Posttraumatic stress disorder: the role of medial prefrontal cortex and amygdala.
Open accessAbstract
Posttraumatic stress disorder (PTSD) is characterized by recurrent distressing memories of an emotionally traumatic event. In this review, the authors present neuroscientific data highlighting the function of two brain areas—the amygdala and ventromedial prefrontal cortex (vmPFC)—in PTSD and related emotional processes. A convergent body of human and nonhuman studies suggests that the amygdala mediates the acquisition and expression of conditioned fear and the enhancement of emotional memory, whereas the vmPFC mediates the extinction of conditioned fear and the volitional regulation of negative emotion. It has been theorized that the vmPFC exerts inhibition on the amygdala, and that a defect in this inhibition could account for the symptoms of PTSD. This theory is supported by functional imaging studies of PTSD patients, who exhibit hypoactivity in the vmPFC but hyperactivity in the amygdala. A recent study of brain-injured and trauma-exposed combat veterans confirms that amygdala damage reduces the likelihood of developing PTSD. But contrary to the prediction of the top-down inhibition model, vmPFC damage also reduces the likelihood of developing PTSD. The putative roles of the amygdala and the vmPFC in the pathophysiology of PTSD, as well as implications for potential treatments, are discussed in light of these results.
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Koenigs et al. found that damage of vmPFC protected a person from PTSD symptoms and that this region actively contributes to the regulation of emotional re-experience in PTSD.
“They found that the damage of vmPFC protected person from PTSD symptoms respectively that this regions actively contributes to the regulation of emotional re-experience in PTSD (Koenigs and Grafman, 2009).”
From Neuroimaging research in posttraumatic stress disorder – Focus on amygdala, hippocampus and prefrontal cortex (2019) · cites this paper as Koenigs and Grafman, 2009
The Discussion of the role of vmPFC in PTSD (page not provided) associates vmPFC damage with resistance to PTSD, supporting the first part of the claim. It proposes that vmPFC involvement in self-reflection may affect distress tied to past events, but does not establish that vmPFC actively regulates emotional re-experience in people with PTSD; the Emotion regulation section describes studies of healthy adults. (LLM, conf=0.86)
Experimental — accuracy not yet measuredChanges in neural circuitry caused by chronic stress are believed to underlie the deficits in learning/memory, mood, motivation, and reward seeking that are characteristic of depression and related disorders.
“these changes in neural circuitry are believed to underlie the deficits in learning/memory, mood, motivation, and reward seeking that are characteristic of depression and related disorders (10, 67–74)”
From Psychedelics and Other Psychoplastogens for Treating Mental Illness. (2021) · cites this paper as [73]
The Emotion regulation section (page unavailable) reports disrupted vmPFC–amygdala coupling during emotion regulation in major depression, supporting a link between neural circuitry and mood. The paper does not attribute that disruption to chronic stress or link it to the claimed deficits in learning/memory, motivation, or reward seeking. (LLM, conf=0.83)
Experimental — accuracy not yet measuredIndividuals with PTSD have shown consistent hyperactivation of subcortical structures compared to healthy individuals in previous neuroimaging studies, particularly at the level of the midbrain in the brainstem.
“First, individuals with PTSD have previously shown consistent hyperactivation of subcortical structures as compared to healthy individuals in previous neuroimaging studies, particularly at the level of the midbrain in the brainstem (Koenigs and Grafman, 2009; Steuwe et al., 2014; Rabellino et al., 2016).”
From How Processing of Sensory Information From the Internal and External Worlds Shape the Perception and Engagement With the World in the Aftermath of Trauma: Implications for PTSD (2021) · cites this paper as Koenigs and Grafman, 2009
The Functional imaging studies of PTSD section (page not supplied) reports elevated amygdala activation in PTSD patients, including a meta-analysis finding significant amygdala hyperactivation. It does not report hyperactivation particularly in the midbrain or brainstem; the paper describes the amygdala as a subcortical structure that projects to brainstem regions, not as a midbrain finding. (LLM, conf=0.88)
Experimental — accuracy not yet measuredPTSD has often been described as a disorder of impaired fear extinction.
“As PTSD has often been described as a disorder of impaired fear extinction (73, 185–187)”
From Psychedelics and Other Psychoplastogens for Treating Mental Illness. (2021) · cites this paper as [73]
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- Authors
- Koenigs, M., & Grafman, J.
- Affiliations
- University of Wisconsin–Madison (US)
- National Institutes of Health (US)
- Corresponding author
- Grafman, Jordan
- Venue
- The Neuroscientist
- Publisher
- SAGE Publications
- Published
- 2009-04-09
- Volume
- 15
- Issue
- 5
- Pages
- 540-548
- ISSN
- 1073-8584 (ISSN-L)
- 1089-4098
- PMC
- PMC2771687
- OpenAlex
- W2147242053
- Cited by
- 368
- References
- 17
- Citations by year
- 2026: 13 · 2025: 23 · 2024: 24 · 2023: 19 · 2022: 17 · 2021: 27 · 2020: 34 · 2019: 19 · 2018: 23 · 2017: 22 · 2016: 27 · 2015: 20 · 2014: 22 · 2013: 26 · 2012: 24
- FWCI
- 2.36
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- The Neuroscientist (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health
- National Institute of Neurological Disorders and Stroke (Z01NS002792)
- Topics
- Social Sciences › Psychology › Clinical Psychology › Posttraumatic Stress Disorder Research
- Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
- Life Sciences › Neuroscience › Cognitive Neuroscience › Memory Processes and Influences
- Keywords
- post-traumatic stress disorder, amygdala, ventromedial prefrontal cortex, fear conditioning, fear extinction, emotional memory, top-down inhibition, amygdala hyperactivity, brain injury, combat veterans, PTSD pathophysiology, PTSD treatment
- MeSH terms
- Amygdala, Animals, Conditioning, Psychological, Fear, Humans, Memory, Models, Neurological, Neural Inhibition, Stress Disorders, Post-Traumatic, Prefrontal Cortex
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