PDF(Pubmed)
Abstract：
UNASSIGNED: Dysregulated reward processing and mood instability are core features of bipolar disorder that have largely been considered separately, with contradictory findings. We sought to test a mechanistic account that emphasizes an excessive tendency in bipolar disorder to enter recursive cycles in which reward perception is biased by signals that the environment may be changing for the better or worse.
UNASSIGNED: Participants completed a probabilistic reward task with functional magnetic resonance imaging. Using an influential computational model, we ascertained whether participants with bipolar disorder (n = 21) showed greater striatal tracking of momentum-biased reward prediction errors (RPEs) than matched control participants (n = 21). We conducted psychophysiological interaction analyses to quantify the degree to which each group modulated functional connectivity between the ventral striatum and left anterior insula in response to fluctuations in momentum.
UNASSIGNED: In participants with bipolar disorder, but not control participants, the momentum-biased RPE model accounted for significant additional variance in striatal activity beyond a standard model of veridical RPEs. Compared with control participants, participants with bipolar disorder exhibited lower insular-striatal functional connectivity modulated by momentum-biased RPEs, an effect that was more pronounced as a function of current manic symptoms.
UNASSIGNED: Consistent with existing theory, we found evidence that bipolar disorder is associated with a tendency for momentum to excessively bias striatal tracking of RPEs. We identified impaired insular-striatal connectivity as a possible locus for this propensity. We argue that computational psychiatric approaches that examine momentary shifts in reward and mood dynamics have strong potential for yielding new mechanistic insights and intervention targets.
Bipolar disorder is characterized by extremes in mood and dysregulated reward processing. Moningka and Mason evaluated a neurocomputational model in which mood disturbances arise from an excessive tendency for momentum over recent experiences to bias reward perception. Using model-based functional MRI, the authors found that in contrast to matched control participants, participants with bipolar disorder exhibited fluctuations in reward-related neural responses that are modulated by momentum. They discuss this excessive neural tracking of momentum as one of the mechanisms that may underlie the propensity to enter recursive mood cycles in bipolar disorder.
UNASSIGNED: Participants completed a probabilistic reward task with functional magnetic resonance imaging. Using an influential computational model, we ascertained whether participants with bipolar disorder (n = 21) showed greater striatal tracking of momentum-biased reward prediction errors (RPEs) than matched control participants (n = 21). We conducted psychophysiological interaction analyses to quantify the degree to which each group modulated functional connectivity between the ventral striatum and left anterior insula in response to fluctuations in momentum.
UNASSIGNED: In participants with bipolar disorder, but not control participants, the momentum-biased RPE model accounted for significant additional variance in striatal activity beyond a standard model of veridical RPEs. Compared with control participants, participants with bipolar disorder exhibited lower insular-striatal functional connectivity modulated by momentum-biased RPEs, an effect that was more pronounced as a function of current manic symptoms.
UNASSIGNED: Consistent with existing theory, we found evidence that bipolar disorder is associated with a tendency for momentum to excessively bias striatal tracking of RPEs. We identified impaired insular-striatal connectivity as a possible locus for this propensity. We argue that computational psychiatric approaches that examine momentary shifts in reward and mood dynamics have strong potential for yielding new mechanistic insights and intervention targets.
Bipolar disorder is characterized by extremes in mood and dysregulated reward processing. Moningka and Mason evaluated a neurocomputational model in which mood disturbances arise from an excessive tendency for momentum over recent experiences to bias reward perception. Using model-based functional MRI, the authors found that in contrast to matched control participants, participants with bipolar disorder exhibited fluctuations in reward-related neural responses that are modulated by momentum. They discuss this excessive neural tracking of momentum as one of the mechanisms that may underlie the propensity to enter recursive mood cycles in bipolar disorder.
摘要：
■奖励处理失调和情绪不稳定是双相情感障碍的核心特征，这些特征在很大程度上被单独考虑，矛盾的发现。我们试图测试一种机械解释，该解释强调了双相情感障碍进入递归循环的过度倾向，在递归循环中，奖励感知因环境可能会变得更好或更坏的信号而产生偏差。
■参与者通过功能磁共振成像完成了概率奖励任务。使用有影响力的计算模型，我们确定了双相情感障碍参与者(n=21)是否比匹配的对照参与者(n=21)表现出更大的纹状体动量偏倚奖励预测误差(RPEs).我们进行了心理生理相互作用分析，以量化每组响应动量波动而调节腹侧纹状体和左前脑岛之间功能连接的程度。
■在患有双相情感障碍的参与者中，但不能控制参与者，动量偏倚RPE模型解释了纹状体活动的显著额外差异,超出了标准的真实RPE模型.与对照参与者相比，双相情感障碍参与者表现出受动量偏倚RPE调节的岛叶-纹状体功能连通性较低，作为当前躁狂症状的功能，效果更明显。
■与现有理论一致，我们发现有证据表明,双相情感障碍与RPE纹状体追踪过度偏倚的动量倾向相关.我们确定了岛叶-纹状体连通性受损是这种倾向的可能位点。我们认为，检查奖励和情绪动态的瞬时变化的计算精神病学方法具有产生新的机械见解和干预目标的强大潜力。
双相情感障碍的特征是情绪极端和奖励处理失调。Moningka和Mason评估了一种神经计算模型，在该模型中，情绪障碍是由于最近的经历过度倾向于偏向奖励感知而引起的。使用基于模型的功能MRI，作者发现，与匹配的对照参与者相反，双相情感障碍参与者表现出奖赏相关神经反应的波动,这些神经反应受动量调节.他们讨论了这种过度的动量神经跟踪，作为可能成为双相情感障碍进入递归情绪周期倾向的基础的机制之一。
■参与者通过功能磁共振成像完成了概率奖励任务。使用有影响力的计算模型，我们确定了双相情感障碍参与者(n=21)是否比匹配的对照参与者(n=21)表现出更大的纹状体动量偏倚奖励预测误差(RPEs).我们进行了心理生理相互作用分析，以量化每组响应动量波动而调节腹侧纹状体和左前脑岛之间功能连接的程度。
■在患有双相情感障碍的参与者中，但不能控制参与者，动量偏倚RPE模型解释了纹状体活动的显著额外差异,超出了标准的真实RPE模型.与对照参与者相比，双相情感障碍参与者表现出受动量偏倚RPE调节的岛叶-纹状体功能连通性较低，作为当前躁狂症状的功能，效果更明显。
■与现有理论一致，我们发现有证据表明,双相情感障碍与RPE纹状体追踪过度偏倚的动量倾向相关.我们确定了岛叶-纹状体连通性受损是这种倾向的可能位点。我们认为，检查奖励和情绪动态的瞬时变化的计算精神病学方法具有产生新的机械见解和干预目标的强大潜力。
双相情感障碍的特征是情绪极端和奖励处理失调。Moningka和Mason评估了一种神经计算模型，在该模型中，情绪障碍是由于最近的经历过度倾向于偏向奖励感知而引起的。使用基于模型的功能MRI，作者发现，与匹配的对照参与者相反，双相情感障碍参与者表现出奖赏相关神经反应的波动,这些神经反应受动量调节.他们讨论了这种过度的动量神经跟踪，作为可能成为双相情感障碍进入递归情绪周期倾向的基础的机制之一。
