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PTSD…

PTSD…. Dr Jon Lane, Franzcp. Ptsd PRIMER. What is PTSD? What causes PTSD? What are the comorbid problems people with PTSD have? How to diagnose PTSD Treatment…. What is psychological trauma?. Trauma - wound or injury To the psyche Potentially Traumatic Event (PTE)

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PTSD…

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  1. PTSD… Dr Jon Lane, Franzcp

  2. Ptsd PRIMER • What is PTSD? • What causes PTSD? • What are the comorbid problems people with PTSD have? • How to diagnose PTSD • Treatment…

  3. What is psychological trauma? Trauma - wound or injury To the psyche Potentially Traumatic Event (PTE) DSM-5 diagnostic criteria Objective Subjective – no longer included Traumatic Event Actual harm

  4. Potential Response to a PTE • The impact of experiencing a PTE on psychological well being may be: Valence: Good, bad, mixed Severity: Negligible, mild, moderate, severe Duration: Brief, long-lasting, permanent • The vast majority of people do not develop long term mental health problems

  5. Resilient Recovery Delayed Persistent Common patterns of response following trauma or disaster

  6. Epidemiology Note that PTE does NOT have to mean PTSD…

  7. PTSD in Women • Lifetime risk is twice as high as men • Probably due to greater likelihood of exposure to PTE’s (rape, abuse) • More likely to be re-victimised than men during later lifetime • There seems to be a genetic vulnerability as well – higher heritability risk, demonstrated by pituitary allelic variation (adenylate cyclase activating polypeptide) • Roughly 39% of sex-risk for women explained by increased exposure and vulnerability

  8. Function of the HPA Axis in ptsd • Increased corticotrophin-releasing hormone from the hypothalamus in ptsd is represented by the thick black line. • Decreased adrenal release of cortisol in ptsd is represented by the thin black line. • Increased negative feedback inhibition of the HPA by cortisol is represented by the thick red lines. • Cortisol binds to the glucocorticoid receptor and modulates gene expression. • Several systems are affected by differential glucocorticoid signalling.

  9. Systemic effects of PTSD • Nervous System – Memory, cognition, stress symptoms • Immune System – suppression of pro-inflammatory cytokines, regulation of immune cell maturation, migration and apoptosis • Cardiovascular system – cardiovascular and metabolic disease • Glucose and liver metabolism – glucose dysregulation, lipid homeostasis, obesity • Reproductive system – epigenetic transmission

  10. Evidence for emerging neurobiological dysregulation in PTSD • Inflammatory mediators (Michopoulos et al, 2016, Gola et al, 2013) • Glucocorticoid receptor sensitivity (de Kloet et al 2007) • Epigenetic changes (Yehuda et al, 2015) • Increased GSR and HR in response to challenge (Costanzo et al, 2016) • Modified lipid metabolism (Michopoulos et al, 2016)

  11. Emotional modulation problems

  12. Emotional Modulation • Emotional Undermodulation – diminished control or heightened emotional and autonomic responses – RE-EXPERIENCING • Include the fear, anger, shame, guilt responses • Emotional overmodulation – increased control of emotional responses, hence related emotional detachment • Includes depersonalisation and derealisation, emotional numbing and analgesia • People can fluctuate between the two states

  13. With diminished prefrontal inhibition of limbic regions during emotional undermodulation, studies have indicated decreased ventromedial prefrontal cortex and rostral anterior cingulate activation and increased amygdala activation in response to trauma and non-trauma-related emotional stimuli in those with PTSD (triggers for re-experiencing and increased emotions) • By contrast, patients who have emotional overmodulation have shown increased activation of medial prefrontal cortex and rostral anterior cingulate regions, which have been suggested to lead to decreased amygdala activation (therefore hypoarousal, detachment, etc)

  14. Consequences of reduced cortisol signalling after trauma

  15. Salience Networks • Central executive network - Cognitive dysfunction • Salience network - Altered arousal and interoception • Default mode network - altered self-referential processing

  16. Primary Construct-Phenomenology of PTSD FEAR CIRCUITS • Intrusive memories • Avoidance - behavioural response • Numbing and loss of pleasure • Difficulty with memory, concentration, irritability • Somatic distress DEFAULT NETWORKS WORKING MEMORY AUTONOMIC DYSFUNCTION

  17. PTSD Diagnosis – DSM 5

  18. The new PTSD – DSM5 cont.

  19. Quality of life issues with ptsd The problem often becomes self-perpetuating, and hence the common development of co-morbid conditions

  20. Common comorbidities Most relevant to chronic PTSD • depression (suicidal ideation/behaviour) • other anxiety disorders • substance use disorders • pain • other medical conditions • occupational impairment • interpersonal problems & relationship breakdown • social withdrawal - disengagement

