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PTSD and the Brain: What Trauma Does to Memory, Fear, and the Prefrontal Cortex.

Trauma does not just leave psychological scars. It physically rewires the brain's fear circuitry, shrinks the hippocampus, silences the prefrontal cortex, and recalibrates the stress axis, creating a system that cannot distinguish past threat from present safety. Here is what the science actually says, and what to do with it.

Section
Arena · Neuroscience
Reading time
22 min read
Sources
34 · reviewed

01Three Millennia Late

PTSD symptoms predate their 1980 diagnosis by three thousand years

The word trauma comes from the Greek for wound, and for most of medical history that was understood literally: a broken bone, a punctured organ, a visible insult to tissue. The psychological meaning arrived late. Symptoms recognisable as post-traumatic stress appear in Mesopotamian cuneiform tablets more than three thousand years old, in accounts of soldiers who could not stop seeing the faces of the men they had killed.[5] The condition was called shell shock in the First World War, combat fatigue in the Second, and was not granted a formal psychiatric diagnosis until the American Psychiatric Association added post-traumatic stress disorder to the DSM-III in 1980, a gap of roughly three millennia between first observation and official recognition.[5]

That delay was not administrative. It reflected a deeper uncertainty about whether the problem was real in the biological sense, whether trauma did something to the brain or merely to the mind. The answer, delivered across three decades of neuroimaging, genomics, neuroendocrinology, and controlled clinical trials, is now unambiguous. Trauma physically reorganises the brain. It shrinks structures, silences circuits, recalibrates hormones, and alters gene expression in ways that can be measured on a scan, quantified in a blood draw, and mapped across a genome.[8][9]

The scale of the problem makes the biology urgent. Benjet and colleagues surveyed 68,894 adults across 24 countries (26 surveys) and found that more than 70 percent had experienced at least one significant traumatic event.[1] Of those exposed, roughly 5.6 percent develop PTSD.[2] In the United States, lifetime prevalence sits at approximately 6 percent, with women twice as likely as men to receive the diagnosis.[4] Among high-exposure populations (combat veterans, first responders, survivors of sexual violence) rates climb to between 20 and 57 percent.[6]

The history

What makes PTSD neuroscience different from the neuroscience of ordinary stress is the direction of change. Acute stress activates systems designed to keep you alive: the amygdala fires a threat alarm, cortisol floods the bloodstream, attention narrows. When the threat passes, the prefrontal cortex reasserts control, cortisol levels normalise, and the brain files the event as a completed experience, a process called fear consolidation. PTSD is what happens when that filing process fails.[8][10]

The result is not heightened anxiety. It is a circuit-level reorganisation in which the brain's alarm system runs unchecked, its contextual memory system cannot distinguish past from present, and its hormonal calibration shifts to a baseline that expects danger at all times.[9][11] The economic consequence is staggering: Davis and colleagues calculated the annual US burden at $232.2 billion, or $19,630 per affected individual, with military per-person costs running 38 percent higher.[3]

That framing matters. Performance culture tends to treat trauma responses as psychological weakness, a failure of mental toughness, a problem of mindset. The PTSD neuroscience literature says something entirely different. It says the brain has been physically remodelled by an event, and the remodelling follows predictable biological rules.

02The Mechanism

The Fear Circuit That Breaks in PTSD

Every brain runs a threat-detection system built from the same basic components. A region called the amygdala, a small, almond-shaped cluster buried in the medial temporal lobe, is the alarm. It receives sensory information before conscious awareness has time to evaluate it, and when it detects a pattern associated with danger, it triggers a cascade: heart rate rises, muscles tense, attention locks onto the source.[8][9] This is not a malfunction. This is the system working as designed.

