Posttraumatic stress disorder (PTSD) is a severe anxiety
disorder that can develop after exposure to any event that 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 ability to cope. As an effect of psychological trauma, PTSD is less frequent
and more enduring than the more commonly seen acute stress response. Diagnostic symptoms
for PTSD include re-experiencing the original trauma(s) through 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-TR and
ICD-10)
require that the symptoms last more than one month and cause significant
impairment in social, occupational, or other important areas of functioning.
Classification
Posttraumatic stress disorder is classified as an anxiety
disorder, characterized by aversive anxiety-related experiences, behaviors,
and physiological
responses that develop after exposure to a psychologically traumatic event
(sometimes months after). Its features persist for longer than 30 days, which
distinguishes it from the briefer acute stress disorder. These persisting
posttraumatic stress symptoms cause significant disruptions of one or more
important areas of life function. It has three sub-forms: acute, chronic, and
delayed-onset.
Causes
Psychological
trauma
PTSD is believed to be caused by experiencing any
of a wide range of events which produces intense negative feelings of
"fear, helplessness or horror" in the observer or participant.
Sources of such feelings may include (but are not limited to):
- experiencing
or witnessing childhood or adult physical,
emotional, or sexual
abuse;
- experiencing
or witnessing physical assault, adult experiences of sexual
assault, accidents, drug
addiction, illnesses, medical complications;
- employment
in occupations exposed to war (such as soldiers) or disaster (such as emergency service workers);
- getting a
diagnosis of a life-threatening illness; or
Children or adults may develop PTSD symptoms by
experiencing bullying
or mobbing.
Approximately 25% of children exposed to family violence can experience PTSD.
Preliminary research suggests that child abuse may interact with
mutations in a stress-related gene to increase the risk of PTSD in adults.
Multiple studies show that parental PTSD and other
posttraumatic disturbances in parental psychological functioning can, despite a
traumatized parent's best efforts, interfere with their response to their child
as well as their child's response to trauma. Parents with
violence-related PTSD may, for example, inadvertently expose their children to
developmentally inappropriate violent media due to their need to manage their
own emotional dysregulation. Clinical findings indicate that a failure to
provide adequate treatment to children after they suffer a traumatic
experience, depending on their vulnerability and the severity of the trauma,
will ultimately lead to PTSD symptoms in adulthood.
Evolutionary
psychology
Evolutionary psychology views different
types of fears and reactions caused by fears as adaptations
that may have been useful in the ancestral environment in order to avoid or
cope with various threats. Mammals generally display several defensive behaviors roughly
dependent on how close the threat is: avoidance, vigilant immobility,
withdrawal, aggressive defense, appeasement, and finally complete frozen
immobility (the last possibly to confuse a predator's attack reflex or to
simulate a dead and contaminated body). PTSD may correspond to and be caused by
overactivation of such fear circuits. Thus, PTSD avoidance behaviors may
correspond to mammal avoidance of and withdrawal from threats. Heightened
memory of past threats may increase avoidance of similar situations in the
future as well as be a prerequisite for analyzing the past threat and develop
better defensive behaviors if the threat should reoccur. PTSD hyperarousal may
correspond to vigilant immobility and aggressive defense. Complex post-traumatic stress
disorder (and phenomena such as the Stockholm syndrome) may in part correspond to
the appeasement stage and possibly the frozen immobility stage.
There may be evolutionary explanations for
differences in resilience to traumatic events. Thus, PTSD is rare following
traumatic fire which may be explained by events such as forest fires long being
part of the evolutionary history of mammals. On the other hand, PTSD is much
more common following modern warfare, which may be explained by modern warfare
being a new development and very unlike the quick inter-group raids that are
argued to have characterized the paleolithic.
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.
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 high, 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
Regions of the brain associated with
stress and posttraumatic stress disorder
Three areas of the brain whose 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 who 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.
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. 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.
