"PTSD" redirects here. For the album by Pharoahe Monch, see P.T.S.D. (Post Traumatic Stress Disorder).
Posttraumatic stress disorder[note 1] (PTSD) may develop after a person is exposed to one or more traumatic events, such as sexual assault, warfare, serious injury, or threats of imminent death.[1] The diagnosis
may be given when a group of symptoms, such as disturbing recurring
flashbacks, avoidance or numbing of memories of the event, and hyperarousal, continue for more than a month after the occurrence of a traumatic event.[1]
Most people having experienced a traumatizing event will not develop PTSD.[2] Women are more likely to experience higher impact events, and are also more likely to develop PTSD than men.[3] Children are less likely to experience PTSD after trauma than adults, especially if they are under ten years of age.[2] War veterans are commonly at risk for PTSD.
Persons considered at risk include, for example, combat military personnel, victims of natural disasters, concentration camp survivors, and victims of violent crime. Individuals frequently experience "survivor's guilt" for remaining alive while others died. Causes of the symptoms of PTSD are the experiencing or witnessing of a stressor event involving death, serious injury or such threat to the self or others in a situation in which the individual felt intense fear, horror, or powerlessness.[11] Persons employed in occupations that expose them to violence (such as soldiers) or disasters (such as emergency service workers) are also at risk.[11]
Children or adults may develop PTSD symptoms by experiencing bullying or mobbing.[12][non-primary source needed][13][non-primary source needed]
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. For example, in two studies by Schechter, one of 67 mothers and another of 25 mothers, this was shown to be the case.[20][non-primary source needed][21][non-primary source needed] 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.[22] 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.[23][dubious ]
PTSD hyperarousal may correspond to vigilant immobility and aggressive defense. Complex posttraumatic stress disorder (and phenomena such as the Stockholm syndrome) may in part correspond to the appeasement stage and possibly the frozen immobility stage.[24][25]
There may be evolutionary explanations for differences in resilience to traumatic events. Thus, PTSD is rare following traumatic fire that may be explained by events such as forest fires' long being part of the evolutionary history of mammals. On the other hand, PTSD is much more common following modern warfare, which may be explained by modern warfare's being a new development and very unlike the quick inter-group raids that are argued to have characterized the paleolithic.[26]
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.[28]
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.[29][30] 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 in medically injured children (that is, dissociation at the time of the birth trauma),[31] which has itself been shown to be predictive of PTSD.[32][33] Furthermore, FKBP5 may be less expressed in those with current PTSD.[34] 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.[35] 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 that requires an environmental event that individuals may have varied responses to so gene-environment studies tend to be the most indicative of their effect on the probability of PTSD then 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 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 is associated with the highest risk of PTSD among those having 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.[28]
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 codon 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 with 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.[28]
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 having 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 then 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.[28]
Genome-wide association study (GWAS) offer an opportunity to identify novel risk variants for PTSD that 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.[dubious ][28]
Posttraumatic stress reactions have not been studied as well in children and adolescents as adults.[2] The rate of PTSD may be lower in children than adults, but in the absence of therapy, symptoms may continue for decades.[2] One estimate suggests that the proportion of children and adolescents having PTSD in a non-wartorn population in a developed country may be 1% compared to 1.5% to 3% of adults, and much lower below the age of 10 years.[2]
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.[37][38][39][40] Peritraumatic dissociation in children is a predictive indicator of the development of PTSD later in life.[28] This effect of childhood trauma, which is not well-understood, may be a marker for both traumatic experiences and attachment problems.[41][42] Proximity to, duration of, and severity of the trauma also make an impact, and interpersonal traumas cause more problems than impersonal ones.[43]
Quasi-experimental studies have demonstrated a relationship between intrusive thoughts and intentional control responses such that suppression increases the frequency of unwanted intrusive thoughts. These results suggest that suppression of intrusive thoughts may be important in the development and maintenance of PTSD.[44]
Yohimbine (not considered specifically appropriate for PTSD) increases arousal by increasing release of endogenous norepinephrine and can worsen PTSD symptoms.[49][clarification needed]
Dubner and Motta (1999)[54] found that 60% of children in foster care having experienced sexual abuse had PTSD, and 42% of those having been physically abused met the PTSD criteria. PTSD was also found in 18% of the children 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.
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.[57][58]
In addition, most people with PTSD also show a low secretion of cortisol and high secretion of catecholamines in urine,[59] with a norepinephrine/cortisol ratio consequently higher than comparable non-diagnosed individuals.[60] 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.[61]
Brain catecholamine levels are high,[62] and corticotropin-releasing factor (CRF) concentrations are high.[63][64] Together, these findings suggest abnormality in the hypothalamic-pituitary-adrenal (HPA) axis.
