Posttraumatic stress disorder (PTSD)

 

Post-traumatic stress disorder (PTSD) is a mental and behavioral disorder 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.

A psychiatric disorder that has an identifiable cause.

Many types of traumatic experiences can lead to PTSD such as rape, physical assault, accidents, disasters, homicides, and suicides.

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.

These symptoms last for more than a month after the event.

A person with PTSD is at a higher risk of suicide and intentional self-harm.

There is an 8.7% lifetime risk, and a 3.5% 12-month risk

Most traumatic experiences do not result in PTSD.

Individuals 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.

Persons experiencing 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.

PTSD  prevention may be possible when counselling those with early symptoms but is not effective when provided to all trauma-exposed individuals whether or not symptoms are present.

The main treatments are psychotherapy and medication.

Antidepressants of the SSRI or SNRI type are the first-line medications used for PTSD and are moderately beneficial for about half of patients.

Medication are less helpful than counseling.

About 3.5% of adults in the US have PTSD in a given year, and 9% of people develop it at some point in their life.

In much of the rest of the world, rates during a given year are between 0.5% and 1%.

Higher rates of PSTD may occur in regions of armed conflict.

PSDT is more common in women than men.

Symptoms of PTSD generally begin within the first three months after the inciting traumatic event.

Symptoms of PSDT, however, may not begin until years later.

Individual with PTSD persistently avoid either trauma-related thoughts, emotions or discussion of the traumatic event.

PTDS may be associated with amnesia of the event.

Commonly the event is relived by intrusive, recurrent recollections, dissociative episodes of reliving the trauma.

These flashbacks, and nightmares occur in 50 to 70% of cases.

Traumatic symptoms must persist and be of a sufficient degree for longer than one month after the trauma to be classified as PTSD.

Such clinically significant dysfunction or distress for less than one month after the trauma is referred to as an acute stress disorder.

Persons whom experience trauma often develop depression, anxiety disorders, and mood disorders in addition to PTSD.

Substance use disorders, commonly accompany PTSD.

The presence of substance abuse disorders may hinder the resolution of PTSD.

Among children and adolescents, there is a strong association between emotional regulation difficulties and post-traumatic stress symptoms, independent of age, gender, or type of trauma: mood swings, anger outbursts, temper tantrums

Moral injuries are is associated with shame and guilt while PTSD is associated with anxiety and fear.

Risk factors for PTSD include:

combat military personnel, victims of natural disasters, concentration camp survivors, victims of violent crime, employment in occupations that expose one to violence or disasters.

High risk occupations include: police officers, firefighters, ambulance personnel, health care professionals, train drivers, divers, journalists, sailors, and workers at banks, post offices or in stores.

PTSD is associated with a wide range of traumatic events, and the risk of developing PTSD after a traumatic event varies by trauma type.

PSTD risk is highest following exposure to sexual violence (11.4%), and particularly rape (19.0%).

Men are more likely to experience a traumatic event of any type.

Women are more likely to experience high-impact traumatic events that can lead to PTSD, such as interpersonal violence and sexual assault.

Children and adult survivors of motor vehicle collisions are at increased risk of PTSD: about 2.6% of adults and children are diagnosed with PTSD following a non-life threatening traffic accident.

Risk of PTSD almost doubles to 4.6% for life-threatening auto accidents.

Females were more likely to be diagnosed with PTSD following a road traffic accident.

The rate of PTSD may be lower in children than adults.

In  the absence of therapy, children’s symptoms may continue for decades.

The proportion of children and adolescents having PTSD in a developed country may be 1% compared to 1.5% to 3% of adults.

16% of children exposed to a traumatic event develop PTSD, that vary by the  type of exposure and gender.

Risk factors for PTSD in children include: female gender, exposure to disasters, negative coping behaviors, and/or lacking proper social support systems.

The risk for PTSD after a traumatic event in adulthood is associated with childhood trauma, chronic adversity, neurobiological differences, and familial stressors.

A peritraumatic dissociation has been a fairly consistent predictive indicator of the development of PTSD.

Proximity to, duration of, and severity of a trauma make an impact on PSTD.

It is suggested that interpersonal traumas cause more problems than impersonal ones.

PTSD risk is increased in individuals who are exposed to physical abuse, physical assault, or kidnapping.

Women who experience physical violence are more likely to develop PTSD than men.

People that have been exposed to domestic violence are predisposed to the development of PTSD. 

A strong association exists between the development of PTSD in mothers that experienced domestic violence during the perinatal period of their pregnancy.

