Thanujaa Subramaniam1, Aditya Jain1, Lance T Hall1, Andrew J Cole1, M Brandon Westover1, Eric S Rosenthal1, Aaron F Struck2. 1. From the Departments of Neurology (T.S., A.F.S.) and Radiology (A.J., L.T.H.), University of Wisconsin-Madison; and Department of Neurology (A.J.C., M.B.W., E.R.), Massachusetts General Hospital, Harvard Medical School, Boston. 2. From the Departments of Neurology (T.S., A.F.S.) and Radiology (A.J., L.T.H.), University of Wisconsin-Madison; and Department of Neurology (A.J.C., M.B.W., E.R.), Massachusetts General Hospital, Harvard Medical School, Boston. afstruck@wisc.edu.
Abstract
OBJECTIVE: To investigate the correlation between characteristics of lateralized periodic discharges (LPDs) and glucose metabolism measured by 18F-fluorodeoxyglucose (FDG)-PET. METHODS: We retrospectively reviewed medical records to identify patients who underwent FDG-PET during EEG monitoring with LPDs present during the FDG uptake period. Two blinded board-certified neurophysiologists independently interpreted EEGs. FDG uptake was measured using standardized uptake value (SUV). Structural images were fused with PET images to aid with localization of SUV. Two PET readers independently measured maximum SUV. Relative SUV values were obtained by normalization of the maximum SUV to the SUV of pons (SUVRpons). LPD frequency was analyzed both as a categorical variable and as a continuous measure. Other secondary variables included duration, amplitude, presence of structural lesion, and "plus" EEG features such as rhythmic or fast sharp activity. RESULTS: Nine patients were identified and 7 had a structural etiology for LPDs. Analysis using frequency as a categorical variable and continuous variable showed an association between increased LPD frequency and increased ipsilateral SUVRpons (p = 0.02). Metabolism associated with LPDs (0.5 Hz as a baseline) increased by a median of 100% at 1 Hz and for frequencies >1 Hz increased by a median of 309%. There were no statistically significant differences in SUVRpons for other factors including duration (p = 0.10), amplitude (p = 0.80), structural etiology (p = 0.55), or "plus" features such as rhythmic or fast sharp activity (p = 0.84). CONCLUSIONS: Metabolic activity increases monotonically with LPD frequency. LPD frequency should be a measure of interest when developing neuroprotection strategies in critical neurologic illness.
OBJECTIVE: To investigate the correlation between characteristics of lateralized periodic discharges (LPDs) and glucose metabolism measured by 18F-fluorodeoxyglucose (FDG)-PET. METHODS: We retrospectively reviewed medical records to identify patients who underwent FDG-PET during EEG monitoring with LPDs present during the FDG uptake period. Two blinded board-certified neurophysiologists independently interpreted EEGs. FDG uptake was measured using standardized uptake value (SUV). Structural images were fused with PET images to aid with localization of SUV. Two PET readers independently measured maximum SUV. Relative SUV values were obtained by normalization of the maximum SUV to the SUV of pons (SUVRpons). LPD frequency was analyzed both as a categorical variable and as a continuous measure. Other secondary variables included duration, amplitude, presence of structural lesion, and "plus" EEG features such as rhythmic or fast sharp activity. RESULTS: Nine patients were identified and 7 had a structural etiology for LPDs. Analysis using frequency as a categorical variable and continuous variable showed an association between increased LPD frequency and increased ipsilateral SUVRpons (p = 0.02). Metabolism associated with LPDs (0.5 Hz as a baseline) increased by a median of 100% at 1 Hz and for frequencies >1 Hz increased by a median of 309%. There were no statistically significant differences in SUVRpons for other factors including duration (p = 0.10), amplitude (p = 0.80), structural etiology (p = 0.55), or "plus" features such as rhythmic or fast sharp activity (p = 0.84). CONCLUSIONS: Metabolic activity increases monotonically with LPD frequency. LPD frequency should be a measure of interest when developing neuroprotection strategies in critical neurologic illness.
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