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  • Published: 28 September 2018

Posttraumatic stress disorder: from diagnosis to prevention

  • Xue-Rong Miao   ORCID: orcid.org/0000-0002-0665-8271 1 ,
  • Qian-Bo Chen 1 ,
  • Kai Wei 1 ,
  • Kun-Ming Tao 1 &
  • Zhi-Jie Lu 1  

Military Medical Research volume  5 , Article number:  32 ( 2018 ) Cite this article

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Posttraumatic stress disorder (PTSD) is a chronic impairment disorder that occurs after exposure to traumatic events. This disorder can result in a disturbance to individual and family functioning, causing significant medical, financial, and social problems. This study is a selective review of literature aiming to provide a general outlook of the current understanding of PTSD. There are several diagnostic guidelines for PTSD, with the most recent editions of the DSM-5 and ICD-11 being best accepted. Generally, PTSD is diagnosed according to several clusters of symptoms occurring after exposure to extreme stressors. Its pathogenesis is multifactorial, including the activation of the hypothalamic–pituitary–adrenal (HPA) axis, immune response, or even genetic discrepancy. The morphological alternation of subcortical brain structures may also correlate with PTSD symptoms. Prevention and treatment methods for PTSD vary from psychological interventions to pharmacological medications. Overall, the findings of pertinent studies are difficult to generalize because of heterogeneous patient groups, different traumatic events, diagnostic criteria, and study designs. Future investigations are needed to determine which guideline or inspection method is the best for early diagnosis and which strategies might prevent the development of PTSD.

Posttraumatic stress disorder (PTSD) is a recognized clinical phenomenon that often occurs as a result of exposure to severe stressors, such as combat, natural disaster, or other events [ 1 ]. The diagnosis of PTSD was first introduced in the 3rd edition of the Diagnostic and Statistical Manual (DSM) (American Psychiatric Association) in 1980 [ 2 ].

PTSD is a potentially chronic impairing disorder that is characterized by re-experience and avoidance symptoms as well as negative alternations in cognition and arousal. This disease first raised public concerns during and after the military operations of the United States in Afghanistan and Iraq, and to date, a large number of research studies report progress in this field. However, both the underlying mechanism and specific treatment for the disease remain unclear. Considering the significant medical, social and financial problems, PTSD represents both to nations and to individuals, all persons caring for patients suffering from this disease or under traumatic exposure should know about the risks of PTSD.

The aim of this review article is to present the current understanding of PTSD related to military injury to foster interdisciplinary dialog. This article is a selective review of pertinent literature retrieved by a search in PubMed, using the following keywords: “PTSD[Mesh] AND military personnel”. The search yielded 3000 publications. The ones cited here are those that, in the authors’ view, make a substantial contribution to the interdisciplinary understanding of PTSD.

Definition and differential diagnosis

Posttraumatic stress disorder is a prevalent and typically debilitating psychiatric syndrome with a significant functional disturbance in various domains. Both the manifestation and etiology of it are complex, which has caused difficulty in defining and diagnosing the condition. The 3rd edition of the DSM introduced the diagnosis of PTSD with 17 symptoms divided into three clusters in 1980. After several decades of research, this diagnosis was refined and improved several times. In the most recent version of the DSM-5 [ 3 ], PTSD is classified into 20 symptoms within four clusters: intrusion, active avoidance, negative alterations in cognitions and mood as well as marked alterations in arousal and reactivity. The diagnosis requirement can be summarized as an exposure to a stressor that is accompanied by at least one intrusion symptom, one avoidance symptom, two negative alterations in cognitions and mood symptoms, and two arousal and reactivity turbulence symptoms, persisting for at least one month, with functional impairment. Interestingly, in the DSM-5, PTSD has been moved from the anxiety disorder group to a new category of ‘trauma- and stressor-related disorders’, which reflects the cognizance alternation of PTSD. In contrast to the DSM versions, the World Health Organization’s (WHO) International Classification of Diseases (ICD) has proposed a substantially different approach to diagnosing PTSD in the most recent ICD-11 version [ 4 ], which simplified the symptoms into six under three clusters, including constant re-experiencing of the traumatic event, avoidance of traumatic reminders and a sense of threat. The diagnosis requires at least one symptom from each cluster which persists for several weeks after exposure to extreme stressors. Both diagnostic guidelines emphasize the exposure to traumatic events and time of duration, which differentiate PTSD from some diseases with similar symptoms, including adjustment disorder, anxiety disorder, obsessive-compulsive disorder, and personality disorder. Patients with the major depressive disorder (MDD) may or may not have experienced traumatic events, but generally do not have the invasive symptoms or other typical symptoms that PTSD presents. In terms of traumatic brain injury (TBI), neurocognitive responses such as persistent disorientation and confusion are more specific symptoms. It is worth mentioning that some dissociative reactions in PTSD (e.g., flashback symptoms) should be recognized separately from the delusions, hallucinations, and other perceptual impairments that appear in psychotic disorders since they are based on actual experiences. The ICD-11 also recognizes a sibling disorder, complex PTSD (CPTSD), composed of symptoms including dysregulation, negative self-concept, and difficulties in relationships based on the diagnosis of PTSD. The core CPTSD symptom is PTSD with disturbances in self-organization (DSO).

In consideration of the practical applicability of the PTSD diagnosis, Brewin et al. conducted a study to investigate the requirement differences, prevalence, comorbidity, and validity of the DSM-5 and ICD-11 for PTSD criteria. According to their study, diagnostic standards for symptoms of re-experiencing are higher in the ICD-11 than the DSM, whereas the standards for avoidance are less strict in the ICD-11 than in the DSM-IV [ 5 ]. It seems that in adult subjects, the prevalence of PTSD using the ICD-11 is considerably lower compared to the DSM-5. Notably, evidence suggested that patients identified with the ICD-11 and DSM-5 were quite different with only partially overlapping cases; this means each diagnostic system appears to find cases that would not be diagnosed using the other. In consideration of comorbidity, research comparing these two criteria show diverse outcomes, as well as equal severity and quality of life. In terms of children, only very preliminary evidence exists suggesting no significant difference between the two. Notably, the diagnosis of young children (age ≤ 6 years) depends more on the situation in consideration of their physical and psychological development according to the DSM-5.

Despite numerous investigations and multiple revisions of the diagnostic criteria for PTSD, it remains unclear which type and what extent of stress are capable of inducing PTSD. Fear responses, especially those related to combat injury, are considered to be sufficient enough to trigger symptoms of PTSD. However, a number of other types of stressors were found to correlate with PTSD, including shame and guilt, which represent moral injury resulting from transgressions during a war in military personnel with deeply held moral and ethical beliefs. In addition, military spouses and children may be as vulnerable to moral injury as military service members [ 6 ]. A research study on Canadian Armed Forces personnel showed that exposure to moral injury during deployments is common among military personnel and represents an independent risk factor for past-year PTSD and MDD [ 7 ]. Unfortunately, it seems that pre- and post-deployment mental health education was insufficient to moderate the relationship between exposure to moral injury and adverse mental health outcomes.

In general, a large number of studies are focusing on the definition and diagnostic criteria of PTSD and provide considerable indicators for understanding and verifying the disease. However, some possible limitations or discrepancies continue to exist in current research studies. One is that although the diagnostic criteria for a thorough examination of the symptoms were explicit and accessible, the formal diagnosis of PTSD using structured clinical interviews was relatively rare. In contrast, self-rating scales, such as the Posttraumatic Diagnostic Scale (PDS) [ 8 ] and the Impact of Events Scale (IES) [ 9 ], were used frequently. It is also noteworthy that focusing on PTSD explicitly could be a limitation as well. The complexity of traumatic experiences and the responses to them urge comprehensive investigations covering all aspects of physical and psychological maladaptive changes.

Prevalence and importance

Posttraumatic stress disorder generally results in poor individual-level outcomes, including co-occurring disorders such as depression and substance use, and physical health problems. According to the DSM-5 reporting, more than 80% of PTSD patients share one or more comorbidities; for instance, the morbidity of PTSD with concurrent mild TBI is 48% [ 8 ]. Moreover, cognitive impairment has been identified frequently in PTSD. The reported incidence rate for PTSD ranges from 5.4 to 16.8% in military service members and veterans [ 10 , 11 , 12 , 13 , 14 ], which is almost double those in the general population. The estimated prevalence of PTSD varies depending on the group of patients studied, the traumatic events occurred, and the measurement method used (Table  1 ). However, it still reflects the profound effect of this mental disease, especially with the rise in global terrorism and military conflict in recent years. While PTSD can arise at any life stage in any population, most research in recent decades has focused on returned veterans; this means most knowledge regarding PTSD has come from the military population. Meanwhile, the impact of this disease on children has received scant attention.

The discrepancy of PTSD prevalence in males and females is controversial. In a large study of OEF/OIF veterans, the prevalence of PTSD in males and females was similar, although statistically more prevalent in men versus women (13% vs. 11%) [ 15 ]. Another study on the Navy and Marine Corps showed a slightly higher incidence for PTSD in the women compared to men (6.6% vs. 5.3%) [ 12 ]. However, the importance of combat exposure is unclear. Despite a lower level of combat exposure than male military personnel, females generally have considerably higher rates of military sexual trauma, which is significantly associated with the development of PTSD [ 16 ].

It is reported that 44–72% of veterans suffer high levels of stress after returning to civilian life. Many returned veterans with PTSD show emotion regulation problems, including emotion identification, expression troubles and self-control issues. Nevertheless, a meta-analytic investigation of 34 studies consistently found that the severity of PTSD symptoms was significantly associated with anger, especially in military samples [ 17 ]. Not surprisingly, high levels of PTSD and emotional regulation troubles frequently lead to poor family functioning or even domestic violence in veterans. According to some reports, parenting difficulties in veteran families were associated with three PTSD symptom clusters. Evans et al. [ 18 ] conducted a survey to evaluate the impact of PTSD symptom clusters on family functioning. According to their analysis, avoidance symptoms directly affected family functioning, whereas hyperarousal symptoms had an indirect association with family functioning. Re-experience symptoms were not found to impact family functioning. Notably, recent epidemiologic studies using data from the Veterans Health Administration (VHA) reported that veterans with PTSD were linked to suicide ideations and behaviors [ 19 ] (e.g., non-suicidal self-injury, NSSI), in which depression as well as other mood disruptions, often serve as mediating factors.

Previously, there was a controversial attitude toward the vulnerability of young children to PTSD. However, growing evidence suggests that severe and persistent trauma could result in stress responses worse than expected as well as other mental and physical sequelae in child development. The most prevalent traumatic exposures for young children above the age of 1 year were interpersonal trauma, mostly related to or derived from their caregivers, including witnessing intimate partner violence (IPV) and maltreatment [ 20 ]. Unfortunately, because of the crucial role that caregivers play in early child development, these types of traumatic events are especially harmful and have been associated with developmental maladaptation in early childhood. Maladaptation commonly represents a departure from normal development and has even been linked to more severe effects and psychopathology. In addition, the presence of psychopathology may interfere with the developmental competence of young children. Research studies have also broadened the investigation to sequelae of PTSD on family relationships. It is proposed that the children of parents with symptoms of PTSD are easily deregulated or distressed and appear to face more difficulties in their psychosocial development in later times compared to children of parents without. Meanwhile, PTSD veterans described both emotional (e.g., hurt, confusion, frustration, fear) and behavioral (e.g., withdrawal, mimicking parents’ behavior) disruption in their children [ 21 ]. Despite the increasing emphasis on the effects of PTSD on young children, only a limited number of studies examined the dominant factors that influence responses to early trauma exposures, and only a few prospective research studies have observed the internal relations between early PTSD and developmental competence. Moreover, whether exposure to both trauma types in early life is associated with more severe PTSD symptoms than exposure to one type remains an outstanding question.

Molecular mechanism and predictive factors

The mechanisms leading to posttraumatic stress disorder have not yet been fully elucidated. Recent literature suggests that both the neuroendocrine and immune systems are involved in the formulation and development of PTSD [ 22 , 23 ]. After traumatic exposures, the stress response pathways of the hypothalamic–pituitary–adrenal (HPA) axis and sympathetic nervous system are activated and lead to the abnormal release of glucocorticoids (GC) and catecholamines. GCs have downstream effects on immunosuppression, metabolism enhancement, and negative feedback inhibition of the HPA axis by binding to the GC receptor (GR), thus connecting the neuroendocrine modulation with immune disturbance and inflammatory response. A recent meta-analysis of 20 studies found increased plasma levels of proinflammatory cytokines tumor necrosis factor-alpha (TNF-a), interleukin-1beta (IL-1b), and interleukin-6 (IL-6) in individuals with PTSD compared to healthy controls [ 24 ]. In addition, some other studies speculate that there is a prospective association of C-reactive protein (CRP) and mitogen with the development of PTSD [ 25 ]. These findings suggest that neuroendocrine and inflammatory changes, rather than being a consequence of PTSD, may in fact act as a biological basis and preexisting vulnerability for developing PTSD after trauma. In addition, it is reported that elevated levels of terminally differentiated T cells and an altered Th1/Th2 balance may also predispose an individual to PTSD.

Evidence indicates that the development of PTSD is also affected by genetic factors. Research has found that genetic and epigenetic factors account for up to 70% of the individual differences in PTSD development, with PTSD heritability estimated at 30% [ 26 ]. While aiming to integrate genetic studies for PTSD and build a PTSD gene database, Zhang et al. [ 27 ] summarized the landscape and new perspective of PTSD genetic studies and increased the overall candidate genes for future investigations. Generally, the polymorphisms moderating HPA-axis reactivity and catecholamines have been extensively studied, such as FKBP5 and catechol-O-methyl-transferase (COMT). Other potential candidates for PTSD such as AKT, a critical mediator of growth factor-induced neuronal survival, were also explored. Genetic research has also made progress in other fields. For example, researchers have found that DNA methylation in multiple genes is highly correlated with PTSD development. Additional studies have found that stress exposure may even affect gene expression in offspring by epigenetic mechanisms, thus causing lasting risks. However, some existing problems in the current research of this field should be noted. In PTSD genetic studies, variations in population or gender difference, a wide range of traumatic events and diversity of diagnostic criteria all may attribute to inconsistency, thus leading to a low replication rate among similar studies. Furthermore, PTSD genes may overlap with other mental disorders such as depression, schizophrenia, and bipolar disorder. All of these factors indicate an urgent need for a large-scale genome-wide study of PTSD and its underlying epidemiologic mechanisms.

It is generally acknowledged that some mental diseases, such as major depressive disorder (MDD), bipolar disorder, and schizophrenia, are associated with massive subcortical volume change. Recently, numerous studies have examined the relationship between the morphology changes of subcortical structures and PTSD. One corrected analysis revealed that patients with PTSD show a pattern of lower white matter integrity in their brains [ 28 ]. Prior studies typically found that a reduced volume of the hippocampus, amygdala, rostral ventromedial prefrontal cortex (rvPFC), dorsal anterior cingulate cortex (dACC), and the caudate nucleus may have a relationship with PTSD patients. Logue et al. [ 29 ] conducted a large neuroimaging study of PTSD that compared eight subcortical structure volumes (nucleus accumbens, amygdala, caudate, hippocampus, pallidum, putamen, thalamus, and lateral ventricle) between PTSD patients and controls. They found that smaller hippocampi were particularly associated with PTSD, while smaller amygdalae did not show a significant correlation. Overall, rigorous and longitudinal research using new technologies, such as magnetoencephalography, functional MRI, and susceptibility-weighted imaging, are needed for further investigation and identification of morphological changes in the brain after a traumatic exposure.

Psychological and pharmacological strategies for prevention and treatment

Current approaches to PTSD prevention span a variety of psychological and pharmacological categories, which can be divided into three subgroups: primary prevention (before the traumatic event, including prevention of the event itself), secondary prevention (between the traumatic event and the development of PTSD), and tertiary prevention (after the first symptoms of PTSD become apparent). The secondary and tertiary prevention of PTSD has abundant methods, including different forms of debriefing, treatments for Acute Stress Disorder (ASD) or acute PTSD, and targeted intervention strategies. Meanwhile, the process of primary prevention is still in its infancy and faces several challenges.

Based on current research on the primary prevention of post-trauma pathology, psychological and pharmacological interventions for particular groups or individuals (e.g., military personnel, firefighters, etc.) with a high risk of traumatic event exposure were applicable and acceptable for PTSD sufferers. Of the studies that reported possible psychological prevention effects, training generally included a psychoeducational component and a skills-based component relating to stress responses, anxiety reducing and relaxation techniques, coping strategies and identifying thoughts, emotion and body tension, choosing how to act, attentional control, emotion control and regulation [ 30 , 31 , 32 ]. However, efficiency for these training has not been evaluated yet due to a lack of high-level evidence-based studies. Pharmacological options have targeted the influence of stress on memory formation, including drugs relating to the hypothalamic-pituitary-adrenal (HPA) axis, the autonomic nerve system (especially the sympathetic nerve system), and opiates. Evidence has suggested that pharmacological prevention is most effective when started before and early after the traumatic event, and it seems that sympatholytic drugs (alpha and beta-blockers) have the highest potential for primary prevention of PTSD [ 33 ]. However, one main difficulty limiting the exploration in this field is related to rigorous and complex ethical issues, as the application of pre-medication for special populations and the study of such options in hazardous circumstances possibly touches upon questions of life and death. Significantly, those drugs may have potential side effects.

