gevirtz, jrv and ptsd
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Transcript of gevirtz, jrv and ptsd
Emerging Applications of Heart Rate Variability Biofeedback: Trauma
Richard Gevirtz, Ph.D., BCIAC
CSPP@ AIU, San Diego, CA
Posttraumatic Stress Disorder Criteria (DSM-IV-TR, 2000) Psychiatric Disorder, Classified as Anxiety Disorder
Criterion A
Traumatic EventOr, series of eventsDirectly or indirectly
experienced
Subjective Response Involve: intense fear, helplessness, or horror
Criterion B
Reexperiencing Symptom Cluster
Intrusive thoughtsDistressing dreamsTrauma cue distress
Criterion C
AvoidantSymptom ClusterAvoid trauma-related
thoughts, places,feelings
Criterion D
Hyperarousal Symptom Cluster
InsomniaIrritability, anger,hypervigilance
The biological message of trauma Remember this moment Never go this way again Be prepared
Severity defined by The breadth of the definition of “this way” The extent of the preparation
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?
Deficit in awareness of internal sensations and being in the present Deficits in frontal sub-cortical circuitry and
Cortico-thalamic integration Vasterling et al., 1998; Clark et al.
2003
Alexithymia Krystal, 1988
Inability to accurately perceive internal states
Evidence from neuro-imaging studies: Exposure to trauma scripts produces:
Increased activity (as measured by blood flow) in: Right medial orbital frontal cortex Insula Amygdala Anterior temporal pole
Deactivation in: Left anterior prefrontal cortex- especially Broca’s area (expressive
speech)Rauch, Van der Kolk, et al, 1966Hull, 2002Lanius, et al., 2001Lindauer et al., 2004
Conditioned fear memories - the lateral nucleus of the amygdala to the central nucleus to the ANS ; Amorapanth,La Doux, et al. 2000
“…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)
Van Der Kolk, 2006
Rostral Anterior
Cingulate ↓
↑ RightAnteriorInsula
Reexperiencing Dissociation
Region implicatedin awareness
of bodily states
Emotional Undermodulation
EmotionalOvermodulatio
n
↓ RightAnteriorInsula
↑ MedialPrefrontal
Cortex
Figure 1: Emotion Dysregulation in PTSD
Regions implicatedin regulation
of emotion and arousal
↓ MedialPrefrontal
Cortex
Amygdala ↑ ↓ Amygdala
Regions implicatedin regulation
of emotion and arousal
RostralAnterior
Cingulate ↑
PTSD Biological Evidence
Neuropsychological Alterations (Charney, et al., 1993; Kolb, 1987; van der Kolk, 2006) Excessive emotional stimulation alters neurological functioning PTSD symptoms are maladaptive neurobiologic sequelae
Low cortisol (Yehuda, Boisoneau, Mason, & Giller, 1993; Yehuda, Kahana, Binder-Brynes K & Southwick, 1995) Paradoxical: Stress = Surge of cortisol Cortisol inhibits, stabilizes stress hormones
Autonomic Nervous System Elevated HR (Buckley and Kaloupek, 2001; Keane et al., 1998) 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)
PTSD: Evidence of Underlying Biological Core?PTSD is Psychophysiological Disorder:
Universal symptom: intrusive memories: not event itself > unique Intrusion > hyperarousal > insomnia > hypervigilance >
exaggerated startle response
Longitudinal study (Schell, Grant, and Jaycox , 2004) Severity of the hyperarousal cluster leads to greater symptom
severity of intrusion +avoidance cluster (12-months). Converse is not true.
John Hughlings Jackson to MacLean:Devolution toTriune brain structure Organization of the CNS-”bottom up” Executive functions (prefrontal cortex) under
ordinary circumstances can inhibit, organize, and modify automatic processes coming from the lower centers
“…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
Elaborated in the 1990 by Mac Lean’s concept of the Triune brain
Developmental perspective Human species unique in their flexibility; abilty to
make choices of how to respond, but these functions develop slowly
Higher function develop during childhood and don’t exist in final form until young adulthood
Vagal development, especially the “smart vagus” follows this develomental sequence
“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
Amygdala and biological salience The amygdala tags incoming stimuli to
determine their biological relevance Action stems from this process 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
Implications for treatment The only empirically based treatments to date are CBT,
CBT/PE, and CPT. Though meta-analyses show that these therapies are better than
placebo, they leave “much room for improvement” Effect sizes are small Hofmann, 2008
“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
A somatic intervention might be a necessary component for PTSD treatment
Interventions that prompt behavioral action may be superior
PTSD Treatment Interventions (cont.)