Genetics
There is evidence that susceptibility to PTSD is
hereditary. For twin pairs exposed to combat in Vietnam
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. Another
recent study found a single SNP in a putative estrogen response element on ADCYAP1R1
(encodes pituitary adenylate cyclase-activating polypeptide type I receptor or
PAC1) to predict PTSD diagnosis and symptoms in females. Incidentally, this SNP
is also associated with fear discrimination. The study suggests that
perturbations in the PACAP-PAC1
pathway are involved in abnormal stress responses underlying PTSD.
Risk factors
Although 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.
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. 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 also make an
impact, and interpersonal traumas cause more problems than impersonal ones.
Military
experience
Schnurr, Lunney, and Sengupta identified risk
factors for the development of PTSD in Vietnam
veterans. Among those are:
- Hispanic
ethnicity, coming from an unstable family, being punished severely
during childhood, childhood asocial behavior, and depression as
pre-military factors
- War-zone
exposure, peritraumatic dissociation,
depression as military factors
- Recent
stressful life events, post-Vietnam
trauma, and depression as post-military factors
They also identified certain protective factors,
such as:
- Japanese-American ethnicity, high school
degree or college education, older age at entry to war, higher
socioeconomic status, and a more positive paternal relationship as
pre-military protective factors
- Social
support at homecoming and current social support as post-military factors.
Other research also indicates the protective effects of social support in
averting PTSD or facilitating recovery if it develops.
There may also be an attitudinal component; for
example, a soldier who believes that they will not sustain injuries may be more
likely to develop symptoms of PTSD than one who anticipates the possibility,
should either be wounded. Likewise, the later incidence of suicide among those
injured in home fires above those injured in fires in the workplace suggests
this possibility.
Foster care
In the Casey Family Northwest Alumni Study,
conducted in conjunction with researchers from the Harvard Medical School in Oregon and
Washington state, the rate of PTSD in adults who were in foster care
for one year between the ages of 14–18 was found to be higher than that of
combat veterans. Up to 25 percent of those in the study meet the diagnostic
criteria for PTSD as compared to 12–13 percent of Iraq
Dubner and Motta (1999) found that 60% of children
in foster care who had experienced sexual abuse had PTSD, and 42% of those who
had been physically abused met the PTSD criteria. PTSD was also found in 18% of
the children who were not abused. These children may have developed PTSD due to
witnessing violence in the home, or as a result of real or perceived parental
abandonment.
Diagnosis
Criteria
The diagnostic criteria for PTSD, stipulated in
the Diagnostic and
Statistical Manual of Mental Disorders IV (Text Revision) (DSM-IV-TR),
may be summarized as:
A: Exposure to a
traumatic event
This must have involved both (a) loss of
"physical integrity", or risk of serious injury or death, to self or
others, and (b) a response to the event that involved intense fear, horror, or
helplessness (or in children, the response must involve disorganized or
agitated behavior). (The DSM-IV-TR criterion differs substantially from the previous
DSM-III-R stressor criterion, which specified the traumatic event should be of
a type that would cause "significant symptoms of distress in almost
anyone," and that the event was "outside the range of usual human
experience.")
B: Persistent
re-experiencing
One or more of these must be present in the
victim: flashback memories, recurring
distressing dreams, subjective re-experiencing of the traumatic event(s), or
intense negative psychological or physiological response to any objective or
subjective reminder of the traumatic event(s).
C: Persistent
avoidance and emotional numbing
This involves a sufficient level of:
- avoidance
of stimuli associated with the trauma, such as certain thoughts or
feelings, or talking about the event(s);
- avoidance
of behaviors, places, or people that might lead to distressing memories;
- inability
to recall major parts of the trauma(s), or decreased involvement in
significant life activities;
- decreased
capacity (down to complete inability) to feel certain feelings;
- an
expectation that one's future will be somehow constrained in ways not
normal to other people.
D: Persistent
symptoms of increased arousal not present before
These are all physiological response issues, such
as difficulty falling or staying asleep, or problems with anger, concentration,
or hypervigilance.
E: Duration of
symptoms for more than 1 month
If all other
criteria are present, but 30 days have not elapsed, the individual is diagnosed
with Acute
stress disorder.
F: Significant impairment
The symptoms reported must lead to
"clinically significant distress or impairment" of major domains of
life activity, such as social relations, occupational activities, or other
"important areas of functioning".
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