In a nationally representative sample of Canadians aged 18 years and over, at least 76% of participants reported being exposed to at least one traumatic event in their lifetime (Van Ameringen, Mancini, Patterson, & Boyle, 2008). Traumatic events are defined by the DSM-5 as “exposure to actual or threatened death, serious injury, or sexual violence” (p. 271). The most commonly reported events were unexpected death of a loved one sexual assault and witnessing someone being seriously harmed or killed. However, only about 8% of Canadians who experience a traumatic event develop PTSD (Canadian Mental Health Association, 2013). Unfortunately, like adults, children are also exposed to high rates of trauma. At least 30% of Canadians self-report that they experienced physical and/or sexual abuse and/or exposure to intimate partner violence before the age of 15 (Afifi et al., 2014; Canadian Centre for Justice Statistics, 2017).

In Canada, the current and lifetime prevalence of PTSD was 2.4% and 9.2%, respectively (Van Ameringen et al., 2008). Rates of PTSD were higher for people living in rural areas, Western Canada, and Ontario, and the risk for developing PTSD was significantly lower among males (Van Ameringen et al., 2008). The rates of PTSD are especially common among Canadian veterans. According to Statistics Canada, the lifetime and 12-month prevalence of PTSD among Canadian Armed Force members was 11.1% and 5.3%, respectively (Caryn, Zamorski, & Janz, 2014). Of concern, the 12-month prevalence for PTSD is twice as high among members who were deployed in Afghanistan compared to those who were not (Caryn et al., 2014).

Symptoms of PTSD

According to the DSM-5, for a person to receive a diagnosis of Post-Traumatic Stress Disorder (PTSD), they must meet the following 8 criteria (APA, 2013). First, as mentioned, the person must have been exposed to a traumatic or stressful event such as actual or threatened death, serious bodily harm, or sexual violence. The person may have experienced the event themselves, witnessed to happening to somebody else, or learned that a close family member or friend was exposed to a trauma (APA, 2013). Second, the person has intrusive symptoms such that they re-experience the trauma, for example through unwanted memories, nightmares, or flashbacks that are related to the traumatic event. These symptoms are not within the person’s control, which can be particularly distressing for those with PTSD.

Third, the person avoids trauma-related stimuli (e.g., thoughts, emotions, reminders) (e.g., people, places, objects). They do so in order to avoid the overwhelming fear response that arises when they are around trauma-related stimuli. For some people with PTSD exposure to trauma-related stimuli can lead to an increase in intrusive thoughts, nightmares, or flashbacks. Some examples of things that people might avoid include certain locations, people, conversations or memories, rooms in their homes, etc.

Fourth, the person experiences negative changes in mood or cognition related to the traumatic event (e.g., inability to remember important parts of the event, exaggerated negative beliefs, negative emotions and the inability to experience positive emotions). Fifth, the person experiences significant changes in arousal and behaviour (e.g., irritability, hypervigilance, sleep disturbance) (APA, 2013). For example, it is not uncommon for individuals with PTSD to experience insomnia or to be hypervigilant to concerns about safety. This overarousal sometimes results in feeling tense, “keyed up” or on edge. It is also common for individuals with PTSD to have exaggerated startle responses, compared to people without PTSD.

Sixth, the disturbances in mood, cognition, and behaviour must occur for at least 1 month, and seventh, and they must cause clinically significant distress or impairment in important areas of functioning (e.g., social, occupational). Eighth, the disturbances should not be better explained by the effects of a substance or another medical condition. In addition to making a diagnosis of PTSD, a psychologist can specify if the person also has symptoms of dissociation and/or if they have delayed expression of symptoms (i.e., full diagnostic criteria are not met until at least 6 months after the traumatic event) (APA, 2013).

The DSM-5 has separate diagnostic criteria for children 6 years and younger. Some important differences are that in young children, intrusive memories may not look the same as they do in adults. In children, intrusive memories can be expressed through repetitive play. Children can also experience less interest in play, an exaggerated startle response, and they may have extreme temper tantrums (APA, 2013).

