Posttraumatic stress disorder (PTSD) is a syndrome resulting from exposure to real or threatened serious injury or sexual assault. The signs and symptoms of PTSD appear to arise from complex interactions of psychological and neurobiological factors. Studies have found alterations in the amygdala, prefrontal cortex, hippocampus, and anterior cingulate, and corpus collosum as well as altered functioning of the hypothalamic pituitary axis (HPA).
Symptoms of posttraumatic stress disorder (PTSD) include the following:
One cannot diagnose PTSD until one month has passed since the traumatic incident. Acute stress disorder, which has similar symptoms, is diagnosed during the first month.
Diagnosing PTSD in adults, adolescents, and children older than 6 years of age using the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5)[1] requires a certain type and level of traumatic event, a combination of required symptoms, and the absence of exclusionary criteria.
A) Causation: The victim was exposed to actual or threatened death, serious injury or sexual violence in one of four ways:
B) The traumatic event is persistently re-experienced:
Children may re-experience the event through repetitive play.
C) Avoidance in one of two ways:
D) Negative alterations in cognition and mood. Two of the following:
E) Hyperarrousal: Two of the following:
F) The duration of symptoms is more than 1 month
G) Disturbance causes clinically significant distress or impairment in functioning
H) The disturbance is not attributable to the physiological effects of a substance or other medical condition
DSM-5 recognizes a “with dissociative symptom” specifier when the PTSD symptoms are accompanied by persistent or recurrent depersonalization or derealization.
The specifier “with delayed expression” should be included if the full criteria for PTSD are not met for more than 6 months following the trauma.
Children may have different reactions to trauma than do adults. Children aged 6–11 years may show extreme withdrawal, disruptive behavior, and/or an inability to pay attention. Regressive behaviors, nightmares, sleep problems, irrational fears, irritability, refusal to attend school, outbursts of anger, and fighting are also common. The child may have somatic complaints with no medical basis. Schoolwork often suffers. Depression, anxiety, feelings of guilt, and emotional numbing are often present. Adolescents aged 12–17 years generally have responses similar to those of adults.[2]
For children aged 6 years or younger, typical reactions to trauma can include regressive behavior, a fear of being separated from a parent, crying, whimpering, screaming, immobility and/or aimless motion, trembling, frightened facial expressions, and excessive clinging. Children are strongly affected by their parents' reactions to the traumatic event and their parents’ ability to provide support.[2] Special criteria for the diagnosis of PTSD in children 6 years of age and under are found in the DSM-5.[1]
Psychological First Aid (PFA) is very important in the immediate aftermath of a traumatic event. PFA includes psychoeducation that the patient's initial symptoms are a normal reaction to an abnormal event and do not mean the person is weak or "going crazy," and that the symptoms will subside with time. First aid also includes providing for the individual’s basic needs (shelter, food, and supportive relationships) and reassurance that support will continue. It is important to avoid making invalidating comments such as: "It's not that big a deal" or "Why are you so upset?"
Evidence-based therapies for PTSD include Trauma Focused Cognitive Behavioral Therapy (TF-CBT) Prolonged Exposure (PE), Cognitive Processing Therapy, and Eye Movement Desensitization and Reprocessing (EMDR). Psychotherapy is clearly more effective than medication. Certain medications may be helpful in increasing the effectivenenss of therapy. D-cycloserine, which enhances memory, may help with extinction learning. Inderal may help to decrease arousal during therapy and may make extinction learning more effective. However, inderal also impairs memory.[3]
The SSRI and SNRI antidepressants appear to be the most effective psychopharmacological interventions for the symptoms of PTSD in adults. Their efficacy in adolescents and children is certainly less and they may not have any efficacy at all. In addition, they carry Black Box warnings for suicidality. Guanfacine and clonidine can be helpful for agitation. Prazosin is sometimes helpful for decreasing trauma-related nightmares and insomnia. Use of inderal in the first few hours may decrease future hyperarrousal symptoms. Use of benzodiazepines has been shown to worsen the course of PTSD.
Playing a visually demanding game such as Tetris shortly after the traumatic event may help to interfere with consolidation of the memory and may decrease the risk of developing PTSD.
