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Abstract Due to extensive connectivity of the parietal lobe, non‐lesional drug‐resistant (DRE) parietal lobe epilepsies (PLEs) are difficult to localize and often imitate other epilepsies. Therefore, patients with PLEs have low rates of seizure freedom following epilepsy surgery. Previous studies have highlighted the need to combine EEG and semiology for more accurate localization of PLEs. As sophisticated tools for localization become more available, the use of multiple different neuroimaging and neurophysiologic diagnostic tests may more readily identify PLE. We hereby report a unique case of a complex localization in a non‐lesional PLE, which was initially falsely localized to frontal lobe. This case underscores the utility of voxel‐based morphometry (VBM) in identifying an epileptogenic lesion on a non‐lesional MRI and the significance of multimodality approach including PET, magnetoencephalopathy (MEG), interictal and ictal EEG, semiology and cortical stimulation for accurate localization of PLEs. Understanding epilepsy through multimodality approach in this fashion can help with accurate localization especially in difficulty to localize and deceptive non‐lesional PLEs. Plain Language Summary Parietal lobe epilepsies are hard to pinpoint in the brain and can mimic other types of epilepsy, especially when brain MRIs appear normal. As sophisticated tools for locating epilepsies in the brain become more available, using multiple diagnostic tests may help identify parietal lobe epilepsies more easily. We describe a unique case of a parietal lobe epilepsy patient with normal brain MRI whose epilepsy was initially misidentified as being in the frontal lobe. Using various advanced diagnostic tests, we accurately found the epilepsy's true location in the parietal lobe and successfully treated the patient with surgery.

Abstract Background and Aim Previous studies conducted at single centers have suggested that patients with cirrhosis are at a greater risk for worse outcomes with COVID‐19. However, there is limited data on a national level in the United States. We aimed to study hospital‐related outcomes and identify the predictors of poor outcomes in patients with cirrhosis and concurrent COVID‐19. Methods We queried 2020 National Inpatient and Readmission databases to identify all hospitalizations due to cirrhosis in adults with a diagnosis of COVID‐19. Primary outcomes included inpatient mortality, mechanical ventilation (MV), and intensive care unit (ICU) utilization. Secondary outcomes included mean length of stay (LOS) and mean hospitalization costs. We classified cirrhosis into compensated (CC) and decompensated (DC) groups. Results We identified 25194 hospitalizations of adult patients due to cirrhosis with a concurrent diagnosis of COVID‐19. These patients had higher mortality (19.50% vs 6.19%, P ≤ 0.01), MV (11.7% vs 2.8%, P ≤ 0.01), ICU utilization (17.3% vs 8.1%, P ≤ 0.01), LOS (8.89 days vs 6.16 days, P ≤ 0.01), and total hospitalization costs ($24 817 vs $18 505, P ≤ 0.01) than those without COVID‐19. On subgroup analysis, patients in the DC group had higher mortality, LOS, and hospitalization costs compared to those in the CC group. On multivariate analysis, we also found that COVID‐19 infection, age, Charlson Comorbidity Index ≥3, acute kidney injury, end‐stage renal disease, septic shock, acute respiratory failure, MV, and ICU status were independent predictors for mortality. Conclusion Our study suggests that COVID‐19 infection is an independent predictor of mortality in patients with cirrhosis, with threefold higher mortality and increased resource utilization. Early intervention through immunizations and advanced COVID‐19 therapies can help improve these outcomes.

Background Preeclampsia is a prominent risk factor for long‐term development of cardiovascular disease. Although existing studies report a strong correlation between preeclampsia and heart failure, the underlying mechanisms are poorly understood. One possibility is the glycoprotein growth factor activin A. During pregnancy, elevated activin A levels are associated with impaired cardiac global longitudinal strain at 1 year, but whether these changes persist beyond 1 year is not known. We hypothesized that activin A levels would remain increased more than 1 year after a preeclamptic pregnancy and correlate with impaired cardiac function. Methods and Results To test our hypothesis, we performed echocardiograms and measured activin A levels in women approximately 10 years after an uncomplicated pregnancy (n=25) or a pregnancy complicated by preeclampsia (n=21). Compared with women with a previously normal pregnancy, women with preeclampsia had worse global longitudinal strain (−18.3% versus −21.3%, P=0.001), left ventricular posterior wall thickness (0.91 mm versus 0.80 mm, P=0.003), and interventricular septal thickness (0.96 mm versus 0.81 mm, P=0.0002). Women with preeclampsia also had higher levels of activin A (0.52 versus 0.37 ng/mL, P=0.02) and activin/follistatin‐like 3 ratio (0.03 versus 0.02, P=0.04). In a multivariable model, the relationship between activin A levels and worsening global longitudinal strain persisted after adjusting for age at enrollment, mean arterial pressure, race, and body mass index (P=0.003). Conclusions Our findings suggest that both activin A levels and global longitudinal strain are elevated 10 years after a pregnancy complicated by preeclampsia. Future studies are needed to better understand the relationship between preeclampsia, activin A, and long‐term cardiac function.

Background Approximately 60% of women have Stage B heart failure 1 year after a preeclamptic delivery. Emerging evidence suggests that the profibrotic growth factor activin A, which has been shown to induce cardiac fibrosis and hypertrophy, is elevated in preeclampsia and may be inhibited by aspirin therapy. We hypothesized that preeclamptic women receiving aspirin would have lower activin A levels and reduced global longitudinal strain (GLS), a sensitive measure of cardiac dysfunction, than women who do not receive aspirin. To test our hypothesis, we performed a cohort study of women with preeclampsia or superimposed preeclampsia and compared activin A levels and GLS in parturients who did or did not receive aspirin. Methods and Results Ninety‐two parturients were enrolled, of whom 25 (27%) received aspirin (81 mg/day) therapy. GLS, plasma activin A, and follistatin, which inactivates activin A, were measured. Women receiving aspirin therapy had lower median (interquartile range) levels of activin A (8.17 [3.70, 10.36] versus 12.77 [8.37, 31.25] ng/mL; P=0.001) and lower activin/follistatin ratio (0.59 [0.31, 0.93] versus 1.01 [0.64, 2.60] P=0.002) than women who did not receive aspirin, which also remained significant after multivariable analysis. Furthermore, GLS was worse in patients who did not receive aspirin (−19.84±2.50 versus −17.77±2.60%; P=0.03) despite no differences in blood pressure between groups. Conclusions Our study suggests that antepartum aspirin therapy reduced serum activin A levels and improved GLS in preeclamptic patients, suggesting that aspirin may mitigate the postpartum cardiac dysfunction seen in women with preeclampsia.