Biological Psychiatry-Cognitive Neuroscience and Neuroimaging最新文献

英文中文

Encoding-Retrieval Similarity Reveals Distinct Neural Reinstatement of Safety Memories Following Counterconditioning in Posttraumatic Stress Disorder 编码-检索相似性揭示了创伤后应激障碍中对抗条件作用后安全记忆的明显神经恢复。

IF 4.8 2区医学 Q1 NEUROSCIENCES

Biological Psychiatry-Cognitive Neuroscience and Neuroimaging

Pub Date : 2025-11-01 DOI: 10.1016/j.bpsc.2025.07.007

Elizabeth A. Bauer , Samuel E. Cooper , Nicole E. Keller , Josh M. Cisler , Joseph E. Dunsmoor

Background

Posttraumatic stress disorder (PTSD) is characterized by deficits in the ability to retrieve extinction memories, which likely contribute to symptom relapse over time. Adapting a hybrid Pavlovian conditioning and episodic memory paradigm, we examined whether counterconditioning produces a more stable and persistent long-term neural memory trace of safety compared with standard extinction in the ventromedial prefrontal cortex (vmPFC)—a region associated with the learning and retrieval of safety.

Methods

Participants consisted of 32 individuals (27 female) who met diagnostic criteria for PTSD and 21 healthy (13 female) comparison participants. Participants completed a multiday Pavlovian conditioning and episodic memory paradigm with standard extinction/counterconditioning.

Results

In healthy adults, we identified overlapping multivariate patterns of functional magnetic resonance imaging activity in the vmPFC associated with the formation and 24-hour retrieval of stimuli that underwent counterconditioning, but neural reinstatement diminished after ∼1 month. This pattern was reversed in PTSD, such that neural reinstatement of counterconditioning was not observed the day after safety learning but did emerge a month later. Interestingly, participants with PTSD showed reinstatement of standard extinction memories in the dorsal anterior cingulate cortex—a region associated with learning and retrieval of threat—both 24 hours and 1 month after safety learning.

Conclusions

These results provide the first evidence that counterconditioning may stabilize a long-term safety memory trace in PTSD. These effects seem to emerge over longer time scales, suggesting that counterconditioning could be an effective strategy for sustained treatment gains.

背景：创伤后应激障碍（PTSD）的特征是恢复消失记忆的能力不足，可能导致症状随着时间的推移而复发。采用巴甫洛夫条件反射和情景记忆的混合模式，我们研究了在与安全学习和检索相关的腹内侧前额叶皮层（vmPFC）中，与标准消退相比，对抗条件反射是否会产生更稳定和持久的长期安全神经记忆痕迹。方法：参与者包括32名符合PTSD诊断标准的个体（27名女性）和21名健康的对照组（13名女性）。参与者完成了为期多日的巴甫洛夫条件反射和情景记忆范式，其中包括标准的消退/对抗条件反射。结果：在健康成人中，我们在vmPFC中发现了重叠的多变量fMRI活动模式，这些模式与经过对抗条件的刺激的形成和24小时恢复有关，但神经恢复在1个月后减弱。这种模式在创伤后应激障碍中被逆转，因此在安全学习后的第二天没有观察到对抗条件作用的神经恢复，但在一个月后确实出现了。有趣的是，创伤后应激障碍参与者在安全学习后24小时和1个月，在背前扣带皮层（dACC）——一个与学习和恢复威胁相关的区域——显示了标准消失记忆的恢复。结论：这些结果提供了第一个证据，证明对抗条件可能稳定PTSD患者的长期安全记忆痕迹。这些影响似乎在更长的时间尺度上出现，这表明对抗条件作用可能是持续治疗效果的有效策略。

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IF 4.8 2区医学 Q1 NEUROSCIENCES

