PTSD 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 or adults may develop PTSD symptoms by experiencing bullying or mobbing.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
PTSD symptoms may result when a traumatic event causes an overactive 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
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
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
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 conflicts. 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.Further animal and clinical
research into the amygdala and fear conditioning may suggest additional treatments
for the condition.
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
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.