The regulation comes from above. The ventromedial prefrontal cortex (vmPFC), the section of prefrontal cortex sitting just behind the bridge of the nose, acts as the brake. Once the amygdala fires, the vmPFC evaluates the context: Is this a real threat? Has this pattern been seen before and found harmless? If the answer is yes, the vmPFC sends inhibitory signals downward, dampening the amygdala's alarm and allowing the body to stand down.[10][14] This process (learning that a previously feared cue is now safe) is called fear extinction, and it depends on the vmPFC and hippocampus working in concert.[15]

In PTSD, this brake fails. Milad and colleagues demonstrated in a controlled fMRI experiment that patients with PTSD show significantly decreased vmPFC activation and greater dorsal anterior cingulate cortex (dACC) activation during extinction recall, meaning the inhibitory circuit that should suppress fear is underactive while the threat-monitoring circuit that should quiet down stays hyperactive.[16] The finding has been replicated in more than 40 subsequent studies.[15][16]

Amygdala 01 alarm misfires Hippocampus 02 context failure vmPFC 03 extinction failure Locus coeruleus 04 NE hyperactivation

The PTSD failure loop: a sensitised amygdala fires on safe cues that a shrunken hippocampus cannot contextualise, the vmPFC brake is too weak to extinguish the alarm, and a hyperactive locus coeruleus keeps norepinephrine elevated, producing chronic hypervigilance and intrusion.

Diagram · HPC

The hippocampus adds a second layer of failure. This structure (critical for episodic memory and contextual processing) tells the amygdala where you are and what that means. A car backfiring in a war zone and a car backfiring in a suburban car park produce the same auditory signal. The hippocampus provides the context that distinguishes them.[10][11]

Logue and colleagues assembled the largest structural neuroimaging dataset in PTSD research: 1,868 individuals across 16 international cohorts in the ENIGMA-PGC consortium. They found significantly smaller hippocampi in PTSD compared with trauma-exposed controls, with a Cohen's d of −0.17 (p = .00054).[11] The effect is modest in magnitude but robust, confirmed simultaneously across 16 independent cohorts, controlling for alcohol use disorder and childhood trauma. Effect sizes vary between military and civilian trauma populations and across PTSD duration, consistent with the understanding that both pre-existing vulnerability and stress-induced atrophy contribute to the finding.[11][12]

Gilbertson's monozygotic twin study resolved the directionality question. By comparing combat-exposed veterans with PTSD to their genetically identical non-combat co-twins, the study found that both brothers shared the same smaller hippocampal volume, establishing that a smaller hippocampus is a pre-existing vulnerability marker, not solely a consequence of trauma.[25]

03Evidence

The 5 Strongest Studies in PTSD Neuroscience

01The claim

The single load-bearing finding

The hero study finds −0.17 Cohen's d.

Not all evidence carries equal weight. A case study and a 16-site mega-analysis both contribute to knowledge, but they contribute differently: in confidence, in generalisability, in the strength of the causal claims they can support. The hierarchy below ranks the five most important studies in the PTSD neuroscience evidence base by methodological rigour, using a 100-point rubric that scores design quality, sample power, measurement precision, causal clarity, replication, and field influence.[8]

Pooled estimate

−0.17 Cohen's d

02How we measured

Grading the PTSD studies

Studies scored on design, sample, rigour, causality, replication, citations.

Because PTSD cannot be induced experimentally in humans, the hardest question is causation: twin and longitudinal designs that separate pre-existing vulnerability from trauma-driven change carry the most inferential weight.

Rubric weights

Design/30
Sample/20
Rigour/15
Causality/15
Replication/10
Citations/10

03The spread

Heterogeneity across 5 studies

Methodological quality across the ranked studies.

The genetic evidence adds a dimension the imaging studies cannot reach. True and colleagues' twin registry study (N = 4,042 pairs) established that genetic factors account for 13–34 percent of variance in PTSD symptom clusters, even after controlling for combat exposure, meaning some individuals are biologically predisposed to develop the disorder when exposed to equivalent trauma.[24]

Rubric spread

89 → 77 /100

Highest to lowest rubric score across the ranked studies.

04What does not hold

Negative knowledge

What the evidence base does not support.