Predictors of PTSD

Why do some individuals, when exposed to trauma, develop PTSD but others do not? In this section we will discuss just a few of the variables that influence the development of PTSD.

Centrality of Events

In Canada, it is estimated that 75.9% of individuals will experience a traumatic event in their lifetime, but the lifetime rate of PTSD in Canada is only 9.2% (Van Ameringen et al., 2008). Therefore, not everyone that is exposed to a traumatic event will develop PTSD. The discrepancy between the rate of trauma exposure and the rate of PTSD has led researchers to try to identify factors that increase the likelihood of developing PTSD after exposure to a trauma. One such identified factor is event centrality (Berntsen & Rubin, 2006), or how central we come to see that event to our lives, memories, and identity. The centrality of events scale (CES) was introduced by Berntsen and Rubin (2006) to measure the extent to which a memory for a trauma becomes a reference point for one’s identity, life story, and the attribution of meaning to other experiences. The CES has a full 20-item version and a short-form 7-item version. Both have high reliability and validity (Berntsen & Rubin, 2006). The CES has three factors. It measures the extent to which the individual’s traumatic memory: 1) becomes a reference point for everyday inferences; 2) represents a turning point in the individual’s life story; and 3) becomes a reference point for their personal identity. Each of these factors are positively related to PTSD (Robinaugh & McNally, 2011).

Berntsen and Rubin (2006) discussed why each factor of the CES may contribute to symptoms of PTSD. Berntsen and Robin (2006) proposed that the availability heuristic (Tversky & Kahnman, 1973) helps to explain the relationship between the first factor and PTSD. For example, if the trauma memories are highly accessible, then the individual will overestimate the frequency of such events in everyday life, leading to unnecessary worries, precautions, and other traumatization symptoms (Berntsen & Rubin, 2006). The second factor was developed from research on how trauma can profoundly change a person’s outlook (Janoff-Bulman, 1989). Berntsen and Rubin (2006) proposed that symptoms of PTSD may be exacerbated when the individual focuses on aspects of their life that can be explained by referencing this turning point in the life story, while discounting aspects that defy these references (Berntsen & Rubin, 2006). Lastly, the third factor was developed from research that suggests that an individual may perceive a trauma as causally related to a stable characteristic of the self (Abramson, Seligman, & Teasdale, 1978; Berntsen & Rubin, 2006). Therefore, this factor is proposed to be related to PTSD when individuals attribute the trauma to stable negative identity characteristics (Berntsen & Rubin, 2006). Overall, research on event centrality supports the autobiographical memory model of PTSD, which purposes that PTSD symptoms result from the over integration of the trauma into one’s memory, identity, and understanding of the world (Berntsen & Rubin, 2006; Rubin, Berntsen, & Bohni, 2008; Rubin, Boals, & Berntsen, 2008).

Since the construction of the centrality of events scale (Berntsen & Rubin, 2006) research has demonstrated a robust positive relationship between event centrality and PTSD for a range of trauma types and participant populations (Gehrt, Berntsen, Hoyle, & Rubin, 2018). For example, the positive relationship between event centrality and PTSD has been found for individuals exposed to child sexual abuse (Robinaugh & McNally, 2011), military combat (Brown, Antonius, Kramer, Root, & Hirst, 2010), terrorist attacks/bombings (Blix, Solberg, & Heir, 2014), physical injury or assault/abuse, illness, exposure to death, sexual assault/abuse, accidents, and natural disasters (Teale Sapach et al., 2019; Barton, Boals, & Knowles, 2013). The positive relationship between event centrality and PTSD has also been found for a range of participant samples, including community members (Rubin, Dennis, & Beckham, 2011; Ogle et al., 2014), undergraduate students (Barton et al., 2013; Berntsen & Rubin, 2006; Broadbridge, 2018; Fitzgerald, Berntsen, & Broadbridge, 2016), treatment-seeking individuals (Boals & Murrel, 2016; Silva et al., 2016), and military veterans (Brown et al., 2010). This relationship between event centrality and PTSD is also evident for adults ranging from 18 to 93 (Barton et al., 2013; Berntsen, Rubin, & Siegler, 2011; Wamser-Nanney, 2019; Ogle et al., 2013; Boals, Hayslip, Knowles, & Banks, 2012). However, there are nuances in the relationship between event centrality and PTSD for certain participant characteristics. For instance, younger adults (Boals et al., 2012) and women (Boals, 2010) are more likely to centralize a traumatic event and develop PTSD compared to older adults and men, respectively. Therefore, the difference in event centrality may help to explain the higher prevalence of PTSD in these populations (i.e., young adults and women; Van Ameringen et al., 2008).

