Post Traumatic Stress Disorder Ptsd What Is It Copied with permission from: http://plrplr.com/56327/post-traumatic-stress-disorder-ptsd-what-is-it/

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Over the past decade, as I have worked with cops, firfighters, abuse victims and children of addicts, I have learned that there are many causes for PTSD. It has also affirmed my belief that PTSD is real and harmful, not only to those who have it, but also to those around them. It impacts the way we act, react, our motivation and our capacity to feel–well, anything.

Terrifying experiences that shatter people’s sense of predictability and invulnerability can profoundly alter their coping skills, relationships and the way they perceive and interact with the world. The criteria for Post Traumatic Stress Disorder (PTSD) are 1) exposure to a traumatic event(s) in which the person witnessed or experienced or were confronted with an event or events that involved actual or threatened death or serious injury, or a threat to the physical integrity of self or others, and 2) the person’s response involved intense fear, helplessness or horror DSM IV p. 427-28). Gradual Onset Traumatic Stress Disorder can be caused by repeated exposure to “sub-critical incidents” such as child abuse, traffic fatalities, rapes and personal assaults.

Nevertheless, not all people exposed to trauma are “traumatized.” Why? In 1998, Pynoos and Nader proposed a theory to assist in explaining why people have different reactions to the same event. They asserted that people are at greater risk of being negatively impacted by traumatic events if any of the following are present: 1) they have experienced other traumatic events within the preceding 6 months, 2) they were already stressed out or depressed at the time of the event, 3) the situation occurred close to their home or somewhere they considered safe, 4) the victims bear a similarity to a family member or friend and 5) they have little social support.

It has been argued that officers, emergency service personnel, children of addicts and abuse victims experience traumatic events or threats to their safety on an almost daily basis. Being abused, not knowing when or if your parents will come home, repeatedly seeing children murdered, people burned in car fires and devastated victims starts to take its toll. People like idealistic officers who joined the force to change the world and protect the innocent begin to feel like nothing they do makes a difference, they cannot even keep their zone safe (criteria 3). This is especially problematic for officers who live in or near their work zone and often leads to frustration and burnout (criteria 2). Children start to feel that the whole world is uncontrollable and unsafe.

It is still not totally accepted within the law enforcement community for officers to discuss the impact of situations on them. Anger, humor and sarcasm are but a brief outlet for what many officers dream about at night. As their condition worsens, many officers withdraw, because they are fearful of seeking help or support for fear it is a one way ticket to a fitness for duty evaluation or will get out and be an obstacle for future promotions. Several studies in recent years have shown that Post Traumatic Stress Disorder (PTSD) is among the most common of psychiatric disorders.

Another thing that distinguishes people who develop PTSD from those who are just temporarily overwhelmed is that people who develop PTSD become “stuck” on the trauma, keep re-living it in thoughts, feelings, or images. It is this intrusive reliving, rather than the trauma itself that many believe is responsible for what we call PTSD. For example, I have worked with officers who have responded to child abuse calls and had a child of their own who was a similar age (criteria 4). In the course of daily life children get hurt and have bad dreams. As parents they have seen looks of pain and fright on their kids faces. This makes it just that much easier to envision the looks of terror and agony on the face of the child as their parent beat them. Sometimes this visualization gets corrupted and officers suddenly they start to see their child in their mental re-enactment of the trauma, obviously a much more powerful memory. These officers are much more likely to be “traumatized” by the incident and potentially get “stuck.”

Traumatized individuals begin organizing their lives around avoiding the trauma. Avoidance may take many different forms: keeping away from reminders, calling in sick to work, or ingesting drugs or alcohol that numb awareness of distress. The sense of futility, hyperarousal, and other trauma-related changes may permanently change how people deal with stress, alter thier self-concept and interfere with their view of the world as a basically safe and predictable place. In the example above, these people often became even more overprotective of their children, suspicious of others, and had difficulty sleeping, because every time they close their eyes they see the child.

One of the core issues in trauma is the fact that memories of what has happened cannot be integrated into one’s general experience. The lack of people’s ability to make this “fit” into their expectations or the way they think about the world in a way that makes sense keeps the experience stored in the mind on a sensory level. When people encounter smells, sounds or other sensory stimuli that remind them of the event, it may trigger a similar response to what the person originally had: physical sensations (such as panic attacks), visual images (such as flashbacks and nightmares), obsessive ruminations, or behavioral reenactments of elements of the trauma. In the example above, sensory triggers that triggered some of the officers memories were certain cries, hearing or seeing a parent spank their child, returning to the same neighborhood for other calls and, of course, television shows or news reports that involved descriptions of abuse.

