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
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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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Psychophysiology measures
• EDA from fingers for skin conductance
response (SCR)
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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
SCR (MICROSIEMENS)
CONTROL
PTSD
1.6
1.4
1.2
1
0.8
0.6
0.4
0.2
0
ACL1 ACL2 ACL3 ACL4 ACL5
NA1
NA2
NA3
NA4
NA5
NA6
NA7
TRIALS
NA1 VS. ACL5, controls, F(1,11)=17.09, p<0.01; PTSD, F(1,14)=10.40, p<0.01 15
NA1 TO NA7, controls, linear F(1,11)=11.67, p<0.01; PTSD, linear F(1,14)=2.44, ns
Results: EMG
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EMG: no group differences in
startle, no habituation
CONTROL
PTSD
STARTLE
(MICROVOLTS)
40
35
30
25
20
15
10
5
0
ACL1 ACL2 ACL3 ACL4 ACL5
NA1
NA2
NA3
NA4
NA5
NA6
NA7
TRIALS
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
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Results: EKG
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EKG: PTSD higher heart-rate than
controls, no effect of startle probes
CONTROL
PTSD
HEART RATE (BPM)
100
95
90
85
80
75
70
65
60
ACL1
ACL2
ACL3
ACL4
ACL5
NA1
NA2
NA3
NA4
NA5
NA6
NA7
TRIALS
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
CONTROL
PTSD
7.00
6.00
5.00
4.00
3.00
2.00
1.00
0.00
ACL1 ACL2 ACL3 ACL4 ACL5 NA1
NA2
NA3
NA4
NA5
NA6
NA7
TRIALS
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CONTROLS VS. PTSD, F(1,25)=7.56, p=0.01
Thank you for your attention!
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