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gevirtz, jrv and ptsd


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  • I am the Associate Director of the Tri-service Integrator of Outpatient Programming Systems (TrIOPS) and work with military programs throughout the country that provide behavioral health treatment for combat related stress conditions (i.e., PTSD, depression, anxiety, etc..). Please feel free to contact me if you have information or experiences you would like to share regarding this area of treatment. There is a much good work taking place with much more work to be done. I am dedicated to learning as much as I can about the system in which care is provided so that resources, products, and services can be developed and utilized by treatment programs working with our Warriors.
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gevirtz, jrv and ptsd

  1. 1. Emerging Applications of Heart Rate Variability Biofeedback: Trauma Richard Gevirtz, Ph.D., BCIAC CSPP@ AIU, San Diego, CA [email_address]
  2. 2. Posttraumatic Stress Disorder Criteria (DSM-IV-TR, 2000) Psychiatric Disorder, Classified as Anxiety Disorder Criterion A Traumatic Event Or, series of events Directly or indirectly experienced Subjective Response Involve: intense fear, helplessness, or horror Criterion B Reexperiencing Symptom Cluster Intrusive thoughts Distressing dreams Trauma cue distress Criterion C Avoidant Symptom Cluster Avoid trauma-related thoughts, places, feelings Criterion D Hyperarousal Symptom Cluster Insomnia Irritability, anger, hypervigilance
  3. 3. The biological message of trauma <ul><li>Remember this moment </li></ul><ul><li>Never go this way again </li></ul><ul><li>Be prepared </li></ul><ul><li>Severity defined by </li></ul><ul><ul><li>The breadth of the definition of “this way” </li></ul></ul><ul><ul><li>The extent of the preparation </li></ul></ul>
  4. 4. Criterion A Traumatic Event Subjective Response Fear, helplessness, or horror Magnitude of subjective response Epidemiological study: PTSD onset depended most on it , not traumatic event (Breslau & Kessler, 2001) Peritraumatic hyperarousal Longitudinal: (elevated HR) to imaginal trauma cues at 1 month and at 3 months was most significant predictor of PTSD onset at 3 months (Elsesser, Sartory, & Tackenberg, 2005) Peritraumatic dissociation Meta-analysis of risk factors: most significant predictor of PTSD, and better predictor than prior events (Ozer, Best, Lipsey, Weiss, 2003) Subjective response CRITICAL to PTSD onset?
  5. 5. Deficit in awareness of internal sensations and being in the present <ul><li>Deficits in frontal sub-cortical circuitry and Cortico-thalamic integration Vasterling et al., 1998; Clark et al. 2003 </li></ul><ul><li>Alexithymia Krystal, 1988 </li></ul><ul><ul><li>Inability to accurately perceive internal states </li></ul></ul>
  6. 6. Evidence from neuro-imaging studies: <ul><li>Exposure to trauma scripts produces: </li></ul><ul><ul><li>Increased activity (as measured by blood flow) in: </li></ul></ul><ul><ul><ul><li>Right medial orbital frontal cortex </li></ul></ul></ul><ul><ul><ul><li>Insula </li></ul></ul></ul><ul><ul><ul><li>Amygdala </li></ul></ul></ul><ul><ul><ul><li>Anterior temporal pole </li></ul></ul></ul><ul><ul><li>Deactivation in: </li></ul></ul><ul><ul><ul><ul><li>Left anterior prefrontal cortex- especially Broca’s area (expressive speech) </li></ul></ul></ul></ul><ul><ul><ul><li>Rauch, Van der Kolk, et al, 1966 </li></ul></ul></ul><ul><ul><ul><li>Hull, 2002 </li></ul></ul></ul><ul><ul><ul><li>Lanius, et al., 2001 </li></ul></ul></ul><ul><ul><ul><li>Lindauer et al., 2004 </li></ul></ul></ul><ul><li>Conditioned fear memories - the lateral nucleus of the amygdala to the central nucleus to the ANS ; Amorapanth,La Doux, et al. 2000 </li></ul>
  7. 7. <ul><li>“… when people are reminded of personal trauma they activate brain regions that support intense emotions, while decreasing activity in brain structures involved in the inhibition of emotions and the translation of experience into communicable language.” (p.278) </li></ul><ul><li>Van Der Kolk, 2006 </li></ul>
