Social anxiety disorder (SAD or SAnD) (DSM-IV 300.23) is an anxiety disorder characterized by intense fear in social situations causing considerable distress and impaired ability to function in at least some parts of daily life. It is a rather extreme form of social phobia (SP), although the latter is sometimes treated synonymously. The diagnosis of social anxiety disorder can be of a specific disorder (when only some particular situations are feared) or a generalized disorder. Generalized social anxiety disorder typically involves a persistent, intense, chronic fear of being judged by others and of being embarrassed or humiliated by one’s own actions. 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. Physical symptoms often accompanying social anxiety disorder include excessive blushing, sweating (hyperhidrosis), trembling, palpitations, nausea, and stammering often accompanied with rapid speech. Panic attacks may 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.

Standardized rating scales such as Social Phobia Inventory can be used for screening social anxiety disorder and measuring severity of social phobia. A person with the disorder may be treated with psychotherapy, medication, or both. Research has shown cognitive behavior therapy, whether individually or in a group, to be effective in treating social phobia. The cognitive and behavioral components seek to change thought patterns and physical reactions to anxiety-inducing situations. Attention given to social anxiety disorder has significantly increased in the United States since 1999 with the approval and marketing of drugs for its treatment. Prescribed medications include several classes of antidepressants: selective serotonin reuptake inhibitors (SSRIs) such as Zoloft, Prozac, and Paxil; serotonin-norepinephrine reuptake inhibitors (SNRIs); and monoamine oxidase inhibitors (MAOIs). Other commonly used medications include beta-blockers and benzodiazepines, as well as newer antidepressants, such as mirtazapine. A herb called kava has also attracted attention as a possible treatment, although safety concerns exist, especially given the unregulated nature of herbs in the United States.

 

History

Literary descriptions of shyness can be traced back to the days of Hippocrates around 400 B.C. Hippocrates described someone who “through bashfulness, suspicion, and timorousness, will not be seen abroad; loves darkness as life and cannot endure the light or to sit in lightsome places; his hat still in his eyes, he will neither see, nor be seen by his good will. He dare not come in company for fear he should be misused, disgraced, overshoot himself in gesture or speeches, or be sick; he thinks every man observes him.”

The first mention of a psychiatric term, social phobia (phobie des situations sociales), was made in the early 1900s. Psychologists used the term “social neurosis” to describe extremely shy patients in the 1930s. After extensive work by Joseph Wolpe on systematic desensitization, research in phobias and their treatment grew. The idea that social phobia was a separate entity from other phobias came from the British psychiatrist Isaac Marks, in the 1960s. This was accepted by the American Psychiatric Association and was first officially included in the third edition of the Diagnostic and Statistical Manual of Mental Disorders. The definition of the phobia was revised in 1989 to allow comorbidity with avoidant personality disorder, and introduced generalized social phobia. Social phobia had been largely ignored prior to 1985.

After a call to action by psychiatrist Michael Liebowitz and clinical psychologist Richard Heimberg, there was an increase in attention to and research on the disorder. The DSM-IV gave social phobia the alternative name social anxiety disorder. Research on the psychology and sociology of everyday social anxiety continued. Cognitive Behavioural models and therapies were developed for social anxiety disorder. In the 1990s, paroxetine became the first prescription drug in the U.S. approved to treat social anxiety disorder, with others following.

Social phobia in many cases can be an extremely debilitating disorder, especially because one who struggles with it often suffers alone.

 

Symptoms

Cognitive aspects

In cognitive models of social anxiety disorder, social phobics experience dread over how they will be presented to others. They may be overly self-conscious, pay high self-attention after the activity, or have high performance standards for themselves. According to the social psychology theory of self-presentation, a sufferer attempts to create a well-mannered impression on others but believes he or she is unable to do so. Many times, prior to the potentially anxiety-provoking social situation, sufferers may deliberately go over what could go wrong and how to deal with each unexpected case. After the event, they may have the perception they performed unsatisfactorily. Consequently, they will review anything that may have possibly been abnormal or embarrassing. These thoughts do not just terminate soon after the encounter, but may extend for weeks or longer. Those with social phobia tend to interpret neutral or ambiguous conversations with a negative outlook and many studies suggest that socially anxious individuals remember more negative memories than those less distressed.

