Posttraumatic stress disorder (commonly referred to by its acronym, PTSD ) is a severe anxiety disorder that can develop after exposure to any event which results in psychological trauma. This event may involve the threat of death to oneself or to someone else, or to one's own or someone else's physical, sexual, or psychological integrity, overwhelming the individual's psychological defenses.
PTSD is a less frequent and more enduring consequence of psychological trauma than the more frequently seen acute stress response. PTSD has also been recognized in the past as railway spine, stress syndrome, shell shock, battle fatigue, traumatic war neurosis, or post-traumatic stress syndrome.
Diagnostic symptoms include re-experiencing original trauma(s), by means of flashbacks or nightmares; avoidance of stimuli associated with the trauma; and increased arousal, such as difficulty falling or staying asleep, anger, and hypervigilance. Formal diagnostic criteria (both DSM-IV and ICD-9) require that the symptoms last more than one month and cause significant impairment in social, occupational, or other important areas of functioning (e.g. problems with work and/or relationships).
Signs and symptoms
PTSD can cause many symptoms. These symptoms can be grouped into three categories:
Re-experiencing
- Flashbacks—reliving the trauma over and over, including physical symptoms like a racing heart or sweating
- Bad dreams
- Frightening thoughts.
Re-experiencing symptoms may cause problems in a person’s everyday routine. They can start from the person’s own thoughts and feelings. Words, objects, or situations that are reminders of the event can also trigger re-experiencing.
Avoidance
- Staying away from places, events, or objects that are reminders of the experience
- Feeling emotionally numb
- Feeling strong guilt, depression, or worry
- Losing interest in activities that were enjoyable in the past
- Having trouble remembering the dangerous event.
Things that remind a person of the traumatic event can trigger avoidance symptoms. These symptoms may cause a person to change his or her personal routine. For example, after a bad car accident, a person who usually drives may avoid driving or riding in a car.
Hyperarousal
- Being easily startled
- Feeling tense or “on edge”
- Having difficulty sleeping, and/or having angry outbursts.
Hyperarousal symptoms are usually constant, instead of being triggered by things that remind one of the traumatic event. They can make the person feel stressed and angry. These symptoms may make it hard to do daily tasks, such as sleeping, eating, or concentrating.
It’s natural to have some of these symptoms after a dangerous event. Sometimes people have very serious symptoms that go away after a few weeks. This is called acute stress disorder, or ASD. When the symptoms last more than a few weeks and become an ongoing problem, they might be PTSD. Some people with PTSD don’t show any symptoms for weeks or months.
Deficient extinction capacity
People with PTSD have deficient extinction capacity relative to those that have been exposed to trauma but who have not developed PTSD. This reduced extinction capacity links to reduced activation during extinction in the hippocampus and bilateral ventromedial prefrontal cortex.
Causes
Psychological trauma
Main article: Psychological traumaPTSD is believed to be caused by either physical trauma or psychological trauma, or more frequently a combination of both. Possible sources of trauma include experiencing or witnessing childhood or adult physical, emotional or sexual abuse. In addition, experiencing or witnessing an event perceived as life-threatening such as physical assault, adult experiences of sexual assault, accidents, drug addiction, illnesses, medical complications, or employment in occupations exposed to war (such as soldiers) or disaster (such as emergency service workers).
Traumatic events that may cause PTSD symptoms to develop include violent assault, kidnapping, sexual assault, torture, being a hostage, prisoner of war or concentration camp victim, experiencing a disaster, violent automobile accidents or getting a diagnosis of a life-threatening illness. Children may develop PTSD symptoms by experiencing bullying or sexually traumatic events like age-inappropriate sexual experiences.
Witnessing traumatic experiences or learning about these experiences may also cause the development of PTSD symptoms.
A preliminary study found that mutations in a stress-related gene interact with child abuse to increase the risk of PTSD in adults.
Neuroendocrinology
PTSD displays 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.
In addition, most people with PTSD also show a low secretion of cortisol and high secretion of catecholamines in urine, with a norepinephrine/cortisol ratio consequently higher than comparable non-diagnosed individuals. 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.
Brain catecholamine levels are low, and corticotropin-releasing factor (CRF) concentrations are high. Together, these findings suggest abnormality in the hypothalamic-pituitary-adrenal (HPA) axis.
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. Some researchers have associated the response to stress in PTSD with long-term exposure to high levels of norepinephrine and low levels of cortisol, a pattern associated with improved learning in animals.
Translating this reaction to human conditions gives a pathophysiological explanation for PTSD by a maladaptive learning pathway to fear response through a hypersensitive, hyperreactive and hyperresponsive HPA axis.
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. 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.
However, there is considerable controversy within the medical community regarding the neurobiology of PTSD. A review of existing studies on this subject showed no clear relationship between cortisol levels and PTSD. Only a slight majority have found a decrease in cortisol levels while others have found no effect or even an increase.
Neuroanatomy
In addition to biochemical changes, PTSD also involves changes in brain morphology. In a study by Gurvits et al., Combat veterans of the Vietnam war with PTSD showed a 20% reduction in the volume of their hippocampus compared with veterans who suffered no such symptoms.
In human studies, the amygdala has been shown to be strongly involved in the formation of emotional memories, especially fear-related memories. Neuroimaging studies in humans have revealed both morphological and functional aspects of PTSD.
The amygdalocentric model of PTSD proposes that it is associated with hyperarousal of the amygdala and insufficient top-down control by the medial prefrontal cortex and the hippocampus particularly during extinction. Further animal and clinical research into the amygdala and fear conditioning may suggest additional treatments for the condition.
Genetics
There is evidence that susceptibility to PTSD is hereditary. 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 having PTSD compared to twins that were dizygotic (non-identical twins).
Recently, it has been found that several single nucleotide polymorphisms (SNPs) in FK506 binding protein 5 (FKBP5) interact with childhood trauma to predict severity of adult PTSD. These findings suggest that individuals with these SNPs who are abused as children are more susceptible to PTSD as adults.
This is particularly interesting given that FKBP5 SNPs have previously been associated with peritraumatic dissociation (that is, dissociation at the time of the trauma), which has itself been shown to be predictive of PTSD. Furthermore, FKBP5 may be less expressed in those with current PTSD.
PTSD has also been interpreted as a syndrome of deficient extinction ability.
Risk and protective factors for PTSD development
See also: Psychological resilienceAlthough most people (50-90%) encounter trauma over a lifetime, only about 8% develop full PTSD. Vulnerability to PTSD presumably stems from an interaction of biological diathesis, early childhood developmental experiences, and trauma severity.
Predic
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