Trauma Type & Social Support

There are certain types of trauma that have a greater impact on the development and maintenance of PTSD. Interpersonal traumatic events that are purposefully caused by other people contribute the most to PTSD risk and symptom severity. Events that occur by accident or by natural disaster have a far less impact on the risk for PTSD compared to interpersonal traumas (Charuvastra & Cloitre, 2008). There are several reasons explaining why interpersonal traumas are so powerful in increasing a person’s risk and severity of PTSD. In interpersonal traumas, the appraisal of threat tends to be higher, and people tend to experience a higher level of distress and decreased sense of safety in the world. In addition, interpersonal traumas can affect people’s ability to effectively interact with others (Charuvastra & Cloitre, 2008).

Social support before and after an exposure to a traumatic event plays an important role in determining a person’s risk and severity of PTSD (Charuvastra & Cloitre, 2008). Social support helps people to effectively regulate their emotions, which is central for recovery from PTSD. If a person is not able to effectively manage intense emotions and memories, they are more likely to re-experience traumatic events and use avoidance as a way to cope with difficult emotional experiences. Social support plays an important role throughout life. In childhood, the bond between the caregiver and child helps to establish a sense of safety and emotion regulation. Abuse during childhood is a significant risk factor for the PTSD later on in life and it plays an important role in dysregulating the stress response system (Charuvastra & Cloitre, 2008).

Positive social interactions act as a protective factor against stress (Charuvastra & Cloitre, 2008). The value of social support lies in the perceived helpfulness and sense of connectedness with others. It is not the quantity of social support that is protective against PTSD, but rather it is the match between what the person needs and the type of support that is offered. Social support can decrease feelings of distress and increase safety and a sense of belonging. If a person feels isolated ostracized, blamed, or feels unsupported by their relationships, this can contribute to the onset and severity of PTSD symptoms (Charuvastra & Cloitre, 2008). Negative relationships can reinforce the belief that the world is a place that is unsafe and harmful.

Genetic & Biological Risk Factors

In a review on the biological risk factors for PTSD, Yahyavi, Zarghami, and Marwah (2014) found that the risk for PTSD can begin in utero. The HPA axis, which plays an important role in the stress response, is greatly affected by early development. Maternal exposure to trauma, for example, can lead to changes in the fetal brain that disrupt gene expression. An example of this is DNA methylation, which re-programs the activity of genes and impacts a person’s response to stress by activating the sympathetic nervous system and causing dysfunction in the HPA axis (Yahyavi et al., 2014). Changes in these biological systems disrupts emotion regulation and the ability to effectively manage stress. However, there is growing consensus that genetic markers do not act in isolation but interact with environmental factors to impact a person’s vulnerability to developing PTSD (Klengel & Binder, 2015). In addition, the genetic risk factors for PTSD are complex and the biologic pathways for this disorder are not fully understood (Sharma & Ressler, 2019).

Treatments for PTSD

The American Psychological Association (APA) has developed a list of empirically supported treatments (ESTs) that are indicated for the treatment of PTSD. Within this list, the APA differentiates between treatments that are conditionally recommended and strongly recommended. Treatments that are conditionally recommended all have evidence that indicates that they can lead to good treatment outcomes. However, the evidence may not be as strong, the balance of treatment benefits and possible harms may be less favorable, or the intervention may be less applicable across treatment settings or subgroups of individuals with PTSD (APA, 2017). Additional research on these conditionally recommended treatments might lead, with time, to a change in the strength of recommendations in future guidelines. Treatments that are strongly recommended all have strong evidence that they lead to good treatment outcomes, that the balance of treatment benefits and possible harms are favorable for the client, and have been found to be applicable across treatment settings and subgroups for individuals with PTSD (APA, 2017).

