Post-traumatic stress disorder is a trauma- and stressor-related psychiatric disorder characterized by intrusive recollections, avoidance, negative mood or cognition changes, and hyperarousal after traumatic exposure.
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Conditions with similar clinical presentations that must be differentiated from Post-Traumatic Stress Disorder:
name: Post-Traumatic Stress Disorder
creation_date: "2026-04-24T20:56:38Z"
updated_date: "2026-04-27T15:25:26Z"
category: Psychiatric
description: >-
Post-traumatic stress disorder is a trauma- and stressor-related psychiatric
disorder characterized by intrusive recollections, avoidance, negative mood
or cognition changes, and hyperarousal after traumatic exposure.
disease_term:
preferred_term: post-traumatic stress disorder
term:
id: MONDO:0005146
label: post-traumatic stress disorder
parents:
- Mental Health Disorder
prevalence:
- population: trauma-exposed populations across PTSD prevalence reviews
percentage: 23.95
notes: >-
Umbrella-review pooled PTSD prevalence across eligible reviews; estimates
vary widely by population, trauma context, and measurement approach.
evidence:
- reference: DOI:10.1017/S0033291724002319
reference_title: "Posttraumatic stress disorder (PTSD) prevalence: an umbrella review"
supports: SUPPORT
evidence_source: HUMAN_CLINICAL
snippet: >-
Overall PTSD prevalence was 23.95% (95% confidence interval 95% CI
20.74-27.15), with no publication bias or significant small-study effects,
but a high level of heterogeneity between meta-analyses.
explanation: >-
Umbrella-review evidence supports PTSD as a common outcome in
trauma-exposed contexts while emphasizing heterogeneity.
- population: civilians residing in armed conflict-affected regions
percentage: 23.70
notes: >-
Meta-analysis estimate for PTSD symptoms among war-afflicted civilians.
evidence:
- reference: DOI:10.1136/gpsych-2023-101438
reference_title: "Prevalence of post-traumatic stress disorder and depressive symptoms among civilians residing in armed conflict-affected regions: a systematic review and meta-analysis"
supports: SUPPORT
evidence_source: HUMAN_CLINICAL
snippet: >-
We estimated a prevalence of 23.70% (95% CI 19.50% to 28.40%) for PTSD
symptoms and 25.60% (95% CI 20.70% to 31.10%) for depressive features
among war-afflicted civilians.
explanation: >-
Conflict-exposed civilian populations have a high pooled PTSD-symptom
burden.
pathophysiology:
- name: Traumatic Stress Exposure
description: >-
Exposure to psychologically threatening or horrific traumatic events is the
initiating environmental context required for PTSD.
biological_processes:
- preferred_term: response to stress
term:
id: GO:0006950
label: response to stress
modifier: ABNORMAL
downstream:
- target: Polygenic Susceptibility to PTSD after Trauma
description: >-
Trauma exposure is required, while inherited liability modifies who
develops persistent PTSD symptoms after exposure.
evidence:
- reference: DOI:10.1038/s41398-023-02313-9
reference_title: Polygenic risk for mental disorders as predictors of posttraumatic stress disorder after mild traumatic brain injury
supports: SUPPORT
evidence_source: HUMAN_CLINICAL
snippet: >-
Many patients with mild traumatic brain injury (mTBI) are at risk for
mental health problems such as posttraumatic stress disorder (PTSD).
explanation: >-
TRACK-TBI frames PTSD risk in a post-trauma cohort and tests genetic
susceptibility in that context.
- target: HPA-Axis Regulation Alteration
description: >-
Traumatic stress activates stress-response pathways that can become
persistently dysregulated in PTSD.
evidence:
- reference: PMID:30790632
reference_title: "HPA axis regulation in posttraumatic stress disorder: A meta-analysis focusing on potential moderators."
supports: SUPPORT
evidence_source: HUMAN_CLINICAL
snippet: >-
Posttraumatic stress disorder (PTSD) is often associated with
alterations in the hypothalamic-pituitary-adrenal (HPA) axis.
explanation: >-
Meta-analysis supports HPA-axis involvement after PTSD develops.
evidence:
- reference: DOI:10.1192/bja.2024.27
reference_title: "Assessment and diagnosis of post-traumatic stress disorders (PTSDs) for medico-legal and other clinical purposes: DSM-5-TR PTSD, ICD-11 PTSD and ICD-11 complex PTSD"
supports: SUPPORT
evidence_source: OTHER
snippet: >-
Given ongoing debate, the article proposes that trauma exposure is best
defined in future iterations of the DSM and ICD as exposure to one or more
psychologically threatening or horrific experiences that are overwhelming.
explanation: >-
The diagnostic review supports traumatic exposure as the initiating
context for PTSD assessment.
- name: Polygenic Susceptibility to PTSD after Trauma
description: >-
Common-variant genetic liability increases the probability of probable PTSD
after traumatic injury, but does not by itself cause PTSD without a trauma
context. PTSD genetic liability overlaps with genetic risk for other
neurodegenerative conditions including REM sleep behavior disorder, suggesting
shared genetic mechanisms underlying trauma response and neurodegenerative
risk.
downstream:
- target: Epigenetic Stress-Response Regulation
description: >-
Genetic and environmental susceptibility are represented as upstream of
molecular regulation systems involved in stress responses.
evidence:
- reference: DOI:10.1038/s41398-023-02313-9
reference_title: Polygenic risk for mental disorders as predictors of posttraumatic stress disorder after mild traumatic brain injury
supports: SUPPORT
evidence_source: HUMAN_CLINICAL
snippet: >-
We used data from individuals of European ancestry with mTBI enrolled in
TRACK-TBI (n = 714), a prospective longitudinal study of level 1 trauma
center patients.
explanation: >-
Prospective trauma-center cohort data support inherited liability as a
post-trauma PTSD risk modifier.
- reference: DOI:10.1038/s41398-023-02313-9
reference_title: Polygenic risk for mental disorders as predictors of posttraumatic stress disorder after mild traumatic brain injury
supports: SUPPORT
evidence_source: HUMAN_CLINICAL
snippet: >-
The adjusted odds of PTSD in the uppermost PTSD-PRS quintile was nearly
four times higher (aOR = 3.71, 95% CI 1.80–7.65) than in the lowest
PTSD-PRS quintile.
explanation: >-
A PTSD polygenic risk score predicted probable PTSD after mild traumatic
brain injury.
- reference: PMID:42168223
reference_title: Genetic associations between post-traumatic stress disorder and REM-sleep behavior disorder.
supports: SUPPORT
evidence_source: HUMAN_CLINICAL
snippet: >-
While not supporting a causal relationship, genetic analyses revealed a
significant association between PTSD and iRBD, consistent with the
exploratory imaging substudy. These findings suggest that individuals
genetically at risk for PTSD may also be at higher risk for iRBD.
explanation: >-
Genome-wide genetic analyses support shared genetic predisposition between
PTSD and isolated REM sleep behavior disorder, with implications for
understanding both psychiatric and neurodegenerative disease mechanisms.
- name: Epigenetic Stress-Response Regulation
description: >-
Trauma and other environmental stressors are associated with epigenetic
mechanisms affecting HPA-axis, neurotrophic, neurotransmitter, and immune
systems relevant to PTSD.
biological_processes:
- preferred_term: chromatin organization
term:
id: GO:0006325
label: chromatin organization
modifier: ABNORMAL
downstream:
- target: HPA-Axis Regulation Alteration
description: >-
Epigenetic changes in HPA-axis-related genes are modeled upstream of
altered endocrine stress regulation.
- target: Neuroimmune Activation
description: >-
Epigenetic changes in immune-function genes are modeled upstream of
altered inflammatory signaling.
evidence:
- reference: DOI:10.1159/000541822
reference_title: "Epigenetic Alterations in Post-Traumatic Stress Disorder: Comprehensive Review of Molecular Markers"
supports: SUPPORT
evidence_source: HUMAN_CLINICAL
snippet: >-
Studies show that environmental stressors can induce various epigenetic
changes that shape the PTSD phenotype.
explanation: >-
Review evidence supports environmentally induced epigenetic regulation as
a PTSD susceptibility and phenotype mechanism.
- reference: DOI:10.1159/000541822
reference_title: "Epigenetic Alterations in Post-Traumatic Stress Disorder: Comprehensive Review of Molecular Markers"
supports: SUPPORT
evidence_source: HUMAN_CLINICAL
snippet: >-
This review investigated gene methylation changes in association with
PTSD, including those related to the hypothalamic-pituitary-adrenal axis,
brain-derived neurotrophic factor, neurotransmitters, and immune system
functioning, as well as the role of histones and regulatory noncoding
RNAs.
explanation: >-
The reviewed molecular systems map directly to HPA, neurotransmission,
and immune pathophysiology nodes.
