TY - JOUR
T1 - The etiology and evolution of magnetic resonance imaging-visible perivascular spaces
T2 - Systematic review and meta-analysis
AU - Okar, Serhat V.
AU - Hu, Fengling
AU - Shinohara, Russell T.
AU - Beck, Erin S.
AU - Reich, Daniel S.
AU - Ineichen, Benjamin V.
N1 - Funding Information:
BI was supported by the UZH FAN Alumni and the Swiss National Science Foundation (SNSF, 407940_206504 and P400PM_183884). EB was supported by a Career Transition Award from the National Multiple Sclerosis Society. RS was partially funded by R01NS112274. This study was partially supported by the Intramural Research Program of NINDS and NIH.
Funding Information:
We thank Mirkka Hiort from the University of Münster, Germany for designing . We thank the UZH FAN Alumni, the Swiss National Science Foundation (SNSF), and the Intramural Research Program of National Institute of Neurological Disorders and Stroke for the financial support. We also thank Igor Iglesias and Arcadi Volodos for their help in data analysis.
Publisher Copyright:
Copyright © 2023 Okar, Hu, Shinohara, Beck, Reich and Ineichen.
PY - 2023
Y1 - 2023
N2 - Objectives: Perivascular spaces have been involved in neuroinflammatory and neurodegenerative diseases. Upon a certain size, these spaces can become visible on magnetic resonance imaging (MRI), referred to as enlarged perivascular spaces (EPVS) or MRI-visible perivascular spaces (MVPVS). However, the lack of systematic evidence on etiology and temporal dynamics of MVPVS hampers their diagnostic utility as MRI biomarker. Thus, the goal of this systematic review was to summarize potential etiologies and evolution of MVPVS. Methods: In a comprehensive literature search, out of 1,488 unique publications, 140 records assessing etiopathogenesis and dynamics of MVPVS were eligible for a qualitative summary. 6 records were included in a meta-analysis to assess the association between MVPVS and brain atrophy. Results: Four overarching and partly overlapping etiologies of MVPVS have been proposed: (1) Impairment of interstitial fluid circulation, (2) Spiral elongation of arteries, (3) Brain atrophy and/or perivascular myelin loss, and (4) Immune cell accumulation in the perivascular space. The meta-analysis in patients with neuroinflammatory diseases did not support an association between MVPVS and brain volume measures [R: −0.15 (95%-CI −0.40–0.11)]. Based on few and mostly small studies in tumefactive MVPVS and in vascular and neuroinflammatory diseases, temporal evolution of MVPVS is slow. Conclusion: Collectively, this study provides high-grade evidence for MVPVS etiopathogenesis and temporal dynamics. Although several potential etiologies for MVPVS emergence have been proposed, they are only partially supported by data. Advanced MRI methods should be employed to further dissect etiopathogenesis and evolution of MVPVS. This can benefit their implementation as an imaging biomarker. Systematic review registration: https://www.crd.york.ac.uk/prospero/display_record.php?RecordID=346564, identifier CRD42022346564.
AB - Objectives: Perivascular spaces have been involved in neuroinflammatory and neurodegenerative diseases. Upon a certain size, these spaces can become visible on magnetic resonance imaging (MRI), referred to as enlarged perivascular spaces (EPVS) or MRI-visible perivascular spaces (MVPVS). However, the lack of systematic evidence on etiology and temporal dynamics of MVPVS hampers their diagnostic utility as MRI biomarker. Thus, the goal of this systematic review was to summarize potential etiologies and evolution of MVPVS. Methods: In a comprehensive literature search, out of 1,488 unique publications, 140 records assessing etiopathogenesis and dynamics of MVPVS were eligible for a qualitative summary. 6 records were included in a meta-analysis to assess the association between MVPVS and brain atrophy. Results: Four overarching and partly overlapping etiologies of MVPVS have been proposed: (1) Impairment of interstitial fluid circulation, (2) Spiral elongation of arteries, (3) Brain atrophy and/or perivascular myelin loss, and (4) Immune cell accumulation in the perivascular space. The meta-analysis in patients with neuroinflammatory diseases did not support an association between MVPVS and brain volume measures [R: −0.15 (95%-CI −0.40–0.11)]. Based on few and mostly small studies in tumefactive MVPVS and in vascular and neuroinflammatory diseases, temporal evolution of MVPVS is slow. Conclusion: Collectively, this study provides high-grade evidence for MVPVS etiopathogenesis and temporal dynamics. Although several potential etiologies for MVPVS emergence have been proposed, they are only partially supported by data. Advanced MRI methods should be employed to further dissect etiopathogenesis and evolution of MVPVS. This can benefit their implementation as an imaging biomarker. Systematic review registration: https://www.crd.york.ac.uk/prospero/display_record.php?RecordID=346564, identifier CRD42022346564.
KW - Virchow-Robin spaces
KW - biomarker
KW - enlarged perivascular spaces
KW - etiology
KW - etiopathogenesis
KW - magnetic resonance imaging
KW - meta-analysis
KW - systematic review
UR - http://www.scopus.com/inward/record.url?scp=85153356631&partnerID=8YFLogxK
U2 - 10.3389/fnins.2023.1038011
DO - 10.3389/fnins.2023.1038011
M3 - Review article
AN - SCOPUS:85153356631
SN - 1662-4548
VL - 17
JO - Frontiers in Neuroscience
JF - Frontiers in Neuroscience
M1 - 1038011
ER -