to trauma.
The characterological use of dissociation by certain personalities underlies the description offered by Allen and Coyne:
Although initially they may have used dissociation to cope with traumatic events, they subsequently dissociate to defend against a broad range of daily stressors, including their own posttraumatic symptoms, pervasively undermining the continuity of their experience (1995, p. 620).
These "initial traumatic events" are embeded in infant relational trauma, the first context in which dissociation is used to autoregulate massive stress.
Dissociation represents a disruption of the monitoring and controlling functions of consciousness. Fonagy et al. describe:
...victims of childhood abuse who coped by refusing to conceive of the contents of their caregiver’s mind and thus successfully avoided having to think about their caregiver’s wish to harm them. This initially defensive disruption of the capacity to depict feelings and thoughts in themselves and others becomes a characteristic response to all subsequent intimate relationships. It also drastically limits their capacity to come to terms with these abusive experiences in later life and creates a vulnerability to interpersonal stress (1996, p. 384).
[T]rauma victims who lack the cognitive and emotional structures to immediately assimilate the experience use the state of consciousness known as dissociation to escape from the full psychological impact of the event (Classen, Koopman, & Spiegel, 1993, p. 179).
It should be pointed out that dissociation may be a more common phenomenon of the psychopathology of everyday life than previously thought. On the Adult Attachment Interview a classification of unresolved (the adult disoriented/disorganized analog) is made when an individual’s narrative of his or her early experiences shows lapses in monitioring, prolonged silences of 20 seconds, and "micro-dissociative processes" (Schuengel et al., 1999). Under a series of dyadic emotional stressors these characterolgical microstates, however, become stabilized attractor macrostates of dissociation.
Such clinical descriptions describe impaired activity of the orbitofrontal system, which acts in the highest level of control of behavior, especially in relation to emotion (Price, Carmichael, & Drevets, 1996), plays a fundamental role in monitoring relevant past and current experiences (Cavada et al., 2000) and in controlling the allocation of attention to possible contents of consciousness (Goldenberg et al., 1989), and allows for choosing appropriate actions in a flexible and purposeful manner in stressful contexts of uncertainty (Elliott, Dolan, & Frith, 2000). These and the above data clearly suggest that a developmentally immature and metabolically inefficient orbitofrontal regulatory system is found in immature personalities who characterolgically use dissociation.
In 1893 Breuer and Freud, citing the recent work of Janet (1889), described dissociation as the major mechanism for "strangulations of affect," but by 1900 and The Interpretation of Dreams Freud discarded this notion and favored repression as the major force of the unconscious. In later writings Freud again hinted of its existence in asserting:
[U]nconscious ideas continue to exist after repression as actual structures in the system Ucs, whereas all that corresponds in that system to unconscious affects is a potential beginning which is prevented from developing (Freud, 1915, p. 178).
With an eye to Freud’s ideas on the negative effects of early truama, Winnicott postulated:
If maternal care is not good enough, then the infant does not really come into existence, since there is no continuity in being; instead, the personality becomes built on the basis of reactions to environmental impingement (1960, p. 54).
Tustin (1981) described this impingement as a "psychological catastrophe," which is responded to by "autistic withdrawal" or "encapsulation," an innate defensive measure against bodily hurt that involves a "shutting out of mind" what can not be handled at the moment. This is an operational definition of the growth inhibiting defense of dissociation, the generator of unconscious affects and the block against potential affective development and the ongoing continuity of existence.
What is maladaptive about this psychic-deadening defense is not only that the individual shifts into dissociation at lower levels of stress, but that it finds difficulty in exiting the state of conservation-withdrawal. Once dissociated it stays in this massive autoregulatory mode for long periods of time. During these intervals it is shut-down to the external environment, and thus totally closed and impermeable (encapsulated) to attachment communications and interactive regulation. If this becomes a basal state, the avoidance of emotional contexts, especially those containing novel and more complex affective information, prevents emotional learning, which in turn precludes any advances of right brain emotional intelligence or what Janet (1889) calls an "enlargement" of personality development. The habitual use of this primitive defense against affect is thus another manifestation of maladaptive infant (and adult) mental health.
