Challenges of post-traumatic stress disorder (PTSD) in Iraq: biochemical network and methodologies. A brief review

Abstract

Abstract Post-traumatic stress disorder (PTSD) is a multifaceted syndrome due to its complex pathophysiology. Signals of illness include alterations in genes, proteins, cells, tissues, and organism-level physiological modifications. Specificity of sensitivity to PTSD suggests that response to trauma depend on gender and type of adverse event being experienced. Individuals diagnosed with PTSD represent a heterogeneous group, as evidenced by differences in symptoms, course, and response to treatment. It is clear that the biochemical mechanisms involved in PTSD need to be elucidated to identify specific biomarkers. A brief review of the recent literature in Pubmed was made to explore the major biochemical mechanisms involved in PTSD and the methodologies applied in the assessment of the disease. PTSD shows pre-exposure vulnerability factors in addition to trauma-induced alterations. The disease was found to be associated with dysfunctions of the hypothalamic–pituitary–adrenal axis (HPA) and hypothalamus–pituitary–thyroid axis. Sympathetic nervous system (SNS) activity play a role in PTSD by releasing norepinephrine and epinephrine. Cortisol release from the adrenal cortex amplifies the SNS response. Cortisol levels in PTSD patients, especially women, are later reduced by a negative feedback mechanism which contributes to neuroendocrine alterations and promotes structural changes in the brain leading to PTSD. Gender differences in normal HPA responsiveness may be due to an increased vulnerability in women to PTSD. Serotonin and dopamine levels were found to be abnormal in the presence of PTSD. Mechanisms such as the induction of neuroinflammation and alterations of mitochondrial energy processing were also associated with PTSD.