IntroductionFluorine-18-fluorodeoxyglucose positron-emission tomography (18F-FDG-PET) is widely used to help localize the hypometabolic epileptogenic focus for presurgical evaluation of drug-refractory epilepsy patients. Two voxel-based brain mapping methods to interpret 18F-FDG-PET, statistical parametric mapping (SPM) and three-dimensional stereotactic surface projection (3D-SSP), improve the detection rate of seizure foci. This study aimed to compare the consistency of epileptic focus detection between SPM and 3D-SSP for 18F-FDG-PET brain mapping analysis.MethodsWe retrospectively reviewed the clinical, electroecephalographic, and brain imaging results of 35 patients with refractory epilepsy. 18F-FDG-PET studies were revaluated by SPM, 3D-SSP, and visual assessment, and the results were compared to the magnetic resonance imaging (MRI) lesion location and to the presumed epileptogenic zone (PEZ) defined by video-electroencephalogram and other clinical data. A second consistency study compared PET analyses to histopathology and surgical outcomes in the 19 patients who underwent lesion resection surgery.ResultsOf the 35 patients, consistency with the PEZ was 29/35 for SPM, 25/35 for 3D-SSP, 14/35 for visual assessment, and 10/35 for MRI. Concordance rates with the PEZ were significantly higher for SPM and 3D-SSP than for MRI (P < 0.05) and visual assessment (P < 0.05). Differences between SPM and 3D-SSP and between visual assessment and MRI were not significant. In the 19 surgical patients, concordance with histopathology/clinical outcome was 14/19 for SPM, 15/19 for 3D-SSP, 14/19 for visual assessment, and 9/19 for MRI (P > 0.05). A favorable Engel outcome (class I/II) was found in 16 of 19 cases (84%), and failure of seizure control was found in 3 of 19 patients (class III/IV).ConclusionVoxel-based 18F-FDG-PET brain mapping analysis using SPM or 3D-SSP can improve the detection rate of the epileptic focus compared to visual assessment and MRI. Consistency with PEZ was similar between SPM and 3D-SSP; according to their own characteristics, 3D-SSP is recommended for primary evaluation due to greater efficiency and operability of the software, while SPM is recommended for high-accuracy localization of complex lesions. Therefore, joint application of both software packages may be the best solution for FDG-PET analysis of epileptic focus localization.
Summary
Objective
We aimed to study the networks’ mechanism of metabolic covariance networks in mesial temporal lobe epilepsy (mTLE), through examining the brain value of fluorine‐18‐fluorodeoxyglucose positron emission tomography (18F‐FDG‐PET).
Methods
18F‐FDG‐PET images from 16 patients with mTLE were analyzed using local and global metabolic covariance network (MCN) approaches, including whole metabolic pattern analysis (WMPA), hippocampus‐based (h‐) MCN, whole brain (w‐) MCN, and edge‐based connectivity analysis (EBCA).
Results
WMPA showed a typical ipsilateral hypometabolism and contralateral hypermetabolism pattern to epileptic zones in mTLE. h‐MCN revealed decreased hippocampus‐based synchronization in contralateral regions. w‐MCN exhibited a disrupted metabolic network with globally increased small‐world properties and regionally decreased nodal metrics in the ipsilateral hemisphere. Hippocampus (h)‐EBCA and whole brain EBCA (w‐EBCA) both detected a reduced‐connectivity dominated metabolic covariant network. Moreover, the reduced interhemisphere connectivity seemingly played a major role in the aberrant epileptic topological pattern.
Conclusion
From a metabolic point of view, we demonstrated the damaging effects with reduced contralateral intranetwork metrics properties and the compensatory effects in contralateral intranetworks with increased network properties. However, the import role of significant reduced interhemisphere connection has rarely been reported in other mTLE studies. Taken together, 18F‐FDG‐PET MCN analysis provides new evidence that the mTLE is a system neurological disorder with disrupted networks.
Rationale:
Dabigatran is a direct thrombin inhibitor that is widely used to prevent the formation of thrombus formation. Amiodarone can increase the plasma concentration of dabigatran.
CES1
(carboxylesterase 1) and
ABCB1
(ATP-binding cassette subfamily B member 1) genetic polymorphisms associate with the pharmacokinetics of dabigatran.
Patient concerns:
A 62-year-old woman was admitted to the hospital due to chest tightness, fatigue, and discomfort despite long-term anticoagulation with dabigatran 110 mg twice daily for 6 months, with concomitant use of amiodarone.
Diagnoses:
Left atrial appendage thrombus formation with a history of atrial fibrillation.
Interventions:
The clinician changed dabigatran to warfarin. To explore the causes of insufficient anticoagulation using dabigatran in this patient, we examined the
ABCB1
and
CES1
genes. Results showed that she carried
ABCB1
variant alleles with 3 heterozygote single nucleotide polymorphisms (SNPs: rs4148738, rs1045642, rs2032582) and
CES1
variant alleles with 2 heterozygote SNPs (rs2244613, rs4580160).
Outcomes:
The left atrial appendage thrombus disappeared.
Lessons:
Multiple mutations in the
ABCB1
and
CES1
genes may influence the pharmacokinetics of dabigatran and could have contributed to the thrombus formation in the left atrial appendage.
The cytochrome P450 2C9 and vitamin K epoxide reductase complex subunit 1 genotypes are associated with anticoagulation control and the clinical events in warfarin therapy. However, the clinical utility of gene-based warfarin dosing (GBWD) is controversial. We compared the anticoagulation control and clinical events related to warfarin with GBWD to those with clinically fixed dosing (CFD). A retrospective cohort study was conducted in a real-world setting. Of the 915 patients who were reviewed, 844 patients met the study-entry criteria; 413 cases were guided by GBWD using the International Warfarin Pharmacogenetic Consortium algorithm; 431 cases were guided by CFD (2.5 mg/day). The primary outcomes were the time needed to achieve the therapeutic International Normalized Ratio (INR) and the time in the therapeutic range (TTR) during a 3-month timeframe. The time needed to achieve the therapeutic INR (in days) for patients in the GBWD group was shorter than that for patients in the CFD group (10.21 ± 4.68 vs. 14.31 ± 8.26, P < 0.001). The overall TTR (Day 4-90) was significantly different between the GBWD group and CFD group (56.86 ± 10.72 vs. 52.87 ± 13.92, P = 0.007).In subgroup analysis, the TTR was also significantly different between the GBWD group and CFD group during the first month of treatment (Day 4-14: 54.28 ± 21.90 vs. 47.01 ± 26.25, P = 0.012; Day 15-28: 59.60 ± 20.12 vs. 51.71 ± 18.96, P = 0.001). However, no significant difference in the TTR was observed after 29 days of treatment. These data suggest that GBWD provided clinical benefits.
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