The Neurobiological Impact of Psychological Trauma:
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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 on the HPA-Axis
~ Identify symptoms of HPA-Axis dysfunction
~ Identify interventions useful for this population
~ Post-traumatic stress disorder: the neurobiological impact of psychological trauma
Dialogues Clin Neurosci. 2011 Sep; 13(3): 263–278.
~ This article lays out the many changes and/or conditions seen in the brain of people with PTSD.
~ As clinicians, awareness of these changes can help us educate patients about their symptoms and find ways of adapting to improve quality of life.
~ Neurobiological abnormalities in PTSD overlap with features found in traumatic brain injury
~ The response of an individual to trauma depends not only on stressor characteristics, but also on factors specific to the individual.
~ Perception of stressor
~ Proximity to safe zones
~ Similarity to victim
~ Degree of helplessness
~ Prior traumatic experiences
~ Amount of stress in the preceding months
~ Current mental health or addiction issues
~ Availability of social support
~ For the vast majority of the population, the psychological trauma is limited to an acute, transient disturbance.
~ The signs and symptoms of PTSD reflect a persistent, abnormal adaptation of neurobiological systems to the witnessed trauma.
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 in the blood during times of stress.
~ Cortisol's main role is in releasing glucose into the bloodstream in order to facilitate the “flight or fight” response. It also suppresses and modulates the immune system, digestive system and reproductive system.
~ The body reduces its HPA axis activation when it appears that further fight/flight may not be beneficial. (Hypocortisolism)
~ 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
~ Fatigue is actually an emotion generated in the brain, which prevents damage to the body when the brain perceives that further exertion could be harmful.
~ Fatigue in sports is largely independent of the state of the muscles themselves and is more related to:
~ Physical factors
~ Core temperature
~ Glycogen levels
~ Oxygen levels in the brain
~ Sleep deprivation
~ Levels of muscle soreness/fatigue
~ Fatigue cont…
~ Psychological factors reducing fatigue
~ Emotional state
~ Knowledge of the endpoint
~ Other competitors/motivation
~ Visual feedback
~ Fatigue is one sign that the body is getting ready to downregulate the HPA-Axis
~ In counseling practice, how can we reduce fatigue and help clients restore HPA-Axis functioning?
Low Cortisol and PTSD
~ Low cortisol has been found to relate to more severe PTSD hyperarousal symptoms.
~ Sensitised negative feedback loop in veterans diagnosed with PTSD by means of a greater gluticorticoid responsiveness. (0-100)
~ Generally low cortisol, but when a threat is perceived there is an exaggerated stress response. (Flat or furious)
~ Evidence points toward a role of trauma experience in sensitizing HPA axis regulation, independent of PTSD development.
~ Those with prior trauma may be more at risk of PTSD from later traumas (Area for prevention)
~ Core endocrine features of PTSD include abnormal regulation of Cortisol and thyroid hormones
~ Hypocortisolism in PTSD occurs due to increased negative feedback sensitivity of the HPA axis.
~ Studies suggest that low Cortisol levels at the time of exposure to psychological trauma may predict the development of PTSD. (Prior trauma exposure may predispose to PTSD)
~ 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, amino acid, peptide, and opioid neurotransmitters, each of which is found in brain circuits that regulate/integrate stress and fear responses.
~ the catecholamine family of neurotransmitters, including dopamine (DA) and norepinephrine (NE), derive from the amino acid tyrosine
~ When a stressor is perceived the HPA Axis releases CRH which interacts with NE to increase fear conditioning and encoding of emotional memories, enhance arousal and vigilance, and integrate endocrine and autonomic responses to stress.
~ there is an abundance of evidence that NF, accounts for certain classic aspects of PTSD symptomatology, including hyperarousal, heightened startle, and increased encoding of fear memories
~ Serotonin (5HT)
~ Poor serotonin transmission in PTSD may cause impulsivity, hostility, aggression, depression, and suicidally
~ Serotonin binding to 5HT1A receptors do not differ between patients with PTSD and controls.