The psychological problems of soldiers in World War II, the Korean War, and the Vietnam War, along with the severe psychological impact of rape, fostered interest and research in the collection of symptoms that became known as posttraumatic stress disorder. PTSD was first included in the Diagnostic and Statistical Manual of Mental Disorders in 1980 when DSM-III was published. The diagnostic criteria have undergone significant revisions with DSM-IV and DSM-5.
Under DSM-III one had to experience an event outside of normal human experience that would cause symptoms in almost anyone. In time, appreciation that the symptom cluster occurred as a result of common experiences, such as car accidents, led to a change in the criteria.
DSM-IV required that the individual respond to the trauma with “intense fear, helplessness, or horror.” Although the DSM-5 contains these as a possible manifestations of PTSD, the requirement for them was dropped. DSM-5 also moved PTSD from the "Anxiety Disorders" category to a new category of disorders referred to as "Trauma- and Stressor-Related Disorders."
Previous criteria focused on the clusters of re-experiencing, avoidance, and hyperarousal. This has been slightly modified in the DSM-5, which now includes intrusive symptoms (similar to the older re-experiencing category), avoidance, negative changes to cognitions and emotions, and altered arousal and reactivity.[1]
Traumatic events had been limited to life-threatening occurrences such as natural disasters, personal assaults, war, or severe accidents.The DSM-5 included the possibility of developing PTSD following sexual violence even if there was no threat of death. For children, a developmentally inappropriate sexual experience may be considered a traumatic event, even though it may not have actually involved violence or physical injury.
The DSM-5 recognizes a new, dissociative subtype of PTSD, with clinical and neurobiological features that distinguish it from the non-dissociative form. This dissociative subtype is described as an over-modulation of affect, or a form of emotional dysregulation mediated by midline prefrontal inhibition of limbic regions. This subtype may require slight differences in treatment.
The DSM-5 now includes differing criteria for diagnosing PTSD in children 6 years of age and younger. Although the criteria are similar to those used in diagnosing PTSD in older populations, there are developmentally appropriate alterations.[1]
The etiology of PTSD is experiencing a serious threat of physical injury or death, or sexual assault. Children who suffer repeated child abuse are at risk for complex trauma. Chronic PTSD represents a failure to recover from the trauma, in part due to inadequate resilience. Considerable effort has been spent in an attempt to determine which individuals will have prolonged, maladaptive responses to trauma. Numerous risk factors have been determined.[1, 4]
Pre-existing factors include the following:
Peritraumatic factors include the following:
Posttraumatic factors include the following:
Exposure to traumatic events is common. Among adults in the United States, as many as 50% of women and 60% of men have experienced a traumatic event. Most of these individuals will not develop PTSD. PTSD has a lifetime prevalence among adults in the United States of roughly 8% (higher in women than men) and accounts for considerable disability and morbidity. These rates vary considerably depending on the specific population being considered.[5]
Prognosis varies based on a number of factors including resilience, secondary stresses, level of support, prior traumatic experiences, ongoing injury, severity of the stressor, and so on.
The child's resilience is an important factor in prognosis.[4]
Three years after Hurricane Katrina, the prevalence of serious emotional disturbance for children in the area with high exposure (serious economic or housing problems, injury or death of someone close to them or victimization) was roughly one in three children.[5]
Child abuse and neglect predispose to personality disorders, affective disorders, substance abuse and medical problems.[6]
Family members of those with PTSD are also impacted by the trauma particularly through the detachment and irritability of the person with PTSD. Family members may desire to be supportive but are not clear what conversations to have or how best to show their concern and support. For many individuals with PTSD, comprehensive treatment includes involvement of the family in some form.
For patient education information, see the Mental Health Center, as well as Post-traumatic Stress Disorder (PTSD) and Stress.