There are several treatment guidelines for patients with PTSD produced by different organizations, including the American Psychiatric Association (APA), the United Kingdom’s National Institute for Health and Clinical Excellence (NICE), the International Society for Traumatic Stress Studies (ISTSS), the Institute of Medicine (IOM), the Australian National Health and Medical Research Council, and the Department of Veterans Affairs and Department of Defense (VA, DoD) [ 34 , 35 , 36 , 37 , 38 ]. Additionally, a large number of research studies are aiming to evaluate an effective treatment method for PTSD. According to these guidelines and research, treatment approaches can be classified as psychological interventions and pharmacological treatments (Fig.  1 ); most of the studies provide varying degrees of improvement in individual outcomes after standard interventions, including PTSD symptom reduction or remission, loss of diagnosis, release or reduction of comorbid medical or psychiatric conditions, quality of life, disability or functional impairment, return to work or to active duty, and adverse events.

figure 1

Psychological and pharmacological strategies for treatment of PTSD. CBT. Cognitive behavioral therapy; CPT. Cognitive processing therapy; CT. Cognitive therapy; CR. Cognitive restructuring; EMDR. Eye movement desensitization and reprocessing; SSRIs. Selective serotonin reuptake inhibitors; SNRIs. Serotonin and norepinephrine reuptake inhibitors; MAO. Monoamine oxidase

Most guidelines identify trauma-focused psychological interventions as first-line treatment options [ 39 ], including cognitive behavioral therapy (CBT), cognitive processing therapy (CPT), cognitive therapy (CT), cognitive restructuring (CR), coping skills therapy (including stress inoculation therapy), exposure-based therapies, eye movement desensitization and reprocessing (EMDR), hypnosis and hypnotherapy, and brief eclectic psychotherapy. These treatments are delivered predominantly to individuals, but some can also be conducted in family or group settings. However, the recommendation of current guidelines seems to be projected empirically as research on the comparison of outcomes of different treatments is limited. Jonas et al. [ 40 ] performed a systematic review and network meta-analysis of the evidence for treatment of PTSD. The study suggested that all psychological treatments showed efficacy for improving PTSD symptoms and achieving the loss of PTSD diagnosis in the acute phase, and exposure-based treatments exhibited the strongest evidence of efficacy with high strength of evidence (SOE). Furthermore, Kline et al. [ 41 ] conducted a meta-analysis evaluating the long-term effects of in-person psychotherapy for PTSD in 32 randomized controlled trials (RCTs) including 2935 patients with long-term follow-ups of at least 6 months. The data suggested that all studied treatments led to lasting improvements in individual outcomes, and exposure therapies demonstrated a significant therapeutic effect as well with larger effect sizes compared to other treatments.

Pharmacological treatments for PTSD include antidepressants such as selective serotonin reuptake inhibitors (SSRIs), serotonin and norepinephrine reuptake inhibitors (SNRIs), and monoamine oxidase (MAO) inhibitors, sympatholytic drugs such as alpha-blockers, antipsychotics, anticonvulsants, and benzodiazepines. Among these medications, fluoxetine, paroxetine, sertraline, topiramate, risperidone, and venlafaxine have been identified as efficacious in treatment. Moreover, in the Jonas network meta-analysis of 28 trials (4817 subjects), they found paroxetine and topiramate to be more effective for reducing PTSD symptoms than most other medications, whereas evidence was insufficient for some other medications as research was limited [ 40 ]. It is worth mentioning that in these studies, efficacy for the outcomes, unlike the studies of psychological treatments, was mostly reported as a remission in PTSD or depression symptoms; other outcomes, including loss of PTSD diagnosis, were rarely reported in studies.

As for the comparative evidence of psychological with pharmacological treatments or combinations of psychological treatments and pharmacological treatments with other treatments, evidence was insufficient to draw any firm conclusions [ 40 ]. Additionally, reports on adverse events such as mortality, suicidal behaviors, self-harmful behaviors, and withdrawal of treatment were relatively rare.

PTSD is a high-profile clinical phenomenon with a complicated psychological and physical basis. The development of PTSD is associated with various factors, such as traumatic events and their severity, gender, genetic and epigenetic factors. Pertinent studies have shown that PTSD is a chronic impairing disorder harmful to individuals both psychologically and physically. It brings individual suffering, family functioning disorders, and social hazards. The definition and diagnostic criteria for PTSD remain complex and ambiguous to some extent, which may be attributed to the complicated nature of PTSD and insufficient research on it. The underlying mechanisms of PTSD involve changes in different levels of psychological and molecular modulations. Thus, research targeting the basic mechanisms of PTSD using standard clinical guidelines and controlled interference factors is needed. In terms of treatment, psychological and pharmacological interventions could relief PTSD symptoms to different degrees. However, it is necessary to develop systemic treatment as well as symptom-specific therapeutic methods. Future research could focus on predictive factors and physiological indicators to determine effective prevention methods for PTSD, thereby reducing its prevalence and preventing more individuals and families from struggling with this disorder.

Abbreviations

American Psychiatric Association

Acute stress disorder

Cognitive behavioral therapy

Catechol-O-methyl-transferase

Cognitive processing therapy

Complex posttraumatic stress disorder

Cognitive restructuring

C-reactive protein

Cognitive therapy

Dorsal anterior cingulate cortex

Diagnostic and Statistical Manual

Disturbances in self-organization

Eye movement desensitization and reprocessing

Glucocorticoids

Glucocorticoids receptor

Hypothalamic–pituitary–adrenal axis

International classification of diseases

Impact of events scale

Interleukin-1beta

Interleukin-6

Institute of Medicine

Intimate partner violence

International Society for Traumatic Stress Studies

Monoamine oxidase

Major depressive disorder

United Kingdom’s National Institute for Health and Clinical Excellence

Non-suicidal self-injury

Posttraumatic diagnostic scale

Posttraumatic stress disorder

Randomized controlled trials

Rostral ventromedial prefrontal cortex

Serotonin and norepinephrine reuptake inhibitors;

Strength of evidence

Selective serotonin reuptake inhibitors

Tumor necrosis factor-alpha

DoD Department of Veterans Affairs and Department of Defense

Veterans Health Administration

World Health Organization

White J, Pearce J, Morrison S, Dunstan F, Bisson JI, Fone DL. Risk of post-traumatic stress disorder following traumatic events in a community sample. Epidemiol Psychiatr Sci. 2015;24(3):1–9.

Article   Google Scholar  

Kendell RE. Diagnostic and statistical manual of mental disorders, 3rd ed., revised (DSM-III-R). America J Psychiatry. 1980;145(10):1301–2.

American Psychiatric Association. Diagnostic and statistical manual of mental disorders : DSM-5. America J Psychiatry. 2013. doi: https://doi.org/10.1176/appi.books.9780890425596.744053 .

Maercker A, Brewin CR, Bryant RA, Cloitre M, Reed GM, Van OM, et al. Proposals for mental disorders specifically associated with stress in the international classification of Diseases-11. Lancet. 2013;381(9878):1683–5.

Brewin CR, Cloitre M, Hyland P, Shevlin M, Maercker A, Bryant RA, et al. A review of current evidence regarding the ICD-11 proposals for diagnosing PTSD and complex PTSD. Clin Psychol Rev. 2017;58(1): 1–15.

Google Scholar  

Nash WP, Litz BT. Moral injury: a mechanism for war-related psychological trauma in military family members. Clin Child Fam Psychol Rev. 2013;16(4):365–75.

Nazarov A, Fikretoglu D, Liu A, Thompson M, Zamorski MA. Greater prevalence of post-traumatic stress disorder and depression in deployed Canadian Armed Forces personnel at risk for moral injury. Acta Psychiatr Scand. 2018;137(4):342–54.

Article   CAS   Google Scholar  

Foa EB, Cashman L, Jaycox L, Perry K. The validation of a self-report measure of posttraumatic stress disorder: the posttraumatic diagnostic scale. Psychol Assess. 1997;9(9):445–51.

Gnanavel S, Robert RS. Diagnostic and statistical manual of mental disorders (5th edit) and the impact of events scale-revised. Chest. 2013;144(6):1974–5.

Reijnen A, Rademaker AR, Vermetten E, Geuze E. Prevalence of mental health symptoms in Dutch military personnel returning from deployment to Afghanistan: a 2-year longitudinal analysis. Eur Psychiatry. 2015;30(2):341–6.

Sundin J, Herrell RK, Hoge CW, Fear NT, Adler AB, Greenberg N, et al. Mental health outcomes in US and UK military personnel returning from Iraq. Br J Psychiatry. 2014;204(3):200–7.

Macera CA, Aralis HJ, Highfill-McRoy R, Rauh MJ. Posttraumatic stress disorder after combat zone deployment among navy and marine corps men and women. J Women's Health (Larchmt). 2014;23(6):499–505.

Macgregor AJ, Tang JJ, Dougherty AL, Galarneau MR. Deployment-related injury and posttraumatic stress disorder in US military personnel. Injury. 2013;44(11):1458–64.

Sandweiss DA, Slymen DJ, Leardmann CA, Smith B, White MR, Boyko EJ, et al. Preinjury psychiatric status, injury severity, and postdeployment posttraumatic stress disorder. Arch Gen Psychiatry. 2011;68(5):496–504.

Seal KH, Bertenthal D, Maguen S, Gima K, Chu A, Marmar CR. Getting beyond "Don't ask; don't tell": an evaluation of US veterans administration postdeployment mental health screening of veterans returning from Iraq and Afghanistan. Am J Public Health. 2008;98(4):714–20.

Street AE, Rosellini AJ, Ursano RJ, Heeringa SG, Hill ED, Monahan J, et al. Developing a risk model to target high-risk preventive interventions for sexual assault victimization among female U.S. army soldiers. Clin Psychol Sci. 2016;4(6):939–56.

Olatunji BO, Ciesielski BG, Tolin DF. Fear and loathing: a meta-analytic review of the specificity of anger in PTSD. Behav Ther. 2010;41(1):93–105.

Evans L, Cowlishaw S, Hopwood M. Family functioning predicts outcomes for veterans in treatment for chronic posttraumatic stress disorder. J Fam Psychol. 2009;23(4):531–9.

Mckinney JM, Hirsch JK, Britton PC. PTSD symptoms and suicide risk in veterans: serial indirect effects via depression and anger. J Affect Disord. 2017;214(1):100–7.

Briggsgowan MJ, Carter AS, Ford JD. Parsing the effects violence exposure in early childhood: modeling developmental pathways. J Pediatric Psychol. 2012;37(1):11–22.

Enlow MB, Blood E, Egeland B. Sociodemographic risk, developmental competence, and PTSD symptoms in young children exposed to interpersonal trauma in early life. J Trauma Stress. 2013;26(6):686–94.

Newport DJ, Nemeroff CB. Neurobiology of posttraumatic stress disorder. Curr Opin eurobiol. 2009;14(1 Suppl 1):13.

Neigh GN, Ali FF. Co-morbidity of PTSD and immune system dysfunction: opportunities for treatment. Curr Opin Pharmacol. 2016;29:104–10.

Passos IC, Vasconcelos-Moreno MP, Costa LG, Kunz M, Brietzke E, Quevedo J, et al. Inflammatory markers in post-traumatic stress disorder: a systematic review, meta-analysis, and meta-regression. Lancet Psychiatry. 2015;2(11):1002.

Eraly SA, Nievergelt CM, Maihofer AX, Barkauskas DA, Biswas N, Agorastos A, et al. Assessment of plasma C-reactive protein as a biomarker of posttraumatic stress disorder risk. JAMA Psychiatry. 2014;71(4):423.

Lebois LA, Wolff JD, Ressler KJ. Neuroimaging genetic approaches to posttraumatic stress disorder. Exp Neurol. 2016;284(Pt B):141–52.

Zhang K, Qu S, Chang S, Li G, Cao C, Fang K, et al. An overview of posttraumatic stress disorder genetic studies by analyzing and integrating genetic data into genetic database PTSD gene. Neurosci Biobehav Rev. 2017;83(1):647–56.

Bolzenius JD, Velez CS, Lewis JD, Bigler ED, Wade BSC, Cooper DB, et al. Diffusion imaging findings in US service members with mild traumatic brain injury and posttraumatic stress disorder. J Head Trauma Rehabil. 2018. https://doi.org/10.1097/HTR.0000000000000378 [Epub ahead of print].

Logue MW, Rooij SJHV, Dennis EL, Davis SL, Hayes JP, Stevens JS, et al. Smaller hippocampal volume in posttraumatic stress disorder: a multi-site ENIGMA-PGC study. Biol. Psychiatry . 2018;83(3):244–53.

Sijaric-Voloder S, Capin D. Application of cognitive behavior therapeutic techniques for prevention of psychological disorders in police officers. Health Med. 2008;2(4):288–92.

Deahl M, Srinivasan M, Jones N, Thomas J, Neblett C, Jolly A. Preventing psychological trauma in soldiers: the role of operational stress training and psychological debriefing. Brit J Med Psychol. 2000;73(1):77–85.

Wolmer L, Hamiel D, Laor N. Preventing children's posttraumatic stress after disaster with teacher-based intervention: a controlled study. J Am Acad Child Adolesc Psychiatry. 2011;50(4):340–8 348.e1–2.

Skeffington PM, Rees CS, Kane R. The primary prevention of PTSD: a systematic review. J Trauma Dissociation. 2013;14(4):404–22.

Jaques H. Introducing the national institute for health and clinical excellence. Eur Heart J. 2012;33(17):2111–2.

PubMed   Google Scholar  

Schnyder U. International Society for Traumatic Stress Studies (ISTSS). Psychosomatik Und Konsiliarpsychiatrie. 2008;2(4):261.

Bulger RE. The institute of medicine. Kennedy Inst Ethics J. 1992;2(1):73–7.

Anderle R, Brown DC, Cyran E. Department of Defense[C]. African Studies Association. 2011;2011:340–2.

Feussner JR, Maklan CW. Department of Veterans Affairs[J]. Med Care. 1998;36(3):254–6.

Sripada RK, Rauch SA, Liberzon I. Psychological mechanisms of PTSD and its treatment. Curr Psychiatry Rep. 2016;18(11):99.

Jonas DE, Cusack K, Forneris CA, Wilkins TM, Sonis J, Middleton JC, et al. Psychological and pharmacological treatments for adults with posttraumatic stress disorder (PTSD). Agency Healthcare Res Quality (AHRQ). 2013;4(1):1–760.

Kline AC, Cooper AA, Rytwinksi NK, Feeny NC. Long-term efficacy of psychotherapy for posttraumatic stress disorder: a meta-analysis of randomized controlled trials. Clin Psychol Rev. 2018;59:30–40.

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We thank Jamie Bono for providing professional writing suggestions.

This work was supported by the National Natural Science Foundation of China (31371084 and 31171013 by ZJL), and the National Natural Science Foundation of China (81100276 by XRM).

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Miao, XR., Chen, QB., Wei, K. et al. Posttraumatic stress disorder: from diagnosis to prevention. Military Med Res 5 , 32 (2018). https://doi.org/10.1186/s40779-018-0179-0

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Received : 20 March 2018

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DOI : https://doi.org/10.1186/s40779-018-0179-0

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research paper on post traumatic stress disorder

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  • Published: 29 March 2022

Post-traumatic stress disorder: clinical and translational neuroscience from cells to circuits

  • Kerry. J. Ressler   ORCID: orcid.org/0000-0002-5158-1103 1 ,
  • Sabina Berretta 1 ,
  • Vadim Y. Bolshakov 1 ,
  • Isabelle M. Rosso 1 ,
  • Edward G. Meloni 1 ,
  • Scott L. Rauch 1 &
  • William A. Carlezon Jr 1  

Nature Reviews Neurology volume  18 ,  pages 273–288 ( 2022 ) Cite this article

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Post-traumatic stress disorder (PTSD) is a maladaptive and debilitating psychiatric disorder, characterized by re-experiencing, avoidance, negative emotions and thoughts, and hyperarousal in the months and years following exposure to severe trauma. PTSD has a prevalence of approximately 6–8% in the general population, although this can increase to 25% among groups who have experienced severe psychological trauma, such as combat veterans, refugees and victims of assault. The risk of developing PTSD in the aftermath of severe trauma is determined by multiple factors, including genetics — at least 30–40% of the risk of PTSD is heritable — and past history, for example, prior adult and childhood trauma. Many of the primary symptoms of PTSD, including hyperarousal and sleep dysregulation, are increasingly understood through translational neuroscience. In addition, a large amount of evidence suggests that PTSD can be viewed, at least in part, as a disorder that involves dysregulation of normal fear processes. The neural circuitry underlying fear and threat-related behaviour and learning in mammals, including the amygdala–hippocampus–medial prefrontal cortex circuit, is among the most well-understood in behavioural neuroscience. Furthermore, the study of threat-responding and its underlying circuitry has led to rapid progress in understanding learning and memory processes. By combining molecular–genetic approaches with a translational, mechanistic knowledge of fear circuitry, transformational advances in the conceptual framework, diagnosis and treatment of PTSD are possible. In this Review, we describe the clinical features and current treatments for PTSD, examine the neurobiology of symptom domains, highlight genomic advances and discuss translational approaches to understanding mechanisms and identifying new treatments and interventions for this devastating syndrome.