Biological Psychiatry-Cognitive Neuroscience and Neuroimaging

Pub Date : 2025-11-01 DOI: 10.1016/S2451-9022(25)00314-3

引用次数: 0

Reward Sensitivity in Patients Receiving Opioid Agonist and Antagonist Treatment for Opioid Use Disorder: An Observational Study 阿片类药物使用障碍患者接受阿片类药物激动剂和拮抗剂治疗的奖励敏感性：一项观察性研究。

IF 4.8 2区医学 Q1 NEUROSCIENCES

Biological Psychiatry-Cognitive Neuroscience and Neuroimaging

Pub Date : 2025-11-01 DOI: 10.1016/j.bpsc.2025.04.013

Martin Trøstheim , Mads Lund Pedersen , Siri Leknes , Lennja Majid Hama , Mathias Nikolai Roland , Philipp Paul Lobmaier , Kristin Klemmetsby Solli , Bente M. Weimand , Lars Tanum , Marie Eikemo

Background

Disrupted reward processing is a core component in neurobiological theories of addictions, including opioid use disorder (OUD). While acute opioid agonist and antagonist administration can modulate reward behavior and experiences, it remains unclear how typical long-term OUD treatment with these medications impacts patients’ sensitivity to substance-free rewards. Therefore, we conducted a cross-sectional study of reward sensitivity in opioid agonist– and antagonist–treated patients with OUD and healthy volunteers.

Methods

Ninety-six patients with OUD on extended-release naltrexone (n = 45) or opioid agonists (n = 51) and 50 healthy volunteers completed a probabilistic reward task (PRT) and self-report measures of anhedonia, depression, preoccupation with immediate consequences, substance craving, and life satisfaction in a single session. We used signal detection analysis and drift diffusion modeling to derive behavioral reward bias measures from PRT performance. Group differences were modeled with beta and linear regression.

Results

Patients reported significantly greater anhedonia (Cohen’s ds ≥ 0.64), depression (ds ≥ 0.53), and preoccupation with immediate consequences (ds ≥ 0.54) than healthy volunteers, but differences between naltrexone- and opioid agonist–treated patients were nonsignificant (ds ≤ 0.26). Group differences in behavioral reward bias were small and nonsignificant (ps = 1, Bayes factor [BF]₀₁s ≥ 84.13). Anhedonia was significantly associated with lower life satisfaction (odds ratio [95% CI], 1.10 [1.04 to 1.17]). There were no other significant associations between reward sensitivity measures and life satisfaction or craving (ps ≥ .31, BF₀₁s ≥ 2.58).

Conclusions

These data support an association between OUD and reduced well-being irrespective of opioid agonist or antagonist treatment, highlighting patients’ need for psychosocial support and/or adjunct interventions. Major detrimental effects of naltrexone treatment on well-being seem unlikely from these and previous results.

背景：中断的奖励加工是成瘾的神经生物学理论的核心组成部分，包括阿片类药物使用障碍（OUD）。虽然急性阿片类激动剂和拮抗剂可以调节奖励行为和体验，但目前尚不清楚这些药物的典型长期OUD治疗如何影响患者对无物质奖励的敏感性。因此，我们对阿片类激动剂和拮抗剂治疗的OUD患者和健康志愿者的奖励敏感性进行了横断面研究。方法：96例服用缓释纳曲酮（n=45）或阿片类激动剂（n=51）的OUD患者和50名健康志愿者在一次疗程中完成了概率奖励任务（PRT）和自我报告的快感缺乏、抑郁、即刻后果的关注、物质渴望和生活满意度。我们使用信号检测分析和漂移扩散模型从PRT的表现中得出行为奖励偏差的度量。组间差异采用beta和线性回归建模。结果：与健康志愿者相比，患者报告的快感缺乏症（Cohen’s ds≥0.64）、抑郁（ds≥0.53）和关注即刻后果（ds≥0.54）显著增加，但纳曲酮和阿片类激动剂治疗患者之间的差异无统计学意义（ds≤0.26）。行为奖励偏差组间差异不显著（ps=1, BF01s≥84.13）。快感缺乏与较低的生活满意度显著相关（OR [95% CI]=1.10[1.04, 1.17]）。奖励敏感性测量与生活满意度或渴望之间无其他显著相关（ps≥0.31,BF01s≥2.58）。结论：这些数据支持不考虑阿片类药物激动剂或拮抗剂治疗的OUD和幸福感下降之间的关联，强调患者需要社会心理支持和/或辅助干预。从这些和以前的结果来看，纳曲酮治疗对健康的主要有害影响似乎不太可能。