Individuals who have experienced sexual assault or rape may develop PTSD.

PTSD symptoms include:  re-experiencing the assault, avoiding things associated with the assault, numbness, and increased anxiety and an increased startle response. 

Sustained symptoms of PTSD is higher following rape if the victim was confined or restrained, if the victim believed the rapist would kill them, if they were very young or very old, and if the rapist was someone they knew. 

Sustained symptoms of PSTD are more likely if people around the survivor ignore, are ignorant of the rape, or blame the rape survivor.

Military service is a risk factor for developing PTSD.

Around 78% of those exposed to combat do not develop PTSD.

In about 25% of military personnel after combat, develop delayed PTSD.

Refugees have an increased risk for PTSD due to their exposure to war, hardships, and traumatic events. 

Sudden, unexpected death of a loved one is the most common traumatic event type reported in cross-national studies of PTSD, although the majority of people who experience this type of event will not develop PTSD. 

There is about a 5.2% risk of developing PTSD after learning of the unexpected death of a loved one.

The unexpected death of a loved one accounts for approximately 20% of PTSD cases worldwide.

PTSD is associated with medical conditions: cancer, heart attack, and stroke.

22% of cancer survivors present with lifelong PTSD like symptoms.

ICU hospitalization is a risk factor for PTSD.

Some women experience PTSD from their experiences related to breast cancer and mastectomy.

Loved ones of those who experience life-threatening illnesses are also at risk for developing PTSD.

Women who experience miscarriage are at risk of PTSD, and  subsequent miscarriages have an increased risk of PTSD compared to those experiencing only one.

PTSD can also occur after childbirth: risk increases if a woman has experienced trauma prior to the pregnancy.

Prevalence of PTSD following normal childbirth is estimated to be between 2.8 and 5.6% at six weeks postpartum.

PTSD rates drop to 1.5% at six months postpartum.

Symptoms of PTSD are common following childbirth, with prevalence of 24-30.1% at six weeks.

Emergency childbirth is also associated with PTSD.

There is evidence that susceptibility to PTSD is hereditary, with approximately 30% of the variance in PTSD is caused from genetics alone.

For twin pairs exposed to combat in Vietnam, identical twins with PTSD are associated with an increased risk of the co-twin’s having PTSD compared to twins that were non-identical twins

Women with a smaller hippocampus are suggested to be more likely to develop PTSD following a traumatic event.

 PTSD shares many genetic influences common to other psychiatric disorders: generalized anxiety disorders, alcohol, nicotine, and drug dependence.

Possible markers for risk of developing PTSD include a smaller hippocampal volume and a heightened and startle response.

A study of soldier’s leukocytes with greater numbers of glucocorticoid receptors indicated they were more prone to developing PTSD after experiencing trauma.

PTSD symptoms may result when a traumatic event causes an over-reactive adrenaline response, and the creation of  deep neurological patterns in the brain. 

Such patterns can persist long after the event that triggered the fear, making an individual hyper-responsive to future fearful situations.

It is proposed that with a traumatic experiences, the high levels of stress hormones secreted suppress hypothalamic activity that may be a major factor toward the development of PTSD.

PTSD causes biochemical changes in the brain and body, differing  from other psychiatric disorders such as major depression. 

PTSD patients respond more strongly to a dexamethasone suppression test than individuals diagnosed with clinical depression.

Most people with PTSD show a low secretion of cortisol and high secretion of catecholamines: with a norepinephrine/cortisol ratio consequently higher than comparable non-diagnosed individuals.

PSTD, is in contrast to the normative fight-or-flight response, which has both  catecholamine and cortisol levels are elevated after exposure to a stressor.

Brain catecholamine levels and corticotropin-releasing factor (CRF) concentrations are high with PTSD, suggesting  abnormality in the hypothalamic-pituitary-adrenal (HPA) axis is present.

The maintenance of fear has been shown to include the HPA axis, that coordinates the hormonal response to stress.

The HPA axis activates the limbic-noradrenergic system, is implicated in the over-consolidation of memories that occurs in the aftermath of trauma, increasing g  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 HPA axis is responsible for coordinating the hormonal response to stress.

There is a 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.

PTSD has been hypothesized to be a maladaptive learning pathway to fear response through a hypersensitive, hyperreactive, and hyperresponsive HPA axis.

Low cortisol levels may predispose individuals to PTSD.

