Dysregulation of the right brain: a fundamental mechanism of traumatic attachment and the psychopathologenisis of posttraumatic stress disorder.

Australian & New Zealand J. of Psychiatry 2002; 36:9-30

Overview : In this paper Allan does a masterful job of achieving his stated objective: to review and integrate attachment theory, affective neuroscience, developmental stress research and infant psychiatry in order to delineate the developmental precursors of posttraumatic stress disorder. Results: data are presented which suggest that traumatic attachments, expressed in episodes of hyper-arousal and dissociation, are imprinted into the developing limbic and autonomic nervous systems of the early maturing right brain. These enduring structural changes lead to the inefficient stress coping mechanisms that lie at the core of infant, child and adult posttraumatic stress disorders. Schore’s conclusions: disorganized-disoriented insecure attachment, a pattern common in infants abused in the first 2 years of life, is psychologically manifest as an inability to generate a coherent strategy for coping with relational stress. Early abuse negatively impacts the developmental trajectory of the right brain, which is dominant for attachment, affect regulation, and stress modulation, thereby setting a template for coping deficits of both mind and body that characterize PTSD symptomatology. These data suggest that early intervention programs can significantly alter the intergenerational transmission of posttraumatic stress disorders.

While 60% of men and 50% of women experience a traumatic event at some point in their lives only 5% of men and 10% of women will experience PTSD. Other research indicated that only one half of those who experience an episode of PTSD develop a chronic form of the disorder. How are these numbers to be understood? A shift has occurred from an exclusive emphasis on the severity of the traumatic event to a correlation between the person’s developmental stage, the specific nature of the trauma and the pre-morbid personality. When these factors are highlighted we have to consider what are the short and long–lasting effects of trauma in the earliest developmental stages, why does this exposure negatively impact the maturation of an individual’s stress coping systems, and how is this related to the genesis of the premorbid personality organizations which are vulnerable to posttraumatic stress disorder? The answer to these questions lie at the intersection of trauma theory and clinical child and adult psychiatry.

As usual, the paper is densely worded and very compacted in its presentation of ideas. I thought a listing of the section headings would give a snapshot of where we are going and help keep Schore’s organization in mind.

I: Attachment and the development of the right brain stress coping mechanisms

Stress and the right hemisphere

Right brain dysregulation, dissociation, and PTSD pathogenesis: introduction

Traumatic attachment, dysregulation, and the pathogenesis of PTSD

II: Overview of the neurobiology of a secure attachment

Attachment and the right cortical regulation of the autonomic nervous system

III: The neurobiology of infant trauma

IV: Disorganized/disoriented attachment neuropsychology

V: Impact of relational trauma on right brain development

Trauma-induced excessive pruning of the right brain circuits

VI: Continuity between infant, childhood and adult PTSD

De-evolution of the right brain limbic circuits and PTSD pathogenesis

I: Attachment and the development of right brain stress coping mechanisms

John Bowlby hypothesized that the infant’s capacity to cope with stress is correlated with certain maternal behaviors and that attachment outcomes have consequences that are vital to the outcome of the species. Modern research has now been able to begin to correlate maternal care and the development of stress responses, thus the influence of maternal factors on the ontogeny of the limbic-hypothalamic-pituitary-adrenal axis. Currently the focus is on the deprivation of maternal care as a source of environmental stress in the development and maturation of neural circuits in the infant’s stress coping systems. In other words there has been a shift away from physical and sexual trauma as being the only significant factors toward including relational trauma as significant contributors to the neurobiology of dysregulated attachment and coping mechanisms.

Stress and the right hemisphere: As we know, it is increasingly clear that the neural circuitry of the stress system is located in the early developing right brain. The hemisphere dominant for those functions that support survival and the human stress response. These coping strategies begin their maturation pre and postnatally, at a time coincident with right brain dominance and rapid right brain growth. Normal adult brain appearance is evident at two years of age, all the major fiber tracts can be identified at three years of age. Thus, attachment experiences of the first two years directly influence the experience-dependent maturation of the right brain.

