**5. Etiology and risk factors**

PTSD is believed to be caused by either physical trauma or psychological trauma, or more frequently a combination of both. Possible sources of trauma include experiencing or witnessing childhood or adult physical, emotional or sexual abuse. Other recognized causes

Posttraumatic stress disorder is classified as an anxiety disorder, characterized by aversive anxiety-related experiences, behaviors, and physiological responses that develop after exposure to a psychologically traumatic event (sometimes months after). Its features persist for longer than 30 days, which distinguishes it from the briefer acute stress disorder. These persisting posttraumatic stress symptoms cause significant disruptions in one or more important areas of life function. It has three sub-forms: acute, chronic, and delayed-onset; based on onset of symptoms after the traumatic event. Acute is of < 1 month, chronic

Complex Post Traumatic Stress Disorder (C-PTSD) is a condition that results from chronic or long-term exposure to emotional trauma over which a victim has little or no control and from which there is little or no hope of escape, such as in cases of domestic emotional, physical or sexual abuse; childhood emotional, physical or sexual abuse; entrapment or kidnapping; slavery or enforced labor and long term imprisonment and torture. When people have been trapped in a situation over which they had little or no control at the beginning, middle or end, they can carry an intense sense of dread even after that situation is removed. This is because they know how bad things can possibly be. And they know that it could possibly happen again. And they know that if it ever does happen again, it might be worse than before. C-PTSD results more from chronic repetitive stress from which there is little chance of escape. PTSD can result from single events, or short term exposure to

PTSD is believed to be caused by either physical trauma or psychological trauma, or more frequently a combination of both. Possible sources of trauma include experiencing or witnessing childhood or adult physical, emotional or sexual abuse. Other recognized causes

Thailand 59 86 30 Indonesia 58 86 30 Philippines 58 86 30 USA 58 86 30 Bangladesh 57 85 29 Egypt 56 83 30 India 56 85 29 Iran 56 83 30 Pakistan 56 85 29 Japan 55 80 31

**PTSD DALY rate, females** 

**PTSD DALY rate, males** 

**Country PTSD DALY rate,** 

Table 1.

**4. Classification** 

extreme stress or trauma.

**5. Etiology and risk factors** 

**overall** 

between 1-3 months and delayed is after 3 months.

of PTSD include experiencing or witnessing an event perceived as life-threatening such as accidents, terminal illnesses, or employment in occupations exposed to war (such as soldiers) or disaster (such as emergency service workers). Traumatic events that may cause PTSD symptoms to develop include violent assault, kidnapping, sexual assault, torture, being a hostage, prisoner of war or concentration camp victim, experiencing a disaster, violent automobile accidents or getting a diagnosis of a life-threatening illness. Children or adults may develop PTSD symptoms by experiencing bullying or mob violence. Preliminary research suggests that child abuse may interact with mutations in a stress-related gene to increase the risk of PTSD in adults[9]. Multiple studies show that parental PTSD and other posttraumatic disturbances in parental psychological functioning can, despite a traumatized parent's best efforts, interfere with their response to their child as well as their child's response to trauma[10,11]. Parents with violence-related PTSD may, for example, inadvertently expose their children to developmentally inappropriate violent media due to their need to manage their own emotional dysregulation[12,13].

Military experience as risk factors for the development of PTSD include coming from an unstable family, being punished severely during childhood, childhood anti-social behavior and depression as pre-military factors, war-zone exposure, peri-traumatic dissociation, depression as military factors and recent stressful life events and depression as post-military factors[14]. Certain protective factors against PTSD in war-conditions include high school degree or college education, older age at entry to war, higher socioeconomic status, and positive paternal relationship as pre-military protective factors and social support at homecoming and current social support as post-military factors[15]. Research also indicates the protective effects of social support in averting and recovery from PTSD[16]. There may also be an attitudinal component; for example, a soldier who believes that they will not sustain injuries may be more likely to develop symptoms of PTSD than one who anticipates the possibility, should either be wounded[15]. Likewise, the later incidence of suicide among those injured in home fires above those injured in fires in the workplace suggests this possibility.

Posttraumatic stress responses have been documented in children who have suffered traumatic loss of their parents, siblings, and peers[17,18,19,20]. Results from a study indicated that knowing someone who was injured or killed, female gender, and bombrelated television viewing or other media exposure were associated with the most severe psychological reactions. Bereaved youths who suffered severe loss (e.g. a parent, sibling, close relative, or friend) as a result of the bombing were more likely to report posttraumatic stress symptoms than did children who did not experience this degree of loss.