Cortisol is normally important in restoring homeostasis after the stress response, it is thought that trauma survivors with low cortisol experience a poorly contained, 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. 

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.

Neuropeptide Y (NPY) has been reported to reduce the release of norepinephrine and has been demonstrated to have anxiolytic properties: Studies have shown people with PTSD demonstrate reduced levels of NPY, possibly indicating their increased anxiety levels.

Individuals suffering 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.

Serotonin also contributes to the stabilization of glucocorticoid production.

Dopamine levels with PTSD can contribute to symptoms.

Low levels of dopamine can contribute to anhedonia, apathy, impaired attention, and motor deficits, while high levels can contribute to psychosis, agitation, and restlessness.

Elevated levels of triiodothyronine in PTSD.may contribute to increased sensitivity to catecholamines and other stress mediators.

Continued exposure to high stress can be associated with  hyperresponsiveness in the norepinephrine system, with overactivation of norepinephrine receptors in the prefrontal cortex: flashbacks and nightmares frequently experienced by those with PTSD. 

There is a decrease in other norepinephrine functions such as the awareness of the current environment in PTSD that prevents the memory mechanisms in the brain from processing the experience.

The emotions a  person experiences during a flashback are not associated with the current environment.

Studies suggest that there is no clear relationship between cortisol levels and PTSD: 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.

Structural MRI studies find an association with reduced total brain volume, intracranial volume, and volumes of the hippocampus, insula cortex, and anterior cingulate in PTSD individuals.

The dorsal and rostral anterior cingulate cortices and the ventromedial prefrontal cortex, areas linked to the experience and regulation of emotion have decreased activity in patients with PTSD.

The amygdala is strongly involved in forming emotional memories, especially those associated with fear-related memories. 

During high stress, the hippocampus and its abilities of placing memories in the correct context of space and time, memory recall, are suppressed.

The hippocampal suppression may be the cause of the flashbacks that can affect people with PTSD.

This  suggests  a patient with PTSD who undergoes stimuli similar to the traumatic event, perceives the event as occurring again because the memory was never properly recorded in the person’s memory.

It is proposed that the amygdala is aroused and insufficiently controlled by the medial prefrontal cortex and the hippocampus, suggesting PTSD as a syndrome of deficient extinction ability.

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. 

A study of Vietnam War combat veterans with PTSD showed a 20% reduction in the volume of their hippocampus compared with veterans having suffered no such symptoms.

PTSD can be difficult to diagnose, because of:

the subjective nature of most of the diagnostic criteria.

the potential for over-reporting-disability benefits, 

PTSD could be a mitigating factor at criminal sentencing.

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.

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

substance use disorders can increase vulnerability to PTSD or exacerbate PTSD symptoms or both

PTSD increases the risk for developing substance use disorders.

PTSD was classified as an anxiety disorder in the DSM-IV, but has since been reclassified as a trauma- and stressor-related disorder in the DSM-5.

PTSD diagnosis includes four symptom clusters: re-experiencing, avoidance, negative alterations in cognition/mood, and alterations in arousal and reactivity.

The International Classification of Diseases and Related Health Problems 10 (ICD-10) classifies PTSD under Reaction to severe stress, and adjustment disorders.

The ICD-10 criteria for PTSD include re-experiencing, avoidance, and either increased reactivity or inability to recall certain details related to the event.

The ICD-11 diagnostic description for PTSD contains three components or symptom groups (1) re-experiencing, (2) avoidance, and (3) heightened sense of threat, but no longer includes verbal thoughts about the traumatic event as a symptom.

A diagnosis of PTSD requires that the person has been exposed to an extreme stressor. 

Any stressor can result in a diagnosis of adjustment disorder and it is an appropriate diagnosis for a stressor and a symptom pattern that does not meet the criteria for PTSD.

Differential diagnosis:

Acute stress disorder must occur and be resolved within four weeks of the trauma.

Obsessive compulsive disorder may be diagnosed for intrusive thoughts that are recurring but not related to a specific traumatic event.

Prolonged, repeated traumatization where there is no viable chance of escape, survivors may develop complex post-traumatic stress disorder, as a result of layers of trauma rather than a single traumatic event, and includes additional symptomatology, such as the loss of a coherent sense of self.

Prevention

Benefits have been seen from early access to cognitive behavioral therapy. 

However, Cochrane review did not find any evidence to support the use of an intervention offered to everyone, and that multiple session interventions may result in worse outcome than no intervention for some individuals.

Recommendations are not to use of benzodiazepines and antidepressants in for acute stress.

