Translational Psychiatry
(2012) 2, e120; doi:10.1038/tp.2012.40
S Cervenka, E Hedman, Y Ikoma, D Radu Djurfeldt, C Rück, C Halldin and N Lindefors
- 1Department of Clinical Neuroscience, Division of Psychiatry, Karolinska Institutet, Stockholm, Sweden
- 2Department of Clinical Neuroscience, Osher Center for Integrative Medicine and Division of Psychology, Karolinska Institutet, Stockholm, Sweden
- 3Molecular Imaging Center, National Institute of Radiological Sciences, Chiba, Japan
Correspondence: Dr S Cervenka, Department of Clinical Neuroscience, Division of Psychiatry, Karolinska Institutet, Karolinska University Hospital Solna, Building R5, 171 76 Stockholm, Sweden. E-mail: [email protected]
Received 19 March 2012; Accepted 10 April 2012
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. (emphasis supplied)