Although most people (50-90%) encounter trauma over a lifetime, only about 8% develop full PTSD[21]. Vulnerability to PTSD presumably stems from an interaction of biological diathesis, early childhood developmental experiences, and trauma severity. Predictor models have consistently found that childhood trauma, chronic adversity, and familial stressors increase risk for PTSD as well as risk for biological markers of risk for PTSD after a traumatic event in adulthood[22]. This effect of childhood trauma, which is not well understood, may be a marker for both traumatic experiences and attachment problems. Proximity to, duration of, and severity of the trauma also make an impact; and interpersonal traumas cause more problems than impersonal ones[21]. People vary in susceptibility to PTSD. Genetic factors may play a significant role in susceptibility. Women develop PTSD at about twice the rate as men, even for the same crimes[21]. Individuals with a prior trauma history or multiple traumas are at increased risk[21]. A premorbid psychiatric history also

Post Traumatic Stress Disorder – An Overview 9

After a month in this heightened state with stress hormones elevated and cortisol levels lowered, further physical changes, such as heightened hearing develop. This cascade of physical changes, one triggering another, suggests that early intervention may be the key to

Given the strong cortisol suppression to dexamethasone in PTSD, HPA axis abnormalities are likely predicated on strong negative feedback inhibition of cortisol, itself likely due to an increased sensitivity of glucocorticoid receptors. Some researchers have associated the response to stress in PTSD with long-term exposure to high levels of norepinephrine and low levels of cortisol, a pattern associated with improved learning in animals. Translating this reaction to human conditions gives a pathophysiological explanation for PTSD by a maladaptive learning pathway to fear response through a hypersensitive, hyperreactive and hyperresponsive HPA axis. Low cortisol levels may predispose individuals to PTSD: Swedish soldiers serving in Bosnia and Herzegovina with low pre-service salivary cortisol levels had a higher risk of reacting with PTSD symptoms, following war trauma, than soldiers with normal pre-service levels[29]. Because cortisol is normally important in restoring homeostasis after the stress response, it is thought that trauma survivors with low cortisol experience a poorly contained—that is, longer and more distressing—response,

However, there is considerable controversy within the medical community regarding the neurobiology of PTSD. A review of existing studies on this subject showed no clear relationship between cortisol levels and PTSD. Only a slight majority have found a decrease in cortisol levels while others have found no effect or even an increase. Decreased brain volume or volume of specific brain structures have been documented in some adults and children with PTSD [30,31]. The biologic correlates have not yet been fully explored, nor are

Three areas of the brain whose function may be altered in PTSD have been identified: the prefrontal cortex, amygdala and hippocampus. Much of this research has utilised PTSD victims from the Vietnam War. For example, a prospective study using the Vietnam Head Injury Study showed that damage to the prefrontal cortex may actually be protective against later development of PTSD [32]. In a study by Gurvits et al, combat veterans of the Vietnam War with PTSD showed a 20% reduction in the volume of their hippocampus compared with veterans who suffered no such symptoms [33,34]. This finding could not be replicated in chronic PTSD patients traumatized at an air show plane crash in 1988 (Ramstein, Germany) [35]. In human studies, the amygdala has been shown to be strongly involved in the formation of emotional memories, especially fear-related memories. Neuroimaging studies in humans have revealed both morphological and functional aspects of PTSD. The amygdalocentric model of PTSD proposes that it is associated with hyperarousal of the amygdala and insufficient top-down control by the medial prefrontal cortex and the hippocampus particularly during extinction. This is consistent with an interpretation of PTSD as a syndrome of deficient extinction ability. Further animal and clinical research into the amygdala and fear conditioning may suggest additional treatments for the condition.

Describing children's responses to trauma, Terr(1991) presents four specific symptoms characteristic of childhood PTSD: repeatedly perceiving memories of the event through visualization, engaging in behavioral re-enactments and repetitive play related to the event,

heading off the effects of post-traumatic stress disorder.

setting the stage for PTSD.

**7. Clinical features** 

the implications for intervention established.

increases the likelihood of developing the disorder[22]. It may be that people who have fewer supports and limited inter-personal coping skills are more likely to develop PTSD[21]. Studies of concentration camp survivors and prisoners of war suggest that even given sufficient trauma intensity and duration most of those who are exposed develop PTSD.

A positive relationship has been found between trauma intensity and the likelihood of PTSD[22]. People who have been injured or perceived the event as life threatening are more likely to develop PTSD than those with less severe trauma. Human caused traumatic events such as assaults and murder have a more powerful impact than accidents and natural disasters. Among crime victims, individuals who have suffered more brutal trauma have higher frequencies of PTSD – torture (54%), rape (49%); badly beaten (32%), and other sexual assault (24%)[21]. Dissociation during the trauma, peritraumatic dissociation, is associated with risk for PTSD[21].

There is evidence that susceptibility to PTSD is hereditary. For twin pairs exposed to combat in Vietnam, having a monozygotic (identical) twin with PTSD was associated with an increased risk of the co-twin having PTSD compared to twins that were dizygotic (nonidentical twins)[23]. Recently, it has been found that several single-nucleotide polymorphisms (SNPs) in FK506 binding protein 5 (FKBP5) interact with childhood trauma to predict severity of adult PTSD[24]. These findings suggest that individuals with these SNPs who are abused as children are more susceptible to PTSD as adults. Another recent study found a single SNP in a putative estrogen response element on ADCYAP1R1 (encodes pituitary adenylate cyclase-activating polypeptide type I receptor or PAC1) to predict PTSD diagnosis and symptoms in females[25].
