Transient focal increase in perihematomal glucose metabolism after acute human intracerebral hemorrhage.

Journal Article (Journal Article)

BACKGROUND AND PURPOSE: Progressive perihematomal cell death over 3 to 4 days has been described after experimental intracerebral hemorrhage (ICH). We investigated whether progressive perihematomal damage occurs in human subjects by measuring relative changes in regional cerebral glucose metabolism with (18)F-fluorordeoxyglucose (FDG) positron emission tomography at multiple time points during the first week after ICH. METHODS: Thirteen subjects with a median hematoma volume of 22 cm(3) were studied 1.0+/-0.3, 2.9+/-0.8, and 6.7+/-1.6 days after ICH. Normalized mean counts in 5 concentric annular 2-mm-thick perihematomal volumes-of-interest (VOIs) were compared to the initial study. Next, automated searches with 0.5 to 5.0 mL spherical VOIs identified maximum focal changes in normalized counts compared to the initial study. RESULTS: No annular or focal decrease in perihematomal FDG uptake developed. Instead, FDG uptake significantly increased at session #2 in the first 3 2-mm annular VOIs (9.2%+/-14.2, 7.8%+/-11.3, 5.9%+/-9.0), returning to baseline at session #3. The VOI search identified focal regions of increased perihematomal FDG uptake relative to the contralateral control hemispheres in 6 subjects, which accounted for the annular increase. CONCLUSIONS: Perihematomal glucose metabolism increased transiently in a subset of patients 2 to 4 days after acute ICH. These transient focal increases in glucose metabolism occurring in the brain after acute ICH demonstrate that there are ongoing processes in response to injury that last for days. Although further studies are needed to elucidate their pathophysiology, these processes may be indicative of a prolonged window for intervention to improve neurological outcome.

Full Text

Duke Authors

Cited Authors

  • Zazulia, AR; Videen, TO; Powers, WJ

Published Date

  • May 2009

Published In

Volume / Issue

  • 40 / 5

Start / End Page

  • 1638 - 1643

PubMed ID

  • 19286594

Electronic International Standard Serial Number (EISSN)

  • 1524-4628

Digital Object Identifier (DOI)

  • 10.1161/STROKEAHA.108.536037


  • eng

Conference Location

  • United States