An example of an instance may be that of an employee presenting to his co-workers. During the presentation, the person may stutter a word, upon which he or she may worry that other people significantly noticed and think that their perceptions of him or her as a presenter have been tarnished. This cognitive thought propels further anxiety which compounds with further stuttering, sweating, and, potentially, a panic attack.

 

Behavioral aspects

Social anxiety disorder is a persistent fear of one or more situations in which the person is exposed to possible scrutiny by others and fears that he or she may do something or act in a way that will be humiliating or embarrassing. It exceeds normal “shyness” as it leads to excessive social avoidance and substantial social or occupational impairment. Feared activities may include almost any type of social interaction, especially small groups, dating, parties, talking to strangers, restaurants, etc. Possible physical symptoms include “mind going blank”, fast heartbeat, blushing, stomach ache, nausea and gagging. Cognitive distortions are a hallmark, and learned about in CBT (cognitive-behavioral therapy). Thoughts are often self-defeating and inaccurate.

According to psychologist B.F. Skinner, phobias are controlled by escape and avoidance behaviors. For instance, a student may leave the room when talking in front of the class (escape) and refrain from doing verbal presentations because of the previously encountered anxiety attack (avoid). Major avoidance behaviors could include an almost pathological/compulsive lying behavior in order to preserve self-image and avoid judgement in front of others. Minor avoidance behaviors are exposed when a person avoids eye contact and crosses arms to avoid recognizable shaking. A fight-or-flight response is then triggered in such events. Preventing these automatic responses is at the core of treatment for social anxiety.

 

Physiological aspects

Physiological effects, similar to those in other anxiety disorders, are present in social phobics. Faced with an uncomfortable situation, children with social anxiety may display tantrums, weeping, clinging to parents, and shutting themselves out. In adults, it may be tears as well as experiencing excessive sweating, nausea, shaking, and palpitations as a result of the fight-or-flight response. The walk disturbance (where a person is so worried about how they walk that they may lose balance and fall) may appear, especially when passing a group of people. Blushing is commonly exhibited by individuals suffering from social phobia. These visible symptoms further reinforce the anxiety in the presence of others. A 2006 study found that the area of the brain called the amygdala, part of the limbic system, is hyperactive when patients are shown threatening faces or confronted with frightening situations. They found that patients with more severe social phobia showed a correlation with the increased response in the amygdala.

 

Prevalence

Country Prevalence

When prevalence estimates were based on the examination of psychiatric clinic samples, social anxiety disorder was thought to be a relatively rare disorder. The opposite was instead true; social anxiety was common but many were afraid to seek psychiatric help, leading to an understatement of the problem. Prevalence rates vary widely because of its vague diagnostic criteria and its overlapping symptoms with other disorders. There has been some debate on how the studies are conducted and whether the illness truly impairs the respondents as laid out in the official criteria. Psychologist Dr. Ray Crozier argues, “it is difficult to ascertain whether the person being interviewed adheres to the DSM-III-R criteria or whether they are merely exhibiting poor social skills or shyness.”

The National Comorbidity Survey of over 8,000 American correspondents in 1994 revealed a 12-month and lifetime prevalence rates of 7.9 percent and 13.3 percent making it the third most prevalent psychiatric disorder after depression and alcohol dependence and the most apparent of the anxiety disorders. According to U.S. epidemiological data from the National Institute of Mental Health, social phobia affects 5.3 million adult Americans in any given year. Cross-cultural studies have reached prevalence rates with the conservative rates at 5 percent of the population. However, other estimates vary within 2 percent and 7 percent of the U.S. adult population.

The mean onset of social phobia is 10 to 13 years. Onset after age 25 is rare and is typically preceded by panic disorder or major depression. Social anxiety disorder occurs in females nearly twice as often as males, although men are more likely to seek help. The prevalence of social phobia appears to be increasing among white, married, and well-educated individuals. As a group, those with generalized social phobia are less likely to graduate from high school and are more likely to rely on government financial assistance or have poverty-level salaries. Surveys carried out in 2002 show the youth of England, Scotland, and Wales have a prevalence rate of 0.4 percent, 1.8 percent, and 0.6 percent, respectively. The prevalence of self-reported social anxiety for Nova Scotians older than 14 years was 4.2 percent in June 2004 with women (4.6 percent) reporting more than men (3.8 percent). In Australia, social phobia is the 8th and 5th leading disease or illness for males and females between 15–24 years of age as of 2003. Because of the difficulty in separating social phobia from poor social skills or shyness, some studies have a large range of prevalence. The table also shows higher prevalence in Brazil.