The prospective biomarker work points toward a future in which vulnerability can be identified before the disorder develops. Harnett and colleagues, using the AURORA study's emergency department cohort, demonstrated that resting-state fMRI patterns at two weeks post-trauma predicted PTSD and depression severity at three months, with the default mode network, central executive network, and salience network each showing differential predictive power.[28] The clinical implication is significant.

The studies

5 trials. One pooled answer.

Below: the anchor study in full; then the forest plot at scale; then the supporting trials in ranked order.

The Key Study Highest rubric · 89/100 · load-bearing

01Anchor

Smaller Hippocampal Volume in Posttraumatic Stress Disorder: A Multisite ENIGMA-PGC Study

Logue 2018 Mega-Analysis · Structural MRI · Multi-Site

The hippocampal volume reduction in PTSD is real, replicable, and not an artefact of measurement inconsistency.

No other PTSD neuroimaging study approaches this sample size or site diversity. The mega-analysis design resolves debates that single-site studies could not.

Rubric breakdown

Design28/30
Sample19/20
Rigour13/15
Causality10/15
Replication10/10
Citations9/10
Total 89/100

The strongest studies, ranked by methodological weight.

Each scored 0–100 against a six-criterion rubric, tagged by design and year; the anchor leads. No study in this set reaches the rubric-90 tier.

050100 01 Logue Mega-analysis · 2018 89 02 Nievergelt 2024 84 03 Milad Neuroimaging · 2009 82 04 Gilbertson 2002 78 05 Morris Meta-analysis · 2012 77 rubric score · out of 100
Anchor (Rank 1) Supporting
Rank Authors & title Journal · Year Finding Score

02

Milad

Neurobiological Basis of Failure to Recall Extinction Memory in Posttraumatic Stress Disorder

2009

PTSD patients showed significantly decreased vmPFC activation and greater dACC activation during extinction recall, directly mapping the symptom of persistent fear to a specific circuit failure. The finding has been replicated in more than 40 subsequent fMRI studies worldwide.

82/100

03

Gilbertson

Smaller hippocampal volume predicts pathologic vulnerability to psychological trauma

2002

Non-combat co-twins of PTSD veterans had hippocampal volumes equivalent to their PTSD brothers, significantly smaller than twin pairs without PTSD. Hippocampal volume predicted PTSD symptom severity in the combat-exposed twin.

78/100

04

Nievergelt

Genome-wide association analyses identify 95 risk loci and provide insights into the neurobiology of PTSD

2024

Identified 95 genome-wide significant loci (80 novel), implicating 43 causal genes across neurotransmitter modulators, synaptic structure genes, and immune regulators. Multi-ancestry design confirms findings generalise beyond European populations. Total sample approximately 1.28 million individuals, including ~150,760 PTSD cases.

84/100

05

Morris

Relations among PTSD, Comorbid Major Depression, and HPA Function: A Systematic Review and Meta-Analysis

2012

PTSD is associated with significantly reduced daily cortisol output (d = −0.36); comorbid PTSD and major depression produces a larger deficit (d = −0.65). Enhanced dexamethasone suppression confirms heightened HPA negative feedback: the opposite pattern from acute stress.

77/100

04Stakes

The Cost of a Brain That Cannot Stand Down

PTSD's circuit failures do not stay inside the skull. They cascade outward into cognition, cardiovascular health, occupational function, and survival itself.

01 System 01 · Cognitive

Verbal Learning and Processing Speed

Scott and colleagues' 60-study meta-analysis (N = 4,108) found the largest neurocognitive deficits in verbal learning (d = −0.62) and information processing speed (d = −0.59).[30] Petzold and Bunzeck's 47-study meta-analysis confirmed medium-magnitude episodic memory impairment (d = −0.50).[31] These deficits are not explained by trauma exposure alone: they are specific to the PTSD diagnosis.

