DSC perfusion-based collateral imaging and quantitative T2 mapping to assess regional recruitment of leptomeningeal collaterals and microstructural cortical tissue damage in unilateral steno-occlusive vasculopathy. Issue 1 (January 2021)

• Record Type: Journal Article
• Authors: Seiler, Alexander; Brandhofe, Annemarie; Gracien, René-Maxime; Pfeilschifter, Waltraud; Hattingen, Elke; Deichmann, Ralf; Nöth, Ulrike; Wagner, Marlies
• Is Part Of: Journal of cerebral blood flow & metabolism. Volume 41:Issue 1(2021)
• Page Start: 67
• Page End: 81
• Publication Date: 2021-01
• Subjects: Chronic cerebral hypoperfusion -- collaterals -- cortical microstructure -- quantitative magnetic resonance imaging -- perfusion-weighted imaging; Cerebral circulation -- Periodicals; Brain -- Metabolism -- Periodicals; Brain -- Blood-vessels -- Periodicals; Cerebrovascular disease -- Periodicals; 612.824
• DOI: 10.1177/0271678X19898148
• Languages: English
• ISSNs: 0271-678X

Abstract

Leptomeningeal collateral supply is considered pivotal in steno-occlusive vasculopathy to prevent chronic microstructural ischaemic tissue damage. The aim of this study was to assess the alleged protective role of leptomeningeal collaterals in patients with unilateral high-grade steno-occlusive vasculopathy using quantitative (q)T2 mapping and perfusion-weighted imaging (PWI)-based collateral abundance. High-resolution qT2 was used to estimate microstructural damage of the segmented normal-appearing cortex. Volumetric abundance of collaterals was assessed based on PWI source data. The ratio relative cerebral blood flow/relative cerebral blood volume (rCBF/rCBV) as a surrogate of relative cerebral perfusion pressure (rCPP) was used to investigate the intravascular hemodynamic competency of pial collateral vessels and the hemodynamic state of brain parenchyma. Within the dependent vascular territory with increased cortical qT2 values ( P = 0.0001) compared to the contralateral side, parenchymal rCPP was decreased ( P = 0.0001) and correlated negatively with increase of qT2 ( P < 0.05). Furthermore, volumetric abundance of adjacent leptomeningeal collaterals was significantly increased ( P < 0.01) and negatively correlated with changes of parenchymal rCPP ( P = 0.01). Microstructural cortical damage is closely related to restrictions of antegrade blood flow despite increased pial collateral vessel abundance. Therefore, increased leptomeningeal collateral supply cannot necessarily be regarded as a sign of effective compensation in patients with high-grade steno-occlusive vasculopathy.