PTSD and the brain

PTSD and the brain

Both the amygdala and insular cortex have been shown to activate in response to emotional stimuli (Shin, 2006; Uddin et al., 2017). In general, the more intense the stimulus, the bigger the activation in these areas.

The volume of the amygdalae (Ousdal et al., 2020) and insular cortices (Chen et al., 2009) of individuals with PTSD has been shown to be significantly reduced. At the same time, increased activation of the amygdalae and insular cortex in cases of PTSD has been demonstrated (Shin & Liberzon, 2009).

Hyperactivation in the amygdala has been directly correlated to the severity of PTSD symptoms (Shin, 2006). In short, it appears that parts of the brain involved in emotional responses are activated more in individuals living with PTSD.

The medial prefrontal cortex (mPFC) has an important role in ‘extinction’ (Giustino et al., 2015), a process of lessening the fear response to stimuli.

Studies have shown that individuals experiencing PTSD tend to have reduced mPFC volumes (Shin, 2006), as well as reduced activation of the mPFC (Giustino et al., 2015). The consequence is reduced emotional regulation.

The hippocampus has been linked to the formation of emotional memories and the contextualisation of those memories. In this respect, the hippocampus is also important in extinction.

Evidence suggests that, as in the case of the mPFC, the volume of the hippocampus is reduced in individuals with PTSD, and the activation of this region of the brain is decreased also (Shin, 2006; Sherin & Nemeroff, 2011).

The evidence seems to suggest that individuals with PTSD may experience an increased emotional response to stimuli, while also being less able to adapt to the stimuli and decrease their emotional response over time.

Understanding how and why these changes come about is key to understanding PTSD and developing potential therapeutic strategies in future.

References

^{Chen, S., Li, L., Xu, B., & Liu, J. (2009). Insular cortex involvement in declarative memory deficits in patients with post-traumatic stress disorder. BMC Psychiatry, 9(1), 39-39. https://doi.org/10.1186/1471-244X-9-39}

^{Giustino, T. F., & Maren, S. (2015). The role of the medial prefrontal cortex in the conditioning and extinction of fear. Frontiers in Behavioral Neuroscience, 9, 298. https://doi.org/10.3389/fnbeh.2015.00298}

^{Ousdal, O. T., Milde, A. M., Hafstad, G. S., Hodneland, E., Dyb, G., Craven, A. R., . . . Hugdahl, K. (2020). The association of PTSD symptom severity with amygdala nuclei volumes in traumatized youths. Translational Psychiatry, 10(1), 1-10. https://doi.org/10.1038/s41398-020-00974-4}

^{Sherin, J. E., & Nemeroff, C. B. (2011). Post-traumatic stress disorder: The neurobiological impact of psychological trauma. Dialogues in Clinical Neuroscience, 13(3), 263-278. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3182008/}

^{Shin, L. M. (2006). Amygdala, medial prefrontal cortex, and hippocampal function in PTSD. Annals of the New York Academy of Sciences, 1071(1), 67-79. doi:10.1196/annals.1364.007}

^{Shin, L. M., & Liberzon, I. (2009). The neurocircuitry of fear, stress, and anxiety disorders. Neuropsychopharmacology (New York, N.Y.), 35(1), 169-191. https://doi.org/10.1038/npp.2009.83}

^{Uddin, L. Q., Nomi, J. S., Hébert-Seropian, B., Ghaziri, J., & Boucher, O. (2017). Structure and function of the human insula. Journal of Clinical Neurophysiology, 34(4), 300-306. doi:10.1097/wnp.0000000000000377}