Current studies conclude that the two dominant forms of maltreatment in childhood, abuse and neglect, are associated with adverse brain development and severe affect dysregulation. It is now believed that relational or social stressors are far more detrimental to brain development than non-social, inanimate or physical stressors. It is now thought that a traumatic and dysfunctional early relationship is the stressor that leads to PTSD and this severe stress can over-ride any genetic, social or psychological resilience factors. Maltreatment and neglect are so damaging because they are ‘ambient’, chronic, repetitive and present from the first interactions with the mother. It is now known that acute stress produces short-lived and reversible deficits while repeated, prolonged chronic stress is associated with long-term patterns of autonomic reactivity, expressed in ‘neuronal structural changes, including atrophy that might lead to permanent damage’. As Schore has already stressed, early relational trauma will have a significant impact on the experience dependent right brain, which is in a critical growth period during the time of dyadic attachment experiences.

As we know, the right brain more than the left, is deeply interconnected with the autonomic, limbic and arousal systems. It is dominant for the processing and communication of social, emotional and bodily information and for the control of spontaneously evoked emotional reactions as well as the regulation and modulation of the ‘primary emotions’.

It has now been shown that perinatal distress leads to a blunting of the stress regulating response of the right prefrontal but not the left prefrontal cortex, this deficit may first become manifest in adulthood. This clearly points to the conclusion that early trauma-induced right brain pathogenesis leads to increased vulnerability to the effects of stress and trauma later in life and to late appearing stress-related psychiatric disorders. In fact, affect regulation is seen as an essential mechanism of all psychiatric disorders.

Since the brain is mutable, its organization reflects the history of the organism. The right brain is dominant for autobiographical memory; it is central for self-recognition and for the ability to maintain a coherent, continuous and unified sense of self. Terr writes that a literal mirroring of traumatic events by behavioral memory can be established at any age including infancy, again buttressing the belief that early relational trauma to the right brain will create an enduring vulnerability to dysregulation during stress and therefore to PTSD.

Right brain dysregulation, dissociation, and PTSD pathogenesis: introduction. In 1996 van der Kolk proposed that the symptoms of PTSD fundamentally reflect an impairment of the right brain, known to be dominant for inhibitory control. Others suggest that the emotional disturbances of PTSD have their origins in the inability of the right prefrontal cortex to modulate amygdala functions, particularly on the right. The right amygdala is known to process frightening faces and ‘unseen fear’. LeDoux concludes that without orbital prefrontal feedback regarding the level of threat, the organism remains in an amygdala-driven defensive response state longer than necessary. And that in humans, conditioned fear acquisition and extinction are a dominant right hemisphere amygdala function, therefore, a defective right orbitofrontal system operates in PTSD.

Parallel to the interest in PTSD there is an interest in the etiology of dissociation – a primitive defense used to cope with overwhelming stress. Again, a disorganized-disoriented insecure attachment, which is a primary risk factor for the development of psychiatric disorders, has been specifically implicated in the etiology of dissociative disorders. Once again, we are observing the long-term effects of early trauma to the developing right brain.

Traumatic attachment, dysregulation and the pathogenesis of PTSD. Thirty years ago Bowlby observed that ‘Since much of the development and organization of [attachment] behavioral systems takes place whilst the individual is immature, there are plenty of occasions when an atypical environment can divert them from developing on an adaptive course’. One hundred years ago Pierre Janet proposed- ‘All [traumatized] patients seem to have the evolution of their lives checked; they are attached to an insurmountable 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 concept of affect regulation and disorders of affect regulation is now shared by the attachment, PTSD and psychiatric literatures. This concept may be a bridging one for an ever-expanding biopsychosocial model of psychiatry. Additionally, a model of the interactive genesis of psychobiological dysregulation also supports a deeper understanding of psychiatric disorders as being caused by a combination of a genetic-constitutional predisposition and environmental or psychosocial stressors, which can overwhelm or activate the inborn neurophysiological vulnerabilities.