- name: HPA-Axis Regulation Alteration
description: >-
PTSD is associated with altered hypothalamic-pituitary-adrenal axis
regulation, including lower morning and 24-hour cortisol in meta-analysis,
though moderator patterns are inconsistent.
biological_processes:
- preferred_term: response to stress
term:
id: GO:0006950
label: response to stress
modifier: ABNORMAL
locations:
- preferred_term: hypothalamus
term:
id: UBERON:0001898
label: hypothalamus
- preferred_term: pituitary gland
term:
id: UBERON:0000007
label: pituitary gland
- preferred_term: adrenal gland
term:
id: UBERON:0002369
label: adrenal gland
downstream:
- target: Neuroimmune Activation
description: >-
Stress-hormone regulation interacts with inflammatory signaling in PTSD
models and clinical studies.
evidence:
- reference: PMID:31991875
reference_title: "Inflammation in Post-Traumatic Stress Disorder (PTSD): A Review of Potential Correlates of PTSD with a Neurological Perspective."
supports: PARTIAL
evidence_source: HUMAN_CLINICAL
snippet: >-
these alterations may further reinforce the related clinical symptoms
of PTSD such as sustained fear and anxiety.
explanation: >-
The review links glucocorticoid signaling, HPA-axis function, immune
function, and PTSD symptoms, but presents a proposed pathway rather than
a single definitive causal experiment.
- target: Threat-Circuit and Fear-Extinction Dysregulation
description: >-
Stress-axis dysregulation affects limbic and prefrontal systems that
regulate fear, anxiety, and memory.
evidence:
- reference: PMID:35927237
reference_title: The role of the immune system in posttraumatic stress disorder.
supports: PARTIAL
evidence_source: HUMAN_CLINICAL
snippet: >-
Importantly, inflammation can influence neural circuits and
neurotransmitter signaling in regions of the brain relevant to fear,
anxiety, and emotion regulation.
explanation: >-
This supports downstream circuit effects through immune signaling;
stress-axis involvement is part of the broader PTSD biology.
evidence:
- reference: PMID:30790632
reference_title: "HPA axis regulation in posttraumatic stress disorder: A meta-analysis focusing on potential moderators."
supports: SUPPORT
evidence_source: HUMAN_CLINICAL
snippet: >-
Morning and 24 h cortisol were significantly lower in PTSD than in
controls (g = -0.21; 95% CI: -0.42-(-0.01); g = -0.31; CI:
-0.60-(-0.03)).
explanation: >-
Meta-analysis supports lower cortisol measures in PTSD compared with
controls.
- name: Neuroimmune Activation
description: >-
PTSD is associated with peripheral inflammatory markers and immune-system
changes that may affect brain circuits involved in fear, anxiety, and
emotion regulation.
cell_types:
- preferred_term: microglial cell
term:
id: CL:0000129
label: microglial cell
- preferred_term: astrocyte
term:
id: CL:0000127
label: astrocyte
biological_processes:
- preferred_term: inflammatory response
term:
id: GO:0006954
label: inflammatory response
modifier: INCREASED
- preferred_term: cytokine production
term:
id: GO:0001816
label: cytokine production
modifier: INCREASED
- preferred_term: cytokine-mediated signaling pathway
term:
id: GO:0019221
label: cytokine-mediated signaling pathway
modifier: ABNORMAL
locations:
- preferred_term: amygdala
term:
id: UBERON:0001876
label: amygdala
- preferred_term: hippocampal formation
term:
id: UBERON:0002421
label: hippocampal formation
- preferred_term: prefrontal cortex
term:
id: UBERON:0000451
label: prefrontal cortex
downstream:
- target: Threat-Circuit and Fear-Extinction Dysregulation
description: >-
Inflammatory markers are associated with structural and functional
alterations in amygdala, hippocampus, and frontal cortex.
evidence:
- reference: PMID:31991875
reference_title: "Inflammation in Post-Traumatic Stress Disorder (PTSD): A Review of Potential Correlates of PTSD with a Neurological Perspective."
supports: SUPPORT
evidence_source: HUMAN_CLINICAL
snippet: >-
neuroimaging-based studies demonstrated that altered inflammatory
markers are associated with structural and functional alterations in
brain regions that are responsible for the regulation of stress and
emotion, including the amygdala, hippocampus, and frontal cortex.
explanation: >-
This directly links inflammatory markers with PTSD-relevant
stress/emotion brain circuitry.
evidence:
- reference: PMID:35927237
reference_title: The role of the immune system in posttraumatic stress disorder.
supports: SUPPORT
evidence_source: HUMAN_CLINICAL
snippet: >-
some individuals with PTSD also exhibit elevated concentrations of
inflammatory markers, including C-reactive protein, interleukin-6, and
tumor necrosis factor-α.
explanation: >-
Review evidence supports inflammatory-marker elevation in a subset of
individuals with PTSD.
- reference: PMID:31991875
reference_title: "Inflammation in Post-Traumatic Stress Disorder (PTSD): A Review of Potential Correlates of PTSD with a Neurological Perspective."
supports: SUPPORT
evidence_source: HUMAN_CLINICAL
snippet: >-
Major findings included elevated levels of serum proinflammatory cytokines
in individuals with PTSD across various trauma types, as compared with
those without PTSD.
explanation: >-
Structured review evidence supports increased proinflammatory cytokines
across trauma contexts.
- name: Threat-Circuit and Fear-Extinction Dysregulation
description: >-
Altered amygdala, hippocampal, and prefrontal cortical function affects
threat detection, emotional regulation, fear reactivity, and traumatic
memory processing.
cell_types:
- preferred_term: neuron
term:
id: CL:0000540
label: neuron
biological_processes:
- preferred_term: learning
term:
id: GO:0007612
label: learning
modifier: ABNORMAL
- preferred_term: memory
term:
id: GO:0007613
label: memory
modifier: ABNORMAL
- preferred_term: modulation of chemical synaptic transmission
term:
id: GO:0050804
label: modulation of chemical synaptic transmission
modifier: ABNORMAL
locations:
- preferred_term: amygdala
term:
id: UBERON:0001876
label: amygdala
- preferred_term: hippocampal formation
term:
id: UBERON:0002421
label: hippocampal formation
- preferred_term: prefrontal cortex
term:
id: UBERON:0000451
label: prefrontal cortex
downstream:
- target: Intrusive Re-experiencing
description: >-
Abnormal threat and memory circuitry contributes to intrusive traumatic
recollections and flashbacks.
evidence:
- reference: PMID:31991875
reference_title: "Inflammation in Post-Traumatic Stress Disorder (PTSD): A Review of Potential Correlates of PTSD with a Neurological Perspective."
supports: PARTIAL
evidence_source: HUMAN_CLINICAL
snippet: >-
Dysfunction in the regions of the prefrontal cortex, amygdala, and
hippocampus are then responsible for functions of executive control,
emotional lability, fear reactivity, and retrieval of traumatic memories
as demonstrated in PTSD.
explanation: >-
The review links dysfunction in these regions to traumatic-memory
retrieval and fear reactivity.
- target: Hyperarousal and Anxiety
description: >-
Altered threat circuitry contributes to persistent threat perception,
hyperarousal, and anxiety.
evidence:
- reference: PMID:31991875
reference_title: "Inflammation in Post-Traumatic Stress Disorder (PTSD): A Review of Potential Correlates of PTSD with a Neurological Perspective."
supports: SUPPORT
evidence_source: HUMAN_CLINICAL
snippet: >-
particular brain regions may be identifiable as neural correlates of PTSD,
including the prefrontal cortex, hippocampus, and amygdala of the brain.
explanation: >-
Review evidence supports amygdala-hippocampal-prefrontal circuitry as a
PTSD-relevant neurobiological substrate.
phenotypes:
- name: Intrusive Re-experiencing
category: Behavioral
description: >-
Recurrent intrusive traumatic memories, flashbacks, and nightmares.
phenotype_term:
preferred_term: Intrusive re-experiencing
diagnostic: true
evidence:
- reference: DOI:10.1159/000541822
reference_title: "Epigenetic Alterations in Post-Traumatic Stress Disorder: Comprehensive Review of Molecular Markers"
supports: SUPPORT
evidence_source: HUMAN_CLINICAL
snippet: >-
PTSD is characterized by nightmares, flashbacks and avoidance of stressors.
explanation: >-
Review abstract supports nightmares and flashbacks as PTSD symptom
features.
