Emerging Applications of Heart Rate Variability Biofeedback: Trauma

Richard Gevirtz, Ph.D., BCIAC

CSPP@ AIU, San Diego, CA

rgevirtz@alliant.edu

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

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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

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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).

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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.