Abstract
The mechanisms behind molecular transport from cerebrospinal fluid to dural lymphatic vessels remain unknown. This study utilized magnetic resonance imaging along with cerebrospinal fluid tracer to visualize clearance pathways to human dural lymphatics in vivo. In 18 subjects with suspicion of various types of cerebrospinal fluid disorders, 3D T2-Fluid Attenuated Inversion Recovery, T1-black-blood, and T1 gradient echo acquisitions were obtained prior to intrathecal administration of the contrast agent gadobutrol (0.5 ml, 1 mmol/ml), serving as a cerebrospinal fluid tracer. Propagation of tracer was followed with T1 sequences at 3, 6, 24 and 48 h after the injection. The tracer escaped from cerebrospinal fluid into parasagittal dura along the superior sagittal sinus at areas nearby entry of cortical cerebral veins. The findings demonstrate that trans-arachnoid molecular passage does occur and suggest that parasagittal dura may serve as a bridging link between human brain and dural lymphatic vessels.
Highlights
The mechanisms behind molecular transport from cerebrospinal fluid to dural lymphatic vessels remain unknown
Lymphatic cerebrospinal fluid (CSF) drainage, and the interplay between the lymphatic- and central nervous system (CNS), gained renewed interest when true lymphatic vessels were shown to reside within the dura mater[3,4]
This study demonstrates for the first time direct efflux of a CSF
Summary
The mechanisms behind molecular transport from cerebrospinal fluid to dural lymphatic vessels remain unknown. The findings demonstrate that trans-arachnoid molecular passage does occur and suggest that parasagittal dura may serve as a bridging link between human brain and dural lymphatic vessels. Lymphatic CSF drainage, and the interplay between the lymphatic- and central nervous system (CNS), gained renewed interest when true lymphatic vessels were shown to reside within the dura mater[3,4]. Impairment of these meningeal lymphatic pathways has been shown to slow paravascular efflux of amyloid-β from interstitial brain fluid and may possibly represent an aggravating factor in Alzheimer’s disease and age-associated cognitive decline[5]. Our aim was to explore how these diverging findings of CSF tracer efflux from animal studies translate into a human cohort
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