All survivors of infant-toddler-child violent trauma and maltreatment share a common ground. Although the information I am presenting here might be difficult for some to read, what is being said here is extremely important. When I say that it isn’t the exact memories of what specifically happened to any one of us that matters most, it is to the kind of information that follows that I am referring to that DOES matter most.
We survivors have always struggled.
Please spend a little time at least skimming through the rest of this post – if you are a survivor of a chaotic, unstable, violent early life I believe you will feel reverberations in your BODY to this topic. I don’t believe we can truly follow our pathway through healing if we don’t truly comprehend the impact of the violent trauma and maltreatment we experienced – and what it did to us on all the levels of our development.
What follows comes from this book:
Handbook of infant mental health By Dr. Charles H. Zeanah, Jr.
Publisher: The Guilford Press; Third Edition (July 15, 2009)
From Chapter 12 – The Effects of Violent Experience
(I present this copyrighted material here for educational purposes only – please refer to the actual book article for exact references to research noted)
“We noted earlier in this chapter that violent trauma early in life – particularly when involving repeated and severe exposure – impacts the central nervous system, brain development, and the overall health of the individual (McEwen, 2003). We now review in greater depth the underlying neurobiology of the sequelae of violence exposure in a developmental and relational context.
“Preclinical studies have shown that areas of the brain that are particularly prone to the adverse effects of maltreatment and violent trauma during the first 3-5 years of life include (1) those that have a prolonged postnatal developmental period, (2) those with a high density of glucocorticoid receptors, and (3) those that have the potential for postnatal neurogenesis (Teicher et al., 2003). These areas include, most prominently, the hippocampus, amygdala, corpus callosum, cerebellar vermis, and the cerebral cortex.
“When a rat infant undergoes severe stress, such as repeated foot shocks, the hippocampus fails to form the expected density of synaptic connections. Normative pruning of these connections nonetheless occurs later in the prepubertal period, so adult animals who were repeatedly stressed in infancy end up with far fewer synaptic connections in this region (Andersen & Teicher, 2004). These results support Carrion et al.’s (2007) findings that differences in hippocampal volume in patients with PTSD are more likely due to the neurotoxicity of stress hormones than to a constitutional size difference. Clinical implications of hippocampal and amygdalar damage due to stress hormones may include increased propensity for confusion of past and present, flashbacks, and dissociative symptoms (Sakamoto et al., 2005).
“The corpus callosum is a heavily myelinated region of the brain that is associated with hemispheric integration. High levels of stress hormones during infancy and early childhood have been associated with suppressed glial cell division, which is critical for myelination (Berrebi et al., 1988). DeBellis et al. (2002) observed that reduced corpus callosum size was the most significant structural finding noted in children with a history of maltreatment and PTSD. Disturbances in the myelination of the corpus callosum and cortex due to excessive exposure to glucocorticoids during the first 3 years of life may explain some of the difficulties that maltreated preschool-age children have in integrating cognitive and emotional information and in taking others’ perspective, in comparison to nonmaltreated age-matched controls (Pears & Fisher, 2005).
“Among the most exciting research that illustrates the interaction of development and traumatic experience is that regarding the differential effects of specific types of maltreatment and violent trauma on the brain at critical periods of development through early adulthood in both animal and human models (Hall, 1998; Teicher, Tomoda, & Andersen, 2006). For example, repeated episodes of sexual and physical abuse were associated in the same group of subjects with reduced hippocampal volume if the abuse was reported to occur in early childhood, but with reduced prefrontal cortex volume if the abuse occurred during adolescence (Teicher, 2005). Similar exposure during different, temporally discrete windows of development may have very different clinical implications.
Effects on Memory
The psychological and neurobiological implications of exposure to traumatic events also involve the infant and young child’s developmentally determined capacity to encode, remember, and recall those events in order to subsequently make meaning of their experience. Recent evidence suggests that even prior to 1 year of age, infants’ capacity to recall events is well underway. By the end of the second year of life, long-term memory is reliably and clearly present, especially when there have been reinforcing memories (i.e., repeated exposures or explicit reminders), which are unfortunately all too common in cases of maltreatment and family violence (Bauer, 2006; Hartshorn & Rovee-Collier, 2003). Based on her review of the literature, Fivush (1998) has noted that traumatic events perceived before the age of 18 months are frequently not verbally accessible, whereas events experienced between 18 and 36 months can often be coherently recounted and retained as long-term memories.
“Early chronic and/or severe exposure to violence and/or maltreatment has also been noted to lead to greater pervasive insult to memory functions and to promote dissociative processes that can interfere with memory retrieval (Howe, Cicchetti, & Toth, 2006; Nelson & Carver, 1998). One mechanism for this biological insult to memory function is thought to be primarily the effect of excessive glucocorticoids, which damage the developing structures involved in memory contextualization and storage, such as the hippocampus (Sapolsky, 2000; Sapolsky, Uno, Rebert, & Finch, 1990). It is clear that over the course of formative development, exposure to violent trauma and maltreatment can affect the degree and nature of changes in the neurobiology of the brain.
