MRI-visible perivascular spaces in basal ganglia but not centrum semiovale or hippocampus were related to deep medullary veins changes. Issue 1 (January 2022)

• Record Type: Journal Article
• Authors: Zhang, Kemeng; Zhou, Ying; Zhang, Wenhua; Li, Qingqing; Sun, Jianzhong; Lou, Min
• Is Part Of: Journal of cerebral blood flow & metabolism. Volume 42:Issue 1(2022)
• Page Start: 136
• Page End: 144
• Publication Date: 2022-01
• Subjects: MRI-visible perivascular spaces -- deep medullary veins -- basal ganglia -- centrum semiovale -- hippocampus -- susceptibility weighted imaging; Cerebral circulation -- Periodicals; Brain -- Metabolism -- Periodicals; Brain -- Blood-vessels -- Periodicals; Cerebrovascular disease -- Periodicals; 612.824
• DOI: 10.1177/0271678X211038138
• Languages: English
• ISSNs: 0271-678X

Abstract

Our purpose is to assess the role of deep medullary veins (DMVs) in pathogenesis of MRI-visible perivascular spaces (PVS) in patients with cerebral small vessel disease (cSVD). Consecutive patients recruited in the CIRCLE study (ClinicalTrials.gov ID: NCT03542734) were included. Susceptibility Weighted Imaging-Phase images were used to evaluate DMVs based on a brain region-based visual score. T2 weighted images were used to evaluate PVS based on the five-point score, and PVS in basal ganglia (BG-PVS), centrum semiovale (CSO-PVS) and hippocampus (H-PVS) were evaluated separately. 270 patients were included. The severity of BG-PVS, CSO-PVS and H-PVS was positively related to the increment of age (all p < 0.05). The severity of BG-PVS and H-PVS was positively related to DMVs score (both p < 0.05). Patients with more severe BG-PVS had higher Fazekas scores in both periventricle and deep white matter (both p < 0.001) and higher frequency of hypertension ( p = 0.008). Patients with more severe H-PVS had higher frequency of diabetes ( p < 0.001). Besides, high DMVs score was an independent risk factor for more severe BG-PVS ( β = 0.204, p = 0.001). Our results suggested that DMVs disruption might be involved in the pathogenesis of BG-PVS.