A positive family history of psychiatric disorders is a consistent risk factor for development of PTSD (Ozer et al., 2003). Preexisting psychiatric disorders, particularly conduct disorder, major depression, and nicotine dependence, also increase PTSD risk (Breslau, 2002). Twin studies have demonstrated that genetic influences common to major depression, generalized anxiety disorder, panic disorder, or substance dependence account for up to 60 % of the genetic variance in PTSD (Koenen et al., 2005). Variants implicated in PTSD also have been associated with other psychiatric conditions (Caspi et al., 2003).

PTSD is highly comorbid with other psychiatric illnesses, including mood disorders such as major depressive disorder (Kessler et al., 1995). It has been suggested that susceptibility to anxiety disorders is associated with increased risk for mood disorders and vice versa (Dilsaver, Akiskal, Akiskal, & Benazzi, 2006). It has been demonstrated that preexisting depression is a risk factor to experience a traumatic event as well as to develop PTSD after trauma exposure (Breslau, Davis, Peterson, & Schultz, 2000). In addition, the development of depression after a traumatic event is more frequent in individuals with PTSD as compared with traumatized individuals without PTSD (Breslau et al., 2000). The accumulating literature suggests common genetic susceptibility factors for the development of PTSD and major depression. For example, Koenen, Moffitt, Poulton, Martin, and Caspi (2007) calculated that a majority of the genetic variance in PTSD is the result of comorbid major depression (Koenen, 2007). In addition, the homozygous S polymorphism of the serotonin transporter has been associated with both PTSD and major depression (Caspi et al., 2003).

It has been frequently demonstrated that women show a greater propensity to develop PTSD following any traumatic event (Testa et al., 2007). Thus, it has been proposed that women may be more vulnerable to aberrant hypothalamus–pituitary–adrenal (HPA) axis responses to stress. For instance, basal cortisol was examined in healthy men and women and following acute exposure to stressors. Among healthy participants, men had higher basal cortisol levels than women. In response to acute stressors, such as carbon dioxide or noise, respectively, cortisol levels were comparable between men and women or higher among women. Cortisol levels were also examined among those with PTSD. Men who have motor vehicle accident-related PTSD demonstrate more aberrant cortisol function, than do their female counterparts. Although these sex differences in cortisol seem to vary with type of stress exposure and/or pathophysiological status of the individual, other hormones may influence cortisol response (Paris et al., 2010).

Furthermore, studies of civilians typically find that female gender is a risk factor for PTSD. In contrast, police and military studies often find no gender differences in PTSD. A study compared female police officers and female civilians on several variables including trauma exposure, peri-traumatic emotional distress, current somatization, and cumulative PTSD symptoms. It was found that despite greater exposure to assaultive violence in the officer group, female civilians reported significantly more severe PTSD symptoms. Elevated PTSD symptoms in female civilians were explained by significantly more intense peri-traumatic emotional distress. However, it was demonstrated that female officers showed a stronger direct relationship between peri-traumatic emotional distress and current somatization. These findings suggest that apparent gender differences in PTSD may result from differences in peri-traumatic emotionality, which influence subsequent PTSD and somatization symptoms. Therefore, emotionality may be more important than biological sex in understanding gender differences in PTSD (Lilly, Pole, Best, Metzler, & Marmar, 2009).

A number of reviews (Fothergill, Maestas, & Darlington, 1999) observed that being a member of an ethnic minority increased the likelihood of developing adverse outcomes following a disaster. Brewin, Andrews, and Valentine (2000) in a meta-analysis of 22 studies with 8,165 subjects confirmed minority status as a risk factor for PTSD following major disasters. In studies assessing the impact of the 9/11 terrorist attacks, Stein et al. (2004) reported more persistent distress in non-whites. Ford, Adams, and Dailey (2005) and Chu, Seery, Ence, Holman, and Cohen-Silver (2006) found Hispanic ethnicity to be a risk factor in reporting psychological problems. Rubin, Brewin, Greenberg, Simpson, and Wessely (2005) reported that being non-white as well as Muslim predicted substantial distress following the 2005 bombing in London. A number of studies have also found that being part of the Arab minority in Israel, during times of ongoing terrorism, is a risk factor. Compared to Jews, Musallam, Ginzburg, Lev-Shalem, and Solomon (2005) found more distress in Arab-Israeli students; Somer et al. (2006) found more PTSD and depression in Arabs in ethnically mixed towns, and Hobfoll, Canetti-Nisim, and Johnson (2006) found more posttraumatic symptomatology in a large sample of urban Arabs compared to Jews.

