Post-traumatic stress disorder From Wikipedia, the free encyclopedia Jump to navigationJump to search "PTSD" redirects here. For other uses, see PTSD (disambiguation). "Post traumatic" redirects here. For the album, see Post Traumatic. Post-traumatic stress disorder A mask, painted by a Marine who attends art therapy to relieve post-traumatic stress disorder symptoms, USMC-120503-M-9426J-001.jpg Art therapy project created by a U.S. Marine with post-traumatic stress disorder Specialty Psychiatry, clinical psychology Symptoms Disturbing thoughts, feelings, or dreams related to the event; mental or physical distress to trauma-related cues; efforts to avoid trauma-related situations; increased fight-or-flight response[1] Complications Self-harm, suicide[2] Duration > 1 month[1] Causes Exposure to a traumatic event[1] Diagnostic method Based on symptoms[2] Treatment Counseling, medication[3] Medication Selective serotonin reuptake inhibitor[4] Frequency 8.7% (lifetime risk); 3.5% (12-month risk) (US)[5] Post-traumatic stress disorder (PTSD)[a] is a mental and behavioral disorder[6] that can develop because of exposure to a traumatic event, such as sexual assault, warfare, traffic collisions, child abuse, domestic violence or other threats on a person's life.[1][7] Symptoms may include disturbing thoughts, feelings, or dreams related to the events, mental or physical distress to trauma-related cues, attempts to avoid trauma-related cues, alterations in the way a person thinks and feels, and an increase in the fight-or-flight response.[1][3] These symptoms last for more than a month after the event.[1] Young children are less likely to show distress, but instead may express their memories through play.[1] A person with PTSD is at a higher risk of suicide and intentional self-harm.[2][8] Most people who experience traumatic events do not develop PTSD.[2] People who experience interpersonal violence such as rape, other sexual assaults, being kidnapped, stalking, physical abuse by an intimate partner, and incest or other forms of childhood sexual abuse are more likely to develop PTSD than those who experience non-assault based trauma, such as accidents and natural disasters.[9][10][11] Those who experience prolonged trauma, such as slavery, concentration camps, or chronic domestic abuse, may develop complex post-traumatic stress disorder (C-PTSD). C-PTSD is similar to PTSD but has a distinct effect on a person's emotional regulation and core identity.[12] Prevention may be possible when counselling is targeted at those with early symptoms but is not effective when provided to all trauma-exposed individuals whether or not symptoms are present.[2] The main treatments for people with PTSD are counselling (psychotherapy) and medication.[3][13] Antidepressants of the SSRI or SNRI type are the first-line medications used for PTSD and are moderately beneficial for about half of people.[4] Benefits from medication are less than those seen with counselling.[2] It is not known whether using medications and counselling together has greater benefit than either method separately.[2][14] Medications, other than some SSRIs or SNRIs, do not have enough evidence to support their use and, in the case of benzodiazepines, may worsen outcomes.[15][16] In the United States, about 3.5% of adults have PTSD in a given year, and 9% of people develop it at some point in their life.[1] In much of the rest of the world, rates during a given year are between 0.5% and 1%.[1] Higher rates may occur in regions of armed conflict.[2] It is more common in women than men.[3] Symptoms of trauma-related mental disorders have been documented since at least the time of the ancient Greeks.[17] During the world wars, the condition was known under various terms including "shell shock" and "combat neurosis".[18] The term "post-traumatic stress disorder" came into use in the 1970s in large part due to the diagnoses of U.S. military veterans of the Vietnam War.[19] It was officially recognized by the American Psychiatric Association in 1980 in the third edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-III).[20] Contents 1 Symptoms 1.1 Associated medical conditions 2 Risk factors 2.1 Trauma 2.2 Genetics 3 Pathophysiology 3.1 Neuroendocrinology 3.2 Neuroanatomy 4 Diagnosis 4.1 Screening 4.2 Assessment 4.3 Diagnostic and statistical manual 4.4 International classification of diseases 4.5 Differential diagnosis 5 Prevention 5.1 Psychological debriefing 5.2 Risk-targeted interventions 6 Management 6.1 Counselling 6.2 Medication 6.3 Other 7 Epidemiology 7.1 United States 8 Veterans 8.1 United States 8.2 Iraq 8.3 United Kingdom 8.4 Canada 9 History 10 Terminology 11 Research 11.1 Psychotherapy 12 Notes 13 References 14 External links Symptoms Service members use art to relieve PTSD symptoms. See also: Psychological stress and sleep Symptoms of PTSD generally begin within the first three months after the inciting traumatic event, but may not begin until years later.[1][3] In the typical case, the individual with PTSD persistently avoids either trauma-related thoughts and emotions or discussion of the traumatic event, and may even have amnesia of the event.[1] However, the event is commonly relived by the individual through intrusive, recurrent recollections, dissociative episodes of reliving the trauma ("flashbacks"), and nightmares (50 to 70%[21]).