  21. The need for clinical staging in PTSD • Different phenotypes that need to be addressed in treatment • Staging is a method for clarifying the issue of longitudinal course and the changing neurobiology McFarlane et al Clinical Psychiatric Reports 2017

  22. Staging model of PTSD 0. Trauma exposed no symptoms but at greater risk with further exposure 1a. Minor symptoms 1b. Subsyndromal PTSD – similar to PTSD 2. First episode of brief duration 3. More enduring or relapsing disorder following treatment 4. Chronic, severe and treatment unresponsive

  23. Preventive Stance of Staging • Emphasis on progression or transition • Not inevitable • Earlier stages of treatment have fewer complications and greater tolerability • Cross sectional and longitudinal biomarkers for the different phenotypes of the disorder • Different treatment strategies at different stages

  24. Australian PTSD Guidelines  Developed in consultation with experts and people affected by PTSD  Supported by the Australian Government and approved by peak health research body - NHMRC  Endorsed by professional associations – RACGP, RANZCP, APS • Available from www.acpmh.unimelb.edu.au

  25. Practice Guidelines – Caveats • Absence of evidence is not evidence of absence • Guidelines support clinical decision-making they do not replace it; they recommend, they do not mandate • Clinical priorities, the impact of comorbid conditions, patient preferences - may influence timing, order and combination of treatments

  26. Guideline Recommendations: Adults • Trauma focussed CBT or EMDR is the treatment of choice for PTSD: • Trauma focused CBT included • In vivo and imaginal exposure • Cognitive therapy or cognitive processing therapy • Medication should not be used as routine 1st line in preference to TF psychological treatment • Where prescribed: • SSRIs • Other newer antidepressants, adjunctive agents

  27. Treatment Context: Three-Level Response to Promoting Recovery following Trauma Level 1: Interventions for all: Psychological first aid (PFA), community development activities (little evidence) Level 2: Interventions for persisting mild/ subclinical problems: Simple intervention strategies for use by primary care, general counsellors, etc (moderate evidence) Level 3: Interventions for disorder: Interventions for use by mental health providers (strong evidence)

  28. Effective psychological treatments: • TFCBT = trauma focused cognitive behavioural therapy • CPT = cognitive processing therapy • EMDR = eye movement desensitisation and reprocessing • To be effective: • Enable patient to confront distressing memories • Manage avoidance responses • Reduce and manage associated arousal & distress

  29. 1: Stabilisation and engagement 2: Education and information 3: Anxiety management 4: Trauma exposure 5: Cognitive restructuring 6: Relapse prevention and maintenance PTSD: Stages of CBT Treatment

  30. How effective are psychological therapies? • Reasonably effective: in most studies, around 70% show substantial symptom reduction • Many people have some residual symptoms and/or vulnerability • Women do better than men, civilians better than veterans, single better than multiple trauma • We need more research on tailoring treatment to clinical presentation • The biggest challenge is dissemination of best treatments and changing clinical practice

  31. Pharmacotherapy for PTSD: Overview There is no “silver bullet” • Medication should not be used as routine 1st line in preference to TF psychological treatment • When medication is used antidepressants are the first line treatment • the evidence is strongest for the SSRI class • The evidence for efficacy of other medications used alone or added to antidepressants is not strong • there is some evidence to support the strategy of adding prazosin or atypical antipsychotic medication to an antidepressant when there is a poor or partial response to antidepressant alone

  32. Role of Antidepressants in PTSD • Need to consider role of peripheral inflammation • Different phenotypes of PTSD (MST, Moral Injury, combat PTSD, etc) • Need a staging model • Different antidepressants may have different impact on these inflammatory systems in PTSD treatment • McFarlane et al Clinical Psychiatric Reports 2017

  33. Antidepressants Act on Peripheral Inflammation Hashimoto Int J Mol Sci 2015

  34. CRP Predicts Differential Response to SSRI vs. SSRI+Bupropion Jah MK et al. Psychoneuroendocrinol2017; 78: 105-13

  35. Meta Analysis of Treatment in Military Populations • Mean post treatment scores for CPT and PE remained at or above clinical criteria for PTSD • Approximately 66% of patients retained their PTSD diagnosis after treatment (range 60-72%) • Prolonged exposure marginally superior compared to non-trauma focused psychotherapies • Need to improve existing treatments and test novel evidence based treatments • Steenkamp et al JAMA 2015, 314;489-500

  36. Evidence Based Care • Important that evidence based treatments are provided • Limitations of the literature • Little comorbidity eg substance abuse • Low levels of suicidality • Need a systematic strategy for how to deal with non response • Issue of multiple versus single trauma • No consideration of phenotypes/personalised approach • Can be used as a method of restricting treatment rather than optimising outcomes

  37. Melatonin Maintenance of circadian cycle Improves sleep Cortical binding Maintenance of somatic self regulation and decreasing arousal Agomelatine can be prescribed through RPBS

  38. Cases?

  39. Questions?

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