SOCIAL ANXIETY
DISORDER
Introduction and Clinical Presentation. Social anxiety disorder (SAD), or social phobia, is characterized by persistent fear of social or performance situations in which an individual will face exposure to unfamiliar people or scrutiny by others. The individual typically fears behaving in an embarrassing or humiliating fashion, or revealing symptoms of anxiety. Exposure to these situations provokes anxiety or panic symptoms, leading the individual to avoid such situations whenever possible. Physical symptoms may include diaphoresis, tachycardia, trembling, nausea, flushing, and difficulty speaking, for example.
DSM-IV criteria stipulate that this condition
contributes to significant functional impairment (for example, in work or
relationships) or distress. Of note, the individual recognizes that the fear is
excessive or unreasonable. Although the diagnosis has been criticized for
ascribing a medical diagnosis to a normal population trait, shyness, the
persistence and severity of these symptoms—and in particular their impact on
functioning—argues otherwise.
Diagnostic criteria distinguish a
generalized form, that is, occurring in most social situations, or a specific
form, that is, one which occurs only in particular circumstances, such as
public speaking or public performance, or writing or eating in front of others.
However, these are not necessarily distinct subtypes, although the generalized
form may be more disabling overall.
Epidemiology. The lifetime prevalence of SAD is ≈12%,
with 12-month prevalence of ≈7%. SAD often has early onset, with about half
of cases presenting by age 11 years; on the other hand, later onset in many
patients provides further support for SAD being some-thing other than the trait
of shyness. As with major depressive disorder, SAD is seen more commonly in
females. As with other psychiatric disorders, rates of comorbidity are high,
having overlap with major depression and substance use disorder, for example.
Treatment of SAD relies on either
cognitivebehavioral therapy, delivered individually or in a group setting, or
pharmacotherapy. Standard medication treatments use selective serotonin
reuptake inhibitors, although other antidepressants, including monoamine-oxidase inhibitors and serotonin-norepinephrine reuptake inhibitors have also
demonstrated efficacy. Anxiolytic medications, such as benzodiazepines, are
sometimes used as well. Scales such as the Liebowitz Social Anxiety Scale may
be used to quantify severity over time.
Pathophysiology. SAD has been noted to be familial, and often
coaggregates with major depression, panic disorder, and agoraphobia. Twin
studies suggest that about 40% of liability is inherited. Although candidate
gene studies have implicated multiple genes, no single association has been
convincingly demonstrated, and genome-wide studies have not been reported. The potential role of neuropeptides involved in
social cognition, such as oxytocin and arginine vasopressin, is also under
active investigation. For example, rodent models illustrate the capacity of
oxytocin to diminish social avoidance, which may inform future treatment
development in SAD.
Functional magnetic resonance imaging (fMRI) implicates the amygdala and insula activation in SAD, for example, on tasks requiring processing of emotional faces. fMRI also suggests there may be abnormal connectivity evident in the resting state, involving frontal and occipital structures. Other studies also suggest basal ganglia dysfunction in SAD; of interest, SAD is seen more commonly in individuals with Parkinson disease, which may provide convergent evidence for the role of basal ganglia in these symptoms.