The goal of treatment is find a way in which people can acknowledge the reality of what has happened and somehow integrate it into their understanding of the world without having to re-experience the trauma all over again. To be able to tell their story, if you will.

The Symptoms of PTSD

Regardless of the origin of the terror, the brain reacts to overwhelming, threatening, and uncontrollable experiences with conditioned emotional responses. For example, rape victims may respond to conditioned stimuli, such as the approach by an unknown man, as if they were about to be raped again, and experience panic.

Remembrance and intrusion of the trauma is expressed on many different levels, ranging from flashbacks, feelings, physical sensations, nightmares, and interpersonal re-enactments. Interpersonal re-enactments can be especially problematic for the officer leading to over-reaction in situations that remind the officer of previous experiences in which she or he has felt helpless. For example, in the child abuse example above, officers may be much more physically and verbally aggressive toward alleged perpetrators and their reports tend to be much more negative and subjective.

Hyperarousal. While people with PTSD tend to deal with their environment by reducing their range of emotions or numbing, their bodies continue to react to certain physical and emotional stimuli as if there were a continuing threat. This arousal is supposed to alert the person to potential danger, but seems to loose that function in traumatized people. This is sort of like when rookie officers start and a hot call is toned out, they usually have an adrenaline rush. After two or three years, the tones hardly have any impact on them. Since traumatized people are always “keyed up” they often do not pay any attention to that feeling which is supposed to warn them of impending danger.

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Numbing of responsiveness. Aware of their difficulties in controlling their emotions, traumatized people seem to spend their energies on avoiding distress. In addition, they lose pleasure in things that previously gave them a sense of satisfaction. They may feel “dead to the world”. This emotional numbing may be expressed as depression, and lack of motivation, or as physical reactions. After being traumatized, many people stop feeling pleasure from involvement in activities, and they feel that they just “go through the motions” of everyday living. Emotional numbness also gets in the way of resolving the trauma in therapy.

Intense emotional reactions and sleep problems. Traumatized people go immediately from incident to reaction without being able to first figure out what makes them so upset. They tend to experience intense fear, anxiety, anger and panic in response to even minor stimuli. This makes them either overreact and intimidate others, or to shut down and freeze. Both adults and children with such hyperarousal will experience sleep problems, because they are unable to settle down enough to go to sleep, and because they are afraid of having nightmares. Many traumatized people report dream-interruption insomnia: they wake themselves up as soon as they start having a dream, for fear that this dream will turn into a trauma-related nightmare. They also are liable to exhibit hypervigilance, exaggerated startle response and restlessness.

Learning difficulties. Being “keyed-up” interferes with the capacity to concentrate and to learn from experience. Traumatized people often have trouble remembering ordinary events. It is helpful to always write things down for them. Often “keyed-up” and having difficulty paying attention, they may display symptoms of attention deficit disorder.

After a trauma, people often regress to earlier modes of coping with stress. In adults, it is expressed in excessive dependence and in a loss of capacity to make thoughtful, independent decisions. In officers, this is often noticed because they suddenly begin making a lot of poor decisions, their reports lose quality and detail and they are unable to focus. In children they may begin wetting their bed, having fears of monsters or having temper tantrums.

Aggression against self and others: Both adults and children who have been traumatized are likely to turn their aggression against others or themselves. Due to their persistent anxiety, traumatized people are almost always “stressed out,” so it does not take much to them set off. This aggression may take many forms ranging from fighting to excessive exercise or obsession about something—anything to keep them from thinking about the trauma.

Psychosomatic reactions. Chronic anxiety and emotional numbing also get in the way of learning to identify and discuss internal states and wishes. May traumatized people report a high frequency of headaches, back and neck aches, gastro-intestinal problems etceteras. Since the stress is being held inside, the body begins to become distressed.

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After a trauma, people realize the limited scope of their safety, power and control in the world, and life can never be exactly the same. The traumatic experience becomes part of a person’s life. Sorting out exactly what happened and sharing one’s reactions with others can make a great deal of difference a person’s recovery. Putting the reactions and thoughts related to the trauma into words is essential in the resolution of post traumatic reactions. This should, however, be done with a professional specializing in PTSD due to the wide range of reactions people have when they start confronting and integrating the memories of the trauma.