Early Relational Trauma and Enduring Right Hemispheric Dysfunction
The orbitofrontal system, which is expanded in the right hemisphere (Falk et al., 1990), acts as an executive control function for the entire right brain. The right prefrontal cortex is critical to the processing and regulation of self functions (Schore, 1994; Keenan, Wheeler, Gallup, & Pascual-Leone, 2000). During its critical period of maturation in the first two years, prolonged episodes of intense and unregulated interactive traumatic stress induce not only heightened negative affect, but chaotic biochemical alterations that produce a developmentally immature, structurally defective right brain. Although very few neuropsychobiological studies on traumatized human infants have yet been done, basic research on trauma in infant mammals and adult humans strongly implicates dysfunction in the right hemisphere, the hemisphere that is dominant in human infancy (Chiron et al., 1997).
And yet compelling theoretical, research, and clinical links have been made between right hemisphere functions and attachment behaviors (Henry, 1993; Schore, 1994), attachment transactions and the regulation of the right brain (Schore, 2000b, c), traumatic stress, attachment and right brain function (Wang, 1997), and the role of impaired right hemispheric activity in very early-forming reactive attachment disorders (Hinshaw-Fuselier, Boris, & Zeanah, 1999), personality disorders (Horton, 1985) and various psychiatric syndromes (Cutting, 1992; Cummings, 1997). The development of attachment, the interactive regulation of biological synchronicity between organisms (Schore, 2000b), allows for the development of emotions, the highest order direct expression of bioregulation in complex organisms (Damasio, 1998).
At the beginning of this two-paper series I cited Damasio’s (1994) description of the fundamental adaptive function of "the brain" - to be be well informed about its own activities, the rest of the body and the environment so that suitable survivable accommodations can be achieved between the organism and the environment. Although the existence of not one but two brains, a left brain and a right brain, was discovered at the dawn of neurology (Harrington, 1985), current neuroscience, armed with neuroimaging technologies, is now detailing the unique functions of the right brain and its critical roles. These systems that contribute to the forementioned adaptive functions are maturing before the advent of language, and are influenced by the attachment relationship.
The right hemisphere, more so than the left, is deeply connected into the limbic system and the sympathetic and parasympathetic components of the ANS, and therefore it plays a predominant role in the physiological and cognitive components of emotional processing (Spence et al., 1996). This "nondominant" (!) hemisphere is specialized for neuroendocrine and autonomic activation (Sullivan & Gratton, 1999), for the secretion of the stress hormones, CRF (Kalogeras et al., 1996) and cortisol (Wittling & Pfluger, 1990), for the human stress response (Wittling, 1997), and for controlling the vital functions supporting survival and enabling the organism to cope with stresses and challenges (Wittling & Schweiger, 1993). Severe developmental impairments of these right brain structure-function relationships are manifest in inefficient and vulnerable coping mechanisms, and they occur in the attachment pathology of disorganized infant and toddlers. I would amend Main’s (1996) assertion that "disorganized" attachment is a primary risk factor for the development of mental disorders to specifically posttraumatic stress, borderline, and sociopathic personality disorders.
Throughout these two papers I have offered interdisciplinary data indicating a developmental right brain etiology of these severe regulatory disorders. Continuing this theme, a juxtaposition of trauma-associated functional deficits in coping strategies and stress tolerance of "type D" infants found in attachment research, right lateralized structural defects from developmental psychobiological studies, and findings on the right brain of normal and abnormal adults from neuroscience can offer more powerful models of the mechanisms by which early relational trauma in the first two years alters the experience-dependent maturation of the right brain and thereby induces a high risk for psychopathogenesis.
Evidence of this lateralization effect is provided by human studies showing that conditioned fear acquisition and extinction are associated with amygdala function, and that this activation is right hemisphere dominant (La Bar, Gore, LeDoux, & Phelps, 1998). In a series of basic psychobological studies Adamec reports that partial kindling of the right and not left amygdala induces long-lasting increases in anxiety-like behavior (1997, 1999), that NMDA receptors mediate transmission from the right amygdala to the ventromedial hypothalamus (Adamec, 1998), and that right amygdala kindling also induces elevated production of the stress hormone CRF (Adamec & McKay, 1993). In parallel research, "type D" infants show "direct indices of apprehension regarding the parent," as manifest in fearful facial expressions (Solomon & George, 1999). These authors document that such infants show asymmetries of facial expression, as in "an extremely swift ‘tic’ which lifts only the left side of the facial musculature," indicating right hemispheric dysfunction. They also describe freezing lasting 20 seconds or more, accompanied by dazed or trance-like facial expressions in "type D" infants. Recall freezing in primate infants is associated with high basal cortisol levels and extreme right frontal EEG activity (Kalin et al., 1998).
