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Psychophysiological Assessment of Stress-related Disorders

COST B27 ENOC Joint WGs Meeting Swansea UK, 16-18 September 2006. Psychophysiological Assessment of Stress-related Disorders. Dragica Kozari ć -Kova č i ć , Tanja Jovanovi ć , Andrea Jambro š i ć -Sakoman, Slavica Esterajher

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Psychophysiological Assessment of Stress-related Disorders

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  1. COST B27 ENOC Joint WGs Meeting Swansea UK, 16-18 September 2006 Psychophysiological Assessment of Stress-related Disorders Dragica 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

  2. Why measure psychophysiology?

  3. 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

  4. 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.

  5. Psychophysiology of fear From Lang, Davis & Öhman (2000), J. Affective Disorders

  6. 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

  7. Baseline psychophysiology

  8. 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

  9. Psychophysiology measures • EDA from fingers for skin conductance response (SCR)

  10. EMG of the obicularis oculi for startle

  11. EKG for heart-rate and respiration for RSA

  12. Apparatus • Acquisition: Biopac MP150 for Windows (Biopac Systems, Inc.) • Stimulus presentation: SuperLab 3.0 (Cedrus, Inc.)

  13. Results: EDA

  14. EDA: Higher SCR to startle probes in both groups, controls habituate NA1 VS. ACL5, controls, F(1,11)=17.09, p<0.01; PTSD, F(1,14)=10.40, p<0.01 NA1 TO NA7, controls, linear F(1,11)=11.67, p<0.01; PTSD, linear F(1,14)=2.44, ns

  15. Results: EMG

  16. 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<0.01 NA1 TO NA7, controls, linear F(1,11)=2.02, ns; PTSD, linear F(1,14)=1.42, ns

  17. Results: EKG

  18. EKG: PTSD higher heart-rate than controls, no effect of startle probes CONTROLS VS. PTSD, F(1,25)=7.56, p=0.01

  19. RSA: PTSD lower HR variability than controls, no effect of probes CONTROLS VS. PTSD, F(1,25)=7.56, p=0.01

  20. Thank you for your attention!

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