To investigate the temporal and spatial patterns of structural brain injury related to deep medullary veins (DMVs) damage.

Due to the reported involvement of perivenous glymphatic drainage in neurodegenerative diseases, pathological changes of cerebral venules have attracted considerable interest, whereas direct evidence from human studies is scarce with inconsistent results. Research is in need to reveal the rich patterns of brain structural alternations related to DMVs’ disruption.

This is a longitudinal analysis in the population-based Shunyi cohort study. Baseline DMVs numbers were identified on susceptibility-weighted imaging. We assessed vertex-wise cortex maps and diffusion maps at both baseline and follow-up using FSL software and the longitudinal FreeSurfer analysis suite. We performed statistical analysis of global measurements and voxel/vertex-wise analysis, to explore the relationship between DMVs number and brain structural measurements.

A total of 977 participants were included in the baseline, of whom 544 completed the MRI follow-up (age 56.77 ± 9.20 years, 34.7% male, mean interval 5.56±0.47 years). A lower DMVs number was associated with a faster disruption of white matter microstructural integrity, presented by increasing mean diffusivity and radial diffusion (β=0.0001 and SE=0.0001 for both, p=0.04 and 0.03, respectively), in extensive deep white matter (TFCE p < 0.05, adjusted for age and sex). Of particular interest, we found a U shape trend association between DMVs number and change in brain volumes. Specifically, participants with mild DMV disruption showed greater cortical enlargement, while those with severe disruption exhibited more significant brain atrophy, primarily involving clusters in the frontal and parietal lobes (multiple comparison corrected p <0.05, adjusted for age, sex, and total intracranial volume).

Our findings posed the complex patten of brain parenchymal lesions related to DMVs injury and shed light on the interactions and chronological roles of various pathological mechanisms.