Association between the Putative Meningeal Lymphatics at the Posterior Wall of the Sigmoid Sinus and Delayed Contrast-agent Elimination from the Cerebrospinal Fluid.

Abstract

Purpose: To investigate the characteristics of the putative meningeal lymphatics located at the posterior wall of the sigmoid sinus (PML-PSS) in human subjects imaged before and after intravenous administration (IV) of a gadolinium-based contrast agent (GBCA). The appearance of the PML-PSS and the enhancement of the perivascular space of the basal ganglia (PVS-BG) were analyzed for an association with gender, age, and clearance of the GBCA from the cerebrospinal fluid (CSF).

Methods: Forty-two patients with suspected endolymphatic hydrops were included. Heavily T2-weighted 3D-fluid attenuated inversion recovery (hT2w-3D-FLAIR) and 3D-real inversion recovery (IR) images were obtained at pre-administration, immediately post-administration, and at 4 and 24 hours after IV-GBCA. The appearance of the PML-PSS and the presence of enhancement in the PVS-BG were analyzed for a relationship with age, gender, contrast enhancement of the CSF at 4 hours after IV-GBCA, and the washout ratio of the GBCA in the CSF from 4 to 24 hours after IV-GBCA.

Results: The PML-PSS and PVS-BG were seen in 23 of 42 and 21 of 42 cases, respectively, at 4 hours after IV-GBCA. In all PML-PSS positive cases, hT2w-3D-FLAIR signal enhancement was highest at 4 hours after IV-GBCA. A multivariate analysis between gender, age, CSF signal elevation at 4 hours, and washout ratio indicated that only the washout ratio was independently associated with the enhancement of the PML-PSS or PVS-BG. The odds ratios (95% CIs; P value) were 4.09 × 10^-5 (2.39 × 10^-8 - 0.07; 0.0078) for the PML-PSS and 1.7 × 10^-4 (1.66 × 10^-7 - 0.174; 0.014) for the PVS-BG.

Conclusion: The PML-PSS had the highest signal enhancement at 4 hours after IV-GBCA. When the PML-PSS was seen, there was also often enhancement of the PVS-BG at 4 hours after IV-GBCA. Both observed enhancements were associated with delayed GBCA excretion from the CSF.