Department of Psychology, Harvard University, Cambridge, MA 02138, USA.
Neuroimage. 2011 Oct 1;58(3):935-45. doi: 10.1016/j.neuroimage.2011.06.059. Epub 2011 Jun 30.
Human beings are social organisms with an intrinsic desire to seek and participate in social interactions. Social anhedonia is a personality trait characterized by a reduced desire for social affiliation and reduced pleasure derived from interpersonal interactions. Abnormally high levels of social anhedonia prospectively predict the development of schizophrenia and contribute to poorer outcomes for schizophrenia patients. Despite the strong association between social anhedonia and schizophrenia, the neural mechanisms that underlie individual differences in social anhedonia have not been studied and are thus poorly understood. Deficits in face emotion recognition are related to poorer social outcomes in schizophrenia, and it has been suggested that face emotion recognition deficits may be a behavioral marker for schizophrenia liability. In the current study, we used functional magnetic resonance imaging (fMRI) to see whether there are differences in the brain networks underlying basic face emotion processing in a community sample of individuals low vs. high in social anhedonia. We isolated the neural mechanisms related to face emotion processing by comparing face emotion discrimination with four other baseline conditions (identity discrimination of emotional faces, identity discrimination of neutral faces, object discrimination, and pattern discrimination). Results showed a group (high/low social anhedonia) × condition (emotion discrimination/control condition) interaction in the anterior portion of the rostral medial prefrontal cortex, right superior temporal gyrus, and left somatosensory cortex. As predicted, high (relative to low) social anhedonia participants showed less neural activity in face emotion processing regions during emotion discrimination as compared to each control condition. The findings suggest that social anhedonia is associated with abnormalities in networks responsible for basic processes associated with social cognition, and provide a starting point for understanding the neural basis of social motivation and our drive to seek social affiliation.
人类是具有内在社交需求的社会生物，渴望寻求并参与社交互动。社交快感缺失是一种人格特质，其特征是社交联系的欲望降低，以及人际互动带来的愉悦感降低。社交快感缺失水平异常升高可预测精神分裂症的发展，并导致精神分裂症患者的预后较差。尽管社交快感缺失与精神分裂症之间存在很强的关联，但个体社交快感缺失差异的神经机制尚未得到研究，因此了解甚少。面部情绪识别缺陷与精神分裂症的社交结局较差有关，有人提出面部情绪识别缺陷可能是精神分裂症易感性的行为标志物。在当前研究中，我们使用功能磁共振成像（fMRI）来观察社交快感缺失程度低和高的社区样本个体在基本面部情绪处理的大脑网络中是否存在差异。我们通过将面部情绪辨别与其他四个基线条件（情绪面孔的身份辨别、中性面孔的身份辨别、物体辨别和图案辨别）进行比较，来分离与面部情绪处理相关的神经机制。结果显示，在前额内侧前额皮质的前部、右侧颞上回和左侧体感皮层中存在组（社交快感缺失程度高/低）与条件（情绪辨别/对照条件）的交互作用。正如预测的那样，与低社交快感缺失程度的参与者相比，高社交快感缺失程度的参与者在进行情绪辨别时，情绪处理区域的神经活动较少。这些发现表明，社交快感缺失与负责与社会认知相关的基本过程的网络异常有关，并为理解社会动机和我们寻求社交联系的驱动力的神经基础提供了一个起点。