Post-traumatic stress disorder (PTSD) is a debilitating neuropsychiatric disorder, characterized by re-experiencing, avoidance, negative emotions and thoughts, and hyperarousal.

PTSD is frequently comorbid with neurological conditions such as traumatic brain injury, post-traumatic epilepsy and chronic headaches.

PTSD has a prevalence of approximately 6–8% in the general population and up to 25% among individuals who have experienced severe trauma.

Many of the neural circuit mechanisms that underlie the PTSD symptoms of fear-related and threat-related behaviour, hyperarousal and sleep dysregulation are becoming increasingly clear.

Key brain regions involved in PTSD include the amygdala–hippocampus–prefrontal cortex circuit, which is among the most well-understood networks in behavioural neuroscience.

Combining molecular–genetic approaches with a mechanistic knowledge of fear circuitry will enable transformational advances in the conceptual framework, diagnosis and treatment of PTSD.

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American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders 5th edn (American Psychiatric Publishing, 2013).

Breslau, N. et al. Trauma and posttraumatic stress disorder in the community: the 1996 Detroit area survey of trauma. Arch. Gen. Psychiatry 55 , 626–632 (1998).

Article   CAS   PubMed   Google Scholar  

Breslau, N., Peterson, E. L., Poisson, L. M., Schultz, L. R. & Lucia, V. C. Estimating post-traumatic stress disorder in the community: lifetime perspective and the impact of typical traumatic events. Psychol. Med. 34 , 889–898 (2004).

Bromet, E., Sonnega, A. & Kessler, R. C. Risk factors for DSM-III-R posttraumatic stress disorder: findings from the National Comorbidity Survey. Am. J. Epidemiol. 147 , 353–361 (1998).

McLaughlin, K. A. et al. Subthreshold posttraumatic stress disorder in the world health organization world mental health surveys. Biol. Psychiatry 77 , 375–384 (2015).

Article   PubMed   Google Scholar  

Jovanovic, T., Kazama, A., Bachevalier, J. & Davis, M. Impaired safety signal learning may be a biomarker of PTSD. Neuropharmacology 62 , 695–704 (2011).

Article   PubMed   PubMed Central   CAS   Google Scholar  

Jovanovic, T. & Ressler, K. J. How the neurocircuitry and genetics of fear inhibition may inform our understanding of PTSD. Am. J. Psychiatry 167 , 648–662 (2010).

Article   PubMed   PubMed Central   Google Scholar  

Morgan, C. A., Grillon, C., Southwick, S. M., Davis, M. & Charney, D. S. Fear-potentiated startle in posttraumatic stress disorder. Biol. Psychiatry 38 , 378–385 (1995).

Rauch, S. L. et al. Exaggerated amygdala response to masked facial stimuli in posttraumatic stress disorder: a functional MRI study. Biol. Psychiatry 47 , 769–776 (2000).

Shin, L. M. et al. A functional magnetic resonance imaging study of amygdala and medial prefrontal cortex responses to overtly presented fearful faces in posttraumatic stress disorder. Arch. Gen. Psychiatry 62 , 273–281 (2005).

Mellman, T. A., Pigeon, W. R., Nowell, P. D. & Nolan, B. Relationships between REM sleep findings and PTSD symptoms during the early aftermath of trauma. J. Trauma. Stress 20 , 893–901 (2007).

Yehuda, R. & LeDoux, J. Response variation following trauma: a translational neuroscience approach to understanding PTSD. Neuron 56 , 19–32 (2007).

Koenen, K. C., Goodwin, R., Struening, E., Hellman, F. & Guardino, M. Posttraumatic stress disorder and treatment seeking in a national screening sample. J. Trauma. Stress 16 , 5–16 (2003).

Koenen, K. C. et al. A high risk twin study of combat-related PTSD comorbidity. Twin Res. 6 , 218–226 (2003).

True, W. R. et al. A twin study of genetic and environmental contributions to liability for posttraumatic stress symptoms. Arch. Gen. Psychiatry 50 , 257–264 (1993).

Stein, M. B. et al. Genome-wide association studies of posttraumatic stress disorder in 2 cohorts of US Army soldiers. JAMA Psychiatry 73 , 695–704 (2016).

Stein, M. B., Jang, K. L., Taylor, S., Vernon, P. A. & Livesley, W. J. Genetic and environmental influences on trauma exposure and posttraumatic stress disorder symptoms: a twin study. Am. J. Psychiatry 159 , 1675–1681 (2002).

Duncan, L. E. et al. Largest GWAS of PTSD ( N =20 070) yields genetic overlap with schizophrenia and sex differences in heritability. Mol. Psychiatry 23 , 666–673 (2018).

Reuveni, I. et al. Anatomical and functional connectivity in the default mode network of post-traumatic stress disorder patients after civilian and military-related trauma. Hum. Brain Mapp. 37 , 589–599 (2015).

Porter, B., Bonanno, G. A., Frasco, M. A., Dursa, E. K. & Boyko, E. J. Prospective post-traumatic stress disorder symptom trajectories in active duty and separated military personnel. J. Psychiatr. Res. 89 , 55–64 (2017).

Ballenger, J. C. et al. Consensus statement update on posttraumatic stress disorder from the international consensus group on depression and anxiety. J. Clin. Psychiatry 65 (Suppl. 1), 55–62 (2004).

PubMed   Google Scholar  

Heim, C. & Nemeroff, C. B. The role of childhood trauma in the neurobiology of mood and anxiety disorders: preclinical and clinical studies. Biol. Psychiatry 49 , 1023–1039 (2001).

Kessler, R. C. et al. Trauma and PTSD in the WHO world mental health surveys. Eur. J. Psychotraumatol. 8 , 1353383 (2017).

Huckins, L. M. et al. Analysis of genetically regulated gene expression identifies a prefrontal PTSD gene, SNRNP35, specific to military cohorts. Cell Rep. 31 , 107716 (2020).

Article   CAS   PubMed   PubMed Central   Google Scholar  

Koenen, K. C. et al. Posttraumatic stress disorder in the World Mental Health Surveys. Psychol. Med. 47 , 2260–2274 (2017).

Kornfield, S. L., Hantsoo, L. & Epperson, C. N. What does sex have to do with it? The role of sex as a biological variable in the development of posttraumatic stress disorder. Curr. Psychiatry Rep. 20 , 39 (2018).

Kessler, R. C., Sonnega, A., Bromet, E., Hughes, M. & Nelson, C. B. Posttraumatic stress disorder in the National Comorbidity Survey. Arch. Gen. Psychiatry 52 , 1048–1060 (1995).

Davis, M. The role of the amygdala in fear and anxiety. Annu. Rev. Neurosci. 15 , 353–375 (1992).

Davis, M. in The Amygdala , Second Edition: A Functional Analysis (ed. Aggleton, J. P.) 213–287 (Oxford Univ. Press, 2000).

LeDoux, J. E., Cicchetti, P., Xagoraris, A. & Romanski, L. M. The lateral amygdaloid nucleus: sensory interface of the amygdala in fear conditioning. J. Neurosci. 10 , 1062–1069 (1990).

Maren, S. The amygdala, synaptic plasticity, and fear memory. Ann. NY Acad. Sci. 985 , 106–113 (2003).

Pitkanen, A. in The Amygdala, Second Edition: A Functional Analysis (ed. Aggleton, J. P.) 31–116 (Oxford Univ. Press, 2000).

Milad, M. R. & Quirk, G. J. Neurons in medial prefrontal cortex signal memory for fear extinction. Nature 420 , 70–74 (2002).

McCullough, K. M., Morrison, F. G. & Ressler, K. J. Bridging the gap: towards a cell-type specific understanding of neural circuits underlying fear behaviors. Neurobiol. Learn. Mem. 135 , 27–39 (2016).

Mobbs, D. et al. Viewpoints: approaches to defining and investigating fear. Nat. Neurosci. 22 , 1205–1216 (2019).

Ressler, K. J. Translating across circuits and genetics toward progress in fear- and anxiety-related disorders. Am. J. Psychiatry 177 , 214–222 (2020).

Fenster, R. J., Lebois, L. A. M., Ressler, K. J. & Suh, J. Brain circuit dysfunction in post-traumatic stress disorder: from mouse to man. Nat. Rev. Neurosci. 19 , 535–551 (2018).

McAllister, T. W. Psychopharmacological issues in the treatment of TBI and PTSD. Clin. Neuropsychol. 23 , 1338–1367 (2009).

Strawn, J. R., Keeshin, B. R., DelBello, M. P., Geracioti, T. D. Jr. & Putnam, F. W. Psychopharmacologic treatment of posttraumatic stress disorder in children and adolescents: a review. J. Clin. Psychiatry 71 , 932–941 (2010).

Abdallah, C. G., Southwick, S. M. & Krystal, J. H. Neurobiology of posttraumatic stress disorder (PTSD): a path from novel pathophysiology to innovative therapeutics. Neurosci. Lett. 649 , 130–132 (2017).

Stojek, M. M., McSweeney, L. B. & Rauch, S. A. M. Neuroscience informed prolonged exposure practice: increasing efficiency and efficacy through mechanisms. Front. Behav. Neurosci. 12 , 281 (2018).

Kelmendi, B., Adams, T. G., Soutwick, S., Abdallah, C. G. & Krystal, J. H. Posttraumatic stress disorder: an integrated overview and neurobiological rationale for pharmacology. Clin. Psychol. 24 , 281–297 (2017).

Google Scholar  

Krystal, J. H. et al. It is time to address the crisis in the pharmacotherapy of posttraumatic stress disorder: a consensus statement of the PTSD Psychopharmacology Working Group. Biol. Psychiatry 82 , e51–e59 (2017).

Stein, D. J. et al. Dissociation in posttraumatic stress disorder: evidence from the world mental health surveys. Biol. Psyhiatry 73 , 302–312 (2013).

Article   Google Scholar  

Lebois, L. A. M. et al. Large-scale functional brain network architecture changes associated with trauma-related dissociation. Am. J. Psychiatry 178 , 165–173 (2021).

Nicholson, A. A. et al. Dynamic causal modeling in PTSD and its dissociative subtype: bottom-up versus top-down processing within fear and emotion regulation circuitry. Hum. Brain Mapp. 38 , 5551–5561 (2017).

Stein, M. B. et al. Genome-wide analyses of psychological resilience in U.S. Army soldiers. Am. J. Med. Genet. B Neuropsychiatr. Genet. 180 , 310–319 (2019).

Nievergelt, C. M. et al. Genomic predictors of combat stress vulnerability and resilience in U.S. Marines: a genome-wide association study across multiple ancestries implicates PRTFDC1 as a potential PTSD gene. Psychoneuroendocrinology 51 , 459–471 (2015).

Thompson, N. J., Fiorillo, D., Rothbaum, B. O., Ressler, K. J. & Michopoulos, V. Coping strategies as mediators in relation to resilience and posttraumatic stress disorder. J. Affect. Disord. 225 , 153–159 (2018).

van Rooij, S. J. H. et al. Hippocampal activation during contextual fear inhibition related to resilience in the early aftermath of trauma. Behav. Brain Res. 408 , 113282 (2021).

Wingo, A. P., Ressler, K. J. & Bradley, B. Resilience characteristics mitigate tendency for harmful alcohol and illicit drug use in adults with a history of childhood abuse: a cross-sectional study of 2024 inner-city men and women. J. Psychiatr. Res. 51 , 93–99 (2014).

Wrenn, G. L. et al. The effect of resilience on posttraumatic stress disorder in trauma-exposed inner-city primary care patients. J. Natl Med. Assoc. 103 , 560–566 (2011).

Astill Wright, L., Horstmann, L., Holmes, E. A. & Bisson, J. I. Consolidation/reconsolidation therapies for the prevention and treatment of PTSD and re-experiencing: a systematic review and meta-analysis. Transl. Psychiatry 11 , 453 (2021).

Linnstaedt, S. D., Zannas, A. S., McLean, S. A., Koenen, K. C. & Ressler, K. J. Literature review and methodological considerations for understanding circulating risk biomarkers following trauma exposure. Mol. Psychiatry 25 , 1986–1999 (2020).

McLean, S. A. et al. The AURORA Study: a longitudinal, multimodal library of brain biology and function after traumatic stress exposure. Mol. Psychiatry 25 , 283–296 (2020).

Iyadurai, L. et al. Preventing intrusive memories after trauma via a brief intervention involving Tetris computer game play in the emergency department: a proof-of-concept randomized controlled trial. Mol. Psychiatry 23 , 674–682 (2018).

Rothbaum, B. O. et al. Early intervention following trauma may mitigate genetic risk for PTSD in civilians: a pilot prospective emergency department study. J. Clin. Psychiatry 75 , 1380–1387 (2014).

Seal, K. H. & Stein, M. B. Preventing the pain of PTSD. Sci. Transl Med. 5 , 188fs122 (2013).

Article   CAS   Google Scholar  

Zohar, J. et al. Secondary prevention of chronic PTSD by early and short-term administration of escitalopram: a prospective randomized, placebo-controlled, double-blind trial. J. Clin. Psychiatry 79 , 16m10730 (2018).

Zohar, J. et al. High dose hydrocortisone immediately after trauma may alter the trajectory of PTSD: interplay between clinical and animal studies. Eur. Neuropsychopharmacol. 21 , 796–809 (2011).

Myers, K. M. & Davis, M. Mechanisms of fear extinction. Mol. Psychiatry 12 , 120–150 (2007).

Ross, D. A. et al. An integrated neuroscience perspective on formulation and treatment planning for posttraumatic stress disorder: an educational review. JAMA Psychiatry 74 , 407–415 (2017).

LaBar, K. S., Gatenby, J. C., Gore, J. C., LeDoux, J. E. & Phelps, E. A. Human amygdala activation during conditioned fear acquisition and extinction: a mixed-trial fMRI study. Neuron 20 , 937–945 (1998).

LeDoux, J. The amygdala. Curr. Biol. 17 , R868–R874 (2007).

Rogan, M. T., Staubli, U. V. & LeDoux, J. E. Fear conditioning induces associative long-term potentiation in the amygdala. Nature 390 , 604–607 (1997).

Myers, K. M. & Davis, M. Behavioral and neural analysis of extinction. Neuron 36 , 567–584 (2002).

Chhatwal, J. P., Myers, K. M., Ressler, K. J. & Davis, M. Regulation of gephyrin and GABAA receptor binding within the amygdala after fear acquisition and extinction. J. Neurosci. 25 , 502–506 (2005).

Herry, C. et al. Switching on and off fear by distinct neuronal circuits. Nature 454 , 600–606 (2008).

Lee, J., An, B. & Choi, S. Longitudinal recordings of single units in the basal amygdala during fear conditioning and extinction. Sci. Rep. 11 , 11177 (2021).

McCullough, K. M. et al. Molecular characterization of Thy1 expressing fear-inhibiting neurons within the basolateral amygdala. Nat. Commun. 7 , 13149 (2016).

Jasnow, A. M. et al. Thy1-expressing neurons in the basolateral amygdala may mediate fear inhibition. J. Neurosci. 33 , 10396–10404 (2013).

Hinrichs, R. et al. Increased skin conductance response in the immediate aftermath of trauma predicts PTSD risk. Chronic Stress 3 , 1–11 (2019).

Milad, M. R. et al. Neurobiological basis of failure to recall extinction memory in posttraumatic stress disorder. Biol. Psychiatry 66 , 1075–1082 (2009).

Etkin, A. & Wager, T. D. Functional neuroimaging of anxiety: a meta-analysis of emotional processing in PTSD, social anxiety disorder, and specific phobia. Am. J. Psychiatry 164 , 1476–1488 (2007).

Steuber, E. R. et al. Thalamic volume and fear extinction interact to predict acute posttraumatic stress severity. Psychiatry Res. 141 , 325–332 (2021).

Kredlow, M. A., Fenster, R. J., Laurent, E. S., Ressler, K. J. & Phelps, E. A. Prefrontal cortex, amygdala and threat processing: implications for PTSD. Neuropsychopharmacology 47 , 247–259 (2022).

Maddox, S. A., Hartmann, J., Ross, R. A. & Ressler, K. J. Deconstructing the gestalt: mechanisms of fear, threat, and trauma memory encoding. Neuron 102 , 60–74 (2019).

Tsvetkov, E., Carlezon, W. A., Benes, F. M., Kandel, E. R. & Bolshakov, V. Y. Fear conditioning occludes LTP-induced presynaptic enhancement of synaptic transmission in the cortical pathway to the lateral amygdala. Neuron 34 , 289–300 (2002).

Josselyn, S. A. et al. Long-term memory is facilitated by cAMP response element-binding protein overexpression in the amygdala. J. Neurosci. 21 , 2404–2412 (2001).

Bremner, J. D. et al. MRI-based measurement of hippocampal volume in patients with combat-related posttraumatic stress disorder. Am. J. Psychiatry 152 , 973–981 (1995).

Bremner, J. D. et al. The environment contributes more than genetics to smaller hippocampal volume in posttraumatic stress disorder (PTSD). J. Psychiatr. Res. 137 , 579–588 (2021).

Logue, M. W. et al. Smaller hippocampal volume in posttraumatic stress disorder: a multisite ENIGMA-PGC study: subcortical volumetry results from posttraumatic stress disorder consortia. Biol. Psychiatry 83 , 244–253 (2018).

