Post traumatic stress disorder (PTSD)
Is an anxiety disorder that can develop after a person is exposed to one or more traumatic events, such as sexual assault, warfare, traffic collisions, terrorism or other threats on a person's life. Symptoms include disturbing recurring flashbacks, avoidance or numbing of memories of the event, and hyperarousal, continue for more than a month after the occurrence of a traumatic event.
Most people who have experienced a traumatizing event will not develop PTSD. People who experience assault-based trauma are more likely to develop PTSD, as opposed to people who experience non-assault based trauma such as witnessing trauma, accidents, and fire events. Children are less likely to experience PTSD after trauma than adults, especially if they are under ten years of age. War veterans are commonly at risk for PTSD. Medications including fluoxetine and paroxetine may improve symptoms a small amount. Most medications do not have enough evidence to support their use. It is unclear as of 2010 if medication and therapy together are better than either alone.
The term "posttraumatic stress disorder"
was coined in the late 1970s in large part due to diagnoses of US
military veterans of the Vietnam War. The concept of stress-induced
mental disorder was already known since at least the 19th century, and
had been referred to previously under various terms including "soldier's
heart", "shell shock" and "battle fatigue"
Classification
Posttraumatic
stress disorder is classified as an anxiety disorder in the DSM IV; the
characteristic symptoms are not present before exposure to the
violently traumatic event. In the typical case, the individual with PTSD
persistently avoids all thoughts and emotions, and discussion of the
stressor event and may experience amnesia for it. However, the event is
commonly relived by the individual through intrusive, recurrent
recollections, flashbacks, and nightmares. The characteristic symptoms
are considered acute if lasting less than three months, and chronic if
persisting three months or more, and with delayed onset if the symptoms
first occur after six months or some years later. PTSD is distinct from
the briefer acute stress disorder, and can cause clinical impairment in
significant areas of functioning
Risk factors
PTSD is
believed to be caused by the experience of a wide range of traumatic
events and, in particular if the trauma is extreme, can occur in persons
with no predisposing conditions. Persons considered at risk include,
for example, combat military personnel, victims of natural disasters,
concentration camp survivors, and victims of violent crime. Individuals
frequently experience "survivor's guilt" for remaining alive while
others died. Causes of the symptoms of PTSD are the experiencing or
witnessing of a stressor event involving death, serious injury or such
threat to the self or others in a situation in which the individual felt
intense fear, horror, or powerlessness. Persons employed in occupations
that expose them to violence (such as soldiers) or disasters (such as
emergency service workers) are also at risk.
Children or adults may develop PTSD symptoms by experiencing bullying. Several
biological indicators have been identified that are related to later
PTSD development. Heightened startle responses and a smaller hippocampal
volume have been identified as biomarkers for the risk of developing
PTSD. Additionally, one study found that soldiers whose leukocytes had
greater numbers of glucocorticoid receptors were more prone to
developing PTSD after experiencing trauma.
Genetics
Genetics of posttraumatic stress disorder
There
is evidence that susceptibility to PTSD is hereditary. Approximately
30% of the variance in PTSD is caused from genetics alone. 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).
There is evidence that those with a genetically smaller hippocampus are
more likely to develop PTSD following a traumatic event. 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.
Trauma
Most
people will experience at least one traumatizing event in their
lifetime. Men are more likely to experience a traumatic event, 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. Posttraumatic stress reactions have not been studied as well
in children and adolescents as adults. The rate of PTSD may be lower in
children than adults, but in the absence of therapy, symptoms may
continue for decades. 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, and much
lower below the age of 10 years. Predictor models have consistently
found that childhood trauma, chronic adversity, and familial stressors
increase risk for PTSD as well as risk for biological markers of risk
for PTSD after a traumatic event in adulthood. Peritraumatic
dissociation in children is a predictive indicator of the development of
PTSD later in life. This effect of childhood trauma, which is not
well-understood, may be a marker for both traumatic experiences and
attachment problems. Proximity to, duration of, and severity of the
trauma make an impact, and interpersonal traumas cause more problems
than impersonal ones.
Quasi-experimental studies have demonstrated a relationship between intrusive thoughts and intentional control responses such that suppression increases the frequency of unwanted intrusive thoughts. These results suggest that suppression of intrusive thoughts may be important in the development and maintenance of PTSD. Foster care, Adults who were in foster care as children have a higher rate of PTSD.
Domestic 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. There is a strong association between the development of
PTSD in mothers that experienced domestic violence during the perinatal
period of their pregnancy.