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引用次数: 0

Altered Striatal Functional Gradients in Obsessive-Compulsive Disorder 强迫症患者纹状体功能梯度改变。

IF 4.8 2区医学 Q1 NEUROSCIENCES

Biological Psychiatry-Cognitive Neuroscience and Neuroimaging

Pub Date : 2025-11-01 DOI: 10.1016/j.bpsc.2025.07.006

Lachlan Webb , Luke J. Hearne , Ye E. Tian , Andrew Zalesky , Conor Robinson , Caitlin V. Hall , Saurabh Sonkusare , Bjorn Burgher , Michael Breakspear , Garance M. Meyer , Andreas Horn , Sebastien Naze , Philip Mosley , Luca Cocchi

Background

Obsessive-compulsive disorder (OCD) is associated with functional alterations in how the striatum interacts with the rest of the brain. However, the characterization of these changes in OCD is incomplete. Mapping functional striatal gradients provides a new opportunity to fill this knowledge gap. These gradients provide a spatial representation of continuous changes in whole-brain connectivity within striatal regions. Thus, OCD-related differences in striatal gradients imply changes in the functional organization of striatal connections.

Methods

We calculated spatial striatal gradients linked to whole-brain activity in 52 people with OCD and 45 control participants. Gradients were computed with individuals at rest and when they underwent a threat-safety reversal task. Using a longitudinal dataset of 47 people with OCD, we investigated possible associations between changes in striatal gradient topology and fluctuations in symptom severity.

Results

Results showed group differences in the main gradient topology at rest, specifically in striatal regions that overlap with the putamen and caudate. Individuals who showed a reduction in symptoms over time tended to change their gradient topology in favor of the control participants’ average topology. Finally, gradients linked to the appraisal of safety reversal, but not threat reversal, showed a group difference in a region separating the right nucleus accumbens and the putamen.

Conclusions

This study advances knowledge of striatal connectivity profiles in OCD, supporting a core role of distinct changes in striatal topology in the expression of symptoms. Collectively, these results encourage studies assessing neural mechanisms that drive the dynamic reorganization of striatal topology and the development of therapies that leverage striatocortical plasticity.

背景：强迫症（OCD）与纹状体与大脑其他部分相互作用的功能改变有关。然而，对强迫症中这些变化的描述是不完整的。绘制功能性纹状体梯度为填补这一知识空白提供了新的机会。这些梯度提供了纹状体区域内全脑连通性连续变化的空间表征。因此，强迫症相关纹状体梯度的差异暗示纹状体连接的功能组织发生了变化。方法：我们计算了52名强迫症患者和45名对照组与全脑活动相关的空间纹状体梯度。梯度是在个体休息时和他们接受威胁-安全逆转任务时计算的。利用47名强迫症患者的纵向数据集，我们研究了纹状体梯度拓扑变化与症状严重程度波动之间的可能关联。结果：结果显示各组在静止状态下的主要梯度拓扑结构存在差异，特别是纹状体区域与壳核和尾状核重叠。随着时间的推移，表现出症状减轻的个体倾向于改变他们的梯度拓扑，以支持对照组参与者的平均拓扑。最后，与安全逆转（而非威胁逆转）评估相关的梯度显示，在右侧伏隔核和壳核之间的区域存在组间差异。结论：本研究提高了对强迫症纹状体连接谱的认识，支持纹状体拓扑结构的明显变化在症状表达中的核心作用。总的来说，这些结果鼓励了评估驱动纹状体拓扑动态重组的神经机制的研究，以及利用纹状体-皮层可塑性的治疗方法的发展。

