Abstracts

Rationale: Lateralized periodic discharges (LPDs) are a common electrographic pattern seen on continuous EEG (cEEG) of patients with acute neurologic illness. The risks and benefits of treating LPDs, particularly when not correlated with clear-cut clinical symptoms, remain unclear. Previous studies have shown that LPDs can be associated with increased local metabolism potentially leading to metabolic failure [1,2]. Here, we examine the correlation between characteristics of LPDs and glucose metabolism imaged by FDG-PET. Methods: We retrospectively reviewed medical records at Massachusetts General Hospital between 2002-2014 to identify patients who underwent FDG-PET during cEEG monitoring and who also had LPDs on EEG during the FDG uptake period. Overall 9 subjects were found. Two board certified neurophysiologists, blinded to both clinical and radiographic data, independently read the EEGs and resolved discrepant interpretations by re-review until reaching consensus. FDG uptake was measured using standardized uptake value (SUV). Structural MRI (8 cases) and CT (1 case) were fused with PET images to aid in localization of SUV in the pons and cortex. Two PET readers (one blinded to all clinical data) independently measured the voxels with maximum SUV (SUVmax) in both pons and cortex. Only three measures had a difference in SUVmax > 0.1; these were resolved by mutual consensus. Relative SUV values were obtained by normalization to the SUVmax of the pons (SUVRpons) (FIGURE 1). The highest cortical SUVRpons ipsilateral to LPDs was used for further analysis. LPD frequency was analyzed both as a categorical variable (bins of 0.5Hz, 1Hz, and 1.5-2.5Hz, here abbreviated as 1Hz) using a permutation-based Kruskal-Wallis test, and as a continuous measure using linear correlation. Other variables assessed with permutation testing included duration, amplitude, presence of structural etiology for LPDs or of “plus” features such as rhythmic or fast sharp activity. Two-tailed testing was performed with an alpha level set at 0.05. Results: Of the 9 patients, 7 had an identifiable structural etiology for the LPDs - either ischemic or hemorrhagic stroke, or posterior reversible encephalopathy syndrome. The remaining two patients had focal epilepsy of unknown etiology and new-onset refractory status epilepticus. Analysis using frequency as a categorical variable showed an association between increased LPD frequency and increased ipsilateral SUVRpons(p=0.02) (FIGURE 2A). Continuous variable analysis also revealed a significant correlation between LPD frequency and SUVRpons (R2 = 0.61, p = 0.01) (FIGURE 2B).There were no statistically significant differences in SUVRpons for other factors including LPDs 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: Our results reveal an association between LPD frequency and increasing metabolic activity in ipsilateral cortex. LPD frequency should be a parameter of interest in future studies of neuroprotection in patients with critical neurological illness.References: 1. Struck, A. F., Westover, M. B., Hall, L. T., Cole, A. J., & Rosenthal, E. S. (2016). Metabolic Correlates of the Ictal-Interictal Continuum: FDG-PET During Continuous EEG. Neurocritical care (3):324-331.2. Witsch J, Frey H.P., Schmidt J.M., Velazquez A, Falo C.M., Reznik M, Roh D, Agarwal S, Park S, Connolly E.S., & Claassen J. (2017). Electroencephalographic Periodic Discharges and Frequency-Dependent Brain Tissue Hypoxia in Acute Brain Injury. JAMA Neurol. 74(3):301-309 Funding: None