Heldt, S. A., Stanek, L., Chhatwal, J. P. & Ressler, K. J. Hippocampus-specific deletion of BDNF in adult mice impairs spatial memory and extinction of aversive memories. Mol. Psychiatry 12 , 656–670 (2007).

Ji, J. & Maren, S. Electrolytic lesions of the dorsal hippocampus disrupt renewal of conditional fear after extinction. Learn. Mem. 12 , 270–276 (2005).

Parsons, R. G. & Ressler, K. J. Implications of memory modulation for post-traumatic stress and fear disorders. Nat. Neurosci. 16 , 146–153 (2013).

Brown, E. S., Rush, A. J. & McEwen, B. S. Hippocampal remodeling and damage by corticosteroids: implications for mood disorders. Neuropsychopharmacology 21 , 474–484 (1999).

Herrmann, L. et al. Long-lasting hippocampal synaptic protein loss in a mouse model of posttraumatic stress disorder. PLoS ONE 7 , e42603 (2012).

Hobin, J. A., Goosens, K. A. & Maren, S. Context-dependent neuronal activity in the lateral amygdala represents fear memories after extinction. J. Neurosci. 23 , 8410–8416 (2003).

Peters, J., Dieppa-Perea, L. M., Melendez, L. M. & Quirk, G. J. Induction of fear extinction with hippocampal-infralimbic BDNF. Science 328 , 1288–1290 (2010).

Milad, M. R. et al. Recall of fear extinction in humans activates the ventromedial prefrontal cortex and hippocampus in concert. Biol. Psychiatry 62 , 446–454 (2007).

Milad, M. R. et al. Thickness of ventromedial prefrontal cortex in humans is correlated with extinction memory. Proc. Natl Acad. Sci. USA 102 , 10706–10711 (2005).

Santhanam, P. et al. Decreases in white matter integrity of ventro-limbic pathway linked to post-traumatic stress disorder in mild traumatic brain injury. J. Neurotrauma 36 , 1093–1098 (2019).

Koch, S. B. J. et al. Decreased uncinate fasciculus tract integrity in male and female patients with PTSD: a diffusion tensor imaging study. J. Psychiatry Neurosci. 42 , 331–342 (2017).

Kennis, M., van Rooij, S. J. H., Reijnen, A. & Geuze, E. The predictive value of dorsal cingulate activity and fractional anisotropy on long-term PTSD symptom severity. Depress. Anxiety 34 , 410–418 (2017).

Sotres-Bayon, F., Sierra-Mercado, D., Pardilla-Delgado, E. & Quirk, G. J. Gating of fear in prelimbic cortex by hippocampal and amygdala inputs. Neuron 76 , 804–812 (2012).

Lanius, R. A., Brand, B., Vermetten, E., Frewen, P. A. & Spiegel, D. The dissociative subtype of posttraumatic stress disorder: rationale, clinical and neurobiological evidence, and implications. Depress. Anxiety 29 , 701–708 (2012).

Mellman, T. A. & Hipolito, M. M. Sleep disturbances in the aftermath of trauma and posttraumatic stress disorder. CNS Spectr. 11 , 611–615 (2006).

Neylan, T. C. et al. Prior sleep problems and adverse post-traumatic neuropsychiatric sequelae of motor vehicle collision in the AURORA study. Sleep 44 , zsaa200 (2021).

van Liempt, S., van Zuiden, M., Westenberg, H., Super, A. & Vermetten, E. Impact of impaired sleep on the development of PTSD symptoms in combat veterans: a prospective longitudinal cohort study. Depress Anxiety 30 , 469–474 (2013).

Pruiksma, K. E. et al. Residual sleep disturbances following PTSD treatment in active duty military personnel. Psychol. Trauma. 8 , 697–701 (2016).

Bryant, R. A., O’Donnell, M. L., Creamer, M., McFarlane, A. C. & Silove, D. Posttraumatic intrusive symptoms across psychiatric disorders. J. Psychiatr. Res. 45 , 842–847 (2011).

Phelps, A. J. et al. Polysomnography study of the post-traumatic nightmares of post-traumatic stress disorder. Sleep 41 , zsx188 (2018).

Harb, G. C. et al. A critical review of the evidence base of imagery rehearsal for posttraumatic nightmares: pointing the way for future research. J. Trauma. Stress 26 , 570–579 (2013).

Norrholm, S. D. et al. Fear load: the psychophysiological over-expression of fear as an intermediate phenotype associated with trauma reactions. Int. J. Psychophysiol. 98 , 270–275 (2015).

Fani, N. et al. Attention bias toward threat is associated with exaggerated fear expression and impaired extinction in PTSD. Psychol. Med. 42 , 533–543 (2012).

Norrholm, S. D. et al. Fear extinction in traumatized civilians with posttraumatic stress disorder: relation to symptom severity. Biol. Psychiatry 69 , 556–563 (2011).

Colvonen, P. J., Straus, L. D., Acheson, D. & Gehrman, P. A review of the relationship between emotional learning and memory, sleep, and PTSD. Curr. Psychiatry Rep. 21 , 2 (2019).

van Liempt, S. et al. Sympathetic activity and hypothalamo-pituitary-adrenal axis activity during sleep in post-traumatic stress disorder: a study assessing polysomnography with simultaneous blood sampling. Psychoneuroendocrinology 38 , 155–165 (2013).

Article   PubMed   CAS   Google Scholar  

Lipinska, G. & Thomas, K. J. F. Rapid eye movement fragmentation, not slow-wave sleep, predicts neutral declarative memory consolidation in posttraumatic stress disorder. J. Sleep. Res. 28 , e12846 (2019).

Onton, J. A., Matthews, S. C., Kang, D. Y. & Coleman, T. P. In-home sleep recordings in military veterans with posttraumatic stress disorder reveal less REM and deep sleep <1 Hz. Front. Hum. Neurosci. 12 , 196 (2018).

Wells, A. M. et al. Effects of chronic social defeat stress on sleep and circadian rhythms are mitigated by kappa-opioid receptor antagonism. J. Neurosci. 37 , 7656–7668 (2017).

Hasler, B. P., Insana, S. P., James, J. A. & Germain, A. Evening-type military veterans report worse lifetime posttraumatic stress symptoms and greater brainstem activity across wakefulness and REM sleep. Biol. Psychol. 94 , 255–262 (2013).

Nestler, E. J. & Carlezon, W. A. Jr. The mesolimbic dopamine reward circuit in depression. Biol. Psychiatry 59 , 1151–1159 (2006).

McCullough, K. M. et al. Nucleus accumbens medium spiny neuron subtypes differentially regulate stress-associated alterations in sleep architecture. Biol. Psychiatry 89 , 1138–1149 (2021).

Sijbrandij, M., Engelhard, I. M., Lommen, M. J., Leer, A. & Baas, J. M. Impaired fear inhibition learning predicts the persistence of symptoms of posttraumatic stress disorder (PTSD). J. Psychiatr. Res. 47 , 1991–1997 (2013).

Rothbaum, B. O. & Davis, M. Applying learning principles to the treatment of post-trauma reactions. Ann. NY Acad. Sci. 1008 , 112–121 (2003).

Ressler, K. J. et al. Post-traumatic stress disorder is associated with PACAP and the PAC1 receptor. Nature 470 , 492–497 (2011).

Ladd, C. O., Plotsky, P. M., Davis, M. in Encyclopedia of Stress 2nd edn (ed. George Fink) 561–568 (Academic, 2007).

Davis, M. Sensitization of the acoustic startle reflex by footshock. Behav. Neurosci. 103 , 495–503 (1989).

Grillon, C., Ameli, R., Woods, S. W., Merikangas, K. & Davis, M. Fear-potentiated startle in humans: effects of anticipatory anxiety on the acoustic blink reflex. Psychophysiology 28 , 588–595 (1991).

Giardino, W. J. & Pomrenze, M. B. Extended amygdala neuropeptide circuitry of emotional arousal: waking up on the wrong side of the bed nuclei of stria terminalis. Front. Behav. Neurosci. 15 , 613025 (2021).

Hinrichs, R. et al. Mobile assessment of heightened skin conductance in posttraumatic stress disorder. Depress Anxiety 34 , 502–507 (2017).

Neylan, T. C., Schadt, E. E. & Yehuda, R. Biomarkers for combat-related PTSD: focus on molecular networks from high-dimensional data. Eur. J. Psychotraumatol. 5 , 23938 (2014).

Yehuda, R., Giller, E. L., Southwick, S. M., Lowy, M. T. & Mason, J. W. Hypothalamic-pituitary-adrenal dysfunction in posttraumatic stress disorder. Biol. Psychiatry 30 , 1031–1048 (1991).

Yehuda, R. et al. Enhanced suppression of cortisol following dexamethasone administration in posttraumatic stress disorder. Am. J. Psychiatry 150 , 83–86 (1993).

Han, X. & Boyden, E. S. Multiple-color optical activation, silencing, and desynchronization of neural activity, with single-spike temporal resolution. PLoS ONE 2 , e299 (2007).

Dunlop, B. W. et al. Corticotropin-releasing factor receptor 1 antagonism is ineffective for women with posttraumatic stress disorder. Biol. Psychiatry 82 , 866–874 (2017).

Jovanovic, T. et al. Psychophysiological treatment outcomes: corticotropin-releasing factor type 1 receptor antagonist increases inhibition of fear-potentiated startle in PTSD patients. Psychophysiology 57 , e13356 (2020).

Galatzer-Levy, I. R. & Bryant, R. A. 636,120 ways to have posttraumatic stress disorder. Perspect. Psychol. Sci. 8 , 651–662 (2013).

Brewin, C. R. The nature and significance of memory disturbance in posttraumatic stress disorder. Annu. Rev. Clin. Psychol. 7 , 203–227 (2011).

Vasterling, J. J. & Arditte Hall, K. A. Neurocognitive and information processing biases in posttraumatic stress disorder. Curr. Psychiatry Rep. 20 , 99 (2018).

Stevens, J. S. & Jovanovic, T. Role of social cognition in post-traumatic stress disorder: a review and meta-analysis. Genes Brain Behav. 18 , e12518 (2019).

Mathias, J. L. & Mansfield, K. M. Prospective and declarative memory problems following moderate and severe traumatic brain injury. Brain Inj. 19 , 271–282 (2005).

Acosta, S. A. et al. Influence of post-traumatic stress disorder on neuroinflammation and cell proliferation in a rat model of traumatic brain injury. PLoS ONE 8 , e81585 (2013).

Elzinga, B. M. & Bremner, J. D. Are the neural substrates of memory the final common pathway in posttraumatic stress disorder (PTSD)? J. Affect. Disord. 70 , 1–17 (2002).

Germine, L. T. et al. Neurocognition after motor vehicle collision and adverse post-traumatic neuropsychiatric sequelae within 8 weeks: initial findings from the AURORA study. J. Affect. Disord. 298 , 57–67 (2022).

Ben-Zion, Z. et al. Neuroanatomical risk factors for posttraumatic stress disorder in recent trauma survivors. Biol. Psychiatry Cogn. Neurosci. Neuroimaging 5 , 311–319 (2020).

Dark, H. E., Harnett, N. G., Knight, A. J. & Knight, D. C. Hippocampal volume varies with acute posttraumatic stress symptoms following medical trauma. Behav. Neurosci. 135 , 71–78 (2021).

van Rooij, S. J. H. et al. The role of the Hippocampus in predicting future posttraumatic stress disorder symptoms in recently traumatized civilians. Biol. Psychiatry 84 , 106–115 (2018).

Girgenti, M. J. et al. Transcriptomic organization of the human brain in post-traumatic stress disorder. Nat. Neurosci. 24 , 24–33 (2021).

Wolf, E. J. et al. Klotho, PTSD, and advanced epigenetic age in cortical tissue. Neuropsychopharmacology 46 , 721–730 (2021).

Olive, I., Makris, N., Densmore, M., McKinnon, M. C. & Lanius, R. A. Altered basal forebrain BOLD signal variability at rest in posttraumatic stress disorder: a potential candidate vulnerability mechanism for neurodegeneration in PTSD. Hum. Brain Mapp. 42 , 3561–3575 (2021).

Mohlenhoff, B. S., O’Donovan, A., Weiner, M. W. & Neylan, T. C. Dementia risk in posttraumatic stress disorder: the relevance of sleep-related abnormalities in brain structure, amyloid, and inflammation. Curr. Psychiatry Rep. 19 , 89 (2017).

Miller, M. W. & Sadeh, N. Traumatic stress, oxidative stress and post-traumatic stress disorder: neurodegeneration and the accelerated-aging hypothesis. Mol. Psychiatry 19 , 1156–1162 (2014).

Mohamed, A. Z., Cumming, P., Gotz, J. & Nasrallah, F., Department of Defense Alzheimer’s Disease Neuroimaging Initiative. Tauopathy in veterans with long-term posttraumatic stress disorder and traumatic brain injury. Eur. J. Nucl. Med. Mol. Imaging 46 , 1139–1151 (2019).

Kaplan, G. B., Vasterling, J. J. & Vedak, P. C. Brain-derived neurotrophic factor in traumatic brain injury, post-traumatic stress disorder, and their comorbid conditions: role in pathogenesis and treatment. Behav. Pharmacol. 21 , 427–437 (2010).

Mojtabavi, H., Saghazadeh, A., van den Heuvel, L., Bucker, J. & Rezaei, N. Peripheral blood levels of brain-derived neurotrophic factor in patients with post-traumatic stress disorder (PTSD): a systematic review and meta-analysis. PLoS One 15 , e0241928 (2020).

Licznerski, P. et al. Decreased SGK1 expression and function contributes to behavioral deficits induced by traumatic stress. PLoS Biol. 13 , e1002282 (2015).

de Kloet, C. S. et al. Assessment of HPA-axis function in posttraumatic stress disorder: pharmacological and non-pharmacological challenge tests, a review. J. Psychiatr. Res. 40 , 550–567 (2006).

Hawn, S. E. et al. GxE effects of FKBP5 and traumatic life events on PTSD: a meta-analysis. J. Affect. Disord. 243 , 455–462 (2019).

Zannas, A. S. & Binder, E. B. Gene-environment interactions at the FKBP5 locus: sensitive periods, mechanisms and pleiotropism. Genes Brain Behav. 13 , 25–37 (2014).

Friend, S. F., Nachnani, R., Powell, S. B. & Risbrough, V. B. C-Reactive protein: marker of risk for post-traumatic stress disorder and its potential for a mechanistic role in trauma response and recovery. Eur. J. Neurosci. https://doi.org/10.1111/ejn.15031 (2020).

Michopoulos, V. et al. Association of prospective risk for chronic PTSD symptoms with low TNFα and IFNγ concentrations in the immediate aftermath of trauma exposure. Am. J. Psychiatry 177 , 58–65 (2020).

Michopoulos, V., Powers, A., Gillespie, C. F., Ressler, K. J. & Jovanovic, T. Inflammation in fear- and anxiety-based disorders: PTSD, GAD, and beyond. Neuropsychopharmacology 42 , 254–270 (2017).

Michopoulos, V. et al. Association of CRP genetic variation and CRP level with elevated PTSD symptoms and physiological responses in a civilian population with high levels of trauma. Am. J. Psychiatry 172 , 353–362 (2015).

Smith, A. K. et al. Differential immune system DNA methylation and cytokine regulation in post-traumatic stress disorder. Am. J. Med. Genet. B Neuropsychiatr. Genet. 156B , 700–708 (2011).

Siegel, C. E. et al. Utilization of machine learning for identifying symptom severity military-related PTSD subtypes and their biological correlates. Transl. Psychiatry 11 , 227 (2021).

Wuchty, S. et al. Integration of peripheral transcriptomics, genomics, and interactomics following trauma identifies causal genes for symptoms of post-traumatic stress and major depression. Mol. Psychiatry 26 , 3077–3092 (2021).

Kuan, P. F. et al. PTSD is associated with accelerated transcriptional aging in World Trade Center responders. Transl. Psychiatry 11 , 311 (2021).

Logue, M. W. et al. An epigenome-wide association study of posttraumatic stress disorder in US veterans implicates several new DNA methylation loci. Clin. Epigenetics 12 , 46 (2020).

Sheerin, C. M. et al. Epigenome-wide study of posttraumatic stress disorder symptom severity in a treatment-seeking adolescent sample. J. Trauma. Stress 34 , 607–615 (2021).

Yang, R. et al. A DNA methylation clock associated with age-related illnesses and mortality is accelerated in men with combat PTSD. Mol. Psychiatry 26 , 4999–5009 (2020).

Smith, A. K. et al. DNA extracted from saliva for methylation studies of psychiatric traits: evidence tissue specificity and relatedness to brain. Am. J. Med. Genet. B Neuropsychiatr. Genet. 168B , 36–44 (2015).

Nievergelt, C. M. et al. International meta-analysis of PTSD genome-wide association studies identifies sex- and ancestry-specific genetic risk loci. Nat. Commun. 10 , 4558 (2019).

Gelernter, J. et al. Genome-wide association study of maximum habitual alcohol intake in >140,000 U.S. European and African American veterans yields novel risk loci. Biol. Psychiatry 86 , 365–376 (2019).

Stein, M. B. et al. Genome-wide association analyses of post-traumatic stress disorder and its symptom subdomains in the Million Veteran Program. Nat. Genet. 53 , 174–184 (2021).

