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Background <p>Hemodynamic abnormalities of the offending vessels may be the main cause of primary hemifacial spasm (HFS). The aim of this study was to explore the mechanism of HFS and provide potential therapeutic strategies by using computational fluid dynamics (CFD).</p> Methods <p>We retrospectively analyzed 74 HFS patients. Based on MRI, 68 symptomatic and 31 asymptomatic neurovascular contact (NVC) models at the root exit zone of the facial nerve were reconstructed. CFD was used to calculate hemodynamic parameters. Time-series parameters were compared between groups by linear mixed-effects models. Receiver operating characteristic curve was used to evaluate non-time-series parameters and determine optimal cutoff values, while restricted cubic spline was applied to those parameters that performed well to assess their nonlinear relationship with HFS.</p> Results <p>At the center of the NVC region, the symptomatic NVC group exhibited significantly higher time-averaged wall shear stress (TAWSS, <i>p</i> &lt; 0.001) and time-averaged wall shear stress ratio (TAWSSR, <i>p</i> &lt; 0.001), while exhibiting significantly lower endothelial cell activation potential (ECAP, <i>p</i> = 0.017) and relative residence time (RRT, <i>p</i> &lt; 0.001). Linear mixed-effects models indicated that, at the NVC center in the symptomatic group, wall shear stress, wall shear stress ratio, and wall pressure gradient were significantly higher throughout the entire cardiac cycle compared with the asymptomatic group (Group-<i>p</i> &lt; 0.001). TAWSSR at the NVC center point (NVCP) showed better discriminatory ability in differentiating symptomatic from asymptomatic cases (AUC = 0.947, DeLong test <i>p</i> &lt; 0.05). However, no statistically robust nonlinear relationship was found between NVCP’s TAWSSR, TAWSS, or RRT and HFS.</p> Conclusion <p>The NVC region in HFS patients suffer greater hemodynamic forces and steeper fluctuations compared to asymptomatic NVC cases, suggesting mechanical effects involved in HFS pathogenesis. Hemodynamic parameters may serve as reliable indicators for diagnosis, localization of the compression site, and guidance of endovascular treatment in HFS.</p>

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Hemodynamic Features of Offending Vessels in Primary Hemifacial Spasm: A Computational Fluid Dynamics Study

  • 期刊论文

  • 发表日期：

    2025年12月27日

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  • You You,
  • Changliang You,
  • Yong Zhang,
  • Xu Wang,
  • Lijia Huang,
  • Haiyang Wang,
  • Zongyi Xie,
  • Qiuguang He

摘要

Background

Hemodynamic abnormalities of the offending vessels may be the main cause of primary hemifacial spasm (HFS). The aim of this study was to explore the mechanism of HFS and provide potential therapeutic strategies by using computational fluid dynamics (CFD).

Methods

We retrospectively analyzed 74 HFS patients. Based on MRI, 68 symptomatic and 31 asymptomatic neurovascular contact (NVC) models at the root exit zone of the facial nerve were reconstructed. CFD was used to calculate hemodynamic parameters. Time-series parameters were compared between groups by linear mixed-effects models. Receiver operating characteristic curve was used to evaluate non-time-series parameters and determine optimal cutoff values, while restricted cubic spline was applied to those parameters that performed well to assess their nonlinear relationship with HFS.

Results

At the center of the NVC region, the symptomatic NVC group exhibited significantly higher time-averaged wall shear stress (TAWSS, p < 0.001) and time-averaged wall shear stress ratio (TAWSSR, p < 0.001), while exhibiting significantly lower endothelial cell activation potential (ECAP, p = 0.017) and relative residence time (RRT, p < 0.001). Linear mixed-effects models indicated that, at the NVC center in the symptomatic group, wall shear stress, wall shear stress ratio, and wall pressure gradient were significantly higher throughout the entire cardiac cycle compared with the asymptomatic group (Group-p < 0.001). TAWSSR at the NVC center point (NVCP) showed better discriminatory ability in differentiating symptomatic from asymptomatic cases (AUC = 0.947, DeLong test p < 0.05). However, no statistically robust nonlinear relationship was found between NVCP’s TAWSSR, TAWSS, or RRT and HFS.

Conclusion

The NVC region in HFS patients suffer greater hemodynamic forces and steeper fluctuations compared to asymptomatic NVC cases, suggesting mechanical effects involved in HFS pathogenesis. Hemodynamic parameters may serve as reliable indicators for diagnosis, localization of the compression site, and guidance of endovascular treatment in HFS.