In fact, EEG studies of one-month-old (Jones et al., 1997) and 3-to 6-month-old (Field, Fox, Pickens, & Nawrocki, 1995) infants of depressed (and therefore potentially neglectful) mothers show this same right frontal EEG asymmetry, a finding that has been interpreted as reflecting a subcortical asymmetry in the amygdala (Calkins & Fox, 1994). At 10 months, infants who express more intense distress to maternal separation display a greater right than left frontal activation (Davidson & Fox, 1989), and this asymmetry is related to emotional reactivity and vulnerability to psychopathology in both infants and adults (Davidson et al., 1990). At 3 to 6 years, children of depressed mothers show a right frontal EEG asymmetry and lack of empathy (Jones, Field, & Davalos, 2000).
Individuals with extreme right frontal activation are thought to exhibit a negative affective response to a very low intensity negative affect elicitor, and to be impaired in the ability to terminate a negative emotion once it has begun (Wheeler, Davidson, & Tomarken, 1993). Fox et al. (1996) report that young children with internalizing and externalizing problems show greater right than left frontal EEG activation, and suggest that this pattern reflects difficulties with affect regulation, whether the affect arousal is extremely negative or positive. At later ages "greater right hemisphericity" is associated with a history of more frequent negative affect and lower self esteem (Persinger & Makarec, 1991), that is, chronic difficulties in affect regulation.
With respect to the association of type D attachments and a predisposition to relational violence (Lyons-Ruth & Jacobvitz, 1999), impaired right hemispheric functioning has also been reported in disinhibited aggressive patients with orbitofrontal brain damage (Starkstein & Robinson, 1997), autonomic physiological studies of high-hostility subjects (Demaree & Harrison, 1997), and neuroimaging research of murderers, where Raine et al. conclude, "reductions in right orbitofrontal functioning may be a particularly important predisposition to violence" (1998a, p. 6).
The right brain circuitry that is involved in the regulation of "primary" emotions (Ross, Homan, & Buck, 1994) and in "intense emotional-homeostatic processes" (Porges et al., 1994) is organized in the first two years of life. Exposure to extensive and long-enduring traumatic states interferes with this organization and predisposes the disorganized/disoriented infant (later, the unresolved/disorganized adult) to a vulnerability, at later points of stress, to develop chronic difficulties in affect regulation. Due to its unique anatomical connections into the reticular formation, the right hemisphere is dominant for the bilateral regulation of arousal (Heilman & Van Den Abell, 1979) and its dysfunction is therefore central to the arousal dysregulation that characterizes the severe coping deficits of fear dysregulation of posttraumatic stress disorders. The right cortex is responsible for maintaining important controls over autonomic activities (Heilman et al., 1977) and for generating the most comprehensive and integrated map of the body state available to the brain (Damasio, 1994). An impairment of the right brain is thus central to the disordered mind-body functions that are found in children and adults who continue to experience the relational trauma of their infancy.
Indeed, van der Kolk (1996) specifically implicates right brain dysfunction in posttraumatic stress disorders, and this lateralization effect is observed in studies that expose the patient to a personal high arousal stressor (Rauch et al., 1996; Shin et al., 1997) and those that induce a stressful startle response (Morgan et al., 1997). Patients with panic disorders show greater activation of a right frontal avoidance-withdrawal system in negatively valenced situations (Wiedemann et al., 1999) and altered GABAergic receptor patterns in the right insula and orbitofrontal cortices (Malizia et al., 1998).
Research may also tell us more about the triggers of right hemispheric dysregulation. It is now thought that traumatic early life events predispose certain individuals to later psychiatric disturbance when they are "rechallenged" with a "matching event" or recurrence of the stressor. Previously I spoke of the right brain imprinting into procedural memory of the abusive caregiver’s threatening face. Current evidence shows that the right amygdala (Morris et al., 1999) is involved in the storage of fearful faces (vs. the left in linguistic threat; Isenberg et al., 1999). The right amygdala is also implicated in the expression of emotionally influenced memory of aversive experiences (Coleman-Mensches & McGaugh, 1995). Similarly, the right orbitofrontal cortex shows an enhanced response to anger expressions that correlate with expression intensity (Blair et al., 1999).