[22] While it is common to have symptoms after any traumatic event, these must persist to a sufficient degree (i.e., causing dysfunction in life or clinical levels of distress) for longer than one month after the trauma to be classified as PTSD (clinically significant dysfunction or distress for less than one month after the trauma may be acute stress disorder).[1][23][24][25] Some following a traumatic event experience post-traumatic growth.[26] Associated medical conditions Trauma survivors often develop depression, anxiety disorders, and mood disorders in addition to PTSD.[27] Substance use disorder, such as alcohol use disorder, commonly co-occur with PTSD.[28] Recovery from post-traumatic stress disorder or other anxiety disorders may be hindered, or the condition worsened, when substance use disorders are comorbid with PTSD. Resolving these problems can bring about improvement in an individual's mental health status and anxiety levels.[29][30] In children and adolescents, there is a strong association between emotional regulation difficulties (e.g. mood swings, anger outbursts, temper tantrums) and post-traumatic stress symptoms, independent of age, gender, or type of trauma.[31] Risk factors No quieren (They do not want to) by Francisco Goya (1746–1828) depicts an elderly woman wielding a knife in defense of a girl being assaulted by a soldier.[32] Persons considered at risk include combat military personnel, victims of natural disasters, concentration camp survivors, and victims of violent crime. Persons employed in occupations that expose them to violence (such as soldiers) or disasters (such as emergency service workers) are also at risk.[33] Other occupations that are at higher risk include police officers, firefighters, ambulance personnel, health care professionals, train drivers, divers, journalists, and sailors, in addition to people who work at banks, post offices or in stores.[34] Trauma Main article: Psychological trauma See also: Psychological resilience PTSD has been associated with a wide range of traumatic events. The risk of developing PTSD after a traumatic event varies by trauma type[35][36] and is highest following exposure to sexual violence (11.4%), particularly rape (19.0%).[37] Men are more likely to experience a traumatic event (of any type), 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.[38] Motor vehicle collision survivors, both children and adults, are at an increased risk of PTSD.[39][40] Globally, about 2.6% of adults are diagnosed with PTSD following a non-life threatening traffic accident, and a similar proportion of children develop PTSD.[37] Risk of PTSD almost doubles to 4.6% for life-threatening auto accidents.[37] Females were more likely to be diagnosed with PTSD following a road traffic accident, whether the accident occurred during childhood or adulthood.[39][40] Post-traumatic stress reactions have been studied in children and adolescents.[41] The rate of PTSD might be lower in children than adults, but in the absence of therapy, symptoms may continue for decades.[42] 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.[42] On average, 16% of children exposed to a traumatic event develop PTSD, varying according to type of exposure and gender.[43] Similar to the adult population, risk factors for PTSD in children include: female gender, exposure to disasters (natural or manmade), negative coping behaviours, and/or lacking proper social support systems.[44] Predictor models have consistently found that childhood trauma, chronic adversity, neurobiological differences, and familial stressors are associated with risk for PTSD after a traumatic event in adulthood.[45][46][47] It has been difficult to find consistently aspects of the events that predict, but peritraumatic dissociation has been a fairly consistent predictive indicator of the development of PTSD.[48] Proximity to, duration of, and severity of the trauma make an impact. It has been speculated that interpersonal traumas cause more problems than impersonal ones,[49] but this is controversial.[50] The risk of developing PTSD is increased in individuals who are exposed to physical abuse, physical assault, or kidnapping.[51][52] Women who experience physical violence are more likely to develop PTSD than men.[51] Intimate partner violence See also: Rape trauma syndrome An individual that has been exposed to domestic violence is predisposed to the development of PTSD. However, being exposed to a traumatic experience does not automatically indicate that an individual will develop PTSD.[53] There is a strong association between the development of PTSD in mothers that experienced domestic violence during the perinatal period of their pregnancy.[54] Those who have experienced sexual assault or rape may develop symptoms of PTSD.[55][56] PTSD symptoms include re-experiencing the assault, avoiding things associated with the assault, numbness, and increased anxiety and an increased startle response. The likelihood of sustained symptoms of PTSD is higher if the rapist confined or restrained the person, if the person being raped believed the rapist would kill them, the person who was raped was very young or very old, and if the rapist was someone they knew. The likelihood of sustained severe symptoms is also higher if people around the survivor ignore (or are ignorant of) the rape or blame the rape survivor.[57] War-related trauma See also: Veteran and Refugee health Military service is a risk factor for developing PTSD.[58] Around 78% of people exposed to combat do not develop PTSD; in about 25% of military personnel who develop PTSD, its appearance is delayed.