Helping Children Cope with Trauma

Individual, family and community perspectives

Ruth Pat-Horenczyk, Danny Brom, Juliet M. Vogel, Ruth Pat-Horenczyk, Danny Brom, Juliet M. Vogel

• Publisher: Routledge
• Year: 2014
• ISBN:
  9781317934660
• Edition: 1
• Topic: Psychology
• Subtopic: Psychotherapy
• Index: Psychology

Helping Children Cope with Trauma bridges theory and practice in examining emerging approaches to enhancing resilience and treating traumatised children. Adopting a child-centred perspective, it highlights the importance of the synergy between individual, family, community and social interventions for recovery from post-traumatic stress.

Consisting of chapters by an international range of contributors, the book is presented in three sections, reflecting the ecological circles of support that facilitate healthy development in the face of traumatic circumstances. Section 1, Individual, addresses the impact of exposure to trauma and loss on post-traumatic adaptation, focusing on biological aspects, attachment patterns, emotion regulation and aggressive behaviour in children. Section 2, Family, looks at the concept of family resilience, the impact of trauma on playfulness in toddlers and parents, innovative models for working with children traumatised by war, domestic violence and poverty and describes the challenges faced by refugee families in the light of intergenerational transmission of trauma. Section 3, Community, broadly explores the concept of community resilience and preparedness, the centrality of the school in the community during times of war and conflict, post-traumatic distress and resilience in diverse cultural contexts and the impact of trauma work on mental health professionals who live and work in shared traumatic realities. The book concludes with a theoretical discussion of the concept of Survival Mode as an organisng principle for understanding post-traumatic phenomena.

Helping Children Cope with Trauma will provide mental health professionals, child welfare workers, educators, child development experts and researchers with a thorough understanding of the needs of children after trauma and how those needs may best be met.

Chapter 1
Developmental trauma from a biophysical perspective

Laura C. Pratchett and Rachel Yehuda

Introduction

Higher rates of childhood trauma (usually defined as chronic and repeated episodes of maltreatment, abuse or neglect, as opposed to single exposures to accidents or disasters) have been found among adults with posttraumatic stress disorder (PTSD) than among similarly exposed individuals who did not develop PTSD (Bremner, Southwick, Johnson, Yehuda, & Charney, 1993; Cloitre, Scarvalone, & Difede, 1997; Follette, Polusny, & Milbeck, 1994; Lang et al., 2008; Rodriguez, Ryan, Vande Kemp, & Foy, 1997; Zlotnick, 1997). Also, among adults who report childhood trauma, rates of PTSD are generally found to range from 72% to 100% (Lindberg & Distad, 1985; Rodriguez et al., 1997), often due to subsequent trauma exposure. These observations support the idea that exposure to childhood trauma is a risk factor for PTSD following trauma in adulthood. Moreover, developmental trauma appears to increase the likelihood of trauma exposure in adulthood, which may lead to the development of PTSD (Brewin, Andrews, & Valentine, 2000; Nishith, Mechanic, & Resick, 2000; Widom, 1999; for a review, see Classen, Palesh, & Aggarwal, 2005). Though not a necessary prerequisite for PTSD in adulthood, developmental trauma is therefore considered a potent risk factor for it.

In recent years, investigation of the biological correlates of childhood trauma has revealed similarities to those found in association with adult PTSD. In particular, the neurobiology of childhood trauma is similar to that of adult PTSD, raising the question of whether the neurobiology of adult PTSD reflects this risk. In this chapter, we evaluate the contribution of developmental trauma to some of the alterations in the hypothalamic-pituitary-adrenal (HPA) axis associated with PTSD. Advances in our understanding of the molecular biology of PTSD also allow us to consider a variety of mechanisms, such as genetic and epigenetic processes, including developmental programming, that may form the foundation for the biological changes observed following both exposure to childhood trauma and the development of PTSD (de Kloet, Joels, & Holsboer, 2005; Jovanovic & Ressler, 2010; Seckl, 2008; Yehuda & Bierer, 2008, 2009; Yehuda & LeDoux, 2007).

Neuroendocrine alterations in PTSD

The HPA axis has been a focus of study in PTSD because of the central role it plays in the neuroendocrine response to acute stress, including responses to fear, which would fit the current conceptualizations of precipitants of PTSD. In response to provocation, the stress response of the HPA axis involves the secretion of corticotropinreleasing hormone (CRH), which activates the release of adrenocorticotropic hormone (ACTH). ACTH, in turn, stimulates the release of glucocorticoids (GCs)—in particular, cortisol in humans—which are essential for the restoration of the biological homeostasis necessary for adaptation and recovery (McEwen, 2002; de Kloet et al., 2005). While older studies focused on hormone release, there has been increased emphasis on receptors and other compounds that affect hormone binding and steroid metabolism, as well as the genes underlying these processes.