The HPA axis is responsible for coordinating the hormonal response to stress.[28] 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.[65]
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.[66]
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.[67] 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 that suffer from PTSD have chronically low levels of serotonin, which contributes to the commonly associated behavioral symptoms such as anxiety, ruminations, irritability, aggression, suicidality, and impulsivity.[18] 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.[18]
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.[18]
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.[28][68]
Most people having experienced a traumatizing event will not develop PTSD.[2] Women are more likely to experience higher impact events, and are also more likely to develop PTSD than men.[3] Children are less likely to experience PTSD after trauma than adults, especially if they are under ten years of age.[2] War veterans are commonly at risk for PTSD.
Classification
Posttraumatic stress disorder is classified as an anxiety disorder in the DSM iV; the characteristic symptoms are not present before exposure to the violently traumatic event. In the typical case, the individual with PTSD persistently avoids all thoughts and emotions, and discussion of the stressor event and may experience amnesia for it. However, the event is commonly relived by the individual through intrusive, recurrent recollections, flashbacks, and nightmares.[4] The characteristic symptoms are considered acute if lasting less than three months, and chronic if persisting three months or more, and with delayed onset if the symptoms first occur after six months or some years later. PTSD is distinct from the briefer acute stress disorder, and can cause clinical impairment in significant areas of functioning.[5][6][7]Causes
PTSD is believed to be caused by the experience of a wide range of traumatic events and, in particular if the trauma is extreme, can occur in persons with no predisposing conditions.[9][10]Persons considered at risk include, for example, combat military personnel, victims of natural disasters, concentration camp survivors, and victims of violent crime. Individuals frequently experience "survivor's guilt" for remaining alive while others died. Causes of the symptoms of PTSD are the experiencing or witnessing of a stressor event involving death, serious injury or such threat to the self or others in a situation in which the individual felt intense fear, horror, or powerlessness.[11] Persons employed in occupations that expose them to violence (such as soldiers) or disasters (such as emergency service workers) are also at risk.[11]
Children or adults may develop PTSD symptoms by experiencing bullying or mobbing.[12][non-primary source needed][13][non-primary source needed]
Family violence
Trauma from family violence can predispose an individual to PTSD. Approximately 25% of children exposed to family violence can experience PTSD in a study of 337 school age children.[14][non-primary source needed] Preliminary research suggests that child abuse may interact with mutations in a stress-related gene to increase the risk of PTSD in adults, in a cross-sectional study of 900 school age children.[15][non-primary source needed][16][unreliable source?][17] However, being exposed to a traumatic experience does not automatically indicate they will develop PTSD.[5] 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.[18] These intrusive memories are mainly characterized by sensory episodes, rather than thoughts. People with PTSD have intrusive re-experiences of traumatic events that lack awareness of context and time. These episodes aggravate and maintain PTSD symptoms, since the individual re-experiences trauma as if it were happening in the present moment.[19]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. For example, in two studies by Schechter, one of 67 mothers and another of 25 mothers, this was shown to be the case.[20][non-primary source needed][21][non-primary source needed] 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.[22] 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.[23][dubious ]
Evolutionary psychology
Evolutionary psychology views different types of fears and reactions caused by fears as adaptations that may have been useful in the ancestral environment in order to avoid or cope with various threats. In general, mammals display several defensive behaviors roughly dependent on how close the threat is: avoidance, vigilant immobility, withdrawal, aggressive defense, appeasement, and finally complete frozen immobility (the last possibly to confuse a predator's attack reflex or to simulate a dead and contaminated body). PTSD may correspond to and be caused by overactivation of such fear circuits. Thus, PTSD avoidance behaviors may correspond to mammal avoidance of and withdrawal from threats. Heightened memory of past threats may increase avoidance of similar situations in the future as well as be a prerequisite for analyzing the past threat and develop better defensive behaviors if the threat should recur.PTSD hyperarousal may correspond to vigilant immobility and aggressive defense. Complex posttraumatic stress disorder (and phenomena such as the Stockholm syndrome) may in part correspond to the appeasement stage and possibly the frozen immobility stage.[24][25]
There may be evolutionary explanations for differences in resilience to traumatic events. Thus, PTSD is rare following traumatic fire that may be explained by events such as forest fires' long being part of the evolutionary history of mammals. On the other hand, PTSD is much more common following modern warfare, which may be explained by modern warfare's being a new development and very unlike the quick inter-group raids that are argued to have characterized the paleolithic.[26]
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's having PTSD compared to twins that were dizygotic (non-identical twins).[27] 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 share greater than 40% genetic similarities.[28]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.[28]