[58] Refugees are also at an increased risk for PTSD due to their exposure to war, hardships, and traumatic events. The rates for PTSD within refugee populations range from 4% to 86%.[59] While the stresses of war affect everyone involved, displaced persons have been shown to be more so than others.[60] Challenges related to the overall psychosocial well-being of refugees are complex and individually nuanced. Refugees have reduced levels of well-being and a high rates of mental distress due to past and ongoing trauma. Groups that are particularly affected and whose needs often remain unmet are women, older people and unaccompanied minors.[61] Post-traumatic stress and depression in refugee populations also tend to affect their educational success.[61] Unexpected death of a loved one Sudden, unexpected death of a loved one is the most common traumatic event type reported in cross-national studies.[37][62] However, the majority of people who experience this type of event will not develop PTSD. An analysis from the WHO World Mental Health Surveys found a 5.2% risk of developing PTSD after learning of the unexpected death of a loved one.[62] Because of the high prevalence of this type of traumatic event, unexpected death of a loved one accounts for approximately 20% of PTSD cases worldwide.[37] Life-threatening illness Medical conditions associated with an increased risk of PTSD include cancer,[63][64][65] heart attack,[66] and stroke.[67] 22% of cancer survivors present with lifelong PTSD like symptoms.[68] Intensive-care unit (ICU) hospitalization is also a risk factor for PTSD.[69] Some women experience PTSD from their experiences related to breast cancer and mastectomy.[70][71][63] Loved ones of those who experience life-threatening illnesses are also at risk for developing PTSD, such as parents of child with chronic illnesses.[72] Pregnancy-related trauma Main article: Childbirth-related post-traumatic stress disorder Women who experience miscarriage are at risk of PTSD.[73][74][75] Those who experience subsequent miscarriages have an increased risk of PTSD compared to those experiencing only one.[73] PTSD can also occur after childbirth and the risk increases if a woman has experienced trauma prior to the pregnancy.[76][77] Prevalence of PTSD following normal childbirth (that is, excluding stillbirth or major complications) is estimated to be between 2.8 and 5.6% at six weeks postpartum,[78] with rates dropping to 1.5% at six months postpartum.[78][79] Symptoms of PTSD are common following childbirth, with prevalence of 24-30.1%[78] at six weeks, dropping to 13.6% at six months.[80] Emergency childbirth is also associated with PTSD.[81] Genetics Main article: Genetics of post-traumatic stress disorder There is evidence that susceptibility to PTSD is hereditary. Approximately 30% of the variance in PTSD is caused from genetics alone.[48] 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).[82] Women with a smaller hippocampus might be more likely to develop PTSD following a traumatic event based on preliminary findings.[83] 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.[48] Several biological indicators have been identified that are related to later PTSD development. Heightened startle responses and, with only preliminary results, a smaller hippocampal volume have been identified as possible biomarkers for heightened risk of developing PTSD.[84] Additionally, one study found that soldiers whose leukocytes had greater numbers of glucocorticoid receptors were more prone to developing PTSD after experiencing trauma.[85] 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.[23][86] During traumatic experiences, the high levels of stress hormones secreted suppress hypothalamic activity that may be a major factor toward the development of PTSD.[87] 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.[88][89] Most people with PTSD show a low secretion of cortisol and high secretion of catecholamines in urine,[90] with a norepinephrine/cortisol ratio consequently higher than comparable non-diagnosed individuals.[91] 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.[92] Brain catecholamine levels are high,[93] and corticotropin-releasing factor (CRF) concentrations are high.[94][95] Together, these findings suggest abnormality in the hypothalamic-pituitary-adrenal (HPA) axis. The maintenance of fear 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 that coordinates the hormonal response to stress,[96] which activates the LC-noradrenergic system, is implicated in the over-consolidation of memories that occurs in the aftermath of trauma.[97] This over-consolidation increases the likelihood of one's 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.[48] The HPA axis is responsible for coordinating the hormonal response to stress.[48] 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.[98] PTSD has been hypothesized to be a maladaptive learning pathway to fear response through a hypersensitive, hyperreactive, and hyperresponsive HPA axis.[99] 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.[100] 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. It is thought that the locus coeruleus-noradrenergic system mediates the over-consolidation of fear memory. High levels of cortisol reduce noradrenergic activity, and because people with PTSD tend to have reduced levels of cortisol, it has been proposed that individuals with PTSD cannot regulate the increased noradrenergic response to traumatic stress.