Combining magnetic resonance fingerprinting with voxel-based morphometric analysis to reduce false positives for focal cortical dysplasia detection.

OBJECTIVE: We aim to improve focal cortical dysplasia (FCD) detection by combining high-resolution, three-dimensional (3D) magnetic resonance fingerprinting (MRF) with voxel-based morphometric magnetic resonance imaging (MRI) analysis. METHODS: We included 37 patients with pharmacoresistant focal epilepsy and FCD (10 IIa, 15 IIb, 10 mild Malformation of Cortical Development [mMCD], and 2 mMCD with oligodendroglial hyperplasia and epilepsy [MOGHE]). Fifty-nine healthy controls (HCs) were also included. 3D lesion labels were manually created. Whole-brain MRF scans were obtained with 1 mm3 isotropic resolution, from which quantitative T1 and T2 maps were reconstructed. Voxel-based MRI postprocessing, implemented with the morphometric analysis program (MAP18), was performed for FCD detection using clinical T1w images, outputting clusters with voxel-wise lesion probabilities. Average MRF T1 and T2 were calculated in each cluster from MAP18 output for gray matter (GM) and white matter (WM) separately. Normalized MRF T1 and T2 were calculated by z-scores using HCs. Clusters that overlapped with the lesion labels were considered true positives (TPs); clusters with no overlap were considered false positives (FPs). Two-sample t-tests were performed to compare MRF measures between TP/FP clusters. A neural network model was trained using MRF values and cluster volume to distinguish TP/FP clusters. Ten-fold cross-validation was used to evaluate model performance at the cluster level. Leave-one-patient-out cross-validation was used to evaluate performance at the patient level. RESULTS: MRF metrics were significantly higher in TP than FP clusters, including GM T1, normalized WM T1, and normalized WM T2. The neural network model with normalized MRF measures and cluster volume as input achieved mean area under the curve (AUC) of .83, sensitivity of 82.1%, and specificity of 71.7%. This model showed superior performance over direct thresholding of MAP18 FCD probability map at both the cluster and patient levels, eliminating ≥75% FP clusters in 30% of patients and ≥50% of FP clusters in 91% of patients. SIGNIFICANCE: This pilot study suggests the efficacy of MRF for reducing FPs in FCD detection, due to its quantitative values reflecting in vivo pathological changes. © 2024 International League Against Epilepsy.

Possible post-COVID epilepsy: A review of epilepsy monitoring unit admissions during the two years of COVID-19 pandemic.

Large scale healthcare data shows that new-onset epilepsy is noted in 0.3 % patients within 6 months of COVID-19 infection. We analyzed diagnostic epilepsy monitoring unit (EMU) evaluations to identify and report such cases. We thoroughly reviewed our EMU database and identified patients having "COVID" or "Corona" virus mention in their medical record from 03/15/2020 to 02/28/2022. Patients with epilepsy prior to COVID infection were excluded. Among 62 patients without prior epilepsy evaluated in the EMU for new-onset spells after confirmed COVID-19 infection, three patients were diagnosed with focal epilepsy. These three women without epilepsy risk factors had seizure onset at the time of, or within one to three months of, COVID-19 diagnosis. Their 3 T MRI imaging was non-lesional but revealed bilateral enlarged perivascular spaces. The video EEG monitoring was consistent with temporal or fronto-temporal lobe epilepsy in all three patients. Two of them developed drug-resistant epilepsy within six months of seizure onset. Our thorough analysis of diagnostic EMU evaluations during the two years of pandemic reveals three cases of post-COVID-19 epilepsy after non-symptomatic to mild disease. Although coincidental epilepsy onset cannot be ruled out, larger multicenter or national database investigations are needed to further analyze the possibility of post-COVID epilepsy.

Digoxin therapy for heart failure: an update.

Digoxin therapy has long been used to treat heart failure; however, its effectiveness was not completely known until recently. Results of the Digitalis Investigation Group trial showed that adding digoxin to standard heart failure therapy had no effect on mortality. However, adding digoxin decreased hospitalizations related to heart failure and improved symptoms in patients treated for heart failure. Reanalyses of the trial's findings have raised new questions about the role of digoxin in heart failure treatment. These new analyses showed that low serum digoxin concentrations used in patients with more severe disease offered the most benefit. Digoxin use in women was associated with increased mortality risk. This finding should be interpreted with caution, however, because it was based on retrospective data, and the cause of this phenomenon has not been fully elucidated. Prospective clinical trials are needed to determine the serum digoxin concentration that is associated with the most clinical benefit and to determine the role of digoxin therapy for women. Digoxin generally does not have a role in the treatment of diastolic heart failure and is not a first-line therapy for managing atrial fibrillation in patients with heart failure.

The less familiar side of heart failure: symptomatic diastolic dysfunction.

Arrange for echocardiography or radionuclide angiography within 72 hours of a heart failure exacerbation. An ejection fraction >50% in the presence of signs and symptoms of heart failure makes the diagnosis of diastolic heart failure probable. To treat associated hypertension, use angiotensin receptor blockers (ARBs), angiotensin-converting enzyme (ACE) inhibitors, beta-blockers, calcium channel blockers, or diuretics to achieve a blood pressure goal of <130/80 mm Hg. When using beta-blockers to control heart rate, titrate doses more aggressively than would be done for systolic failure, to reach a goal of 60 to 70 bpm. Use ACE inhibitors/ARBs to decrease hospitalizations, decrease symptoms, and prevent left ventricular remodeling.

Ezetimibe for hypercholesterolemia.

Ezetimibe (Zetia) is a novel, selective cholesterol absorption inhibitor. Ezetimibe blocks the absorption of dietary and biliary cholesterol within the brush-border enzyme system of the small intestine. Ezetimibe does not appear to alter or decrease the absorption of bile acids, fatty acids, fat-soluble vitamins, or triglycerides. It is labeled for use in the treatment of primary hypercholesterolemia, either as monotherapy or in combination with statins. It also is labeled for the treatment of homozygous familial hypercholesterolemia in conjunction with statins and as adjunctive therapy to diet in the treatment of homozygous sitosterolemia (a rare, inherited, plant sterol storage disease).