The following websites also provide valuable information for patients and their families:
In addition to the psychological impact of experiencing a traumatic event, PTSD frequently leads to changes in the anatomy and neurophysiology of the brain. Reduced size of the hippocampus is probably both a predisposing factor and a result of trauma. The amygdala, which is involved in processing emotions and modulating the fear response, seems to be overly reactive in patients with PTSD. The medial prefrontal cortex (mPFC), which exhibits inhibitory control over the stress response and emotional reactivity of the amygdala, appears to be smaller and less responsive in individuals with PTSD.[7, 8, 9, 10]
Alterations in neurohormonal and neurotransmitter functioning have also been found. Individuals with PTSD tend to have normal to low circulating levels of cortisol despite their ongoing stress and elevated levels of Corticotropin Releasing Factor (CRF). Cortisol leads to decreased production of CRF. If cortisol is low then CRF continues to be high and stimulates norepinephrine release by the anterior cinculate cortex. Individuals with PTSD demonstrate hyperactivity of the sympathetic branch of the autonomic nervous system, as evidenced by changes in heart rate, blood pressure, skin conductance level, and other psychophysiological measures. They also have elevated noradrenergic reactivity to pharmacological challenges. A variety of other neurotransmitter systems, such as the serotonin, GABA, glutamate, neuropeptide Y, and endogenous opioids, show altered functioning in individuals with PTSD.
Further insight into the pathophysiology of PTSD may be found in the Dual Representational Theory. This understanding highlights the presence of two separate systems for memory. Verbally accessible memory (first recorded in the hippocampus and later in general brain memory storage) is able to be modified by reflection. This is characteristic of most non-traumatic memories. Situationally accessible memory, on the other hand, is non-verbal and associated with very strong emotions and the amygdala. Traumatic memories tend to be stored as situationally accessible memories, which are harder to process, are readily triggered by associations, and more likely to cause emotional distress when activated. Individuals may struggle to integrate these traumatic experiences with the rest of their life narrative thereby resulting in the traumatic memory having a significant impact on their views of the world and themselves.[11, 12]
In the 1990s, Van Der Kolk and others began promoting the concept of “Complex PTSD.” It is also referred to as Disorder of Extreme Stress Not Otherwise Specified (DESNOS). DESNOS arises from severe, protracted abuse, most notably childhood sexual abuse, victims of torture, and living in a war zone. This type of trauma often leads to the use of primitive defense mechanisms (splitting and dissociation), which causes significant interpersonal problems and emotional struggles in addition to the standard symptoms of PTSD. Complex PTSD often leads to poor resilience, increased risk of depressive and anxiety disorders, and somatization. Numerous situations will trigger these individuals and lead to very strong adverse emotional reactions. The great majority of individuals who develop Borderline Personality Disorder or Dissociative Identity Disorder suffered complex trauma during childhood. Although many clinicians find this to be a useful conceptualization, it does not appear in the DSM-5.[13]
Freyd and others have developed the concept of betrayal trauma. Betrayal trauma does not fulfill the diagnostic criteria for PTSD because it does not entail a serious threat of injury or sexual assault. Nevertheless, betrayal, such as a spouse having an affair or abandonment by a parent can result in most of the same symptoms that PTSD can cause.[14, 15] Symonds argued that some of the symptoms we normally attribute to the initial traumatic event are actually the result of the individual feeling betrayed by those (s)he expected to provide support. Child abuse includes betrayal trauma because parents and teachers are supposed to protect children, not abuse them.
The diagnosis of posttraumatic stress disorder (PTSD) is based on evidence of having experienced a serious threat of physical injury or a sexual assault followed by the symptoms of PTSD. Because of the frequent comorbidities, providers should also ask about the following:
Patients may display physiological arousal (e.g., tremor, sweating, agitation) when they are discussing their trauma. Individuals may also present with physical injuries related to the trauma (e.g., traumatic amputation from an explosion or bruises in victims of ongoing domestic abuse). Those who have experienced a head injury should be checked for evidence of neurological impairment.
Autonomic arousal in the immediate aftermath of the traumatic events indicates an increased risk of PTSD.[16]
Factors discovered during the mental status examination may help confirm the diagnosis of PTSD. These may include:
Psychiatric and medical comorbidities are common with PTSD. Among individuals with PTSD there are increased rates of:
Substance abuse is a particular problem for individuals with PTSD. Studies have found that up to 51.9% of men with PTSD concomitantly misuse alcohol. In one study, men with PTSD reported an earlier age of onset of alcohol dependence, greater alcohol use intensity and craving, and more severe legal problems due to alcohol use. In the same study, PTSD more often preceded alcohol dependence in women than men and women were more likely to test positive for cocaine upon entering treatment.[17] Use of analgesic medications (opiate and non-opiate) may be raised among individuals with PTSD.[18]
Primary care and mental health providers can efficiently screen for PTSD using readily available self-administered tests. This should become standard of care as one study found that nearly half (48%) of the patients in general medical practices with PTSD were receiving no mental health treatment. One primary reason for this lack of treatment was providers not recognizing the diagnosis and recommending treatment.[22] Mental health providers who do not ask about trauma may also miss the key role that PTSD plays in their patient’s symptoms.
