Casper Regina C
Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, 401 Quarry Road, Room 2365, CA 94305-5723, USA.
J Affect Disord. 2006 May;92(1):99-107. doi: 10.1016/j.jad.2005.12.039. Epub 2006 Jan 31.
This paper discusses the hypothesis that a 'drive for activity" in the presence of physiological and endocrine changes consistent with starvation is a characteristic symptom of acute anorexia nervosa (AN). This 'drive for movement', along with alertness and lack of fatigue, so unlike the motor slowing and loss of energy observed in simple starvation has been recognized in AN throughout history, but has received little attention in the past fifty years. Clinical reports and experimental evidence suggest that 'restlessness' and a 'drive for activity' vary in intensity, they appears to be starvation-dependent and to wane with food intake. Central nervous system (CNS) systems known to be involved in mediating activity and arousal levels that are altered by the negative energy expenditure in AN are reviewed. Among these, the corticotropin-releasing hormone (CRH) system, the melanocyte stimulating hormone/agouti-related protein (MSH/AGRP) system and the norepinephrine/epinephrine (NE/EPI) and dopamine (DA) system may contribute to the 'drive for activity' and alertness in AN. AN appears to represent a disorder of gene/environment interaction. Future research will reveal whether in individuals predisposed to AN, the 'drive for activity' reflects the reactivation of mechanisms important in food scarcity, controlled by one or more evolutionary conserved genes including those regulating foraging behavior. Recognition of the 'drive for activity' as a diagnostic symptom of AN and its assessment prior to re-nutrition would permit clarification of its role in the etiology of AN.
本文探讨了一种假说，即在存在与饥饿相一致的生理和内分泌变化的情况下，“活动驱力”是急性神经性厌食症（AN）的一个特征性症状。这种“运动驱力”，连同警觉性和缺乏疲劳感，与单纯饥饿时观察到的运动迟缓及能量丧失截然不同，在神经性厌食症的整个历史中都已被认识到，但在过去五十年里却很少受到关注。临床报告和实验证据表明，“坐立不安”和“活动驱力”在强度上有所不同，它们似乎依赖于饥饿，并会随着食物摄入而减弱。本文回顾了已知参与调节活动和觉醒水平的中枢神经系统（CNS）系统，这些系统会因神经性厌食症中的负能量消耗而发生改变。其中，促肾上腺皮质激素释放激素（CRH）系统、促黑素细胞激素/刺鼠相关蛋白（MSH/AGRP）系统以及去甲肾上腺素/肾上腺素（NE/EPI）和多巴胺（DA）系统可能促成了神经性厌食症中的“活动驱力”和警觉性。神经性厌食症似乎代表了一种基因/环境相互作用的紊乱。未来的研究将揭示，在易患神经性厌食症的个体中，“活动驱力”是否反映了在食物短缺时重要的机制的重新激活，这些机制受一个或多个进化保守基因控制，包括那些调节觅食行为的基因。将“活动驱力”识别为神经性厌食症的一种诊断症状，并在重新营养之前对其进行评估，将有助于阐明其在神经性厌食症病因学中的作用。