 

Comorbidity

There is a high degree of comorbidity with other psychiatric disorders. Social phobia often occurs alongside low self-esteem and clinical depression, due to lack of personal relationships and long periods of isolation from avoiding social situations. To try to reduce their anxiety and alleviate depression, people with social phobia may use alcohol or other drugs, which can lead to substance abuse. It is estimated that one-fifth of patients with social anxiety disorder also suffer from alcohol dependence. The most common complementary psychiatric condition is unipolar depression. In a sample of 14,263 people, of the 2.4 percent of persons diagnosed with social phobia, 16.6 percent also met the criteria for clinical depression. Besides depression, the most common disorders diagnosed in patients with social phobia are panic disorder (33 percent), generalized anxiety disorder (19 percent), post-traumatic stress disorder (36 percent), substance abuse disorder (18 percent), and attempted suicide (23 percent). In one study of social anxiety disorder among patients who developed comorbid alcoholism, panic disorder, or depression, social anxiety disorder preceded the onset of alcoholism, panic disorder and depression in 75 percent, 61 percent, and 90 percent of patients, respectively. Avoidant personality disorder is also highly correlated with social phobia. Because of its close relationship and overlapping symptoms with other illnesses, treating social phobics may help understand underlying connection in other psychiatric disorders.

There is research indicating that social anxiety disorder is often correlated with bipolar disorder. Some researchers believe they share an underlying cyclothymic-anxious-sensitive disposition. In addition, studies show that more socially phobic patients treated with anti-depressant medication develop hypomania than non-phobic controls. This can be seen as the medication creating a new problem, and also has this adverse effect in a proportion of those without social phobia.

 

Causes and perspectives

Research into the causes of social anxiety and social phobia is wide-ranging, encompassing multiple perspectives from neuroscience to sociology. Scientists have yet to pinpoint the exact causes. Studies suggest that genetics can play a part in combination with environmental factors.

 

Genetic and family factors

It has been shown that there is a two to threefold greater risk of having social phobia if a first-degree relative also has the disorder. This could be due to genetics and/or due to children acquiring social fears and avoidance through processes of observational learning or parental psychosocial education. Studies of identical twins brought up (via adoption) in different families have indicated that, if one twin developed social anxiety disorder, then the other was between 30 percent and 50 percent more likely than average to also develop the disorder. To some extent this ‘heritability’ may not be specific – for example, studies have found that if a parent has any kind of anxiety disorder or clinical depression, then a child is somewhat more likely to develop an anxiety disorder or social phobia. Studies suggest that parents of those with social anxiety disorder tend to be more socially isolated themselves (Bruch and Heimberg, 1994; Caster et al., 1999), and shyness in adoptive parents is significantly correlated with shyness in adopted children (Daniels and Plomin, 1985);

Adolescents who were rated as having an insecure (anxious-ambivalent) attachment with their mother as infants were twice as likely to develop anxiety disorders by late adolescence, including social phobia.

A related line of research has investigated ‘behavioural inhibition’ in infants – early signs of an inhibited and introspective or fearful nature. Studies have shown that around 10–15 percent of individuals show this early temperament, which appears to be partly due to genetics. Some continue to show this trait in to adolescence and adulthood, and appear to be more likely to develop social anxiety disorder.

 

Social experiences

A previous negative social experience can be a trigger to social phobia, perhaps particularly for individuals high in ‘interpersonal sensitivity’. For around half of those diagnosed with social anxiety disorder, a specific traumatic or humiliating social event appears to be associated with the onset or worsening of the disorder; this kind of event appears to be particularly related to specific (performance) social phobia, for example regarding public speaking (Stemberg et al., 1995). As well as direct experiences, observing or hearing about the socially negative experiences of others (e.g. a faux pas committed by someone), or verbal warnings of social problems and dangers, may also make the development of a social anxiety disorder more likely. Social anxiety disorder may be caused by the longer-term effects of not fitting in, or being bullied, rejected or ignored (Beidel and Turner, 1998). Shy adolescents or avoidant adults have emphasised unpleasant experiences with peers or childhood bullying or harassment (Gilmartin, 1987). In one study, popularity was found to be negatively correlated with social anxiety, and children who were neglected by their peers reported higher social anxiety and fear of negative evaluation than other categories of children. Socially phobic children appear less likely to receive positive reactions from peers and anxious or inhibited children may isolate themselves.