There are a number of self-report scales that can be used for screening or management:[23, 24, 25]
There are no lab studies that are currently recommended for diagnosing PTSD, but they may be helpful in assessing for the substance use disorders, which commonly accompany PTSD.
Cortisol levels may be decreased, while norepinephrine and CRF levels may be elevated; however, these findings are currently used only for research.
While there are some consistent anatomical and functional studies in individuals with PTSD such as small hippocampi, decreased corpus collosum, decreased prefrontal cortex, increased reactivity in the amygdala, and decreased activity in the prefrontal cortex, these are currently used only for research.
Although increased arousal is not a required criterion for diagnosis, it might be measurable through studies of autonomic functioning (e.g., heart rate monitoring, electromyography, sweat gland activity).
Increased heart rate shortly after the traumatic event indicates an increased risk of PTSD.
Secondary prevention consists of interventions designed to decrease the rate of PTSD in individuals exposed to traumatic events.
While no definitive studies exist, it is commonly believed that Psychological First Aid (PFA) may decrease rates of PTSD following a natural disaster or mass casualty situation. PFA includes emotional support, decreasing stress by reassuring the victim that shelter, food, and access to loved ones is guaranteed. Helping the person find a tolerable meaning for the trauma, reducing ideas leading to shame or guilt, avoiding invalidating comments such as "it's not that bad," and reassuring the victim that their strong emotional reaction is normal and does not mean they are weak or will forever feel this way can all be helpful.
Controlled trials have not found that single individual or group debriefings done in the immediate aftermath of traumas have been successful in preventing the development of PTSD. They also risk flooding victims. Pressuring a victim to participate can retraumatize them. Group treatment of trauma victims runs the risk of victims becoming worse as a result of flooding from hearing the stories of other members. Group treatment for PTSD must have very careful selection of group members to avoid this. Forcing victims to speak about the event, as has happened through required debriefing sessions, can be very harmful.
Brief cognitive-behavioral therapy (CBT) started within a few weeks of a traumatic event has been shown to decrease the rate of subsequent PTSD. Brief CBT appears to have the biggest impact in patients who have the most symptoms.
Attempts to decrease the formation of PTSD through pharmacology continues to be studied. Aggressive pain control is important to avoid increasing the trauma to the individual. Hydrocortisone has been shown to be effective. Individuals with low cortisol levels at the time of the trauma are at greater risk for the development of PTSD. Low cortisol levels lead to increased production of CRF, which increases norepinephrine release by the anterior cingulate. Some research has shown that propranolol given in the first hours after the traumatic event leads to reduced hyperarousal in the future. One study found that PTSD patients who actively recalled their traumatic event under the influence of propranolol showed a substantial decrease in symptom ratings on the Clinician-Administered PTSD Scale (CAPS) and the patient-rated PTSD Checklist–Specific (PCL-S) measures compared with patients who received placebo.[26] Trials of escitalopram, temazepam, and gabapentin have been unsuccessful in preventing PTSD following trauma. Benzodiazepines appear to be harmful.
High levels of emotional support and help with basic needs for shelter, food, clothing, and economic issues likely decrease the risk of PTSD.