A number of reasons have been proposed as to why minorities are more at risk for mental health sequelae following traumatic exposure. For example, minorities often have higher exposure rates (Beals et al., 2002) and live in at-risk areas. They often have high mortality, morbidity and injury rates (Hobfoll et al., 2006), and less health care following disasters (Ford, 2005). Empirical studies suggest that minorities may have higher risk perceptions, more motion focused coping (Chu et al., 2006), less behavioral adaptation to terror (Goltz, Russell, & Bourque, 1992), and less psychological resources (Zeidner, Klingman, & Itskowitz, 1993), all conducive to more distress. Economic and social–political factors such as less education and economic resources (Goltz et al., 1992), closed and overburdened social networks (Kaniasty & Norris, 1993), acculturation stress (Perilla, Norris, & Lavizzio, 2002), racism (Loo, Fairbank, & Chemtob, 2005), and political stress may also compound the burden on these populations. However, following 19 months of terrorism, Arab Israelis and Jewish Israelis reacted similarly. This is in line with a number of previous studies that have also found no (Adams & Boscarino, 2005) or only minor differences in the way most minorities reacted in the aftermath of the 9/11 events (Galea et al., 2003). One might assume an equalizing mechanism, whereby national or community stress impacts in a way that overshadows certain risk factors usually closely associated with traumatic reactions such as ethnicity (Somer, Ruvio, Soref, & Sever, 2005), education (Lewin, Carr, & Webster, 1998), and socioeconomic status (Kaniasty & Norris, 1995). This situation changed over 44 months of terror. In the Jewish population some symptoms worsened, some remained unchanged, and others improved. In the Arab population, outcome measures worsened significantly. These results suggest that traumatic events may impact over time differentially in minorities and majorities (Palinkas, Petterson, Russell, & Downs, 2004). Resilience eroding factors such as dual allegiance, feelings of political and social oppression, and internal pressure to actively support terrorist activities may have elevated the Arab population’s level of stress to a point where available material, societal, and psychological resources become inadequate to meet the threat of terror.

Further, issues about the impact of traumatic experiences on minority soldiers and veterans have been initially raised in the context of the Vietnam era studies.

Findings from the American troops in Operation Desert Storm, who were of a more diverse ethnicity than in previous military operations, supported findings from studies of Vietnam veterans that ethnic minorities are more vulnerable to traumatic stress following war-zone duty (Sutker, Davis, Uddo, & Ditta, 1995). Veterans from ethnic minority backgrounds may have different experiences during service, such as higher levels of combat stressors (MacDonald, Chamberlain, & Long, 1997) and exposure to adverse race-related events (Loo et al., 2005), as well as added difficulties in the readjustment period following discharge (Brende, 1983).

Breslau (2002) noted, “Personality traits of neuroticism and extroversion, early conduct problems, a family history of psychiatric disorders, and preexisting psychiatric disorders are associated with increased risk for exposure to traumatic events”. Thus, a portion of the psychopathology observed following trauma may simply represent an extension of preexisting risk factors for exposure (Zeidner et al., 1993).

A prospective study examined constitutional and contextual factors leading to the development of PTSD in a cohort of children aged 3–5 years, who were followed into adulthood. Constitutional factors were defined as within-individual capacities, such as childhood cognitive ability, early temperament and behavior, and juvenile mental disorders. Contextual factors were defined as aspects of the child’s social environment, such as maternal depression, poverty, and residential instability.

It has been shown that childhood IQ assessed as early as age 5 was inversely associated with risk for developing PTSD by age 32. No association was found between PTSD and other neurodevelopmental factors assessed in this cohort, including number of perinatal insults or gross motor skills in childhood. This suggested that the IQ-PTSD association was specific to cognitive ability and not a marker of broader neurodevelopmental deficits. Lower childhood IQ was not associated with increased risk of later trauma exposure. The authors have posited that individuals with greater cognitive ability are better able to translate their traumatic event into a narrative and make meaning out of it, both of which are thought to be important in recovery from PTSD (Koenen et al., 2007).