[87] Intrusive memories and conditioned fear responses are thought to be a result of the response to associated triggers. Neuropeptide Y (NPY) 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.[48] 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.[101] Serotonin also contributes to the stabilization of glucocorticoid production. Dopamine levels in a person with PTSD can contribute to symptoms: low levels can contribute to anhedonia, apathy, impaired attention, and motor deficits; high levels can contribute to psychosis, agitation, and restlessness.[101] Several studies described elevated concentrations of the thyroid hormone triiodothyronine in PTSD.[102] This kind of type 2 allostatic adaptation may contribute to increased sensitivity to catecholamines and other stress mediators. Hyperresponsiveness in the norepinephrine system can also 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 the experience, and emotions the person is experiencing during a flashback are not associated with the current environment.[101] There is considerable controversy within the medical community regarding the neurobiology of PTSD. A 2012 review showed no clear relationship between cortisol levels and PTSD. 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.[48][103] Neuroanatomy Regions of the brain associated with stress and post-traumatic stress disorder[104] A meta-analysis of structural MRI studies found an association with reduced total brain volume, intracranial volume, and volumes of the hippocampus, insula cortex, and anterior cingulate.[105] Much of this research stems from PTSD in those exposed to the Vietnam War.[106][107] People with PTSD have decreased brain activity in the dorsal and rostral anterior cingulate cortices and the ventromedial prefrontal cortex, areas linked to the experience and regulation of emotion.[108] The amygdala is strongly involved in forming emotional memories, especially fear-related memories. During high stress, the hippocampus, which is associated with placing memories in the correct context of space and time and memory recall, is suppressed. According to one theory this suppression may be the cause of the flashbacks that can affect people with PTSD. When someone with PTSD undergoes stimuli similar to the traumatic event, the body perceives the event as occurring again because the memory was never properly recorded in the person's memory.[48][109] The amygdalocentric model of PTSD proposes that the amygdala is very much aroused and insufficiently controlled by the medial prefrontal cortex and the hippocampus, in particular during extinction.[110] This is consistent with an interpretation of PTSD as a syndrome of deficient extinction ability.[110][111] 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) of the amygdala, which elaborates the fear response, (including behavioral response to threat and elevated startle response). Descending inhibitory inputs from the medial prefrontal cortex (mPFC) regulate the transmission from the BLA to the CeA, which is hypothesized to play a role in the extinction of conditioned fear responses.[48] While as a whole, amygdala hyperactivity is reported by meta analysis of functional neuroimaging in PTSD, there is a large degree of heterogeniety, more so than in social anxiety disorder or phobic disorder. Comparing dorsal (roughly the CeA) and ventral(roughly the BLA) clusters, hyperactivity is more robust in the ventral cluster, while hypoactivity is evident in the dorsal cluster. The distinction may explain the blunted emotions in PTSD (via desensitization in the CeA) as well as the fear related component.[112] In a 2007 study Vietnam War combat veterans with PTSD showed a 20% reduction in the volume of their hippocampus compared with veterans having suffered no such symptoms.[113] This finding was not replicated in chronic PTSD patients traumatized at an air show plane crash in 1988 (Ramstein, Germany).[114] Evidence suggests that endogenous cannabinoid levels are reduced in PTSD, particularly anandamide, and that cannabinoid receptors (CB1) are increased in order to compensate.[115] There appears to be a link between increased CB1 receptor availability in the amygdala and abnormal threat processing and hyperarousal, but not dysphoria, in trauma survivors. A 2020 study found no evidence for conclusions from prior research that suggested low IQ is a risk factor for developing PTSD.[116] Diagnosis PTSD can be difficult to diagnose, because of: the subjective nature of most of the diagnostic criteria (although this is true for many mental disorders); the potential for over-reporting, e.g., while seeking disability benefits, or when PTSD could be a mitigating factor at criminal sentencing[117] the potential for under-reporting, e.g., stigma, pride, fear that a PTSD diagnosis might preclude certain employment opportunities; symptom overlap with other mental disorders such as obsessive compulsive disorder and generalized anxiety disorder;[118] association with other mental disorders such as major depressive disorder and generalized anxiety disorder; substance use disorders, which often produce some of the same signs and symptoms as PTSD; and substance use disorders can increase vulnerability to PTSD or exacerbate PTSD symptoms or both; and PTSD increases the risk for developing substance use disorders. the differential expression of symptoms culturally (specifically with respect to avoidance and numbing symptoms, distressing dreams, and somatic symptoms)[119] Screening There are a number of PTSD screening instruments for adults, such as the PTSD Checklist for DSM-5 (PCL-5)[120][121] and the Primary Care PTSD Screen for DSM-5 (PC-PTSD-5).[122] There are also several screening and assessment instruments for use with children and adolescents. These include the Child PTSD Symptom Scale (CPSS),[123][124] Child Trauma Screening Questionnaire,[125][126] and UCLA Post-traumatic Stress Disorder Reaction Index for DSM-IV.[127][128] In addition, there are also screening and assessment instruments for caregivers of very young children (six years of age and younger). These include the Young Child PTSD Screen,[129] the Young Child PTSD Checklist,[129] and the Diagnostic Infant and Preschool Assessment.[130]