Strongly Recommended Treatments

At present, the APA strongly recommends four treatments for individuals with PTSD, all which are variations of Cognitive Behavioural Therapy (CBT). These treatments include: Prolonged Exposure Therapy, Cognitive Processing Therapy, Cognitive Therapy, and traditional Cognitive Behavioural Therapy (APA, 2017). CBT is a form of therapy that focuses on how individuals’ thoughts, behaviours, and emotions are interrelated. The therapist works with the client to identify thoughts, behaviours, and emotions which might be having negative effects on the client’s wellbeing and uses various skills to alter these as needed. As applied to trauma, oftentimes this takes the form of helping clients learn how to modify and challenge unhelpful beliefs related to the trauma. Modifying and challenging these unhelpful beliefs is meant to modify the client’s emotional and behavioural reactions into ones that are more positive. Oftentimes a technique called exposure is incorporated into the abovementioned treatments. Exposure is a process whereby the client gradually approaches trauma-related memories, feelings, and situations. It can be conducted in a number of ways, including describing the trauma narrative aloud, listening to an audio recording of the trauma narrative, writing out the trauma narrative and/or reading it aloud, and physically going to situations which are feared and/or reminders of the trauma. These different methods of exposure are often referred to as imaginal exposure (occurring within the imagination), and in-vivo exposure (occurring in real life). By facing what has been avoided, the client presumably will learn that the trauma-related memories and cues are not dangerous and do not need to be avoided. By extension, any associated distressing thoughts, feelings, and sensations will be diminished.

There have been various studies performed with the intention of understanding how well these treatments for PTSD work and, as mentioned, they all have strong evidence to support them.

Individuals randomly assigned to exposure therapy have significantly greater pre- to posttreatment reductions in PTSD symptoms compared to supportive counseling (Bryant, et al., 2003; Bryant, et al., 2008; Schnurr et al., 2007), relaxation training (Marks et al.,1998; Taylor et al., 2003), and treatment as usual including pharmacotherapy (Asukai et al., 2010). A meta-analysis on the effectiveness of PTSD showed that clients treated with PE fared better than 86% of patients in control conditions on PTSD symptoms at the end of treatment (Powers et al., 2010). Furthermore, among PE participants, 41% to 95% lost their PTSD diagnosis at the end of treatment (Jonas et al., 2016), and 66% more participants treated with exposure therapy achieved loss of PTSD diagnosis, compared to those in waitlist control groups (Jonas et al., 2016).

CPT has been found to influence a clinically significant reduction in PTSD, depression, and anxiety symptoms in sexual assault and Veteran samples, with results maintained at 5 and 10 year post treatment follow-up (Cusack et al., 2016; Resick et al., 2008; Watts et al., 2013). Furthermore, rates of participants who no longer met PTSD diagnosis criteria ranged from 30% to 97% and 51% more participants treated with CPT achieved loss of PTSD diagnosis, compared to waitlist, self-help booklet and usual care control groups (Jonas et al., 2016).

Traditional CBTs have also been shown to be more effective than a waitlist (Power et al., 2002), supportive therapy (Blanchard et al., 2003) and a self-help booklet (Ehlers et al., 2003). Researchers have also compared various components of CBT (i.e., imaginal exposure, in vivo exposure, cognitive restructuring) with some mixed results. Marks et al. (1998) compared exposure therapy (that included five sessions of imaginal exposure and five sessions of in vivo exposure), cognitive restructuring, combined exposure therapy and cognitive restructuring, and relaxation in an RCT. Exposure and cognitive restructuring were each effective in reducing PTSD symptoms and were superior to relaxation. Exposure and cognitive restructuring were not mutually enhancing when combined. Furthermore, research suggests that 61% to 82.4% of participants treated with traditional CBT lost their PTSD diagnosis and 26% more CBT participants than waitlist or supportive counseling achieved loss of PTSD diagnosis (Jonas et al., 2016).