 

Social/cultural influences

Cultural factors that have been related to social anxiety disorder include a society’s attitude towards shyness and avoidance, affecting ability to form relationships or access employment or education, and shame. One study found that the effects of parenting are different depending on the culture – American children appear more likely to develop social anxiety disorder if their parents emphasize the importance of others’ opinions and use shame as a disciplinary strategy (Leung et al., 1994), but this association was not found for Chinese/Chinese-American children. In China, research has indicated that shy-inhibited children are more accepted than their peers and more likely to be considered for leadership and considered competent, in contrast to the findings in Western countries. Purely demographic variables may also play a role – for example there are possibly lower rates of social anxiety disorder in Mediterranean countries and higher rates in Scandinavian countries, and it has been hypothesized that hot weather and high density may reduce avoidance and increase interpersonal contact.

Problems in developing social skills, or ‘social effectiveness’, may be a cause of some social anxiety disorder, through either inability or lack of confidence to interact socially and gain positive reactions and acceptance from others. The studies have been mixed, however, with some studies not finding significant problems in social skills while others have. What does seem clear is that the socially anxious perceive their own social skills to be low. It may be that the increasing need for sophisticated social skills in forming relationships or careers, and an emphasis on assertiveness and competitiveness, is making social anxiety problems more common, at least among the ‘middle classes’. An interpersonal or media emphasis on ‘normal’ or ‘attractive’ personal characteristics has also been argued to fuel perfectionism and feelings of inferiority or insecurity regarding negative evaluation from others. The need for social acceptance or social standing has been elaborated in other lines of research relating to social anxiety

 

Evolutionary context

A long-accepted evolutionary explanation of anxiety is that it reflects an in-built ‘fight or flight’ system, which errs on the side of safety. One line of research suggests that specific dispositions to monitor and react to social threats may have evolved, reflecting the vital and complex importance of social living and social rank in human ancestral environments. Charles Darwin originally wrote about the evolutionary basis of shyness and blushing, and modern evolutionary psychology and psychiatry also addresses social phobia in this context. It has been hypothesized that in modern day society these evolved tendencies can become more inappropriately activated and result in some of the cognitive ‘distortions’ or ‘irrationalities’ identified in cognitive-behavioral models and therapies

 

Substance induced

While alcohol initially helps social phobia, excessive alcohol misuse can worsen social phobia symptoms and can cause panic disorder to develop or worsen during alcohol intoxication and especially during alcohol withdrawal syndrome. This effect is not unique to alcohol but can also occur with long term use of drugs which have a similar mechanism of action to alcohol such as the benzodiazepines which are sometimes prescribed as tranquillisers. Benzodiazepines possess anti-anxiety properties and can be useful for the short-term treatment of severe anxiety. Like the anticonvulsants, they tend to be mild and well tolerated, although extremely addictive. Benzodiazepines are usually administered orally for the treatment of anxiety; however, occasionally lorazepam or diazepam may be given intravenously for the treatment of panic attacks.

The World Council of Anxiety does not recommend benzodiazepines for the long term treatment of anxiety due to a range of problems associated with long term use of benzodiazepines including tolerance, psychomotor impairment, cognitive and memory impairments, physical dependence and a benzodiazepine withdrawal syndrome upon discontinuation of benzodiazepines. Despite increasing focus on the use of antidepressants and other agents for the treatment of anxiety, benzodiazepines have remained a mainstay of anxiolytic pharmacotherapy due to their robust efficacy, rapid onset of therapeutic effect, and generally favorable side effect profile. Treatment patterns for psychotropic drugs appear to have remained stable over the past decade, with benzodiazepines being the most commonly used medication for panic disorder.

