Post traumatic stress disorder pathophysiology: Difference between revisions
Sapan Patel (talk | contribs) |
Sapan Patel (talk | contribs) No edit summary |
||
| Line 1: | Line 1: | ||
__NOTOC__ | __NOTOC__ | ||
{{ Post traumatic stress disorder}} | {{Post traumatic stress disorder}} | ||
{{CMG}} | {{CMG}} | ||
Revision as of 19:38, 17 April 2013
|
Post traumatic stress disorder Microchapters |
|
Differentiating Post Traumatic Stress Disorder from other Diseases |
|---|
|
Diagnosis |
|
Treatment |
|
Case Studies |
|
Post traumatic stress disorder pathophysiology On the Web |
|
American Roentgen Ray Society Images of Post traumatic stress disorder pathophysiology |
|
Directions to Hospitals Treating Post traumatic stress disorder |
|
Risk calculators and risk factors for Post traumatic stress disorder pathophysiology |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Neurochemistry
PTSD displays biochemical changes in the brain and body, which are different from other psychiatric disorders such as major depression.
In PTSD patients, the dexamethasone cortisol suppression is strong, while it is weak in patients with major depression. In most PTSD patients the urine secretion of cortisol is low, at the same time as the catecholamine secretion is high, and the norepinephrine/cortisol ratio is increased. Brain catecholamine levels are low, and corticotropin-releasing factor (CRF) concentrations are high. There is also an increased sensitivity of the hypothalamic-pituitary-adrenal (HPA) axis, with a strong negative feedback of cortisol, due to a generally increased sensitivity of cortisol receptors.[1]
In addition to biochemical changes, PTSD also involves changes in the brain itself. Combat veterans of the Vietnam war with PTSD showed an 8% reduction in the volume of their hippocampus in comparison with veterans who suffered no such symptoms.[2]
Cortisol
The association of PTSD with cortisol levels is controversial within the medical community.
Some researchers have associated the response to stress in PTSD with long-term high levels of norepinephrine, at the same time as cortisol levels are low, a pattern associated with facilitated learning in animals. Translating this reaction to human conditions gives a pathophysiological explanation for PTSD by a maladaptive learning pathway to fear response.[3] With this deduction follows that the clinical picture of hyperreactivity and hyperresponsiveness in PTSD is consistent with the sensitive HPA-axis.
Low cortisol levels are also discussed as a possible pre-existing condition that neurochemically predisposes a person to PTSD. Swedish United Nation soldiers serving in Bosnia 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.[4]
There is considerable controversy within the medical community regarding the neurobiology of PTSD. A review of existing studies on this subject showed no clear relation between cortisol levels and PTSD. For example, only a slight majority of studies have found a decrease in cortisol levels; many others have found no effect or even an increase.[5]
Neuroanatomy
In animal research as well as 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. Further animal and clinical research into the amygdala and fear conditioning may suggest additional treatments for the condition.
References
- ↑ Yehuda, 2001
- ↑ July issue of the American Journal of Psychology
- ↑ Yehuda 2002
- ↑ Aardal-Eriksson 2001
- ↑ Lindley SE, Carlson EB, Benoit M (2004). "Basal and dexamethasone suppressed salivary cortisol concentrations in a community sample of patients with posttraumatic stress disorder". Biol. Psychiatry. 55 (9): 940–5. doi:10.1016/j.biopsych.2003.12.021. PMID 15110738.