Conditionally Recommended Treatments

There are also a number of treatments which the APA indicates are conditionally recommended for the treatment of PTSD. These include Eye Movement Desensitization and Reprocessing Therapy (EMDR), Narrative Exposure Therapy (NET) and Medication (APA, 2017). When utilizing EMDR, the client is asked to focus on the trauma memory while simultaneously experiencing bilateral stimulation (typically tracking the therapist’s finger with their eye; (APA, 2017). This is thought to be associated with a reduction in the vividness and emotion associated with the trauma memories (APA, 2017). With NET, a client establishes a chronological narrative of their life. They are told to concentrate mainly on their traumatic experience(s), but also incorporate some positive events (APA, 2017). NET therapists posit that this process contextualizes the network of cognitive, affective and sensory memories of a client’s trauma (APA, 2017). When the client expresses the narrative, they are able to fill in details of the trauma memories, which are often fragmented, and this helps them to develop a coherent autobiographical story (APA, 2017). In so doing, the memory of a traumatic episode is refined and understood, and symptoms are believed to be reduced (APA, 2017).

In additional to psychological treatments, four medications have received a conditional recommendation for use in the treatment of PTSD. These include the Selective Serotonin Reuptake Inhibitors (SSRIs) sertraline, paroxetine, and fluoxetine and the selective serotonin and norepinephrine reuptake inhibitor (SNRI) venlafaxine (APA, 2017). Currently only sertraline (Zoloft) and paroxetine (Paxil) are approved by the Food and Drug Administration (FDA) for PTSD (APA, 2017). From the FDA perspective, all other medication uses are “off label,” though there are differing levels of evidence supporting their use. These medications work by inhibiting the presynaptic reuptake of serotonin and norepinephrine (neurotransmitters), respectively, thereby increasing the presence of these neurotransmitters in the brain.

As noted above, the evidence for the efficacy of these three treatments is conditional. EMDR received a conditional recommendation there is a low strength of evidence for the critical outcome of PTSD symptom reduction (APA, 2017). However, research suggests that EMDR is effective for loss of PTSD diagnosis, and prevention/reduction of comorbid depression (APA, 2017). Thus, the APA (2017) recommends that clinicians offer EMDR compared to no intervention. With regards to NET, it has received a conditional recommendation, because despite evidence of a large/medium magnitude of benefit for the critical outcome of PTSD symptom reduction, there was low or insufficient/very low strength of evidence for all other important benefit outcomes (e.g., remission or loss of PTSD diagnosis or reduction/prevention of comorbid depression). However, research suggests that NET is effective at reducing PTSD symptoms (APA, 2017). Similarly, the APA (2017), suggests that clinicians offer NET, as opposed to no treatment.

Last, with regards to psychopharmacological treatments, the APA (2017) suggests that the medications noted above all be offered, compared to no intervention. Fluoxetine has been found to reduce PTDS symptoms and prevent/reduce comorbid depression and anxiety (APA, 2017), with the benefits slightly outweighing the harms. Paroxetine has been found to reduce PTSD symptoms, contribute to PTSD remission, and prevent/reduce comorbid depression and disability/functional impairment, with the benefits clearly outweighing the harms (APA, 2017). Sertaline has been found to assist with PTSD symptom reduction, with benefits slightly outweighing the harms (APA, 2017). Last, Venlafaxine has been found to assist with PTSD symptoms reduction, and to assist with remission, with the benefits slightly outweighing the harms (2017).

Overall, the APA (2017) posits that their findings from the panel recommendations, would be unlikely to change if the meta-analyses reported in the systematic review were updated to include the new trials. However, the note that EMDR and NET are exceptions to this, and that it is possible that their recommendations might change, pending additional research on these two treatment modalities.

