Findings from research on psychiatric epidemiology, disaster effects, discrepancies in service use, and cross-cultural psychology are reviewed to generate guidelines for culturally responsive postdisaster interventions. Ethnicity and culture influence mental health care at various points: on need for help; on availability and accessibility of help; on help-seeking comfort (stigma, mistrust), and on the probability that help is provided appropriately. There are aspects of disaster mental health practice that may ameliorate many of barriers that contribute to ethnic disparities in service use. It is proposed that interventions should give greater attention to socially engaged emotions and functioning. To promote disaster recovery, practitioners are advised to: assess community needs early and often; provide easily accessible services; work collaboratively and proactively to reduce stigma and mistrust and engage minorities in care; validate and normalize distress and help-seeking; value interdependence as well as independence as an appropriate developmental goal; promote community action; and advocate for, facilitate, or conduct treatment and evaluation research. Notwithstanding the pain and stress they cause, disasters create opportunities to de-stigmatize mental health needs and build trust between providers and minority communities.

Patients with psychiatric disorders have an increased rate of cardiovascular morbidity and mortality compared with the general population. Metabolic issues such as weight gain, dyslipidemia, diabetes mellitus, diabetic ketoacidosis, and pancreatitis have been reported with the use of antipsychotic agents. Although atypical antipsychotics have not been linked directly to the development of metabolic syndrome, these medications have been shown to increase risk factors that can lead to metabolic and endocrine disturbances. Therefore, clinicians should provide ongoing monitoring for patients who are being treated for psychiatric disorders with these agents. According to the 2004 Consensus Report on Antipsychotics, screening measures should include baseline and follow-up monitoring of personal/family histories, weight (body mass index), waist circumference, blood pressure, fasting plasma glucose, and fasting lipid profile.

Social anxiety disorder (SAD) is a common, chronic psychiatric disorder characterized by a persistent fear of social or performance situations in which embarrassment can occur. This disorder typically appears during the mid-adolescent years and is unremitting throughout life if not properly treated. SAD presents as two subtypes: the more common and debilitating generalized form, and the nongeneralized form, which consists predominantly of performance anxiety. The majority of patients with SAD have comorbid mental disorders, including mood, anxiety, and substance abuse. No single development theory has been proposed to account for the origins of SAD, although current understanding of the etiology of SAD posits an interaction between psychological and biological factors. Risk factors include environmental and parenting influences and dysfunctional cognitive and conditioning events in early childhood. The neurobiology of SAD appears to involve neurochemical dysfunction, as evidenced by studies of neuroreceptor imaging, neuroendocrine function, and profiles of response to specific medications. Clinical trials have demonstrated that benzodiazepines and antidepressants are effective in the treatment of SAD. The selective serotonin reuptake inhibitors are emerging as the first-line treatment for SAD, based on their proven safety, tolerability, and efficacy. Goals for ongoing future research include development of approaches to achieve remission, to convert nonresponders and partial responders to full responders, and to prevent relapse and maintain long-term efficacy.

This monograph explores the epidemiology, clinical presentation, and differential diagnosis of SAD, with a focus on neural circuitry of social relationships and neurochemical dysfunction. The prevalence, rates of recognition and treatment, patterns of comorbidity, quality-of-life issues, and natural history of SAD are discussed as well as pharmacologic and psychosocial treatment strategies for SAD.