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). When survivors were exposed to traumatic images or sounds, the results showed an increase in PTSD symptoms, decreased blood flow, and/or failure of activating the medial prefrontal cortex and the anterior cingulate, including Brodmann’s area 25 (subcallosal gyrus), 32 and 24.
Additional trauma exposure studies have shown decreased function in the hippocampus, visual association cortex, parietal cortex, and inferior frontal gyrus, and increased function in the amygdala, posterior cingulate, and parahippocampal gyrus (Bremner, 2006). The physiological change to the hippocampus of a PTSD patient results decreases in declarative memory, fragmentation of memories, and trauma-related amnesia; while the physiological change to the amygdala results increases in conditioning and sensitization, and enhanced traumatic memories. With the physiological change in the prefrontal cortex of a PTSD patient, the patient shows failure to inhibit irrelevant cognitions, decreased working memory and inhibition of emotion, increased intrusions, and deficits in both attention and concentration (Elzinga & Bremner, 2002). Stress-induced hippocampal damage may be an example of sacrificing long-term function for short-term survival (Bremner, 1999). Antidepressant medication, which is given to some PTSD patients, has been shown to block the effects of stress and promote neurogenesis (Bremner, 2006).
References
Bremner, J. D. (1999). Does Stress Damage the Brain? Biological Psychiatry , 45, 797-805.
Bremner, J. D. (2006). Traumatic stress: effects on the brain. Dialogues in Clinical Neuroscience , 8 (4), 335-355.
Bremner, J. D., Vermetten, E., Afzal, N., & Vythilingam, M. (2004). Deficits in Verbal Declarative Memory Function in Women with Childhood Sexual Abuse-Related Posttraumatic Stress Disorder. The Journal of Nervous and Mental Disease , 192 (10), 643-649.
Elzinga, B., & Bremner, J. (2002). Are the neural substrates of memory the final common pathway in posttraumatic stress disorder (PTSD)? Journal of Affective Disorders , 70, 1-17.
Izenberg, N., & Dowsher, S. (2001). Human Diseases and Conditions; Behavioral Health Supplement. New York: Gale Group.
Nixon, R. D., Nishith, P., & Resick, P. A. (2004). The Accumulative Effect of Trauma Exposure on Short-Term and Delayed Verbal Memory in a Treatment-Seeking Sample of Female Rape Victims. Journal of Traumatic Stress , 17 (1), 31-35.
Williams, L., & Banyard, V. (1999). Trauma and Memory. In General Memory Functioning at Pre- and Posttreatment in Female Rape Victims with Posttraumatic Stress Disorder (pp. 47-56). Sage Publications.
Wolfe, J., & Schlesinger, L. (1997). Performance of PTSD Patients on Standard Tests of Memory. Annals New York Academy of Sciences , 821 (1), 208-218.
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Elizabeth Stannard Gromisch received her bachelor’s of science degree in neuroscience from Trinity College in Hartford, CT in May 2009. She is the Hartford Women's Health Examiner.