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Background <p>Chronic migraine (CM) carries high disability, yet interictal MRI phenotypes that distinguish CM from episodic migraine (EM), particularly in medication-overuse headache (MOH)-inclusive cohorts, remain incompletely characterized. We tested whether periventricular diffusivity (PVeD), an indirect MRI marker of tissue-water properties at the ventricular-parenchymal interface, is associated with CM and headache burden.</p> Methods <p>In this cross-sectional 3.0-T multimodal MRI study, 289 adults with complete structural MRI, diffusion MRI, and resting-state fMRI were analyzed: 67 healthy controls, 162 EM, and 60 CM. MOH was diagnosed and retained in the CM group. MRI was acquired during verified interictal evening sessions; participants with headache within 24 hours before or after MRI were excluded. The primary contrast was age- and sex-adjusted CM versus EM for PVeD. Secondary analyses examined MOH strata, headache-frequency strata, partial Spearman correlations, Firth logistic regression for CM status, and HIT-6 models.</p> Results <p>Age- and sex-adjusted PVeD was lower in CM than EM (adjusted difference, −0.011; 95% CI, −0.017 to −0.006; standardized difference, −0.71; <i>p</i> &lt; 0.001) and healthy controls (−0.014; 95% CI, −0.021 to −0.007; standardized difference, −0.88; <i>p</i> &lt; 0.001), with no EM-control difference. Both CM participants with and without MOH had lower PVeD than EM. In migraine participants, lower PVeD correlated with higher headache frequency, HIT-6, and MIDAS and with larger choroid plexus volume and smaller thalamic, nucleus accumbens, and putaminal volumes. In the expanded clinical-plus-MRI Firth model, each 1-SD higher PVeD was associated with lower CM odds (OR, 0.59; 95% CI, 0.38 to 0.89; <i>p</i> = 0.011). Higher PVeD was associated with lower HIT-6 after adjustment for headache frequency or MOH.</p> Conclusions <p>CM was associated with lower PVeD at the ventricular-parenchymal interface, and lower PVeD was linked to patient-centered burden in this MOH-inclusive cohort. PVeD is not yet a diagnostic or treatment-selection biomarker, but may help define an MRI phenotype for future chronification-risk and treatment-response studies after longitudinal and external validation.</p>

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Periventricular diffusivity at the ventricular-parenchymal interface across healthy controls, episodic migraine, and chronic migraine: a cross-sectional multimodal MRI study

  • 期刊论文

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  • 发表日期：

    2026年6月19日

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  • Fangwang Fu,
  • Chenyu Dai,
  • Chenyu Lin,
  • Xiaoqing Liu,
  • Zi Tao,
  • Xiaojie Zhang,
  • Xinhao Li,
  • Mengqian Ye,
  • Tong Xu,
  • Yixuan Hu,
  • Kun Liu,
  • Yungang Cao,
  • Keyang Chen,
  • Beilei Hu,
  • Xiaozheng Liu,
  • Jing Sun,
  • Yan Li

摘要

Background

Chronic migraine (CM) carries high disability, yet interictal MRI phenotypes that distinguish CM from episodic migraine (EM), particularly in medication-overuse headache (MOH)-inclusive cohorts, remain incompletely characterized. We tested whether periventricular diffusivity (PVeD), an indirect MRI marker of tissue-water properties at the ventricular-parenchymal interface, is associated with CM and headache burden.

Methods

In this cross-sectional 3.0-T multimodal MRI study, 289 adults with complete structural MRI, diffusion MRI, and resting-state fMRI were analyzed: 67 healthy controls, 162 EM, and 60 CM. MOH was diagnosed and retained in the CM group. MRI was acquired during verified interictal evening sessions; participants with headache within 24 hours before or after MRI were excluded. The primary contrast was age- and sex-adjusted CM versus EM for PVeD. Secondary analyses examined MOH strata, headache-frequency strata, partial Spearman correlations, Firth logistic regression for CM status, and HIT-6 models.

Results

Age- and sex-adjusted PVeD was lower in CM than EM (adjusted difference, −0.011; 95% CI, −0.017 to −0.006; standardized difference, −0.71; p < 0.001) and healthy controls (−0.014; 95% CI, −0.021 to −0.007; standardized difference, −0.88; p < 0.001), with no EM-control difference. Both CM participants with and without MOH had lower PVeD than EM. In migraine participants, lower PVeD correlated with higher headache frequency, HIT-6, and MIDAS and with larger choroid plexus volume and smaller thalamic, nucleus accumbens, and putaminal volumes. In the expanded clinical-plus-MRI Firth model, each 1-SD higher PVeD was associated with lower CM odds (OR, 0.59; 95% CI, 0.38 to 0.89; p = 0.011). Higher PVeD was associated with lower HIT-6 after adjustment for headache frequency or MOH.

Conclusions

CM was associated with lower PVeD at the ventricular-parenchymal interface, and lower PVeD was linked to patient-centered burden in this MOH-inclusive cohort. PVeD is not yet a diagnostic or treatment-selection biomarker, but may help define an MRI phenotype for future chronification-risk and treatment-response studies after longitudinal and external validation.