In order to provide additional evidence and to verify the proposed impaired fear inhibition, validation is needed in a clinical sample of anxiety disorder patients. In the present study, inhibition of fear of PTSD patients will be compared with…
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Source
Brief title
Condition
- Psychiatric disorders
Synonym
Research involving
Sponsors and support
Intervention
Outcome measures
Primary outcome
1. *Startle* respons is measured by exposure to the *startle probe*. Door
middel van deze respons wordt de mate van angst en uiteindelijk de mate van
inhibitie gemeten. De *startle probe* (akoestische stimulus) wordt binauraal
door een koptelefoon geleverd. De *startle probe* bestaat uit een witte ruis
(alle frequenties omvattende) geluidsstimulus met een geluidsdrukniveau van
104-dbA en een duur van 40 msec.
2. Cognitive expectancy/contingency awareness: the online US expectancy is
measured on a 11- point scale from certainly no electrical pulse to uncertain
to *certain a elektric pulse'. After every stimulus presentation the online
expectancy is registered.
3. Propositional knowledge: after the computertask is finished the
questionnaire about the obtained knowledge about the stimuli are answered.
Secondary outcome
Using the human fear conditioning paradigm it is demonstrated that the effects
of extinction are largely confined to the context in which the extinction
procedure took place (Vansteenwegen, Hermans, Vervliet et al., 2005).
From the clinical viewpoint, it is suggested that changes in the constellation
of the therapy context contribute to the sometimes reported Return of fear
(Rachman, 1989) following successful therapy completion (see also Bouton, 2002)
Bouton and colleagues (e.g. Bouton & Nelson)
For these reasons, the effects of context on (transfer of) inhibition
performance will be tested. It will be hypothesized that patients with PTSD
will show less transfer of inhibition to another test context than controls. In
other words, patients regard the safety cue in another context as less
inhibitory.
Background summary
There is substantial evidence that neuroticism or trait anxiety poses a risk
factor for the development of anxiety disorders, but the mechanism remains
unclear. It is often assumed that mechanisms underlying experimental fear
conditioning play a fundamental role in the aetiology and maintenance of
anxiety disorders. Therefore, studies using fear-conditioning paradigm will
provide essential insights in the underlying mechanisms of pathological anxiety
and as a consequence, acquired knowledge could lead to improved treatment
techniques. The prevailing hypothesis that may account for the etiological
contribution of trait anxiety states that it may give rise to increased
excitatory fear learning. Although this hypothesis is appealing, evidence for
this hypothesis is scarce. As children grow up, they normally experience a
range of fears that wax and wane following a predictive pattern. The presence
of fears is not restricted to the vulnerable children. It is hypothesized that
the transition from normal fears to anxiety disorders may be better explained
by impaired fear inhibition of the fear-response even in the presence of safety
signals than by increased fear acquisition. A crucial element of anxiety may be
the distrust of safety signals instead of the overestimation of threat stimuli.
Study objective
In order to provide additional evidence and to verify the proposed impaired
fear inhibition, validation is needed in a clinical sample of anxiety disorder
patients. In the present study, inhibition of fear of PTSD patients will be
compared with trauma exposed non-PTSD individuals. This patient group can be
depicted by excessive anxiety and a failure to overcome these emotions.
Impaired fear inhibition could be related to the onset or maintenance of these
symptoms. It is predicted that patients with PTSD will show impaired fear
inhibition in a fear-potentiated startle paradigm (AX+/BX). If patients with
PTSD show impaired fear inhibition, this provides further evidence for the
mediating role of impaired fear inhibition in the etiology of anxiety
disorders.
Study design
This study embrace a clinical experimental study design. In order to test the
fear inhibition hypothesis, a recently developed AX+/BX- procedure (Myers &
Davis, 2004; Jovanovic et al., 2005) was used that allows for an independent
evaluation of excitation and inhibition of fear.
Fase Component
Habituation [NA (4)]¹
[NA (4)]²
Conditioning fase [AX+ (6)]¹
[BX- (6)]¹
[NA (6)]
Testfase 1 [AB- (3)]¹ of [AC- (3)]¹
[NA (3)]¹
Re-conditioning fase 1 [AX+ (3)]¹
[BX- (3)]¹
[NA (3)]¹
Testfase 2 [AC- (3)]¹ of [AB- (3)]¹
[NA (3)] ¹
Re-conditioning fase 2 [AX+ (2)]¹
[BX- (2)]¹
[NA (2)]¹
Testfase 3 [AB- (3)] ²
[NA (3)] ²
[]¹ = context 1, light
[]² = context 2, dark
CS+ = with US (electric pulse)
CS- = without US
NA = *noise alone*
AX+ = color combination followed by adverse stimulus (US)
BX-., AB, AC = color combination not followed by adverse stimulus (US)
Study burden and risks
Although some people could experience the experiment as aversive, the
experiment involves no risks,the burden is minimal and the computer task only
takes 25 minutes.
Roetersstraat
1018 WB Amsterdam
Nederland
Roetersstraat
1018 WB Amsterdam
Nederland
Listed location countries
Age
Inclusion criteria
All subjects have experienced a work-related trauma. The main inclusion criteria for the experimental group is to meet the DSM IV criteria for PTSD as a consequence of a work related trauma.
Exclusion criteria
The main exclusion criteria all subjects are; severe concentration problems, visual problems, hearing problems, pregancy, cardiovascular complaints and epilepsy. ;Exclusion criteria for the experimental group is severe comorbidity and PTSD as a consequence of complex trauma. Exclusion criteria of the control group are any DSM IV diagnosis.
Design
Recruitment
Followed up by the following (possibly more current) registration
No registrations found.
Other (possibly less up-to-date) registrations in this register
No registrations found.
In other registers
Register | ID |
---|---|
CCMO | NL19049.018.07 |