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Integration of Neurobiological and Psychosocial Processes
a Pediatric Bipolar Disorders Program, Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, Stanford, California, USA
Key Words: bipolar disorders • children • prevention • neurobiology • genetics
Address for correspondence: Kiki D. Chang, M.D., Stanford University School of Medicine, Division of Child and Adolescent Psychiatry, 401 Quarry Road, Stanford, CA 94305-5540. Voice: 650-725-0956; fax: 650-723-5531. e-mail: kchang88{at}stanford.edu
Bipolar disorder (BD) is a prevalent condition in the United States that typically begins before the age of 18 years and is being increasingly recognized in children and adolescents. Despite great efforts in discovering more effective treatments for BD, it remains a difficult-to-treat condition with high morbidity and mortality. Therefore, it appears prudent to focus energies into developing interventions designed to prevent individuals from ever fully developing BD. Such interventions early in the development of the illness might prevent inappropriate interventions that may worsen or hasten development of BD, delay the onset of first manic episode, and/or prevent development of full BD. Studies of populations at high-risk for BD development have indicated that children with strong family histories of BD, who are themselves experiencing symptoms of attention-deficit/hyperactive disorder (ADHD) and/or depression or have early mood dysregulation, may be experiencing prodromal states of BD. Understanding the neurobiological and genetic underpinnings that create risk for BD development would help with more accurate identification of this prodromal population, which could then lead to suitable preventative interventions. Such interventions could be pharmacologic or psychosocial in nature. Reductions in stress and increases in coping abilities through psychosocial interventions could decrease the chance of a future manic episode. Similarly, psychotropic medications may decrease negative sequelae of stress and have potential for neuroprotective and neurogenic effects that may contribute to prevention of fully expressed BD. Further research into the biologic and environmental mechanisms of BD development as well as controlled early intervention studies are needed to ameliorate this significant public health problem.
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