Serotonin Receptors (Soap Box)
• Blood Pressure
• Heart Rate
• Sexual Behavior
• Sexual Behavior
• GI Motility
• Sexual Behavior
• GI Motility
~ GABA has profound anxiolytic effects in part by inhibiting the CRH/NE circuits
~ Patients with PTSD exhibit decreased peripheral benzodiazepine binding sites.
~ 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
~ NMDA Receptors
~ 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 increase the sensitivity of NMDA receptors, rendering the brain more vulnerable to excitoxic insults at times of stress.
~ Points to ponder
~ It may take clients with PTSD more time to master new skills
~ If the brain becomes excitotoxic during stress, inhibiting learning and memory, then exposure therapies may also be dangerous.
~ Endogenous opioids act upon the same CNS receptors activated by exogenous opioids such as morphine or heroin.
~ Opioids (depressants) exert inhibitory influences on the HPA axis.
~ Alterations in endogenous opioids may be involved in certain PTSD symptoms such as numbing, stress-induced analgesia, and dissociation.
~ Naltrexone, appears to be effective in treating symptoms of dissociation and flashbacks in traumatized persons.
~ Highlights the risk for opiate abuse of persons with PTSD
~ How can we assist with physical and emotional distress tolerance
Changes? In Brain Structure
~ A hallmark feature of PTSD is reduced hippocampal volume.
~ The hippocampus is implicated in the control of stress responses, memory, and contextual aspects of fear conditioning.
~ Prolonged exposure to stress and high levels of glucocorticoids damages the hippocampus
~ Hippocampal volume reduction in PTSD may reflect the accumulated toxic effects of repeated exposure to increased glucocorticoid levels (Flat or Furious)
~ Decreased hippocampal volumes might be a pre-existing vulnerability factor for developing PTSD.
Changes? In Brain Structure
~ The amygdala is a limbic structure involved in emotional processing and is critical for the acquisition of fear responses.
~ Functional imaging studies have revealed hyper-responsiveness in PTSD during the presentation of stressful scripts, cues, and/or trauma reminders.
~ PTSD patients further show increased amygdala responses to general emotional stimuli that are not trauma-associated, such as emotional faces.
~ So clients with PTSD may be more emotionally responsive across the board (dysregulation)
Changes? In Brain Structure
~ Early adverse experience, including prenatal stress and stress throughout childhood, has profound and long-lasting effects on the development of neurobiological systems, thereby “programming” subsequent stress reactivity and vulnerability to develop PTSD.
~ Adult women with childhood trauma histories exhibit sensitization of both neuroendocrine, and autonomic stress responses
~ A variety of changes take place in the brains and nervous systems of persons with PTSD
~ Pre-existing issues causing hypocortisolism (the brain has already down regulated) increases the likelihood of the development of PTSD
~ This points to the importance of prevention and early intervention of adverse childhood experiences
~ People with hypocorticolism may or may not have PTSD
~ Hypocorticolism sets the stage for the Flat and the Furious toxic levels of glutamate upon exposure to stressors reduction of hippocampal volume persistent negative brain changes
~ People with PTSD are more reactive to emotional stimuli, even stimuli unrelated to trauma
~ Hypocorticolism results when the brain perceives that continued effort is futile.
~ Feelings of “fatigue” set in (akin to reduced stress tolerance)
~ Reducing fatigue can be accomplished, in part, with psychological factors including
~ Motivation/Knowledge of “competitors”
~ Feedback (frequent successes)
~ Knowledge of an endpoint
~ 46% of people in the US are exposed to adverse childhood experiences. (Early Intervention)
~ Instruction in skills to handle emotional dysregulation
~ Vulnerability prevention and awareness
~ Emotion Regulation
~ Distress Tolerance
~ Problem Solving
~ Of those exposed to trauma, education about and normalization of heightened emotional reactivity and susceptibility to PTSD in the future may be helpful
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