This article is an excerpt from my thesis “Learning, Memory and Attention Deficits in Female College-Age Sexual Assault Survivors with Posttraumatic Stress Disorder”
Multiple human and animal research studies suggest that extreme and/or chronic stress can lead to impaired memory performance, thus having a physiological effect on the hippocampus (Nixon, Nishith, & Resick, 2004). In the same animal testing study, abnormal levels of stress were associated with damage to the neurons in the CA3 region of the hippocampus. In addition, during extraordinary levels of stress, a large enough amount of cortisone is released that it has a negative effect on the hippocampus, thus impacting memory and recall. Survivors with PTSD tend to have abnormal levels of stress-involved hormones after the traumatic event: levels of cortisol are lower than normal, while levels of epinephrine and norepinephrine are higher (Izenberg & Dowsher, 2001).
In addition, even after the danger that caused the stressor has passed, there are still high levels of opiates, which are correlated with the emotional numbness symptom of PTSD. Other PTSD brain dysfunction hypotheses in literature include an alteration in noradrenergic function and damage to the limbic structure due to elevated levels of glucocorticoids (Bremner, Vermetten, Afzal, & Vythilingam, 2004). Due to the measured deficits noted in the prefrontal cortex in the same study, the neural circuits connecting the hippocampus to the prefrontal cortex are most likely also affected by the high level of stress.
Fear is processed through the sensory pathways in the subcortical brain systems, which sends the information to the thalamus and the amygdala; thus, when a PTSD survivor experiences fear, as from a flashback or panic attack, there could be deficits in cognitive processing (Wolfe & Schlesinger, 1997). Memories of traumatic experiences are hierarchically organized cognitive structures and are easily triggered when exposed to trauma-related cues (Williams & Banyard, 1999).