Biological Researchers conclude:
Treatment interventions need to address core neuronal and psychophysiological abnormalities (Charney, 1993; van der Kolk, 2006)
Neuropsychological abnormalities limit the “main staples” of
psychotherapy, understanding and insight as well as the ability to
communicate thoughts and feelings (van der Kolk, 2006)
Foa’s Emotional Processing Theory Fear represented in memory as cog structure
that is a “program” for escaping danger. This includes: Fear responses (e.g. heart acceleration) Meaning of stimuli (“This man is dangerous” Cognitive responses (“My fast heartrate means
that I am afraid.”
Fear structure becomes pathological when:
Associations are inaccurate Physiological and escape/avoidance responses
are evoked by harmless stimuli Excessive and easily triggered responses
interfere with adaptive behavior Harmless stimuli and elements are associated
with threat meaning
The mechanisms of CPTSD treatment The connection of fear to its source The creation of safety The de-stigmatization of fear and its
consequences
The role of “relaxation” Historically preserved as part of the original
Exposure and PE packages Not seen as important by theoreticians Relied on by clinicians
Would the role of relaxation by enhanced by the addition of HRV technology?
Mechanics of Exposure Treatment: TRI Model Typical treatment program consisted of 10-15
weekly treatment sessions of 90 minutes each TRI Model adds
2 ACT sessions 1 preliminary HRV psychoeducation session
The ACT Model supplementation Recognizing that escape and avoidance will
not work, and have not worked. Control of emotion is the problem
The principle of addition vs subtraction Stopping the struggle Commitment to action
Sessions 5-10 Imaginal exposure Homework assignments from in vivo
exposure Processing of exposure Reminder of ACT principles Evaluation of HRV progress about every 3
sessions
Session 11-15 Moving away from imaginal exposure, and
focusing more on in vivo exposure Acceptance of remaining anxiety as normal
reactions (ACT)
Why include HRV training: 1 As Foa et al. (2002) point out, a minority of patients in
PE show a reliable increase in symptoms 21.1% exacerbation of anxiety symptoms 10.5% increase in PTSD symptoms Exacerbation doesn’t mean dropout or poor outcome.
The average dropout rate in CT or PT is 20-30%. Therefore there is some evidence that management of
the anxiety of treatment is a problem in current treatment.
Why include HRV training Both alexithymia and dissociation are highly
comorbid with PTSD. Therefore one cannot count on the patient
being able to reliably describe their internal state of anxiety during PTSD treatment.
Why include HRV training: 3 Hyperventilation and Hyperventilation syndrome
are comorbid with PTSD (particularly PTSD with panic)
The experience of hyperventilation syndrome mimics anxiety and dissociative syndromes
Hyperventilation syndrome is curable with high success rates by HRV training.
