Social anxiety disorder (SAD) is considered to be one of the most common anxiety disorders. Despite its high prevalence, the disorder is still considerably underdiagnosed and undertreated. SAD shows a typically early onset in childhood or early adolescence and generally becomes chronic. The disease places a massive burden on patients lives, affecting not only their social interactions but also their educational and professional activities, thereby constituting a severe disability. Although substantial progress in the study of the etiology of SAD has been made, no commonly accepted model has emerged yet. Data from genetic and neuroimaging studies point towards a contribution of several neurotransmitter systems (i.e. norepinephrine, dopamine and serotonin) to the pathophysiology of this disorder. Functional magnetic resonance imaging studies have repeatedly emphasized the central role of the amygdalae and insula in the neural circuitry of the disorder. Selective serotonin reuptake inhibitors (SSRI) are commonly accepted as first line therapy, however other substance classes like serotonin norepineprine reuptake inhibitors (SNRI), monoamine oxidase inhibitors (MAOI), benzodiazepines and several other agents have also proved effective. There is still a substantial lack of data on therapeutic options in cases of non-responsive SAD as well as on add-on therapy. A combined treatment-approach including psychotherapy (e.g. cognitive behavioural therapy) may prove useful.