OBJECTIVES. Enhancing Hope for Change Krista K. Krebs, PhD September 2017

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1 Enhancing Hope for Change Krista K. Krebs, PhD September 2017 OBJECTIVES To augment confidence/understanding of the neurobiology of PTSD To augment willingness to talk about PTSD with both Veterans and families in cognitive, behavioral, emotional, spiritual and biological terms in a clear and accessible way Through the first 2 objectives, we can develop Veterans motivation to engage in the treatments that are most effective 1

2 NUMBERS Of 22 million Veterans living today, 16.5 million, or 75%, served in Wartime (7 million Vietnam Era) floor estimates of PTSD by era: 13-20% of Operation Iraqi Freedom (OIF) and Enduring Freedom (OEF) Veterans given year 12% of first Gulf War Veterans given year 30% of Vietnam Era Veterans have had PTSD in their lifetime. (National Center for PTSD: PTSD Monthly Update, Nov 2015) Why do we need to know? We have good treatments for PTSD, but getting Veterans to agree and motivating them to complete them is often difficult: Stigma both within and outside military circles Fear of emotional response of course! Avoidance is the natural urge when something hurts, and can become a way of life Talking about this disorder from a biological perspective creates another opportunity to break down barriers to and increase motivation for treatment. 2

3 Veterans Need to Know Every behavior and experience is related to the Central Nervous System Talking about neurological reasons for behavioral problems: Reduces stigma Induces HOPE NOTE: There is a National PTSD Brain Bank Nash, W. P., Silva, C., & Litz, B. T. (2009). Brave New Brain Science for MH? Will we one day be able to individually tailor our treatments to the recipient s unique genes/brain? Will medication and psychotherapeutic techniques be melded effectively, so medications may be developed to augment psychotherapy Example: D- cycloserine (NMDA agonist) studies with phobia and PTSD recovery Concepts related to neuroplasticity are key the idea that what we do can change our brain and that we can structure interventions accordingly 3

4 NeuroplasFcity and Neurogenesis the ability of the brain to reorganize itself, both physically and functionally, throughout life due to one s environment, behavior, thinking, etc. The brain is much more plastic during the early years and capacity declines with age, plasticity happens throughout your life. Example: new brain connectivity and neurons are formed in the hippocampus daily, most of them do not survive if not used Neuroimaging Techniques and Data Neuroimaging techniques map structures or functions by: blood flow, electrical output, O2 or glucose uptake PET and SPECT scans MRI and fmri NIRS and fnirs (near- infrared spectroscopy) Use of innovative contrast agents for real time mapping 4

5 Neurobiologically speaking PTSD (and many other disorders) are clearly associated with specific neural functional and structural changes Theory chronic exposure to stress hormones and other mechanisms result in neural atrophy that plays a part in failure to recover A flat heart rate variability profile with fear vs. safety stimuli Over- activity of the HPA axis (hypothalamic- pituitary- adrenal) Specific Neural Effects of PTSD Hyperactivity: amygdala (threat detection) Hypoactivity: PreFrontal Cortex Hypoactivity: Anterior Cingulate Cortex(r?) Hypoactivity & volume: Hippocampi (r?) Chronic high levels of cortisol may also result in death of neurons in the hippocampi, which compounds the problem as those neurons usually inhibit adrenal production of cortisol Severe stress can reduce the expression of helpful genes or increase the expression of unhelpful genes (epigentic changes) 5

6 Unique?: kids, adults who dissociate emotional under- modulation = PFC failing to quiet the limbic system the dissociative subtype of PTSD may be a form of emotion dysregulation that involves emotional over- modulation These findings [indicate] the need to assess patients with PTSD for dissociative symptoms and to incorporate the treatment of dissociative symptoms into stage- oriented trauma treatment. Lanius, et al (2010) Chicken and the Egg A reciprocal process genetic predispositions interact with damage due to the disorder itself Many recent studies demonstrated changes in brain structure and function after TF- CBT or EMDR Some studies indicate that favorable gene expression occurs after treatment The best examples are RCTs with control groups that are also trauma- exposed but did not develop PTSD 6

7 Recent Texts and Reviews Indicate reversibility of damage Arden, J. B. (2015) Brain2Brain: Enacting client change through the persuasive power of neuroscience. Bremner, J.D. (2016). Posttraumatic Stress Disorder: From Neurobiology to Treatment. Liberzon, I. & Ressler, K. (Eds). (2016). Neurobiology of PTSD: From Brain to Mind. Barsaglini, et al (2014) review of therapy effects Lack of support for benzodiazepine: impairs recovery from EBPs Potential for abuse Impairs neuroplasticity Rothbaum et al, (2014) FuncFonal Change post- tx Examples Goossens L, Sunaert S, Peeters R, Griez EJ, Schruers KR. (2007): amygdala over- activity normalizes after exposure therapy for specific phobias Dickie EW, Brunet A, Akerib V, Armony JL (2011): increased activation in the hippocampi and the anterior cingulate cortex, and increased activity in the PreFrontal Cortex with reduced activity in amygdala. Thomaes et al (2014) 7

8 Structural Change post- Tx Levy- Gigi, Szabo, Kelemen, Keri (2013). significantly increased FKBP5 expression and increased hippocampal volume in patients with PTSD. At follow- up, patients did not differ from control subjects [trauma- exposed] in hippocampal volume. See also Helpman et al (2016) racc changes post- therapy SO, severe experiences can result in Increased amygdala activation (over- reactive threat detector) Chronic flat HRV (danger and safety feel the same) Hippocampal volume loss and decreased function (no context for then versus now) Reduced volume and activity in the PFC (runaway threat detector train has no engineer) Due (at least) to chronic exposure to glucocorticoids and imbalance in specific neurotransmitters (cortisol and adrenaline and the like) 8

9 Talking with Veterans and families PTSD affects the brain directly it s not your fault Painful new set points (example, adrenaline response) Treatments help to re- calibrate the set point Treatments lead to recovery or reversal of brain structure damage or functional impairment Engaging in EBPs is analogous to physical therapy for a physical injury Avoidance is really avoidance of specific internal experiences All healing hurts Teach healing the brain Respond to memories based on new learning build your hippocampus give homework that requires PFC use (e. g. alternative explanations homework) increase motivation and hope for change through discussion of how psychotherapy changes the brain reduce dropout Increase safety learning develop a strong vagal tone (opposite of a flat HRV) yoga, mindfulness practice, loving/kindness meditation, exercise 9