Researchers from the Department of Clinical Neuroscience, Division of Psychiatry, at Karolinska Institute in Stockholm, Sweden looked at whether the dopamine system plays a role in social anxiety disorder (SAD). The complete, free article can be found here.

In the past, molecular imaging studies have shown reduced levels of striatal dopaminergic markers in SAD patients, as compared with control subjects.  But the dopamine system has not been examined in frontal and limbic brain regions, which are considered to be central in the pathophysiology of SAD.
In this study, investigators hypothesized that extra-striatal dopamine D2-receptor (D2-R) levels, as measured by PET scan, 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 [(11)C]FLB 457, before and after 15 weeks of CBT. Symptom levels were assessed using the anxiety subscale of the Liebowitz Social Anxiety Scale (LSAS(anx)).

At post-treatment, 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 × LSAS(anx) change on D2-R-binding potential (BP(ND)) were shown (P<0.05).

In a subsequent region-by-region analysis, negative correlations between change in D2-R BP(ND) and LSAS(anx) 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 15 weeks of psychological treatment (CBT) and a marker of brain neurotransmission.  Using an intra-individual comparison design, the study supports a significant role for the dopamine system in cortical and limbic brain regions in the pathophysiology of SAD.

Citation:  S Cervenka, E Hedman, Y Ikoma, D Radu Djurfeldt, C Rück, C Halldin, and N Lindefors Changes in dopamine D2-receptor binding are associated to symptom reduction after psychotherapy in social anxiety disorder. Translational Psychiatry. 2012 May 22;2:e120. doi: 10.1038/tp.2012.40. [email protected]