Cerebral control of social behaviour in social anxiety disorder

Social anxiety disorder (SAD) is characterized by persistent fear and avoidance
in social situations. Although several studies have addressed the neural bases
of threat processing in SAD, almost nothing is known on how the behavioral fear
responses evoked by the threat stimuli (such as approach and avoidance
responses) are controlled. Social approach-avoidance behavior can be reliably
measured using computer tasks, in which participants either approach or avoid
visually presented facial expressions by pulling or pushing a joystick,
respectively. Generally, response latencies are shorter for affect-congruent
(happy-approach; angry-avoid), as compared to affect-incongruent
response-conditions (angry-approach; happy-avoid). Recently, these behavioral
AA congruency-effects have been found to be accompanied by increased activation
in the left orbitofrontal cortex in healthy participants (Roelofs et al., in
Press). In addition, a behavioral study demonstrated that patients with SAD
show increased behavioural AA congruency-effects for angry faces in relation to
increased cortisol levels (Roelofs et al., 2008). We hypothesize that increased
AA-congruency-effects in clinical social anxiety result from a failure in the
cortical regulation of social fear behavior.

To assess differences in brain activation during the AA task in participants
with SAD.

A static group comparison design (patients versus matched healthy volunteers).

All participants will be tested inside a MRI scanner. The Donders Institute for
brain, cognition and behavior: centre for cognitive neuroimaging has a lot of
experience with the type of research we are proposing in this protocol and
there are no special risks associated with this kind of research.
Although there is no direct benefit to the participants from this proposed
research, this study can increase insight in the neurobiological background of
failing control of social fear behavior in patients with social anxiety
disorder (SAD). A greater understanding of the neurobiological control
mechanisms of social fear behavior is of crucial importance for the development
of both psychological and pharmacological interventions in SAD. The study is
not only relevant for SAD, but also for other anxiety disorders characterized
by a failure to regulate fear and fear behavior, such as Post Traumatic Stress
Disorder (PTSD) and General Anxiety Disorder (GAD).