The first published study of PTSD illustrated lower levels of basal cortisol in veterans with PTSD than among veterans with other psychiatric diagnoses (Mason, Giller, Kosten, Ostroff, & Podd, 1986). This observation was unexpected in light of numerous findings of elevated cortisol in individuals with both chronic stress and depression (Holsboer, 2003; Strohle & Holsboer, 2003). However, this finding has been replicated in numerous other studies that have substantially increased our understanding of the neuroendocrinology of PTSD. To summarize these many reports, studies of the HPA axis in PTSD revealed a profile in which CRH levels are increased (Bremner et al., 1997; Baker et al., 1999) while levels of cortisol are often lower than in controls (e.g., Bremner, Vermetten, & Kelley, 2007; Thaller, Vrkljan, Hotujac, & Thakore, 1999; Vythilingam et al., 2010; Yehuda et al., 1990; Yehuda, Teicher, Trestman, Levengood, & Siever, 1996). Increased cortisol suppression in response to dexamethasone (DEX), a synthetic GC, has also been repeatedly observed, suggesting increased sensitivity of glucorticoid receptors (GRs), and reflecting enhanced negative feedback inhibition (for a review, de Kloet et al., 2006; Yehuda, 2002, 2009). In PTSD, then, the HPA axis is dysregulated in a way that suggests an increased cortisol signaling capacity, so that lower GC levels efficiently suppress the HPA axis, leading to reduced levels of cortisol, which may contribute to increased sympathetic activation (de Kloet et al., 2005; Raison & Miller, 2003; Yehuda, 2002). Thus, although cortisol levels at baseline may be lower, the enhanced responsiveness of GR—the major regulatory elements of the HPA axis—may render the individual hyperresponsive to some types of provocations.

Neuroendocrine alterations associated with childhood trauma

Neuroendocrine alterations in adults with PTSD who report childhood trauma

Results of studies of adults diagnosed with PTSD who report a history of childhood trauma have been somewhat conflicting, but this may reflect the fact that childhood trauma is also a risk factor for depression, which has some hormonal similarities with PTSD (e.g., CRH) but also some differences from it (e.g., cortisol). Lemieux and Coe (1995) observed significantly higher cortisol, norepinephrine (noradrenaline) and epinephrine (adrenaline) levels in women with PTSD than in women without it, among a sample of women who reported child hood sexual abuse. The subjects in that study who reported abuse also tended to be more obese, particularly if they had PTSD, which might be one of the factors contributing to higher am bient hormone levels. In comparison, Bremner et al. (2003) found lower cortisol levels among women with both reported abuse and current PTSD than among those who did not have PTSD, whether or not they reported childhood abuse. However, the ACTH response to CRH administration was blunted in women with PTSD only, in comparison to the women who did not report abuse, while no such differences were observed in comparison to abused women without PTSD. Lower cortisol levels (and higher cortisol pulsatility) was also observed by Bremner et al. (2007) in women with PTSD and a history of childhood abuse compared to women without PTSD, whether or not they reported abuse. Thus, there are some similarities in the observed HPA axis abnormalities associated with PTSD due to childhood abuse and adult traumatization, and certainly target hormones such as cortisol and norepinephrine are impacted. However, further work is needed to understand the differences and discover whether they are associated with factors such as comorbidity with depression or type of trauma, the period of development when the trauma(s) occurred and the longitudinal course from childhood trauma to adulthood. It is of particular interest that these studies also show that HPA axis dysfunction may be associated with a history of childhood abuse even in the absence of PTSD.

