Post-traumatic stress disorder (PTSD) is a distressing illness that can pose a serious debilitation if not promptly and adequately treated. It is habitually followed by substantial comorbidities including depression, substance abuse, and elevated suicidal risk; the lifetime prevalence of PTSD among adult American is 6.8% with women having high proportion likelihood as high as twice of men to suffer from PTSD (Ponomareva & Ressler, 2021). Both its diagnosis and treatment can reveal to be challenging. The aim purpose of this assignment is to explain the neurobiological basis for PTSD illness, discuss its diagnosis according to Diagnostic and Statistical Manual of Mental Disorders fifth edition (DSM-5) and its treatment approaches. Neurobiological Basis for Post-traumatic Stress Disorder Illness The perception of stressful event and the ability to cope with it, also referred to as perceived stress, has been shown to be an essential factor for physical and mental outcomes including PTSD. Growing evidence has suggested that stress may be considered as a specific neurobiological factor in the PTSD genesis. Recent studies have highlighted the implication of alterations in functional connectivity of important brain regions including connectivity between the prefrontal cortex, the amygdala and its complexes, the insula, and the periaqueductal gray (Lanius et al., 2018). Other studies have acknowledged association of limbic system and prefrontal cortex structures including medial prefrontal cortex, orbitofrontal cortex with stress; some of the limbic system include hippocampus and amygdala (Guo et la., 2023). The hippocampus is believed to be the central region of brain that regulates the release of stress as it contains considerable number of receptors for stress hormones including glucocorticoids; the regulation is done through the hormones’ action on the hypothalamic-pituitary- adrenal (HPA) axis that promotes adaptation to stressors (Guo et la., 2023). Recent studies propose that multiple genomic mechanisms, including pathways involved in glucocorticoid signaling, HPA axis regulation, immune response, and epigenetic regulation are involved in the pathogenesis of the PTSD (Ponomareva & Ressler, 2021)
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