Social anxiety disorder (SAD), also known as social phobia, is the most common anxiety disorder.[1] It is one of the most common psychiatric disorders, with 12% of Americans having experienced it in their lifetime.[2] It is characterized by intense fear in one or more social situations,[3] causing considerable distress and impaired ability to function in at least some parts of daily life. These fears can be triggered by perceived or actual scrutiny from others. While the fear of social interaction may be recognized by the person as excessive or unreasonable, overcoming it can be quite difficult. Some people suffering from social anxiety disorder fear a wide range of social situations while others may only show anxiety in performance situations. In the latter case, the specifier "performance only" is added to the diagnosis.
Social anxiety disorder is known to appear at an early age in most cases. Fifty percent of those who develop this disorder have developed it by the age of 11 and 80% have developed it by age 20. This early age of onset may lead to people with social anxiety disorder being particularly vulnerable to depressive illnesses, drug abuse and other psychological conflicts.[1] Physical symptoms often accompanying social anxiety disorder include excessive blushing, sweating (hyperhidrosis), trembling, palpitations and nausea. Stammering may be present, along with rapid speech. Panic attacks can also occur under intense fear and discomfort. An early diagnosis may help minimize the symptoms and the development of additional problems, such as depression. Some sufferers may use alcohol or other drugs to reduce fears and inhibitions at social events. It is common for sufferers of social phobia to self-medicate in this fashion, especially if they are undiagnosed, untreated, or both; this can lead to alcoholism, eating disorders or other kinds of substance abuse. SAD is sometimes referred to as an 'illness of lost opportunities' where 'individuals make major life choices to accommodate their illness.'[4][5] Standardized rating scales such as the Social Phobia Inventory, the SPAI-B and Liebowitz Social Anxiety Scale can be used to screen for social anxiety disorder and measure the severity of anxiety.[6][7][8][9][10] [11]
Mechanisms
There are many studies investigating neural bases of social anxiety disorder.[70][71] Although the exact neural mechanisms have not been found yet, there is evidence relating social anxiety disorder to imbalance in some neurochemicals and hyperactivity in some of brain areas.
Dopamine[edit]
Sociability is closely tied to dopamine neurotransmission.[72] Misuse of stimulants like amphetamines to increase self-confidence and improve social performance is common.[citation needed] In a recent study a direct relation between social status of volunteers and binding affinity of dopamine D2/3 receptors in the striatum was found.[73] Other research shows that the binding affinity of dopamine D2 receptors in the striatum of social anxiety sufferers is lower than in controls.[74] Some other research shows an abnormality in dopamine transporter density in the striatum of social anxiety sufferers.[75][76] However, some researchers have been unable to replicate previous findings of evidence of dopamine abnormality in social anxiety disorder.[77] Studies have shown high prevalence of social anxiety in Parkinson's disease and schizophrenia. In a recent study, social phobia was diagnosed in 50% of Parkinson's disease patients.[78] Other researchers have found social phobia symptoms in patients treated with dopamine antagonists like haloperidol, emphasizing the role of dopamine neurotransmission in social anxiety disorder.[79]Also, concentration problems, mental and physical fatigue, anhedonia and decreased self-confidence are seen in those with social anxiety disorder.
Other neurotransmitters[edit]
Some evidence points to the possibility that social anxiety disorder involves reduced serotonin receptor binding.[80] A recent study reports increased serotonin transporter binding in psychotropic medication-naive patients with generalized social anxiety disorder.[75] Although there is little evidence of abnormality in serotonin neurotransmission, the limited efficacy of medications which affect serotonin levels may indicate the role of this pathway. Paroxetine and sertraline are two SSRIs that have been confirmed by the FDA to treat social anxiety disorder. Some researchers believe that SSRIs decrease the activity of the amygdala.[70] There is also increasing focus on other candidate transmitters, e.g. norepinephrine and glutamate, which may be over-active in social anxiety disorder, and the inhibitory transmitter GABA, which may be under-active in the thalamus.[70][81]
Brain areas[edit]
The amygdala is part of the limbic system which is related to fear cognition and emotional learning. Individuals with social anxiety disorder have been found to have a hypersensitive amygdala; for example in relation to social threat cues (e.g. perceived negative evaluation by another person), angry or hostile faces, and while waiting to give a speech.[82] Recent research has also indicated that another area of the brain, theanterior cingulate cortex, which was already known to be involved in the experience of physical pain, also appears to be involved in the experience of 'social pain', for example perceiving group exclusion.[83]
Treatment
The first line treatment for social anxiety disorder is cognitive behavioral therapy with medications such as selective serotonin reuptake inhibitors(SSRIs) used only in those who are not interested in therapy.[12]
Given the evidence that social anxiety disorder may predict subsequent development of other psychiatric disorders such as depression, early diagnosis and treatment is important.[87][88] Social anxiety disorder remains under-recognized in primary care practice, with patients often presenting for treatment only after the onset of complications such as clinical depression or substance abuse disorders.[89][90][91]
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