In practice

difficulty concentrating, words slipping away mid-sentence, reading the same paragraph three times

02 System 02 · Cardiovascular

Heart Disease and Stroke

Edmondson's meta-analysis of 402,274 individuals found PTSD confers a 55 percent increased risk of coronary heart disease (HR = 1.55), with 27 percent remaining after controlling for depression.[32] Padhi's 20-study analysis found stroke risk more than doubles (HR = 2.07).[33] PTSD is an independent cardiovascular risk factor, not mediated entirely through depression or lifestyle.

In practice

unexplained chest tightness, elevated resting heart rate, a body perpetually braced for impact

03
System 03 · Substance Use and Occupation

Comorbidity and Work Capacity

Approximately 46.4 percent of PTSD patients meet criteria for a co-occurring substance use disorder, a rate 2–4 times higher than the non-PTSD population.[34] Brenner and colleagues found that 74.6 percent of PTSD patients and 87.5 percent of those with complex PTSD were unable to work.[35] The occupational impact alone makes PTSD a workforce-level economic event.

In practice

self-medicating to sleep, calling in sick, the slow erosion of professional identity

04 System 04 · Mortality

Suicide Risk

Fox and colleagues' nationwide Swedish cohort (N = 3.1 million) found that PTSD independently doubles the risk of death by suicide after full adjustment for prior psychiatric diagnoses: HR = 2.16 (95% CI: 1.86–2.50).[36] Crude mortality rates (53.9 versus 12.9 per 100,000) illustrate the raw incidence gap, though the adjusted figure is the defensible risk estimate. This is not comorbid depression driving the finding. It is PTSD itself.

95% This is not comorbid depression driving the finding. It is PTSD itself.
In practice

exhaustion that sleep cannot fix, a narrowing of reasons to continue, the conviction that nothing will change

05Protocol

An Evidence-Based PTSD Recovery Protocol

Every evidence-based PTSD treatment works by the same underlying mechanism: repeated exposure to the threat cue in a context where the prefrontal cortex can re-learn safety. The steps differ in method. The biology is identical.

The protocol, as a sequence.

Weeks 1–15 → Alternative → Adjunct → Ongoing

Weeks 1–15 01 Trauma-FocusedPsychotherapy Alternative 02 EMDR as First-LineEquivalent Adjunct 03 PharmacotherapyWhen Needed Ongoing 04 Neuroplasticity Support
01 Step 01 · Weeks 1–15

Trauma-Focused Psychotherapy

Engage in Prolonged Exposure or Cognitive Processing Therapy with a trained clinician: 8–15 weekly sessions.

Why

PE retrains the vmPFC's inhibitory control through direct confrontation with trauma memories, a process called imaginal exposure; CPT targets the maladaptive appraisals maintaining the threat state. Schnurr's 916-patient RCT (the largest PTSD psychotherapy trial) found PE produced large symptom reductions (SMD = 0.99); Asmundson's meta-analysis found the average CPT patient fared better than 89 percent of controls.[38][40]

15week Engage in Prolonged Exposure or Cognitive Processing Therapy with a trained…
Common mistake

Avoiding trauma-focused therapy out of fear of symptom worsening. Avoidance maintains the fear circuit. Controlled exposure under therapeutic support is the corrective mechanism.

02 Step 02 · Alternative

EMDR as First-Line Equivalent

Consider EMDR (6–12 sessions) as a guideline-endorsed alternative with equivalent effect sizes.

Why

Chen's 26-RCT meta-analysis found significant PTSD symptom reduction (Hedges' g = −0.662) and depression reduction (g = −0.643).[41] International guidelines (APA, NICE, ISTSS) endorse EMDR as a first-line treatment equivalent to trauma-focused CBT.[42] The specific contribution of the eye movement component remains scientifically contested; efficacy does not depend on resolving that question.

Common mistake

Dismissing EMDR as "alternative medicine." The effect sizes are equivalent to PE and CPT in head-to-head comparisons.

