Emotion & Development Branch, National Institute of Mental Health, National Institutes of Health, Bethesda, Maryland.
Department of Psychology, University of Otago, Dunedin, New Zealand.
JAMA Psychiatry. 2019 Jun 1;76(6):624-633. doi: 10.1001/jamapsychiatry.2019.0020.
Anhedonia can present in children and predict detrimental clinical outcomes.
To map anhedonia in children onto changes in intrinsic large-scale connectivity and task-evoked activation and to probe the specificity of these changes in anhedonia against other clinical phenotypes (low mood, anxiety, and attention-deficit/hyperactivity disorder [ADHD]).
DESIGN, SETTING, AND PARTICIPANTS: Functional magnetic resonance imaging (fMRI) data were from the first annual release of the Adolescent Brain Cognitive Development study, collected between September 2016 and September 2017 and analyzed between April and September 2018. Cross-sectional data of children aged 9 to 10 years from unreferred, community samples during rest (n = 2878) and during reward anticipation (n = 2874) and working memory (n = 2745) were analyzed.
Alterations in fMRI data during rest, reward anticipation, and working memory were examined, using both frequentist and Bayesian approaches. Functional MRI connectivity within large-scale networks, between networks, and between networks and subcortical regions were examined during rest. Functional MRI activation were examined during reward anticipation and working memory using the monetary incentive delayed and N-back tasks, respectively.
Among 2878 children with adequate-quality resting-state fMRI data (mean [SD] age, 10.03 [0.62] years; 1400 girls [48.6%]), children with anhedonia (261 [9.1%]), compared with those without anhedonia (2617 [90.9%]), showed hypoconnectivity among various large-scale networks and subcortical regions, including between the arousal-related cingulo-opercular network and reward-related ventral striatum area (mean [SD] with anhedonia, 0.08 [0.10] vs without anhedonia, 0.10 [0.10]; t2,876 = 3.33; P < .001; q[false discovery rate] = 0.03; ln[Bayes factor10] = 2.85). Such hypoconnectivity did not manifest among children with low mood (277 of 2878 [9.62%]), anxiety (109 of 2878 [3.79%]), or ADHD (459 of 2878 [15.95%]), suggesting specificity. Similarly, among 2874 children (mean [SD] age, 10.03 [0.62] years; 1414 girls [49.2%]) with high-quality task-evoked fMRI data, children with anhedonia (248 of 2874 [8.63%]) demonstrated hypoactivation during reward anticipation in various areas, including the dorsal striatum and areas of the cingulo-opercular network. This hypoactivity was not found among children with low mood (268 of 2874 [9.32%]), anxiety (90 of 2874 [3.13%]), or ADHD (473 of 2874 [16.46%]). Moreover, we also found context- and phenotype-specific double dissociations; while children with anhedonia showed altered activation during reward anticipation (but not working memory), those with ADHD showed altered activation during working memory (but not reward anticipation).
Using the Adolescent Brain Cognitive Development study data set, phenotype-specific alterations were found in intrinsic large-scale connectivity and task-evoked activation in children with anhedonia. The hypoconnectivity at rest and hypoactivation during reward anticipation complementarily map anhedonia onto aberrations in neural-cognitive processes: lack of intrinsic reward-arousal integration during rest and diminishment of extrinsic reward-arousal activity during reward anticipation. These findings help delineate the pathophysiological underpinnings of anhedonia in children.
快感缺失可发生于儿童，并预测不良的临床结局。
将儿童快感缺失映射到内在的大规模连接和任务诱发的激活变化上，并在快感缺失与其他临床表型（情绪低落、焦虑和注意缺陷多动障碍[ADHD]）之间特异性地探测这些变化。
设计、地点和参与者：功能磁共振成像（fMRI）数据来自青少年大脑认知发展研究的第一次年度发布，于 2016 年 9 月至 2017 年 9 月间收集，并于 2018 年 4 月至 9 月间分析。分析了来自未转介的社区样本的 9 至 10 岁儿童的静息（n=2878）、奖励预期（n=2874）和工作记忆（n=2745）的横断面数据。
使用频率论和贝叶斯方法检查了静息、奖励预期和工作记忆期间的 fMRI 数据变化。在静息期间检查了大尺度网络内、网络间和网络与皮质下区域间的功能磁共振连接。使用货币奖励延迟和 N 回任务分别在奖励预期和工作记忆期间检查了功能磁共振激活。
在 2878 名具有足够质量的静息态 fMRI 数据的儿童中（平均[标准差]年龄，10.03[0.62]岁；1400 名女孩[48.6%]），有快感缺失（261 名[9.1%]）的儿童与无快感缺失（2617 名[90.9%]）的儿童相比，在各种大尺度网络和皮质下区域之间显示出连接减少，包括唤醒相关扣带回-前运动皮层网络和奖励相关腹侧纹状体区域之间（有快感缺失的平均[标准差]，0.08[0.10]与无快感缺失的，0.10[0.10]；t2,876=3.33；P<.001；q[假发现率] =0.03；ln[贝叶斯因子 10]=2.85）。在有情绪低落（277 名/2878 名[9.62%]）、焦虑（109 名/2878 名[3.79%]）或 ADHD（459 名/2878 名[15.95%]）的儿童中没有表现出这种连接减少，表明具有特异性。同样，在 2874 名（平均[标准差]年龄，10.03[0.62]岁；1414 名女孩[49.2%]）具有高质量任务诱发 fMRI 数据的儿童中，有快感缺失（248 名/2874 名[8.63%]）的儿童在奖励预期期间显示出各个区域的激活减少，包括背侧纹状体和扣带回-前运动皮层网络的区域。在有情绪低落（268 名/2874 名[9.32%]）、焦虑（90 名/2874 名[3.13%]）或 ADHD（473 名/2874 名[16.46%]）的儿童中没有发现这种低激活。此外，我们还发现了与背景和表型特异性的双重分离；当有快感缺失的儿童在奖励预期期间显示出激活改变（但在工作记忆期间没有）时，有 ADHD 的儿童在工作记忆期间显示出激活改变（但在奖励预期期间没有）。
使用青少年大脑认知发展研究数据集，在有快感缺失的儿童中发现了内在大尺度连接和任务诱发激活的表型特异性改变。静息时的低连接性和奖励预期时的低激活性互补地将快感缺失映射到神经认知过程的异常：静息时内在奖励唤醒整合缺失，奖励预期时外在奖励唤醒活动减少。这些发现有助于描绘儿童快感缺失的病理生理学基础。