- name: Avoidance of Trauma Reminders
category: Behavioral
description: >-
Avoidance of trauma-related internal experiences or external reminders.
phenotype_term:
preferred_term: Avoidance of trauma reminders
diagnostic: true
evidence:
- reference: DOI:10.1159/000541822
reference_title: "Epigenetic Alterations in Post-Traumatic Stress Disorder: Comprehensive Review of Molecular Markers"
supports: SUPPORT
evidence_source: HUMAN_CLINICAL
snippet: >-
PTSD is characterized by nightmares, flashbacks and avoidance of stressors.
explanation: >-
The abstract identifies avoidance as a core PTSD symptom feature.
- name: Hyperarousal and Anxiety
category: Behavioral
description: >-
Persistent threat perception, heightened arousal, fearfulness, and anxiety.
phenotype_term:
preferred_term: Anxiety
term:
id: HP:0000739
label: Anxiety
diagnostic: true
evidence:
- reference: DOI:10.1192/bja.2024.27
reference_title: "Assessment and diagnosis of post-traumatic stress disorders (PTSDs) for medico-legal and other clinical purposes: DSM-5-TR PTSD, ICD-11 PTSD and ICD-11 complex PTSD"
supports: SUPPORT
evidence_source: OTHER
snippet: >-
the clinical presentation of PTSDs; psychological models of PTSDs; how to
approach assessment and differential diagnosis
explanation: >-
The diagnostic review supports clinical presentation and assessment of
PTSD symptom clusters, including arousal and threat-related symptoms.
- name: Depressive Symptoms
category: Behavioral
description: >-
Depressive symptoms can co-occur with PTSD and complicate assessment,
functioning, and outcomes.
phenotype_term:
preferred_term: Depression
term:
id: HP:0000716
label: Depression
evidence:
- reference: DOI:10.1136/gpsych-2023-101438
reference_title: "Prevalence of post-traumatic stress disorder and depressive symptoms among civilians residing in armed conflict-affected regions: a systematic review and meta-analysis"
supports: SUPPORT
evidence_source: HUMAN_CLINICAL
snippet: >-
We estimated a prevalence of 23.70% (95% CI 19.50% to 28.40%) for PTSD
symptoms and 25.60% (95% CI 20.70% to 31.10%) for depressive features
among war-afflicted civilians.
explanation: >-
Meta-analysis supports frequent depressive features in a high-risk PTSD
context.
diagnosis:
- name: Clinician-administered PTSD assessment
presence: >-
PTSD diagnosis is established by clinical assessment using diagnostic
criteria and validated clinician-administered interviews, with screening
questionnaires used as aids rather than stand-alone diagnostics.
diagnosis_term:
preferred_term: clinical assessment
term:
id: MAXO:0000487
label: clinical assessment
evidence:
- reference: DOI:10.1192/bja.2024.27
reference_title: "Assessment and diagnosis of post-traumatic stress disorders (PTSDs) for medico-legal and other clinical purposes: DSM-5-TR PTSD, ICD-11 PTSD and ICD-11 complex PTSD"
supports: SUPPORT
evidence_source: OTHER
snippet: >-
This article provides an overview and critique of key topics, literature
and principles to inform comprehensive and meticulous assessment of PTSDs.
explanation: >-
Diagnostic review supports comprehensive clinical assessment for PTSD.
- reference: DOI:10.1002/jts.23013
reference_title: "A clinician's guide to the 2023 VA/DoD Clinical Practice Guideline for Management of Posttraumatic Stress Disorder and Acute Stress Disorder"
supports: SUPPORT
evidence_source: OTHER
snippet: >-
The CPG recommendations are accompanied by a clinical algorithm, which
incorporates principles of evidence-based practice, shared
decision-making, and functional and contextual assessments of goals and
outcomes.
explanation: >-
Guideline summary supports structured clinical algorithms and contextual
functional assessment.
- name: Biomarker and neuroimaging research is not diagnostic
presence: >-
Inflammatory, endocrine, imaging, and genetic markers support mechanistic
research but are not established as stand-alone diagnostic tests.
diagnosis_term:
preferred_term: clinical assessment
term:
id: MAXO:0000487
label: clinical assessment
evidence:
- reference: PMID:31991875
reference_title: "Inflammation in Post-Traumatic Stress Disorder (PTSD): A Review of Potential Correlates of PTSD with a Neurological Perspective."
supports: SUPPORT
evidence_source: HUMAN_CLINICAL
snippet: >-
Future studies that utilize both central and peripheral inflammatory
markers are warranted to elucidate the underlying neurological pathway of
the pathophysiology of PTSD.
explanation: >-
The review frames biomarkers as needing further study for mechanisms,
not as current diagnostic replacements.
differential_diagnoses:
- name: Acute stress disorder
description: >-
Acute stress disorder is considered when trauma-related symptoms occur in
the immediate post-trauma period before persistence thresholds for PTSD are
met.
disease_term:
preferred_term: acute stress disorder
term:
id: MONDO:0003763
label: acute stress disorder
evidence:
- reference: DOI:10.1002/jts.23013
reference_title: "A clinician's guide to the 2023 VA/DoD Clinical Practice Guideline for Management of Posttraumatic Stress Disorder and Acute Stress Disorder"
supports: SUPPORT
evidence_source: OTHER
snippet: >-
The 2023 Department of Veterans Affairs /Department of Defense Clinical
Practice Guideline for Management of Posttraumatic Stress Disorder and
Acute Stress Disorder is described herein.
explanation: >-
The guideline covers PTSD and acute stress disorder together, supporting
the distinction in post-trauma assessment.
- name: Adjustment disorder
description: >-
Adjustment disorder can follow stressors and cause distress or impairment,
but does not require the full PTSD trauma and symptom-cluster profile.
disease_term:
preferred_term: adjustment disorder
term:
id: MONDO:0003265
label: adjustment disorder
evidence:
- reference: DOI:10.1192/bja.2024.27
reference_title: "Assessment and diagnosis of post-traumatic stress disorders (PTSDs) for medico-legal and other clinical purposes: DSM-5-TR PTSD, ICD-11 PTSD and ICD-11 complex PTSD"
supports: PARTIAL
evidence_source: OTHER
snippet: >-
A range of topics relevant to assessment are discussed, including: the
complex relationship between trauma and PTSDs; DSM-5-TR PTSD and ICD-11
PTSD and complex PTSD diagnoses and the similarities and differences
between them; the clinical presentation of PTSDs; psychological models of
PTSDs; how to approach assessment and differential diagnosis
explanation: >-
The abstract supports differential-diagnosis assessment, but does not
specifically name adjustment disorder.
- name: Major depressive disorder
description: >-
Depressive symptoms frequently co-occur in trauma-exposed populations and
can overlap with PTSD negative mood and cognition symptoms.
disease_term:
preferred_term: major depressive disorder
term:
id: MONDO:0002009
label: major depressive disorder
evidence:
- reference: DOI:10.1136/gpsych-2023-101438
reference_title: "Prevalence of post-traumatic stress disorder and depressive symptoms among civilians residing in armed conflict-affected regions: a systematic review and meta-analysis"
supports: SUPPORT
evidence_source: HUMAN_CLINICAL
snippet: >-
This meta-analysis aims to estimate the prevalence of post-traumatic
stress disorder (PTSD) and depressive symptoms among civilians residing in
armed conflict-affected regions.
explanation: >-
The meta-analysis supports close assessment of depressive symptoms in
PTSD-prone trauma contexts.
