Abstract
The dopamine system has been suggested to play a role in social anxiety disorder (SAD), partly based on molecular imaging studies showing reduced levels of striatal dopaminergic markers in patients compared with control subjects. However, the dopamine system has not been examined in frontal and limbic brain regions proposed to be central in the pathophysiology of SAD. In the present study, we hypothesized that extrastriatal dopamine D2-receptor (D2-R) levels measured using positron emission tomography (PET) would predict symptom reduction after cognitive behavior therapy (CBT). Nine SAD patients were examined using high-resolution PET and the high-affinity D2-R antagonist radioligand [11C]FLB 457, before and after 15 weeks of CBT. Symptom levels were assessed using the anxiety subscale of Liebowitz Social Anxiety Scale (LSASanx). At posttreatment, there was a statistically significant reduction of social anxiety symptoms (P<0.005). Using a repeated measures analysis of covariance, significant effects for time and time × LSASanx change on D2-R-binding potential (BPND) were shown (P<0.05). In a subsequent region-by-region analysis, negative correlations between change in D2-R BPND and LSASanx change were found for medial prefrontal cortex and hippocampus (P<0.05). This is the first study to report a direct relationship between symptom change after psychological treatment and a marker of brain neurotransmission. Using an intra-individual comparison design, the study supports a role for the dopamine system in cortical and limbic brain regions in the pathophysiology of SAD.
Highlights
The dopamine system is involved in social behavior, learning and emotional regulation, predicting a role in the pathophysiology of social anxiety disorder (SAD)
This has been due to methodological limitations, as the first generation D2-receptor (D2-R) positron emission tomography (PET) radioligands such as [11C]raclopride have insufficient affinity for measurements in low-density extrastriatal brain regions
We assessed the role of the extrastriatal dopamine system in SAD, by examining changes in dopamine D2-R binding as a function of symptom change after cognitive behavior therapy (CBT)
Summary
The dopamine system is involved in social behavior, learning and emotional regulation, predicting a role in the pathophysiology of social anxiety disorder (SAD). Molecular imaging studies have provided preliminary support for this hypothesis, showing reduced levels of striatal dopaminergic markers both pre- and postsynaptically in patients compared with control subjects.[1,2,3] negative results have been reported.[4] A possible explanation for this inconsistency may be that none of the studies performed far have examined the dopamine system in limbic or prefrontal brain regions, which have shown to be involved in SAD based on brain activation studies For SAD, cognitive behavior therapy (CBT) leads to clinical improvement in up to 75% of patients.[7,8]
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