 Some evidence supports the use of hydrocortisone for prevention in adults.

Trauma-exposed individuals often receive treatment called psychological debriefing in an effort to prevent PTSD, which consists of interviews that are meant to allow individuals to directly confront the event and share their feelings with the counselor and to help structure their memories of the event: Meta-analyses find that psychological debriefing is unhelpful and is potentially harmful.

Management:

Combination therapy (psychological and pharmacotherapy) is no more effective than psychological therapy alone.

Approaches with the strongest evidence include behavioral and cognitive-behavioral therapies such as prolonged exposure therapy,

cognitive processing therapy, and eye movement desensitization and reprocessing.

Children with PTSD are far more likely to pursue treatment at school (because of its proximity and ease) than at a free clinic.

Cognitive behavioral therapy

Cognitive behavioral therapy seeks to change the way a person feels and acts by changing the patterns of thinking or behavior, or both, responsible for negative emotions. 

CBT is a proven effective treatment for PTSD and is currently considered the standard of care.

PTSD patients learn to identify thoughts that make them feel afraid or upset and replace them with less distressing thoughts. 

Exposure therapy is a type of cognitive behavioral therapy that involves assisting trauma survivors to re-experience distressing trauma-related memories and reminders in order to facilitate habituation and successful emotional processing of the trauma memory. 

Most exposure therapy programs include both imaginative confrontation with the traumatic memories and real-life exposure to trauma reminders.

Exposure therapy is well supported by clinical evidence.

Eye movement desensitization and reprocessing (EMDR) is a form of psychotherapy that is used when one is thinking about disturbing memories and the eyes are moving rapidly.

When eye  movements are brought under control while thinking, the thoughts are less distressing.

EMDR closely resembles cognitive behavior therapy as it combines exposure by re-visiting the traumatic event, working on cognitive processes and relaxation/self-monitoring.

Exposure by way of being asked to think about the experience rather than talk about it.

There is moderate strength evidence to support the efficacy of EMDR for reduction in PTSD symptoms, loss of diagnosis, and reduction in depressive symptoms.

Evidence concludes that thinking of upsetting memories and simultaneously doing a task that facilitates eye movements reduces the vividness and distress associated with the upsetting memories.

Interpersonal psychotherapy reported high rates of remission from PTSD symptoms without using exposure.

The medications fluoxetine, paroxetine, and venlafaxine have a small to modest benefit over placebo.

With the use of many medications, residual PTSD symptoms following treatment is the rule rather than the exception.

Selective serotonin reuptake inhibitors (SSRIs) and serotonin-norepinephrine reuptake inhibitors (SNRIs) have some benefit for PTSD symptoms.

Tricyclic antidepressants are equally effective for PSTD but are less well tolerated.

Sertraline, fluoxetine, paroxetine, and venlafaxine fourmedications are considered to be first-line medications for PTSD.

Benzodiazepines are not recommended for the treatment of PTSD:  lack of evidence of benefit and risk of worsening PTSD symptoms.

Benzodiazepines may reduce the effectiveness of psychotherapeutic interventions.

Benzodiazepines may contribute to the development and chronification of PTSD, by worsening and prolong the course of illness, worsening psychotherapy outcomes, and causing or exacerbating aggression, depression and substance use.

Prazosin, an alpha-1 adrenergic antagonist, has been used with PTSD to reduce nightmares. 

Glucocorticoids may be useful for short-term therapy to protect against neurodegeneration caused by the extended stress response of PTSD.

Cannabinoid nabilone is sometimes used for nightmares in PTSD. 

Repetitive play can also be one way a child relives traumatic events, and that can be a symptom of trauma in a child or young person.

The National Comorbidity Survey Replication has estimated that the lifetime prevalence of PTSD among adult Americans is 6.8%, with women (9.7%) more than twice as likely as men (3.6%) to have PTSD at some point in their lives.

More than 60% of men and more than 60% of women experience at least one traumatic event in their life. 

The most frequently reported traumatic events reported by men are rape, combat, and childhood neglect or physical abuse. 

Women most frequently report instances of rape, sexual molestation, physical attack, being threatened with a weapon and childhood physical abuse.

88% of men and 79% of women with lifetime PTSD have at least one comorbid psychiatric disorder:most commonly major depressive disorder, alcohol use disorder or dependence are the most common comorbid disorders.

A large majority of Vietnam veterans suffered from PTSD symptoms, but not the disorder itself.