In the quest to understand the links between pre/perinatal adverse events or stressors and adult psychiatric outcomes Schore suggests that, recent theoretical models linking developmental affective neuroscience, attachment theory, updated basic research in biological psychiatry on stress mechanisms and current advances in psychophysiology on the survival functions of the autonomics nervous system may offer us a deeper understanding of the underlying mechanisms by which early childhood trauma massively dysregulates and thereby alters the developmental trajectory of the right hemisphere. This results in an immature personality organization with vulnerable coping capacities, one predisposed to the pathological hyper-arousal and dissociation that characterizes PTSD at later points of stress. These psycho-neuro-biological models which link infant, child, adolescent and adult psychiatry can be tested by clinical and experimental research.

II: Overview of the neurobiology of a secure attachment

This section of the paper is so beautifully and simply written I will read much of it directly.

The essential task of the first year of life is the creation of a secure attachment bond of emotional communication between the infant and the primary caregiver. In order to enter into this communication, the mother must be psychologically attuned to the dynamic crescendos and decrescendos of the infant’s bodily based internal states of autonomic arousal. During the sequential signaling of play episodes mother and infant show sympathetic cardiac acceleration and then parasympathetic deceleration in response to the smile of the other, and thus the language of the mother and infant consist of signals produced by the autonomic, involuntary nervous system in both parties. The attachment relationship mediates the dyadic regulation of emotion, wherein the mother co-regulates the infant’s postnatally developing autonomic nervous system.

In heightened affective moments each partner learns the rhythmic structures of the other and modifies his or her behavior to fit that structure, thereby co-creating a specially fitted interaction. In play episodes of affect synchrony, the pair are in affective resonance, and in such a state, an amplification of vitality affects and a positive state occurs particularly when the rhythms of the mother matches the infant’s endogenous rhythms. Similarly positive feelings occur in moments of interactive repair by the ‘good enough caregiver’. In this way maternal sensitivity acts as an external organizer of the infant’s biobehavioral regulation.

If attachment is seen as regulation by interactive synchrony, stress can be defined as asynchrony in an interactional sequence. When asynchrony is followed by a period of reestablished synchrony stress recovery and coping occur. The repeated sequence of synchrony, asynchrony and reliable interactive repair are the building blocks of a secure attachment. Resilience in the face of stress is the ultimate indicator of secure attachment. Attachment is the outcome of the child’s genetically encoded predispositions and the particular caregiver environment.

Secure attachment experiences directly influence the maturation of the central nervous system (CNS) and limbic system. The CNS processes and regulates social-emotional stimuli and the autonomic nervous system (ANS), which generates the somatic aspects of emotion. As we already know the higher regulatory systems of the right hemisphere form extensive reciprocal connections with the lower limbic and autonomic nervous systems. The right brain, the CNS and the ANS continue to develop postnatally, the assembly of these limbic-autonomic circuits is directly influenced by the attachment relationship. Thus, as Bowlby suggested, the mother shapes the infant’s coping system.

Attachment and right cortical regulation of the autonomic nervous system. Bowlby described a neurophysiological control system that is centrally involved in regulating instinctive attachment behavior. Schore believes this system in located in the righ orbitofrontal area and in its cortical and subcortical connections. This area of the brain because of its location and connections sits at the apex of many systems, including:

1. It is at the interface of the cortex and subcortex.

2. It sits at the highest level of the limbic system.

3. It connects directly into the subcortical reticular formation, thus regulating arousal.

4. It acts as the highest level of control of behavior, particularly emotional behavior.

5. As the “thinking part of the emotional brain”, it is situated at the hierarchical apex of the ‘rostral limbic system’ or ‘anterior limbic prefrontal network’, which includes the anterior cingulate and the amygdala.

6. This ‘Senior Executive’ of the social emotional brain comes to act in the capacity of an executive control function for the entire right brain. The center of the emotional self.

7. It represents the apex of the hierarchy of control of the autonomic nervous system. This is due to its direct connections into the hypothalamus, the head ganglion of the ANS, it functions as the cortical control center of involuntary bodily functions. This represents the somatic components of all emotional states, controlling the autonomic responses associated with emotional events.

8. Central and integral to the autonomous processing and regulation of self-related information and information about the corporeal self.