(Pages 203 – 205)
The Relational Context
“The violent traumatization of an infant or very young child, whether due to maltreatment or exposure to familial, community, war, or terrorist violence, is most significantly a breach in safety. Unlike older children or adults, very young children experience their world contextually, from within the embrace of the primary attachment relationship (Scheeringa & Zeanah, 2001). Their sense and expectation of safety are therefore inherently bound to the caregiver. To appreciate the effects of violence on young children requires an understanding of the goals and mechanisms involved in the attachment relationship as well as the ways in which trauma impacts attachment.”
Attachment, Safety, and Violence
“In the anchoring concept of attachment theory, the ethological wisdom of a caregiver-infant behavioral system is seen as ensuring species’ survival (Bowlby, 1969). The infant’s drive to maintain safety is paramount and is expressed in attachment behaviors that may phenotypically change over time but that serve the same purposeful goal of achieving “felt security” (Bretherton, 1990). Perturbations in the infant’s ability to achieve felt security necessarily result in adaptations that may be more or less pernicious, depending on the quality and degree of frustration. In response to the primary attachment figure’s track record of providing “felt” security, the infant constructs an “internal working model” of self and other. This internal representation consolidates over the first 3 years of life and guides the infant’s expectations and behaviors in times of stress.
“The experience of violence, with its attendant physiological “felt anxiety” might therefore be conceptualized as the exact affective opposite of felt security. The young child does not yet have the cognitive ability to mediate feelings of fear that result when exposed to violence, either as a victim or witness. For young children, the caregiver’s role is to function as external regulator of negative or overwhelming internal affect and sensation. Several violence scenarios may be imagined in which the caregiver is unavailable to soothe infant anxiety: when the caregiver is being victimized, when the caregiver is a witness to violence and becomes too hyperaroused or too dissociated/avoidant to provide safety, or when the caregiver is the source of the violence – as in the case of parental child abuse (Carlson, 2000). A toddler who has internalized a working model in which he or she is unprotected and repeatedly left subject to overwhelming fear – one of the definitional criterion for trauma – may develop what has been termed distortions in secure-base behavior (Lieberman & Pawl, 1990). Such distortions are, in fact, attempts by the child to manage unmanageable anxiety without the actual or “real time” mentally represented assistance of the caregiver.
“If early childhood is characterized by a relational context in which the child’s ability to manage stress is determined by caregiver response, then the mental health status of the caregiver becomes a vital concern. Fraiberg, Adelson, and Shapiro (1975) called attention to the profound effects of maternal mental health on the developing child. The “ghosts in the nursery” that Fraiberg et al. described were malevolent internalized attachment figures who had subjected the caregiver to various forms of maltreatment during his or her own childhood. Fraiberg et. al. observed that caregiver traumatization in the past resulted in (1) his or her present-day inability to respond appropriately to infant anxiety, or (2) his or her engagement in behavior that actually induced anxiety. From an attachment perspective, the infant’s working model of self and other is thereby shaped by the caregiver’s disturbed attachment representations.
“Exploring representational models, Fonagy et. al. (Fonagy, Moran, Steele, Steele, & Higgitt, 1991; Fonagy, Steele, Moran, Steele, & Higgitt, 1993) identified the capacity for “reflective functioning” as an awareness of a meaningful relationship between underlying mental states (feelings, thoughts, motivations, intentions) and behavior in and between both self and others. Fonagy’s group found that caregiver reflective functioning was significantly predictive of infant attachment classification. The caregiver’s capacity to “read” infant mental states accurately, and with inference of meaning, allows for sensitively attuned responses that create a subjective experience of security/safety and support the infant’s developing capacity for self-regulation (Bretherton & Munholland, 1999). However, when engaging in reflective functioning leads to the experiencing of highly negative affect, certain aspects of mental functioning may be defensively inhibited (Fonagy, Steele, Steele, Higgitt, & Target, 1994) or excluded (Bretherton, 1990). A caregiver in a state of defensive inhibition will be incapable of accurately responding to and reflecting the child’s mental state, leaving the child to manage states of arousal and anxiety on his or her own. Consistent with this formulation is the finding that young children assessed as having a disorganized attachment have caregivers who are often unresolved with respect to past traumatic experience (Lyons-Ruth & Jacobvitz, 1999). In short, caregiver history of attachment relationships and of trauma exposure determines not only the dyad’s quality of attachment, via reflective functioning, but additionally the manner in which trauma exposure will be processed by both child and caregiver.
“Thus, traumatic violence can interfere with the initial development of a secure and organized attachment or derail a previously secure attachment if the caregiver is sufficiently adversely affected. Disturbances in attachment, in turn, confer increased [sic] for (1) recovery from trauma exposure by the child and/or caregiver (Fisher, Gunnar, Dozier, Bruce, & Pears, 2006), (2) enactment of maltreatment by the traumatized caregiver (Cicchetti, Rogosch, & Toth, 2006), (3) child exposure to trauma via inadequate caregiver monitoring (Schechter, 2006; Schechter, Brunelli, Cunningham, Brown, & Baca, 2002; Schechter et al., 2005), and (4) subsequent repetition and transmission of risk by the traumatized child and/or caregiver (Weinfield, Whaley, & Egeland, 2004). Such evidence supports the contention that we must view infant mental health disturbances through the dual conceptual lenses of attachment theory and trauma theory (Lieberman, 2004).” (pages 205 – 206)
Like all psychological functions, the child’s expectations in relation to attachment figures have neurobiological correlates. In addition to the effects of cortisol noted earlier, physical abuse, compounding its clear effects on emotion regulation and separation anxiety within the context of attachment, has been found to be associated with attentional dysregulation and selective biases to angry and negative affect (Pollak & Torrey-Schell, 2003).