It was also found that children characterized as exhibiting externalizing temperament and behavior, defined as having difficult temperaments aged 3–5 or manifesting antisocial behavior and hyperactivity aged 5–11, were at increased risk of developing PTSD (Koenen et al., 2007). This increased risk was explained, in part, by an association between externalizing and increased risk of trauma exposure. However, even among the trauma exposed, externalizing increased risk of PTSD. One explanation for this association is that externalizing tendencies might interfere with tolerating the emotions (e.g., fear) necessary for processing the traumatic event, and thus impede recovery. Anger, which is a characteristic of individuals with externalizing tendencies, has been associated with reduced likelihood of recovery from PTSD, both in treatment settings (Koenen et al., 2007) and in the community (Koenen et al., 2007).

Only 15 % of the trauma exposed with no juvenile mental disorder history developed PTSD. In contrast, 41 % of those with one juvenile diagnosis and 48 % of those with two or more developed PTSD. This effect was not specific to any one juvenile diagnosis. The longitudinal findings of this study also suggest that characteristics of the child’s early social context may sensitize them to the adverse effects of later trauma. Specifically, children raised in poverty were predisposed to developing PTSD by age 32 when exposed to a traumatic event, as compared with children of high socioeconomic status. Residential instability, defined as moving three or more times before age 11, was also a strong contributor to PTSD risk. Other factors that contributed to the development of PTSD were maternal depression and parent changes before age 11. It was speculated that these factors—poverty, residential instability, maternal depression, and caregiver changes—result in an unpredictable and uncontrollable environments that have adverse life course effects.

Childhood adversity in human studies is associated with HPA axis dysregulation in adulthood (Watson et al., 2007). Thus, HPA axis dysregulation is a potential biological mechanism linking the association between an unpredictable and uncontrollable childhood environment and the later development of PTSD.

To summarize: developmental factors may be useful in identifying individuals who are at high risk and should be monitored more carefully for persistent symptoms. Identification of high-risk groups is particularly important in natural and human-made disasters where large numbers of individuals are trauma exposed but resources are limited for follow-up. A better understanding of the role of developmental factors in PTSD may also help inform resiliency training for persons in professions with a high probability of trauma exposure, such as the military, police, firefighters, or other first responders. Finally, prevention efforts aimed at addressing some of these developmental capacities, such as externalizing temperament and behavior or at improving conditions of childhood adversity, may ultimately reduce risk of PTSD.

It has been postulated that the severity of initial reaction to stress may be predictive of subsequent development of PTSD (Goltz et al., 1992). Thus, it was demonstrated that a significant portion of injured traffic accident victims manifested PTSD one year after the event. Development of PTSD at one year can be predicted as early as 1 week after the accident, on the basis of the existence and severity of early PTSD-related symptoms. However, the first 3 months following the accident appear to be the critical period for the development of PTSD (Koren, Arnon, & Klein, 1999). This study examined the prevalence of peri-traumatic and persistent panic symptoms following trauma. Panic attacks were experienced by 77 % of participants during their trauma, and 47 % reported recurrent panic attacks post-trauma. Individuals suffering from Acute Stress Disorder (ASD) demonstrated more panic symptoms during and after their trauma than those not diagnosed with ASD. Posttraumatic panic was most strongly associated with anxiety sensitivity. There is increasing evidence that panic attacks play a role in psychopathological response to trauma. A significant proportion of people with panic disorder report a history of trauma (Nixon & Bryant, 2003). Moreover, two-thirds of trauma survivors report panic attacks within the previous 2 weeks (Nixon & Bryant, 2003). There is also evidence that people with PTSD display elevated levels of anxiety sensitivity (Nixon & Bryant, 2003). ASD is a useful framework in which to investigate the role of panic in posttraumatic stress because ASD describes acute responses to trauma that are strongly predictive of chronic PTSD (Nixon & Bryant, 2003).