Post-traumatic stress disorder
| Post-traumatic stress disorder | |
|---|---|
 | |
| Art therapy project created by a U.S. Marine with post-traumatic stress disorder | |
| Specialty | Psychiatry, clinical psychology |
| Symptoms | Disturbing thoughts, feelings, or dreams related to the event; mental or physical distress to trauma-related cues; efforts to avoid trauma-related situations; increased fight-or-flight response[1] |
| Complications | Self-harm, suicide[2] |
| Duration | > 1 month[1] |
| Causes | Exposure to a traumatic event[1] |
| Diagnostic method | Based on symptoms[2] |
| Treatment | Counseling, medication[3] |
| Medication | Selective serotonin reuptake inhibitor[4] |
| Frequency | 8.7% (lifetime risk); 3.5% (12-month risk) (US)[5] |
Post-traumatic stress disorder (PTSD)[a] is a mental and behavioral disorder[6] that can develop because of exposure to a traumatic event, such as sexual assault, warfare, traffic collisions, child abuse, domestic violence or other threats on a person's life.[1][7] Symptoms may include disturbing thoughts, feelings, or dreams related to the events, mental or physical distress to trauma-related cues, attempts to avoid trauma-related cues, alterations in the way a person thinks and feels, and an increase in the fight-or-flight response.[1][3] These symptoms last for more than a month after the event.[1] Young children are less likely to show distress, but instead may express their memories through play.[1] A person with PTSD is at a higher risk of suicide and intentional self-harm.[2][8]
Most people who experience traumatic events do not develop PTSD.[2] People who experience interpersonal violence such as rape, other sexual assaults, being kidnapped, stalking, physical abuse by an intimate partner, and incest or other forms of childhood sexual abuse are more likely to develop PTSD than those who experience non-assault based trauma, such as accidents and natural disasters.[9][10][11] Those who experience prolonged trauma, such as slavery, concentration camps, or chronic domestic abuse, may develop complex post-traumatic stress disorder (C-PTSD). C-PTSD is similar to PTSD but has a distinct effect on a person's emotional regulation and core identity.[12]
Prevention may be possible when counselling is targeted at those with early symptoms but is not effective when provided to all trauma-exposed individuals whether or not symptoms are present.[2] The main treatments for people with PTSD are counselling (psychotherapy) and medication.[3][13] Antidepressants of the SSRI or SNRI type are the first-line medications used for PTSD and are moderately beneficial for about half of people.[4] Benefits from medication are less than those seen with counselling.[2] It is not known whether using medications and counselling together has greater benefit than either method separately.[2][14] Medications, other than some SSRIs or SNRIs, do not have enough evidence to support their use and, in the case of benzodiazepines, may worsen outcomes.[15][16]
In the United States, about 3.5% of adults have PTSD in a given year, and 9% of people develop it at some point in their life.[1] In much of the rest of the world, rates during a given year are between 0.5% and 1%.[1] Higher rates may occur in regions of armed conflict.[2] It is more common in women than men.[3] Symptoms of trauma-related mental disorders have been documented since at least the time of the ancient Greeks.[17] During the world wars, the condition was known under various terms including "shell shock" and "combat neurosis".[18] The term "post-traumatic stress disorder" came into use in the 1970s in large part due to the diagnoses of U.S. military veterans of the Vietnam War.[19] It was officially recognized by the American Psychiatric Association in 1980 in the third edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-III).[20]
Symptoms
Symptoms of PTSD generally begin within the first three months after the inciting traumatic event, but may not begin until years later.[1][3] In the typical case, the individual with PTSD persistently avoids either trauma-related thoughts and emotions or discussion of the traumatic event, and may even have amnesia of the event.[1] However, the event is commonly relived by the individual through intrusive, recurrent recollections, dissociative episodes of reliving the trauma ("flashbacks"), and nightmares (50 to 70%[21]).[22] While it is common to have symptoms after any traumatic event, these must persist to a sufficient degree (i.e., causing dysfunction in life or clinical levels of distress) for longer than one month after the trauma to be classified as PTSD (clinically significant dysfunction or distress for less than one month after the trauma may be acute stress disorder).[1][23][24][25] Some following a traumatic event experience post-traumatic growth.[26]
Associated medical conditions