- name: Substance use disorder
description: >-
Substance use disorder commonly co-occurs with PTSD and can complicate
symptom attribution, treatment planning, and outcomes.
disease_term:
preferred_term: substance-related disorder
term:
id: MONDO:0002494
label: substance-related disorder
evidence:
- reference: DOI:10.1002/jts.23049
reference_title: "State of the Science: Treatment of comorbid posttraumatic stress disorder and substance use disorders"
supports: SUPPORT
evidence_source: HUMAN_CLINICAL
snippet: >-
Posttraumatic stress disorder (PTSD) and substance use disorders (SUDs)
co-occur at high rates, with research showing that up to nearly 60% of
individuals with PTSD also suffer from an alcohol and/or drug use disorder.
explanation: >-
Co-occurrence at high rates supports assessment for SUD during PTSD
differential and comorbidity evaluation.
treatments:
- name: Trauma-focused psychotherapy
description: >-
First-line trauma-focused psychotherapies for PTSD include exposure therapy
such as prolonged exposure, cognitive processing therapy, trauma-focused
cognitive behavioral therapy, EMDR, and narrative exposure therapy.
treatment_term:
preferred_term: cognitive behavior therapy
term:
id: MAXO:0000883
label: cognitive behavior therapy
target_phenotypes:
- preferred_term: Intrusive re-experiencing
- preferred_term: Avoidance of trauma reminders
- preferred_term: Anxiety
term:
id: HP:0000739
label: Anxiety
evidence:
- reference: PMID:26574151
reference_title: "Psychological treatments for adults with posttraumatic stress disorder: A systematic review and meta-analysis."
supports: SUPPORT
evidence_source: HUMAN_CLINICAL
snippet: >-
Evidence supports efficacy of exposure therapy (high SOE) including the
manualized version Prolonged Exposure (PE); cognitive therapy (CT),
cognitive processing therapy (CPT), cognitive behavioral therapy
(CBT)-mixed therapies (moderate SOE); eye movement desensitization and
reprocessing (EMDR) and narrative exposure therapy (low-moderate SOE).
explanation: >-
Systematic review evidence supports trauma-focused psychotherapy options
including PE, CPT, CBT-based therapies, EMDR, and narrative exposure
therapy for adults with PTSD.
- reference: PMID:35044471
reference_title: "Comparison of Prolonged Exposure vs Cognitive Processing Therapy for Treatment of Posttraumatic Stress Disorder Among US Veterans: A Randomized Clinical Trial."
supports: SUPPORT
evidence_source: HUMAN_CLINICAL
snippet: >-
This randomized clinical trial found that although PE was statistically
more effective than CPT, the difference was not clinically significant,
and improvements in PTSD were meaningful in both treatment groups.
explanation: >-
A large randomized trial supports both prolonged exposure and cognitive
processing therapy as effective PTSD psychotherapies.
- name: Serotonergic antidepressant pharmacotherapy
description: >-
SSRI and SNRI pharmacotherapy can be used for PTSD symptom reduction,
including sertraline, paroxetine, and venlafaxine.
treatment_term:
preferred_term: Pharmacotherapy
term:
id: NCIT:C15986
label: Pharmacotherapy
therapeutic_agent:
- preferred_term: sertraline
term:
id: CHEBI:9123
label: sertraline
- preferred_term: paroxetine
term:
id: CHEBI:7936
label: paroxetine
- preferred_term: venlafaxine
term:
id: CHEBI:9943
label: venlafaxine
target_phenotypes:
- preferred_term: Anxiety
term:
id: HP:0000739
label: Anxiety
evidence:
- reference: PMID:34992738
reference_title: "Pharmacological therapy for post-traumatic stress disorder: a systematic review and meta-analysis of monotherapy, augmentation and head-to-head approaches."
supports: SUPPORT
evidence_source: HUMAN_CLINICAL
snippet: >-
For individual monotherapy agents compared to placebo in two or more
studies, we found small statistically significant evidence for the
antidepressants fluoxetine, paroxetine, sertraline, venlafaxine and the
antipsychotic quetiapine.
explanation: >-
Systematic review and meta-analysis evidence supports several
antidepressant monotherapies for reducing PTSD symptom severity,
including paroxetine, sertraline, and venlafaxine.
clinical_trials:
- name: NCT06947538
phase: NOT_APPLICABLE
status: RECRUITING
description: >-
SMART stepped-care trial testing adaptive sequences of digital and brief
trauma- or skills-focused interventions for PTSD treatment access,
engagement, and effectiveness in routine care.
target_phenotypes:
- preferred_term: Anxiety
term:
id: HP:0000739
label: Anxiety
- preferred_term: Intrusive re-experiencing
evidence:
- reference: clinicaltrials:NCT06947538
reference_title: "Adaptive Interventions to Improve Posttraumatic Stress Disorder (PTSD) Treatment Access, Engagement, and Effectiveness in Routine Care"
supports: SUPPORT
snippet: >-
The adaptive intervention sequences a digital mental health intervention
(DMHI) and brief trauma- and skills-focused treatments for PTSD.
explanation: >-
ClinicalTrials.gov record supports stepped-care intervention testing for
PTSD symptoms.
- name: NCT04044534
phase: PHASE_II
status: RECRUITING
description: >-
Phase 2 clinical trial evaluating intranasal insulin for reducing PTSD
symptoms.
target_phenotypes:
- preferred_term: Anxiety
term:
id: HP:0000739
label: Anxiety
evidence:
- reference: clinicaltrials:NCT04044534
reference_title: Intranasal Insulin for Treating Posttraumatic Stress Disorder
supports: SUPPORT
snippet: >-
To evaluate if intranasal insulin is effective in reducing PTSD symptoms.
explanation: >-
ClinicalTrials.gov summary states the intervention target.
- name: NCT05517304
phase: NOT_APPLICABLE
status: RECRUITING
description: >-
Trial of transcutaneous cervical vagal nerve stimulation versus sham
stimulation in veterans with PTSD, including brain imaging, physiology, and
PTSD symptom outcomes.
target_phenotypes:
- preferred_term: Anxiety
term:
id: HP:0000739
label: Anxiety
evidence:
- reference: clinicaltrials:NCT05517304
reference_title: Transcutaneous Vagal Nerve Stimulation in Veterans With Posttraumatic Stress Disorder
supports: SUPPORT
snippet: >-
This study effects the effects of transcutaneous cervical vagal nerve
stimulation (tcVNS) or a sham control on brain, physiology, and PTSD
symptoms in Veterans with posttraumatic stress disorder (PTSD).
explanation: >-
ClinicalTrials.gov summary supports neuromodulation testing with symptom
and physiologic outcomes.
- name: NCT05729789
phase: NOT_APPLICABLE
status: RECRUITING
description: >-
Pilot study of online group written exposure therapy for PTSD, compared
with group cognitive processing therapy outcomes.
target_phenotypes:
- preferred_term: Intrusive re-experiencing
evidence:
- reference: clinicaltrials:NCT05729789
reference_title: "Investigating Group Written Exposure Therapy for Posttraumatic Stress Disorder: A Pilot Study"
supports: SUPPORT
snippet: >-
The goal of this clinical trial is to test if Written Exposure Therapy
(WET) works well in a group setting in patients with post-traumatic stress
disorder (PTSD).
explanation: >-
ClinicalTrials.gov summary documents a PTSD psychotherapy trial.
datasets:
- accession: DOI:10.1038/s41398-023-02313-9
title: Polygenic risk for mental disorders as predictors of posttraumatic stress disorder after mild traumatic brain injury
description: >-
TRACK-TBI prospective level 1 trauma-center cohort with European-ancestry
mild traumatic brain injury participants, PTSD symptom outcome at 6 months,
and PTSD polygenic-risk-score analysis.
organism:
preferred_term: Homo sapiens
term:
id: NCBITaxon:9606
label: Homo sapiens
sample_count: 714
conditions:
- mild traumatic brain injury
- probable post-traumatic stress disorder
publication: DOI:10.1038/s41398-023-02313-9
evidence:
- reference: DOI:10.1038/s41398-023-02313-9
reference_title: Polygenic risk for mental disorders as predictors of posttraumatic stress disorder after mild traumatic brain injury
supports: SUPPORT
evidence_source: HUMAN_CLINICAL
snippet: >-
We used data from individuals of European ancestry with mTBI enrolled in
TRACK-TBI (n = 714), a prospective longitudinal study of level 1 trauma
center patients.
explanation: >-
The publication describes a reusable cohort for post-trauma PTSD genetic
risk modeling.
findings:
- statement: Higher PTSD polygenic risk predicted probable PTSD 6 months after mild traumatic brain injury.
evidence:
- reference: DOI:10.1038/s41398-023-02313-9
reference_title: Polygenic risk for mental disorders as predictors of posttraumatic stress disorder after mild traumatic brain injury
supports: SUPPORT
evidence_source: HUMAN_CLINICAL
snippet: >-
One hundred and sixteen mTBI patients (16.3%) had probable PTSD (PCL-5
score ≥33) at 6 months post-injury.
explanation: >-
The cohort captured a clinically relevant PTSD outcome after traumatic
injury.
