Meza-Concha Nicolás, Arancibia Marcelo, Salas Felicia, Behar Rosa, Salas Germán, Silva Hernán, Escobar Rocío
Escuela de Medicina, Facultad de Medicina, Universidad de Valparaíso, Valparaíso, Chile. Address: Angamos 655, Reñaca, Viña del Mar, Región de Valparaíso, Chile. Email:
Centro de Investigaciones Biomédicas, Universidad de Valparaíso, Valparaíso, Chile; Centro Colaborador de la Red Cochrane Iberoamericana, Universidad de Valparaíso, Valparaíso, Chile.
Medwave. 2017 May 29;17(4):e6960. doi: 10.5867/medwave.2017.04.6960.
Although the specialized literature on the etiology of alexithymia is controversial, neurobiological research has shown relevant advances. The aim of this review is to analyze the available evidence regarding the neurophysiological bases of alexithymia. A comprehensive review of available articles from Medline/PubMed, EBSCO and SciELO was conducted. Previously, alexithymia was linked to a reduced interhemispheric brain connection. From a childhood traumatic perspective, the right prefrontal cortex and the default mode network would experience alterations, first hypermetabolic (dopaminergic and glutamatergic dysregulation) and then hypometabolic-dissociative (serotonergic and opioid dysregulation), resulting in a distorted interoceptive and emotional awareness. Mirror neurons are the essential neurobiological substrate of theory of mind and social cognition, intrinsically linked to alexithymia, involving parietal, temporal, premotor, and cingulate cortices, and inferior frontal gyrus. Other structures involved are the amygdala (facial expression and emotional reactivity), the insula (interoception, emotional integration and empathy) and the cerebellum (limbic cerebellum and somatosensory awareness). Molecular genetics has detected polymorphisms in genes of the serotonin transporter, in the enzyme genes of dopaminergic metabolism and brain-derived neurotrophic factor, while the role of oxytocin is controversial. To sum up, we found several studies demonstrating the overwhelming evidence of a neurobiological basis underlying alexithymia; nevertheless, research is still inconclusive and must include environmental, traumatic, social, and psychological factors that contribute to the origin of the alexithymia.
尽管关于述情障碍病因的专业文献存在争议，但神经生物学研究已取得了相关进展。本综述的目的是分析有关述情障碍神经生理学基础的现有证据。我们对来自Medline/PubMed、EBSCO和SciELO的现有文章进行了全面综述。以前，述情障碍与大脑半球间连接减少有关。从童年创伤的角度来看，右侧前额叶皮质和默认模式网络会发生改变，首先是代谢亢进（多巴胺能和谷氨酸能失调），然后是代谢减退 - 解离（血清素能和阿片样物质失调），导致内感受和情绪意识扭曲。镜像神经元是心理理论和社会认知的重要神经生物学基础，与述情障碍有着内在联系，涉及顶叶、颞叶、运动前区、扣带回皮质和额下回。其他涉及的结构包括杏仁核（面部表情和情绪反应）、脑岛（内感受、情绪整合和同理心）和小脑（边缘小脑和体感意识）。分子遗传学已在血清素转运体基因、多巴胺能代谢酶基因和脑源性神经营养因子中检测到多态性，而催产素的作用存在争议。总之，我们发现多项研究证明了述情障碍存在神经生物学基础的压倒性证据；然而，研究仍无定论，必须纳入有助于述情障碍起源的环境、创伤、社会和心理因素。
