Confirmatory Efficacy Clinical Trial of Amygdala Neurofeedback for Depression

杏仁核神经反馈治疗抑郁症的疗效临床试验

• 批准号: 10633760
• 负责人: Kym Young
• 金额: $ 74.42万
• 依托单位: UNIVERSITY OF PITTSBURGH AT PITTSBURGH
• 依托单位国家: 美国
• 财政年份: 2023
• 资助国家: 美国
• 起止时间: 2023-06-01 至 2028-05-31
• 项目状态: 未结题
• 来源: https://reporter.nih.gov/project-details/10633760
• 关键词: Adopted; Affect; Alexithymias; Amygdaloid structure; Anhedonia; Antidepressive Agents; Autobiography; Brain; Brain region; Clinical; Clinical Trials; Communities; Control Groups; Data; Diagnosis; Disease; Dissemination and Implementation; Double-Blind Method; Emotional; Ensure; Evaluation; Feedback; Functional Magnetic Resonance Imaging; Gender; Goals; Individual; Intervention; Literature; Major Depressive Disorder; Measures; Mediating; Memory; Mental Depression; Outcome; Participant; Patient Self-Report; Patients; Pharmaceutical Preparations; Phase; Process; Provider; Proxy; Public Health; Quality of life; Randomized; Recovery; Rest; Sampling; Scientist; Series; Signal Transduction; Specificity; Stimulus; Symptoms; Time; Training; Translational Research; Treatment Efficacy; Work; clinical effect; clinically relevant; confirmatory clinical trial; confirmatory trial; depressive symptoms; design; efficacy evaluation; experimental group; follow-up; future implementation; hemodynamics; implementation determinants; improved; indexing; intervention refinement; memory recall; neurofeedback; novel therapeutics; pharmacologic; process evaluation; psychologic; public health relevance; randomized, clinical trials; reduce symptoms; response; stakeholder perspectives; success; symptomatic improvement; treatment response

Abstract Up to two-thirds of patients diagnosed with major depressive disorder (MDD) will not respond to standard pharmacological and psychological interventions, suggesting a need to develop novel therapeutics. Decreased reactivity to positive stimuli, indexed by low amygdala reactivity to positive autobiographical memory recall, may be a causal mechanism interfering with recovery from MDD. Previous work suggests that individuals who do respond to antidepressant medications show increased amygdala activity to positive stimuli that is indistinguishable from controls, while those who do not respond fail to show this increase in amygdala activity. In several small studies we have shown that MDD participants are able to increase their amygdala response during positive memory recall via real-time fMRI neurofeedback (rtfMRI-nf) training, and that this increase is associated with large and rapid reductions in depressive symptoms. Here, we propose to evaluate the efficacy of this intervention in a large-scale confirmatory R01 clinical trial. N=200 MDD individuals will be randomly assigned under double-blind conditions to the amygdala rtfMRI-nf intervention or to a control rtfMRI-nf intervention where they receive yoked sham neurofeedback (instead of their own brain activity they see the signal from another participant who underwent amygdala rtfMRI-nf). We propose to use the same neurofeedback paradigm as our prior studies, with one critical difference. Rather than using a control condition that involves training another brain region, we will adopt a yoked sham control group in order to demonstrate that our findings are robust to the type of control condition used. We additionally aim to determine whether we can use self-report mechanisms to assess who might need the proposed neurofeedback intervention and whether they are likely to be successful in using it. Finally, we will work with implementation scientists to obtain feedback from end-users and clinicians to understand contextual influences on outcomes and increase intervention acceptability. Success will confirm a new non-pharmacological, non-invasive intervention for MDD individuals.

抽象的 多达三分之二的被诊断为重度抑郁症（MDD）的患者不会对标准做出反应 药理和心理干预措施，表明需要开发新的治疗疗法。减少 对阳性刺激的反应性，由低杏仁核对阳性自传记忆的反应性索引， 可能是一种因果机制，会干扰从MDD恢复。以前的工作表明 对抗抑郁药的反应表明，杏仁核活性增加了阳性刺激 与控件无法区分，而那些反应不反应的人则无法显示杏仁核活动的增加。 在几项小型研究中，我们表明MDD参与者能够增加其杏仁核反应 在积极记忆中通过实时fMRI神经反馈（RTFMRI-NF）训练进行回忆，并且这种增加是 与抑郁症状的大量和快速减少有关。在这里，我们建议评估功效 这项干预大规模确认性R01临床试验。 n = 200 MDD个人将是随机的 在双盲条件下分配给杏仁核RTFMRI-NF干预或对照RTFMRI-NF 干预措施会接受Yoked假神经反馈（而不是自己的大脑活动，他们会看到 来自另一个接受杏仁核RTFMRI-NF的参与者的信号。我们建议使用相同的 神经反馈范式作为我们先前的研究，具有一个关键差异。而不是使用控制条件 这涉及培训另一个大脑区域，我们将采用一个Yok them对照组，以证明 我们的发现对所使用的控制条件的类型具有鲁棒性。我们还旨在确定我们是否 可以使用自我报告机制来评估谁可能需要提议的神经反馈干预和 他们是否可能成功使用它。最后，我们将与实施科学家合作，以获取 最终用户和临床医生的反馈，以了解上下文对结果的影响并增加 干预可接受性。成功将确认MDD的新的非药理，非侵入性干预 个人。