03 Step 03 · Adjunct

Pharmacotherapy When Needed

Use sertraline or paroxetine as adjuncts when psychotherapy alone is insufficient, not as a substitute for trauma-focused therapy.

Why

Jia's 52-RCT meta-analysis found an overall pharmacological response rate of 39 percent, substantially lower than the psychotherapy response rates.[45] Prazosin, which targets the noradrenergic arousal circuit, showed promise in a smaller trial (N = 67) but a larger NEJM trial (N = 304) found null results on all primary outcomes: clinician discretion is warranted rather than routine prescription.[43][44]

Common mistake

Using medication as a replacement for trauma-focused therapy. Pharmacotherapy manages symptoms; only exposure-based therapy addresses the circuit deficit that maintains the disorder.

04 Step 04 · Ongoing

Neuroplasticity Support

Sustain the biological conditions that enable hippocampal neurogenesis and prefrontal recovery: aerobic exercise (>=150 min/week), consistent sleep architecture (+/-30 min), alcohol avoidance.

Why

Bremner's data showed SSRI treatment (paroxetine) produced a 5 percent hippocampal volume increase at 9 months alongside 30 percent verbal memory improvement, demonstrating that the brain retains structural plasticity post-trauma.[46] Preliminary fMRI evidence suggests PE restores amygdala-hippocampus-vmPFC connectivity.[47]

150min Sustain the biological conditions that enable…
Common mistake

Treating PTSD as purely psychological. The biological substrate (hippocampal volume, cortisol calibration, synaptic connectivity) is modifiable, and modifying it supports the psychological work.

06Verdict

The verdict.

Bottom line

The brain that learned danger can learn safety again. The question is no longer whether: it is how soon and for how many.

The neuroscience of PTSD has reached a level of convergence that leaves no reasonable doubt: trauma physically reorganises the brain's threat-processing infrastructure, shrinking the hippocampus, silencing the prefrontal brake on fear, hyperactivating the noradrenergic arousal system, and recalibrating the stress axis to a baseline that expects danger as the permanent condition. These are not metaphors. They are findings replicated across mega-analyses of thousands of individuals, confirmed in controlled experiments, mapped across the genome, and quantified in meta-analyses of neuroendocrine function. The mechanism also explains why treatment works: every evidence-based PTSD therapy (Prolonged Exposure, Cognitive Processing Therapy, EMDR) operates by restoring the vmPFC's capacity to inhibit the amygdala and allowing the hippocampus to consolidate new safety memories. Understanding the circuit is not academic. It is the shortest path to knowing what to fix.

The old framing (that PTSD is a failure of mental toughness, a deficit of character, a problem that willpower should resolve) does not survive contact with the evidence. A brain whose vmPFC cannot inhibit its amygdala is not weak. It is operating according to a threat model that was accurate at the moment of trauma and has not been updated because the circuit responsible for updating it is the same circuit that was damaged.

That distinction has practical consequences. It means avoidance (the most common coping strategy among trauma survivors) is not just unhelpful but mechanistically counterproductive. Avoidance prevents the vmPFC from encountering the feared cue in a safe context, which is the only condition under which extinction learning can occur. Every day of avoidance is a day the circuit stays locked.

It also means the window for intervention is real but not infinite. The prospective biomarker work suggests that circuit-level vulnerability can be identified within two weeks of trauma exposure.[28] Early, targeted intervention during this window (before the dysregulated circuit consolidates into a chronic state) represents the most promising frontier in PTSD treatment. The science no longer asks whether trauma changes the brain. It asks how quickly we can change it back.

Same disorder. Comorbidity doubles the deficit.

PTSD depletes cortisol. Depression compounds it.