Memory of the traumatic event (MTE) is considered a central component of trauma-related disorders, including PTSD. It has been suggested that the psychopathology of PTSD is closely related to abnormal memory processes, namely, that in PTSD patients, traumatic events create pathogenic (“toxic”) memories. These memories, rather than the events themselves, are responsible for generating the characteristic symptoms of the disorder. Traumatic memories share both explicit and implicit features and are believed to be processed differently than ordinary memories (Brewin, 2001). This results in a failure to organize the traumatic event into a coherent verbally represented narrative (Brewin, 2001). The abnormal nature of traumatic memories is considered to be a central feature of PTSD. This is manifested by two well-documented and seemingly contradictory observations of traumatized individuals: hypermnesic symptoms, such as re-experiencing, intrusive thoughts, nightmares, and flashbacks, on the one hand, and impaired memory for certain aspects of the traumatic event in the form of amnesia and delayed recall, on the other hand. Furthermore, it appears that traumatic memories tend to be disorganized and fragmented. Patients with PTSD provide less coherent memories, exhibiting extra repetitions and nonconsecutive memory chunks (Halligan, Michael, Clark, & Ehlers, 2003). Their memories are characterized by dissociation and sensory verbal representation, namely, frequent use of sensory symbols. These abnormal features of memory (i.e., repetition and nonconsecutive chunks) were found to predict PTSD severity (Halligan et al., 2003) as well as to contribute to the preservation of PTSD, by interfering with processing and resolution of the traumatic memory (Ehlers & Clark, 2000). On the other hand, Foa, Molnar, and Cashman (1995) found that participants who exhibited a decrease in narrative fragmentation over time reported a reduction in trauma-related anxiety.

Preclinical and clinical data suggest that amnesia of the traumatic event is associated with a decreased prevalence of PTSD. Clinical data include following up on traumatic brain injury and examination of the frequency of PTSD in individuals with amnesia as compared to non-amnesic patients. Klein, Caspi, and Gil (2003) examined 120 patients with mild traumatic brain injury. Patients’ memory of the traumatic event was recorded (24-h post-trauma), and they were assessed for PTSD symptoms 1 week, 3 months, and 6 months later. Rates of PTSD 6 months following the traumatic event were found to be significantly lower in patients with no memory of the traumatic event (6 % PTSD) than in patients with memory of the event (23 % PTSD).

Along these lines, psychological defense mechanisms which mimic amnesia (such as repression) might be predicted as useful. Indeed, a study of repressive coping styles after myocardial infarction revealed this to be the case (Ginzburg, Solomon, & Bleich, 2002). In this study, 116 myocardial infarction patients were assessed for repressive coping style within a week of their myocardial infarction. These patients were divided into four groups: high anxious, low anxious, defensive, and repressors. Patients were also assessed at this point for symptoms of ASD, and for symptoms of PTSD at 7 months. The repressor group displayed fewer symptoms of both ASD and PTSD, implying that repression is indeed useful in buffering against the potential consequences of trauma.

Dissociation is a common feature of PTSD (van der Kolk et al., 1996). It involves disruptions in, and fragmentation of, the usually integrated functions of consciousness, memory, identity, body awareness, and perception of the self and the environment (American Psychiatric Association, 1994). Alterations in memory encoding and storage occur in dissociation, leading to fragmentation and compartmentalization of memory and impairments in memory retrieval (Spiegel & Cardena, 1991). Chronic psychological, sexual, and physical trauma as well as emotional neglect, including parental psychological unavailability, has been etiologically related to dissociation (Loewenstein & Putnam, 2004). Even though dissociative symptoms are often observed following exposure to chronic psychological trauma, acute traumatic events can also lead to dissociative experiences, often referred to as peri-traumatic dissociation. For example, a number of studies of individuals experiencing danger or life threat have shown specific peri-traumatic dissociative changes, including alterations in time sense, perception, attentional focus, and awareness of pain among others (Morgan et al., 2001). In addition, depersonalization has been described in a significant percentage of individuals facing acute life threat (Ironson et al., 1997). Information related to traumatic experiences is often differently encoded in these altered states, resulting in decreased access to information about the trauma, once the person returns to his or her baseline state. This may give a subjective sense of “compartmentalization” of the trauma and lead to cognitive fragmentation or emotional detachment from the experience. The cost of this detachment may be avoidance of necessary cognitive and affective processing of trauma in its aftermath (Spiegel & Cardena, 1991). Acute dissociative responses to psychological trauma have been found to predict the development of chronic PTSD (Marmar et al., 1994). Moreover, a chronic pattern of dissociation in response to reminders of the original trauma and minor stressors develops in persons who experience acute dissociative responses to psychological trauma (Butler, Duran, Jasiukaitis, Koopman, & Spiegel, 1996).

