Research/Empirical Evidence

Developmental Psychopathology Model of Childhood Traumatic Stress

Because of its complexity, it is rare for studies to examine all aspects of the developmental psychopathology model of childhood traumatic stress simultaneously. We review empirical evidence for various aspects and pathways in this model, including the role of the event and exposure to it, child characteristics, and the ecology of post-crisis environment, which can also be conceptualized in terms of internal and external vulnerability and protective factors.

Event and Exposure

There is ample research supporting the fact that the nature of the crisis event has a differential impact on traumatic responses. Human-caused events, especially those that are interpersonal and intentional, are more likely to cause PTSD than severe illnesses, injuries, natural disasters, or accidents (American Psychiatric Association, 2013; Feldman & Vengrober, 2011). For example, adolescents who have been raped are more than six times as likely to have PTSD compared with those who have experienced a natural disaster (McLaughlin et al., 2013). This is not to say that a natural disaster cannot be traumatic, as the duration, consequences, and intensity of the exposure all contribute to the likelihood of developing PTSD and other mental health disorders (Ayub et al., 2012; Ghazali, Elklit, Yaman, & Ahmad, 2013).

The more direct the physical exposure in terms of seeing or hearing an event, the greater the risk of psychological trauma (Ma et al., 2011). In addition, knowing someone who was exposed to a crisis event also impacts individuals, likely because it elevates their fear for the safety of the other (Ma et al., 2011; Ying, Wu, Lin, & Chen, 2013).

Child Characteristics

Children’s risk and protective factors predict how traumatized they may be after a crisis. People with pre-existing mental health disorders or history of previous traumas are also more vulnerable to traumatic stressors and acute symptomatology (Mullett-Hume, Anshel, Guevara, & Cloitre, 2008; Nemeroff, 2004; Trickey, Siddaway, Meiser-Stedman, Serpell, & Field, 2012). For example, a direct doseresponse relationship between trauma exposure and adverse symptomology was found in children who witnessed the 9/11 attack, with those experiencing moderate to high levels of cumulative life traumas displaying significantly more PTSD symptoms (Mullett-Hume et al., 2008).

Young children are especially vulnerable to trauma in terms of language and cognitive development, emotion regulation, and appropriate functioning within the classroom (Paccione-Dyzlewski, 2016). Low developmental and/or cognitive levels also can contribute to more psychological trauma (Banks & Weems, 2014). In some cases, this can actually be protective if the individual’s cognitive development is such that he or she does not understand the threat or its negative implications (Stallard & Salter, 2003). Social withdrawal or using avoidance coping as a longterm strategy also relates to increased traumatic stress (Trickey et al., 2012).

Although most research has focused on risk factors, it is critical to consider resilience, or the capacity to withstand or recover from trauma (Masten, 2011). Experiencing trauma need not define a person, and many youth with trauma histories do not experience the reactions we might expect or may recover and enjoy a healthy subjective well-being. Skills associated with resilience include selfregulation, self-efficacy and problem solving, ability to manage and cope with stress, and feelings of hope (Masten, Herbers, Cutuli, & Lafavor, 2008).

Ecology/post-crisis Environment

External vulnerabilities, as well as protective factors such as family, other social support systems (Lai, Kelley, Harrison, Thompson, & Self-Brown, 2015; Trickey et al., 2012), and resources are also important determinants of traumatic stress reactions. Students living in the Bronx following the 9/11 attacks who reported experiencing financial difficulty and those who reported psychosocial resource losses (e.g., social support and self-efficacy) were significantly more likely to have PTSD than their peers who did not experience these stressors (Calderoni Aiderman, Silver, & Bauman, 2006). In addition, the presence of an alcoholic parent in the home also increases the likelihood of experiencing other adverse child experiences (Dube et al., 2001).

The post-crisis environment can also be protective. Central to resilience are the relationships that children have with significant others such as family members, peers (e.g., friends, romantic partners), and other prosocial adults and institutions (e.g., faith communities; Masten et al., 2008). For example, having a sensitive caregiver can buffer children from experiencing heightened physiological responses to stressful situations (Gilissen et al., 2007).

Biological Theory

Psychiatrists, psychologists, and neuropsychologists have increasingly focused their attention on the child traumatic stress response and its impact (Wilson, Hansen, & Li, 2011). In a traumatic stress response, the brain exaggerates a form of pattern recognition in which traumatic reminders (i.e., sight, smell, sound, or other sensory input) bring forth neuroendocrine responses, resulting in the behavioral response (Bremner et al., 2003).

Multiple studies have demonstrated that traumatic life experiences in early life can alter brain systems and structure (Carpenter et al. 2004; Heim, Newport, Wagner, Wilcox, Miller, & Nemeroff, 2002). R. A. Cohen et al. (2006) found that individuals who experienced a higher number of adverse childhood experiences (ACES), compared with those who did not have any ACEs, had smaller right and left volumes of the caudate nuclei, as well as the right and left volume for the hippocampus. Global gray matter was also significantly higher among the no-ACE group (R.A. Cohen et al., 2006). Specific traumatic experiences led to more severe effects; individuals who had lost a parent or family member, witnessed domestic violence in their homes, or experienced sexual abuse had significantly smaller anterior cingulated cortexes and caudate nuclei (R.A. Cohen et al., 2006). These alterations can in turn affect long-term mental health, physical health, and behavior, including sleep, affect, substance use and abuse, early intercourse, promiscuity', impaired memory of childhood, difficulty' controlling anger, intimate partner violence, suicide, teen pregnancy, and impaired work performance (Anda et al., 2006).

Cognitive Theories

Particularly relevant for cognitive theories is the notion of threat perceptions with regard to a crisis or traumatic event, which is a central aspect of both the

SAMHSA (2014) conceptualization of trauma and the PREPaRE Model (Brock et al., 2009; Brock et al., 2016) of factors that increase vulnerability. There is a large research base showing that children’s subjective experiences of an event predict their psychological trauma (Ellis, Nixon, & Williamson, 2009; Lai et al., 2015; Trickey et al., 2012). Children’s threat perceptions and functioning after a crisis relate to reactions of important adults in their lives. If adults perceive an event as highly traumatic (regardless of the actual level of threat), younger children will respond similarly (DeVoe, Klein, Bannon, & Miranda-Julian, 2011; Masten & Gewirtz, 2006). This likely is because parents and other adult caregivers serve as “external regulators” for young children in terms of their ability to manage their emotional reactions to traumatic stress (Kaufman-Shriqui et al., 2013, p. 429).

In addition to perceived threat, causal attributions play an important role in the development of PTSD. Having a poor sense of self-efficacy (believing one has a limited ability to cope with the crisis; Bomyea, Risbrough, & Lang, 2012) and an external locus of control, or belief that the outcome is out of one’s own control, are also associated with increased traumatic stress symptoms (Zhang, Jiang, Ho, & Wu, 2011). Relatedly, being pessimistic, including dwelling on negative emotions and attributing events to internal, stable, and global causes, contributes to increased vulnerability (Bomyea et al., 2012; Ehlers & Steil, 1995).

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