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Case report reveals intense FDG activity in the brain from cerebral hypoperfusion, suggesting compensatory mechanisms.
We describe FDG PET/CT and PET/MRI findings in a case with severe stenosis of the left posterior cerebral artery and impaired perfusion of the left posterior cerebral artery territory as evidenced by CT angiography and CT perfusion. FDG PET/CT and PET/MRI showed a wedge-shaped intense activity in the left posterior cerebral artery territory with mild parenchymal atrophy and no infarction. The intense FDG activity in the left posterior cerebral artery territory may be caused by activation of glucose transporters and elevated glycolytic activity as compensation for hypoperfusion resulting from the stenosis of the left posterior cerebral artery.
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Liu et al. (2026) studied this question.
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