Family cohesion and quality of life significantly affecting personality changes in adult epilepsy patients: a case-control study.

OBJECTIVE: The goal of epilepsy treatment is not only to control convulsive seizures but also to improve the quality of life of patients. This study aimed to investigate personality changes and the risk factors for their development in adult epilepsy patients. METHODS: A case-control study in a Class III, Class A hospital. The study comprised 206 adult epilepsy patients admitted to the Neurology Department at the First Hospital of Jilin University between October 2019 and December 2021, while the control group consisted of 154 community volunteers matched with the epilepsy group based on age, sex, and education. No additional treatment interventions were determined to be relevant in the context of this study. RESULTS: There is a significantly higher incidence of personality changes in epilepsy than in the general population, and patients with epilepsy were more likely to become psychoticism, neuroticism, and lie. Epilepsy patient's employment rate and average quality of life score were significantly lower than that of the general population and had strong family intimacy but poor adaptability in this study. There are many factors affecting personality change: sleep disorders, economic status, quality of life, use of anti-seizure drugs, family cohesion and adaptability. The independent risk factors were quality of life and family cohesion.

Exploring causal correlations between systemic inflammatory cytokines and epilepsy: A bidirectional Mendelian randomization study.

BACKGROUND: Inflammation plays a role in the development and advancement of epilepsy, but the relationship between inflammatory cytokines and epilepsy is still not well understood. Herein, we use two-sample Mendelian randomization (MR) to examine the causal association between systemic inflammatory cytokines and epilepsy. METHODS: We conducted a bidirectional two-sample MR analysis based on genome-wide association study data of 41 serum cytokines from 8293 Finnish individuals with various epilepsy subtypes from the International League against Epilepsy Consortium. RESULTS: Our study showed that three inflammatory cytokines were associated with epilepsy, five were associated with generalized epilepsy, four were associated with focal epilepsy, one was associated with focal epilepsy-documented lesion negative, three were associated with juvenile absence epilepsy, one was associated with childhood absence epilepsy, two were associated with focal epilepsy-documented lesion other than hippocampal sclerosis, and two were associated with juvenile myoclonic epilepsy. Furthermore, the expression of systemic inflammatory cytokines was unaffected by genetically predicted epilepsy. CONCLUSION: This study suggested that several inflammatory cytokines are probably the factors correlated with epilepsy. Additional research is required to ascertain if these biomarkers have therapeutic potential to prevent or manage epilepsy.

Effect of intranasal and oral administration of levetiracetam on the temporal and spatial distributions of SV2A in the KA-induced rat model of SE.

To investigate the effectiveness of nasal delivery of levetiracetam (LEV) on the distributions of synaptic vesicle protein 2 isoform A (SV2A) in epileptic rats with injection of kainic acid (KA) into amygdala. A total of 138 rats were randomly divided into four groups, including the Sham surgery group, the epilepsy group (EP), and the LEV oral administration (LPO) and nasal delivery (LND) groups. The rat intra-amygdala KA model of epilepsy was constructed. Pathological changes of rat brain tissue after status epilepticus (SE) were detected using haematoxylin and eosin staining. Expression of SV2A in rat hippocampus after SE was evaluated using the western blotting analysis. Expression and distribution of SV2A in rat hippocampus after SE were detected based on immunofluorescence staining. The EP group showed evident cell loss and tissue necrosis in the CA3 area of hippocampus, whereas the tissue damage in both LPO and LND groups was significantly reduced. Western blotting analysis showed that the expressions of SV2A in the hippocampus of both EP and LND groups were significantly decreased 1 week after SE, increased to the similar levels of the Sham group in 2 weeks, and continuously increased 4 weeks after SE to the level significantly higher than that of the Sham group. Results of immunofluorescence revealed largely the same expression patterns of SV2A in the CA3 area of hippocampus as those in the entire hippocampus. Our study revealed the same antiepileptic and neuronal protective effects by the nasal and oral administrations of LEV, without changing the expression level of SV2A.

Modified Manual Chest Compression for Prevention and Treatment of Respiratory Depression in Patients Under Deep Sedation During Upper Gastrointestinal Endoscopy: Two Randomized Controlled Trials.

