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

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.