Structural and Functional Neuroplasticity in Relation to Traumatic Stress

The body’s stress response is an essential adaptive and protective mechanism to cope with threatening situations. However, chronic or traumatic stress leads to structural and functional alterations in the traumatized brain. We argue for a building-block effect: Exposure to different types of traumatic events increases the probability of developing posttraumatic stress disorder (PTSD), via incremental enlargement of a fear network. We summarize evidence of brain changes in PTSD, including recent results from research on animal models of stress-related neuroplastic remodeling, with an emphasis on structural and functional changes in the hippocampus, the amygdala, and the medial prefrontal cortex. KEYWORDS—amygdala; hippocampus; neuroplasticity; posttraumatic stress disorder; stress The human brain and body are capable of dealing with stressors such as danger or violent experiences in a flexible and adaptive way. Chronic or repeated traumatic stress, however, can damage organs, including the brain, and may weaken regulatory functional systems such as the hypothalamic-pituitary-adrenal (HPA) axis. The hippocampus and the HPA axis are involved in the feedback regulation of the stress hormone cortisol and thus in the body’s reaction to danger. Regulatory dysfunctions in these systems in the aftermath of highly stressful life events may result in mental illness. Whereas stressful life events like bereavement or role changes can lead to depressive disorders, exposure to extreme (traumatic) stress may lead to posttraumatic stress disorder (PTSD). PTSD is characterized by ongoing, intrusive (i.e., uncontrollable) memories, including nightmares; a constant state of alarm (hyperarousal); and avoidance symptoms, including emotional numbing. Sleep disturbances, substance abuse, depression, and enhanced risk for suicide are common consequences, as are poor self-reported well-being, poor physical health, and increased health-care utilization. Traumatic stress refers to potentially harmful experiences eliciting feelings of helplessness, intense fear, or horror, with an associated alarm response (cf. Elbert, Rockstroh, Kolassa, Schauer, & Neuner, 2006)—that is, the acute release of stress hormones. Each such experience is appropriately referred to as a trauma (Greek for ‘‘wound’’); traumas render a person more vulnerable to develop PTSD in a cumulative manner. BUILDING BLOCKS: DIFFERENT TRAUMATIC STRESSORS ADD UP TO PRODUCE PTSD Investigating more than 3,000 war refugees with varying degrees of traumatic stress exposure, Neuner et al. (2004) found that the greater the number of various types of traumatic events experienced by an individual (e.g., torture, fighting, shelling, abduction, abuse/rape, forcible female circumcision), the more likely the individual was to have PTSD, with more pronounced symptoms. PTSD prevalence rates reached 100% for individuals having experienced 28 or more different traumatic-event types (Fig. 1)—a ‘‘building block’’ effect. Neuner et al. interpreted this to mean that nearly anyone would develop PTSD if they were exposed to a sufficiently high number of different traumatic stressors. This building-block effect may be a direct result of the development of a neural fear network, which is strengthened and extended in response to each new traumatic event (cf. Elbert et al., 2006). During a traumatic event, perceptual and emotional features of the situation are stored in memory—autobiographical context information (dates, external circumstances) as neutral or ‘‘cold’’ memories and sensory-perceptual information (fear, helplessness, high pulse) as emotionally charged or ‘‘hot’’ Address correspondence to Iris-Tatjana Kolassa, Department of Psychology, Clinical & Neuropsychology, University of Konstanz, 78457 Konstanz, Germany; e-mail: [email protected].