More on the Physiology of Post Traumatic Stress Disorder

In this second article on the topic of PTSD I go through more of the biochemistry behind the symptoms.
In the next article I will look at available alternative and complementary remedies.

To understand the differences between the origins, pathways and hormones involved in PTSD, and why their action can become chronic and debilitating, one must first review the alarm phase and resistance phase reactions. In a sudden 'fight or flight' situation nerve impulses go from the hypothalamus to the sympathetic Nervous System (SNS) to alert the brain, activate the mobilization of huge amounts of glucose and oxygen and the shutting down of non essential body functions such as digestion . Via the SNS the adrenal medulla produces epinephrine and norepinephrine and also, through visceral effectors, activates all of the alarm phase responses.

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

The differences between normal resistance and PTSD symptoms originate from different sources. One researcher points out that in resistance the prolonged stressor stimulates an increased release of CRH by hypothalamic neurons which axons terminate on capillary beds in the infundibulum. However, it is thought that PTSD symptoms may arise from an activation of the fear-related brain systems such as the amygdala and its neuronal projections into the brain stem, hypothalamus and medulla, which extremely produce exaggerated SNS activity 'and do not switch into the PNS pathways.

In 1998 le Doux described the differences thus. "The body's fear response is coordinated by the amygdala – now seen as the site of a bodily representation of the trauma, and it activates a fear response to any remote match of the trauma, without the central cortex being aware of what is being responded to The hippocampus is part of the cerebral cortex and is responsible for long term explicit memory (declarative memory) and for filing away new memories, locating them in time and space. The problem is that there is a motorway between the amygdala and the hippocampus, going there, but only a back road the other way, suggesting that over ride may not always be possible. " Scott et al. refer to this as being 'hijacked' by the amygdala (Scott & Stradling 2001: 3).

Thus, it has been found that in PTSD sufferers the sensory input from the traumatic event is transmitted to the amygdala and following cortical input leads to activation of these responses, which are a combination and an exaggeration of the alarm phase responses.

Note from Jude: Ok, that may have contained a whole lot of biochem stuff you did not need but it does explain triggers and the highway analogy is especially helpful. If you think of the fact that its all over-production of chemicals that have probably been over-produced before (in many cases of PTSD there is a history of trauma in early childhood) .. or that the choke was left open in an old car engine .. then you can start working at looking at ways of reducing the effect, both chemically and by a variety of natural, alternative and / or complementary methods.