Trauma survivors often develop depression, anxiety disorders, and mood disorders in addition to PTSD.[27]
Substance use disorder, such as alcohol use disorder, commonly co-occur with PTSD.[28] Recovery from post-traumatic stress disorder or other anxiety disorders may be hindered, or the condition worsened, when substance use disorders are comorbid with PTSD. Resolving these problems can bring about improvement in an individual's mental health status and anxiety levels.[29][30]
In children and adolescents, there is a strong association between emotional regulation difficulties (e.g. mood swings, anger outbursts, temper tantrums) and post-traumatic stress symptoms, independent of age, gender, or type of trauma.[31]
Risk factors
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Persons considered at risk include combat military personnel, victims of natural disasters, concentration camp survivors, and victims of violent crime. Persons employed in occupations that expose them to violence (such as soldiers) or disasters (such as emergency service workers) are also at risk.[33] Other occupations that are at higher risk include police officers, firefighters, ambulance personnel, health care professionals, train drivers, divers, journalists, and sailors, in addition to people who work at banks, post offices or in stores.[34]
Trauma
PTSD has been associated with a wide range of traumatic events. The risk of developing PTSD after a traumatic event varies by trauma type[35][36] and is highest following exposure to sexual violence (11.4%), particularly rape (19.0%).[37] Men are more likely to experience a traumatic event (of any type), 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.[38]
Motor vehicle collision survivors, both children and adults, are at an increased risk of PTSD.[39][40] Globally, about 2.6% of adults are diagnosed with PTSD following a non-life threatening traffic accident, and a similar proportion of children develop PTSD.[37] Risk of PTSD almost doubles to 4.6% for life-threatening auto accidents.[37] Females were more likely to be diagnosed with PTSD following a road traffic accident, whether the accident occurred during childhood or adulthood.[39][40]
Post-traumatic stress reactions have been studied in children and adolescents.[41] The rate of PTSD might be lower in children than adults, but in the absence of therapy, symptoms may continue for decades.[42] 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.[42] On average, 16% of children exposed to a traumatic event develop PTSD, varying according to type of exposure and gender.[43] Similar to the adult population, risk factors for PTSD in children include: female gender, exposure to disasters (natural or manmade), negative coping behaviours, and/or lacking proper social support systems.[44]
Predictor models have consistently found that childhood trauma, chronic adversity, neurobiological differences, and familial stressors are associated with risk for PTSD after a traumatic event in adulthood.[45][46][47] It has been difficult to find consistently aspects of the events that predict, but peritraumatic dissociation has been a fairly consistent predictive indicator of the development of PTSD.[48] Proximity to, duration of, and severity of the trauma make an impact. It has been speculated that interpersonal traumas cause more problems than impersonal ones,[49] but this is controversial.[50] The risk of developing PTSD is increased in individuals who are exposed to physical abuse, physical assault, or kidnapping.[51][52] Women who experience physical violence are more likely to develop PTSD than men.[51]
Intimate partner violence
An individual that has been exposed to domestic violence is predisposed to the development of PTSD. However, being exposed to a traumatic experience does not automatically indicate that an individual will develop PTSD.[53] There is a strong association between the development of PTSD in mothers that experienced domestic violence during the perinatal period of their pregnancy.[54]
Those who have experienced sexual assault or rape may develop symptoms of PTSD.[55][56] PTSD symptoms include re-experiencing the assault, avoiding things associated with the assault, numbness, and increased anxiety and an increased startle response. The likelihood of sustained symptoms of PTSD is higher if the rapist confined or restrained the person, if the person being raped believed the rapist would kill them, the person who was raped was very young or very old, and if the rapist was someone they knew. The likelihood of sustained severe symptoms is also higher if people around the survivor ignore (or are ignorant of) the rape or blame the rape survivor.[57]
Military service is a risk factor for developing PTSD.[58] Around 78% of people exposed to combat do not develop PTSD; in about 25% of military personnel who develop PTSD, its appearance is delayed.[58]
Refugees are also at an increased risk for PTSD due to their exposure to war, hardships, and traumatic events. The rates for PTSD within refugee populations range from 4% to 86%.[59] While the stresses of war affect everyone involved, displaced persons have been shown to be more so than others.[60]
Challenges related to the overall psychosocial well-being of refugees are complex and individually nuanced. Refugees have reduced levels of well-being and a high rates of mental distress due to past and ongoing trauma. Groups that are particularly affected and whose needs often remain unmet are women, older people and unaccompanied minors.[61] Post-traumatic stress and depression in refugee populations also tend to affect their educational success.[61]