References

Abramson, L., Seligman, M., & Teasdale, J. (1978). Learned helplessness in humans: Critique and reformulation. Journal of Abnormal Psychology, 87, 49-74.

Afifi, T. O. MacMillan, H. L., Boyle, M., Taillieu, T., Cheung, K. & Sareen, J. (2014). Child abuse and mental disorders in Canada. Canadian Medical Association Journal, 186(9), E324-E332. doi:https://doi.org/10.1503/cmaj.131792

American Psychiatric Association (2013). Diagnostic and statistical manual of mental disorders (5th ed.). Washington, DC: Author.

American Psychological Association (2017, February 24). Clinical Practice Guidelines for the Treatment of PTSD. https://www.apa.org/ptsd-guideline/ptsd.pdf.

American Psychological Association (2017, July 31). PTSD Treatments. https://www.apa.org/ptsd-guideline/treatments/index

Asukai, N., Saito, A., Tsuruta, N., Kishimoto, J., & Nishikawa, T. (2010). Efficacy of exposure therapy for Japanese patients with posttraumatic stress disorder due to mixed traumatic events: a randomized controlled study. Journal of Traumatic Stress, 23, 744–750.

Barton, S., Boals, A., & Knowles, L. (2013). Thinking about trauma: The unique contributions of event centrality and posttraumatic cognitions in predicting PTSD and posttraumatic growth. Journal of Traumatic Stress, 26, 718-726.

Berntsen, D., & Rubin, D. C. (2006). The centrality of event scale: A measure of integrating a trauma into one’s identity and its relation to post-traumatic stress disorder symptoms. Behaviour Research and Therapy, 44, 219-231.

Berntsen, D., Rubin, D. C., & Siegler, I. C. (2011). Two versions of life: Emotionally negative and positive life events have different roles in the organization of life story and identity. Emotion, 11, 1190.

Blanchard, E. B., Hickling, E. J., Devineni, T., Veazey, C. H., Galovski, T. E., Mundy, E., Malta, L.S. & Buckley, T.C. (2003). A controlled evaluation of cognitive behavioral therapy for posttraumatic stress in motor vehicle accident survivors. Behavaviour Research and Therapy, 41, 79–96.

Blix, I., Solberg, &., & Heir, T. (2014). Centrality of event and symptoms of posttraumatic stress disorder after the 2011 Oslo bombing attack. Applied Cognitive Psychology, 28, 249-253.

Boals, A. (2010). Events that have become central to identity: Gender differences in the centrality of events scale for positive and negative events. Applied Cognitive Psychology, 24(1), 107-121.

Boals, A., & Murrell, A. R. (2016). I am > trauma: Experimentally reducing event centrality and PTSD symptoms in a clinical trial. Journal of Loss and Trauma, 21, 471-483.

Boals, A., Hayslip Jr, B., Knowles, L. R., & Banks, J. B. (2012). Perceiving a negative event as central to one’s identity partially mediates age differences in posttraumatic stress disorder symptoms. Journal of Aging and Health, 24, 459-474.

Broadbridge, C. L. (2018). Is the centralization of potentially traumatic events always negative? An expansion of the Centrality of Events Scale. Applied Cognitive Psychology, 32, 315-325.

Brown, A., Antonius, D., Kramer, M., Root, J., & Hirst, W. (2010). Trauma centrality and PTSD in veterans returning from Iraq and Afghanistan. Journal of Traumatic Stress, 23, 496-499.

Bryant, R. A., Moulds, M. L., Guthrie, R. M., Dang, S. T., Mastrodomenico, J., Nixon, R. D., Felmingham, K.L., Hopwood, S. & Creamer, M. (2008). A randomized controlled trial of exposure therapy and cognitive restructuring for posttraumatic stress disorder. Journal of Consulting & Clinical Psychology, 76, 695–703.

Bryant, R. A., Moulds, M. L., Guthrie, R. M., Dang, S. T., & Nixon, R. D. V. (2003). Imaginal exposure alone and imaginal exposure with cognitive restructuring in treatment of posttraumatic stress disorder. Journal of Consulting & Clinical Psychology, 71, 706–712.