  8. 8. Rostral Anterior Cingulate ↓ ↑ Right Anterior Insula Reexperiencing Dissociation Region implicated in awareness of bodily states ↓ Right Anterior Insula ↑ Medial Prefrontal Cortex Figure 1: Emotion Dysregulation in PTSD Regions implicated in regulation of emotion and arousal ↓ Medial Prefrontal Cortex Amygdala ↑ ↓ Amygdala Regions implicated in regulation of emotion and arousal Rostral Anterior Cingulate ↑ Emotional Undermodulation Emotional Overmodulation
  9. 9. PTSD Biological Evidence <ul><li>Neuropsychological Alterations (Charney, et al., 1993; Kolb, 1987; van der Kolk, 2006) </li></ul><ul><ul><li>Excessive emotional stimulation alters neurological functioning </li></ul></ul><ul><ul><li>PTSD symptoms are maladaptive neurobiologic sequelae </li></ul></ul><ul><li>Low cortisol ( Yehuda , Boisoneau, Mason, & Giller, 1993; Yehuda , Kahana, Binder-Brynes K & Southwick, 1995) </li></ul><ul><ul><li>Paradoxical: Stress = Surge of cortisol </li></ul></ul><ul><ul><li>Cortisol inhibits, stabilizes stress hormones </li></ul></ul><ul><li>Autonomic Nervous System </li></ul><ul><ul><li>Elevated HR (Buckley and Kaloupek, 2001; Keane et al., 1998) </li></ul></ul><ul><ul><li>Low HRV (autonomic dysregulation) (Cohen, Kotler, Matar, & Kaplan, 1997; Cohen, et al, 1998; Hopper, Spinazzola, Simpson, & van der Kolk, 2006; Sack et al., 2004; Sahar, Shalev, & Porges, 2001) </li></ul></ul>
  10. 10. PTSD: Evidence of Underlying Biological Core? <ul><li>PTSD is Psychophysiological Disorder: </li></ul><ul><li>Universal symptom: intrusive memories: not event itself > unique </li></ul><ul><ul><li>Intrusion > hyperarousal > insomnia > hypervigilance > exaggerated startle response </li></ul></ul><ul><ul><li>Longitudinal study (Schell, Grant, and Jaycox , 2004) </li></ul></ul><ul><ul><ul><li>Severity of the hyperarousal cluster leads to greater symptom severity of intrusion +avoidance cluster (12-months). </li></ul></ul></ul><ul><ul><ul><li>Converse is not true. </li></ul></ul></ul>
  11. 11. John Hughlings Jackson to MacLean: Devolution toTriune brain structure <ul><li>Organization of the CNS-”bottom up” </li></ul><ul><li>Executive functions (prefrontal cortex) under ordinary circumstances can inhibit, organize, and modify automatic processes coming from the lower centers </li></ul><ul><li>“… the higher nervous arrangements inhibit (or control) the lower, and thus, when the higher are suddenly rendered functionless, the lower rise in activity.” J.H. Jackson in Taylor, 1958 </li></ul><ul><li>Elaborated in the 1990 by Mac Lean’s concept of the Triune brain </li></ul>
  12. 12. Developmental perspective <ul><li>Human species unique in their flexibility; abilty to make choices of how to respond, but these functions develop slowly </li></ul><ul><li>Higher function develop during childhood and don’t exist in final form until young adulthood </li></ul><ul><li>Vagal development, especially the “smart vagus” follows this develomental sequence </li></ul><ul><li>“ The rational mind, while able to organize feelings and impulses, does not seem to be able to abolish emotions, thoughts, and impulses.” Van der Kolk, 2006, p.279 </li></ul>
  13. 13. Amygdala and biological salience <ul><li>The amygdala tags incoming stimuli to determine their biological relevance </li></ul><ul><li>Action stems from this process </li></ul><ul><li>As Sperry said in 1981: “ The brain is the organ of and for movement: The brain is the organ that moves the muscles. It does many other things, but all of them secondary to making our bodies move.” Sperry, 1952 </li></ul>
  14. 14. Implications for treatment <ul><li>The only empirically based treatments to date are CBT, CBT/PE, and CPT. </li></ul><ul><ul><li>Though meta-analyses show that these therapies are better than placebo, they leave “much room for improvement” </li></ul></ul><ul><ul><li>Effect sizes are small Hofmann, 2008 </li></ul></ul><ul><li>“ One thing is clear: the rational, executive brain, the mind, the part that needs to be functional in order to engage in the process of psychotherapy, has very limited capacity to squelch sensations, control emotional arousal, or change action patterns” Van der Kolk, 2006, p.281 </li></ul><ul><li>A somatic intervention might be a necessary component for PTSD treatment </li></ul><ul><li>Interventions that prompt behavioral action may be superior </li></ul>