PTSD diagnosis increased significantly when troops were stationed in combat zones, had tours of longer than a year, experienced combat, or were injured. 

Military personnel serving in combat zones are 12  percentage points more likely to receive a PTSD diagnosis than their active-duty counterparts in non-combat zones. 

Overall prevalence of PTSD after 911 was highest immediately following the attacks and decreased over time. 

The rate of PTSD for first responders was lowest directly after the attacks and increased from ranges of 4.8-7.8% to 7.4-16.5% between the 5-6 year follow-up and a later assessment.

When comparing traditional responders to volunteers, the probable PTSD prevalence 2.5 years after the initial visit was greater in volunteers with estimates of 11.7% and 17.2% respectively.

Volunteer participation in tasks atypical to the defined occupational role is a significant risk factor for PTSD.

Other risk factors included exposure intensity, earlier start date, duration of time spent on site, and constant, negative reminders of the trauma.

Almost 50% of World Trade Center workers who self-identified as alcohol users reported drinking more during the rescue efforts.

Traumas most commonly associated with PTSD are combat exposure and witnessing among men and rape and sexual molestation among women.

Trauma-focused psychotherapies for PTSD prolonged exposure therapy (PE), eye movement desensitization and reprocessing (EMDR), and cognitive-reprocessing therapy (CPT).

These measures have the most for efficacy and are recommended as first-line treatment for PTSD.

Many trauma-focused psychotherapies evince high drop-out rates.

Psychotherapies for PTSD, most of which are trauma-focused therapies, are more effective than pharmacotherapy.

There are reviews that suggest exposure-based psychotherapies for PTSD and pharmacotherapy are equally effective.

Following an accidental injury 8-39% of patients have PTSD over the following weeks and months.

Diagnosis requires exposure to a dramatic or stressful event.

Diagnosis is based on self reporting symptoms.

Diagnosis requires symptoms must be apparent for at least one month, and the patient must experience significant distress or impaired social, occupational, or other areas of functioning.

Patients must either directly experience a traumatic event, witness someone else directly experiencing an event, learn the event occurred to a close family member or friend, or experience repeated extreme exposure to aversive details of the event.

12 month prevalence in the US is 3.5% and lifetime prevalence is 8.7%.

88% of men and 79% of women with lifetime PTSD have at least one comorbid psychiatric disorder. 

A disorder in which 1 or more traumatic events give rise to 4 symptom clusters: recurrent and painful reexperiencing of the event, phobic avoidance of trauma-related situations and memories, emotional numbing and withdrawal, and hyperarousal.

Although characterized as a traumatic disorder, the causal event is psychological.

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.

Some studies have indicated neuroanatomical changes in PTSD patients such as increased size and activity of the amygdala, decreased volume of the prefrontal cortex, and decreased volume of the hippocampus.

Neurobiologic changes may exist including heightened sympathetic nervous system responses and alterations in the hypothalamic-pituitary-adrenal axis being the most often noted.

Most perceived as being the result from exposure to disturbing events such as military combat, sexual assault, or man made or natural disasters.

At least 50% of the population experiences a traumatic event, and approximately 20% of such patients go on to develop PTSD.

In a twins study discordant for exposure in Vietnam, combat veterans with PTSD had smaller hippocampi than combat veterans without PTSD (Gilbertson MW).

US veterans with PTSD associated with the development of dementia.

32-34% of patients suffer from PTSD after traffic accidents.

5 years after a traffic accident 8% of patients have PTSD.

Up to 62% of patients with substance dependence experience comorbid PTSD, and up to 65% of patients with PTSD have a comorbid substance abuse disorder.

Higher rates of comorbid psychiatric illness including: pressure, anxiety, substance-abuse, attention deficit hyperactivity disorder and borderline personality disorder.

Patients often experience other medical problems including chronic pain, sleep problems, sexual dysfunction, and cognitive dysfunction.

Associated with functional impairments and quality-of-life deficits.

There is a 2-3 increase in suicide attempts among such patients.

Associated with more and longer hospitalizations and greater use of mental health care.

Estimated that, on average, a person with PTSD will endure 20 years of active symptoms and will experience almost only 2 day a week of work impairment.

Lifetime prevalence in the range of 8%, with women affected twice as often as men.

Lifetime prevalence 6.8%.

Lifetime prevalence amid is 3.6% versus 9.7% in women.

Women are somewhat less likely than men to experience the true Maddock event, could have a lifetime prevalence rates aproximally twice that of men.