Approximately half of patients attending mental health services for conditions including anxiety disorders such as panic disorder or social phobia are the result of alcohol or benzodiazepine dependence. Sometimes anxiety pre-existed alcohol or benzodiazepine dependence but the alcohol or benzodiazepine dependence act to keep the anxiety disorders going and often progressively making them worse. Many people who are addicted to alcohol or prescribed benzodiazepines when it is explained to them they have a choice between ongoing ill mental health or quitting and recovering from their symptoms decide on quitting alcohol and/or their benzodiazepines. It was noted that every individual has an individual sensitivity level to alcohol or sedative hypnotic drugs and what one person can tolerate without ill health another will suffer very ill health and that even moderate drinking can cause rebound anxiety syndromes and sleep disorders. A person who is suffering the toxic effects of alcohol or benzodiazepines will not benefit from other therapies or medications as they do not address the root cause of the symptoms. Symptoms may temporarily worsen however, during alcohol withdrawal or benzodiazepine withdrawal.

 

Psychological factors

Research has indicated the role of ‘core’ or ‘unconditional’ negative beliefs (e.g. I am inept) and ‘conditional’ beliefs nearer to the surface (e.g. If I show myself, I will be rejected). They are thought to develop based on personality and adverse experiences and to be activated when the person feels under threat. One line of work has focused more specifically on the key role of self-presentational concerns. The resulting anxiety states are seen as interfering with social performance and the ability to concentrate on interaction, which in turn creates more social problems, which strengthens the negative schema. Also highlighted has been a high focus on and worry about anxiety symptoms themselves and how they might appear to others. A similar model emphasizes the development of a distorted mental representation of their self and over-estimates of the likelihood and consequences of negative evaluation, and of the performance standards that others have. Such cognitive-behavioral models consider the role of negatively-biased memories of the past and the processes of rumination after an event, and fearful anticipation before it. Studies have also highlighted the role of subtle avoidance and defensive factors, and shown how attempts to avoid feared negative evaluations or use ‘safety behaviors’ (Clark & Wells, 1995) can make social interaction more difficult and the anxiety worse in the long run. This work has been influential in the development of Cognitive Behavioral Therapy for social anxiety disorder, which has been shown to have efficacy.

 

Neural mechanisms

There are many researches investigating neural bases of social anxiety disorder. Although the exact neural mechanisms are not found yet there is evidence relating social anxiety disorder to imbalance in some neurochemicals and hyperactivity in some of brain areas.

 

Dopamine

Sociability is closely tied to dopamine neurotransmission. Misuse of stimulants like amphetamines to increase self-confidence and improve social performance is common. 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. Other research shows that the binding affinity of dopamine D2 receptors in the striatum of social anxiety sufferers is lower than controls. Some other researches show an abnormality in dopamine transporter density in the striatum of social anxiety sufferers. However, some researchers do not replicate previous findings of evidence of dopamine abnormality in social anxiety disorder. 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. 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. Also, concentration problems, mental and physical fatigue, Anhedonia and decreased self-confidence are seen in those with social anxiety disorder.

 

Other neurotransmitters

Some scientists hypothesize that social phobia is related to an imbalance of the brain chemical serotonin. A recent study report increased Serotonin transporter binding in psychotropic medication-naive patients with generalized social anxiety disorder. Although there are not many evidences 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 FDA to treat social anxiety disorder. Some researchers believe that SSRIs decrease activity of Amygdala. 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 is subsequently lacking.

 

Brain areas

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. someone might be evaluating you negatively), angry or hostile faces, and while just waiting to give a speech. Recent research has also indicated that another area of the brain, the anterior 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.

 

Treatment

The most important clinical point to emerge from studies of social anxiety disorder is the benefit of early diagnosis and treatment. 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.

Research has provided evidence for the efficacy of two forms of treatment available for social phobia: certain medications and a specific form of short-term psychotherapy called Cognitive-behavioral therapy (CBT), the central component being gradual exposure therapy.

 

Psychosocial Treatment

Basic Principles

In the case of an agoraphobic patient, the clinician might have the patient imagine (perhaps in hypnotic trance, but this does not seem to add to the effectiveness of treatment) taking a fearful trip, remaining in the anxiety-producing fantasy as long as possible, then “returning” to the therapist’s office. This is repeated a number of times, and the patient is instructed to perform the same exercise as often as possible between sessions. Family members are frequently engaged to assist in the process and monitor the “homework.” Written journals and diaries may also be used.

