Roybal Donna J, Singh Manpreet K, Cosgrove Victoria E, Howe Meghan, Kelley Ryan, Barnea-Goraly Naama, Chang Kiki D
Department of Psychiatry and Behavioral Sciences, School of Medicine, Stanford University, Stanford, California, U.S.A.
Isr J Psychiatry Relat Sci. 2012;49(1):28-43.
Bipolar disorder (BD) is a chronic illness with high morbidity and mortality. Pediatric onset BD has a more severe course of illness with higher rates of relapse and psychosocial impairment. Discovering interventions early in the course of BD in youth is paramount to preventing full illness expression and improve functioning in these individuals throughout the lifespan. It is therefore important to understand the mechanisms involved in the development of BD in order to determine which youth are at most risk and provide biological targets for early intervention. To serve this cause, we propose a neurodevelopmental model of BD, based on the existing data that implicate prefrontal-subcortical network dysfunction, caused by pre-existing genetic susceptibility and triggered by pathological reactions to stress and chronic inflammatory processes.
双相情感障碍（BD）是一种发病率和死亡率都很高的慢性疾病。儿童期发病的双相情感障碍病程更为严重，复发率和社会心理损害率更高。在青少年双相情感障碍病程早期发现干预措施对于预防疾病全面发作以及改善这些个体一生的功能至关重要。因此，了解双相情感障碍发展过程中涉及的机制，以确定哪些青少年风险最高，并为早期干预提供生物学靶点，这一点很重要。为了实现这一目标，我们基于现有数据提出了一种双相情感障碍的神经发育模型，这些数据表明前额叶 - 皮质下网络功能障碍是由预先存在的遗传易感性引起的，并由对压力和慢性炎症过程的病理反应触发。