- accession: DOI:10.1017/S0033291724002319
title: "Posttraumatic stress disorder (PTSD) prevalence: an umbrella review"
description: >-
Umbrella-review dataset synthesizing 59 reviews of PTSD prevalence across
trauma-exposed contexts, diagnostic instruments, and trauma-event types.
organism:
preferred_term: Homo sapiens
term:
id: NCBITaxon:9606
label: Homo sapiens
conditions:
- post-traumatic stress disorder
- trauma exposure
publication: DOI:10.1017/S0033291724002319
evidence:
- reference: DOI:10.1017/S0033291724002319
reference_title: "Posttraumatic stress disorder (PTSD) prevalence: an umbrella review"
supports: SUPPORT
evidence_source: HUMAN_CLINICAL
snippet: >-
Fifty-nine reviews met the criteria of this umbrella review.
explanation: >-
The publication documents the evidence base for a synthesized PTSD
prevalence dataset.
findings:
- statement: PTSD prevalence estimates were heterogeneous but pooled at approximately 24% across included reviews.
evidence:
- reference: DOI:10.1017/S0033291724002319
reference_title: "Posttraumatic stress disorder (PTSD) prevalence: an umbrella review"
supports: SUPPORT
evidence_source: HUMAN_CLINICAL
snippet: >-
Overall PTSD prevalence was 23.95% (95% confidence interval 95% CI
20.74-27.15), with no publication bias or significant small-study
effects, but a high level of heterogeneity between meta-analyses.
explanation: >-
Captures the principal prevalence finding and heterogeneity caveat.
notes: >-
This curation keeps the pathophysiology granular: trauma exposure,
polygenic susceptibility, epigenetic regulation, HPA-axis regulation,
neuroimmune activation, and threat-circuit dysregulation are separate nodes
connected by downstream edges.
Question: You are an expert researcher providing comprehensive, well-cited information.
Provide detailed information focusing on: 1. Key concepts and definitions with current understanding 2. Recent developments and latest research (prioritize 2023-2024 sources) 3. Current applications and real-world implementations 4. Expert opinions and analysis from authoritative sources 5. Relevant statistics and data from recent studies
Format as a comprehensive research report with proper citations. Include URLs and publication dates where available. Always prioritize recent, authoritative sources and provide specific citations for all major claims.
Please provide a comprehensive research report on Post-Traumatic Stress Disorder covering all of the disease characteristics listed below. This report will be used to populate a disease knowledge base entry. Be thorough and cite primary literature (PMID preferred) for all claims.
For each section, suggested databases/resources are listed. These are the first places you should search for information on each topic.
Search first: OMIM, Orphanet, ICD-10/ICD-11, MeSH, PubMed
Search first: PubMed, Cochrane Library, UpToDate, clinical guidelines, ClinVar, ClinGen, GWAS Catalog, PheGenI, CTD, CDC, WHO, epidemiological databases
Search first: PubMed, Cochrane Library, clinical trial databases, GWAS Catalog, gnomAD, WHO, CDC, nutrition databases
Search first: CTD, PubMed, PheGenI, GxE databases
Search first: HPO (Human Phenotype Ontology), OMIM, Orphanet, PubMed, clinicaltrials.gov, MedDRA, SNOMED CT, DECIPHER, LOINC
For each phenotype, provide: - Phenotype type: symptoms, clinical signs, physical manifestations, behavioral changes, or laboratory abnormalities
For symptoms/signs: HPO, OMIM, Orphanet, PubMed For behavioral changes: HPO, DSM, RDoC (Research Domain Criteria), PubMed For laboratory abnormalities: LOINC, SNOMED CT, LabTests Online, PubMed - Phenotype characteristics: Search first: OMIM, Orphanet, HPO, PubMed - Age of symptom onset (neonatal, childhood, adult-onset, late-onset) - Symptom severity (mild, moderate, severe, variable) - Symptom progression (stable, progressive, episodic, fluctuating) - Frequency among affected individuals (percentage or qualitative) - Quality of life impact: Effects on daily functioning and well-being (per-phenotype when possible) Search first: EQ-5D database, SF-36, WHO QOL databases, PubMed - Suggest HPO (Human Phenotype Ontology) terms for each phenotype
Search first: OMIM, ClinVar, HGMD, Ensembl, NCBI Gene
Search first: ENCODE, Roadmap Epigenomics, MethBase, DiseaseMeth
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Search first: ImmPort, Immunome Database, IEDB, Gene Ontology
Search first: PubMed, Gene Ontology, Reactome
Search first: BRENDA, UniProt, KEGG, OMIM, PubMed
Search first: ENCODE, Roadmap Epigenomics, MethBase, DiseaseMeth
For each mechanism, describe: - The causal chain from initial trigger to clinical manifestation - Which mechanisms are upstream vs downstream - What cell types and biological processes are involved - Suggest GO terms for biological processes and CL terms for cell types
Search first: Uberon, FMA (Foundational Model of Anatomy), OMIM, HPO, ICD-11, MeSH, SNOMED CT
Search first: Uberon, Human Protein Atlas, Cell Ontology, Human Cell Atlas, CellMarker, PanglaoDB
Search first: Gene Ontology (Cellular Component), UniProt, Human Protein Atlas
Search first: OMIM, Orphanet, HPO, PubMed
Search first: Disease registries, longitudinal cohort databases, natural history studies, PubMed, Orphanet, OMIM
Search first: Orphanet, CDC, WHO, GBD (Global Burden of Disease), national registries, SEER, disease registries
Search first: GTR (Genetic Testing Registry), GeneReviews, ClinGen
For each treatment, suggest MAXO (Medical Action Ontology) terms where applicable.
Search first: CDC vaccine schedules, WHO immunization, FDA vaccine database
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Search first: Clinical guidelines, FDA approvals, PubMed
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Structure your response as a comprehensive narrative organized by the sections above. For each section, provide: - Factual content with specific details (numbers, percentages, gene names, variant nomenclature) - Ontology term suggestions (HPO, GO, CL, UBERON, CHEBI, MAXO, MONDO) where applicable - Evidence citations with PMIDs - Direct quotes from abstracts to support key claims - Clear indication when information is not available or not applicable for this disease
This report will be used to populate a disease knowledge base entry with: - Pathophysiology descriptions with causal chains - Gene/protein annotations (HGNC, GO terms) - Phenotype associations (HP terms) with frequencies - Cell type involvement (CL terms) - Anatomical locations (UBERON terms) - Chemical entities (CHEBI terms) - Treatment annotations (MAXO terms) - Evidence items with PMIDs and exact abstract quotes - Epidemiology, prognosis, diagnostic, and prevention information - Animal model descriptions with phenotype recapitulation details
Post-traumatic stress disorder (PTSD) is a trauma- and stressor-related psychiatric disorder characterized by persistent re-experiencing of a traumatic event, avoidance of reminders, and alterations in threat detection/arousal and mood/cognition that cause functional impairment. Contemporary research and guidelines emphasize (i) heterogeneity across diagnostic frameworks (DSM-5-TR vs ICD-11), (ii) strong evidence for trauma-focused psychotherapies as first-line treatment, (iii) robust epidemiologic burden in conflict and displacement settings, and (iv) emerging but not-yet-clinically-validated biological markers implicating HPA-axis dysregulation and neuroimmune activation. (bisson2024posttraumaticstressdisorder pages 1-2, schincariol2024posttraumaticstressdisorder pages 2-3, lang2024acliniciansguide pages 5-5, lawrence2024posttraumaticstress pages 5-5)
A compact, citation-rich snapshot suitable for knowledge-base ingestion is provided in the embedded table below.
