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Define and explain the HPA-Axis
Identify the impact of trauma on the HPA Axis
Identify the impact of chronic stress/cumulative trauma and addiction on the HPA-Axis
Identify symptoms of HPA-Axis dysfunction
Identify interventions useful for this population
Neurobiological abnormalities in resulting from trauma overlap with features found in traumatic brain injury, including that from addictive behaviors
Abuse of stimulants, alcohol and process addictions increase excitotoxicity in the brain
Excessive use of depressants and opioids, respiration may be impaired causing hypoxia
During alcohol withdrawal blood pressure increases and can cause stroke
Alcohol use can also cause WKS due to reduced levels of thiamine in the brain.
What is the HPA Axis
Hypothalamic-Pituitary-Adrenal Axis AKA the Threat Response System
Controls reactions to stress and regulates many body processes, including digestion, the immune system, mood and emotions, sexuality, and energy storage and expenditure
The ultimate result of the HPA axis activation is to increase levels of cortisol and glutamate during times of stress.
Both intoxication and withdrawal from substances trigger the stress response
Cortisol’s main role is in releasing glucose into the bloodstream in order to facilitate the “flight or fight” response.
Glutamate is the main excitatory neurotransmitter
The body reduces its HPA axis activation when it appears that further fight/flight may not be beneficial. (Hypocortisolism)
In addiction this is often part of tolerance
Hypocortisolism seen in stress-related disorders such as CFS, burnout and PTSD is actually a protective mechanism designed to conserve energy during threats that are beyond the organism’s ability to cope.
Dysfunctional HPA axis activation will result in
Abnormal immune system activation
Increased inflammation and allergic reactions
IBS symptoms such as constipation and diarrhea,
Reduced tolerance to physical and mental stresses (including pain)
Altered levels of sex hormones
Low Cortisol and PTSD
Low cortisol has been found to relate to more severe PTSD hyperarousal symptoms.
Glucocorticoids interfere with the retrieval of traumatic memories, an effect that may
Independently prevent or reduce symptoms of PTSD
Or contribute to difficulty treating PTSD
Core neurochemical features of PTSD include abnormal regulation of catecholamine, serotonin, glutamate, amino acid, peptide, and opioid neurotransmitters, each of which is found in brain circuits that regulate/integrate stress and fear responses.
Poor serotonin transmission may cause impulsivity, hostility, aggression, depression, and suicidally
GABA has profound anxiolytic effects in part by inhibiting the CRH/NE circuits
May indicate the usefulness of emotion regulation and distress tolerance skills due to potential emotional dysregulation
We need to reduce excitotoxicity in order to reduce distress, improve stress tolerance and enable the acquisition of new skills
The NMDA receptor system has been implicated in synaptic plasticity, as well as learning and memory
Glutamate binds to NMDA receptors. High levels of glutamate are secreted during high levels of stress
Overexposure of neurons to glutamate is known to be excitotoxic, and may contribute to the loss of neurons in the hippocampus of patients with PTSD
Elevated glucocorticoids (Cortisol) increase the sensitivity of NMDA receptors, rendering the brain more vulnerable to excitoxic insults at times of stress.
It may take clients with brain damage from PTSD or addiction more time to master new skills
If the brain becomes excitotoxic during stress, inhibiting learning and memory, then exposure therapies may also be dangerous.
Early adverse experience has profound and long-lasting effects on the development of neurobiological systems, thereby “programming” subsequent stress reactivity and vulnerability to develop PTSD.
The impact of addictive behaviors on the adolescent brain is exaggerated in comparison to that of adults
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