Recent advances in understanding anorexia nervosa.
Recent advances in understanding anorexia nervosa.
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DOI：
10.12688/f1000research.17789.1
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发表时间：
2019-01-01
期刊：
影响因子：
--
通讯作者：
DeGuzman, Marisa C
中科院分区：
文献类型：
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作者：
Frank, Guido K W;Shott, Megan E;DeGuzman, Marisa C
神经性厌食症是一种复杂的精神疾病，与食物限制和高死亡率有关。最近对患有神经性厌食症的青少年和成年人的大脑研究使用了更大的样本量，与早期测试特定大脑回路的研究和任务相比。这些研究产生了更有力的结果，并提高了我们对可能有助于神经性厌食症发展和维持的潜在生物学机制的了解。现在人们认识到，营养不良和脱水会导致整个大脑的大脑结构发生动态变化，随着体重的恢复，大脑结构会正常化。一些结构变化可能是特征因素，但需要复制。脑功能成像和行为研究表明，与学习相关的大脑回路可能与神经性厌食症的饮食限制有关。最值得注意的是，这些环路涉及纹状体、岛叶和额叶皮质区域，这些区域驱动从奖惩中学习，以及习惯学习。这些电路中的干扰可能会导致恶性循环，阻碍复苏。其他研究已经开始探索神经性厌食症患者内部感觉或社会互动的神经生物学，以及大脑区域之间的连接是否发生了变化。总之，这些研究建立在早期研究的基础上，这些研究表明神经性厌食症患者存在神经递质异常，并帮助我们建立起支撑神经性厌食症的独特神经生物学模型。
Anorexia nervosa is a complex psychiatric illness associated with food restriction and high mortality. Recent brain research in adolescents and adults with anorexia nervosa has used larger sample sizes compared with earlier studies and tasks that test specific brain circuits. Those studies have produced more robust results and advanced our knowledge of underlying biological mechanisms that may contribute to the development and maintenance of anorexia nervosa. It is now recognized that malnutrition and dehydration lead to dynamic changes in brain structure across the brain, which normalize with weight restoration. Some structural alterations could be trait factors but require replication. Functional brain imaging and behavioral studies have implicated learning-related brain circuits that may contribute to food restriction in anorexia nervosa. Most notably, those circuits involve striatal, insular, and frontal cortical regions that drive learning from reward and punishment, as well as habit learning. Disturbances in those circuits may lead to a vicious cycle that hampers recovery. Other studies have started to explore the neurobiology of interoception or social interaction and whether the connectivity between brain regions is altered in anorexia nervosa. All together, these studies build upon earlier research that indicated neurotransmitter abnormalities in anorexia nervosa and help us develop models of a distinct neurobiology that underlies anorexia nervosa.