More on the Physiology of Post Traumatic Stress Disorder

In the second article on the topic of PTSD I went through more biochemistry behind the symptoms.

In the next article I will look at alternative and complementary alternatives.

To understand the differences between the origins, pathways and hormones involved in PTSD, and why their actions can be chronic and debilitating, one must review the alarm phase and resistance phase. Suddenly 'struggle or flight' The impulse nerve state travels from the hypothalamus to the Sympathetic Nervous System (SNS) to alert the brain, activates the release of large amounts of glucose and oxygen and disrupts vital body functions such as digestion. Through the SNS, the adrenal medulla produces epinephrine and norepinephrine and also, through the auditory sensors, activates all phase-response responses.

Meanwhile in the CRH hormone releasing the hypothalamus Corticotropin, growth hormone releasing hormone (GHRH) and Thyrotropin-releasing hormone (TRH) are produced. When the body moves to the resistance phase, the SNS is turned off and replaced by the Parasympathetic Nervous System (PNS) which acts to bring the body back to homeostasis. In the anterior pituitary, three hormones stimulate ACTH, hGH and TSH. ACTH stimulates the adrenal cortex, stimulates lipolysis, gluconeogenesis and protein catabolism, thereby releasing more cortisol. Acting through insulin growth factors, hGH stimulates lipolysis and glycogenolysis to produce more glucose. TSH promotes the secretion of thyroid hormones T3 and T4 which stimulate glucose uptake to produce ATP. The result of all these reactions is that the body produces more glucose, fatty acids and amino acids, more cortisol and ATP are needed to maintain energy while the pressure continues, to repair damaged cells and reduce inflammation.

The difference between normal resistance and PTSD symptoms comes from different sources. One researcher showed that prolonged stress resistance stimulated increased CRH release by hypothalamic neurons whose axons terminated in the capillary bed in the infundibulum. However, it is thought that PTSD symptoms may arise from activation of the brain-related nervous system such as the amygdala and its projection of neurons into the brainstem, hypothalamus and medulla, which eventually results in excessive SNS activity & # 39; s and does not turn into a PNS path.

In 1998, Le Doux described the difference. The body's fear response is coordinated by the amygdala - now seen as the site of trauma representation, and it activates the fear response to any long-distance trauma match, without the central cortex realizing what the Hippocampus is responding to is part of the cerebral cortex and responsible for long-term memory clear length (declarative memory) and to forge new memories, find them in time and space. There is a connection between the amygdala and the hippocampus. The amygdala The problem is that there is a highway between the amygdala and the hippocampus, going there, but only the other way back, indicating that more travel is not possible. "Scott et al. refer to this as 'seized' (Scott & Stradling 2001: 3).

Therefore, it is found that in PTSD sensory input from traumatic events is transmitted to the amygdala and following cortical input leads to activation of this response, which is a combination of and exacerbates the alarm phase.

Note from Jude: Ok, that may contain a lot of biochemical material you don't need but it does explain the triggers and analogy of the highway is very helpful. If you think about the fact that all of the chemical production may have been fruitful before (in many cases PTSD has a history of childhood trauma) .. or the choking was left open long ago by car engines .. then you can start working on ways to reduce the effects , both chemically and with a variety of natural, alternative and / or complementary methods.

More on the Physiology of Post Traumatic Stress Disorder


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