The neurobiology of social anxiety disorder is poorly understood, alth
ough preliminary research has suggested several possible biological ab
normalities. Challenge studies have demonstrated that subjects with so
cial anxiety disorder have a sensitivity to carbon dioxide, cholecysto
kinin, and caffeine somewhere between that of panic disorder patients
and normal controls. Serotonergic pathways may play a role in social a
nxiety disorder, as shown by the clinical effectiveness of selective s
erotonin reuptake inhibitors, plus fenfluramine and m-chlorophenylpipe
razine challenge studies. Dopaminergic function and striatal dopamine
uptake appear to be reduced in social anxiety disorder. There is also
evidence for cardiovascular and adrenergic abnormalities. Recently, po
sitron emission tomography has begun to identify brain regions that ap
pear to be uniquely activated in this condition. These results offer t
he promise of an understanding of the brain mechanisms of social anxie
ty disorder, but much further research is needed to fully elucidate th
e neurobiological cause(s) that exist.