Center for Depression, Anxiety and Stress Research, McLean Hospital, Belmont; Department of Psychiatry, Harvard Medical School, Boston, Massachusetts.
Center for Depression, Anxiety and Stress Research, McLean Hospital, Belmont; Department of Psychiatry, Harvard Medical School, Boston, Massachusetts; Department of Psychology, University of California Los Angeles, Los Angeles, California.
Biol Psychiatry Cogn Neurosci Neuroimaging. 2018 Nov;3(11):959-967. doi: 10.1016/j.bpsc.2017.10.008. Epub 2017 Nov 16.
Reward processing deficits have been increasingly associated with trauma exposure and are a core feature of posttraumatic stress disorder (PTSD). While altered resting-state functional connectivity (rsFC) of ventral striatal regions, including the nucleus accumbens (NAcc), has been associated with anhedonia in some stress-related disorders, relationships between NAcc rsFC and anhedonia have not previously been investigated in trauma-exposed individuals. Additionally, relationships between anhedonia and reward-related decision making remain unexplored in relation to trauma exposure. We hypothesized that elevated anhedonia would be associated with altered rsFC between NAcc and default mode network regions and with increased delay discounting.
The sample included 51 participants exposed to a DSM-IV PTSD Criterion A event related to community trauma. Participants completed the Clinician Administered PTSD Scale, the Snaith-Hamilton Pleasure Scale, the Beck Depression Inventory, a computerized delay discounting paradigm, and resting-state functional magnetic resonance imaging. rsFC data were analyzed in SPM12 and CONN.
Higher levels of anhedonia were associated with increased rsFC between seed regions of bilateral NAcc and areas of right dorsomedial prefrontal cortex. This relationship remained significant after accounting for Clinician Administered PTSD Scale total scores, Beck Depression Inventory total scores, or diagnostic group in the regression. Additionally, anhedonia was associated with elevated (increased) delay discounting.
Greater anhedonia was related to higher positive connectivity between NAcc and right dorsomedial prefrontal cortex and to increased delay discounting, i.e., greater preference for smaller immediate versus larger delayed rewards. These findings contribute to a growing body of literature emphasizing the importance of anhedonia in trauma-exposed individuals.
奖赏处理缺陷与创伤暴露越来越相关，是创伤后应激障碍（PTSD）的核心特征。虽然腹侧纹状体区域（包括伏隔核（NAcc））的静息态功能连接（rsFC）改变与一些与应激相关的障碍中的快感缺失有关，但 NAcc rsFC 与快感缺失之间的关系以前并未在创伤暴露个体中进行研究。此外，快感缺失与奖赏相关的决策之间的关系与创伤暴露有关仍未得到探索。我们假设，快感缺失增加与 NAcc 与默认模式网络区域之间的 rsFC 改变以及延迟折扣增加有关。
该样本包括 51 名经历过与社区创伤相关的 DSM-IV PTSD 标准 A 事件的参与者。参与者完成了临床管理的创伤后应激障碍量表、Snaith-Hamilton 快感量表、贝克抑郁量表、计算机化的延迟折扣范式和静息状态功能磁共振成像。rsFC 数据在 SPM12 和 CONN 中进行分析。
更高水平的快感缺失与双侧 NAcc 种子区域与右侧背内侧前额叶皮层区域之间的 rsFC 增加有关。在回归中考虑到临床管理的创伤后应激障碍量表总分、贝克抑郁量表总分或诊断组后，这种关系仍然显著。此外，快感缺失与延迟折扣增加有关。
更大的快感缺失与 NAcc 和右侧背内侧前额叶皮层之间更高的正连接有关，并且与增加的延迟折扣有关，即对较小的即时奖励与较大的延迟奖励更大的偏好。这些发现为强调快感缺失在创伤暴露个体中的重要性的不断增长的文献做出了贡献。