The "visuospatial" right hemisphere contains a "nonverbal affect lexicon" of facial expressions (Bowers, Bauer, & Heilman, 1993), and these are imprinted in mother-infant affective transactions. This hemisphere appraises facial expression at levels beneath awareness (Schore, 1994; 1998b, 1999a; in press a, b), and if a match is registered with a stored image an affective response occurs. Autonomic changes in the body are evoked when angry facial expressions are subliminally presented to the right, and not the left hemisphere (Johnsen & Hugdahl, 1991). Right hemispheric impairments in processing facial (Deldin et al., 2000) and vocal affective-prosodic (Snow, 2000) interpersonal stimuli have profound consequences for interpersonal behavior, isolating the individual from the social environment. A growing literature demonstrates that neglected children have difficulty in recognizing emotion in faces, and that physically abused children dis[play a response bias for angry facial expressions (Pollak, Cicchetti, Hornung, & Reed, 2000).
I suggest that visual and auditory stressors that are nonconsciously processed (Mogg, Bradley, Williams, & Mathews, 1993) in an inefficient right hemisphere, especially the perception or memory of images and sounds of threatening and humiliating faces are potent triggers of dysregulation and dissociation in early traumatized patients. In support of this, Main (1995) reports the dissociative responses of disorganized/disoriented children to the faces of a family photograph:
One child, happily interacting with the examiner just previously, bent silently over the photograph for 12 seconds, then looked up, silent and depressed. Another looked into the photograph for some time then murmured softly, "Where are you, Mama? For children who had been disorganized/disoriented with mother in infancy, then, the visual presentation of the parent, self, or family presented within the photograph seemed to have an overwhelming and absorbing quality that drew attention away from the immediate situation (p. 435).
Furthermore, the infant’s transactions with an emotionally misattuned and unresponsive caregiver who induces traumatic states and provides poor interactive repair are stored in the infant’s developing corticolimbic circuitries as imagistic, visceral, and nonverbal implicit-procedural memories. Interpersonal contexts of interactive repair contain facially expressed safety signals that can be associated with "switching off" the traumatized state, and so the lack of such internal representations deprives the traumatized individual of an internal regulatory mechanism that can terminate the traumatic reaction.
Kiersky and Beebe (1994) state that nonverbal presymbolic forms of relating constitute adult versions of the early interaction structures that protected the infant from trauma and continue to be used by patients to avoid retraumatization. Fonagy (1991) asserts that the mental representations of early traumatic interactions with an abusive parent lead the child to defensively disregard perceptions of the thoughts and feelings of the parent. These unconscious working models of disorganized-disoriented attachment encode an enduring prototypical cognitive-affective schema of a dysregulated-self-in-interaction-with-a-misattuning-other (Schore, 1994, 1997b, c, in press b).
Such "pathological" representations are accessed when the individual is stressed, and they are stored in the right hemisphere which is dominant for unconscious processes (Schore, 1994; 1997b, 1999; in press a) and for episodic and autobiographical memory (Fink et al., 1996). Early abusive memories are recorded in the right hemisphere outside of conscious awareness, and this realm represents the traumatic memories in imagistic form along with the survival behavior employed as a result of the abuse. The cortical hemispheres contain two different types of representational processes and separate, dissociable memory systems (Zaidel, Esiri, & Beardsworth, 1998), and this allows for the fact that early emotional learning of the right, especially of stressful, threatening experiences, can be unknown to the left (Joseph, 1982). In clinical psychoanalytic writings Bromberg describes:
Dissociated experience thus tends to remain unsymbolized by thought and language, exists as a separate reality outside of self-expression, and is cut off from authentic human relatedness and deadened to full participation in the life of the rest of the personality (1991, p. 405).
A limited representational capacity is thus another deficit derived from early relational trauma. According to Reid,
Where trauma has occurred in infancy, before there is adequate differentiation of self from other, and before the development of the capacity to symbolize, the child cannot withdraw into daydreaming and fantasy, which has been noted in adults and children suffering from post-traumatuc stress disorders (1999, pp. 99-100).