| Category | Key points | Key citations |
|---|---|---|
| Identifiers/Definitions | Disease: Post-traumatic stress disorder (PTSD), a trauma- and stressor-related mental disorder that may develop after exposure to exceptionally threatening/horrifying events. DSM-5-TR vs ICD-11: DSM-5-TR requires qualifying trauma exposure and 4 symptom clusters—intrusion, avoidance, negative alterations in cognition/mood, and arousal/reactivity—with duration >1 month and functional impairment; ICD-11 defines 3 core clusters—re-experiencing, avoidance, and persistent sense of current threat—with symptoms lasting several weeks and impairment. ICD-11 additionally distinguishes PTSD and complex PTSD (CPTSD) as sibling diagnoses. Recent population work found DSM-5 and ICD-11 prevalence can be similar overall but identify only partially overlapping cases (κ=0.62). URLs: https://doi.org/10.1192/bja.2024.27 (Aug 2024); https://doi.org/10.1136/bmj.h6161 (Nov 2024); https://doi.org/10.1017/S2045796025100164 (Aug 2025). | Siddaway 2024, BJPsych Advances, doi:10.1192/bja.2024.27; Bisson et al. 2024, BMJ, doi:10.1136/bmj.h6161; Pettrich et al. 2025, Epidemiol Psychiatr Sci, doi:10.1017/S2045796025100164 (siddaway2024assessmentanddiagnosis pages 1-2, siddaway2024assessmentanddiagnosis pages 3-4, bisson2024posttraumaticstressdisorder pages 1-2, pettrich2025theprevalenceof pages 1-2) |
| Epidemiology | General burden: Umbrella review of 59 reviews found pooled PTSD prevalence 23.95% (95% CI 20.74–27.15), with wide heterogeneity across trauma contexts; lifetime global prevalence cited around 5.6%. General adult estimates: BMJ review reports point prevalence about 3% and lifetime prevalence 1.9%–8.8%. Context-specific: armed-conflict civilians 23.70% (95% CI 19.50–28.40%); displaced people in Africa 55.64% (95% CI 42.76–68.41%); internally displaced persons in Africa 51% (95% CI 38–64); Ethiopian war-affected communities 48.4% (95% CI 37.1–59.8%). German general population: trauma exposure 47.2%; probable PTSD 4.7% by both DSM-5 and ICD-11 algorithms. URLs: https://doi.org/10.1017/S0033291724002319 (Sep 2024); https://doi.org/10.1136/gpsych-2023-101438 (Jun 2024); https://doi.org/10.3389/fpsyt.2024.1336665 (Mar 2024); https://doi.org/10.1371/journal.pone.0300894 (Apr 2024); https://doi.org/10.3389/fpsyt.2024.1399013 (May 2024). | Schincariol et al. 2024, Psychol Med, doi:10.1017/S0033291724002319; Ahmed et al. 2024, Gen Psychiatry, doi:10.1136/gpsych-2023-101438; Andualem et al. 2024, Front Psychiatry, doi:10.3389/fpsyt.2024.1336665; Tesfaye et al. 2024, PLoS One, doi:10.1371/journal.pone.0300894; Tinsae et al. 2024, Front Psychiatry, doi:10.3389/fpsyt.2024.1399013; Pettrich et al. 2025, doi:10.1017/S2045796025100164 (schincariol2024posttraumaticstressdisorder pages 1-2, ahmed2024prevalenceofposttraumatic pages 1-2, andualem2024prevalenceofposttraumatic pages 1-2, tesfaye2024posttraumaticstressdisorder pages 1-2, tinsae2024posttraumaticstressdisorder pages 1-2, pettrich2025theprevalenceof pages 1-2) |
| Risk factors | Sex: female sex repeatedly increases risk—OR 2.2 (95% CI 1.2–4.3) in Ethiopian war-affected communities; pooled OR 1.99 (95% CI 1.65–2.32) in African IDPs. Trauma severity/cumulative trauma: witnessing murder of a loved one OR 3.0; close family member killed/seriously injured OR 3.1; moderate/high perceived threat to life OR 3.4. In IDPs, dose-response for traumatic events: 4–7 events OR 2.09, 8–11 events OR 3.15, 12–16 events OR 5.37. Social/contextual: poor social support OR 4.4; no longer married OR 1.93; unemployment OR 1.92; repeated displacement OR 2.13; illness without medical care OR 1.92. Comorbidity: depression OR 2.97 in IDPs; depression symptoms OR 2.8 and anxiety symptoms OR 3.4 in Ethiopian war-affected communities. Interpersonal trauma is noted to produce more severe/lasting PTSD than many non-intentional events. | Tinsae et al. 2024, Front Psychiatry, doi:10.3389/fpsyt.2024.1399013; Tesfaye et al. 2024, PLoS One, doi:10.1371/journal.pone.0300894; Schincariol et al. 2024, doi:10.1017/S0033291724002319 (tinsae2024posttraumaticstressdisorder pages 1-2, tinsae2024posttraumaticstressdisorder pages 10-11, tesfaye2024posttraumaticstressdisorder pages 15-16, tesfaye2024posttraumaticstressdisorder pages 1-2, schincariol2024posttraumaticstressdisorder pages 2-3) |
| Diagnostics | Diagnostic approach: validated clinician-administered interviews should be used to establish diagnosis; screening tools should not be used alone to diagnose PTSD. Structured interviews: CAPS-5, CAPS-CA-5, PSSI-5. Self-report measures: PCL-5, PDS-5. ICD-11 PTSD/CPTSD tools: International Trauma Questionnaire (ITQ), ITQ-CA; International Trauma Interview validation also cited. Assessment caveats: PCL-5-based prevalence depends strongly on cut-off; one general-population study found cut-off methods aligned more with DSM-5 than ICD-11. PCL-5 lacks depersonalization/derealization items, so DSM-5 dissociative subtype may be missed. Questionnaires are faster but more bias-prone; interviews are more comprehensive but time-consuming. URLs: https://doi.org/10.1002/jts.23013 (Jan 2024); https://doi.org/10.1192/bja.2024.27 (Aug 2024); https://doi.org/10.1002/cpp.3012 (May 2024). | Lang et al. 2024, J Trauma Stress, doi:10.1002/jts.23013; Siddaway 2024, doi:10.1192/bja.2024.27; Sarr et al. 2024, Clin Psychol Psychother, doi:10.1002/cpp.3012; Pettrich et al. 2025, doi:10.1017/S2045796025100164 (lang2024acliniciansguide pages 4-4, siddaway2024assessmentanddiagnosis pages 10-11, sarr2024asystematicreview pages 35-35, pettrich2025theprevalenceof pages 6-7, pettrich2025theprevalenceof pages 1-2) |
| Treatment | 2023 VA/DoD first-line (“strong for”): trauma-focused psychotherapies CPT, EMDR, PE; first-line medications paroxetine, sertraline, venlafaxine. Trauma-focused psychotherapy is preferred first-line because meta-analyses show larger and more persistent improvement. Other options: Ehlers’ cognitive therapy, present-centered therapy, written exposure therapy (WET), and mindfulness-based stress reduction have weaker/supportive roles; prazosin is suggested against for overall PTSD but suggested for nightmares. Strong against: benzodiazepines and cannabis/cannabis derivatives. Guideline also suggests against invasive interventions such as ECT and vagus nerve stimulation for routine PTSD treatment because of limited efficacy evidence/harms. Some brief treatment formats in implementation/research: trauma-focused treatments often 8–16 sessions; WET can be 5 sessions. URLs: https://doi.org/10.1002/jts.23013 (Jan 2024); Figure summary from guideline article page 22. | Lang et al. 2024, J Trauma Stress, doi:10.1002/jts.23013; Koven 2024, Eur J Med Health Res, doi:10.59324/ejmhr.2024.2(5).01; BMJ review 2024, doi:10.1136/bmj.h6161 (lang2024acliniciansguide pages 5-5, koven2024ptsdtreatmentliterature pages 1-2, koven2024ptsdtreatmentliterature pages 2-3, lang2024acliniciansguide media 0f51705c, geter2024posttraumaticstress pages 41-47) |
| Mechanisms | Core pathophysiology: dysregulation of stress systems links limbic threat circuitry to endocrine and immune abnormalities. Canonical HPA cascade: amygdala/limbic input → hypothalamic CRH → pituitary ACTH → adrenal cortisol. Reviews report low cortisol / hypocortisolism, enhanced glucocorticoid receptor sensitivity, and stronger negative feedback in many PTSD cohorts. Inflammation/immune: elevated IL-6, TNF-α, IL-1β, chemokine changes, interferon-related gene expression, and reduced anti-inflammatory/regulatory cytokines. Neuroimmune mechanisms: microglia, astrocytes, mast cells, NLRP3-related signaling, COX-2/PGE2 pathways, endothelial-brain microvasculature signaling. Affected circuits/regions: amygdala, hippocampus, prefrontal cortex, PVN; consequences include impaired fear extinction, altered memory/emotion regulation, and possible neurodegenerative/somatic disease links. Epigenetics/genetics: FKBP5 and glucocorticoid signaling are repeatedly implicated; epigenetic reviews also highlight NR3C1, BDNF, and SLC6A4-related alterations. URLs: https://doi.org/10.1016/j.bbih.2024.100849 (Nov 2024); https://doi.org/10.1007/s11481-023-10064-z (Apr 2023); https://doi.org/10.1159/000541822 (Nov 2024). | Lawrence & Scofield 2024, Brain Behav Immun Health, doi:10.1016/j.bbih.2024.100849; Govindula et al. 2023, J Neuroimmune Pharmacol, doi:10.1007/s11481-023-10064-z; Golubeva et al. 2024, Complex Psychiatry, doi:10.1159/000541822 (lawrence2024posttraumaticstress pages 5-5, lawrence2024posttraumaticstress pages 1-2, lawrence2024posttraumaticstress pages 2-4, govindula2023emphasizingthecrosstalk pages 1-2) |
| Trials | Representative active/recent trials from ClinicalTrials.gov: STEPPS (NCT06947538; recruiting; Boston Medical Center; posted Apr 27 2025) tests a SMART stepped-care model using webSTAIR, coaching, Brief STAIR, and WET; nonresponse defined as <15-point decrease on PCL-5. Intranasal insulin for PTSD (NCT04044534; phase 2; recruiting; VA Connecticut; posted Aug 5 2019, updated Sep 16 2025) tests 40 IU twice daily with CAPS-5 outcome and amygdala hyperactivation rationale. tcVNS in Veterans with PTSD (NCT05517304; recruiting; VA ORD; posted Aug 26 2022, updated Mar 3 2026) evaluates PTSD symptoms, PET-measured insula activation, and IL-6. Group WET (NCT05729789; recruiting; St. Joseph’s Healthcare Hamilton; posted Feb 15 2023, updated Apr 17 2024) evaluates 6-session online group WET, hypothesizing low dropout (<10%) and symptom reduction. URLs: https://clinicaltrials.gov/study/NCT06947538 ; https://clinicaltrials.gov/study/NCT04044534 ; https://clinicaltrials.gov/study/NCT05517304 ; https://clinicaltrials.gov/study/NCT05729789 | ClinicalTrials.gov records: NCT06947538; NCT04044534; NCT05517304; NCT05729789 (NCT06947538 chunk 1, NCT04044534 chunk 1, NCT05517304 chunk 1, NCT05729789 chunk 1) |
Table: This table compiles high-yield PTSD facts for a knowledge base entry, including diagnostic frameworks, epidemiology, risk factors, diagnostics, treatment recommendations, mechanisms, and active clinical trials. It is designed to provide a compact but citation-rich snapshot anchored to the gathered evidence.
