Biological Mechanism of Traumatic Stress Response

The Biological Stress System

The stress system is activated when the subject's environment is perceived as threatening. Sensory environmental cues reach the brain and are processed by the amygdala, important in the brain's “fear circuitry.” In case of danger, the hypothalamic-pituitary-adrenal (HPA) axis and the sympathetic nervous system (SNS) are activated through neural signaling, producing multiple effects. Through SNS activation, within seconds hormones called catecholamines are released into the blood from the adrenal glands, causing, for example, an increase in heart rate, blood pressure, and glucose levels, resulting in arousal for “fight or flight.” When the hypothalamus is stimulated, it releases neuropeptides, which in turn results in cortisol release. Cortisol has important negative feedback roles. Via binding to glucocorticoid receptors in the brain, cortisol dampens stress responses.

Stress responses function to adapt to threat and to restore the body's balance. However, severe stress directly influences the system's functionality, and may lead to stress-related symptoms such as PTSD.

Heterogeneity of Biological Responses: Acute and Chronic PTSD Predictors

Research illustrated that acute and chronic biological reactions to trauma are heterogeneous. These differences may explain why the minority does, but the majority does not, develop symptoms after traumatization, and they may reflect vulnerability factors for psychopathology development.

Since PTSD is characterized by hyperarousal, prospective studies assessed associations between physiological measures acutely after traumatization and subsequent PTSD symptoms. These studies yielded evidence that increased heart rate in the acute phase post trauma is predictive of PTSD development.

Regarding HPA measures, an acute low cortisol response is generally associated with an increased PTSD risk. However, altered hormonal responses after trauma and subsequent increased PTSD risk seem to be closely related to prior trauma exposure. In victims of rape, only women with a history of assault showed acute hypocortisolism and had an increased likelihood to suffer from PTSD. These and similar findings led researchers to hypothesize that early life stress alters the relationship between SNS and HPA hormones, increasing the risk for PTSD development to subsequent trauma. The diminished cortisol response fails to attenuate the sympathetic response. Since stress hormones in the brain play important roles in memory consolidation, this altered stress response may causally contribute to overconsolidated traumatic memories, which are manifested in PTSD symptoms.

Generally, similar findings of increased SNS activity and HPA alterations are found in PTSD, although results have been mixed.

Brain Mechanisms of Traumatic Stress

In humans, researchers using functional magnetic resonance imaging (fMRI) techniques have studied brain regions associated with traumatic responses. Most attention has been paid to structural and functional changes in the hippocampus, amygdala, and medial prefrontal cortex (mPFC). These areas are important in stress regulation and memory. Processing emotional memories with contextual [Page 48]information requires amygdala-hippocampus interaction, and the mPFC plays an important role in fear extinction by inhibiting the amygdala. Smaller hippocampal volumes have been associated with PTSD and trauma exposure in general. In PTSD patients, the amygdala shows hyperreactivity to trauma-related and other amygdala-activating stimuli. Furthermore, the functional connection between the amygdala and mPFC is diminished in PTSD. Also, decreased volumes of the mPFC have been reported.

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