Autism is demanding increased attention by professional and lay audiences; prevalence seems to be increasing. There are differing opinions about whether the increase is due to greater recognition and reporting, diagnostic expansion and substitution, or increasing acceptability. On the other hand, the increase may be a consequence of environmental toxins or infectious and immune vulnerability and epigenetics or perhaps a combination of social and environmental factors.
Clearly, autism has a large genetic component and multiple genes are involved in various combinations. Nevertheless, the prevalence of autism in the United States and in other countries has increased exponentially; this trend would not happen with a purely genetic disorder. Most autism researchers accept a theory of etiology that starts with a genetic neurodevelopmental vulnerability combined with an environmental stressor through such epigenetic processes as immune function.1
Increasingly, researchers and clinicians refer to autism to describe a wide variety of phenotypes that start with genes and gene expression and range through a variety of metabolic functions to symptoms that cluster diagnostically but have a great deal of individuality.
Symptoms can range from mild to severe and may be associated with mental retardation; GI and neurological involvement; and behavioral, emotional, cognitive, and whole body pathology.2Here we discuss diagnostic assessment and classification, co-occurring or comorbid psychiatric disorders and their differential diagnosis, the medical workup, and possible medical comorbidities. We also review a model for psychosocial treatment as well as psychopharmacological and alternative treatments. We conclude with a brief look at the future of research and treatment.
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http://www.psychiatrictimes.com/display/article/10168/1694995">Psychiatric Times