Gelernter, J. et al. Genome-wide association study of post-traumatic stress disorder reexperiencing symptoms in >165,000 US veterans. Nat. Neurosci. 22 , 1394–1401 (2019).

Logue, M. W. et al. The Psychiatric Genomics Consortium Posttraumatic Stress Disorder Workgroup: posttraumatic stress disorder enters the age of large-scale genomic collaboration. Neuropsychopharmacology 40 , 2287–2297 (2015).

Pape, J. C. et al. DNA methylation levels are associated with CRF 1 receptor antagonist treatment outcome in women with post-traumatic stress disorder. Clin. Epigenetics 10 , 136 (2018).

Mizuno, Y. More than 20 years of the discovery of Park2. Neurosci. Res. 159 , 3–8 (2020).

Shaltouki, A. et al. Mitochondrial alterations by PARKIN in dopaminergic neurons using PARK2 patient-specific and PARK2 knockout isogenic iPSC lines. Stem Cell Rep. 4 , 847–859 (2015).

Binder, E. B. et al. Association of FKBP5 polymorphisms and childhood abuse with risk of posttraumatic stress disorder symptoms in adults. JAMA 299 , 1291–1305 (2008).

Heim, C., Owens, M. J., Plotsky, P. M. & Nemeroff, C. B. Persistent changes in corticotropin-releasing factor systems due to early life stress: relationship to the pathophysiology of major depression and post-traumatic stress disorder. Psychopharmacol. Bull. 33 , 185–192 (1997).

CAS   PubMed   Google Scholar  

Bremner, J. D. et al. Elevated CSF corticotropin-releasing factor concentrations in posttraumatic stress disorder. Am. J. Psychiatry 154 , 624–629 (1997).

Dias, B. G. & Ressler, K. J. PACAP and the PAC1 receptor in post-traumatic stress disorder. Neuropsychopharmacology 38 , 245–246 (2013).

Ross, R. A. et al. Circulating PACAP peptide and PAC1R genotype as possible transdiagnostic biomarkers for anxiety disorders in women: a preliminary study. Neuropsychopharmacology 45 , 1125–1133 (2020).

Bangasser, D. A. et al. Sex differences in corticotropin-releasing factor receptor signaling and trafficking: potential role in female vulnerability to stress-related psychopathology. Mol. Psychiatry 15 , 896–904 (2010).

Jovanovic, T. et al. PAC1 receptor (ADCYAP1R1) genotype is associated with dark-enhanced startle in children. Mol. Psychiatry 18 , 742–743 (2013).

Miles, O. W. & Maren, S. Role of the bed nucleus of the stria terminalis in PTSD: insights from preclinical models. Front. Behav. Neurosci. 13 , 68 (2019).

Stroth, N., Holighaus, Y., Ait-Ali, D. & Eiden, L. E. PACAP: a master regulator of neuroendocrine stress circuits and the cellular stress response. Ann. NY Acad. Sci. 1220 , 49–59 (2011).

Ramikie, T. S. & Ressler, K. J. Mechanisms of sex differences in fear and posttraumatic stress disorder. Biol. Psychiatry 83 , 876–885 (2018).

Mercer, K. B. et al. Functional evaluation of a PTSD-associated genetic variant: estradiol regulation and ADCYAP1R1. Transl. Psychiatry 6 , e978 (2016).

Klengel, T. et al. Allele-specific FKBP5 DNA demethylation mediates gene-childhood trauma interactions. Nat. Neurosci. 16 , 33–41 (2013).

Fani, N. et al. FKBP5 and attention bias for threat: associations with hippocampal function and shape. JAMA Psychiatry 70 , 392–400 (2013).

Galatzer-Levy, I. R. et al. A cross species study of heterogeneity in fear extinction learning in relation to FKBP5 variation and expression: implications for the acute treatment of posttraumatic stress disorder. Neuropharmacology 116 , 188–195 (2017).

Yun, J. Y., Jin, M. J., Kim, S. & Lee, S. H. Stress-related cognitive style is related to volumetric change of the hippocampus and FK506 binding protein 5 polymorphism in post-traumatic stress disorder. Psychol. Med. https://doi.org/10.1017/S0033291720002949 (2020).

Hartmann, J. et al. Mineralocorticoid receptors dampen glucocorticoid receptor sensitivity to stress via regulation of FKBP5. Cell Rep. 35 , 109185 (2021).

Herrmann, L. et al. Analysis of the cerebellar molecular stress response led to first evidence of a role for FKBP51 in brain FKBP52 expression in mice and humans. Neurobiol. Stress 15 , 100401 (2021).

Young, K. A., Thompson, P. M., Cruz, D. A., Williamson, D. E. & Selemon, L. D. BA11 FKBP5 expression levels correlate with dendritic spine density in postmortem PTSD and controls. Neurobiol. Stress 2 , 67–72 (2015).

Abdallah, C. G. et al. The neurobiology and pharmacotherapy of posttraumatic stress disorder. Annu. Rev. Pharmacol. Toxicol. 59 , 171–189 (2019).

Watts, B. V. et al. Meta-analysis of the efficacy of treatments for posttraumatic stress disorder. J. Clin. Psychiatry 74 , e541–e550 (2013).

Krystal, J. H. et al. Adjunctive risperidone treatment for antidepressant-resistant symptoms of chronic military service-related PTSD: a randomized trial. JAMA 306 , 493–502 (2011).

Han, C. et al. The potential role of atypical antipsychotics for the treatment of posttraumatic stress disorder. J. Psychiatr. Res. 56 , 72–81 (2014).

Cipriani, A. et al. Comparative efficacy and acceptability of pharmacological treatments for post-traumatic stress disorder in adults: a network meta-analysis. Psychol. Med. 48 , 1975–1984 (2018).

Adamou, M., Puchalska, S., Plummer, W. & Hale, A. S. Valproate in the treatment of PTSD: systematic review and meta analysis. Curr. Med. Res. Opin. 23 , 1285–1291 (2007).

Andrus, M. R. & Gilbert, E. Treatment of civilian and combat-related posttraumatic stress disorder with topiramate. Ann. Pharmacother. 44 , 1810–1816 (2010).

Hertzberg, M. A. et al. A preliminary study of lamotrigine for the treatment of posttraumatic stress disorder. Boil. Psychiatry 45 , 1226–1229 (1999).

Wang, H. R., Woo, Y. S. & Bahk, W. M. Anticonvulsants to treat post-traumatic stress disorder. Hum. Psychopharmacol. 29 , 427–433 (2014).

Davis, L. L. et al. Divalproex in the treatment of posttraumatic stress disorder: a randomized, double-blind, placebo-controlled trial in a veteran population. J. Clin. Psychopharmacol. 28 , 84–88 (2008).

Lindley, S. E., Carlson, E. B. & Hill, K. A randomized, double-blind, placebo-controlled trial of augmentation topiramate for chronic combat-related posttraumatic stress disorder. J. Clin. Psychopharmacol. 27 , 677–681 (2007).

Taylor, F. B. et al. Prazosin effects on objective sleep measures and clinical symptoms in civilian trauma posttraumatic stress disorder: a placebo-controlled study. Biol. Psychiatry 63 , 629–632 (2008).

Raskind, M. A. et al. A parallel group placebo controlled study of prazosin for trauma nightmares and sleep disturbance in combat veterans with post-traumatic stress disorder. Biol. Psychiatry 61 , 928–934 (2007).

Khachatryan, D., Groll, D., Booij, L., Sepehry, A. A. & Schütz, C. G. Prazosin for treating sleep disturbances in adults with posttraumatic stress disorder: a systematic review and meta-analysis of randomized controlled trials. Gen. Hosp. Psychiatry 39 , 46–52 (2016).

Brudey, C. et al. Autonomic and inflammatory consequences of posttraumatic stress disorder and the link to cardiovascular disease. Am. J. Physiol. Regul. Integr. Comp. Physiol. 309 , R315–R321 (2015).

Raskind, M. A. et al. The alpha1-adrenergic antagonist prazosin ameliorates combat trauma nightmares in veterans with posttraumatic stress disorder: a report of 4 cases. J. Clin. Psychiatry 61 , 129–133 (2000).

Porter-Stransky, K. A. et al. Noradrenergic transmission at alpha1-adrenergic receptors in the ventral periaqueductal gray modulates arousal. Biol. Psychiatry 85 , 237–247 (2019).

Mallick, B. N., Singh, S. & Pal, D. Role of alpha and beta adrenoceptors in locus coeruleus stimulation-induced reduction in rapid eye movement sleep in freely moving rats. Behav. Brain Res. 158 , 9–21 (2005).

Germain, A. et al. Placebo-controlled comparison of prazosin and cognitive-behavioral treatments for sleep disturbances in US Military Veterans. J. Psychosom. Res. 72 , 89–96 (2012).

Raskind, M. A. et al. A trial of prazosin for combat trauma PTSD with nightmares in active-duty soldiers returned from Iraq and Afghanistan. Am. J. Psychiatry 170 , 1003–1010 (2013).

Raskind, M. A. et al. Trial of prazosin for post-traumatic stress disorder in military veterans. N. Engl. J. Med. 378 , 507–517 (2018).

Dutkiewics, S. Efficacy and tolerability of drugs for treatment of benign prostatic hyperplasia. Int. Urol. Nephrol. 32 , 423–432 (2001).

Lewis, C., Roberts, N. P., Andrew, M., Starling, E. & Bisson, J. I. Psychological therapies for post-traumatic stress disorder in adults: systematic review and meta-analysis. Eur. J. Psychotraumatol. 11 , 1729633 (2020).

Powers, M. B., Halpern, J. M., Ferenschak, M. P., Gillihan, S. J. & Foa, E. B. A meta-analytic review of prolonged exposure for posttraumatic stress disorder. Clin. Psychol. Rev. 30 , 635–641 (2010).

Pavlov, I. P. & Anrep, G. V. Conditioned Reflexes; An Investigation of the Physiological Activity of the Cerebral Cortex (Oxford Univ. Press, 1927).

Singewald, N., Schmuckermair, C., Whittle, N., Holmes, A. & Ressler, K. J. Pharmacology of cognitive enhancers for exposure-based therapy of fear, anxiety and trauma-related disorders. Pharmacol. Ther. 149 , 150–190 (2015).

Keynan, J. N. et al. Electrical fingerprint of the amygdala guides neurofeedback training for stress resilience. Nat. Hum. Behav. 3 , 63–73 (2019).

Chen, B. K. et al. Sex-specific neurobiological actions of prophylactic (R,S)-ketamine, (2R,6R)-hydroxynorketamine, and (2S,6S)-hydroxynorketamine. Neuropsychopharmacology 45 , 1545–1556 (2020).

Van’t Veer, A. & Carlezon, W. A. Jr. Role of kappa-opioid receptors in stress and anxiety-related behavior. Psychopharmacology 229 , 435–452 (2013).

Smith, A. K. et al. Epigenome-wide meta-analysis of PTSD across 10 military and civilian cohorts identifies methylation changes in AHRR. Nat. Commun. 11 , 5965 (2020).

Mellon, S. H. et al. Metabolomic analysis of male combat veterans with post traumatic stress disorder. PLoS ONE 14 , e0213839 (2019).

Bremner, J. D. Neuroimaging in posttraumatic stress disorder and other stress-related disorders. Neuroimaging Clin. N. Am. 17 , 523–538 (2007).

Britton, J. C., Phan, K. L., Taylor, S. F., Fig, L. M. & Liberzon, I. Corticolimbic blood flow in posttraumatic stress disorder during script-driven imagery. Biol. Psychiatry 57 , 832–840 (2005).

Insel, T. R. The NIMH Research Domain Criteria (RDoC) Project: precision medicine for psychiatry. Am. J. Psychiatry 171 , 395–397 (2014).

Hyman, S. Mental health: depression needs large human-genetics studies. Nature 515 , 189–191 (2014).

Bale, T. L. et al. The critical importance of basic animal research for neuropsychiatric disorders. Neuropsychopharmacology 44 , 1349–1353 (2019).

Baker, J. T., Germine, L. T., Ressler, K. J., Rauch, S. L. & Carlezon, W. A. Jr. Digital devices and continuous telemetry: opportunities for aligning psychiatry and neuroscience. Neuropsychopharmacology 43 , 2499–2503 (2018).

Cakmak, A. S. et al. Classification and prediction of post-trauma outcomes related to PTSD using circadian rhythm changes measured via wrist-worn research watch in a large longitudinal cohort. IEEE J. Biomed. Health Inf. 25 , 2866–2876 (2021).

Tsanas, A., Woodward, E. & Ehlers, A. Objective characterization of activity, sleep, and circadian rhythm patterns using a wrist-worn actigraphy sensor: insights into posttraumatic stress disorder. JMIR Mhealth Uhealth 8 , e14306 (2020).

Thompson, R. S. et al. Repeated fear-induced diurnal rhythm disruptions predict PTSD-like sensitized physiological acute stress responses in F344 rats. Acta Physiol. 211 , 447–465 (2014).

Phillips, A. G., Geyer, M. A. & Robbins, T. W. Effective use of animal models for therapeutic development in psychiatric and substance use disorders. Biol. Psychiatry 83 , 915–923 (2018).

Van’t Veer, A., Yano, J. M., Carroll, F. I., Cohen, B. M. & Carlezon, W. A. Jr. Corticotropin-releasing factor (CRF)-induced disruption of attention in rats is blocked by the kappa-opioid receptor antagonist JDTic. Neuropsychopharmacology 37 , 2809–2816 (2012).

Vogel, S. C. et al. Childhood adversity and dimensional variations in adult sustained attention. Front. Psychol. 11 , 691 (2020).

White, S. F. et al. Increased cognitive control and reduced emotional interference is associated with reduced PTSD symptom severity in a trauma-exposed sample: a preliminary longitudinal study. Psychiatry Res. Neuroimaging 278 , 7–12 (2018).

Beard, C. et al. Abnormal error processing in depressive states: a translational examination in humans and rats. Transl. Psychiatry 5 , e564 (2015).

Robble, M. A. et al. Concordant neurophysiological signatures of cognitive control in humans and rats. Neuropsychopharmacology 46 , 1252–1262 (2021).

Der-Avakian, A. et al. Social defeat disrupts reward learning and potentiates striatal nociceptin/orphanin FQ mRNA in rats. Psychopharmacology 234 , 1603–1614 (2017).

Lokshina, Y., Nickelsen, T. & Liberzon, I. Reward processing and circuit dysregulation in posttraumatic stress disorder. Front. Psychiatry 12 , 559401 (2021).

Lori, A. et al. Transcriptome-wide association study of post-trauma symptom trajectories identified GRIN3B as a potential biomarker for PTSD development. Neuropsychopharmacology 46 , 1811–1820 (2021).

Pacella, M. L., Hruska, B., Steudte-Schmiedgen, S., George, R. L. & Delahanty, D. L. The utility of hair cortisol concentrations in the prediction of PTSD symptoms following traumatic physical injury. Soc. Sci. Med. 175 , 228–234 (2017).

McCullough, K. M. et al. Genome-wide translational profiling of amygdala Crh-expressing neurons reveals role for CREB in fear extinction learning. Nat. Commun. 11 , 5180 (2020).

Boyden, E. S., Zhang, F., Bamberg, E., Nagel, G. & Deisseroth, K. Millisecond-timescale, genetically targeted optical control of neural activity. Nat. Neurosci. 8 , 1263–1268 (2005).

Zhang, F. et al. Multimodal fast optical interrogation of neural circuitry. Nature 446 , 633–639 (2007).

Chow, B. Y. et al. High-performance genetically targetable optical neural silencing by light-driven proton pumps. Nature 463 , 98–102 (2010).

Han, X. et al. A high-light sensitivity optical neural silencer: development and application to optogenetic control of non-human primate cortex. Front. Syst. Neurosci. 5 , 18 (2011).

Luchkina, N. V. & Bolshakov, V. Y. Diminishing fear: optogenetic approach toward understanding neural circuits of fear control. Pharmacol. Biochem. Behav. 174 , 64–79 (2018).

Gradinaru, V. et al. Molecular and cellular approaches for diversifying and extending optogenetics. Cell 141 , 154–165 (2010).

Coward, P. et al. Controlling signaling with a specifically designed Gi-coupled receptor. Proc. Natl Acad. Sci. USA 95 , 352–357 (1998).

Dong, S., Rogan, S. C. & Roth, B. L. Directed molecular evolution of DREADDs: a generic approach to creating next-generation RASSLs. Nat. Protoc. 5 , 561–573 (2010).

Roth, B. L. DREADDs for neuroscientists. Neuron 89 , 683–694 (2016).

Lin, M. Z. & Schnitzer, M. J. Genetically encoded indicators of neuronal activity. Nat. Neurosci. 19 , 1142–1153 (2016).

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Acknowledgements

This work was supported by NIH awards P50-MH115874 (to W.C./K.J.R.), R01-MH108665 (to K.J.R.), R01-MH063266 (to W.C.), R01-MH123993 (to V.Y.B.), and the Frazier Institute at McLean Hospital (to K.J.R.). I.R. was partially supported by (R01-MH120400).