Trauma-focused CBT and eye movement desensitization and reprocessing (EMDR) have been shown to be most effective in treating patients with PTSD.[27, 28, 29, 30, 31, 32, 33, 34]
Studies have suggested that even a single CBT session for sleep abnormalities can significantly improve daytime PTSD symptoms, as can pharmacologic treatments for sleep abnormalities.[35, 36]
In 2013, the World Health Organization (WHO) issued new clinical protocols and guidelines for addressing the mental health consequences of PTSD, acute stress, and bereavement. The new protocols allow primary healthcare workers to offer basic psychosocial support to refugees as well as people exposed to trauma or loss in other situations. Types of support offered may include Psychological First Aid, stress management, and helping affected people to identify and strengthen positive coping methods and social supports. Referral for advanced treatments such as CBT or EMDR should also be considered. Benzodiazepine use for the reduction of acute traumatic stress symptoms or sleep problems in the first month after a potentially traumatic event is not recommended.[37, 38]
Psychotherapy
Trauma-focused psychotherapies appear to be effective treatment for PTSD. A systematic review and meta-analysis of 55 clinical trials found that evidence-based trauma-focused psychotherapy (TFP) outperformed medications when looking at pre-/post-treatment symptoms and at 9-month follow-up. In this meta-analysis, TFP included trauma-focused CBT, prolonged exposure, cognitive processing therapy, eye movement desensitization and reprocessing (EMDR), and imaginal exposure. There is limited data supporting more generalized CBT approaches such as stress inoculation training and relaxation training.[27, 28, 38, 31, 32, 33, 34]
There are ongoing efforts to assess variations of psychotherapy and psychotherapies that target specific symptoms such as insomnia. A trial study of service members with PTSD caused by the traumatic events of September 11, 2001, or by Operation Iraqi Freedom, found that self-managed, Internet-based CBT led to a greater reduction in PTSD symptoms than did Internet-based supportive counseling.[39] Studies have suggested that even a single CBT session for sleep abnormalities can significantly improve daytime PTSD symptoms.[35, 36]
Trauma-focused CBT is effective in treating PTSD in children and adolescents. There is insufficient evidence, however, to definitively compare one form of psychotherapy to another.[32] The most recent research says therapy shortens the course of those who will recover but does not change the long-term course.[40]
Other research suggests that adding 3,4-methylenedioxymethamphetamine (MDMA), also known as ecstasy, to intensive psychotherapy can significantly mitigate symptoms of PTSD. According to results of an FDA-regulated phase 2 trial of 28 chronic PTSD sufferers, 43% of patients no longer met criteria for PTSD after one month of MDMA-assisted psychotherapy, and 76% of participants no longer had PTSD 12 months after MDMA-assisted psychotherapy.[41]
Psychopharmacology
Recommendations for pharmacological treatment vary depending on the source. The United Kingdom’s National Institute for Health and Care Excellence (NICE) and the World Health Organization (WHO) do not recommend any medications as first-line treatment for PTSD. The American Psychiatric Association and the US Department of Veterans Affairs and Department of Defense Clinical Practice Guidelines both recommend antidepressants (particularly SSRIs) as first-line treatment for PTSD. Both organizations also support the use of prazosin for trauma-related nightmares and insomnia. Benzodiazepine use for the reduction of acute traumatic stress symptoms or sleep problems after a potentially traumatic event is not recommended.[37, 38] Although benzodiazepines may be popular with patients and lead to a transient decrease in anxiety symptoms, research indicates that they not only are not effective, but may prolong the course of PTSD.
Inpatient care may be necessary if the patient becomes an acute danger to themselves or others. Individuals with severe PTSD from childhood abuse may need inpatient care to help learn emotional regulation and then treat the PTSD.
Active treatment should occur until symptoms have abated. In addition to monitoring symptoms and social and occupational functioning, providers should continue to assess for the emergence of suicidal ideation or substance abuse. Some traumas (such as childhood sexual abuse) may result in delayed exacerbations as individuals reach developmental milestones such as marriage or having children.
Mental health providers who encounter individuals with PTSD need to assess for the common comorbidities and may have to consult other clinicians in order to provide comprehensive care. Providers who are not trained in the specific trauma-focused psychotherapies should refer patients to those who are competent in them. General psychiatrists and other mental health providers may need to consult child and adolescent psychiatrists and psychologists when encountering younger victims of trauma.
It is important for people with PTSD to try to stay active lest their lives become increasingly restricted and things they fear increase.
While a large number of medications have been tried, few have been shown to have any efficacy. The SSRIs and SNRIs are generally the first-line medications for adults, but only sertraline and paroxetine have FDA approval. Their efficacy in children and adolescents is not proven. Moreover, they have significant side effects. They carry Black Box warnings for suicidal ideation. Benzodiazepines increase the risk of PTSD developing.[42, 43, 44, 45, 33, 46]
Agitation is best treated with clonidine and guanfacine.