Applications II: New ideas and challenges In addition to affecting autonomic
homeostasis, it is possible that the HRV biofeedback technique can affect: Mood/Dysphoria Anxiety Immune and inflammatory systems Limbic emotional regulation (mindfulness)
HRV Biofeedback
04/11/23 Gevirtz 29
RFT : Notice trend from three waves to a dominant .1 Hz Wave
04/11/23 Gevirtz 30
Evidence of efficacy, HRV Biofeedback Asthma-Lehrer et al., Chest, 2004 COPD- Giardino et al., APB, 2004 CAD- Del Pozo et al. (AHJ, 2004), van Dixhoorn et al. Performance- Strack et al., Gruzelier’s group (APB, 2005) Stress, performance, etc., McCraty et al (Har. Bus Rev, 2003; Physio Beh
Sci, 1999; numerous HeartMath reports) IBS/RAP- Humphreys & Gevirtz (JPGN, 2000) Sowder, Gevirtz,et al. (2007) FM- Hasset et al. APB,(2007) Altitude sickness-Bernardi (2001& in press) MDD, Karavadis et al., APB, (2007), Zucker et al.(2007), Rene et al.(2007) Congestive Heart Failure-(Bernardi, 2002, Circulation) Swanson, Gevirtz, et
al. (2007) Hypertension- (Schein et al, 2001, J. Human Hypertension; Herbs & Gevirtz,
1994, Abstract, APB; Lehrer et al.,( 2004) Reinke, Gevirtz, et al. (2007) PTSD Zucker et al., White et al.,(2008) GAD Murphy, Hoffmann et al. (2008)
Mechanisms Baroreflex gain Vagal Afferent stimulation Shift towards mindfulness Enhanced visceral perception Reduced limbic drive Enhanced frontal inhibitory circuits
04/11/23 Gevirtz 33
04/11/23 Gevirtz 34
Baroreceptor Sensitivity A rise in BP stimulates the baroreceptor to
signal to the SA node through the PNS to brake the HR.
A drop in BP stimulates the baroreceptor to increase HR through the SNS.
The ability of BP to regulate HR is called “Baroreceptor Sensitivity” (BRS).
04/11/23 Gevirtz 35
Baroreflex Sensitivity (BRS) Sensitive prognostic indicator of
cardiovascular health (Osterzeil et al., 1995, Br. Heart J, 73, 517-522)
Can be reliably estimated with .1 Hz paced breathing (Davies et al., 2002, Am. Heart J, 143,441-7)
Measure IBI (in msec) from valley to peak during .1 Hz paced breathing
Correlates r=.81 with finipres methods Superior to: Bolus phenylephrine, alpha
index, and sequence method (Davies et al., 1999, Clinical Science, 97, 515-522)
Baroreceptor Reflex Sensitivity for both Groups over Sessions
0
2
4
6
8
10
12
1 5 10 11
Session
BR
S (m
s/m
mH
g)
TreatmentComparison
Antihypertensive Medication Changes by Group
0
2
4
6
8
10
12
Increase Same Decrease
Num
ber o
f Pat
ients
TreatmentComparison
Vagal Afferents
04/11/23 Gevirtz 39
Vagal Nerve Stimulation Medication resistant Depression
42% response rates after two years adjunctive treatment; Nahas et al. 2005
Treatment resistant Epilepsy“Therefore VNS is safe and effective therapy and has a long-term sustained effect in refractory epilepsy.” Abubakr and
Wambacq, 2007
,
Abuhuziefa Abubakr , a,
and Ilse Wambacq
Slow diaphragmatic breathing “… 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
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?
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
Pathways for Vagal Afferent Stimulation
“ 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”
(Gerbarg and Brown, J. of Family Practice, 4, 2005)
Effect of Stress eraser vs. PMR on traumatized vets- White & Gevirtz, 2008
Within Non-dissociative veterans, SE reduced trauma symptoms to a significantly better PMR.
Limbic Emotional Regulation
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)
TM
Mindfulness: an important active ingredient in psychotherapy Do resonant frequency breathing techniques
promote mindfulness? “Moving from judging to witnessing” Anecdotal reports:
ACT DBT Yoga Meditation Prayer
.
Some prliminary data
BDI-II Score Pre to Post for the two Groups (Zucker et al., 2008)
TM
Post Traumatic Stress Disorder Checklist (PCL-C)
Score Pre to Post for the two Groups (Zucker et al., 2008)
TM
Relationship between SDNN increaseand trauma symptom decrease, Pre to Post
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
Treatment success over time
The effect of HRV Biofeedback vs TAU on PCL
Trauma Scores in PTSD Vets Tan et al. 2008
48
50
52
54
56
58
60
62
64
66
Pre Post
HRVtxControl
The Effect of HRV Biofeedback vs. TAU on Memory Recall
(total list learning) in PTSD Vets Ginsberg, 2009
52
53
54
55
56
57
58
59
Pre Post
HRVControl
Conclusions The addition of HRV biofeedback to
empirically based PTSD treatment represents a promising step forward in treatment efficacy.
Results of a study in our lab, just getting under way where we are adding HRV biofeedback to PE therapy should allow further inference.