  15. 15. PTSD Treatment Interventions (cont.) <ul><li>Biological Researchers conclude: </li></ul><ul><li>Treatment interventions need to address core neuronal and psychophysiological abnormalities (Charney, 1993; van der Kolk, 2006) </li></ul><ul><li>Neuropsychological abnormalities limit the “ main staples ” of </li></ul><ul><ul><li>psychotherapy, understanding and insight as well as the ability to </li></ul></ul><ul><ul><li>communicate thoughts and feelings (van der Kolk, 2006) </li></ul></ul>
  16. 16. Foa’s Emotional Processing Theory <ul><li>Fear represented in memory as cog structure that is a “program” for escaping danger. This includes: </li></ul><ul><ul><li>Fear responses (e.g. heart acceleration) </li></ul></ul><ul><ul><li>Meaning of stimuli (“This man is dangerous” </li></ul></ul><ul><ul><li>Cognitive responses (“My fast heartrate means that I am afraid.” </li></ul></ul>
  17. 17. Fear structure becomes pathological when: <ul><li>Associations are inaccurate </li></ul><ul><li>Physiological and escape/avoidance responses are evoked by harmless stimuli </li></ul><ul><li>Excessive and easily triggered responses interfere with adaptive behavior </li></ul><ul><li>Harmless stimuli and elements are associated with threat meaning </li></ul>
  18. 18. The mechanisms of CPTSD treatment <ul><li>The connection of fear to its source </li></ul><ul><li>The creation of safety </li></ul><ul><li>The de-stigmatization of fear and its consequences </li></ul>
  19. 19. The role of “relaxation” <ul><li>Historically preserved as part of the original Exposure and PE packages </li></ul><ul><li>Not seen as important by theoreticians </li></ul><ul><li>Relied on by clinicians </li></ul><ul><ul><li>Would the role of relaxation by enhanced by the addition of HRV technology? </li></ul></ul>
  20. 20. Mechanics of Exposure Treatment: TRI Model <ul><li>Typical treatment program consisted of 10-15 weekly treatment sessions of 90 minutes each </li></ul><ul><li>TRI Model adds </li></ul><ul><ul><li>2 ACT sessions </li></ul></ul><ul><ul><li>1 preliminary HRV psychoeducation session </li></ul></ul>
  21. 21. The ACT Model supplementation <ul><li>Recognizing that escape and avoidance will not work, and have not worked. </li></ul><ul><li>Control of emotion is the problem </li></ul><ul><ul><li>The principle of addition vs subtraction </li></ul></ul><ul><li>Stopping the struggle </li></ul><ul><li>Commitment to action </li></ul>
  22. 22. Sessions 5-10 <ul><li>Imaginal exposure </li></ul><ul><li>Homework assignments from in vivo exposure </li></ul><ul><li>Processing of exposure </li></ul><ul><li>Reminder of ACT principles </li></ul><ul><li>Evaluation of HRV progress about every 3 sessions </li></ul>
  23. 23. Session 11-15 <ul><li>Moving away from imaginal exposure, and focusing more on in vivo exposure </li></ul><ul><li>Acceptance of remaining anxiety as normal reactions (ACT) </li></ul>
  24. 24. Why include HRV training: 1 <ul><li>As Foa et al. (2002) point out, a minority of patients in PE show a reliable increase in symptoms </li></ul><ul><ul><li>21.1% exacerbation of anxiety symptoms </li></ul></ul><ul><ul><li>10.5% increase in PTSD symptoms </li></ul></ul><ul><ul><li>Exacerbation doesn’t mean dropout or poor outcome. </li></ul></ul><ul><li>The average dropout rate in CT or PT is 20-30%. </li></ul><ul><li>Therefore there is some evidence that management of the anxiety of treatment is a problem in current treatment. </li></ul>
  25. 25. Why include HRV training <ul><li>Both alexithymia and dissociation are highly comorbid with PTSD. </li></ul><ul><li>Therefore one cannot count on the patient being able to reliably describe their internal state of anxiety during PTSD treatment. </li></ul>
  26. 26. Why include HRV training: 3 <ul><li>Hyperventilation and Hyperventilation syndrome are comorbid with PTSD (particularly PTSD with panic) </li></ul><ul><li>The experience of hyperventilation syndrome mimics anxiety and dissociative syndromes </li></ul><ul><li>Hyperventilation syndrome is curable with high success rates by HRV training. </li></ul>
