Posttraumatic Stress Disorder

Posttraumatic Stress Disorder

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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:

Persistent re-experiencing of the event: intrusive thoughts related to the traumatic event, nightmares or distressing dreams, persistent or recurrent involuntary memories, dissociation (including flashbacks) and intense, negative emotional or physiological reaction on exposure to reminders (traumatic triggers)

Avoidance of traumatic triggers or of thinking/talking about the experience

Negative alterations in cognition and mood: inability to recall important aspects of the trauma; persistent negative beliefs and expectations about oneself, others, and the world; inappropriate blaming of oneself for the trauma; exaggerated negative beliefs about the consequences of the trauma; persistent negative emotional state (sadness, horror, guilt); a paucity of positive emotional experiences; loss of interest or participation in important activities; and detachment from people.

Increased arousal or reactivity: irritability, problems with sleep or concentration, increased startle reaction, increased vigilance for potential danger, self-harming acts, or recklessness

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:

Directly experiencing the traumatic event(s)

Witnessing, in person, the event(s) as it occurred to others

Learning that the traumatic event(s) occurred to a close family member or friend

Experiencing repeated or extreme exposure to aversive details of the traumatic event(s); this does not apply to exposure through media such as television, movies, or pictures

B) The traumatic event is persistently re-experienced:

Nightmares

Intrusive thoughts of the traumatic event

Flashbacks

Marked emotional distress when exposed to traumatic reminders

Strong physiologic reaction when exposed to traumatic reminders

Children may re-experience the event through repetitive play.

C) Avoidance in one of two ways:

Avoidance of thoughts, feelings, or conversations associated with the event

Avoidance of people, places, or activities that may trigger recollections of the event

D) Negative alterations in cognition and mood.  Two of the following:

Inability to remember an important aspect of the event(s)

Persistent and exaggerated negative beliefs about oneself, others, or the world

Persistent distorted cognitions about the cause or consequences of the event(s)

Persistent negative emotional state

Markedly diminished interest or participation in significant activities

Feelings of detachment or estrangement from others

Persistent inability to experience positive emotions

E) Hyperarrousal: Two of the following:

Irritable behavior and angry outbursts

Reckless or self-destructive behavior

Hypervigilance

Exaggerated startle response

Concentration problems

Sleep disturbance

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.

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T Allen Gore, MD, MBA, CMCM, DFAPA Volunteer Associate Professor, Department of Psychiatry, Howard University School of Medicine; Senior Psychiatrist and Director, Medical Education, Comprehensive Psychiatric Emergency Program, District of Columbia Department of Mental Health

T Allen Gore, MD, MBA, CMCM, DFAPA is a member of the following medical societies: American Psychiatric Association, National Association of Managed Care Physicians, National Medical Association

Disclosure: Serve(d) as a speaker or a member of a speakers bureau for: Alkermes, Inc.

Joel Z Lucas, MD Senior Medical Writer, Reckitt Benckiser Pharmaceuticals, Inc

Joel Z Lucas, MD is a member of the following medical societies: American College of Physicians, American Medical Student Association/Foundation, Student National Medical Association

Disclosure: Received salary from Johnson & Johnson for employment.

Roy H Lubit, MD, PhD Private Practice

Roy H Lubit, MD, PhD is a member of the following medical societies: American Academy of Child and Adolescent Psychiatry

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

David Bienenfeld, MD Professor, Departments of Psychiatry and Geriatric Medicine, Wright State University, Boonshoft School of Medicine

David Bienenfeld, MD is a member of the following medical societies: American Medical Association, American Psychiatric Association, Association for Academic Psychiatry

Disclosure: Nothing to disclose.

The authors would like to thank all colleagues and students who contributed to this article. We are especially grateful to the following individuals:

Georgianna M Richards-Reid, MD, Staff Physician, Department of Neurology, Howard University Hospital, Howard University College of Medicine

Zachary Osborne, MD; Ross University School of Medicine

Bobbi Adams, BS; University of Alabama

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