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Psychophysiological Assessment of Stress-related

DisordersDragica Kozarić-Kovačić, Tanja Jovanović,

Andrea Jambrošić-Sakoman, Slavica Esterajher

University Hospital Dubrava, Croatian Ministry of Health Referral Center for the Stress-related Disorders, Regional Center for Psychotrauma

COST B27 ENOC Joint WGs Meeting Swansea UK, 16-18 September 2006

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Why measure psychophysiology?

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Rationale

• Posttraumatic stress disorder (PTSD) and acute stress disorder (ASD) can develop after exposure to traumatic events

• Due to the fact that the diagnosis is based on the patients' self-report of symptoms, a diagnosis of PTSD is difficult to make with certainty, and can be malingered

• There is a need to include more objective assessment techniques in a multimodal approach

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• The psychophysiological reaction to stressful stimuli is under the control of the sympathetic nervous system and is difficult to malinger

• In ASD and PTSD reminders of the traumatic experience induce exaggerated fear and subsequent physiological symptoms.

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Psychophysiology of fear

From Lang, Davis & Öhman (2000), J. Affective Disorders

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Aims of the project

• To see whether PTSD patients have increased psychophysiological arousal to trauma stimuli compared to controls

• To see whether psychophysiological response in ASD will be related to the development of PTSD

• To see whether a lack of association between arousal and PTSD symptoms will be correlated with malingering

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Baseline psychophysiology

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Methods• Participants:

– 15 male subjects with chronic PTSD • (age=39.5±4.7 years)

– 12 male healthy control subjects• (age=41.3±10.7 years)

• Trials:– ACL: 3 minutes acclimation period—no stimuli– NA: 7 startle probes, 108 dB [A] SPL, 40ms

white noise burst

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• EDA from fingers for skin conductance response (SCR)

Psychophysiology measures

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• EMG of the obicularis oculi for startle

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• EKG for heart-rate and respiration for RSA

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Apparatus

• Acquisition: Biopac MP150 for Windows (Biopac Systems, Inc.)

• Stimulus presentation: SuperLab 3.0 (Cedrus, Inc.)

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Results: EDA

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EDA: Higher SCR to startle probes in both groups, controls habituate

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0.2

0.4

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0.8

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1.2

1.4

1.6

ACL1 ACL2 ACL3 ACL4 ACL5 NA1 NA2 NA3 NA4 NA5 NA6 NA7

TRIALS

SC

R (

MIC

RO

SIE

ME

NS

)

CONTROL PTSD

NA1 VS. ACL5, controls, F(1,11)=17.09, p<0.01; PTSD, F(1,14)=10.40, p<0.01NA1 TO NA7, controls, linear F(1,11)=11.67, p<0.01; PTSD, linear F(1,14)=2.44, ns

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Results: EMG

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EMG: no group differences in startle, no habituation

NA1 VS. ACL5, controls, F(1,11)=5.01, p<0.05; PTSD, F(1,14)=9.50, p<0.01NA1 TO NA7, controls, linear F(1,11)=2.02, ns; PTSD, linear F(1,14)=1.42, ns

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5

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25

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ACL1 ACL2 ACL3 ACL4 ACL5 NA1 NA2 NA3 NA4 NA5 NA6 NA7

TRIALS

ST

AR

TL

E

(MIC

RO

VO

LT

S)

CONTROL PTSD

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Results: EKG

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EKG: PTSD higher heart-rate than controls, no effect of startle probes

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ACL1 ACL2 ACL3 ACL4 ACL5 NA1 NA2 NA3 NA4 NA5 NA6 NA7

TRIALS

HE

AR

T R

AT

E (

BP

M)

CONTROL PTSD

CONTROLS VS. PTSD, F(1,25)=7.56, p=0.01

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RSA: PTSD lower HR variability than controls, no effect of probes

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ACL1 ACL2 ACL3 ACL4 ACL5 NA1 NA2 NA3 NA4 NA5 NA6 NA7

TRIALS

CONTROL PTSD

CONTROLS VS. PTSD, F(1,25)=7.56, p=0.01

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Thank you for your attention!