Neurobiology of Retraumatization
Epidemiological studies ¢nd that one of the strongest risk factors predicting who will develop posttraumatic stress disorder (PTSD) after exposure to a given trauma is whether individuals have experienced other traumas previously in their lifetime (Breslau, Davis, Andreski, & Peterson, 1991; Kessler, Sonnega, Bromet, Hughes, & Nelson, 1995; Koenen et al., 2002). Thus, the phenomenon of retraumatization appears to be of great importance in shaping how people respond to trauma and in predicting the development of PTSD subsequent to trauma. Although the evidence directly investigating retraumatization in humans is currently limited, this chapter will review existing data on the neurobiology of childhood trauma and adult PTSD, which is, in general, consistent with the idea that the experience of trauma may have neurobiological consequences that lead to additional risk upon retraumatization. This chapter will examine existing knowledge about the neurobiology of trauma and the effects of trauma on brain, autonomic nervous system, and neuroendocrine system functions that could underlie the impact of multiple lifetime traumas on PTSD risk. We will review a number of neurobiological systems within which effects of trauma and PTSD have been documented. Human and animal models of the neurobiology of trauma will be reviewed because of the potential all these models have to increase our understanding of how the experience of previous traumas affects responses to subsequent trauma. Trauma and other childhood adversity appear to be associated with particular risk for PTSD; this suggests that childhood trauma could lead to lifelong patterns of reactivity to stress and traumas that might underlie adult PTSD risk. The accumulating neurobiological data in humans is reviewed,
with particular emphasis placed on the possible associated childhood trauma exposure to alterations in adult neuroendocrine function, structural alterations in related limbic and cortical brain regions, and differences in functional activity in neurocircuitry implicated in threat detection, emotional regulation, and fear conditioning and extinction. Models of early life adversity in rodents which show lifelong alterations in anxiety behaviors, neuroendocrine responses, and patterns of brain gene expression will also be discussed, with emphasis placed on those mechanisms that potentially serve as mediators or moderators of the relation of early life trauma to PTSD vulnerability. The hypothesis that early life trauma and adversity may lead to lifelong imprinting of brain function and stress responses through neurodevelopmental, and possibly through epigenetic, changes has potentially important implications for understanding the neurobiology of trauma and PTSD.