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<p>Pain sensitivity variations represent a critical frontier in pain neuroscience, where advanced neuroimaging has mapped cerebral correlates of nociception for decades, yet conventional brain-centric models persistently overlook the spinal cord’s hub role in pain gating and amplification. Here we show that a corticospinal pain sensitivity signature, a pattern of functional connectivity from simultaneous corticospinal magnetic resonance imaging, predicts individual pain sensitivity and clinical pain. Trained on resting-state data and validated across independent healthy (n = 723) and patient cohorts (<i>n</i> = 46), the model generalized to new datasets, distinguished pain from non-pain, and outperformed brain-centric models. Crucially, transcranial magnetic stimulation perturbation revealed a causal axis where enhanced motor cortex-spinal connectivity directly changes pain perception (r = 0.55). These results indicate a previously unknown corticospinal biomarker that bridges laboratory pain measures and patient symptoms, providing insights into translating pain mechanisms from healthy individuals to clinical populations and informing neuromodulation approaches.</p>

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A corticospinal signature for interindividual pain sensitivity

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年12月11日

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  • Xiao-Min Lin,
  • Ling-Fei Guo,
  • Bing Ni,
  • Jiu-Quan Zhang,
  • Xiao-Shuo Zhang,
  • Li-Bo Zhang,
  • Zhao-Xing Wei,
  • Yun-Yun Duan,
  • Li Hu,
  • Ming Zhang,
  • Jing-Yi Zhang,
  • Min Shao,
  • Zai-Ying Jiang,
  • Yun-Jian Huang,
  • Ji-Xin Liu,
  • Li-Ming Cheng,
  • Jonathan C. W. Brooks,
  • Tor D. Wager,
  • Irene Tracey,
  • Ya-Ou Liu,
  • Ya-Zhuo Kong

摘要

Pain sensitivity variations represent a critical frontier in pain neuroscience, where advanced neuroimaging has mapped cerebral correlates of nociception for decades, yet conventional brain-centric models persistently overlook the spinal cord’s hub role in pain gating and amplification. Here we show that a corticospinal pain sensitivity signature, a pattern of functional connectivity from simultaneous corticospinal magnetic resonance imaging, predicts individual pain sensitivity and clinical pain. Trained on resting-state data and validated across independent healthy (n = 723) and patient cohorts (n = 46), the model generalized to new datasets, distinguished pain from non-pain, and outperformed brain-centric models. Crucially, transcranial magnetic stimulation perturbation revealed a causal axis where enhanced motor cortex-spinal connectivity directly changes pain perception (r = 0.55). These results indicate a previously unknown corticospinal biomarker that bridges laboratory pain measures and patient symptoms, providing insights into translating pain mechanisms from healthy individuals to clinical populations and informing neuromodulation approaches.