Post Traumatic Stress Disorder
Posttraumatic stress disorder (also known as post-traumatic stress disorder or 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.
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.
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.
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 of PTSD
Psychological trauma PTSD
is believed to be caused by either physical trauma or psychological trauma, or more frequently a combination of both. According to Atkinson et al. (2000) PTSD is more likely to be caused by physical or psychological trauma caused by humans such as rape, war, or terrorist attack than trauma caused by natural disasters. 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. 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.
Neuroendocrinology 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 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.[citation needed]
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 disorderThree 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. 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. 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.