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K.J.R. has received consulting income from Alkermes, Bionomics, Bioxcel and Jazz Pharmaceuticals, and is on scientific advisory boards for the Army STARRS Project, Janssen, the National Center for PTSD, Sage Therapeutics and Verily. He has also received sponsored research support from Brainsway and Takeda. He also serves on the Boards of ACNP and Biological Psychiatry. W.C. has received consulting income from Psy Therapeutics and has a sponsored research agreement with Cerevel Therapeutics. He is the editor-in-chief for Neuropsychopharmacology and serves on the board of ACNP. None of this work is directly related to the work presented here. S.L.R. receives compensation as a Board member of Community Psychiatry and for his role as Secretary of SOBP. He also serves on the Boards of ADAA and NNDC. He has received royalties from Oxford University Press and APPI.

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A core feature of post-traumatic stress disorder (PTSD) that includes irritability, panic and disruptions in sleep and cognitive function.

A reflex that occurs rapidly and unconsciously in response to an external stimulus such as a noise burst.

A core feature of post-traumatic stress disorder (PTSD) characterized by a heightened state of active threat assessment.

A method of inducing alterations in gene expression involving the ability of the enzyme Cre-recombinase to induce site-specific recombination of genetic material.

A theoretical representation of a neural unit of memory storage.

A muscle located in the eyelid, activity of which is often an end point in human fear conditioning research.

Secondary phenotypes that reliably co-occur as a sub-feature of a broader primary phenotype.

Two or more biological processes that are modulated (activated, suppressed) in parallel by a common upstream factor.

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Ressler, K.J., Berretta, S., Bolshakov, V.Y. et al. Post-traumatic stress disorder: clinical and translational neuroscience from cells to circuits. Nat Rev Neurol 18 , 273–288 (2022). https://doi.org/10.1038/s41582-022-00635-8

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research paper on post traumatic stress disorder

Post-traumatic stress disorder: evidence-based research for the third millennium

Affiliation.

  • 1 David Geffen School of Medicine at UCLA, USA.
  • PMID: 16322808
  • PMCID: PMC1297500
  • DOI: 10.1093/ecam/neh127

The stress that results from traumatic events precipitates a spectrum of psycho-emotional and physiopathological outcomes. Post-traumatic stress disorder (PTSD) is a psychiatric disorder that results from the experience or witnessing of traumatic or life-threatening events. PTSD has profound psychobiological correlates, which can impair the person's daily life and be life threatening. In light of current events (e.g. extended combat, terrorism, exposure to certain environmental toxins), a sharp rise in patients with PTSD diagnosis is expected in the next decade. PTSD is a serious public health concern, which compels the search for novel paradigms and theoretical models to deepen the understanding of the condition and to develop new and improved modes of treatment intervention. We review the current knowledge of PTSD and introduce the role of allostasis as a new perspective in fundamental PTSD research. We discuss the domain of evidence-based research in medicine, particularly in the context of complementary medical intervention for patients with PTSD. We present arguments in support of the notion that the future of clinical and translational research in PTSD lies in the systematic evaluation of the research evidence in treatment intervention in order to insure the most effective and efficacious treatment for the benefit of the patient.

SYSTEMATIC REVIEW article

Post-traumatic stress disorder in the ethiopian population dwelling in war-affected communities: a systematic review and meta-analysis.

Techilo Tinsae*

  • 1 Department of Psychiatry, College of Medicine and Health Science, University of Gondar, Gondar, Ethiopia
  • 2 Department of Psychiatry, School of Medicine, College of Medicine and Health Sciences, University of Gondar, Gondar, Ethiopia
  • 3 Department of Psychiatry, Mattu University, Mettu, Ethiopia

Background: Post-traumatic stress disorder (PTSD) is a significant mental health concern globally, particularly prevalent in populations exposed to war and conflict. This systematic review and meta-analysis aim to examine the prevalence and factors associated with PTSD among the Ethiopian population residing in war-affected communities.

Methods: The review was reported according to the PRISMA guidelines. Related eligible published articles were searched in electronic online databases such as PubMed, Scopus, Web of Science, MEDLINE/PubMed, Scopus, Embase, Science Direct, Web of Science, Google Scholar, and Google, which reported the prevalence and risk factors of PTSD among people dwelling in the war-affected area until January 2024. The relevant data was extracted using a Microsoft Excel spreadsheet. The meta-analysis was conducted using STATA version 11. The estimated pooled prevalence and risk factors were estimated using a random effect model. The potential risk of publication bias was checked using a funnel plot and Egger’s statistical test.

Results: A total of nine published studies with 6107 participants were analyzed in this meta-analysis. The estimated pooled prevalence of PTSD among people living in war-affected areas was 48.4%, with a 95% CI (37.1, 59.8). This study found a higher prevalence of PTSD among women than men. Being female (OR= 2.2, 95% CI: 1.2, 4.3), witnessing a murder of a loved one (OR= 3.0, 95% CI: 1.2, 7.5), depression symptoms (OR= 2.8, 95% CI: 1.4, 5.6), and anxiety symptoms (OR= 3.4, 95% CI: 1.4, 8.0), a close family member killed or seriously injured (OR= 3.1, 95% CI: 1.2, 7.7), a moderate and high perceived threat to life (OR= 3.4, 95% CI: 1.3, 9.1), and poor social support (OR= 4.4, 95% CI: 1.1, 18.7) were associated with post-traumatic stress disorder.

Conclusion: The result of this study shows the high prevalence rate of PTSD in people living in war-affected areas. disparities in PTSD prevalence, with women being at higher risk, and identified risk factors were witnessing the murder of a loved one, experiencing depression and anxiety, and perceived threat to life. Addressing PTSD in war-affected communities requires comprehensive interventions that consider both individual and contextual factors.

Systematic review registration: www.crd.york.ac.uk/PROSPERO/ , identifier CRD42024501384.

Introduction

Post-traumatic stress disorder (PTSD) is a common, disabling disorder that occurs after exposure to traumatic events ( 1 ). Post-traumatic stress can cause a pattern of symptoms that includes a delayed response to an acutely stressful and life-threatening situation or event, such as combat exposure during wartime ( 2 ). These symptoms could occur either during or immediately after the occurrence of the traumatic event, or even several days later. The symptoms of traumatic events include initially intense fear or instability, horror, nightmares, and hopelessness. Later, the individual could develop a response to traumatic events that are characterized by persistently re-experiencing the traumatic events, avoidance and hyper-arousal, agitation, anxiety, sleep disturbance, and avoidance of the reminder ( 3 – 5 ). These symptoms of PTSD should persist for more than a month and could cause significant functional impairment.

For the last five years, Ethiopia has experienced multiple internal conflicts, deaths, and injuries. Ethiopia’s history of conflict, including the Derg regime, the Eritrean War of Independence, and recent conflicts in regions like Tigray and Amhara has left a legacy of trauma and psychological distress among its population. The cumulative effects of these conflicts have deeply impacted individuals, families, and communities, necessitating comprehensive efforts to address the mental health needs of war-affected populations and promote healing and reconciliation within Ethiopian society ( 6 ). According to studies, war-related victims had a higher rate of PTSD ( 7 , 8 ) than the general population. According to World Health Organization reports, 21.7% of people in conflict situations have PTSD ( 9 ). According to a meta-analysis carried out in war conflict-affected areas, the population that has settled in the affected area has a pooled prevalence of PTSD of 23.5% ( 10 ). Another systematic review and meta-analysis were conducted in sub-Saharan African countries in conflict-exposed regions, where the pooled prevalence of PTSD was 30% ( 11 ), and in a recent cross-sectional survey conducted in Ukraine, the prevalence of post-traumatic stress disorder (PTSD) was found to be 23.5% ( 12 ).

The majority of people affected by conflict may experience several traumas such as the death of a loved one or family member, severe physical harm, sexual or emotional trauma, socioeconomic disadvantages, poverty, altered family dynamics, loss of social support, difficulty obtaining education, encountering hostility and racism, and living in an extremely congested area ( 13 – 15 ). PTSD is linked to the risk of developing physical health problems such as sleep disturbances, parenting difficulties, and interpersonal problems and is most strongly associated with comorbid depression, substance use, and suicidal behavior ( 16 , 17 ). It is also linked with decreased well-being and unemployment when it persists unremittingly for years ( 18 – 20 ).

Various studies were conducted to show the rate and potential risk factors of PTSD in Ethiopia, which range from 19.4% ( 21 ) to 67.5% ( 22 ), but they demonstrated great variation across geographical settings. Based on this fact, there was a need for nationally representative data on the rate and determinant factors of PTSD among war-exposed individuals in the country. In addition, the existing epidemiological data on post-traumatic stress disorder in residents of conflict-affected areas is desperately needed to assess the precise burden of prevalence and risk factors for PTSD to allocate resources for health care appropriately and effectively. Given the lack of concrete coverage regarding the prevalence and determinants of post-traumatic stress disorder (PTSD) in conflict-affected regions of Ethiopia, this systematic review and meta-analysis aimed to address this gap. The primary objective was to provide an estimation of the pooled prevalence of PTSD and identify determinant risk factors among individuals residing in war-affected communities in Ethiopia.

Searching strategy

The detailed protocol of this systematic review and meta-analysis was registered in PROSPERO with a reference number of CRD42024501384. This study was reported according to the preferred Reporting Items for Systematic Review and Meta-analysis (PRISMA) guideline. Before reporting the meta-analysis, the relevant published articles were searched in public electronic databases such as MEDLINE/PubMed, Scopus, Embase, Science Direct, Web of Science, Google Scholar, and Google, which reported the prevalence and risk factors of PTSD among people dwelling in the war-affected area until January 2024. The search process was performed in the English language using appropriate keywords, including post-trauma stress disorder, trauma, post-trauma, stress, conflict, war-affected area, trauma disorder, post-trauma disorder, stress-related disorder, trauma-related disorder, post-conflict, prevalence of PTSD, and determinants of PTSD. In addition, the AND/OR operator was also used to obtain more comprehensive access to all articles. PubMed searching strategies: ((((((((post-trauma stress disorder [title/abstract]) OR post-trauma [title/abstract]) AND stress-related disorder OR trauma-related disorder [title/abstract]) OR war-affected area [title/abstract]) OR PTSD (title/abstract]) OR post-conflict [title/abstract]) AND prevalence of PTSD [title/abstract]) OR determinant of PTSD [title/abstract]) OR Ethiopia.

Eligibility criteria

Inclusion criteria.

The studies’ inclusion criteria include observational studies (cross-sectional and survey studies), in which the original published paper reports the prevalence and risk factors of PTD. The population lives in war-affected areas. Eligible literature published in the English language. Literature conducted in Ethiopia, available up to January 2024, met the inclusion criteria.

Exclusion criteria

Case reports, interventional studies, qualitative studies, studies without full-text accessibility, editor’s letters, studies with inadequate data, studies unrelated to the topic, review studies, and duplicate studies are among the exclusion criteria in this research.

Data extraction and quality assessment

Two authors (author one and author four) were individually involved in the extraction of relevant studies from the databases. All the eligible studies were screened. After the selection of eligible studies, study characteristics, and relevant data, the name of the author, publication year, study location and setting, study design, sampling method, sample size, response rate, screening tool, and prevalence were extracted. We contacted authors through email for additional information whenever required. In cases of disagreement between two reviewers, arbitration was made by other authors. The authors used the Newcastle-Ottawa Scale (NOS) ( 23 ) critical appraisal checklist adopted for a cross-sectional study. The scale is used to score the articles under three categories: (i) selection (score 0−5); (ii) comparability (score 0−2); and (iii) outcome (score 0−3); the total score range is 0−10. The selection category consists of parameters, such as representativeness of the sample, adequacy of the sample size, non-response rate, and use of a validated measurement tool to gather data on exposure. The comparability category examines whether subjects in different outcome groups are comparable based on the study design and analysis and whether confounding factors were controlled for or not. The outcome category includes whether data on outcome (s) were collected by independent blind assessment, through records, or by self-reporting. The outcome category also includes whether the statistical tests used to analyze the data were clearly described and whether these tests were appropriate or not. Stars were assigned to evaluate study quality: 9–10 stars indicate ‘ very good’ quality, 7–8 stars ‘good’ quality, 5–6 stars ‘satisfactory’ quality, and 0–4 stars ‘unsatisfactory’ quality ( 23 ).

Outcome variables

The primary outcome of this systematic review and meta-analysis was to assess the prevalence and risk factors of PTSD in people dwelling in war-affected areas.

Heterogeneity and publication bias

The existence of heterogeneity was checked by inverse variance (I 2 ) was used to quantify it. The values of statistics of 25%, 50%, and 75% were used to declare low, moderate, and high heterogeneity, respectively ( 24 ). The publication bias was checked visually by funnel plot, and objectively using Egger’s statistical test. In addition, a p-value less than 0.05 was used to declare the presence of heterogeneity across studies and publication bias ( 25 ). to declare the absence of publication bias. Trim and fill analyses were conducted to manage the publication bias.

Statistical analysis

The data were retrieved in Microsoft Excel spreadsheet format. The analysis was conducted using STATA version 11 statistical software. The logarithm and standard error of the odds ratio (OR) for each included study were generated using the generate command on STATA. The pooled prevalence of PTSD and its risk factors were presented in the form of a forest plot. The presence of heterogeneity among the included studies was checked by the inverse variance index (I 2 ), and the authors considered I 2 values > 50% to represent significant heterogeneity ( 26 ). An estimated pooled prevalence and associated risk factors of PTSD Random effect model were computed to estimate the pooled prevalence and associated risk factors of PTSD among people dwelling in war-affected communities using a forest plot diagram with a corresponding 95% CI and OR. A funnel plot was used to check the presence of publication bias. In addition, Egger’s statistical test was used to check the statistical significance of publication bias. The sensitivity analysis was done with the random effect model to observe the effect of a single study on the overall pooled estimate.

Literature searching

The search strategy retrieved 6345 articles. After the removal of duplication articles, 268 articles remained. Based on the eligibility criteria 34 full-text articles were accessed for eligibility, 19 were excluded due to unrelated titles, and 6 articles due to lack of outcome interest. Finally, 9 eligible full-text articles were used to analyze this meta-analysis ( Figure 1 ).

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Figure 1 Study selection process.

Characteristics of the included studies

In this systematic review and meta-analysis, nine primary studies were involved. Among the included studies, eight studies were from the Amhara region ( 21 , 22 , 27 – 31 ), and one study was from the Southern Nations, Nationalities, and Peoples’ Region (SNNPR) ( 32 ) ( Table 1 ). All of the articles were published in the most recent four-year period (2020-2023). All of the articles were conducted using a cross-sectional study design. Most of the studies were assessed using the PTSD checklist for DSM-5 (PCL-5) measurement tool. Regarding study settings of the primary study, seven eligible studies were conducted in community-based settings whereas two studies were conducted in internally displaced people (IDP) settings.

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Table 1 Characteristics of included studies among people dwelling in war-affected areas, in Ethiopia (n = 9).

Qualities of studies

The Newcastle-Ottawa Scale (NOS) was used to assess the quality of the included studies methodologically. In the evaluation, we assessed 9 articles to satisfy the quality assessment in terms of selection, outcome measurement, and statistical test. The risk of bias in each study was assessed using kappa values, which range from 0.88 to 1 ( Table 2 ).

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Table 2 The quality and agreed level of bias and level of agreement on the method qualities include articles in this systematic review and meta-analysis based on a sample, outcome, objective, response rate, and analysis method (n = 9) .

The estimated pooled prevalence of post-traumatic stress disorder

Based on the random effect model, the overall pooled prevalence of post-traumatic stress disorder among people dwelling in war-affected areas was 48.42% with a 95% CI (37.08, 59.77) ( Figure 2 ). From records of this meta-analysis, we observed the highest prevalence rate of PTSD in women (48.3% with a 95% CI of 35.6, 61.0) ( Figure 3 ) than in men (37.1% with a 95% CI of 27.3, 46.9) ( Figure 4 ).

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Figure 2 Forest Plot describing the pooled prevalence of PTSD among people dwelling in war-affected areas in Ethiopia with a 95% CI.

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Figure 3 Forest Plot describing the pooled prevalence of PTSD among women dwelling in war-affected areas in Ethiopia with a 95% CI.

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Figure 4 Forest Plot describing the pooled prevalence of PTSD among men dwelling in war-affected areas in Ethiopia with a 95% CI.

Subgroup analysis

Subgroup analysis was conducted based on the study setting of the primary studies, which were done in community-based and IDP settings. According to the findings, we observed a higher prevalence of PTSD in IDP settings (62.94% with a 95% CI of 54.02-71.85) than in community-based studies (44.32% with a 95% CI of 31.98-56.65) ( Figure 5 ).

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Figure 5 Subgroup analysis based on the study settings of PTSD among people dwelling in war-affected areas.

Publication bias and sensitivity analysis

The included studies were checked to assess the potential publication bias visually by funnel plot. The funnel plot is a symmetrical distribution. This indicates the absence of publication bias since the included studies fell within the triangular region ( Figure 6 ). In addition, the results of Egger’s test showed the presence of publication bias (P-value< 0.05) ( Table 3 ). So, we used trim and fill analysis to manage this publication bias ( Figure 7 ). The sensitivity analysis was done with the random effect model to observe the effect of a single study on the overall pooled estimate. The result showed that the included did not show significant differences ( Figure 8 ).

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Figure 6 Funnel plot with a pseudo95% confidence interval that describes the heterogeneity of the pooled prevalence of PTSD among people dwelling in war-affected areas in Ethiopia.

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Table 3 Egger’s test of PTSD among people dwelling in war-affected areas in Ethiopia.

