What Exactly Does PTSD Do to the Brain?

Post-traumatic stress disorder (PTSD) is a trauma and stressor-related disorder that results in improper processing and storage of traumatic memories. Because of the way these memories are stored, patients with PTSD exhibit symptoms such as recurrent memories regarding the event; traumatic nightmares; dissociative flashbacks; hypervigilance; engaging in risk-taking behavior; and an exaggerated startle response.

Certain structures of the brain are closely related to some of the symptoms of PTSD. These structures include the amygdala and hippocampus (which are part of the limbic system); several parts of the prefrontal cortex (PFC); the mid-anterior cingulate cortex and the right inferior frontal gyrus. PTSD causes the hyper-activation of some of these structures while other parts of the brain become hypoactive.

Both the amygdala and the mid-anterior cingulate cortex become over-stimulated when a person suffers with PTSD. However, the hippocampus, right inferior frontal gryus, ventromedial PFC, dorsolateral PFC and orbitofrontal cortex all become hypoactive, some to the point of atrophy.

Very generally, the amygdala controls some mating functions; the assessment of threat-related stimuli (basically what in the environment is considered a danger); the formation and storage of emotional memories; fear conditioning; and memory consolidation.

The primary function of the mid-anterior cingulate cortex (ACC) is to monitor conflict. The ACC also plays a role in emotional awareness (particularly empathy); registering physical pain, and regulating autonomic functions like heart rate and blood pressure.

The hippocampus helps regulate smell, spatial coding, and memory.

More specifically the hippocampus helps store long-term memories, basically helping to decide what goes from being a short-term memory to what becomes a long-term memory. This process of turning a short-term memory into a long-term memory is what is referred to as memory consolidation. Damage to the hippocampus can also release excess cortisol (a stress hormone).

The right inferior frontal gyrus is involved in modulating risk aversion. Studies show that transcranial magnetic stimulation (TMS) of this brain region may reduce some risk-taking behavior.

The ventromedial PFC helps suppress negative emotion, as well as playing a role in personal and social decision-making. It also plays a major role in the later part of memory consolidation, as well as regulating extinction – the weakening and eventual dissipation of a conditioned response.

The dorsolateral PFC modulates decision making and working memory. Working memory actively holds transitory information before it becomes part of the long-term memory during memory consolidation.

The orbitofrontal cortex, one of the least understood parts of the brain, seems to be involved in sensory integration and signaling expected rewards and/or punishments in a given situation. It also modulates emotion and decision making.

As a whole, the prefrontal cortex is interconnected to many brain functions, including memory consolidation and regulating slow-wave sleep (non-REM sleep, referred to as "deep sleep").
The function of the entire prefrontal cortex is particularly dependent on its neurochemical environment. 

When examining the functions of the various structures of the brain, the correlation between change to those structures’ activity levels and some PTSD symptoms becomes clearer. For example, the hippocampus is involved in "explicit memory processes and in the encoding of context during fear conditioning." When the hippocampus fails to function optimally, it impacts the way a person remembers and recalls memories, especially memories that contain a fear element – such as those related to a trauma. Symptomatically, this presents as recurrent memories regarding the event; distorted negative beliefs; and dissociative flashbacks. Changes to the right inferior frontal gyrus help to explain why PTSD patients suddenly engage in high-risk activities. The over-activity of the amygdala presents as symptoms of hypervigilance and the exaggerated startle response.

When thoroughly examining the relationship between brain function and symptomatology, it becomes easier to understand many of the complex manifestations of PTSD. Although understanding the brain in this way may not provide direct symptomatic relief to someone suffering from PTSD, it can be helpful in understanding why the symptoms are happening, and in helping the medical community continue to develop more effective interventions.


Fecteau S, Pascual-Leone A, et al. Activation of Prefrontal Cortex by Transcranial Direct Current Stimulation Reduces Appetite for Risk during Ambiguous Decision Making. Journal of Neuroscience 2007 Jun 6;27(23):6212-8.

Hayes JP1, Vanelzakker MB, Shin LM. Emotion and cognition interactions in PTSD: a review of neurocognitive and neuroimaging studies. Frontiers of Integrated Neuroscience, 2012 Oct 9;6:89.

Mander BA, Rao V, et al. Prefrontal atrophy, disrupted NREM slow waves and impaired hippocampal-dependent memory in aging. Nature Neuroscience, 2013 Mar;16(3):357-64.

Shin, L., Rauch, S., and Pitman, R. Amygdala, Medial Prefrontal Cortex, and Hippocampal Function in PTSD. Annals of the New York Academy of Sciences, 2006 Jul;1071:67-79.

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