Immediate peri-traumatic dissociative responses have been noted in police and emergency personnel attending to catastrophes (Marmar et al., 1999), as well as fire victims (Koopman, Classen, & Spiegel, 1994), victims of earthquakes (Cardena & Spiegel, 1993), and combat soldiers (Marmar et al., 1994). Dissociative responses to trauma have also been correlated with increased dissociative response to reminders of trauma (Bremner et al., 1998), increased dissociative responses to subsequent traumas and stressors, and long-term PTSD and dissociative pathology (Bremner & Brett, 1997). Prospective studies in healthy military personnel have also revealed that severe stress leads to heightened dissociation (Morgan et al., 2001).

Bremner (1999) has hypothesized that there may be two subtypes of acute trauma response that represent unique pathways to chronic stress-related psychopathology: one is primarily dissociative, and the other predominantly intrusive and hyperaroused. Data from neuroimaging studies have shown that two subtypes of response can persist in persons with chronic PTSD and are associated with distinct patterns of neural activation upon exposure to reminders of traumatic events (Lanius, Bluhm, Lanius, & Pain, 2006). It should be noted that these response patterns are not completely distinct, and that individual patients with PTSD may show both response patterns either simultaneously, or at different time points. However, PTSD patients with prolonged traumatic experiences, such as chronic childhood abuse or combat trauma, often show a clinical syndrome that is characterized by chronic symptoms of dissociation (Pervanidou, 2008) as opposed to patients who have suffered from more acute traumatic experiences.

Psychobiological responses to recalling traumatic experiences can differ significantly among patients with chronic PTSD (Breslau, Davis, Andreski, Peterson, & Schultz, 1997). Approximately 70 % of patients had subjective experiences of reliving their traumatic experience and showed an increase in heart rate while recalling the traumatic memory (Lanius et al., 2006). The other 30 % of PTSD subjects had a dissociative response. The latter predominantly involved subjective states of depersonalization and derealization with no significant concomitant increase in heart rate (Hopper, Frewen, van der Kolk, & Lanius, 2007).

Terr (1991) proposed two types of traumatic experiences. Type I trauma refers to traumatic conditions that result from single traumatic experiences and include predominantly full and vividly detailed memories, cognitive reappraisals, and misperceptions. In contrast, Type II trauma was hypothesized to be associated with long-standing or repeated exposure to extreme stressors, and includes dissociation, denial and numbing, states of self-hypnosis, and rage. Further support for these hypotheses comes from a study by van der Kolk et al. (1996) which, as part of a DSM-IV field trial, examined a sample of 395 traumatized treatment-seeking subjects and 125 non-treatment-seeking subjects who had been exposed to traumatic experiences. Results showed that participants who had suffered early-onset interpersonal abuse (age ≤14 years) had significantly higher percentages of endorsements of dissociative symptoms than participants with late-onset interpersonal abuse and disaster survivors. Moreover, subjects with dissociative symptoms continued to suffer from dissociation even after they no longer met criteria for PTSD. This suggests that severe, chronic dissociative symptoms develop in response to early-onset interpersonal violence.

