YouTube. https://www.youtube.com/watch?v=RkSv_zPH-M4 Briefly explain the neurobiological basis for PTSD illness. Discuss the DSM-5-TR diagnostic criteria for PTSD and relate these criteria to the symptomology presented in the case study. Does the video case presentation provide sufficient information to derive a PTSD diagnosis? Justify your reasoning. Do you agree with the other diagnoses in the case presentation? Why or why not? Discuss one other psychotherapy treatment option for the client in this case study. Explain whether your treatment option is considered a “gold standard treatment” from a clinical practice guideline perspective, and why using gold standard, evidence-based treatments from clinical practice guidelines is important for psychiatric-mental health nurse practitioners.

Posttraumatic Stress Disorder (PTSD)

The Neurobiological Basis for PTSD Illness

The neurobiological basis for PTSD illness includes complex changes in the neuroendocrine and the neurochemical environment, as well as neuroanatomical changes. The neuroendocrine leading to the development of PTSD occur in the hypothalamic-pituitary-adrenal (HPA) axis. The HPA axis plays a central role in how individuals respond to stress. Exposure to or experiencing traumatic events, which are highly stressful events in an unexpected way, causes the hypothalamus to secrete corticotropin-releasing hormone (CRH), stimulating the release of adrenocorticotropin hormone (ACH) (Dunlop & Wong, 2019). ACH is responsible for stimulating the release of glucocorticoids, such as cortisol. As cortisol is responsible for the HPA’s negative feedback control and stress response, sustained cortisol exposure due to traumatic events heightens the HPA’s negative feedback sensitivity, high CRH and low ACH response to the CRH. Therefore, there is a dysregulation of glucocorticoid release, hence low levels of cortisol, which are associated with the development of PTSD (Rauch et al., 2020).

The changes in the neurochemical environment that occur due to exposure to traumatic events forming the basis for PTSD illness involve the dysregulation in neurotransmitter production such as serotonin and dopamine affect how the individual gets aroused and reacts to stress. There is a varying degree in the decrease or increase of the neurotransmitters responsible for reactivity to stress and anxiety during traumatic experiences. For instance, serotonin concentration decreases in the dorsal/median raphe, influencing the inability to regulate moods. With low levels of serotonin, the individual may become more aggressive, impulsive, more vigilant, with development of intrusive thoughts associated with PTSD. Another neurotransmitter, noradrenaline, responsible for stress response, can increase with exposure to extreme stress, leading to fear conditioning and the development of emotional memories. Genetic variances can influence the production of neurotransmitters such as dopamine, which is responsible for managing anxiety and can predict the development of PTSD (Dunlop & Wong, 2019). Exposure to high levels of stress also alters the functioning of other neurotransmitter systems, such as GABA and glutamate, affecting how an individual develops memories, interprets experiences, and responds to stress and anxiety, hence the risk of developing PTSD (Mann & Marwaha, 2023).

The neurochemical changes in the brain due to exposure to traumatic events are related to the neuroanatomical changes leading to the development of stress. The main neuroanatomical changes due to sustained exposure to stress occur majorly in the amygdala, the hippocampus, and the prefrontal cortex. Sustained stress increases the activity of the amygdala responsible for processing emotions such as fear, which increases the hyper-emotional response to stress. Hippocampal damage can occur due to elevated glucocorticoid levels with exposure to traumatic and stressful events (Vedantham et al., 2000). The hippocampus can shrink, affecting its functional capacity, hence functional memory deficits and risk for intrusive memories. Additionally, as exposure to traumatic events dysregulates emotional control and increases reactivity and impulsivity, the sustained stress exposure tends to make the medial prefrontal cortex grow smaller and less active in emotional regulation, hence the inability of people with PTSD to manage their fears (Mann & Marwaha, 2023).