The Neurobiological Impact of Trauma and Addiction



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Objectives
 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
Introduction
 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
HPA-Axis Dysfunction
 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.
 Serotonin (5HT)
 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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