More recently, Ginzburg et al. (2006) employed signal detection analyses to identify high and low dissociation PTSD subgroups in a sample of 122 women who were seeking treatment for childhood sexual abuse. Specifically, three PTSD symptoms, including hypervigilance, sense of foreshortened future, and sleep difficulties, discriminated between high and low dissociation subgroups. In addition, Zucker, Spinazzola, Blaustein, and van der Kolk (2006) examined differences in dissociative symptoms in subjects with PTSD, versus subjects with PTSD who also met criteria for disorders of extreme stress not otherwise specified. Criteria for disorders of extreme stress not otherwise specified were developed to characterize traumatized individuals who suffer “complex” forms of PTSD-related multiple episodes of trauma over several developmental epochs, with symptoms of dissociation, emotion dysregulation, somatization, altered relationships and attachments, and alterations in systems of meaning (Cash, 1993). Subjects with both PTSD and disorders of extreme stress not otherwise specified exhibited chronic symptoms of dissociation, as evidenced by higher scores on the Dissociative Experiences Scale, than participants who were suffering from PTSD only. Prospective longitudinal studies have shown that trauma leads to heightened dissociation in children (Putnam, Helmers, Horowitz, & Trickett, 1995). Cross-sectional studies have also consistently show a heightened level of dissociation in children whose trauma histories have been objectively confirmed compared to non-traumatized children (Valentino, Cicchetti, Rogosch, & Toth, 2008).

Vietnam combat veterans with PTSD (N = 40) scored significantly higher on all five aspects of dissociation as measured by the clinician administered SCID-D (Steinberg, Rounsaville, & Cicchetti, 1990) compared to Vietnam veterans without PTSD (Bremner, Steinberg, Southwick, Johnson, & Charney, 1993). In fact, the symptom with the greatest difference between PTSD and non-PTSD patients was amnesia. Furthermore, prospective, longitudinal research showed that individuals presenting to emergency rooms resulting from acute assaults and with ASD retrieved fewer specific autobiographical memories than those without ASD 2 weeks post-assault (Kleim & Ehlers, 2008). In addition, reduced memory specificity at 2 weeks predicted PTSD at 6 months over and above what could be predicted by initial diagnoses and symptom severity.

Studies in combat-related PTSD also point to a dissociative subtype of PTSD. Taxometric analyses in a sample of 316 Vietnam veterans consistently revealed a taxon/subtype (subgroup identified by scores that are discontinuous with a dimensional distribution) of highly dissociative individuals. The dissociative subtype of PTSD was also associated with more severe PTSD (Creamer et al., 2001). Furthermore, Putnam et al. (1996) examined whether mean dissociation scores, as measured by the Dissociative Experiences Scale, resulted from uniform distributions of scores in a group of 166 predominantly combat-related PTSD patients. Results showed that the diagnostic group’s mean Dissociative Experiences Scale scores were a function of the proportion of subjects within the group who were high dissociators, thus suggesting the existence of a distinct dissociative subtype. An earlier study of Vietnam veterans also reported that chronic dissociative symptoms are an important element of long-term psychological responses to combat trauma, which is often repetitive in nature (Bremner et al., 1992).

Exposure-based treatments for PTSD (Institute of Medicine, 2007) have the strongest empirical support and involve repeated imaginary and in vivo exposure to trauma-related stimuli. However, exposure treatments should be used with caution in patients with significant emotional over modulation, such as dissociative and numbing symptoms. Foa and Kozak (1986) have suggested that such symptoms can prevent emotional engagement with trauma-related information and thus reduce treatment effectiveness (Jaycox, Foa, & Morral, 1998). In fact, a more recent study (Waelde, Silvern, & Fairbank, 2005) suggests that levels of dissociation are an important negative predictor of psychotherapy outcome in patients with borderline personality disorder, a disorder that has often been associated with childhood abuse (Ball & Links, 2009). Therefore, it is crucial, before commencing exposure-based treatments, to assess levels of dissociative psychopathology and to provide interventions to reduce dissociative symptomatic responses to trauma-related stimuli. Failure to do so may lead to an actual increase in PTSD and related symptoms, including dissociation, emotional dysregulation, and an increase in the patient’s overall distress and functional impairment.

As far as psychological mechanisms are concerned, the most direct hypothesis is that bodily injury intensifies the perceived threat to one’s life or physical integrity during the trauma. According to the literature (Shalev, 1992), trauma survivors’ perceived level of danger is a better predictor of PTSD than the objective severity of the traumatic event. However, this hypothesis may be overly simplistic due to data (Koren, Norman, Cohen, Berman, & Klein, 2005), suggesting that the heightened level of perceived threat is not directly correlated with the severity of injury. These findings suggest that the effect of bodily injury on perceived threat is moderated by other factors, such as sense of control and the ability to effectively function and cope during the traumatic event (Asmundson, Coons, Taylor, & Katz, 2002).