Dopamine transporter binding in social anxiety disorder: the effect of treatment with escitalopram

• DOI: 10.1007/s11011-012-9280-3
• Publication Date: 2012-02-15T02:13:06Z
• Authors: J. M. Warwick; P. D. Carey; N. Cassimjee; C. Lochner; S. Hemmings; H. Moolman-Smook; E. Beetge; P. Dupont; D. J. Stein
• Keywords: Adult; Male; Genotype; Dopamine; 150; Citalopram; Neuropsychological Tests; Imaging; 03 medical and health sciences; 0302 clinical medicine; Image Processing, Computer-Assisted; SSRI; Humans; Social anxiety disorder; Tomography, Emission-Computed, Single-Photon; Dopamine Plasma Membrane Transport Proteins; Brain; DAT; Middle Aged; Diagnostic and Statistical Manual of Mental Disorders; Phobic Disorders; SPECT; Antidepressive Agents, Second-Generation; Female; Radiopharmaceuticals; Tropanes

Social anxiety disorder (SAD) is characterised by fear of social or performance situations where the individual is exposed to unfamiliar people or to possible scrutiny by others. The literature on dopamine ligands and dopamine genotypes in SAD is however inconsistent. In this study we measured the effects of SSRI pharmacotherapy on dopamine transporter (DAT) binding in patients with SAD, also addressing variability in DAT genotype. Adult subjects meeting DSM-IV criteria for generalised SAD were studied before and after 12 weeks of pharmacotherapy with the selective serotonin reuptake inhibitor (SSRI) escitalopram. DAT single photon emission computed tomography (SPECT) using (123)I-FP-CIT was performed at baseline, and repeated at 12 weeks. Striatal DAT binding was analysed for changes following therapy, and for correlations with clinical efficacy, in the whole group as well as for a subgroup with the A10/A10 DAT genotype. The study included 14 subjects (9 male, 5 female) with a mean (SD) age of 41 (±13) years. The subjects' Liebowitz Social Anxiety Scale (LSAS) score was significantly decreased following pharmacotherapy. In the combined group the left caudate and left putamen showed clusters of increased DAT binding after therapy. The left caudate changes were also observed in the subgroup of 9 A10/A10 homozygotes. However no correlation was found between improved symptoms and DAT binding. The changes found in DAT binding in the caudate and putamen may be due to serotonergic activation of dopamine function by SSRI therapy. This is consistent with previous work indicating decreased DAT binding in SAD, and increased DAT binding after SSRI administration.