Post-traumatic Stress Disorder (PTSD)

Introduction

Post-traumatic stress disorder (PTSD) is a potentially debilitating anxiety disorder related to exposure to severe psychological trauma. PTSD first appeared in the Diagnostic and Statistical Manual of Psychiatric Disorders (DSM-III) in 1980, arising from studies of the Vietnam war and civilian victims of disasters. The disorder alone in psychiatry requires an external stimulus, the traumatic experience, resulting in many symptoms. Important traumatic events causing PTSD include war, violent personal assault, being taken hostage or kidnapped, confinement as a prisoner of war, terrorist attack, or severe car accidents.

Based on its duration, PTSD can be categorized into two types of acute and chronic PTSD: if symptoms persist for less than three months, it is termed acute PTSD; otherwise, it is called chronic PTSD. There is also delayed-onset PTSD, which refers to the disease onset at least six months after the traumatic event. After experiencing a trauma, an individual reaction may often have a complex cause. Individual, societal, and contextual conditions all contribute to emotional problems. The likelihood of developing PTSD also varies according to gender, age, the severity of the injury, prior victimization, and previous mental illness.

Comorbidity of PTSD and Depression

PTSD is comorbid with many other psychiatric disorders. Individuals diagnosed with comorbid PTSD and depression may suffer from a particular psychobiological condition termed post-traumatic mood disorder. This condition results from trauma have features of both disorders and are more severe than PTSD alone or depression alone.

Fig.1 The hypothalamic-pituitary-adrenal axis is the major response system for stress. (Sherin, 2011)

Genetic Risk Factors for PTSD

Genetically determined variations in brain function may mediate the pathological response to trauma and the vulnerability to the effects of stress. Multiple reports suggest that genetic factors are associated with susceptibility to PTSD. One study has linked a polymorphism in the DA transporter gene to PTSD risk. In this study, PTSD patients were found to have an excess of the SLC6A39 repeat allele. This finding suggests that genetically determined features of DA transmission may contribute to the development of PTSD among trauma survivors. Genetic variation of the glucocorticoid receptor cochaperone protein, FKBP5, moderates the risk of developing PTSD about childhood abuse. The FKBP5 genotype can enhance glucocorticoid receptor sensitivity.

Inflammation in PTSD

Many studies review for alteration in proinflammatory cytokines in association with PTSD. For instance, alteration in proinflammatory cytokines, including IL-6, due to psychosocial stress may disrupt the relationship between proinflammatory cytokines and glucocorticoid receptors. These alterations further reinforce the related clinical symptoms of PTSD, such as sustained fear and anxiety. Further research investigating the pathogenesis of PTSD through a multi-level approach of inflammatory responses, clinical symptoms, and brain structural and functional changes can help determine the detailed underlying pathway of PTSD and open novel strategies of assessment and intervention for the disorder.

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Reference

1. Sherin, J. E.; Nemeroff, C. B. Post-traumatic stress disorder: the neurobiological impact of psychological trauma. Dialogues in clinical neuroscience. 2011, 13(3), 263.