0 0.2 0.4 0.6 0.8 cortisol deficit (Cohen's d, absolute value) PTSD + COMORBID DEPRESSION · CORTISOL DEFICIT (47 STUDIES, N = 6,008) d = 0.65 PTSD ALONE · CORTISOL DEFICIT (47 STUDIES, N = 6,008) d = 0.36
01Claim

Circuit, Not Character

PTSD is a measurable failure of the brain's threat-processing infrastructure: a hyperactive amygdala, a silenced prefrontal cortex, a structurally compromised hippocampus, and a recalibrated stress axis. The evidence base includes the largest neuroimaging consortium study, the cleanest controlled fMRI experiment, and the most comprehensive GWAS ever conducted for the disorder.

Claim
02Consequence

Cascade Beyond the Brain

Left unaddressed, the circuit failure cascades into cognitive impairment, cardiovascular disease, substance dependence, occupational disability, and a more than doubled risk of death by suicide. The annual US economic burden exceeds $232 billion, a figure that understates the human cost.

Consequence
03Lever

Re-learning Safety

Every evidence-based treatment works by the same mechanism: restoring the prefrontal cortex's authority to inhibit fear and providing the hippocampus with conditions for structural recovery. The circuit that learned danger can learn safety, but only through controlled exposure, not avoidance.

Lever

Editorial confidence

High · 34 sources · Convergent evidence from mega-analysis neuroimaging, controlled fMRI experiments, multi-ancestry GWAS, neuroendocrine meta-analyses, and large-scale RCTs, replicated across independent research groups worldwide

- 30 -

Put it to work

Where this science goes next on HPC

AssessmentCrisis AssessmentScore where you actually standProtocol90-Day Crisis Readiness ProtocolTurn the mechanism into practice

07Bibliography

The bibliography.

34 sources · ~5h est. corpus read · 34 visible

RCT · 1 Meta · 8 Review · 3 Cohort · 3 Journal · 19
Type
Sort
  1. 01 Cohort

    Benjet, C., Bromet, E., Karam, E. G., Kessler, R. C., McLaughlin, K. A., Ruscio, A. M., et al2016

    The epidemiology of traumatic event exposure worldwide: results from the World Mental Health Survey Consortium

    Psychological Medicine46(2) · 327–343

    doi: 10.1017/S0033291715001981
  2. 02 Journal

    Koenen, K. C., Ratanatharathorn, A., Ng, L., McLaughlin, K. A., Bromet, E. J., Stein, D. J., et al2017

    Posttraumatic stress disorder in the World Mental Health Surveys

    Psychological Medicine47(13) · 2260–2274

    doi: 10.1017/S0033291717000708
  3. 03 Journal

    Davis, L. L., Schein, J., Cloutier, M., Gagnon-Sanschagrin, P., Maitland, J., Urganus, A., Guerin, A., Lefebvre, P., & Houle, C. R2022

    The Economic Burden of Posttraumatic Stress Disorder in the United States From a Societal Perspective

    Journal of Clinical Psychiatry83(3)

    doi: 10.4088/JCP.21m14116
  4. 04 Cohort

    Kessler, R. C., Sonnega, A., Bromet, E., Hughes, M., & Nelson, C. B1995

    Posttraumatic stress disorder in the National Comorbidity Survey

    Archives of General Psychiatry52(12) · 1048–1060

    doi: 10.1001/archpsyc.1995.03950240066012
  5. 05 Journal

    Crocq, M. A., & Crocq, L2000

    From shell shock and war neurosis to posttraumatic stress disorder: a history of psychotraumatology

    Dialogues in Clinical Neuroscience2(1) · 47–55

    doi: 10.31887/DCNS.2000.2.1/macrocq
  6. 06 Review

    Obuobi-Donkor, G., Oluwasina, F., Nkire, N., & Agyapong, V. I. O2022

    A Scoping Review on the Prevalence and Determinants of Post-Traumatic Stress Disorder among Military Personnel and Firefighters

    International Journal of Environmental Research and Public Health19(3)

    doi: 10.3390/ijerph19031565
  7. 08 Review

    Pitman, R. K., Rasmusson, A. M., Koenen, K. C., Shin, L. M., Orr, S. P., Gilbertson, M. W., Milad, M. R., & Liberzon, I2012