Failure to approach trauma related material gradually is likely to make things worse. Often, talking about the trauma is not enough: trauma survivors need to take some action that symbolizes triumph over helplessness and despair. The Holocaust Memorial in Jerusalem and the Vietnam Memorial in Washington, DC, are good examples of symbols for survivors to mourn the dead and establish the historical and cultural meaning of the traumatic events. There are several events for survivors of traumas that officers can also take part in. These events remind survivors of the fact that there are others who have shared similar experiences. Other symbolic actions may take the form of writing a book, taking political action or helping other victims.

PTSD is real, and can be resolved with time, patience and compassion.

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This entry was posted in Time Management and tagged children, officers, people, ptsd, trauma, traumatic, traumatized.

PTSD

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Posttraumatic stress disorder(PTSD) is a severe anxiety disorder that can develop after exposure to any event that results in psychological trauma. This event may involve the threat of death to oneself or to someone else, or to one’s own or someone else’s physical, sexual, or psychological integrity,overwhelming the individual’s ability to cope. As an effect of psychological trauma, PTSD is less frequent and more enduring than the more commonly seen post traumatic stress (also known as acute stress response). Diagnostic symptoms for PTSD include re-experiencing the original trauma(s) through flashbacks or nightmares, avoidance of stimuli associated with the trauma, and increased arousal—such as difficulty falling or staying asleep, anger, and hypervigilance. Formal diagnostic criteria (both DSM-IV-TR and ICD-10) require that the symptoms last more than one month and cause significant impairment in social, occupational, or other important areas of functioning.

Classification

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 and are disruptive to all aspects of life.It has three sub-forms: acute, chronic, and delayed-onset.

Causes

Psychological trauma

PTSD is believed to be caused by experiencing any of a wide range of events  which produces intense negative feelings of “fear, helplessness or horror”in the observer or participant.  Sources of such feelings may include (but are not limited to):

• experiencing or witnessing childhood or adult physical, emotional, or sexual abuse;
• experiencing or witnessing physical assault, adult experiences of sexual assault, accidents, drug addiction, illnesses, medical complications;
• employment in occupations exposed to war (such as soldiers) or disaster (such as emergency service workers);
• getting a diagnosis of a life-threatening illness

Children or adults may develop PTSD symptoms by experiencing bullying or mobbing. Approximately 25% of children exposed to family violence can experience PTSD.  Preliminary research suggests that child abuse may interact with mutations in a stress-related gene to increase the risk of PTSD in adults. However, being exposed to a traumatic experience doesn’t automatically indicate they will develop PTSD.It has been shown that the intrusive memories, such as flashbacks, nightmares, and the memories themselves, are greater contributors to the biological and psychological dimensions of PTSD than the event itself.These intrusive memories are mainly characterized by sensory episodes, rather than thoughts. People with PTSD have intrusive re-experiences of traumatic events which lack awareness of context and time. These episodes aggravate and maintain PTSD symptoms since the individual re-experiences trauma as if it was happening in the present moment.

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. 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.Clinical findings indicate that a failure to provide adequate treatment to children after they suffer a traumatic experience, depending on their vulnerability and the severity of the trauma, will ultimately lead to PTSD symptoms in adulthood.

Neuroendocrinology

PTSD symptoms may result when a traumatic event causes an over-reactive adrenaline response, which creates deep neurological patterns in the brain. These patterns can persist long after the event that triggered the fear, making an individual hyper-responsive to future fearful situations. During traumatic experiences the high levels of stress hormones secreted suppress hypothalamic activity which may be a major factor towards the development of PTSD.

PTSD causes biochemical changes in the brain and body that differ from other psychiatric disorders such as major depression. Individuals diagnosed with PTSD respond more strongly to a dexamethasone suppression test than individuals diagnosed with clinical depression.^[30][31]

In addition, most people with PTSD also show a low secretion of cortisol and high secretion of catecholamines in urine,with a norepinephrine/cortisol ratio consequently higher than comparable non-diagnosed individuals.This is in contrast to the normative fight-or-flight response, in which both catecholamine and cortisol levels are elevated after exposure to a stressor.

Brain catecholamine levels are high, and corticotropin-releasing factor (CRF) concentrations are high. Together, these findings suggest abnormality in the hypothalamic-pituitary-adrenal (HPA) axis.

The HPA axis is responsible for coordinating the hormonal response to stress. 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.^{[citation needed]}

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: Following war trauma, 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.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, setting the stage for PTSD.

