Background
Accumulating data have suggested seizures occur frequently in patients with neuronal surface antibody‐mediated autoimmune encephalitis. We aimed to evaluate seizure outcomes and potential factors associated with the development of epilepsy in patients with anti‐N‐methyl‐D‐aspartate receptor (NMDAR), anti‐leucine‐rich glioma‐inactivated 1 (LGI1), and anti‐gamma‐aminobutyric‐acid B receptor (GABABR) encephalitis.
Methods
Patients with anti‐NMDAR, anti‐LGI1, and anti‐GABABR encephalitis were prospectively recruited from 2014 to June 2019, with a median follow‐up period of 30.5 months (range 8–67 months). Seizure outcomes were assessed and risk factors of epilepsy were analyzed.
Results
A total of 119 patients with anti‐NMDAR, anti‐LGI1, and anti‐GABABR encephalitis were included, and 83 (69.7%) of them developed new‐onset seizures. By the end of follow‐up, 17 (21.3%) of 80 patients had seizure relapses after intermittent seizure remission or exhibited uncontrolled seizure episodes, contributing to epilepsy. Immunotherapy delay and interictal epileptic discharges (IEDs) were identified to be associated with the development of epilepsy in patients with anti‐NMDAR, anti‐LGI1, and anti‐GABABR encephalitis, particularly anti‐NMDAR encephalitis. Furthermore, multivariate logistic regression analysis demonstrated that immunotherapy delay was an independent predictor for epilepsy.
Conclusion
Our study suggested that immunotherapy delay and IEDs were associated with the development of epilepsy in patients with anti‐NMDAR, anti‐LGI1, and anti‐GABABR encephalitis. Early diagnosis and treatment were required, and particular consideration should be given to patients with these risk factors.
Parkinson's disease (PD) is a common neurodegenerative movement disorder associated with substantial morbidity and mortality 1 , and the number of persons affected is expected to increase dramatically in coming years 2 . Although the exact cause of the selective dopaminergic cell death that underlies PD is still unknown, oxidative stress is regarded as a potential mechanism in the pathogenesis 3 and evidence of oxidative damage, such as DNA and protein damage and lipid peroxidation, has been found at autopsy of PD brains 4,5 . Urate is thought to be a potent antioxidant that effectively scavenges oxygen radicals and reactive nitrogen 6 , and its potential protective effects on PD have been reported in prior studies. Some studies suggested that persons with high serum urate level have a markedly lower risk of developing PD 7,8 , while others showed no such benefits or negative effect 9,10 . Characterized by deposition of monosodium urate crystals in individuals with high serum urate level, gout is ABSTRACT: Objective: Serum urate may exert protective effects against Parkinson's disease (PD) through its antioxidant capacities. In this article, we examine the hypothesis that high serum urate levels are associated with lower risk of PD. Methods: We searched NCbI (PubMed), ISI Web of Science and eMbASe for studies that reported the risk of PD associated with serum urate. Fixed or random effects meta-analysis was used to pool results across studies, and further analysis was used to assess the effects by gender. Results: Six studies met the inclusion criteria involving a total of 33 185 participants. Overall, we found a 33% reduction in PD incidence among persons with high serum urate level (relative risk [RR]=0.67; 95% confidence interval [CI], 0.50-0.91). Subgroup analysis was performed with 20 641 men and 12 544 women included, indicating statistically significant protective effects of serum urate in men (RR=0.60; 95% CI, 0.40-0.90) but not in women. A dose-response trend of serum urate to reduce PD risk was also observed involving 11 795 participants (RR=0.77; 95% CI, 0.68-0.88). Additionally, high serum urate levels seemed to slow the clinical decline of PD patients (RR=0.56; 95% CI, 0.43-0.72). Conclusions: In light of these findings, our study confirms previous findings of a robust association between high serum urate level and PD risk, especially in men. It also suggests that long-term exposure to high serum urate may be linked to the delay of PD progression, however more well-designed investigations are needed.
We demonstrated the presence of BRAF V600E mutation in Chinese epileptic patients with GNTs, which was significantly correlated with gender and multiple seizure types. Large sample studies and long-term follow-up are required for further confirmation.
Cerebral venous collagenosis has been implicated in leading to white matter hyperintensities (WMHs) via venous ischemia. We sought to determine whether cerebral venous dilation or ischemia correlate with the severity of WMHs by quantitative in vivo imaging techniques. This was an investigator-initiated prospective single-center study. We reviewed clinical, laboratory data from 158 consecutive WMHs patients and 50 controls, and measured the number of voxels of deep medullary veins (DMVs) on susceptibility-weighted image and assessed the WMH volume (as a marker of the severity of WMHs) on a 3-T magnetic resonance system. We then performed the logistic-regression analysis and partial Pearson’s correlation analysis to examine the association between the venous voxel count and WMH volume. The number of voxels of DMVs was significantly higher in WMHs than in controls. Increased number of voxels of DMVs was independently associated with both WMH volume of the whole brain and coregistered regional WMH volume after adjusting for age and number of lacunes. Our study indicates that cerebral deep venous insufficiency or ischemia play a role in the pathogenesis of WMHs, which may provide prognostic information on patients with WMHs and may have implications for therapeutic interventions.
These results suggested that ABCB1 rs1045642 and UGT2B7 rs7439366 may affect OXC pharmacokinetics and therapeutic efficacy in Han Chinese patients with epilepsy. However, further studies in larger populations and other ethnic groups are required.
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