    Biological studies of post-traumatic stress disorder

    Nature Reviews Neuroscience13(11) · 769–787

    doi: 10.1038/nrn3339
  8. 09 Journal

    Shin, L. M., & Liberzon, I2010

    The neurocircuitry of fear, stress, and anxiety disorders

    Neuropsychopharmacology35(1) · 169–191

    doi: 10.1038/npp.2009.83
  9. 10 Journal

    Liberzon, I., & Abelson, J. L2016

    Context Processing and the Neurobiology of Post-Traumatic Stress Disorder

    Neuron92(1) · 14–30

    doi: 10.1016/j.neuron.2016.09.039
  10. 11 Journal

    Logue, M. W., van Rooij, S. J. H., Dennis, E. L., Davis, S. L., Hayes, J. P., Stevens, J. S., et al2018

    Smaller Hippocampal Volume in Posttraumatic Stress Disorder: A Multisite ENIGMA-PGC Study

    Biological Psychiatry83(3) · 244–253

    doi: 10.1016/j.biopsych.2017.09.006
  11. 12 Meta

    Bromis, K., Calem, M., Reinders, A. A. T. S., Williams, S. C. R., & Kempton, M. J2018

    Meta-Analysis of 89 Structural MRI Studies in Posttraumatic Stress Disorder and Comparison With Major Depressive Disorder

    American Journal of Psychiatry175(10) · 989–998

    doi: 10.1176/appi.ajp.2018.17111199
  12. 14 Journal

    Milad, M. R., Wright, C. I., Orr, S. P., Pitman, R. K., Quirk, G. J., & Rauch, S. L2007

    Recall of fear extinction in humans activates the ventromedial prefrontal cortex and hippocampus in concert

    Biological Psychiatry61(9) · 1016–1023

    doi: 10.1016/j.biopsych.2006.10.011
  13. 15 Review

    Milad, M. R., & Quirk, G. J2012

    Fear extinction as a model for translational neuroscience: Ten years of progress

    Annual Review of Psychology129–151

    doi: 10.1146/annurev.psych.121208.131631
  14. 16 Journal

    Milad, M. R., Pitman, R. K., Ellis, C. B., Gold, A. L., Shin, L. M., Lasko, N. B., Zeidan, M. A., Handwerger, K., Orr, S. P., & Rauch, S. L2009

    Neurobiological Basis of Failure to Recall Extinction Memory in Posttraumatic Stress Disorder

    Biological Psychiatry66(12) · 1075–1082

    doi: 10.1016/j.biopsych.2009.06.026
  15. 24 Journal

    True, W. R., Rice, J., Eisen, S. A., Heath, A. C., Goldberg, J., Lyons, M. J., & Nowak, J1993

    A twin study of genetic and environmental contributions to liability for posttraumatic stress disorder

    Archives of General Psychiatry50(4) · 257–264

    doi: 10.1001/archpsyc.1993.01820160019002
  16. 25 Journal

    Gilbertson, M. W., Shenton, M. E., Ciszewski, A., Kasai, K., Lasko, N. B., Orr, S. P., & Pitman, R. K2002

    Smaller hippocampal volume predicts pathologic vulnerability to psychological trauma

    Nature Neuroscience5(11) · 1242–1247

    doi: 10.1038/nn958
  17. 28 Journal

    Harnett, N. G., Finegold, K. E., Lebois, L. A. M., van Rooij, S. J. H., Ely, T. D., Murty, V. P., et al2021

    Prognostic neuroimaging biomarkers of trauma-related psychopathology: resting-state fMRI shortly after trauma predicts future PTSD and depression symptoms in the AURORA study

    Neuropsychopharmacology46(7) · 1263–1271

    doi: 10.1038/s41386-020-00946-8
  18. 30 Meta

    Scott, J. C., Matt, G. E., Wrocklage, K. M., Crnich, C., Jordan, J., Southwick, S. M., Krystal, J. H., & Schweinsburg, B. C2014