  27. 27. Applications II: New ideas and challenges <ul><li>In addition to affecting autonomic homeostasis, it is possible that the HRV biofeedback technique can affect: </li></ul><ul><ul><li>Mood/Dysphoria </li></ul></ul><ul><ul><li>Anxiety </li></ul></ul><ul><ul><li>Immune and inflammatory systems </li></ul></ul><ul><ul><li>Limbic emotional regulation (mindfulness) </li></ul></ul>
  28. 28. HRV Biofeedback
  29. 29. 12/20/09 Gevirtz RFT : Notice trend from three waves to a dominant .1 Hz Wave
  30. 30. 12/20/09 Gevirtz
  31. 31. Evidence of efficacy, HRV Biofeedback <ul><li>Asthma-Lehrer et al., Chest, 2004 </li></ul><ul><li>COPD- Giardino et al., APB, 2004 </li></ul><ul><li>CAD- Del Pozo et al. (AHJ, 2004), van Dixhoorn et al. </li></ul><ul><li>Performance- Strack et al., Gruzelier’s group (APB, 2005) </li></ul><ul><li>Stress, performance, etc., McCraty et al (Har. Bus Rev, 2003; Physio Beh Sci, 1999; numerous HeartMath reports) </li></ul><ul><li>IBS/RAP- Humphreys & Gevirtz (JPGN, 2000) Sowder, Gevirtz,et al. (2007) </li></ul><ul><li>FM- Hasset et al. APB,(2007) </li></ul><ul><li>Altitude sickness-Bernardi (2001& in press) </li></ul><ul><li>MDD, Karavadis et al., APB, (2007), Zucker et al.(2007), Rene et al.(2007) </li></ul><ul><li>Congestive Heart Failure-(Bernardi, 2002, Circulation) Swanson, Gevirtz, et al. (2007) </li></ul><ul><li>Hypertension- (Schein et al, 2001, J. Human Hypertension; Herbs & Gevirtz, 1994, Abstract, APB; Lehrer et al.,( 2004) Reinke, Gevirtz, et al. (2007) </li></ul><ul><li>PTSD Zucker et al., White et al.,(2008) </li></ul><ul><li>GAD Murphy, Hoffmann et al. (2008) </li></ul>
  32. 32. <ul><li>Mechanisms </li></ul><ul><ul><li>Baroreflex gain </li></ul></ul><ul><ul><li>Vagal Afferent stimulation </li></ul></ul><ul><ul><li>Shift towards mindfulness </li></ul></ul><ul><ul><li>Enhanced visceral perception </li></ul></ul><ul><ul><li>Reduced limbic drive </li></ul></ul><ul><ul><li>Enhanced frontal inhibitory circuits </li></ul></ul>
  33. 33. 12/20/09 Gevirtz
  34. 34. Baroreceptor Sensitivity <ul><li>A rise in BP stimulates the baroreceptor to signal to the SA node through the PNS to brake the HR. </li></ul><ul><li>A drop in BP stimulates the baroreceptor to increase HR through the SNS. </li></ul><ul><li>The ability of BP to regulate HR is called “Baroreceptor Sensitivity” (BRS). </li></ul>12/20/09 Gevirtz
  35. 35. Baroreflex Sensitivity (BRS) <ul><li>Sensitive prognostic indicator of cardiovascular health (Osterzeil et al., 1995, Br. Heart J, 73, 517-522) </li></ul><ul><li>Can be reliably estimated with .1 Hz paced breathing (Davies et al., 2002, Am. Heart J, 143,441-7) </li></ul><ul><li>Measure IBI (in msec) from valley to peak during .1 Hz paced breathing </li></ul><ul><li>Correlates r=.81 with finipres methods </li></ul><ul><li>Superior to: Bolus phenylephrine, alpha index, and sequence method (Davies et al., 1999, Clinical Science, 97, 515-522) </li></ul>12/20/09 Gevirtz
  36. 38. Vagal Afferents
  37. 39. 12/20/09 Gevirtz
  38. 40. Vagal Nerve Stimulation <ul><li>Medication resistant Depression </li></ul><ul><li>42% response rates after two years adjunctive treatment; Nahas et al. 2005 </li></ul><ul><li>Treatment resistant Epilepsy </li></ul><ul><li>“ Therefore VNS is safe and effective therapy and has a long-term sustained effect in refractory epilepsy.” Abubakr and Wambacq, 2007 </li></ul><ul><li>, </li></ul>Abuhuziefa Abubakr     , a ,     and Ilse Wambacq
  39. 41. Slow diaphragmatic breathing <ul><li>“… voluntary control of breath patterns can affect ANS functions via vagal afferents to brainstem nuclei (nucleus tractus solitarius, parabrachial nucleus, locus coeruleus)…Our neurophysiologic model postulates that vagal afferents activate hypothalamic vigilance areas and enhance and enhance attention and alertness, whereas pathways through the thalamus quiet frontal cortical activity and reduce anxious worrying” Gersbarg and Brown, 2005 </li></ul>
  40. 42. VNS=vagal nerve stimulation; NTS=nucleus tractus solitarius; PBN=parabrachial nucleus; MRS=mesolimbic reward system; SMR=sensori-motor rhythm; PRS=post-reinforcement synchronization (Adapted and reproduced with permission from John Wiley & Sons, Ltd.) 19 ( Italics mine) HRV biofeedback?