In a similar description, Meares (1993) demonstrates that in cases of early abuse, the older child’s capacity for positively charged symbolic play is not adequately established. Slade reports that insecurely attached children have fewer episodes, shorter periods, and less complex symbolic play (1994), and emphasizes the links between play, the consolidation of affect, meaning, and representation (1987). These essential capacities to generate and maintain postively charged autoregulatory representations heavily depend upon efficient right hemispheric activity.
Another right hemispheric cognitive activity may be detrimentally affected by relational trauma during its initial period of maturation. In light of the known involvement of the right hemisphere in attention (Tucker & Derryberry, 1994; Posner & Peterson, 1990; Coule et al., 1996; Sturm et al., 1999) and joint attention (Kingstone, Friesen, & Gazzaniga, 2000), it is tempting to speculate that joint attention experiences in the first year tune the attentional mechanisms of these right laterlized circuits. Unmedicated children with attention-deficit hyperactivity disorder (ADHD) show a disruption of right hemispheric attentional systems, due to a difficulty sustaining attention over short time intervals and a failure of inhibition (Carter et al., 1995; Castellanos et al., 1996; Epstein et al., 1997; Pliszka, Liotti, & Woldorff, 2000). Elevated dopamine levels in right midbrain areas that control attention are correlated with symptom severity (Ernst et al., 1999).
Very recent evidence suggests that developmental dyslexia is a left hemispheric dysfunction, while developmental hyperactivity is a right hemispheric dysfunction (Braun et al., 2000). A number of researchers have been describing this latter clinical entity. In early work Weintraub and Mesulam documented right hemispheric learning disability as:
a syndrome of early right hemisphere dysfunction...that is associated with introversion, poor social perception, chronic emotional difficulties, inability to display affect, and impairments in visuospatial representation (1983, p. 468).
In more recent work, this group differentiates children with left hemisphere dyslexia from right hemisphere social emotional processing disorder, the latter displaying difficulties in interpreting and producing nonverbal aspects of communication including prosody, facial expression, and gesture, as well as poor emotional adjustment and psychiatric disorder (Manoach et al., 1997). Similar descriptions are seen in developmental right hemisphere syndrome, expressed in emotional and interpersonal problems and avoidance of eye contact (Gross-Tsur et al., 1995), right hemispheric learning disability, showing episodic dyscontrol and psychiatric disorders (Grace & Malloy, 1992), and nonverbal learning disability, who in adolescence are high risk for depression and suicide (Rourke, Young, & Leenars, 1989). Recent neuroimaging research indicates that metabolic rate of the right amygdala correlates with negative affect in depressed patients (Abercrombie et al., 1998). I suggest that these more severely disturbed right brain learning disabilities are "type D" attachments.
One other defining clinical feature occurs in individuals who are high risk for later developing pathological traumatic reactions. Relational trauma in the second year would induce a severe pruning of the right hemispheric orbitofrontal callosal axons that are growing towards their counterparts in the left hemisphere. This would produce an interhemispheric organization in which facial expressions, bodily states, and affective information implicitly processed in the right brain would be inefficiently transmitted to the left hemisphere for semantic processing. Maltreated toddlers show a dramatic inability to talk about their emotions and internal states (Cicchetti, Ganiban, & Barnett,1991).
This represents the early expression of alexithymia, "no words for feelings," a common symptom of trauma patients (Taylor et al., 1997, 1999). Neuropsychological studies of alexithymia now demonstrate a right hemispheric dysfunction and a specific right to left deficit of callosal transfer (Dewaraja & Sasaki, 1990). A physiological disconnection of the two hemispheres results in an inability of the affective and symbolic energies of the right hemisphere to be externalized through the verbal expression of the left hemisphere. A hyporesponsivity in the prefrontal and orbital circuits has been suggested to underlie alexithymia (Hommer et al., 1997).
Indeed both alexithymia and PTSD share similar altered neuroendocrine patterns (Henry et al., 1992), and the extensive overlap between the two has been emphasized (Taylor et al., 1997). Alexithymic personalities manifest a deficit in the capacity for symbolization of emotions, a tendency for impulsive behavior, avoidance of social relationships, abnormal physiology resulting in disease, and an impaired capacity for self-care and self-regulation. Miller (1986, p. 138) points out that the noninsightful constricted mental state of the alexithymic resembles "the retraction of the field of consciousness" discussed by Janet (1924), as well as the dissociative reactions described in hysterical patients by Breuer and Freud (1893). Right hemisphere invovlement in hysterical paresthesia (Tiihonen et al., 1995) and somatization (Min & Lee, 1997) is now reported.
