Neuroscience of Stress
Stress reaction is any physiological or psychological reaction to physical, mental, or emotional stress that disturbs the organism's homeostasis.
Stress alters brain chemistry, create hormonal imbalances, increase heart rate, raise blood pressure, and negatively affect both metabolic and immune function. It is also important to recognize that although stress itself is not a disease, it can worsen any number of already serious physical conditions (170).
High levels of stress hormones, like adrenaline, can stop it from working properly – like “blowing a fuse”. This means that flashbacks and nightmares continue because the memories of the trauma can’t be processed.
Adrenaline is a hormone our bodies produce when we are under stress. It “pumps up” the body to prepare it for action. When the stress disappears, the level of adrenaline should go back to normal. In PTSD, it may be that the vivid memories of the trauma keep the levels of adrenaline high. This will make a person tense, irritable, and unable to relax or sleep well.
If the stress goes away, and the adrenaline levels get back to normal. The disturbing memories can then be processed and the flashbacks and nightmares will slowly disappear (126).
The brain stress systems
The brain stress systems involved the pituitary gland, nucleus of the stria terminalis, the adrenal gland, hippocampus, the central nucleus of the amygdala.
The hippocampus is a part of the brain that processes memories. Atrophy of the hippocampus in humans reduces the memory resources available to help a body formulate appropriate reactions to stress; exposes to severe stress caused by prolonged exposure to high concentrations of glucocorticoids.
Stressors can be of many different types, including social and physical stressors. Both types activate the HPA axis, though via different pathways. Monoamine neurotransmitters are important in regulating the HPA axis, especially dopamine, serotonin and norepinephrine.
Pre-pubertal stress in early life determines the capacity of the adult hypothalamus to respond to an acute stressor.
HPA axis stress system: Anatomical connections between brain areas such as the amygdala, hippocampus, and hypothalamus facilitate activation of the HPA axis. Sensory information at the lateral aspect of the amygdala, is processed and conveyed to the central nucleus, which projects to several parts of the brain involved in responses to fear; at the hypothalamus, fear-signalling impulses activate both the sympathetic nervous system and the modulating systems of the HPA axis; cortisol mediates alarm reactions to stress.
Extrahypothalamic stress system: Stressful stimuli activate CRF systems in the basal forebrain, notably the bed nucleus of the stria terminalis and the central nucleus of the amygdala, to help mediate behavioural responses to stressors and to mediate sympathetic activation associated with stressors.
Corticotrophin-Releasing Factor (CRF): Stressful stimuli increase Corticotrophin-Releasing Factor (CRF), which in turn stimulates adrenocorticotrophic hormone (ACTH) release from the pituitary, which results in enhanced release of glucocorticoids from the adrenal gland. High levels of glucocorticoids, through negative feedback, decrease CRF synthesis at the level of the paraventricular nucleus (PVN) but activate CRF activity at the level of the central nucleus of the amygdala.
In an adaptive phase of a general adaptation syndrome alarm reactions, including the immune response, are suppressed, allowing the body to attempt countermeasures.
If the stress goes away, and the adrenaline levels get back to normal, the brain is able to repair the damage itself, like other natural healing processes in the body.
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