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Figure 7 Trim and fill analysis of PTSD among people dwelling in war-affected areas in Ethiopia, 2024.

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Figure 8 The sensitivity analysis for the pooled estimate of PTSD among people dwelling in war-affected areas in Ethiopia.

Factors associated with post-traumatic stress disorder

Of nine included studies seven studies that conveyed the factors associated with post-traumatic stress disorder among people that dwell in war-affected areas were incorporated in this systematic review and meta-analysis. Based on the random effect model, the following factors were associated with the occurrence of post-traumatic stress disorder among conflict victim individuals. The odds of being female (POR = 2.25: 95% CI: 1.16, 4.35), the odds of having witnessed a murder of a loved one (POR = 2.98; 95% CI: 1.19, 7.49), Conflict victim individuals who had depression symptoms (POR =2.78: 95% CI: 1.38, 5.61) and anxiety symptoms (POR = 3.36; 95% CI: 1.42, 7.99), the odds of a close family member killed or seriously injured (POR = 3.05; 95% CI: 1.21, 7.74), conflict victim individuals who had a moderate and high perceived threat to life (POR = 3.41; 95% CI: 1.28, 9.08) and (POR = 4.94; 95% CI: 1.47, 16.52), conflict victim individual who had poor social support (POR = 4.45; 95%: 1.06, 18.71) were associated with post-traumatic stress disorder ( Figure 9 ).

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Figure 9 Factors associated with PTSD among people dwelling in war-affected areas in Ethiopia.

This systematic review and meta-analysis tried to ascertain the concrete pooled evidence on the prevalence and associated risk factors of PTSD among people living in war-affected areas in Ethiopia. For the last six years, Ethiopia has experienced multiple internal conflicts. Even though different scholars attempted to show the prevalence and associated risk factors of PTSD, aggregated pooled evidence was not presented. In our study, around nine relevant, eligible primary studies with 6107 participants were incorporated to conduct this analysis. This meta-analysis showed that the estimated pooled prevalence of PTSD among people dwelling in war-affected areas was 48.42% with a 95% CI (37.08, 59.77). Additionally, our research verified that eight common factors exacerbate the occurrence of PTSD in people dwelling in war-affected areas —being female, having witnessed a loved one’s murder, experiencing symptoms of depression or anxiety, having a close family member killed or gravely injured, feeling that one’s life is in danger, and having inadequate social support—are linked to post-traumatic stress disorder (PTSD). These show that in creating plans to stop and treat PTSD in war-affected communities, related variables need to be taken into account.

According to this meta-analysis, we found a higher prevalence rate of PTSD among women than men living in war-affected areas. The results of this finding are supported by previous meta-analyses done in war-affected areas ( 33 – 37 ). The possible justification for this discrepancy might be the fact that men and women may utilize different coping strategies in response to trauma. Women may be more likely to ruminate on traumatic events or seek social support, while men may be more inclined to use avoidance or substance abuse as coping mechanisms. Societal norms and gender roles can influence how men and women cope with traumatic events. Women may face greater stigma or barriers to seeking help, leading to higher rates of untreated PTSD, or women may experience different types of trauma compared to men during conflicts. They might be more likely to experience sexual violence, which can lead to a higher risk of developing PTSD or hormonal differences between men and women may play a role in the development and manifestation of PTSD symptoms. For example, fluctuations in estrogen levels can affect the stress response and emotional regulation. Therefore, addressing these disparities requires a multifaceted approach that considers gender-specific needs and challenges in mental health support and intervention programs.

The overall pooled prevalence of post-traumatic stress disorder (PTSD) in our study was 48.42%. The finding result of this study is similar to previous meta-analysis studies done on African migrants, accounting for 37.9% ( 38 ), Ethiopia at 39% ( 14 ), Africa at 55.64% ( 39 ), and the meta-analysis conducted among immigration at 42% ( 40 ). It suggested that the similarity in prevalence rates across different studies validates the reliability and robustness of the findings, strengthening the evidence base for the prevalence of PTSD in these contexts. This consistency also highlights the urgency of addressing the mental health needs of vulnerable populations, particularly those exposed to trauma in war-affected areas. However, the prevalence of PTSD in the current systematic review is higher than in previous systematic reviews conducted in the war-affected area, with a point prevalence of around 26.51% ( 41 ); systematic reviews and meta-analyses carried out among Palestinian children and adolescents exposed to political violence (36% ( 42 );, another systematic review and meta-analysis were carried out in youth exposed to the Syrian crisis; the pooled prevalence of PTSD was 36%, 36.9% ( 43 , 44 ); and another systematic review was carried out in individuals involved in armed conflict; the pooled prevalence was approximately 31% ( 45 ). The possible justification for this discrepancy might be due to the nature of traumatic experiences can vary widely across different conflict-affected populations. For example, populations experiencing systematic persecution, genocide, or mass displacement may be exposed to more severe and pervasive trauma compared to those facing localized conflict or political unrest. The severity and complexity of traumatic experiences can contribute to higher rates of PTSD. The severity of PTSD can be influenced by the intensity and frequency of trauma exposure. Populations experiencing more severe and frequent traumatic events, such as direct combat exposure, prolonged displacement, or mass atrocities, may have higher rates of PTSD compared to those exposed to less severe trauma. The cumulative impact of multiple traumatic events over time can exacerbate the risk of developing PTSD. Populations exposed to ongoing or recurrent violence, displacement, and human rights abuses may experience cumulative trauma, leading to higher rates of PTSD compared to those exposed to isolated traumatic events. Sociocultural norms and beliefs surrounding trauma, mental health, and help-seeking behaviors can vary widely across different populations. The stigma surrounding mental illness, particularly PTSD, may vary, affecting the likelihood of individuals reporting symptoms and seeking treatment. Therefore, considering the severity of traumatic events is essential for understanding the variation in PTSD prevalence estimates across different conflict-affected populations. It highlights the importance of addressing the underlying determinants of trauma exposure and providing comprehensive support and intervention strategies to mitigate the impact of severe trauma on mental health outcomes.

According to the subgroup analysis report a higher prevalence of PTSD was found among participants in IDP settings than in community-based study settings. This finding of this result is supported by previous studies conducted in Africa ( 46 , 47 ). The possible justification for this discrepancy might be due to trauma exposure which is an individual in IDP settings may have experienced higher levels of trauma due to forced displacement, conflict, or natural disasters compared to those in stable community settings. The ongoing stressors and uncertainties in IDP settings can contribute to a higher prevalence of PTSD. On the other hand, it might be due to social support factors because community-based studies may include individuals with stronger social support networks, which can act as protective factors against developing PTSD. Conversely, IDP settings may lack such support networks due to disrupted social structures and loss of community ties, thereby increasing vulnerability to PTSD. In addition, this might be due to environmental effects hence living conditions in IDP settings, such as overcrowding, lack of necessities, and exposure to ongoing violence or threats, can exacerbate stress levels and contribute to the development or persistence of PTSD symptoms.

Factors associated with this systematic review and meta-analysis: being female was the risk factor for developing post-traumatic stress disorder in people dwelling in war-affected communities. This finding is supported by previous studies ( 48 – 54 ). The possible reason is that women may be more likely to experience certain types of trauma during conflicts than men, such as sexual violence, intimate partner violence, or gender-based discrimination. These types of traumatic experiences can increase the risk of developing PTSD. Sociocultural factors may play a major role in the development of PTSD, such as sociocultural norms and expectations surrounding gender roles can influence how men and women perceive and respond to traumatic events. Women may face additional stressors related to caregiving responsibilities, social roles, and cultural expectations, which can impact their risk of developing PTSD. Biological factors that might be exacerbating the occurrence of PTSD, such as hormonal differences between men and women, can influence the stress response and susceptibility to PTSD. For example, fluctuations in estrogen levels in women may affect the regulation of stress hormones and contribute to increased vulnerability to PTSD.

Among participants, having a history of witnessing the murder of a loved one or being seriously injured increases three times the risk of developing post-traumatic stress disorder in people living in war-affected communities compared to their counterparts. This finding was supported by studies conducted previously ( 27 , 55 ). The possible reason could be the fact that the severity of the traumatic events may increase the occurrence of PTSD because individuals who have witnessed the murder of a loved one or experienced serious injury often face more severe and direct exposure to traumatic events compared to their counterparts. The intensity and severity of traumatic exposure can significantly impact the risk of developing PTSD, with more severe traumas associated with a higher risk. Also, this might be due to the nature of traumatic events, such as witnessing the murder of a loved one or experiencing serious injury represents traumatic events that involve a high degree of violence, threat to life, and loss. These types of traumas are known to be particularly distressing and are associated with a higher risk of developing PTSD compared to other types of traumatic experiences, or they might be due to survivor guilt; hence, individuals who survive traumatic events in which loved ones are killed or seriously injured may experience survivor guilt, feeling guilty for having survived while others did not, or the reason might be due to psychological effects. Traumatic events involving the murder of a loved one or serious injury can have profound psychological effects, including feelings of helplessness, horror, grief, guilt, and betrayal. These psychological reactions can significantly increase the risk of developing PTSD.

Depression and anxiety were other risk factors associated with PTSD compared to those who did not have depression and anxiety symptoms in war-affected areas. These results are supported by the previous study ( 56 – 58 ). The possible reason might be that individuals with a predisposition to depression and anxiety may also be more susceptible to developing PTSD following exposure to traumatic events. These conditions may interact and exacerbate each other, leading to greater symptom severity and impairment, or they might be due to depression, which may arise from feelings of hopelessness, worthlessness, and loss of interest or pleasure in activities. Anxiety may manifest as persistent worry, hyperarousal, and avoidance of trauma-related stimuli. These psychological responses can co-occur with PTSD symptoms and contribute to the complexity of trauma-related mental health issues, or they might be due to impairment of coping functioning, hence; depression and anxiety symptoms can impair individuals’ ability to cope with traumatic stressors and regulate their emotions effectively. Persistent feelings of sadness, worry, and fear may interfere with adaptive coping strategies and exacerbate PTSD symptoms. Conversely, PTSD symptoms such as intrusive memories, hypervigilance, and avoidance behaviors can exacerbate depression and anxiety.

In addition, individuals who had a moderate and high perceived threat to life were associated with risk factors for PTSD compared with their counterparts in war-affected areas. This might be due to the intensity of traumatic events because a perceived threat to life represents a significant aspect of traumatic experiences in war-affected areas. Individuals who perceive themselves to be in imminent danger or at risk of death during conflict-related events are more likely to experience intense fear, helplessness, and horror, which are core features of PTSD, or it might be due to a sense of control and safety; hence, perceived threats to life can undermine individuals’ sense of control and safety, leading to feelings of vulnerability and powerlessness. The loss of control and perceived inability to protect oneself or loved ones during traumatic events can exacerbate feelings of trauma and increase the risk of developing PTSD. Also, this might be due to the psychological impact of traumatic events because a perceived threat to life can have profound psychological effects, including heightened arousal, hypervigilance, and intrusive thoughts or memories related to the traumatic event. Individuals who perceive a moderate to high threat to their lives may experience persistent anxiety, fear, and distress, which increase the risk of developing PTSD symptoms.

Poor social support had four times higher odds of having post-traumatic stress disorder than those who had strong social support in war-affected areas. This finding is supported by previous studies ( 59 , 60 ). The possible reason is that social support serves as a buffer against the adverse effects of trauma and stress. Strong social support networks provide individuals with emotional, instrumental, and informational support, which can help them, cope with traumatic experiences and mitigate the risk of developing PTSD. Conversely, poor social support can leave individuals feeling isolated, unsupported, and unable to effectively cope with trauma, increasing their vulnerability to PTSD. Furthermore, this might be due to social support fosters a sense of belonging and connectedness, which are essential for psychological well-being. Individuals with strong social support networks feel valued, cared for, and connected to others, reducing feelings of loneliness and isolation. In contrast, poor social support can exacerbate feelings of alienation, detachment, and disconnection, which are risk factors for the development of PTSD. Overall, the association between poor social support and higher odds of PTSD in war-affected areas underscores the importance of strengthening social support networks and implementing interventions aimed at enhancing social connectedness and support in these communities. Addressing social isolation and promoting social cohesion are essential components of trauma-informed care and mental health support services in war-affected areas.

The findings may not be generalizable to all war-affected populations, as the study focused specifically on Ethiopia. Other countries may have different sociocultural contexts and levels of trauma. Another limitation of this study is that the primary studies included in the meta-analysis may have used different methodologies, assessment tools, and criteria for diagnosing PTSD, leading to heterogeneity in the results. Furthermore, there may be a bias toward publishing studies with significant findings, which could influence the overall prevalence estimate. In addition, the limitation of this study is its narrow scope, which included studies involving only internally conflict-affected individuals. Moreover, all of the studies in this systematic review and meta-analysis had cross-sectional study designs.

The result of this study shows the high prevalence rate (48.42%) of PTSD in people living in war-affected areas. The research underscores gender disparities in PTSD prevalence, with women being at higher risk. This suggests the importance of gender-sensitive approaches in mental health interventions. Identified risk factors such as witnessing the murder of a loved one, experiencing depression and anxiety, perceived threat to life, and poor social support highlight the complex interplay of individual, social, and environmental factors in PTSD development. Addressing PTSD in war-affected communities requires comprehensive interventions that consider both individual and contextual factors. Strategies should include trauma-informed care, psychosocial support, and efforts to strengthen social support networks. Despite the findings, further research is needed to better understand the nuanced experiences of PTSD in diverse war-affected populations and to develop targeted interventions tailored to their specific needs.

Data availability statement

The raw data supporting the conclusions of this article will be made available by the authors, without undue reservation.

Author contributions

TT: Formal analysis, Investigation, Software, Supervision, Validation, Visualization, Writing – review & editing. SS: Investigation, Methodology, Supervision, Visualization, Writing – review & editing. GT: Investigation, Methodology, Validation, Visualization, Writing – review & editing. GM: Methodology, Software, Validation, Visualization, Writing – review & editing. GR: Formal analysis, Investigation, Validation, Writing – review & editing. MM: Methodology, Visualization, Writing – review & editing. FA: Formal analysis, Software, Writing – review & editing. GN: Investigation, Methodology, Visualization, Writing – review & editing. TS: Investigation, Methodology, Writing – review & editing. SK: Formal analysis, Methodology, Writing – review & editing. SF: Investigation, Supervision, Visualization, Writing – review & editing. WG: Formal analysis, Investigation, Methodology, Supervision, Validation, Visualization, Writing – review & editing.

The author(s) declare that no financial support was received for the research, authorship, and/or publication of this article.

Conflict of interest

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Publisher’s note

All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article, or claim that may be made by its manufacturer, is not guaranteed or endorsed by the publisher.

Abbreviations

PRISMA, Preferred Reporting Items for Systematic Reviews and Meta-Analyses; NOS, Newcastle-Ottowa Scale; POR, Pooled odds Ratio; CI, Confidence Interval; PCL-5, PTSD Checklist for DSM-5; PCSS-SR, PTSD Symptom Scale-Self Report; PTSD, post-trauamtic stress disorder; SNNPR, Southern Nations, Nationalities, and Peoples’ Region.

1. Nemeroff CB, Bremner JD, Foa EB, Mayberg HS, North CS, Stein MB. Posttraumatic stress disorder: a state-of-the-science review. J Psychiatr Res . (2006) 40:1–21. doi: 10.1016/j.jpsychires.2005.07.005

PubMed Abstract | CrossRef Full Text | Google Scholar

2. Lavoie S, Talbot LR, Mathieu L. Post-traumatic stress disorder symptoms among emergency nurses: their perspective and a 'tailor-made' solution. J advanced nursing . (2011) 67:1514–22. doi: 10.1111/j.1365-2648.2010.05584.x

CrossRef Full Text | Google Scholar

3. Risser HJ, Hetzel-Riggin MD, Thomsen CJ, McCanne TR. PTSD as a mediator of sexual revictimization: the role of reexperiencing, avoidance, and arousal symptoms. J traumatic stress . (2006) 19:687–98. doi: 10.1002/jts.20156

4. Kuijpers KF, van der Knaap LM, Winkel FW. PTSD symptoms as risk factors for intimate partner violence revictimization and the mediating role of victims' violent behavior. J traumatic stress . (2012) 25:179–86. doi: 10.1002/jts.21676

5. American Psychiatric Association A, Association AP. Diagnostic and statistical manual of mental disorders: DSM-IV . Washington, DC: American Psychiatric Association (1994).