Alexithymic individuals become disorganized under stress, and the regulatory disturbance is manifest in dramatic outbursts of emotion that end as quickly as they begin as though a valve is turning on and shutting off (Nemiah & Sifneos, 1970), affective blocking in the face of unbearably intense pain during overwhelming experiences (Krystal, 1988), and deficits in spontaneous nonverbal expressions of negative affect (McDonald & Prkachin,1990). Alexithymia is thus fundamentally an impairment in emotional information processing (Lane et al., 1997), specifically a deficit in the cognitive processing and regulation of emotions (Taylor, 2000), and is manifest in posttraumatic stress disorder, borderline personality disorders, substance abuse disorders, and somatoform disorders (Taylor et al., 1997). Developmental traumatic stress and neurobiological deficits in the anterior cingulate and orbitofrontal cortices (Lane et al., 1997) and in the right hemisphere (Taylor et al., 1997) have been implicated in alexithymic symptomatology.
In discussing the etiology of alexithyma Rotenberg concludes:
[The] functional deficiency of the right hemisphere...may be caused by the lack of emotional relationships between the child and the parents. Such emotional relationships...stimulate the development of the right hemisphere functions and correspond to these functions as a key to the lock. If these emotional relationships are insufficient, the right hemisphere will become inefficient, its contribution in psychological defense mechanisms and emotional stabilization will be lost, and there will be a general predisposition to subsequent mental and psychosomatic disorders (1995, p. 59).
The right hemisphere ends its growth phase in the second year, when the left hemisphere begins one, but it cycles back into growth phases at later periods of the life cycle (Thatcher, 1994). This allows for potential continuing reorganization of the emotion-processing right brain. The orbitofrontal regions, which are involved in "emotion-related learning" (Rolls, Hornak, Wade, & McGrath, 1994) are unique in that they retain the neuroanatomic and biochemical features of early development, and for this reason they are the most plastic areas of the cortex (Barbas, 1995). If, however, in its earliest organizational history this system is exposed to frequent and intense caregiver-induced dysregulation, its primordial organization will be poorly capable of coping with the stresses inherent in human relationships. Maladaptive infant mental health describes a system that early on becomes static and closed, and due to its inability to respond to novel stimuli and challenging situations it does not expose itself to new forms of socioemotional experiences that are required for the continuing experience-dependent growth of the right brain.
Implications for Models of Early Intervention
It is important to remember that "type D" behaviors are found in neurologically impaired infants, and infants with early neurological insults to the orbitofrontal cortex show long-term deficits, despite optimal environments. This means that relational trauma can not be automatically inferred from deflections, even severe deflections of a normal developmental course. That being the case, the opportunity for a maturing individual, even one with a constitutional deficit, to optimize its developmental trajectory is greatly enhanced by forming a dyadic system with a primary caregiver who is sensitive to its unique strategies of processing and expressing social emotional information.
Orbitofrontal deficiencies and affect regulatory disturbances are not solely found in patients with severe relational trauma. This system is also impaired in neurological patients (Brazzelli, Colombo, Della Sala, & Spinnler, 1994), schizophrenia (Norman et al., 1997), autism (Baron-Cohen, 1995), manic state of bipolar disorder (Blumberg et al., 1999), unipolar (Biver et al., 1994) and major (Biver et al., 1997) depression, obsessive-compulsive disorder (Mcguire et al., 1994; Rauch et al., 1994), and, indeed, Alzheimer’s disease (van Hoesen, Parvizi, & Chu, 2000). It is also dysfunctional in alcoholism (Hommer et al. 1997; Volkow et al., 1999; Volkow et al., 1997) and drug addiction (London et al., 2000; Volkow & Fowler, 2000), and it is tempting to speculate that the origins of a predisposition to addiction lie in prenatal exposure to maternal drug use during pregnancy (Jacobson et al., 1996; Espy et al 1999) and postnatal relational stressors embedded in "type D" parenting (O’Connor, Sigman, & Brill, 1987).
