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Published on: April 23, 2021
Deep medullary vein dysfunction is associated with cerebral microbleeds in cerebral small vessel disease
Haiyuan Lan1, Xinjun Lei1, Zhihua Xu2
1Department of Radiology, Lishui Hospital of Traditional Chinese Medicine Affiliated Zhejiang Chinese Medical University, Lishui, China.
Objective:
This study investigated the association between deep medullary vein (DMV) dysfunction and the development of cerebral microbleeds (CMB) in patients with cerebral small vessel disease (CSVD), with a particular focus on the contribution of extracellular fluid accumulation.
Methods:
This was a cross sectional study. Clinical and imaging data from 176 patients with CSVD were consecutively collected between July 2024 and May 2025. DMV visibility was scored on a scale of 0-18 using susceptibility-weighted imaging (SWI). CMB were quantified on SWI magnitude images and categorized into three groups: absent CMB, mild CMB (1-2 lesions), and extensive CMB (≥3 lesions). Extracellular fluid volume was estimated using free water (FW) values derived from diffusion tensor imaging. Associations between DMV scores, FW values, and CMB burden were evaluated.
Results:
DMV scores were moderate positively correlated with both CMB burden and FW values (r = 0.460, P < 0.001; r = 0.549, P < 0.001, respectively), as well as between FW values and CMB burden (r = 0.561, P < 0.001). Patients in the extensive CMB group had significantly higher DMV scores and FW values compared to those in the absent CMB and mild CMB groups. Mediation analysis demonstrated that FW acted as a partial mediator in the relationship between DMV scores and CMB burden (β = 0.088, 95% CI: 0.048-0.152, P < 0.05). This mediating effect remained statistically significant after adjusting for age, sex, hypertension, diabetes, smoking, and hyperlipidemia (β = 0.054, 95% CI: 0.022-0.107, P < 0.05).
Conclusion:
DMV dysfunction is positively associated with CMB burden in CSVD, partially mediated by increased extracellular fluid accumulation. These findings suggest that impaired venous drainage and interstitial fluid retention may play a role in the pathogenesis of CMB.
Insights
Deep medullary vein (DMV) dysfunction is linked to cerebral microbleeds (CMB) in cerebral small vessel disease (CSVD). Extracellular fluid accumulation partially mediates this association, suggesting impaired venous drainage contributes to CMB development.
Area of Science:
- Neurology
- Radiology
- Vascular Biology
Background:
- Cerebral small vessel disease (CSVD) is a major cause of stroke and cognitive decline.
- Cerebral microbleeds (CMB) are common in CSVD and associated with increased risk of stroke and dementia.
- Deep medullary vein (DMV) dysfunction has been implicated in CSVD pathogenesis, but its direct role in CMB development remains unclear.
Purpose of the Study:
- To investigate the association between deep medullary vein (DMV) dysfunction and cerebral microbleed (CMB) burden in patients with CSVD.
- To determine the role of extracellular fluid accumulation, specifically free water (FW) values, in mediating the relationship between DMV dysfunction and CMB.
Main Methods:
- A cross-sectional study of 176 patients with CSVD was conducted.
- Deep medullary vein (DMV) visibility was assessed using susceptibility-weighted imaging (SWI).
- Cerebral microbleeds (CMB) were quantified, and extracellular fluid volume was estimated using free water (FW) derived from diffusion tensor imaging.
Main Results:
- DMV scores showed moderate positive correlations with CMB burden (r=0.460) and FW values (r=0.549).
- Patients with extensive CMB had significantly higher DMV scores and FW values.
- Free water (FW) partially mediated the association between DMV scores and CMB burden (β=0.088, P<0.05), even after adjusting for covariates.
Conclusions:
- Deep medullary vein (DMV) dysfunction is associated with increased cerebral microbleed (CMB) burden in CSVD.
- Extracellular fluid accumulation partially mediates this relationship, highlighting the potential role of impaired venous drainage and interstitial fluid retention in CMB pathogenesis.
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