Background and Purpose
Hyperintense FLAIR signal in the cerebral sulci (SSI) of anesthetized children is attributed to supplemental oxygen (FiO2), but resembles FLAIR hypersignal associated with perfusion abnormalities in Moyamoya and carotid stenosis. We investigated whether cerebral perfusion, known to be altered by anesthesia, contributes to diffuse SSI in children, and explored the relative contributions of supplemental oxygen, cerebral perfusion and anesthesia to SSI.
Methods
Supraventricular SSI on pre- and post-contrast T2-FLAIR images of 24 propofol-sedated (6.20 ± 3.28 years) breathing supplemental oxygen and 18 non-sedated (14.28 ±2.08 years) children breathing room air was graded from 0 to 3. Spearman correlation of SSI with FiO2 and age in 42 subjects, and with DSC measures of cortical CBF, CBV and MTT available in 25 subjects, were evaluated overall and compared between subgroups. Factors most influential on SSI were identified by stepwise logistic regression.
Results
CBV was more influential on non-contrast FLAIR SSI than FiO2 or age in propofol-sedated children (CBV: r=0.612, p=0.026; FiO2: r=−0.418, p=0.042; Age: r=0.523, p=0.009) and overall (CBV: r=0.671, p=0.0002; FiO2: r=0.442, p=0.003; Age: r=−0.374, p=0.015); MTT (CBV/CBF) was influential in the overall cohort (r=0.461, p=0.020). SSI increased with contrast in 45% of subjects, decreased in none, and was greater (p<0.0001) in younger propofol-sedated subjects, in whom SSI increased with age post-contrast (r=0.600, p=0.002).
Conclusion
Elevated cortical CBV appears to contribute to increased SSI on non-contrast FLAIR in propofol-sedated children. Effects of propofol on age-related cerebral perfusion and vascular permeability may play a role.