Other studies indicate that people who suffer from PTSD have chronically low levels of serotonin which contributes to the commonly associated behavioral symptoms such as anxiety, ruminations, irritability, aggression, suicidal, and impulsivity. Serotonin also contributes to the stabilization of glucocorticoid production.

Dopamine levels in patients with PTSD can help contribute to the symptoms associated. Low levels of dopamine can contribute to anhedonia, apathy, impaired attention, and motor deficits. Increased levels of dopamine can cause psychosis, agitation, and restlessness.

Hyperresponsiveness in the norepinephrine system can be caused by continued exposure to high stress. Overactivation of norepinephrine receptors in the prefrontal cortex can be connected to the flashbacks and nightmares frequently experienced by those with PTSD. A decrease in other norepinephrine functions (awareness of the current environment) prevents the memory mechanisms in the brain from processing that the experience, and emotions the person is experiencing during a flashback are not associated with the current environment.

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. However the majority of reports indicate people with PTSD have elevated levels of corticotropin-releasing hormone, lower basal cortisol levels, and enhanced negative feedback suppression of the HPA axis by dexamethasone

Neuroanatomy

Regions of the brain associated with stress and posttraumatic stress disorder

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. 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.This finding could not be replicated in chronic PTSD patients traumatized at an air show plane crash in 1988 (Ramstein, Germany).

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. However during high stress times the hippocampus, which is associated with the ability to place memories in the correct context of space and time, and with the ability to recall the memory, is suppressed. This suppression is hypothesized to be the cause of the flashbacks that often plague PTSD patients. When someone with PTSD undergoes a stimuli similar to the traumatic event the body perceives the event as occurring again because the memory was never properly recorded in the patients memory.

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. A study at the European Neuroscience Institute-Goettingen (Germany) found that fear extinction-induced IGF2/IGFBP7 signalling promotes the survival of 17–19-day-old newborn hippocampal neurons. This suggests that therapeutic strategies that enhance IGF2 signalling and adult neurogenesis might be suitable to treat diseases linked to excessive fear memory such as PTSD. Further animal and clinical research into the amygdala and fear conditioning may suggest additional treatments for the condition.

The maintenance of the fear involved with PTSD has been shown to include the HPA axis, the locus coeruleus-noradrenergic systems, and the connections between the limbic system and frontal cortex. The HPA axis which coordinates the hormonal response to stresswhich activates the LC-noradrenergic system is implicated in the over consolidation of memories that occurs in the aftermath of trauma. This over consolidation increases the likelihood of developing PTSD. The amygdala is responsible for threat detection and the conditioned and unconditioned fear responses that are carried out as a response to a threat. The medial prefrontal cortex, part of the amygdala, can inhibit the conditioned fear responses during trauma.

The LC-noradrenergic system has been hypothesized to mediate the over-consolidation of fear memory in PTSD. High levels of cortisol reduces noradrenergic activity it is proposed that individuals with PTSD fail to regulate the increased noradrenergic response to traumatic stress. It is thought that the intrusive memories and conditioned fear responses to associated triggers is a result of this response. Neuropeptide Y has been reported to reduce the release of norepinephrine and has been demonstrated to have anxiolytic properties in animal models. Studies have shown people with PTSD demonstrate reduced levels of NPY, possibly indicating their increased anxiety levels.

The basolateral nucleus (BLA) of the amygdala is responsible for the comparison and development of associations between unconditioned and conditioned responses to stimuli which results in the fear conditioning present in PTSD. The BLA activates the central nucleus (CeA) which elaborates the fear response, (including behavioral response to threat and elevated startle response). Descending inhibitory inputs form the medial prefrontal cortex (mPFC) regulates the transmission from the BLA to the CeA which is hypothesized to play a role in the extinction of conditioned fear responses.

Genetics

There is evidence that susceptibility to PTSD is hereditary. Approximately 30% of the variance in PTSD is caused from genetics alone. 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  (non-identical twins).There is also evidence that those with a genetically smaller hippocampus are more likely to develop PTSD following a traumatic event. Research has also found that PTSD shares many genetic influences common to other psychiatric disorders. Panic and generalized anxiety disorders and PTSD share 60% of the same genetic variance. Alcohol, nicotine, and drug dependence shares greater than 40% genetic similarities.