  41. 43. SUDS results from client (Dalenberg) Event SUDS 1 SUD2 SUDS3 SUDS4 1 25 15 5 0 2 35 0 5 0 3 55 35 5 5 4 65 55 15 5 5 75 75 45 5 6 85 85 45 25 7 90 90 40 30
  42. 44. Pathways for Vagal Afferent Stimulation <ul><ul><li>“ Evidence suggests that voluntary control of breath patterns can affect ANS functions via the vagal afferents to brainstem nuclei (nucleus tractus sollitarius, parabrachial nucleus, and locus coeruleus) … Our neurophysiologic model postulates that vagal afferents activate hypothalamic vigilance areas and enhance attention and alertness, whereas pathways through the thalamus quiet frontal cortical activity and reduce worrying” </li></ul></ul><ul><ul><li>(Gerbarg and Brown, J. of Family Practice, 4, 2005) </li></ul></ul>
  43. 45. Effect of Stress eraser vs. PMR on traumatized vets- White & Gevirtz, 2008 <ul><li>Within Non-dissociative veterans, SE reduced trauma symptoms to a significantly better PMR. </li></ul>
  44. 46. Limbic Emotional Regulation <ul><li>Recent StressEraser study for anxiety control indicated EEG patterns that are consistent with reductions in arousal at the level of the Limbic System (Sherlin et al., 2008) </li></ul>TM
  45. 47. Mindfulness: an important active ingredient in psychotherapy <ul><li>Do resonant frequency breathing techniques promote mindfulness? </li></ul><ul><ul><li>“ Moving from judging to witnessing” </li></ul></ul><ul><ul><li>Anecdotal reports: </li></ul></ul><ul><ul><ul><li>ACT </li></ul></ul></ul><ul><ul><ul><li>DBT </li></ul></ul></ul><ul><ul><ul><li>Yoga </li></ul></ul></ul><ul><ul><ul><li>Meditation </li></ul></ul></ul><ul><ul><ul><li>Prayer </li></ul></ul></ul><ul><li>. </li></ul>
  46. 48. Some prliminary data
  47. 49. BDI-II Score Pre to Post for the two Groups (Zucker et al., 2008) TM
  48. 50. Post Traumatic Stress Disorder Checklist (PCL-C) Score Pre to Post for the two Groups (Zucker et al., 2008) TM
  49. 51. Relationship between SDNN increase and trauma symptom decrease, Pre to Post
  50. 52. Dalenberg, 2008 Rx N Dropout % nonclin % subjective PE 189 14 81 71 PE+ACT 74 10 83 82 PE+ ACT + HRV 77 4 94 88
  51. 53. Treatment success over time
  52. 54. The effect of HRV Biofeedback vs TAU on PCL Trauma Scores in PTSD Vets Tan et al. 2008
  53. 55. The Effect of HRV Biofeedback vs. TAU on Memory Recall (total list learning) in PTSD Vets Ginsberg, 2009
  54. 56. Conclusions <ul><li>The addition of HRV biofeedback to empirically based PTSD treatment represents a promising step forward in treatment efficacy. </li></ul><ul><li>Results of a study in our lab, just getting under way where we are adding HRV biofeedback to PE therapy should allow further inference. </li></ul>