PTSD is defined in authoritative clinical reviews as “a mental disorder that may develop after exposure to exceptionally threatening or horrifying events.” (BMJ, Nov 2024, DOI: https://doi.org/10.1136/bmj.h6161). (bisson2024posttraumaticstressdisorder pages 1-2)
This report integrates aggregated disease-level sources: clinical guidelines/summaries, umbrella/systematic reviews and meta-analyses, and clinical trial registry records; it does not derive from individual EHR case reports (though some evidence relates to EHR/biobank approaches in the broader retrieved corpus). (lang2024acliniciansguide pages 5-5, schincariol2024posttraumaticstressdisorder pages 1-2, NCT06947538 chunk 1)
PTSD requires exposure to a traumatic stressor (Criterion A–type exposure in DSM-5-TR; “extremely threatening or horrific event(s)” in ICD-11). (bisson2024posttraumaticstressdisorder pages 1-2, siddaway2024assessmentanddiagnosis pages 3-4)
Conflict/displacement settings show particularly high pooled prevalence and strong associations with social/clinical risk factors. - War-affected Ethiopian communities (meta-analysis; May 2024; Frontiers in Psychiatry): pooled prevalence 48.4% (95% CI 37.1–59.8) with risk factors including female sex (OR 2.2), poor social support (OR 4.4), depression symptoms (OR 2.8), anxiety symptoms (OR 3.4), and threat/severity indicators (e.g., perceived threat to life OR 3.4). (https://doi.org/10.3389/fpsyt.2024.1399013). (tinsae2024posttraumaticstressdisorder pages 1-2) - Internally displaced persons (IDPs) in Africa (systematic review/meta-analysis; Apr 2024; PLOS ONE): pooled PTSD prevalence 51% (95% CI 38–64) and dose–response with number of traumatic events (e.g., 12–16 events OR 5.37). Other pooled risk factors include female sex (OR 1.99), depression (OR 2.97), repeated displacement (OR 2.13), and illness without medical care (OR 1.92). (https://doi.org/10.1371/journal.pone.0300894). (tesfaye2024posttraumaticstressdisorder pages 1-2) - Displaced people in Africa (Mar 2024; Frontiers in Psychiatry): pooled PTSD prevalence 55.64% (95% CI 42.76–68.41%); associated factors included female sex, unemployment, and depression. (https://doi.org/10.3389/fpsyt.2024.1336665). (andualem2024prevalenceofposttraumatic pages 1-2)
Direct quantitative protective-factor synthesis was limited in retrieved evidence. However, poor social support was strongly associated with PTSD in war-affected communities (OR 4.4), implying that strong social support is plausibly protective in those contexts. (tinsae2024posttraumaticstressdisorder pages 1-2)
PTSD risk is partly genetically influenced and interacts with traumatic exposures. - In a prospective cohort of mild traumatic brain injury (TRACK-TBI; Translational Psychiatry; Jan 2023; DOI: https://doi.org/10.1038/s41398-023-02313-9), probable PTSD at 6 months occurred in 16.3% (116/714; PCL-5 ≥33). A PTSD polygenic risk score (PRS) significantly predicted PTSD: top PRS quintile vs lowest aOR 3.71 (95% CI 1.80–7.65), and adding PRS improved discrimination (AUC 0.687→0.733). Authors interpret PRS as potentially actionable for enhanced follow-up/early intervention, pending prospective validation. (stein2023polygenicriskfor pages 3-5)
DSM-5-TR groups symptoms into four clusters: intrusion; avoidance; negative alterations in cognitions and mood; and alterations in arousal and reactivity, with persistence >1 month and functional impairment. (schincariol2024posttraumaticstressdisorder pages 2-3, bisson2024posttraumaticstressdisorder pages 1-2)
ICD-11 defines PTSD with three core clusters: re-experiencing in the present; avoidance; and a persistent perception of heightened current threat, with symptoms lasting several weeks and causing distress/impairment; ICD-11 additionally recognizes complex PTSD (CPTSD) as a sibling diagnosis. (schincariol2024posttraumaticstressdisorder pages 2-3, siddaway2024assessmentanddiagnosis pages 3-4)
(These are ontology suggestions; exact mapping should be verified against HPO.) - Intrusive memories/flashbacks → Recurrent intrusive memories; Flashback (HPO suggestion). - Nightmares → Nightmares (HPO suggestion). - Avoidance → Avoidant behavior (HPO suggestion). - Hypervigilance / exaggerated startle → Hypervigilance; Increased startle response (HPO suggestion). - Sleep disturbance/insomnia (not core ICD-11 but common DSM-5-TR symptom content) → Insomnia (HPO suggestion). (schincariol2024posttraumaticstressdisorder pages 2-3, bisson2024posttraumaticstressdisorder pages 1-2)
No monogenic causal genes were supported in the retrieved evidence; PTSD is treated as a polygenic and multifactorial disorder with environmental necessity (trauma exposure). (barr2025multivariategenomewideassociation pages 1-4, stein2023polygenicriskfor pages 3-5)
A recent multivariate GWAS preprint summarizing background evidence reports twin-based heritability around 30–40% and SNP-based variance explained roughly 5–9% for PTSD (interpret cautiously as preprint/background). (barr2025multivariategenomewideassociation pages 1-4)
A 2024 epigenetics review emphasizes that environmental stressors can induce epigenetic changes relevant to PTSD, focusing on DNA methylation/chromatin regulation/noncoding RNA and highlighting gene systems related to HPA-axis regulation, neurotrophins, neurotransmission, and immune function. (Complex Psychiatry; Nov 2024; DOI: https://doi.org/10.1159/000541822). (hu2025thecentralrole pages 3-5)
The retrieved 2023–2024 corpus did not include a primary, large PTSD GWAS locus paper with a complete locus list; thus, locus-level curation is incomplete in this report.
Specific lifestyle exposures (diet, exercise) were not directly quantified in retrieved evidence; substance use is addressed under comorbidity and treatment evidence. (back2024stateofthe pages 3-4)
Not applicable as a primary cause in the evidence retrieved.