Canadian Centre for Justice Statistics (2017). Family violence in Canada: A statistical profile, 2015. Retrieved April 13, 2020 from https://www150.statcan.gc.ca/n1/daily-quotidien/170216/dq170216b-eng.htm

Canadian Mental Health Association. (2013). Posttraumatic stress disorder. Retrieved April 12, 2020 from https://cmha.bc.ca/documents/post-traumatic-stress-disorder-2/

Caryn, P. Zamorski, M., & Janz T. (2014). Mental health of the Canadian Armed Forces Health at a Glance. Statistics Canada Catalogue no. 82-624-X. Retrieved April 12, 2020 from https://www150.statcan.gc.ca/n1/pub/82-624-x/2014001/article/14121-eng.htm#n7

Charuvastra, A., & Cloitre, M. (2008). Social bonds and posttraumatic stress disorder. Annual Review of Psychology, 59, 301-328. Retrieved from https://doi.org/10.1146/annurev.psych.58.110405.085650.

Cusack, K., Jonas, D. E., Forneris, C. A., Wines, C., Sonis, J., Middleton, J. C., Feltner, C., Brownley, K.A., Olmsted, K.R., Greenblatt, A. & Weil, A. (2016). Psychological treatments for adults with posttraumatic stress disorder: a systematic review and meta-analysis. Clinical Psychology Review, 43, 128–141.

Ehlers, A., Clark, D. M., Hackmann, A., McManus, F., Fennell, M., Herbert, C., & Mayou, A. (2003). A randomized controlled trial of cognitive therapy, a self-help booklet, and repeated assessments as early interventions for posttraumatic stress disorder. Archives of General Psychiatry, 60, 1024–1032.

Fitzgerald, J., Berntsen, D., & Broadbridge, C. (2016). The influences of event centrality in memory models of PTSD. Applied Cognitive Psychology, 30, 10-21.

Gehrt, T. B., Berntsen, D., Hoyle, R. H., & Rubin, D. C. (2018). Psychological and clinical correlates of the Centrality of Event Scale: A systematic review. Clinical Psychology Review, 65, 57-80.

Janoff-Bulman, R. (1989). Assumptive worlds and the stress of traumatic events: Applications of the schema construct. Social Cognition, 7, 113-136.

Jonas, D. E., Cusack, K., Forneris, C. A., Wilkins, T. M., Sonis, J., Middleton, J. C., Feltner, C., Meredith, D., Cavanaugh, J., Brownley, K.A. & Olmsted, K.R. (2016). Psychological and pharmacological treatments for adults with posttraumatic stress disorder (PTSD). Rockville (MD): Agency for Healthcare Research and Quality (US); 2013 April. Comparative Effectiveness Review No. 92. Journal of Clinical Psychiatry, 77, e580-e587.

Klengel, T., & Binder, E. B. (2015). Epigenetics of Stress-Related Psychiatric Disorders and Gene x Environment Interactions. Neuron, 86(6), 1343–1357.

Marks, I., Lovell, K., Noshirvani, H., Livanou, M., & Thrasher, S. (1998). Treatment of posttraumatic stress disorder by exposure and/or cognitive restructuring: a controlled study. Cochrane Database Syst. Rev. 55:CD004780.

Ogle, C. M., Rubin, D. C., & Siegler, I. C. (2014). Cumulative exposure to traumatic events in older adults. Aging & Mental Health, 18, 316-325.

Ogle, C. M., Rubin, D. C., Berntsen, D., & Siegler, I. C. (2013). The frequency and impact of exposure to potentially traumatic events over the life course. Clinical Psychological Science, 1, 426-434.

Power, K., McGoldrick, T., Brown, K., Buchanan, R., Sharp, D., Swanson, V., & Karatzias, A. (2002). A controlled comparison of eye movement desensitization and reprocessing versus exposure plus cognitive restructuring versus waiting list in the treatment of post-traumatic stress disorder. Clinical Psychology & Psychotherapy, 9, 299–318.

