The Neuroscience of Trauma and Addiction | PTSD & cPTSD Interventions

The Neuroscience of Trauma and Addiction

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Objectives
 Define&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

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