Neuroendocrine alterations in traumatized children

There are studies that have attempted to clarify the association between childhood abuse and HPA-axis dysfunction by removing longitudinal elements as a variable and studying children with recent abuse and maltreatment. As is the case in individuals with adult trauma and PTSD, low levels of cortisol have been observed in some groups of traumatized children: those in foster care due to maltreatment (Bruce, Fisher, Pears, & Levine, 2009; Gunnar & Vazquez, 2001); those being raised in Romanian orphanages under presumably deprived, if not previously abusive, conditions (Carlson & Earls, 1997); sexually abused girls (King, Mandansky, King, Fletcher, & Brewer, 2001); children suffering from the loss of family members or their home at the epicenter of a devastating earthquake (Goenjian et al., 1996); and children who have experienced peer victimization or witnessed violence (Kliewer, 2006). In addition, low cortisol levels have been observed among children with a more general history of trauma (Bevans, Cerbone, & Overstreet, 2008). However, multiple studies have found elevated morning cortisol in maltreated children (reviewed in Tarullo & Gunnar, 2006). Despite a trend for low cortisol in physically abused children, Cicchetti and Rogosch (2001) found elevated cortisol levels in children who had suffered both physical and sexual abuse, and De Bellis et al. (2000) found that both cortisol and cate cholamines were higher in maltreated children with PTSD than in normal control subjects. Interestingly, a recent study that followed sexually abused children longitudinally from age 6 to age 30 demonstrated a progressive attenuation in cortisol activity starting in adolescence, with significantly lower levels of cortisol appearing only in early adulthood (Trickett, Noll, Susman, Shenk, & Putnam, 2010).

Neuroendocrine alterations in adults reporting childhood trauma

Other attempts to better clarify and understand the complex biological responses to trauma have focused on adults without PTSD who report a history of childhood abuse. Blunted diurnal variation of cortisol has been identified among women with a reported history of childhood physical or sexual abuse (Brewer-Smyth & Burgess, 2008; Weissbecker, Floyd, Dedert, Salmon, & Sephton, 2006) and among adults who were adopted in childhood following extreme abuse or neglect (van der Vegt, van der Ende, Kirschbaum, Verhulst, & Tiemeier, 2009). Increased ACTH responses to the administration of CRH have been observed in women with histories of childhood abuse (Newport, Heim, Bonsall, Miller, & Nemeroff, 2004). Attenuated cortisol response to either a stress test or DEX was reported in association with severe childhood maltreatment (Carpenter et al., 2007; MacMillan et al., 2009), emotional neglect (Watson et al., 2007), emotional abuse (Carpenter et al., 2009) and sexual abuse (Stein, Yehuda, Koverola, & Hanna, 1997; Newport et al., 2004), suggesting similarities in negative feedback inhibition in the HPA as is observed in PTSD. However, some studies have suggested that HPA axis dysregulation as a consequence of childhood abuse is present only in adults with depression (Heim, Plotsky, & Nemeroff, 2004; Heim, Newport, Mletzko, Miller, & Nemeroff, 2008). The exact nature of the relationship between childhood trauma and HPA axis dysfunction is thus complex and unclear. What does seem clear is childhood trauma is associated with HPA axis dysfunction, which, at least for some individuals, may reflect the kind of dysfunction observed among individuals with PTSD subsequent to adult trauma. The fluctuating directionality of the findings may reflect the cross-sectional nature of biological studies. Indeed, findings showing extreme high or low HPA axis activity may reflect a system that is more dynamic or hyperresponsive (Yehuda et al., 1996).

HPA axis dysfunction as a risk for adult PTSD

Although prospective longitudinal studies are required to delineate the mechanisms and associations involved in the progression from childhood trauma to biological changes and adult PTSD, the previous literature offers one plausible hypothesis—that early life trauma produces HPA axis sensitization, which serves as the risk factor for PTSD in the face of later trauma. Indeed, the inconsistencies in the literature may reflect the complexity of how environmental events shape biological responses to stress. Clearly, there may be many significant contributors, including the nature of the trauma, the point in development when the event occurred, the nature of the child's parental attachment and countervailing resilience and coping mechanisms.

This would be consistent with our current understanding of the nature of low cortisol as a risk factor for PTSD. Although cortisol findings in PTSD were initially interpreted as reflecting pathophysiology of the disorder resulting from trauma exposure and/or chronic symptoms, data from prospective longitudinal studies have raised the possibility that low cortisol levels reflect pre-traumatic predictors of PTSD. For example, several prospective longitudinal studies have demonstrated that lower cortisol levels in the acute aftermath of trauma were associated with either the subsequent development of PTSD or the risk factor of prior trauma exposure (Delahanty, Raimonde, & Spoonster, 2000; McFarlane, Atchison, & Yehuda, 1997; Resnick, Yehuda, Pitman, & Foy, 1995; Yehuda, McFarlane, & Shalev, 1998). Low cortisol levels at the time of the trauma could compromise the inhibition of stress-induced biologic responses to trauma, such as catecholamines, resulting in prolonged physiological arousal and distress, leading to PTSD (Yehuda, 2002). The idea that reduced cortisol levels might reflect HPA dysfunction associated with pre-exposure vulnerability provides a plausible explanation for discrepant observations in PTSD. Cortisol levels may be low only in PTSD asso...