Social Anxiety Disorder

By | March 23, 2015

Epidemiology of Social Anxiety Disorder (SAD)

SAD (social anxiety disorder) (social anxiety disorder), also known as social phobia, is characterised by excessive fear of embarrassment or humiliation in social situations, which in turn leads to marked distress or avoidance of these situations and functional impairment as described in DSM-IV-TR.

It is a common disorder with early onset, significant comorbidity and functional impairment.

SAD (social anxiety disorder) has been ranked as one of the top ten chronic disorders ― mental or physical ― in terms of its effects on objective outcomes, such as days of work lost and reduced health-related quality of life. According to the National Comorbidity Survey, social anxiety disorder is the most reported anxiety disorder and has a lifetime prevalence of 12%, with considerable coexisting psychiatric disorders, such as depression, anxiety, and substance-related disorders. Lifetime prevalence of social anxiety disorder among Turkish university students was 23%. Co-occurring social anxiety disorder and depression carry a substantial risk of suicide, which further complicates treatment. social anxiety disorder symptoms normally emerge during early adolescence and continue throughout adulthood; they affect women more often than men. In clinical samples the ratio of male and female changes in the favour of males.. Trials suggest that social anxiety even below the diagnostic threshold is clearly associated with adverse outcomes like elevated risk for comorbid disorders and associated with impairment in diverse areas of life.

Despite the growing understanding of this condition, information is lacking on key aspects of the disorder and many individuals, including doctors, psychiatrists and patients, unaware about this condition.

Children and Adolescents

SAD (social anxiety disorder), which so often begins in childhood, precedes other comorbid disorders and may be a direct or indirect risk factor for other disorders, such as depression and substance abuse. Epidemiologic findings show that in the pediatric primary healthcare setting anxiety disorders are very common ranging from 1% to 10%, but are unrecognized and under-treated. In community settings, rates of social anxiety disorder in youth range from 0.5% to 4% and from 3% to 6.8% in primary care settings. Recent research suggest that lifetime prevalence rates in adolescents in the US and Germany are between 5% and 15%). Although the age of onset is usually in the early teens with a mean age of onset of 15.5 years children as young as 8 years old have been diagnosed with the disorder.

Shyness, behavioral inhibition and selective mutism can be considered in spectrum of social anxiety disorder in childhood. Children who are rated by their parents as having a shy temperament in infancy or in early childhood had an approximately 2 or 3 times increased probability of having an anxiety disorder in adolescence. In a five year longitudinal study, researchers found that behavioral inhibition-which can be described as a tendency to demonstrate tearfulness or resistance when faced with an unfamiliar stimuli, in pre-school children appeared to be a predictor for social anxiety in middle school. Selective mutism can be considered an extreme form of social anxiety including features of shyness and behavioral inhibition, where the most prominent feature is the inhibition of speech in select situations. Comorbidity rates between selective mutism and social anxiety disorder range from 70-95% and characteristics such as shyness, anxiousness, withdrawal and seriousness are used to describe both selective mutism and social anxiety alike.

Studies have shown that in children aged 7-13 years with social anxiety disorder (SAD), 60% had an additional psychiatric diagnosis, of whom 36% had an anxiety disorder as follows: generalized anxiety disorder 10%; attention deficit hyperactivity disorder 10%; specific phobia 10%; and selective mutism 8%. Those individuals who develop comorbid disorders will also have an increased risk of suicidal ideation and suicide attempts. In treatment of social anxiety disorders in childhood and adolecence, most practitioners advise the initial use of psychological interventions followed by pharmacotherapy when necessary. Specific treatments have employed cognitive-behavioral group therapy for social anxiety disorder in adolescents, social effectiveness therapy for children and ‘coping cat’ child behavior therapy. Overall, most clinical researchers now believe that cognitive behavioural therapy is the treatment of choice for youth with internalizing disorders including social anxiety disorder.

There are very few pharmacotherapy trials in general and even fewer randomized, double-blind, placebo-controlled trials in childhood anxiety disorders. Studies with both open-label and double blind placebo control groups have shown promising results ranging from 36-100% success rates. Selective serotonin reuptake inhibitors (SSRI) and serotonin norepinephrine reuptake inhibitors (SNPI) are defined as first line pharmacotherapy for social anxiety disorders in youth with a careful assessessment of suicidal ideation before starting these antidepressants.

The development of comorbid mental disorders such as depression and substance abuse, children and adolescents with this illness are at risk for educational or occupational under-achievement, and failure to achieve financial and emotional independence. The challenge of preventing the consequences of social anxiety disorder lies in early diagnosis.

Organic Etiology of Social Anxiety Disorder

Although the etiology of social anxiety disorder is poorly understood, emerging evidence indicates multidimensional causes. It is a distinct psychiatric disorder with genetic underpinnings and is associated with neurobiological and environmental mechanisms.

Over the past two decades, numerous neurobiological methods have been used in studies of social anxiety disorder including structural, functional and receptor brain imaging, pharmacological trials, candidate gene investigations and studies of psychophysiological, endocrine, biochemical and behavioral responses to stressful challenges. It has been hypothesized that affect regulation is compromised in individuals with social anxiety disorder (SAD), either due to hyperactivity in emotion triggering areas like the amygdala and insula, or hypoactivity in modulatory regions like the anterior cingulate and prefrontal cortices. It also has been hypothesized that social anxiety disorder patients would show exaggerated amygdala responses to angry or threatening faces in comparison to healthy control subjects and that amygdala hyperresponsivity is associated with enhanced fear conditionability in social anxiety disorder.

A range of neurotransmitters may be important in social anxiety disorder including the monoamines, glutamate, GABA, and several neuropeptides, but to date, the serotonergic and dopaminergic transmission systems have received most of the attention.

