Anxiety Disorders ____________________________________________________________________________
GAD, and nicotine dependence [39]. One study followed 711 participants with anxiety disorder diagnoses over 15 years. At baseline, those with early-onset (≤20 years of age) panic disorder were more likely to have comorbid major depressive disorder, GAD, and SAD. Those with early- onset panic disorder with agoraphobia were less likely to be married and more likely to have comorbid GAD and SAD. Dur- ing follow-up, persons with panic disorder with agoraphobia were significantly more likely to have illness recurrence after periods of recovery, while findings for the other disorders failed to reach significance. This was thought to reflect differences in typical age of onset among anxiety disorders. The onset of panic disorder with or without agoraphobia is usually early adulthood; earlier onsets are relatively uncommon and may signal a particularly pernicious form of illness. The results further support the particularly adverse effects of early-onset psychiatric illness [40].
Brain profiles of children with behavioral inhibition show distinct patterns, including electroencephalography asym- metry, functional differences in amygdala response to facial expression challenge, and structural differences in the ventral prefrontal cortex. Roughly 40% of children with behavioral inhibition eventually develop SAD, and childhood behavioral inhibition is a primary predictor of SAD. Other components of SAD probably appear later in development, including social- evaluative concerns and coping skills deficits that contribute to functional impairment [44; 45]. A bi-directional relationship exists between parenting style and childhood anxiety. Parenting styles of criticism, over-protection, over-control, and lack of warmth can create insecure attach- ment and risk for SAD. Likewise, temperamentally introverted and anxious children may shape and change parenting styles, with parents becoming over-protective or over-controlling [42]. Studies suggest that challenging parenting behavior (especially in fathers) may play a protective role in anxiety development in the most vulnerable children [46; 47]. Early childhood anxiety disorders, especially separation anxiety and other phobias, are associated with elevated SAD risk in adulthood. SAD is highly comorbid with other anxiety disor- ders, mood disorders, and substance use disorders; substance abuse is often used to regulate anxiety symptoms and social skills [48]. Multiple social cues can develop the capacity to elicit anxiety- related symptoms. Learned escape and avoidance behaviors maintain anxiety, interfere with skill development, and can lead to functional impairment and disability over time. Simi- larly, safety behaviors, such as only entering social situations with a trusted companion, averting eye contact, and staying on the periphery of social gatherings, may maintain anxiety-related impairments. Selective attention to social cues of negative evaluation and internal cues supporting danger perception
Social Anxiety Disorder Epidemiology
SAD can develop at any time during a lifespan, but the aver- age age of onset is during late childhood and adolescence. The prevalence of SAD in pre-adolescence is 3.5%, with rates increasing to about 14% during adolescence [41]. The lifetime prevalence of SAD is 13%, and the prevalence in primary care settings (7%) is high compared with that of other anxiety disorders encountered in general practice [19; 350]. Gender distribution is generally equal during pre-adolescence and becomes increasingly more common in girls/women through adolescence and adulthood. An estimated 70% to 80% of individuals with SAD have comorbid anxiety, mood, or substance use disorders. There are cultural variants in Asian and Eastern cultures that involve fears of offending others or making others uncomfortable [2]. Risk Factors A combination of biologic, familial, environmental, and cultural risk factors drive the development of SAD. Life transi- tions, personal loss, poverty, and experiences of humiliation or embarrassment contribute to SAD risk [42]. Compared with data from the general population, first-degree relatives are as much as six times more likely to be at risk of SAD. Concordance rates are 24% in monozygotic twins and 15% in dizygotic twins [43]. Behavioral inhibition, shyness, introversion, and anxiety sen- sitivity are all common among patients with SAD. Emerging early in life, behavioral inhibition is a heritable trait, and 15% to 20% of young children with behavior inhibition exhibit extreme signs. Relative to children without behavioral inhibi- tion, these patients are typically shy, fearful, and cautious and show elevated physiologic arousal signs at rest, such as higher heart rate, increased pupil dilation, and higher cortisol levels.
may develop [49; 50]. Primary Prevention
Childhood presence of fearfulness and behavioral inhibition can lead to chronic, disabling SAD. Early recognition of child- hood impairments and evidence-based treatment intervention may offset the SAD trajectory of persisting into and through adulthood. Educational-behavioral interventions involving older children/adolescents, parents, school staff, and health- care providers have been found to reduce the development of social anxiety [51; 52; 53]. Clinical Course SAD tends to run a chronic course of long duration, associated with substantial impairment of work productivity, and has a reported recovery rate of only 38% [54].
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