Abnormalities in the limbic system, in the frontal lobe, temporal lobe, basal ganglia, reticular formation, and the hypothalamic-pituitary-adrenal axis connectivity play a critical role in the pathophysiology of each of these disorders, but which limbic circuit and what point in a circuit is metabolically unstable and inefficient would determine the particular expression of affect dysregulation of a specific psychiatric syndrome. The most severe disturbances would involve cell death of dopamine or noradrenaline or hypothalamic neurons at the base of the hierarchical circuits, since disruption of their trophic functions would lead to widespread alterations of subcortical and cortical structures. Less severe would be loss of the receptors for these bioagents, many of which are found on astrocyes that regulate the metabolic activity and connectional plasticity of brain synapses (Laming et al., 2000). The postnatal proliferation and growth of astrocytic processes that surround synapses is influenced by events in the social environment (Jones & Greenough, 1996).
It should also be remembered that the process of prefrontal-subcortical parcellation continues over the life stages (Keshavan, Anderson, & Pettegrew, 1994), and this process, for example, as the brain reorganizes in adolescence may pare down an already thinned cortical-subcortical system, and therefore result in the massive dysregulatory symptoms of the psychopathologies that "first appear" at this time. Yet the early regulatory deficts of social-emotional information processing of these disorders are manifest in attachment disturbances in infancy, and may be treatable at this early time.
Although I have mainly focused upon disorganized insecure attachments, what of the the other insecure categories? Insecure organized attachments also express partial orbitofrontal hypo- or hypermetabolic disturbances under stress (see Schore, 1994, 1996 for insecure resistant/ambivalent and avoidant brain organizations). However, these involve stress impairments of only one of the two limbic circuits, the sympathetic ventral tegmental limbic forebrain-midbrain circuit or the parasympathetic lateral tegmental limbic forebrain-midbrain circuit. The insecure avoidant infant/dismissing adult and insecure resistant-ambivalent/preoccupied adult organizations show inhibitory or excitatory biased orbitofrontal systems. Under stress the former can access a passive coping strategy of autoregulation, the latter an active coping capacity of interactive regulation, while the disoriented, neither. The availability of single circuit strategy is limiting, yet it allows for an organized if limited coping mechanism. The affect regulating dysfunctions of insecure organized personalities are not as severe as the disorganized-disoriented insecures, but as Main (1996) points out, these attachments are also high risk for psychiatric disorders.
I want to stress the point that I do not believe that only trauma in the first two years of life is psychopathogenic or self-disorganizing. I also am not undervaluing the long-term negative impact that an abusing father can have on the the developing child. Indeed most forms of sexual abuse are perpetrated by the father. What I am saying is that what a particular individual appraises to be stressful, how he or she characteristically consciously and especially unconsciously responds to stressors, and how efficiently he or she psychobiologically copes with these stressors, are uniquely and indelibly influenced by events in early and late infancy, especially events that involve abuse by the primary caregiver, who in the vast majority of cases is the mother. What’s more, these early interactive experiences determine whether, in later times of crisis, the individual can allow himself to go to others for interpersonal support, that is, to avail himself of interactive regulation within an intimate or psychotherapeutic relationship when his own autoregulatory mechanisms have temporarily failed.
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 life span as possible. Osofsky and her colleagues demonstrate that effective therapeutic interventions can be made in traumatized 2 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, b, c). This context can alter attachment patterns from "insecurity" to "earned security" (Phelps, Belsky, & Crnic, 1998).
A recently published fMRI study (Hariri et al., 2000) provides evidence that higher regions of specifically the right prefrontal cortex attenuate emotional responses at the most basic levels in the brain, that such modulating processes are "fundamental to most modern psychotherapeutic methods" (p. 43), that this lateralized neocortical network is active in "modulating emotional experience through interpreting and labeling emotional expressions" (p. 47), and that "this form of modulation may be impaired in various emotional disorders and may provide the basis for therapies of these same disorders" (p. 48). Furthermore, the co-construction of a coherent narrative of the trauma may emerge in a relational context which promotes a callosal transfer of affective information from the right to left orbitofrontal regions. This structural advance allows for left hemispheric retrieval and explicit semantic processing of right hemispheric emotional states encoded in implicit-procedural memory (Schore, in press, b).
This model also has practical implications for programs of early prevention. 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 which 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’s 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 co-creates 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 co-creation 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 lifelong 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.
Originally published in: Infant Mental Health Journal, 2001, 22, 201-269.
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