Alteration of brain metabolism in lacunar stroke based on 18F-FDG-PET/MRI analysis

TL;DR

This study finds that lacunar stroke causes changes in brain metabolism and network connectivity, suggesting broader brain dysfunction beyond the stroke site.

Contribution

The study reveals novel metabolic and network-level brain alterations in lacunar stroke patients using 18F-FDG-PET/MRI.

Findings

LS patients showed higher glucose uptake in the right postcentral gyrus compared to healthy controls.

LS patients had lower metabolic connectivity between the right postcentral gyrus and several brain regions.

LS patients exhibited altered network properties, including higher clustering coefficient and global efficiency.

Abstract

Lacunar stroke (LS) is caused by occlusion of the penetrating branches of the major cerebral arteries and includes small and deep infarcts. Our study aimed to explore brain metabolic alterations in LS.

Seventy individuals with LS (aged 53.89 ± 1.198 years, 52 males) and 70 healthy controls (HCs; aged 50.34 ± 0.737 years, 42 males) underwent brain 18F-fluorodeoxyglucose positron emission tomography/magnetic resonance imaging. Glucose uptake, metabolic connectivity, and metabolic networks at the group level were analyzed.

Compared with HCs, LS patients exhibited a higher standardized uptake value in the right postcentral gyrus (p < 0.001) and lower metabolic connectivity between the right postcentral gyrus and the right caudate nucleus, left amygdala, left hippocampus, and left supramarginal gyrus (p < 0.001). In the analysis of network properties, compared with HCs, LS patients demonstrated higher clustering coefficient (p < 0.001), global efficiency (p < 0.001), local efficiency (p < 0.001), gamma (p = 0.024), and lambda (p = 0.016), as well as a shorter path length (p < 0.001). Additionally, we observed a higher degree in the right superior temporal gyrus (p = 0.002), greater efficiency in the middle part of the right superior frontal gyrus (p = 0.004), and a lower degree in the left insula (p = 0.002).

Our study identified that LS is not merely localized brain damage; it also involves broader dysfunction across brain networks, thereby affecting advanced cognitive functions. The observed compensatory increase in global network efficiency in LS patients might serve to maintain cerebral glucose metabolism. These findings may indicate new target areas for future treatments.

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