A consistent contemporary mechanistic model is: 1) Trauma exposure initiates stress responses and threat-learning processes (diagnostic prerequisite). (bisson2024posttraumaticstressdisorder pages 1-2) 2) Stress-system dysregulation: the limbic system (including amygdala) influences hypothalamic CRH release → pituitary ACTH → adrenal cortisol; PTSD is often associated with low cortisol and heightened glucocorticoid receptor sensitivity and enhanced negative feedback. (Brain, Behavior, & Immunity–Health; Nov 2024; DOI: https://doi.org/10.1016/j.bbih.2024.100849). (lawrence2024posttraumaticstress pages 5-5) 3) Neuroimmune activation: elevated pro-inflammatory cytokines (e.g., IL-6, TNF-α, IL-1β) and reduced regulatory cytokines occur alongside stress physiology; immune signaling can influence brain function through endothelial/microglial/astrocytic mechanisms. (lawrence2024posttraumaticstress pages 5-5, govindula2023emphasizingthecrosstalk pages 1-2) 4) Circuit-level manifestations: altered function in hippocampus/amygdala/prefrontal cortex contributes to dysregulated fear extinction, emotional processing, memory re-experiencing, hypervigilance, and impaired executive control. (lawrence2024posttraumaticstress pages 5-5)
(These are ontology suggestions; verify in GO for exact labels.) - HPA axis signaling / glucocorticoid response: “response to glucocorticoid”; “regulation of hormone secretion”. (lawrence2024posttraumaticstress pages 5-5) - Inflammatory signaling: “cytokine-mediated signaling pathway”; “inflammatory response”; “interferon signaling”. (lawrence2024posttraumaticstress pages 5-5, govindula2023emphasizingthecrosstalk pages 1-2) - COX-2/PGE2 axis: “prostaglandin biosynthetic process”; “cyclooxygenase pathway” (suggested). (govindula2023emphasizingthecrosstalk pages 1-2)
Primary neuroanatomical structures repeatedly implicated include: - Amygdala (UBERON suggestion) (lawrence2024posttraumaticstress pages 5-5) - Hippocampus (UBERON suggestion) (lawrence2024posttraumaticstress pages 5-5) - Prefrontal cortex (UBERON suggestion) (lawrence2024posttraumaticstress pages 5-5) - Hypothalamic paraventricular nucleus (PVN) (UBERON suggestion) (govindula2023emphasizingthecrosstalk pages 1-2)
An example of ongoing mechanistically motivated neuromodulation research targets insula activation via imaging outcomes (see tcVNS trial). (NCT05517304 chunk 1)
A 2024 umbrella review reports that World Mental Health Surveys estimate 25–40% recover within 12 months (many within 6 months), while meta-analyses suggest nearly 50% may develop chronic PTSD if untreated. (schincariol2024posttraumaticstressdisorder pages 2-3)
A 2024 systematic review on PTSD recurrence concludes terminology/definitions are inconsistent and meta-analysis was not possible, indicating uncertainty around recurrence prevalence and predictors. (schincariol2024posttraumaticstressdisorder pages 2-3)
Pooled evidence in African displacement/war-affected meta-analyses shows higher risk for women (e.g., OR 1.99 in IDPs; OR 2.2 in Ethiopian war-affected communities). (tesfaye2024posttraumaticstressdisorder pages 1-2, tinsae2024posttraumaticstressdisorder pages 1-2)
Polygenic risk contributes to susceptibility (see PRS evidence), but no Mendelian inheritance pattern is supported. (stein2023polygenicriskfor pages 3-5)
No validated, scalable diagnostic biomarkers were established in the evidence. Reviews highlight cortisol-axis markers and inflammatory cytokines (e.g., IL-6, TNF-α) as biologically plausible but heterogeneous across studies and sensitive to sampling and comorbidity. (lawrence2024posttraumaticstress pages 2-4, lawrence2024posttraumaticstress pages 5-5)
Quantitative prognosis evidence in the retrieved corpus is limited; the umbrella review-derived course estimates suggest substantial early recovery for a subset (25–40% within 12 months) but substantial chronicity risk if untreated (~50%). (schincariol2024posttraumaticstressdisorder pages 2-3)
A clinician’s guide to the 2023 VA/DoD Clinical Practice Guideline (Journal of Traumatic Stress; Jan 2024; DOI: https://doi.org/10.1002/jts.23013) emphasizes trauma-focused psychotherapies as first-line and recommends starting with one of three recommended trauma-focused treatments when feasible, using shared decision-making. (lang2024acliniciansguide pages 5-5)
From the guideline summary figure, “strong for” interventions include: - Psychotherapies: Cognitive Processing Therapy (CPT), Eye Movement Desensitization and Reprocessing (EMDR), Prolonged Exposure (PE). (lang2024acliniciansguide media 0f51705c) - Medications: paroxetine, sertraline, venlafaxine. (lang2024acliniciansguide media 0f51705c)
“Strong against” includes benzodiazepines and cannabis/cannabis derivatives. (lang2024acliniciansguide media 0f51705c, lang2024acliniciansguide pages 5-5)
The guideline also suggests additional psychotherapies (e.g., Written Exposure Therapy; Present-Centered Therapy; Ehlers’ cognitive therapy) and mind–body approaches such as mindfulness-based stress reduction. (lang2024acliniciansguide pages 5-5)
The guideline suggests against prazosin for overall PTSD treatment but suggests prazosin for PTSD-related nightmares. (lang2024acliniciansguide pages 5-5)
A 2024 state-of-the-science review reports that rigorously conducted trials support individual, manualized, trauma-focused treatments for PTSD/SUD, and that patients do not need to be abstinent to benefit. It highlights COPE (integrating Prolonged Exposure with CBT for SUD) as the most studied integrated treatment, with evidence for reductions in PTSD symptoms and substance use and improved remission outcomes, delivered in-person and via telehealth. (Journal of Traumatic Stress; Jun 2024; DOI: https://doi.org/10.1002/jts.23049). (back2024stateofthe pages 3-4)
(Verify exact MAXO IDs in downstream curation.) - Trauma-focused psychotherapy; prolonged exposure therapy; cognitive processing therapy; EMDR; SSRI administration; SNRI administration; prazosin administration for nightmares; shared decision-making in care planning. (lang2024acliniciansguide media 0f51705c, lang2024acliniciansguide pages 5-5)
The VA/DoD clinician guide states that no pharmacological interventions had sufficient evidence to recommend for prevention of PTSD or acute stress disorder. (lang2024acliniciansguide pages 5-5)
A SMART stepped-care trial (STEPPS; NCT06947538; first posted Apr 27 2025; recruiting) aims to improve PTSD treatment access/engagement via a sequence of a digital intervention (webSTAIR), coaching, and brief clinician-administered treatments (Brief STAIR, WET), reflecting real-world implementation priorities in routine care. (ClinicalTrials.gov: https://clinicaltrials.gov/study/NCT06947538). (NCT06947538 chunk 1)
PTSD is a human psychiatric diagnosis; however, mechanistic evidence relies heavily on preclinical stress models.
Preclinical support for inflammation-linked mechanisms: A 2024 review cites rodent evidence that PTSD-like symptoms were reduced after chronic inflammation treatment with ibuprofen, supporting a causal role for inflammation in symptom expression (preclinical). (lawrence2024posttraumaticstress pages 5-5)
Detailed model-organism cataloging was not retrieved; available evidence supports that animal stress paradigms are used to interrogate inflammatory mediators (e.g., COX-2/PGE2 signaling and cytokines) and HPA-axis dysregulation in PTSD-like phenotypes. (govindula2023emphasizingthecrosstalk pages 1-2)
1) Guideline evolution and implementation focus: The 2023 VA/DoD guideline (described in 2024) centers trauma-focused psychotherapy first-line, shared decision-making, and cautions against benzodiazepines/cannabis; this directly influences real-world care systems (e.g., VA and civilian implementation projects) and informs stepped-care/digital delivery research. (lang2024acliniciansguide pages 5-5, lang2024acliniciansguide media 0f51705c, NCT06947538 chunk 1)
2) High-burden humanitarian contexts: 2024 meta-analyses quantify PTSD prevalence in armed conflict and displacement, supporting prioritization of scalable, culturally sensitive services in LMIC and conflict settings. (ahmed2024prevalenceofposttraumatic pages 1-2, tesfaye2024posttraumaticstressdisorder pages 1-2, andualem2024prevalenceofposttraumatic pages 1-2)
3) Precision mental health directions: 2023 evidence indicates polygenic risk scores can stratify risk for PTSD after a defined trauma exposure (mTBI), suggesting an emerging path toward targeted follow-up and early intervention trials. (stein2023polygenicriskfor pages 3-5)
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