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引用次数: 0

Trading Fear for Safety 用恐惧换取安全

IF 4.8 2区医学 Q1 NEUROSCIENCES

Biological Psychiatry-Cognitive Neuroscience and Neuroimaging

Pub Date : 2025-11-01 DOI: 10.1016/j.bpsc.2025.09.009

Kai Zhang, Lihan Cui, Mohammed R. Milad

引用次数: 0

Ketosis Modulates Neurotransmitters, Antioxidants, and Energy Metabolism to Improve Brain Network Stability in Humans 酮症调节神经递质、抗氧化剂和能量代谢，以改善人类大脑网络的稳定性

IF 4.8 2区医学 Q1 NEUROSCIENCES

Biological Psychiatry-Cognitive Neuroscience and Neuroimaging

Pub Date : 2025-11-01 DOI: 10.1016/j.bpsc.2025.09.004

Dongjian Wu , Miaomiao Zhao , Chunyan Chen , Xiaoxian Xie

引用次数: 0

Sensorimotor Feedback Control Dysfunction as a Marker of Posttraumatic Stress Disorder 作为创伤后应激障碍标志的感觉运动反馈控制功能障碍

IF 4.8 2区医学 Q1 NEUROSCIENCES

Biological Psychiatry-Cognitive Neuroscience and Neuroimaging

Pub Date : 2025-11-01 DOI: 10.1016/j.bpsc.2024.07.010

Jonathon R. Howlett , Heekyeong Park , Martin P. Paulus

Background

Posttraumatic stress disorder (PTSD) is characterized not only by its direct association with traumatic events but also by a potential deficit in inhibitory control across emotional, cognitive, and sensorimotor domains. Recent research has shown that a continuous sensorimotor feedback control task, the rapid assessment of motor processing paradigm, can yield reliable measures of individual sensorimotor control performance. This study used this paradigm to investigate control deficits in PTSD compared with both a healthy volunteer group and a non-PTSD psychiatric comparison group.

Methods

We examined control processing using the rapid assessment of motor processing paradigm in a sample of 40 individuals with PTSD, matched groups of 40 individuals with mood and anxiety complaints, and 40 healthy control participants. We estimated K_p (drive) and K_d (damping) parameters using a proportional-derivative control modeling approach.

Results

The K_p parameter was lower in the PTSD group than in the healthy control (Cohen’s d = 0.86) and mood and anxiety (Cohen’s d = 0.63) groups. After controlling for color-word inhibition, K_p remained lower in the PTSD group than in the healthy control (Cohen’s d = 0.79) and mood and anxiety (Cohen’s d = 0.62) groups. Mediation analysis showed that K_d significantly mediated the relationship between PTSD and control deficits in the K_p parameter, with 96% of the effect being mediated by K_d.

Conclusions

These findings underscore the potential of using dynamic control paradigms to elucidate the control dysfunctions in PTSD and suggest that different psychiatric conditions may distinctly influence subcomponents of sensorimotor control.