Gamma-aminobutyric acid (GABA) is the major inhibitory neurotransmitter in the brain. A recent study reported significant interactions between three polymorphisms in the GABA alpha-2 receptor gene and the severity of childhood trauma in predicting PTSD in adults. A study found those with a specific genotype for G-protein signaling 2 (RGS2), a protein that decreases G protein-coupled receptor signaling, and high environmental stress exposure as adults and a diagnosis of lifetime PTSD. This was particularly prevalent in adults with prior trauma exposure and low social support.

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. These findings suggest that individuals with these SNPs who are abused as children are more susceptible to PTSD as adults.

This is particularly interesting given that FKBP5 SNPs have previously been associated with peritraumatic dissociation (that is, dissociation at the time of the trauma), which has itself been shown to be predictive of PTSD. Furthermore, FKBP5 may be less expressed in those with current PTSD.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.Incidentally, this SNP is also associated with fear discrimination. The study suggests that perturbations in the PACAP-PAC1 pathway are involved in abnormal stress responses underlying PTSD.

PTSD is a psychiatric disorder which requires an environmental event which individuals may have varied responses to so gene-environment studies tend to be the most indicative of their effect on the probability of PTSD than studies of the main effect of the gene. Recent studies have demonstrated the interaction between PFBP5 and childhood environment to predict the severity of PTSD. Polymorphisms in FKBP5 have been associated with peritraumatic dissociation in mentally ill children. A study of highly traumatized African-American subjects from inner city primary care clinics indicated 4 polymorphisms of the FKBP5 gene, each of these were functional. The interaction between the polymorphisms and the severity of childhood abuse predicts the severity of the adult PTSD symptoms. A more recent study of the African-American population indicated that the TT genotype of the FKBP5 gene was associated with the highest risk of PTSD among those who experienced childhood adversity, however those with this genotype that experienced no childhood adversity had the lowest risk of PTSD. In addition alcohol dependence interacts with the FKBP5 polymorphisms and childhood adversity to increase the risk of PTSD in these populations. Emergency room expression of the FKPB5 mRNA following trauma was shown to indicate a later development of PTSD.

Catechol-O-methyl transferase (COMT) is an enzyme that catalyzes the extraneuronal breakdown of catecholamines. The gene that codes for COMT has a functional polymorphism in which a valine has been replaced with a methionine at condon 158. This polymorphism has lower enzyme activity and has been tied to slower breakdown of the catecholamines. A study, of Rwandan Genocide survivors, indicated that carriers of the Val allel demonstrated the expected response relationship between the higher number of lifetime traumatic events and a lifetime diagnosis of PTSD. However those who were homozygotes for the Met/Met genotype demonstrated a high risk of lifetime PTSD independent of the number of traumatic experiences. Those with Met/Met genotype also demonstrated a reduced extinction of conditioned fear responses with may account for the high risk for PTSD experienced by this genotype.

Many genes impact the limbic-frontal neurocircuitry as a result of its complexity. The main effect of the D2A1 allele of the dopamine receptor D2 (DRD2) has a strong association with the diagnosis of PTSD. The D2A1 allele has also shown a significant association to PTSD in those who engaged in harmful drinking. In addition a polymorphism in the dopamine transporter SLC6A3 gene has a significant association with chronic PTSD. A polymorphism of the serotonin receptor 2A gene has been associated with PTSD in Korean women. The short allele of the promoter region of the serotonin transporter (5-HTTLPR) has been shown to be less efficient than the long allele and is associated with the amygdala response for extinction of fear conditioning. However the short allele is associated with a decreased risk of PTSD in a low risk environment but a high risk of PTSD in a high risk environment. The s/s genotype demonstrated a high risk for development of PTSD even in response to a small number of traumatic events but those with the l allele demonstrate increasing rates of PTSD with increasing traumatic experiences.

Genome-wide association study (GWAS) offer an opportunity to identify novel risk variants for PTSD which will in turn inform our understanding of the etiology of the disorder. Early results indicate the feasibility and potential power of GWAS to identify biomarkers for anxiety-related behaviors that suggest a future of PTSD. These studies will lead to the discovery of novel loci for the susceptibility and symptomatology of anxiety disorders including PTSD.