“Moreover, from early infancy, children are dependent on their attachment figures to reflect back to them how they are feeling and to make sense of their experience. Expectation of the contingent responsiveness during early infancy has been described empirically in the work of Gergely and Watson (1996), who also first described the “marking” of the infant’s affect by the primary caregiver – the processing and modulation of that affect, which feeds back a sense of empathy as well as serving a modulatory function for the baby, beginning in the period of the second to fifth months of life. Subsequently, Gergely (2001) noted that lack of marking and overidentification with the child’s perspective may interfere with affect regulation, particularly around crises and trauma.
“We now know that specific neural circuits in the developing brain, among which the mirror neuron system figures prominently, are crucial to the development of social cognition, self-awareness, affect regulation, and learning (Jacoboni & Dapretto, 2006). The functional implications of these cortical pre-motor planning and parietal structures in the context of early development are only just beginning to be understood. The impact of violence exposure on the development of these circuits with respect to expression of aggression remains to be studied.
“Myron Hofer (1984) has described multiple “hidden regulators” embedded within the attachment system across mammalian species. The need for mutual regulation of emotion and arousal in humans lasts approximately as long as it takes for integrative structures in the brain to myelinate and prefrontal cortical areas to develop, all of which serve to assist the child in self-regulation in the face of stress and fear. In other words, the primary caregiver is, during the first 5 years of life, crucial to the infant’s developing self-regulation. The hidden regulators embedded within the attachment system include those of sleep, feeding, digestion, and excretion as well as higher functions of emotion, arousal, and attention. The literature contains many examples of how the sequelae of a caregiver’s experience of violent trauma and maltreatment, PTSD, affective disorders, severe personality disorders, and substance abuse can impair this fundamental regulatory function during formative stages of development, both at the representational and behavioral levels of attachment. (Lyons-Ruth & Block, 1996; Schechter et al., 2005; Theran, Levendosky, Bogat, & Huth-Bocks, 2005), and contribute to intergenerational transmission of violent trauma and maltreatment.
“Neurobiologically based studies of primates, specifically, macaque monkeys, have helped to elucidate the role of attachment in interrupting versus promoting intergenerational transmission of maltreatment (Barr et al., 2004; Maestripieri, 2005; Shannon et al., 2005). In Shannon et al.’s study (2005), maternal absence (i.e., neglect) was associated with decreased serotonin replenishment, a finding associated with mood and impulse disorders, as well as with increased alcohol consumption (in Barr e al.’s study, 2004).
“Recent research has also supported transgenerational transmission of biological response to trauma. Whether this finding proves ultimately to be a risk or resilience factor remains a question. An affected mother’s exposure to violent trauma during pregnancy (i.e., the 9/11 terrorist attacks on the World Trade Center in New York City) and her glucocorticoid stress response were linked to the glucocorticoid levels, upregulation of the receptor setpoint, and behavior of her infant by 9 months of life (Yehuda et al., 2005)…. Could this transmission of response to shared stress during pregnancy be one example at the very beginning of the organism’s life of adaptation in the service of evolution? Is the mother’s biology preparing the offspring for expectation of threat? If so, can one say that the development of PTSD (and/or other posttraumatic psychopathology) is a form of risk if no further threat actually exists, or resilience in the form of potentially beneficial hypervigilance to actual subsequent threat? [bold type is mine]
“As the hypothalamic-midbrain-limbic-paralimbic-cortical circuits in the caregiver respond jointly to infant stimuli, as has been found in recent neuroimaging studies among normative mother-infant dyads (Swain, Lorberbaum, Kose, & Strathearn, 2007), one can imagine a cycle of dysregulation in which unquelled infant distress becomes a stressor particularly for a traumatized parent. Indeed, while watching video clips of their children during separation and other stressful moments, group differences between violence-exposed mothers of toddlers and nonexposed mothers have been noted with respect to measures of integrative behavior, autonomic nervous system activity, and brain activation (Schechter, 2006).
“We know that an important determinant of the effects of traumatic exposure (e.g., how long they endure) is the primary caregiver’s ability to help restore a sense of safety via regulation of infant emotion, sleep, arousal, and attention (Laor, Wolmer, & Cohen, 2001; Scheeringa & Zeanah, 2001). These emerging findings may illuminate the ways in which the experience of violent trauma and its sequelae interfere with this primary caregiving function. On a positive note, we have also begun to understand how new relationships, most dramatically that of foster care, can curb if not reverse at least some of the effects of early violent trauma exposure (Fisher et al., 2006; Zeanah et al., 2001).
(Pages 206 – 208)