背景：创伤后应激障碍（PTSD创伤后应激障碍（PTSD）的特点不仅在于它与创伤事件的直接联系，还在于它在情绪、认知和感觉运动领域的抑制控制方面可能存在缺陷。最近的研究表明，一种连续的感觉运动反馈控制任务--运动处理快速评估（RAMP）范式--可以对个体的感觉运动控制表现进行可靠的测量。本研究利用该范式调查了创伤后应激障碍患者相对于健康志愿者和非创伤后应激障碍精神疾病对比组的控制缺陷：方法：我们使用 RAMP 范式对 40 名创伤后应激障碍患者以及 40 名情绪和焦虑（MA）症状患者和 40 名健康对照组（HC）进行了控制处理研究。我们使用比例-衍生（PD）控制模型方法估算了Kp（驱动）和Kd（阻尼）参数：结果：与 HC 组（Cohen's d = 0.86）和 MA 组（Cohen's d = 0.63）相比，创伤后应激障碍组的 Kp 参数较低。在对颜色词抑制进行控制后，创伤后应激障碍组的 Kp 仍低于 HC 组（Cohen's d = 0.79）和 MA 组（Cohen's d = 0.62）。中介分析表明，Kd对创伤后应激障碍与Kp参数控制缺陷之间的关系有明显的中介作用，96%的影响由Kd中介：这些发现强调了使用动态控制范式来阐明创伤后应激障碍中的控制功能障碍的潜力，并表明不同的精神疾病可能会对感觉运动控制的子组件产生不同的影响。

{"title":"Sensorimotor Feedback Control Dysfunction as a Marker of Posttraumatic Stress Disorder","authors":"Jonathon R. Howlett , Heekyeong Park , Martin P. Paulus","doi":"10.1016/j.bpsc.2024.07.010","DOIUrl":"10.1016/j.bpsc.2024.07.010","url":null,"abstract":"<div><h3>Background</h3><div><span>Posttraumatic stress disorder<span> (PTSD) is characterized not only by its direct association with traumatic events<span> but also by a potential deficit in inhibitory control across emotional, cognitive, and sensorimotor domains. Recent research has shown that a continuous sensorimotor feedback control task, the rapid assessment of motor processing paradigm, can yield reliable measures of individual </span></span></span>sensorimotor control performance. This study used this paradigm to investigate control deficits in PTSD compared with both a healthy volunteer group and a non-PTSD psychiatric comparison group.</div></div><div><h3>Methods</h3><div>We examined control processing using the rapid assessment of motor processing paradigm in a sample of 40 individuals with PTSD, matched groups of 40 individuals with mood and anxiety complaints, and 40 healthy control participants. We estimated <em>K</em><sub><em>p</em></sub> (drive) and <em>K</em><sub><em>d</em></sub> (damping) parameters using a proportional-derivative control modeling approach.</div></div><div><h3>Results</h3><div>The <em>K</em><sub><em>p</em></sub> parameter was lower in the PTSD group than in the healthy control (Cohen’s <em>d</em> = 0.86) and mood and anxiety (Cohen’s <em>d</em> = 0.63) groups. After controlling for color-word inhibition, <em>K</em><sub><em>p</em></sub> remained lower in the PTSD group than in the healthy control (Cohen’s <em>d</em> = 0.79) and mood and anxiety (Cohen’s <em>d</em><span> = 0.62) groups. Mediation analysis showed that </span><em>K</em><sub><em>d</em></sub> significantly mediated the relationship between PTSD and control deficits in the <em>K</em><sub><em>p</em></sub> parameter, with 96% of the effect being mediated by <em>K</em><sub><em>d</em></sub>.</div></div><div><h3>Conclusions</h3><div>These findings underscore the potential of using dynamic control paradigms to elucidate the control dysfunctions in PTSD and suggest that different psychiatric conditions may distinctly influence subcomponents of sensorimotor control.</div></div>","PeriodicalId":54231,"journal":{"name":"Biological Psychiatry-Cognitive Neuroscience and Neuroimaging","volume":"10 11","pages":"Pages 1117-1124"},"PeriodicalIF":4.8,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141763220","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

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IF 4.8 2区医学 Q1 NEUROSCIENCES

Biological Psychiatry-Cognitive Neuroscience and Neuroimaging

Pub Date : 2025-11-01 DOI: 10.1016/S2451-9022(25)00313-1

引用次数: 0

Does Reward Insensitivity in Anhedonia Result From Limitations in Cognitive Capacity? 快感缺乏症的奖励不敏感是认知能力限制的结果吗？