Unexpected death of a loved one
Sudden, unexpected death of a loved one is the most common traumatic event type reported in cross-national studies.[37][62] However, the majority of people who experience this type of event will not develop PTSD. An analysis from the WHO World Mental Health Surveys found a 5.2% risk of developing PTSD after learning of the unexpected death of a loved one.[62] Because of the high prevalence of this type of traumatic event, unexpected death of a loved one accounts for approximately 20% of PTSD cases worldwide.[37]
Life-threatening illness
Medical conditions associated with an increased risk of PTSD include cancer,[63][64][65] heart attack,[66] and stroke.[67] 22% of cancer survivors present with lifelong PTSD like symptoms.[68] Intensive-care unit (ICU) hospitalization is also a risk factor for PTSD.[69] Some women experience PTSD from their experiences related to breast cancer and mastectomy.[70][71][63] Loved ones of those who experience life-threatening illnesses are also at risk for developing PTSD, such as parents of child with chronic illnesses.[72]
Women who experience miscarriage are at risk of PTSD.[73][74][75] Those who experience subsequent miscarriages have an increased risk of PTSD compared to those experiencing only one.[73] PTSD can also occur after childbirth and the risk increases if a woman has experienced trauma prior to the pregnancy.[76][77] Prevalence of PTSD following normal childbirth (that is, excluding stillbirth or major complications) is estimated to be between 2.8 and 5.6% at six weeks postpartum,[78] with rates dropping to 1.5% at six months postpartum.[78][79] Symptoms of PTSD are common following childbirth, with prevalence of 24-30.1%[78] at six weeks, dropping to 13.6% at six months.[80] Emergency childbirth is also associated with PTSD.[81]
Genetics
There is evidence that susceptibility to PTSD is hereditary. Approximately 30% of the variance in PTSD is caused from genetics alone.[48] 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).[82] Women with a smaller hippocampus might be more likely to develop PTSD following a traumatic event based on preliminary findings.[83] 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.[48]
Several biological indicators have been identified that are related to later PTSD development. Heightened startle responses and, with only preliminary results, a smaller hippocampal volume have been identified as possible biomarkers for heightened risk of developing PTSD.[84] Additionally, one study found that soldiers whose leukocytes had greater numbers of glucocorticoid receptors were more prone to developing PTSD after experiencing trauma.[85]
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.[23][86] During traumatic experiences, the high levels of stress hormones secreted suppress hypothalamic activity that may be a major factor toward the development of PTSD.[87]
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.[88][89]
Most people with PTSD show a low secretion of cortisol and high secretion of catecholamines in urine,[90] with a norepinephrine/cortisol ratio consequently higher than comparable non-diagnosed individuals.[91] 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.[92]
Brain catecholamine levels are high,[93] and corticotropin-releasing factor (CRF) concentrations are high.[94][95] Together, these findings suggest abnormality in the hypothalamic-pituitary-adrenal (HPA) axis.
The maintenance of fear 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 that coordinates the hormonal response to stress,[96] which activates the LC-noradrenergic system, is implicated in the over-consolidation of memories that occurs in the aftermath of trauma.[97] This over-consolidation increases the likelihood of one's 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.[48]
The HPA axis is responsible for coordinating the hormonal response to stress.[48] 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.[98] PTSD has been hypothesized to be a maladaptive learning pathway to fear response through a hypersensitive, hyperreactive, and hyperresponsive HPA axis.[99]
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.[100] 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.
It is thought that the locus coeruleus-noradrenergic system mediates the over-consolidation of fear memory. High levels of cortisol reduce noradrenergic activity, and because people with PTSD tend to have reduced levels of cortisol, it has been proposed that individuals with PTSD cannot regulate the increased noradrenergic response to traumatic stress.[87] Intrusive memories and conditioned fear responses are thought to be a result of the response to associated triggers. Neuropeptide Y (NPY) 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.[48]
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.[101] Serotonin also contributes to the stabilization of glucocorticoid production.
Dopamine levels in a person with PTSD can contribute to symptoms: low levels can contribute to anhedonia, apathy, impaired attention, and motor deficits; high levels can contribute to psychosis, agitation, and restlessness.[101]
Several studies described elevated concentrations of the thyroid hormone triiodothyronine in PTSD.[102] This kind of type 2 allostatic adaptation may contribute to increased sensitivity to catecholamines and other stress mediators.