Military experience
Early
intervention appears to be a critical preventive measure. Studies have
shown that soldiers prepared for the potential of a traumatic experience
are more prepared to deal with the stress of a traumatic experience and
therefore less likely to develop PTSD. Among American troops in
Vietnam a greater portion of women experienced high levels of war-zone
stress compared to theater men—39.9 percent versus 23.5 percent. The key
to this fact is that the vast majority (6,250 or 83.3%) of the women
who served in the war zone were nurses who dealt almost daily with
death. Black veterans had nearly 2.5 fold the risk of developing war
zone-related PTSD as compared to white/other veterans. Hispanics had
more than three times the risk. But the most revealing fact, theater
veterans injured or wounded in combat had nearly four times the risk of
developing PTSD compared to those not injured/wounded according to two
key studies—the August 2014 National Vietnam Veterans Longitudinal Study
(NVVLS). Paired with the late 1980s National Vietnam Veterans
Readjustment Study (NVVRS). The long-term medical consequence of PTSD
among male veterans who served in the Vietnam War was that they were
almost twice as likely to die in the quarter of a century between the
two key studies than those who did not have PTSD. It was also found
those with PTSD were more likely to die of chronic conditions such as
cancer, nervous system disorders, and musculoskeletal problems. The
etiology of this relationship is not certain other than lingering stress
from combat such as nightmares, intrusive memories, and hyper-vigilance
are aggravating factors contributing to psychological and physiological
illnesses. The racial similarity between Hispanic and Vietnamese
soldiers, and the discrimination Hispanic soldiers faced from their own
military, made it difficult for Hispanic soldiers to dehumanize their
enemy. Hispanic veterans who reported experiencing racial discrimination
during their service displayed more symptoms of PTSD than Hispanic
veterans who did not.
PTSD is under-diagnosed in female veterans.
Sexual assault in the military is a leading cause for female soldiers
developing PTSD; a female soldier who is sexually assaulted while
serving in the military is nine times more likely to develop PTSD than a
female soldier who is not assaulted. A soldier's assailant may be her
colleague or superior officer, making it difficult for her to both
report the crime and to avoid interacting with her assailant again.
Until the Tailhook scandal drew attention to the problem, the role that
sexual assault in the military plays in female veterans developing PTSD
went largely unstudied.
Protective effects include social support,
which also helps with recovery if PTSD develops. For more aggravating
factors to recovery once home, see social alienation among returning war
veterans.
Drug and substance abuse
Drug abuse and alcohol abuse
commonly co-occur with PTSD. Recovery from posttraumatic stress disorder
or other anxiety disorders may be hindered, or the condition worsened,
by medication or substance overuse, abuse, or dependence; resolving
these problems can bring about a marked improvement in an individual's
mental health status and anxiety levels.
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. During 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, 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 high, and
corticotropin-releasing factor (CRF) concentrations are high. Together,
these findings suggest abnormality in the hypothalamic-pituitary-adrenal
(HPA) axis.
The HPA axis is responsible for coordinating the hormonal response to stress. 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.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. 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. Serotonin also contributes to the stabilization of glucocorticoid production.
Dopamine levels in a
person with PTSD can help contribute to the symptoms associated. Low
levels of dopamine can contribute to anhedonia, apathy, impaired
attention, and motor deficits. Increased levels of dopamine can cause
psychosis, agitation, and restlessness. Hyperresponsiveness in the
norepinephrine system can 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 that the experience, and
emotions the person is experiencing during a flashback are not
associated with the current environment.
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. However,
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
Neuroanatomy
Three
areas of the brain in which function may be altered in PTSD have been
identified: the prefrontal cortex, amygdala, and hippocampus. Much of
this research has utilised PTSD victims from the Vietnam War. For
example, a prospective study using the Vietnam Head Injury Study showed
that damage to the prefrontal cortex may actually be protective against
later development of PTSD. 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 having suffered no such
symptoms. This finding could not be replicated in chronic PTSD patients
traumatized at an air show plane crash in 1988 (Ramstein, Germany).
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. However, during high stress times the hippocampus, which is associated with the ability to place memories in the correct context of space and time, and with the ability to recall the memory, is suppressed. This suppression is hypothesized to be the cause of the flashbacks that often 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.
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 in particular during extinction. This is consistent with
an interpretation of PTSD as a syndrome of deficient extinction
ability. A study at the European Neuroscience Institute-Goettingen
(Germany) found that fear extinction-induced IGF2/IGFBP7 signalling
promotes the survival of 17–19-day-old newborn hippocampal neurons. This
suggests that therapeutic strategies that enhance IGF2 signalling and
adult neurogenesis might be suitable to treat diseases linked to
excessive fear memory such as PTSD. Further animal and clinical research
into the amygdala and fear conditioning may suggest additional
treatments for the condition.
The maintenance of the fear involved
with PTSD 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, which activates the LC-noradrenergic system, is
implicated in the over-consolidation of memories that occurs in the
aftermath of trauma. 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.
The LC-noradrenergic system has been hypothesized to mediate the over-consolidation of fear memory in PTSD. High levels of cortisol reduce noradrenergic activity, and because people with PTSD tend to have reduced levels of cortisol, it is proposed that individuals with PTSD fail to regulate the increased noradrenergic response to traumatic stress. It is thought that the intrusive memories and conditioned fear responses to associated triggers is a result of this response. Neuropeptide Y 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.
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.
Studies have also shown that PTSD patients show hypoactiviation or 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