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.[29][30] 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 in medically injured children (that is, dissociation at the time of the birth trauma),[31] which has itself been shown to be predictive of PTSD.[32][33] Furthermore, FKBP5 may be less expressed in those with current PTSD.[34] 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.[35] 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 that requires an environmental event that individuals may have varied responses to so gene-environment studies tend to be the most indicative of their effect on the probability of PTSD then 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 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 is associated with the highest risk of PTSD among those having 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.[28]
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 codon 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 with 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.[28]
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 having 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 then 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.[28]
Genome-wide association study (GWAS) offer an opportunity to identify novel risk variants for PTSD that 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.[dubious ][28]
Epigenetics
Gene and environment studies alone fail to explain the importance the developmental stressor timing exposure to the phenotypic changes associated with PTSD. Epigenetic modification is the environmentally induced change in DNA that 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 that 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 has not 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-responsivity 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.[28]Risk factors
See also: Psychological resilience
Most people (more than half) will experience at least one traumatizing event in their lifetime.[36]
Men are more likely to experience a traumatic event, but women are more
likely to experience the kind of high impact traumatic event that can
lead to PTSD, such as interpersonal violence and sexual assault.[2]
Only a minority of people who are traumatized will develop PTSD, but
they are more likely to be women. The average risk of developing PTSD
after trauma is around 8% for men, while for women it is just over 20%.[2] The risk is believed to be higher in young urban populations (24%): 13% for men and 30% for women.[2]
Rates of PTSD are higher in combat veterans than other men, with a rate
estimated at up to 20% for veterans returning from Iraq and
Afghanistan.[36]Posttraumatic stress reactions have not been studied as well in children and adolescents as adults.[2] The rate of PTSD may be lower in children than adults, but in the absence of therapy, symptoms may continue for decades.[2] One estimate suggests that the proportion of children and adolescents having PTSD in a non-wartorn population in a developed country may be 1% compared to 1.5% to 3% of adults, and much lower below the age of 10 years.[2]
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.[37][38][39][40] Peritraumatic dissociation in children is a predictive indicator of the development of PTSD later in life.[28] This effect of childhood trauma, which is not well-understood, may be a marker for both traumatic experiences and attachment problems.[41][42] Proximity to, duration of, and severity of the trauma also make an impact, and interpersonal traumas cause more problems than impersonal ones.[43]
Quasi-experimental studies have demonstrated a relationship between intrusive thoughts and intentional control responses such that suppression increases the frequency of unwanted intrusive thoughts. These results suggest that suppression of intrusive thoughts may be important in the development and maintenance of PTSD.[44]
Military experience
Schnurr, Lunney, and Sengupta[33] identified risk factors for the development of PTSD in Vietnam veterans. The subjects were 68 women and 414 men of whom 88 were white, 63 black, 80 Hispanic, 90 Native Hawaiian, and 93 Japanese American. Among their findings were:- 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
- 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.[45] Other research also indicates the protective effects of social support in averting PTSD or facilitating recovery if it develops.[46][47]
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, perceptional, 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.[5]
Drug misuse
Alcohol abuse and drug abuse commonly co-occur with PTSD.[49] Recovery from posttraumatic stress disorder or other anxiety disorders may be hindered, or the condition worsened, by medication or substance overuse, abuse, or dependence; resolving these problems can bring about a marked improvement in an individual's mental health status and anxiety levels.[50][51]Yohimbine (not considered specifically appropriate for PTSD) increases arousal by increasing release of endogenous norepinephrine and can worsen PTSD symptoms.[49][clarification needed]
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.[52][53]Dubner and Motta (1999)[54] found that 60% of children in foster care having experienced sexual abuse had PTSD, and 42% of those having been physically abused met the PTSD criteria. PTSD was also found in 18% of the children 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.
Pathophysiology
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.[5][55] During traumatic experiences the high levels of stress hormones secreted suppress hypothalamic activity that may be a major factor toward the development of PTSD.[56]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.[57][58]
In addition, most people with PTSD also show a low secretion of cortisol and high secretion of catecholamines in urine,[59] with a norepinephrine/cortisol ratio consequently higher than comparable non-diagnosed individuals.[60] 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.[61]
Brain catecholamine levels are high,[62] and corticotropin-releasing factor (CRF) concentrations are high.[63][64] Together, these findings suggest abnormality in the hypothalamic-pituitary-adrenal (HPA) axis.
The HPA axis is responsible for coordinating the hormonal response to stress.[28] 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.[65]
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.[66]
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.[67] 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 that suffer from PTSD have chronically low levels of serotonin, which contributes to the commonly associated behavioral symptoms such as anxiety, ruminations, irritability, aggression, suicidality, and impulsivity.[18] 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.[18]
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.[18]
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.[28][68]
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