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Early-Onset Bipolar Disorder 337next 5 to 10 years we will be able to use a set of 10 or so factors to quantify riskfor BD development. Such a set could include current symptomatology, familyhistory, and genetic and brain markers. Ideally, the degree of risk would then becorrelated with degree of intervention needed—none, psychotherapy only, orpsychotherapy combined with medications.The most tantalizing aspect of prevention is that early intervention would leadto a change in trajectory of brain development, such that a normal trajectory wouldbe achieved and the brain, which typically continues to develop through earlyadulthood, would “heal itself.” Then such medication or psychosocial interventionscould be removed, with the child/adolescent/adult continuing to function freeof psychiatric symptomatology. This is a far cry from the current recommendationsregarding the treatment of children and adolescents with fully developed BD:Most experts agree that such patients usually require lifelong treatment with medicationsand psychotherapy (Kowatch et al., 2005). This dire outcome highlightsthe significant need for further research geared toward preventing this debilitatingand life-threatening disorder from ever reaching this irreversible state in atriskindividuals.ReferencesAkiskal, H. S. (1996). The prevalent clinical spectrum of bipolar disorders: Beyond DSM-IV. Journal of Clinical Psychopharmacology, 16(2 Suppl. 1), 4S–14S.Akiskal, H. S., Bourgeois, M. L., Angst, J., Post, R., Moller, H., & Hirschfeld, R. (2000).Re-evaluating the prevalence of and diagnostic composition within the broad clinicalspectrum of bipolar disorders. Journal of Affective Disorders, 59 Suppl 1, S5–S30.Altshuler, L. L., Bartzokis, G., Grieder, T., Curran, J., Jimenez, T., Leight, K., et al. (2000).An MRI study of temporal lobe structures in men with bipolar disorder or schizophrenia.Biological Psychiatry, 48(2), 147–162.American Psychiatric Association. (1994). Diagnostic and statistical manual of mentaldisorders (4th ed.). Washington, DC: Author.Baumer, F., Howe, M., Gallelli, K., Chang, K.D. (2006). A Pilot Study of antidepressantinducedmania in pediatric bipolar disorder: characteristics, risk factors, and the serotonintransporter gene. Biological Psychiatry, 60, 1005–1012.Bellivier, F., Golmard, J. L., Henry, C., Leboyer, M., & Schurhoff, F. (2001). Admixtureanalysis of age at onset in bipolar I affective disorder. Archives of General Psychiatry,58(5), 510–512.Biederman, J., Faraone, S., Mick, E., Wozniak, J., Chen, L., Ouellette, C., et al. (1996).Attention-deficit hyperactivity disorder and juvenile mania: An overlooked comorbidity?Journal of the American Academy of Child and Adolescent Psychiatry, 35(8), 997–1008.Blumberg, H. P., Charney, D. S., & Krystal, J. H. (2002). Frontotemporal neural systemsin bipolar disorder. Seminars in Clinical Neuropsychiatry, 7(4), 243–254.Blumberg, H. P., Kaufman, J., Martin, A., Whiteman, R., Zhang, J. H., Gore, J. C., et al.(2003). Amygdala and hippocampal volumes in adolescents and adults with bipolardisorder. Archives of General Psychiatry, 60(12), 1201–1208.Blumberg, H. P., Leung, H. C., Skudlarski, P., Lacadie, C. M., Fredericks, C. A., Harris,