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Epigenetics

Gene and environment studies alone fail to explain the importance the developmental stressors timing exposure to the phenotypic changes associated with PTSD. Epigenetic modification is the environmentally induced change in DNA which alters the function rather than the structure of the gene. The biological mechanism of epigenetic modification typically involves the methylation of cytosine within a gene which produces decreased transcription of that segment of DNA. The neuroendocrine alteration seen in animal models parallel those of PTSD in which low basal cortisol and enhanced suppression of cortisol in response to synthetic glucocorticoid becomes hereditary. Lower levels of glucocorticoid receptor (GR) mRNA have been demonstrated in the hippocampus of suicide victims with histories of childhood abuse. It hasn’t been possible to monitor the state of methylation over time however the interpretation is early developmental methylation changes are long-lasting and enduring. It is hypothesized that epigenetic-mediated changes in the HPA axis could be associated with an increased vulnerability to PTSD following traumatic events. These findings support the mechanism in which early life trauma strongly validates as a risk factor for PTSD development in adulthood by recalibrating the set point and stress-responsiveness of the HPA axis. Studies have reported an increased risk for PTSD and low cortisol levels in the offspring of female holocaust survivors with PTSD. Epigenetic mechanisms may also be relevant to the intrauterine environment. Mothers with PTSD produced infants with lower salivary cortisol levels only if the traumatic exposure occurred during the third trimester of gestation. These changes occur via transmission of hormonal responses to the fetus leading to a reprogramming of the glucocorticoid  responsivity in the offspring.^[38]

Risk factors

See also: Psychological resilience

Although most people (50–90%) encounter trauma over a lifetime,  about 20-30% develop PTSD but over half of these people will recover without treatment.  Vulnerability to PTSD presumably stems from an interaction of biological diathesis, early childhood developmental experiences, and trauma severity.  A person that never established secure relationships and learned coping skills as a young child if exposed to a traumatic experience is more likely to develop PTSD than one that developed good coping skills and has a support network.

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.Peri-traumatic dissociation in children is a predictive indicator of the development of PTSD later in life. 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.

Military experience

Schnurr, Lunney, and Senguptaidentified risk factors for the development of PTSD in Vietnam veterans. Among those are:

• Hispanic ethnicity, coming from an unstable family, being punished severely during childhood, childhood asocial behavior, and depression as pre-military factors
• War-zone exposure, peritraumatic dissociation, depression as military factors
• Recent stressful life events, post-Vietnam trauma, and depression as post-military factors

They also identified certain protective factors, such as:

• Japanese-American ethnicity, high school degree or college education, older age at entry to war, higher socioeconomic status, and a more positive paternal relationship as pre-military protective factors.
• Social support at homecoming and current social support as post-military factors.Other research also indicates the protective effects of social support in averting PTSD or facilitating recovery if it develops.

Glass and Jones found early intervention to be a critical preventive measure:

“PTSD symptoms can follow any serious psychological trauma, such as exposure to combat, accidents, torture, disasters, criminal assault and exposure to atrocities or to the sequelae of such extraordinary events. Prisoners of war exposed to harsh treatment are particularly prone to develop PTSD. In their acute presentation these symptoms, which include subsets of a large variety of affective, cognitive, perceptions, emotional and behavioral responses which are relatively normal responses to gross psychological trauma. If persistent, however, they develop a life of their own and may be maintained by inadvertent reinforcement. Early intervention and later avoidance of positive reinforcement (which may be subtle) for such symptoms is a critical preventive measure.

Studies have shown that those prepared for the potential of a traumatic experience are more prepared to deal with the stress of a traumatic experience and therefore less likely to develop PTSD.

Foster care

In the Casey Family Northwest Alumni Study, conducted in conjunction with researchers from the Harvard Medical School in Oregon and Washington state, the rate of PTSD in adults who were in foster care for one year between the ages of 14–18 was found to be higher than that of combat veterans. Up to 25% of those in the study meet the diagnostic criteria for PTSD as compared to 12–13% of Iraq war veterans and 15% of Vietnam War veterans, and a rate of 4% in the general population. The recovery rate for foster home alumni was 28.2% as opposed to 47% in the general population.

Dubner and Motta (1999)found that 60% of children in foster care who had experienced sexual abuse had PTSD, and 42% of those who had been physically abused met the PTSD criteria. PTSD was also found in 18% of the children who were not abused. These children may have developed PTSD due to witnessing violence in the home, or as a result of real or perceived parental abandonment.

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Refrance Wikki

• Posttraumatic stress disorder at the Open Directory Project
• PTSD professional associations at the Open Directory Project
• Management of PTSD in adults and children by the National Institute for Health and Clinical Excellence (UK)
• Practice guidelines from the American Psychiatric Association
• Post Traumatic Stress Disorder Information Resource from The University of Queensland School of Medicine