IF 4.8 2区医学 Q1 NEUROSCIENCES

Biological Psychiatry-Cognitive Neuroscience and Neuroimaging

Pub Date : 2025-11-01 DOI: 10.1016/j.bpsc.2025.09.008

Vanessa M. Brown

引用次数: 0

Computationally Informed Insights Into Anhedonia and Treatment by Kappa Opioid Receptor Antagonism 通过k-阿片受体拮抗剂对快感缺乏症和治疗的计算信息见解。

IF 4.8 2区医学 Q1 NEUROSCIENCES

Biological Psychiatry-Cognitive Neuroscience and Neuroimaging

Pub Date : 2025-11-01 DOI: 10.1016/j.bpsc.2025.05.011

Bilal A. Bari , Andrew D. Krystal , Diego A. Pizzagalli , Samuel J. Gershman

Background

Anhedonia, the loss of pleasure, is prevalent and impairing. Parsing its computational basis promises to explain its transdiagnostic character. One manifestation of anhedonia, reward insensitivity, may be linked to limited memory. Furthermore, the need to economize on limited memory engenders a perseverative bias toward frequently chosen actions. Anhedonia may also be linked with deviations from optimal perseveration for a given memory capacity, a pattern that causes inefficiency because it results in less reward for the same memory cost.

Methods

To test these hypotheses, we applied a theory of optimal decision making under memory constraints that decomposes behavior into a memory component and an efficiency component. We applied this theory to behavior on the Probabilistic Reward Task, a reward learning paradigm that has been validated in anhedonia, and performed secondary analysis of a randomized controlled trial testing kappa opioid receptor (KOR) antagonism for anhedonia (n = 24 KOR; n = 31 placebo), as well as analyses of 3 other datasets (n = 100, 66, 24, respectively). We fit a resource-bounded reinforcement learning model to behavior.

Results

Across clinical and nonclinical populations, anhedonia was associated with deficits in efficiency but not memory. The reinforcement learning models demonstrated that deficits in efficiency arise from the inability to perseverate optimally. KOR antagonism, which likely elevates tonic dopamine, increases both memory and efficiency, and the model demonstrated that this arises from increased reward sensitivity and perseveration.

Conclusions

Therefore, KOR antagonism has distinct cognitive effects, only one related to anhedonia. These findings have potential implications for the applications of KOR antagonists.

背景：快感缺乏，即快乐的丧失，是一种普遍且有害的现象。分析其计算基础有望解释其跨诊断特性。快感缺乏的一种表现——奖励不敏感——可能与记忆有限有关。此外，为了节省有限的记忆，人们对频繁选择的行为产生了持久的偏见。快感缺乏症也可能与对给定记忆容量的最佳持久性的偏离有关，这种模式导致效率低下，因为它导致相同记忆成本的奖励更少。方法：为了验证这些假设，我们应用记忆约束下的最优决策理论，将行为分解为记忆成分和效率成分。我们将这一理论应用于概率奖励任务（Probabilistic Reward Task）的行为，这是一种奖励学习范式，在快感缺乏症中得到了验证，并对一项随机对照试验进行了二次分析，该试验测试了κ-阿片受体（KOR）对快感缺乏症的拮抗作用(N=24 KOR；N=31安慰剂)，以及其他三个数据集的分析（N=100, 66, 24）。我们将资源有限的强化学习模型应用于行为。结果：在临床和非临床人群中，快感缺乏与效率缺陷有关，但与记忆缺陷无关。强化学习模型表明，效率的缺陷来自于无法保持最佳状态。KOR拮抗剂可能会增加强直性多巴胺，从而增加记忆和效率，该模型表明，这是由于奖励敏感性和持久性的增加。结论：因此，KOR拮抗剂具有明显的认知作用，只有一种与快感缺乏有关。这些发现对KOR拮抗剂的应用具有潜在的意义。

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