In most patients, panic attacks can be treated at the same time, in the same way. Sometimes attention to the physiologic cues of panic or mounting anxiety helps the patient to recognize and control panic symptoms.

 

Psychotherapy

Psychotherapy can be a useful part of the treatment of the anxious or phobic patient. The term “psychotherapy” implies a wide variety of kinds of therapist-patient interaction, overlapping considerably with the behavioral treatments. It is almost impossible to work with a patient in any context without providing considerable interest, support, and understanding. Beyond this, the patient who has given up a symptom may suffer feelings of loss for the symptom itself, for the “equilibrium” of life-style which has existed surrounding the symptom, or both. The opportunity for continuing counseling may be valuable.

Research has shown that cognitive behavioral therapy (CBT) can be highly effective for several anxiety disorders, particularly specific phobias, obsessive compulsive disorder, panic disorder and social anxiety disorder. CBT, as its name suggests, has two main components, cognitive and behavioral. In cases of social anxiety, the cognitive component can help the patient question how they can be so sure that others are continually watching and harshly judging them. The behavioral component seeks to change people’s reactions to anxiety-provoking situations. As such it serves as a logical extension of cognitive therapy, whereby people are shown proof in the real world that their dysfunctional thought processes are unrealistic. A key element of this component was gradual exposure, in which the patient was confronted by the things they fear in a structured, sensitive manner. Gradual exposure is an inherently unpleasant technique; and had high drop out rates. Ideally it involves exposure to a feared social situation that is anxiety provoking but bearable, for as long as possible, two to three times a week. Often, a hierarchy of feared steps is constructed and the patient is exposed each step sequentially. Now modern CBT treatments have been enhanced by focusing treatment on cognitive process, e.g., behavioral experiment with attentional focus, video feedback experiments, addressing fears of negative evaluation, identifying & removing safety seeking behaviors, etc. The aim is to learn from acting differently and observing reactions. This is intended to be done with support and guidance, and when the therapist and patient feel they are ready. Cognitive-behavioral therapy for social phobia for few patients now includes anxiety management training, which may include techniques such as deep breathing and muscle relaxation exercises, which may be practiced ‘in-situ’. These early interventions, for some, can be useful but for most can become safety seeking behaviors (and thus unhelpful) so need to be suggested in a considered case conceptualization (i.e., individualized understanding of the cognitive and behavioral factors that are maintaining the problem). CBT can also be conducted partly in group sessions, facilitating the sharing of experiences, a sense of acceptance by others and undertaking behavioral challenges in a trusted environment (Heimberg).

Those patients who do not respond to the briefer treatments often benefit from more in depth psychodynamic psychotherapy. The typical patient after such treatment was in better condition than 77% of untreated controls evaluated at the same time. The various modes examined included psychodynamic, cognitive, and humanistic, as well as behavioral and social, therapies.

 

Behavior Therapy

The behavioral technique of “exposure” is an effective treatment, both short- and long-term, for agoraphobics and many other phobia patients. The use of exposure in fantasy, presenting increasingly anxiety-producing situations as discomfort dissipates at each level, is a form of systematic desensitization. Exposure in vivo also involves gradual adaptation to anxiety-producing objects or situations, but the objects or situations are actually present during the treatment. Flooding, rapid exposure to almost overwhelming volumes of phobic material, also known as implosion, may be used either in fantasy or in vivo.

In general, the behavioral treatments, perhaps coupled with appropriate psychotherapy, have the greatest likelihood of effectiveness, and should be tried before medication is prescribed on any chronic basis.

Some studies have suggested social skills training can help with social anxiety. However, it is not clear whether specific social skills techniques and training are required, rather than just support with general social functioning and exposure to social situations.

Additionally, a recent study has suggested that interpersonal therapy, a form of psychotherapy primarily used to treat depression, may also be effective in the treatment of social phobia.