Google Scholar

6. Siyum BA. Underlying Causes of Conflict in Ethiopia: Historical, Political, and Institutional? Diamond Scientific Publishing (2021). Available at: https://www.dpublication.com/wp-content/uploads/2021/10/N-856.pdf

7. Tol WA, Barbui C, Galappatti A, Silove D, Betancourt TS, Souza R, et al. Mental health and psychosocial support in humanitarian settings: linking practice and research. Lancet (London England) . (2011) 378:1581–91. doi: 10.1016/S0140-6736(11)61094-5

8. Njenga FG, Nguithi AN, Kang'ethe RN. War and mental disorders in Africa. World Psychiatry . (2006) 5:38–9.

PubMed Abstract | Google Scholar

9. Charlson F, van Ommeren M, Flaxman A, Cornett J, Whiteford H, Saxena S. New WHO prevalence estimates of mental disorders in conflict settings: a systematic review and meta-analysis. Lancet (London England) . (2019) 394:240–8. doi: 10.1016/S0140-6736(19)30934-1

10. Lim I, Tam WWS, Chudzicka-Czupała A, McIntyre RS, Teopiz KM, Ho RC, et al. Prevalence of depression, anxiety and post-traumatic stress in war- and conflict-afflicted areas: A meta-analysis. Front Psychiatry . (2022) 13:978703. doi: 10.3389/fpsyt.2022.978703

11. Ng LC, Stevenson A. National and regional prevalence of posttraumatic stress disorder in sub-Saharan Africa: A systematic review and meta-analysis. PloS Med . (2020) 17:e1003090. doi: 10.1371/journal.pmed.1003090

12. Roberts B, Makhashvili N, Javakhishvili J, Karachevskyy A, Kharchenko N, Shpiker M, et al. Mental health care utilization among internally displaced persons in Ukraine: results from a nation-wide survey. Epidemiol Psychiatr Sci . (2019) 28:100–11. doi: 10.1017/S2045796017000385

13. Sheikh TL, Mohammed A, Agunbiade S, Ike J, Ebiti WN, Adekeye O. Psycho-trauma, psychosocial adjustment, and symptomatic post-traumatic stress disorder among internally displaced persons in Kaduna, Northwestern Nigeria. Front Psychiatry . (2014) 5:127. doi: 10.3389/fpsyt.2014.00127

14. Melkam M, Tinsae T, Andualem F, Nakie G. Post-traumatic stress disorder and associated factors among adults exposed to stress in Ethiopia: A meta-analysis and systematic review. SAGE Open Med . (2023) 11:20503121231160884. doi: 10.1177/20503121231160884

15. Sheikh TL, Mohammed A, Eseigbe E, Adekeye T, Nuhu FT, Lasisi M, et al. Descriptive characterization of psycho-trauma, psychological distress, and post-traumatic stress disorder among children and adolescent internally displaced persons in Kaduna, Nigeria. Front Psychiatry . (2016) 7:219866. doi: 10.3389/fpsyt.2016.00179

16. Sareen J. Posttraumatic stress disorder in adults: impact, comorbidity, risk factors, and treatment. Can J Psychiatry Rev Can psychiatrie . (2014) 59:460–7. doi: 10.1177/070674371405900902

17. Mouthaan J, Sijbrandij M, Reitsma JB, Luitse JS, Goslings JC, Gersons BP, et al. The role of early pharmacotherapy in the development of posttraumatic stress disorder symptoms after traumatic injury: an observational cohort study in consecutive patients. Gen Hosp Psychiatry . (2015) 37:230–5. doi: 10.1016/j.genhosppsych.2015.02.010

18. Qi W, Gevonden M, Shalev A. Prevention of post-traumatic stress disorder after trauma: current evidence and future directions. Curr Psychiatry Rep . (2016) 18:20. doi: 10.1007/s11920-015-0655-0

19. Forbes D, Creamer M, Phelps A, Bryant R, McFarlane A, Devilly GJ, et al. Australian guidelines for the treatment of adults with acute stress disorder and post-traumatic stress disorder. Aust New Z J Psychiatry . (2007) 41:637–48. doi: 10.1080/00048670701449161

20. Hoge EA, Worthington JJ, Nagurney JT, Chang Y, Kay EB, Feterowski CM, et al. Effect of acute posttrauma propranolol on PTSD outcome and physiological responses during script-driven imagery. CNS Neurosci Ther . (2012) 18:21–7. doi: 10.1111/j.1755-5949.2010.00227.x

21. Anbesaw T, Zenebe Y, Asmamaw A, Shegaw M, Birru N. Post-traumatic stress disorder and associated factors among people who experienced traumatic events in Dessie town, Ethiopia, 2022: a community-based study. Front Psychiatry . (2022) 13:1026878. doi: 10.3389/fpsyt.2022.1026878

22. Makango B, Alemu ZA, Solomon T, Lemma N, Girma T, Mohammednur T, et al. Prevalence and factors associated with post-traumatic stress disorder among internally displaced people in camps at Debre Berhan, Amhara Region, Ethiopia: a cross-sectional study. BMC Psychiatry . (2023) 23:81. doi: 10.1186/s12888-023-04570-w

23. Stang A. Critical evaluation of the Newcastle-Ottawa scale for the assessment of the quality of nonrandomized studies in meta-analyses. Eur J Epidemiol . (2010) 25:603–5. doi: 10.1007/s10654-010-9491-z

24. Higgins JP, Thompson SG, Deeks JJ, Altman DG. Measuring inconsistency in meta-analyses. BMJ (Clinical Res ed) . (2003) 327:557–60. doi: 10.1136/bmj.327.7414.557

25. Duval S, Tweedie R. A nonparametric “trim and fill” method of accounting for publication bias in meta-analysis. J Am Stat Assoc . (2000) 95:89–98. doi: 10.1080/01621459.2000.10473905

26. Schünemann HJ, Oxman AD, Higgins JP, Vist GE, Glasziou P, Guyatt GH. Presenting results and “Summary of findings” tables. in: Higgins JPT Green S Cochrane handbook for systematic reviews of interventions. Hoboken: Wiley. (2008) NJ2008: 335–58..

27. Teshome AA, Abebe EC, Mengstie MA, Seid MA, Yitbarek GY, Molla YM, et al. Post-traumatic stress disorder and associated factors among adult war survivors in Northwest Ethiopia: Community-based, cross-sectional study. Front Psychiatry . (2023) 14:1083138. doi: 10.3389/fpsyt.2023.1083138

28. Ali D, Azale T, Wondie M, Tadesse J. About six in ten survivors of the november 2020 maikadra massacre suffer from posttraumatic stress disorder, in northwest Ethiopia. Psychol Res Behav Manage . (2022) 15:251–60. doi: 10.2147/PRBM.S338823

29. Kassaye A, Demilew D, Fanta B, Mulat H, Ali D, Seid J, et al. Post-traumatic stress disorder and its associated factors among war-affected residents in Woldia town, North East Ethiopia, 2022; community-based cross-sectional study. PloS One . (2023) 18:e0292848. doi: 10.1371/journal.pone.0292848

30. Biset G, Goshiye D, Melesse N, Tsehay M. Post-traumatic stress disorders among children and adolescents in conflict-affected zones of Amhara region, February 2022. Front Psychol . (2022) 13:1052975. doi: 10.3389/fpsyg.2022.1052975

31. Birhan Z, Deressa Y, Shegaw M, Asnakew S, Mekonen T. Posttraumatic stress disorder in a war-affected area of Northeast Ethiopia: a cross-sectional study. BMC Psychiatry . (2023) 23:627. doi: 10.1186/s12888-023-05116-w

32. Madoro D, Kerebih H, Habtamu Y, Gtsadik M, Mokona H, Molla A, et al. Post-traumatic stress disorder and associated factors among internally displaced people in south Ethiopia: A cross-sectional study. Neuropsychiatr Dis Treat . (2020) 16:2317–26. doi: 10.2147/NDT.S267307

33. Morina N, Stam K, Pollet TV, Priebe S. Prevalence of depression and posttraumatic stress disorder in adult civilian survivors of war who stay in war-afflicted regions. A systematic review and meta-analysis of epidemiological studies. J Affect Disord . (2018) 239:328–38. doi: 10.1016/j.jad.2018.07.027

34. Ainamani HE, Elbert T, Olema DK, Hecker T. Gender differences in response to war-related trauma and posttraumatic stress disorder – a study among the Congolese refugees in Uganda. BMC Psychiatry . (2020) 20:17. doi: 10.1186/s12888-019-2420-0

35. Koshe T, Jarso MH, Walde MT, Ebrahim J, Mamo A, Esmael A, et al. A post-traumatic stress disorder among internally displaced people in sub-Saharan Africa: a systematic review. Front Psychiatry . (2023) 14:1261230. doi: 10.3389/fpsyt.2023.1261230

36. Valentine SE, Marques L, Wang Y, Ahles EM, Dixon De Silva L, Alegría M. Gender differences in exposure to potentially traumatic events and diagnosis of posttraumatic stress disorder (PTSD) by racial and ethnic group. Gen Hosp Psychiatry . (2019) 61:60–8. doi: 10.1016/j.genhosppsych.2019.10.008

37. Vishnevsky T, Cann A, Calhoun LG, Tedeschi RG, Demakis GJ. Gender differences in self-reported posttraumatic growth: A meta-analysis. Psychol Women Quarterly . (2010) 34:110–20. doi: 10.1111/j.1471-6402.2009.01546.x

38. James PB, Renzaho AMN, Mwanri L, Miller I, Wardle J, Gatwiri K, et al. The prevalence of anxiety, depression, and post-traumatic stress disorder among African migrants: A systematic review and meta-analysis. Psychiatry Res . (2022) 317:114899. doi: 10.1016/j.psychres.2022.114899

39. Andualem F, Melkam M, Takelle GM, Nakie G, Tinsae T, Fentahun S, et al. Prevalence of posttraumatic stress disorder and associated factors among displaced people in Africa: a systematic review and meta-analysis. Front Psychiatry . (2024) 15:1336665. doi: 10.3389/fpsyt.2024.1336665

40. Verhülsdonk I, Shahab M, Molendijk M. Prevalence of psychiatric disorders among refugees and migrants in immigration detention: systematic review with meta-analysis. BJPsych Open . (2021) 7:e204. doi: 10.1192/bjo.2021.1026

41. Hoppen TH, Priebe S, Vetter I, Morina N. Global burden of post-traumatic stress disorder and major depression in countries affected by war between 1989 and 2019: a systematic review and meta-analysis. BMJ Global Health . (2021) 6. doi: 10.1136/bmjgh-2021-006303

42. Agbaria N, Petzold S, Deckert A, Henschke N, Veronese G, Dambach P, et al. Prevalence of post-traumatic stress disorder among Palestinian children and adolescents exposed to political violence: A systematic review and meta-analysis. PLoS One . (2021) 16(8):e0256426. doi: 10.1371/journal.pone.0256426

43. Kanan J, Leão T. Post-traumatic stress disorder in youth exposed to the Syrian conflict: A systematic review and meta-analysis of prevalence and determinants. (2022), 13591053221123141. doi: 10.1177/13591053221123141

44. Kakaje A, Al Zohbi R, Hosam Aldeen O, Makki L, Alyousbashi A, Alhaffar MBA. Mental disorder and PTSD in Syria during wartime: a nationwide crisis. BMC Psychiatry . (2021) 21:2. doi: 10.1186/s12888-020-03002-3

45. Mesa-Vieira C, Haas AD, Buitrago-Garcia D, Roa-Diaz ZM, Minder B, Gamba M, et al. The mental health of migrants with pre-migration exposure to armed conflict: a systematic review and meta-analysis. Lancet Public Health . (2022) 7:e469–e81. doi: 10.1016/S2468-2667(22)00061-5

46. Tesfaye AH, Sendekie AK, Kabito GG, Engdaw GT, Argaw GS, Desye B, et al. Post-traumatic stress disorder and associated factors among internally displaced persons in Africa: A systematic review and meta-analysis. PloS One . (2024) 19:e0300894. doi: 10.1371/journal.pone.0300894

47. Johnson RJ, Antonaccio O, Botchkovar E, Hobfoll SE. War trauma and PTSD in Ukraine’s civilian population: comparing urban-dwelling to internally displaced persons. Soc Psychiatry Psychiatr Epidemiol . (2022), 1–10. doi: 10.1007/s00127-021-02176-9

48. Kim GS, Uddin M. Sex-specific and shared expression profiles of vulnerability and resilience to trauma in brain and blood. Biol sex differences . (2020) 11:13. doi: 10.1186/s13293-020-00288-6

49. Keller SM, Schreiber WB, Staib JM, Knox D. Sex differences in the single prolonged stress model. Behav Brain Res . (2015) 286:29–32. doi: 10.1016/j.bbr.2015.02.034

50. Reuben KE, Stanzione CM, Singleton JL. Interpersonal trauma and posttraumatic stress in autistic adults. Autism adulthood: challenges management . (2021) 3:247–56. doi: 10.1089/aut.2020.0073

51. Haskell SG, Gordon KS, Mattocks K, Duggal M, Erdos J, Justice A, et al. Gender differences in rates of depression, PTSD, pain, obesity, and military sexual trauma among Connecticut War Veterans of Iraq and Afghanistan. J women's Health (2002) . (2010) 19:267–71. doi: 10.1089/jwh.2008.1262

52. Ditlevsen DN, Elklit A. The combined effect of gender and age on post-traumatic stress disorder: do men and women show differences in the lifespan distribution of the disorder? Ann Gen Psychiatry . (2010) 9:32. doi: 10.1186/1744-859X-9-32

53. Norris FH, Friedman MJ, Watson PJ. 60,000 disaster victims speak: Part II. Summary and implications of the disaster mental health research. Psychiatry . (2002) 65:240–60. doi: 10.1521/psyc.65.3.240.20169

54. Zhou X, Kang L, Sun X, Song H, Mao W, Huang X, et al. Prevalence and risk factors of post-traumatic stress disorder among adult survivors six months after the Wenchuan earthquake. Compr Psychiatry . (2013) 54:493–9. doi: 10.1016/j.comppsych.2012.12.010

55. Badri A, Crutzen R, Van den Borne HW. Exposures to war-related traumatic events and post-traumatic stress disorder symptoms among displaced Darfuri female university students: an exploratory study. BMC Public Health . (2012) 12:603. doi: 10.1186/1471-2458-12-603

56. Roze M, Melchior M, Vuillermoz C. Post-traumatic stress disorder in homeless migrant mothers of the paris region shelters. (2020) 17(13):. doi: 10.3390/ijerph17134908

57. Tsujiuchi T, Yamaguchi M, Masuda K, Tsuchida M, Inomata T, Kumano H, et al. High prevalence of post-traumatic stress symptoms in relation to social factors in affected population one year after the fukushima nuclear disaster. PloS One . (2016) 11:e0151807. doi: 10.1371/journal.pone.0151807

58. Jenkins R, Othieno C, Omollo R, Ongeri L, Sifuna P, Mboroki JK, et al. Probable post traumatic stress disorder in Kenya and its associated risk factors: A cross-sectional household survey. Int J Environ Res Public Health . (2015) 12:13494–509. doi: 10.3390/ijerph121013494

59. Price M, Lancaster CL, Gros DF, Legrand AC, van Stolk-Cooke K, Acierno R. An examination of social support and PTSD treatment response during prolonged exposure. Psychiatry . (2018) 81:258–70. doi: 10.1080/00332747.2017.1402569

60. Wang Y, Chung MC, Wang N, Yu X, Kenardy J. Social support and posttraumatic stress disorder: A meta-analysis of longitudinal studies. Clin Psychol Review . (2021) 85:101998. doi: 10.1016/j.cpr.2021.101998

Keywords: PTSD, internal conflict, trauma, conflict, war

Citation: Tinsae T, Shumet S, Tadesse G, Takelle GM, Rtbey G, Melkam M, Andualem F, Nakie G, Segon T, Koye S, Fentahun S and Alemu WG (2024) Post-traumatic stress disorder in the Ethiopian population dwelling in war-affected communities: a systematic review and meta-analysis. Front. Psychiatry 15:1399013. doi: 10.3389/fpsyt.2024.1399013

Received: 11 March 2024; Accepted: 19 April 2024; Published: 09 May 2024.

Reviewed by:

Copyright © 2024 Tinsae, Shumet, Tadesse, Takelle, Rtbey, Melkam, Andualem, Nakie, Segon, Koye, Fentahun and Alemu. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY) . The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

*Correspondence: Techilo Tinsae, [email protected]

Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.

Title: Supervised learning models to predict mental illness and its severity from Reddit posts

Authors : Neha Arun Angadi; Navya Eedula; Kshitij Prit Gopali; R. Jayashree

Addresses : Department of Computer Science, PES University, Bangalore, Karnataka, India ' Department of Computer Science, PES University, Bangalore, Karnataka, India ' Department of Computer Science, PES University, Bangalore, Karnataka, India ' Department of Computer Science, PES University, Bangalore, Karnataka, India

Abstract : Given the growing popularity of free dialogue on social media, this paper presents a methodology for identifying mental illnesses from Reddit posts where users describe their experiences with illnesses like bipolar disorder, borderline personality disorder (BPD), depression, eating disorders, obsessive-compulsive disorder (OCD), panic disorder, post-traumatic stress disorder (PTSD), and schizophrenia. After data cleaning and pre-processing with the standard NLP techniques on the posts, hyperparameter tweaking helped evaluate multiple different supervised classification models, from which the LinearSVC model delivered the best results with 78.25% accuracy. CalibratedClassifierCV helped with probabilistic calibration for the model. If the findings revealed that multiple mental diseases had comparable probability, a second step of classification was performed using a questionnaire that described the user's conditions, which the model used to determine the mental illness. The final step is to assess the severity of the sickness, which helps analyse the next plan-of-action to tackle the mental disorder.

Keywords : supervised machine learning; probability calibration; text pre-processing; mental illness; Reddit posts; severity detection.

DOI : 10.1504/IJCSE.2024.138417

International Journal of Computational Science and Engineering, 2024 Vol.27 No.3, pp.352 - 363

Received: 03 Oct 2022 Accepted: 11 Jun 2023 Published online: 03 May 2024 *

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