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

Resick, P. A., Galovski, T. E., Uhlmansiek, M. O., Scher, C. D., Clum, G. A., & Young-Xu, Y. (2008). A randomized clinical trial to dismantle components of cognitive processing therapy for posttraumatic stress disorder in female victims of interpersonal violence. Journal of Consulting and Clinical Psychology, 76, 243–258.

Robinaugh, D. J., & McNally, R. J. (2011). Trauma centrality and PTSD symptom severity in adult survivors of childhood sexual abuse. Journal of Traumatic Stress, 24, 483-486.

Rubin, D. C., Berntsen, D., & Bohni, M. K. (2008). A memory-based model of posttraumatic stress disorder: Evaluating basic assumptions underlying the PTSD diagnosis. Psychological Review, 115, 985.

Rubin, D. C., Boals, A., & Berntsen, D. (2008). Memory in posttraumatic stress disorder: Properties of voluntary and involuntary, traumatic and non-traumatic autobiographical memories in people with and without PTSD symptoms. Journal of Experimental Psychology: General, 137, 591–614.

Rubin, D., Dennis, M., & Beckham, J. (2011). Autobiographical memory for stressful events: The role of autobiographical memory in posttraumatic stress disorder. Consciousness and Cognition, 20, 840-856.

Schnurr, P. P., Friedman, M., Engel, C. C., Foa, E. B., Shea, M. T., Chow, B. K., Resick, P.A., Thurston, V., Orsillo, S.M., Haug, R., & Turner, C. (2007). Cognitive behavioral therapy for posttraumatic stress disorder in women: a randomized controlled trial. JAMA, 297, 820–830.

Sharma, S., & Ressler, K. J. (2019). Genomic updates in understanding PTSD. Progress in Neuro-Psychopharmacology & Biological Psychiatry, 90, 197-203. Retrieved from https://doi.org/10.1016/j.pnpbp.2018.11.010.

Silva, T., Donat, J., Lorenzonni, P., Souza, L., Gauer, G., & Kristensen, C. (2016). Event centrality in trauma and PTSD: Relations between event relevance and posttraumatic symptoms. Psicologia: Reflexão E Crítica, 29, 1-7.

Taylor, S., Thordarson, D. S., Maxfield, L., Fedoroff, I. C., Lovell, K., & Ogrodniczuk, J. (2003). Comparative efficacy, speed and adverse effects of three PTSD treatments: exposure therapy, EMDR, and relaxation training. Journal of Consulting and Clinical Psychology., 71, 330–338.

Teale Sapach, M., Horswill, J., Parkerson, N., Asmundson, S., & Carleton, C. (2019). Centrality of traumatic events: Double edged sword or matter of valence? Cognitive Therapy and Research, 43, 374-386.

Tversky, A., & Kahneman, D. (1973). Availability: A heuristic for judging frequency and probability. Cognitive Psychology, 5, 207-232.

Van Ameringen, M., Mancini, C., Patterson, B., & Boyle, M. H. (2008). Post-traumatic stress disorder in Canada. CNS Neuroscience & Therapeutics, 14, 171-181. https://doi.org/10.1111/j.1755-5949.2008.00049.x

Wamser‐Nanney, R. (2019). Event centrality: Factor structure and links to posttraumatic stress disorder symptom clusters. Journal of Traumatic Stress, 32, 516-525.

Watts, B. V., Schnurr, P. P., Mayo, L., Young-Xu, Y., Weeks, W. B., & Friedman, M. J. (2013). Meta-analysis of the efficacy of treatments for posttraumatic stress disorder. Journal of Clinical Psychiatry, 74, e541–e550.

Yahyavi, S. T., Zarghami, M., & Marwah, U. (2014). A review on the evidence of transgenerational transmission of posttraumatic stress disorder vulnerability. Revista Brasileira de Psiquiatria, 36, 89-94. Retrieved from https://doi.org/10.1590/1516-4446-2012-0995