 

Pharmacological treatments

SSRIs

Selective serotonin reuptake inhibitors (SSRIs), a class of antidepressants, are considered by many to be the first choice medication for generalised social phobia. These drugs elevate the level of the neurotransmitter serotonin, among other effects. The first drug formally approved by the Food and Drug Administration was paroxetine, sold as Paxil in the U.S. or Seroxat in the UK. Compared to older forms of medication, there is less risk of tolerability and drug dependency. However, their efficacy and increased suicide risk has been subject to controversy.

In a 1995 double-blind, placebo-controlled trial, the SSRI paroxetine was shown to result in clinically meaningful improvement in 55 percent of patients with generalized social anxiety disorder, compared with 23.9 percent of those taking placebo. An October 2004 study yielded similar results. Patients were treated with either fluoxetine, psychotherapy, fluoxetine and psychotherapy, placebo and psychotherapy, or a placebo. The first four sets saw improvement in 50.8 to 54.2 percent of the patients. Of those assigned to receive only a placebo, 31.7 percent achieved a rating of 1 or 2 on the Clinical Global Impression-Improvement scale. Those who sought both therapy and medication did not see a boost in improvement.

General side-effects are common during the first weeks while the body adjusts to the drug. Symptoms may include headaches, nausea, insomnia and changes in sexual behavior. Treatment safety during pregnancy has not been established. In late 2004 much media attention was given to a proposed link between SSRI use and juvenile suicide. For this reason, the use of SSRIs in pediatric cases of depression is now recognized by the Food and Drug Administration as warranting a cautionary statement to the parents of children who may be prescribed SSRIs by a family doctor. Recent studies have shown no increase in rates of suicide. These tests, however, represent those diagnosed with depression, not necessarily with social anxiety disorder. However, it should be noted that due to the nature of the conditions, those taking SSRIs for social phobias are far less likely to have suicidal ideation than those with depression.

 

Other drugs

Although SSRIs are often the first choice for treatment, other prescription drugs are also used, sometimes only if SSRIs fail to produce any clinically significant improvement.

In 1985, before the introduction of SSRIs, anti-depressants such as monoamine oxidase inhibitors (MAOIs) were frequently used in the treatment of social anxiety. Their efficacy appears to be comparable or sometimes superior to SSRIs or benzodiazepines. However, because of the dietary restrictions required, high toxicity in overdose, and incompatibilities with other drugs, its usefulness as a treatment for social phobics is now limited. Some argue for their continued use, however, or that a special diet does not need to be strictly adhered to. A newer type of this medication, Reversible inhibitors of monoamine oxidase subtype A (RIMAs) inhibit the MAO enzyme only temporarily, improving the adverse-effect profile but possibly reducing their efficacy.

Benzodiazepines such as alprazolam and clonazepam are an alternative to SSRIs. These drugs are often used for short-term relief of severe, disabling anxiety. Although benzodiazepines are still sometimes prescribed for long-term everyday use in some countries, there is some concern over the development of drug tolerance, dependency and misuse. It has been recommended that benzodiazepines are only considered for individuals who fail to respond to safer medications. Benzodiazepines augment the action of GABA, the major inhibitory neurotransmitter in the brain; effects usually begin to appear within minutes or hours.

The novel antidepressant mirtazapine has been proven effective in treatment of social anxiety disorder. This is especially significant due to mirtazapine’s fast onset and lack of many unpleasant side-effects associated with SSRIs (particularly, sexual dysfunction).

In Japan, the serotonin-norepinephrine reuptake inhibitor (SNRI), Milnacipran is used in the treatment of Taijin kyofusho a Japanese variant of social anxiety disorder.

Some people with a form of social phobia called performance phobia have been helped by beta-blockers, which are more commonly used to control high blood pressure. Taken in low doses, they control the physical manifestation of anxiety and can be taken before a public performance.

A novel treatment approach has recently been developed as a result of translational research. It has been shown that a combination of acute dosing of d-cycloserine (DCS) with exposure therapy facilitates the effects of exposure therapy of social phobia. DCS is an old antibiotic medication used for treating tuberculosis and does not have any anxiolytic properties per se. However, it acts as an agonist at the glutamatergic N-methyl-D-aspartate (NMDA) receptor site, which is important for learning and memory. It has been shown that administering a small dose acutely 1 hour before exposure therapy can facilitate extinction learning that occurs during therapy.