    A quantitative meta-analysis of neurocognitive functioning in posttraumatic stress disorder

    Psychological Bulletin141(1) · 105–140

    doi: 10.1037/a0038039
  19. 31 Meta

    Petzold, M., & Bunzeck, N2022

    Impaired episodic memory in PTSD patients, A meta-analysis of 47 studies

    Frontiers in Psychiatry

    doi: 10.3389/fpsyt.2022.909442
  20. 32 Meta

    Edmondson, D., Kronish, I. M., Shaffer, J. A., Falzon, L., & Burg, M. M2013

    Posttraumatic stress disorder and risk for coronary heart disease: A meta-analytic review

    American Heart Journal166(5) · 806–814

    doi: 10.1016/j.ahj.2013.07.031
  21. 33 Meta

    Padhi, B. K., Khatib, M. N., Abu Serhan, H., Gaidhane, A. M., Rustagi, S., Zahiruddin, Q. S., Sharma, R. K., & Satapathy, P2024

    Cardiovascular impact of post-traumatic stress disorder: A systematic review and meta-analysis

    Current Problems in Cardiology49(8)

    doi: 10.1016/j.cpcardiol.2024.102632
  22. 34 Journal

    McCauley, J. L., Killeen, T., Gros, D. F., Brady, K. T., & Back, S. E2012

    Posttraumatic stress disorder and co-occurring substance use disorders: Advances in assessment and treatment

    Clinical Psychology: Science and Practice19(3) · 283–304

    doi: 10.1111/cpsp.12006
  23. 35 Journal

    Brenner, L., Köllner, V., & Bachem, R2019

    Symptom burden and work-related impairment among patients with PTSD and complex PTSD

    European Journal of Psychotraumatology10(1)

    doi: 10.1080/20008198.2019.1694766
  24. 36 Cohort

    Fox, V., Dalman, C., Dal, H., Hollander, A.-C., Kirkbride, J. B., & Pitman, A2021

    Suicide risk in people with post-traumatic stress disorder: A cohort study of 3.1 million people in Sweden

    Journal of Affective Disorders609–616

    doi: 10.1016/j.jad.2020.10.009
  25. 38 RCT

    Schnurr, P. P., Chard, K. M., Ruzek, J. I., Chow, B. K., Resick, P. A., Foa, E. B., et al2022

    Comparison of Prolonged Exposure vs Cognitive Processing Therapy for Treatment of PTSD Among US Veterans: A Randomized Clinical Trial

    JAMA Network Open5(1)

    doi: 10.1001/jamanetworkopen.2021.36921
  26. 39 Journal

    McLean, C. P., & Foa, E. B2024

    State of the science: Prolonged exposure therapy for the treatment of posttraumatic stress disorder

    Journal of Traumatic Stress37(4) · 535–550

    doi: 10.1002/jts.23046
  27. 40 Meta

    Asmundson, G. J. G., Thorisdottir, A. S., Roden-Foreman, J. W., et al2019

    A meta-analytic review of cognitive processing therapy for adults with posttraumatic stress disorder

    Cognitive Behaviour Therapy48(1) · 1–14

    doi: 10.1080/16506073.2018.1522371
  28. 41 Meta

    Chen, Y.-R., Hung, K.-W., Tsai, J.-C., et al2014

    Efficacy of eye-movement desensitization and reprocessing for patients with posttraumatic-stress disorder: A meta-analysis of randomized controlled trials

    PLoS One9(8)

    doi: 10.1371/journal.pone.0103676
  29. 42 Journal

    de Jongh, A., de Roos, C., & El-Leithy, S2024

    State of the science: Eye movement desensitization and reprocessing (EMDR) therapy

    Journal of Traumatic Stress37(2) · 205–216

    doi: 10.1002/jts.23012
  30. 43 Journal

    Raskind, M. A., Peterson, K., Williams, T., et al2013

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