BACKGROUND: We aimed to determine the preventive and therapeutic efficacy of modified manual chest compression (MMCC), a novel noninvasive and device-independent method, in reducing oxygen desaturation events in patients undergoing upper gastrointestinal endoscopy under deep sedation. METHODS: A total of 584 outpatients who underwent deep sedation during upper gastrointestinal endoscopy were enrolled. In the preventive cohort, 440 patients were randomized to the MMCC group (patients received MMCC when their eyelash reflex disappeared, M1 group) or control group (C1 group). In the therapeutic cohort, 144 patients with oxygen desaturation of a Sp o2 < 95% were randomized to MMCC group (patients who subsequently received MMCC, M2 group) or the conventional treatment group (C2 group). The primary outcomes were the incidence of desaturation episodes with an Sp o2 < 95% for the preventive cohort and the time spent below 95% Sp o2 for the therapeutic cohort. Secondary outcomes included the incidence of gastroscopy withdrawal and diaphragmatic pause. RESULTS: In the preventive cohort, MMCC reduced the incidence of desaturation episodes <95% (14.4% vs 26.1%; RR, 0.549; 95% confidence interval [CI], 0.37-0.815; P = .002), gastroscopy withdrawal (0% vs 2.29%; P = .008), and diaphragmatic pause at 30 seconds after propofol injection (74.5% vs 88.1%; RR, 0.846; 95% CI, 0.772-0.928; P < .001). In the therapeutic cohort, patients who received MMCC had a significantly shorter time spent below 95% Sp o2 (40 [20-69] seconds vs 91 [33-152] seconds, median difference [95% CI], -39 [-57 to -16] seconds, P < .001), a lower incidence of gastroscopy withdrawal (0% vs 10.4%, P = .018), and more enhanced diaphragmatic movement at 30 seconds after Sp o2 <95% (1.11 [0.93-1.4] cm vs 1.03 [0.7-1.24] cm; median difference [95% confidence interval], 0.16 [0.02-0.32] cm; P = .015). CONCLUSIONS: MMCC may exert preventive and therapeutic effects against oxygen desaturation events during upper gastrointestinal endoscopy.

The JAK-STAT Signaling Pathway in Epilepsy.

Epilepsy is defined as spontaneous recurrent seizures in the brain. There is increasing evidence that inflammatory mediators and immune cells are involved in epileptic seizures. As more research is done on inflammatory factors and immune cells in epilepsy, new targets for the treatment of epilepsy will be revealed. The Janus kinase-signal transducer and transcriptional activator (JAKSTAT) signaling pathway is strongly associated with many immune and inflammatory diseases, At present, more and more studies have found that the JAK-STAT pathway is involved in the development and development of epilepsy, indicating the JAK-STAT pathway's potential promise as a target in epilepsy treatment. In this review, we discuss the composition, activation, and regulation of the JAK-STAT pathway and the relationship between the JAK-STAT pathway and epilepsy. In addition, we summarize the common clinical inhibitors of JAK and STAT that we would expect to be used in epilepsy treatment in the future.

Circulating malondialdehyde level in patients with epilepsy: A meta-analysis.

PURPOSE: Malondialdehyde (MDA) is an oxidative stress marker that determines the impact of oxidation on MDA levels in patients with epilepsy (PWE) and healthy controls. METHODS: A meta-analysis was performed on 15 published studies. A total of 559 PWE and 853 healthy controls were included to evaluate the MDA levels in erythrocytes, serum, and plasma, respectively. RESULTS: Meta-analysis showed that MDA levels were significantly higher in PWE than in healthy controls. Moreover, the meta-analysis demonstrated that MDA levels were increased in three subgroups of serum, plasma, and red blood cells from epileptic patients compared with the control group. Differentiating the subgroups according to the proportion of female patients, region, and MDA detection method showed that MDA levels in epileptic patients were higher than in healthy controls. In addition, MDA levels were significantly higher in the Asian subgroup than in the non-Asian subgroup. There was no potential publication bias. The age of the patients, the proportion of female patients, the region, and methods for measuring MDA of the included studies did not cause heterogeneity. CONCLUSION: Our results showed increased MDA levels in erythrocytes, serum, and plasma in PWE, which may be an indicator of oxidative damage in epilepsy. This is the first meta-analysis of circulating MDA levels in PWE and healthy controls.

Spontaneous Spinal Epidural Hematoma Complicated by Pulmonary Embolism During Pregnancy: A Case Report.

Background: Spontaneous spinal epidural hematoma, without discernable underlying conditions, is considered a neurological emergency, and is rare during pregnancy. Case Presentation: We report the case of a 24-year-old patient at 37 weeks of gestation. She had back pain that progressed to paraplegia of both lower limbs within 2 days. Thoracic magnetic resonance imaging revealed a lesion behind the spinal cord at the T5-T6 level, suggestive of spontaneous spinal epidural hematoma. Due to the rapid recovery of muscle strength in her lower limbs after an emergency cesarean section, we used methylprednisolone therapy to reduce spinal edema rather than decompression of the spinal canal. We incidentally found that the patient's left pulmonary artery was occluded. In consideration of spontaneous spinal epidural hematoma as relative contraindication to anticoagulation, and in the absence of pulmonary embolism symptoms, including good partial oxygen pressure, we did not administer anticoagulant therapy. The patient's condition improved rapidly in the following week. Conclusion: Spontaneous spinal epidural hematoma concomitant with pulmonary artery embolism is an extremely rare manifestation during pregnancy. As exemplified by our case, desirable treatment outcomes are possible under such cases.

Migraine and the risk of dementia: a meta-analysis and systematic review.