Hyperresponsiveness in the norepinephrine system can also 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 the experience, and emotions the person is experiencing during a flashback are not associated with the current environment.[101]
There is considerable controversy within the medical community regarding the neurobiology of PTSD. A 2012 review showed no clear relationship between cortisol levels and PTSD. 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.[48][103]
Neuroanatomy
A meta-analysis of structural MRI studies found an association with reduced total brain volume, intracranial volume, and volumes of the hippocampus, insula cortex, and anterior cingulate.[105] Much of this research stems from PTSD in those exposed to the Vietnam War.[106][107]
People with PTSD have decreased brain activity in the dorsal and rostral anterior cingulate cortices and the ventromedial prefrontal cortex, areas linked to the experience and regulation of emotion.[108]
The amygdala is strongly involved in forming emotional memories, especially fear-related memories. During high stress, the hippocampus, which is associated with placing memories in the correct context of space and time and memory recall, is suppressed. According to one theory this suppression may be the cause of the flashbacks that can affect people with PTSD. When someone with PTSD undergoes stimuli similar to the traumatic event, the body perceives the event as occurring again because the memory was never properly recorded in the person's memory.[48][109]
The amygdalocentric model of PTSD proposes that the amygdala is very much aroused and insufficiently controlled by the medial prefrontal cortex and the hippocampus, in particular during extinction.[110] This is consistent with an interpretation of PTSD as a syndrome of deficient extinction ability.[110][111]
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) of the amygdala, which elaborates the fear response, (including behavioral response to threat and elevated startle response). Descending inhibitory inputs from the medial prefrontal cortex (mPFC) regulate the transmission from the BLA to the CeA, which is hypothesized to play a role in the extinction of conditioned fear responses.[48] While as a whole, amygdala hyperactivity is reported by meta analysis of functional neuroimaging in PTSD, there is a large degree of heterogeniety, more so than in social anxiety disorder or phobic disorder. Comparing dorsal (roughly the CeA) and ventral(roughly the BLA) clusters, hyperactivity is more robust in the ventral cluster, while hypoactivity is evident in the dorsal cluster. The distinction may explain the blunted emotions in PTSD (via desensitization in the CeA) as well as the fear related component.[112]
In a 2007 study Vietnam War combat veterans with PTSD showed a 20% reduction in the volume of their hippocampus compared with veterans having suffered no such symptoms.[113] This finding was not replicated in chronic PTSD patients traumatized at an air show plane crash in 1988 (Ramstein, Germany).[114]
Evidence suggests that endogenous cannabinoid levels are reduced in PTSD, particularly anandamide, and that cannabinoid receptors (CB1) are increased in order to compensate.[115] There appears to be a link between increased CB1 receptor availability in the amygdala and abnormal threat processing and hyperarousal, but not dysphoria, in trauma survivors.
A 2020 study found no evidence for conclusions from prior research that suggested low IQ is a risk factor for developing PTSD.[116]
Diagnosis
PTSD can be difficult to diagnose, because of:
- the subjective nature of most of the diagnostic criteria (although this is true for many mental disorders);
- the potential for over-reporting, e.g., while seeking disability benefits, or when PTSD could be a mitigating factor at criminal sentencing[117]
- the potential for under-reporting, e.g., stigma, pride, fear that a PTSD diagnosis might preclude certain employment opportunities;
- symptom overlap with other mental disorders such as obsessive compulsive disorder and generalized anxiety disorder;[118]
- association with other mental disorders such as major depressive disorder and generalized anxiety disorder;
- substance use disorders, which often produce some of the same signs and symptoms as PTSD; and
- substance use disorders can increase vulnerability to PTSD or exacerbate PTSD symptoms or both; and
- PTSD increases the risk for developing substance use disorders.
- the differential expression of symptoms culturally (specifically with respect to avoidance and numbing symptoms, distressing dreams, and somatic symptoms)[119]
Screening
There are a number of PTSD screening instruments for adults, such as the PTSD Checklist for DSM-5 (PCL-5)[120][121] and the Primary Care PTSD Screen for DSM-5 (PC-PTSD-5).[122]
There are also several screening and assessment instruments for use with children and adolescents. These include the Child PTSD Symptom Scale (CPSS),[123][124] Child Trauma Screening Questionnaire,[125][126] and UCLA Post-traumatic Stress Disorder Reaction Index for DSM-IV.[127][128]
In addition, there are also screening and assessment instruments for caregivers of very young children (six years of age and younger). These include the Young Child PTSD Screen,[129] the Young Child PTSD Checklist,[129] and the Diagnostic Infant and Preschool Assessment.[130]
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