Although the pathophysiology of posttraumatic stress disorder (PTSD) has not been fully established, as of today many interesting research findings have been accumulated.
Results of studies on the pathophysiological basis of PTSD
Specifically, studies using magnetic resonance imaging have shown that patients with PTSD have reduced volume of the hippocampus, left amygdala, and anterior cingulate cortex compared to controls.
Other results showed:
- increased levels of norepinephrine in the central nervous system with decreased regulation of central adrenergic receptors;
- chronically decreased levels of glucocorticoids with upregulation of their receptors (this may explain some data that such patients have a higher incidence of autoimmune diseases);
- hemispheric lateralization, in which there is a relative lack of function of the left hemisphere (this may be an explanation for the violation of the temporal reproduction of the sequence of traumatic events).
Researchers believe that genetics may contribute to a person’s susceptibility to PTSD due to interactions with environmental factors. Large-scale genetic studies demonstrate that PTSD is a highly polygenic phenotype that is likely to be influenced by thousands of loci across the genome.
An example of a potential gene-environment interaction may be the presence of one of four polymorphisms in the stress-related gene FKBP5, which is associated with an increased risk of developing PTSD in patients with a history of child abuse, but not in patients without a history of child abuse.
Previous exposure to trauma, possibly, increases the risk of developing PTSD following subsequent traumatic events. The mechanism by which this “sensitization” occurs is unclear. A study of victims of severe accidents, who were healthy before the injury, found that their frequency of developing PTSD was low.
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