Serotonin has been implicated in animal models of fear and anxiety and the therapeutic efficacy of SSRIs strongly suggests that serotonin has a crucial role in social anxiety disorder (SAD). Allelic variation in serotonin-related genes modulate amygdala responsivity both in healthy volunteers and in patients with social anxiety disorder. Lanzenberger et al. demonstrated a significantly lower serotonin-1 A receptor binding potential in social anxiety disorder patients relative to controls in the amygdala, anterior cingulate cortex, insula, and dorsal raphe nuclei in their PET study. Serotonergic involvement is also supported by neuroendocrine challenges studies.

Dopamine is known to play a central role in motivation and reward-seeking behaviors and several lines of evidence point to a dysfunction of this transmitter system in social anxiety disorder like patients with Parkinson’s Disease, which is associated with dopamine hypofunction, appear to have enhanced risk for developing social anxiety disorder. Abnormal central dopaminergic neurotransmission has also been reported in animal trials relevant to social anxiety disorder (SAD), such as studies of social subordination in primates. Two independent SPECT studies also point directly to an altered dopamine system activity in social anxiety disorder (SAD). Tiihonen et al. reported that the striatal dopamine reuptake site density was markedly lower in patients with social anxiety disorder than controls, presumably reflecting a smaller number of dopaminergic synapses and neurons in the basal ganglia. Schneier et al. also observed that striatal dopamine D2 receptor binding was significantly lower in subjects with social anxiety disorder than in comparison subjects.

Genetically-oriented studies of social anxiety disorder and related constructs such as behavioral inhibition, neuroticism, introversion and harm-avoidance suggest that genetic factors play at least a moderate role in the etiology of excessive social anxiety. The short (s) allele of the promoter polymorphism of the human serotonin transporter gene (the 5-HTT-linked polymorphic region; 5-HTTLPR) has been associated with anxiety-related personality traits, increased fear conditionability, and life-stress-induced aff ective disorder.

Diagnosis And Assessment Of Social Anxiety Disorder

The first challenge in the treatment of social anxiety disorder is making a correct diagnosis. There is evidence that social anxiety disorder is under-diagnosed and under-treated in primary care and specialist settings alike. Possible reasons for this may be lack of diagnostic awareness, lack of diagnostic threshold clarity or the presence of co-morbid disorders. Moreover, as consultation with a clinician may be perceived as social interaction, the nature of the disorder may cause patients to delay seeking help, and when they eventually do, it is often with physical complaints or psychiatric comorbidity.

During the initial evaluation it is important to find out severity of symptoms as well as the degree of avoidance and functional impairment present. Rating scales such as the Liebowitz social anxiety scale that is translated and validated to Turkish also, may be helpful in assessing both feared situations and avoidance and can be used to monitor the patient’s treatment progress. A range of other social anxiety disorder scales are also available, like the Brief Social Phobia Scale (clinician rated) and the Social Phobia Inventory (patient rated).

Comorbidity Of Social Anxiety And Mood Disorders

Significant comorbidity of social anxiety and mood disorders have been consistently shown in the literature. Social anxiety has also been linked to severity and persistence of mood disorders. Also comorbid mood disorders have worsen social anxiety symptoms and result in greater impairment in patients with social anxiety disorder. A significant number of patients presenting with social anxiety will have a secondary anxiety disorder, particularly panic disorder with agoraphobia and generalized anxiety disorder. Comorbid depressive or anxiety disorders complicate social anxiety disorder (SAD), the severity of symptoms and suicidality should be assessed and hospitalisation considered if indicated. In such cases, the treatment of choice should ideally target both the mood and the anxiety components.

Social phobia and avoidant personality disorder were introduced in the DSM classification system nearly 30 years ago. Since then it has been shown that these two disorders can be found highly comorbid in patients, in some trials as high as 89%. Some researchers have interpreted this high rate of overlap to mean that social phobia and avoidant personality disorder reflect a spectrum of social anxiety.

Social anxiety disorder is associated with high rates of alcohol use disorders. Almost half of the patients with lifetime social anxiety disorder meet criteria for lifetime prevalence of an alcohol use disorder and it is a significantly high rate when compared to general population. Among the anxiety disorders, social anxiety disorder shows a particularly problematic risk profile for comorbid alcohol use disorders, as social anxiety disorder is associated with higher rates of alcohol use disorders relative to most other anxiety disorders.

Recently, researchers have identified that individuals with social anxiety disorder appear particularly vulnerable to marijuana-related problems too. Data from the National Comorbidity Study suggest that individuals with social anxiety disorder are 7 times more likely to experience marijuana dependence relative to the general population and undergraduates with higher social anxiety appear to be particularly vulnerable to marijuana use problems. In a study, adolescents with social anxiety disorder were nearly 5 times more likely to develop marijuana dependence as young adults compared to adolescents without social anxiety disorder.

Treatment of Social Anxiety Disorder

Social Anxiety Disorder: Conclusion

SAD (social anxiety disorder) is a prevalent and disabling disorder that often remains undetected unless the clinicaian takes a careful history. Present consensus supports that SSRIs can currently be regarded as first-line treatment in social anxiety disorder because of their proven efficacy, tolerability and bility to treat co-morbid conditions such as depression or other anxiety disorders. There is a recent evidence venlafaxine XR may also be considered in the first-line. Second-line treatments include MAOIs (e.g. phenelzine) and RIMAs (e.g.moclobemide).

The combination of cognitive behavioural therapy and an SSRI is often espoused as best practice, unfortunately there is little hard evidence supporting this (despite considerable face validity). Future studies taking a good look at combination therapies of this type are encouraged and also future research should focus on complicated and treatment refractory social anxiety disorder and treatment strategies in special populations (e.g.children and adolescents).