Some research has shown that propranolol given in the first hours after the traumatic event leads to reduced hyperarousal in the future. One study found that PTSD patients who actively recalled their traumatic event under the influence of propranolol showed a substantial decrease in symptom ratings on the Clinician-Administered PTSD Scale (CAPS) and the patient-rated PTSD Checklist–Specific (PCL-S) measures compared with patients who received placebo.[26]
Insomnia is a common problem for patients with PTSD. It may be treated though reinforcing sleep hygiene and CBT. Clonidine and prazosin may be helpful. Prazosin decreases trauma-related nightmares.[36] Trazodone may be helpful.
Antipsychotics and anticonvulsants have been tried. One study shows that adding risperidone to standard antidepressant therapy significantly improves outcomes in patients with PTSD without causing additional adverse effects. A meta-analysis of almost 400 patients showed that those who received risperidone as an add-on treatment not only experienced significant improvements in overall and key aspects of PTSD symptoms but also demonstrated significant reductions in anxiety scores compared to those who received placebo.[47]
There is a huge placebo effect for medication. You are likely to find benefit with whatever you give, but it is probably placebo effect.
Clinical Context: Sertraline is an SSRI that is FDA approved for the treatment of PTSD, panic disorder, social anxiety, and obsessive-compulsive disorder. It may be particularly useful in women who have experienced sexual or physical assaults.
Clinical Context: Paroxetine is FDA approved to treat PTSD. It is used to reduce symptom severity of PTSD. It is a potent, selective inhibitor of neuronal serotonin reuptake. It also has a weak effect on norepinephrine and dopamine neuronal reuptake. It is also FDA approved for panic disorder, depression, social anxiety disorder, and obsessive-compulsive disorder.
Clinical Context: Fluoxetine selectively inhibits presynaptic serotonin reuptake with minimal or no effect on the reuptake of norepinephrine or dopamine. SSRIs such as fluoxetine have less sedation, cardiovascular, and anticholinergic effects than the tricyclic antidepressants (TCAs). Studies have shown this drug to be superior for measures of PTSD severity, disability, and high end-state function.
The selective serotonin reuptake inhibitors (SSRIs) work by blocking the reuptake of serotonin. SSRIs such sertraline (Zoloft) and paroxetine (Paxil) have been FDA approved to treat PTSD as well as other disorders.
Clinical Context: Propranolol is a nonselective beta-adrenergic receptor blocking agent. It has been found to relieve exaggerated startle response, explosiveness, nightmares, and intrusive reexperiencing in some patients with PTSD. Propranolol has not been FDA approved for these indications.
Beta-blockers such as propranolol are useful in controlling some symptoms of PTSD caused by hyperarousal. A pilot study revealed propranolol is effective for decreasing physiological signs of hyperarousal for up to 1 week when used shortly after patients with PTSD reexperience their traumatic event.[48] Ideally, propranolol is to be used within 6 hours of the initial traumatic event, well before a diagnosis of PTSD is made. Larger randomized, placebo-controlled studies are warranted to confirm these findings.
Clinical Context: Prazosin is an alpha-1 adrenergic blocker that is indicated for hypertension. Studies indicate that a nighttime dose of prazosin (10-15 mg) decreases nightmares and sleep disturbances in combat veterans with PTSD and increases normal dreaming patterns. Additional pilot trials have suggested that a midmorning dose of prazosin also helps to decrease daytime PTSD symptoms in civilian and military patients. However, larger, randomized, placebo-controlled trials are needed to confirm these results.
Novel pilot studies in combat veterans suggest alpha-1 antagonists have efficacy on the sleep-associated symptoms of PTSD. Alpha-1 antagonists have not been FDA approved for this indication.
Clinical Context: Clonidine is a central alpha-adrenergic agonist that is commonly used as an antihypertensive agent. It stimulates alpha2-adrenoreceptors in the brain stem and activates an inhibitory neuron, resulting in a decrease in vasomotor tone and heart rate. Clonidine may have potential effects on the hyperarousal symptoms of PTSD. It may also help in patients experiencing nightmares.
Agents in this class may decrease vasomotor tone and heart rate by stimulating alpha2-adrenoreceptors in the brain stem and activating an inhibitory neuron.