OBJECTIVES: To conduct a comprehensive systematic review and meta-analysis to explore the correlation between migraine and the risk of dementia. METHODS: The PubMed, EMBASE, and Cochrane library databases were searched systematically. We selected cohort studies (prospective and retrospective) and case-control studies that reported migraine in patients with dementia, including vascular dementia. The pooled effects were analyzed to evaluate relative risk with 95% confidence intervals. RESULTS: In total, nine studies (two case-control and seven cohort studies) including 291,549 individuals were identified. These studies indicated that people with migraine (relative risk = 1.33; 95% confidence interval: 1.16-1.53) have an increased risk of all-cause dementia. Additionally, the pooled results of four studies showed that migraine is associated with an increased risk of vascular dementia (relative risk = 1.85; 95% confidence interval: 1.22-2.81; P = 0.004). CONCLUSIONS: Data from observational studies suggest that migraine may be a risk factor for dementia, particularly vascular dementia. More studies are warranted to explore the association between migraine and dementia and the potential common pathophysiological mechanisms.

Influence of nanoparticle size on blood-brain barrier penetration and the accumulation of anti-seizure medicines in the brain.

Anti-seizure medicines constitute a common yet important modality to treat epilepsy. However, some of them are associated with serious side effects including hepatotoxicity and hypersensitivity. Furthermore, the blood-brain barrier (BBB) is an insurmountable obstacle for brain drug delivery. Fortunately, the introduction of the nanoparticles for drug delivery is a feasible approach to overcome these obstacles. Encapsulating drugs into nanoparticles and delivering them to specific sites shows great potential for improving the efficiency of drug delivery and reducing systemic toxicity. Several in vivo studies have investigated the effect of nanoparticle size on biodistribution in mice, but very few have investigated its effects on efficient drug delivery while crossing the BBB. Therefore, we designed a methoxy poly(lactide-co-glycolide)-b-poly(ethylene glycol) methyl ether (mPEG-PLGA) nanoparticle delivery system and explored the cell uptake efficiency of nanoparticles with different sizes and their ability to penetrate the BBB while carrying carbamazepine (CBZ). CBZ-loaded nanoparticles could significantly reduce the cytotoxicity of CBZ to L929 cells at high concentrations. Results from the endocytosis experiment involving human cerebral microvessel endothelial cell/D3 showed that the DiR-loaded mPEG5K-PLGA10K nanoparticles possessed the highest cell uptake efficiency. The endocytosis efficiency was 90% at 30 min, which far exceeded that of the other groups. Moreover, similar results were obtained from subsequent experiments where fluorescence images of the isolated organs of the mice were acquired. To summarize, our study demonstrated that drug delivery to the brain using nanocarriers is size dependent. Nanoparticles with the smallest particle size can be internalized more effectively, and easily penetrate the BBB, and accumulate in the brain.

Epilepsy Associated With Mitochondrial Encephalomyopathy, Lactic Acidosis, and Stroke-Like Episodes.

Objectives: The present study explored the clinical characteristics and prognostic factors of epilepsy in patients with mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes (MELAS). Methods: Thirty-four MELAS patients were included in the present study. They were diagnosed by clinical characteristics, genetic testing, muscle biopsy, and retrospective analysis of other clinical data. The patients were divided into three groups according to the effects of treatment after at least 2 years of follow-up. Results: Epilepsy was more common in male MELAS patients than in females (20/14). The age of onset ranged from 0.5 to 57 years, with an average of 22.6 years. Patients with epilepsy and MELAS had various forms of seizures. Focal seizures were the most common type affecting 58.82% of patients, and some patients had multiple types of seizures. The abnormal EEG waves were mainly concentrated in the occipital (69.57%), frontal (65.22%) and temporal lobes (47.83%). Overall, the prognosis of patients with epilepsy and MELAS was poor. Poor prognosis was associated with brain atrophy (P = 0.026), status epilepticus (P < 0.001), and use of anti-seizure medications with high mitochondrial toxicity (P = 0.015). Interpretation: Avoiding the application of anti-seizure medications with high mitochondrial toxicity, controlling seizures more actively and effectively, and delaying the occurrence and progression of brain atrophy as much as possible are particularly important to improve the prognosis of patients with MELAS and epilepsy.

Cerebral venous sinus thrombosis and subdural hematoma in a female patient with systemic lupus erythematosus: a case report and literature review.

Cerebral venous sinus thrombosis (CVST) and subdural hematoma (SDH) are extremely rare in patients with systemic lupus erythematosus (SLE), and when conditions are severe, it can endanger the life of the patients. We report a case of a 44-year-old woman who was admitted to our hospital due to multiple paroxysmal headaches, dizziness, and seizures for 20 days. In the past 2 years, she had severe thrombocytopenia. Her brain computed tomography (CT) and magnetic resonance venography (MRV) demonstrated CVST and a SDH near the right parietal occipital lobe and left temporal parietal lobe. After admission, she was eventually diagnosed with SLE based on the seizures, thrombocytopenia, positive antinuclear antibodies, and anti-ds DNA antibodies. After treatment, the patient's headaches and symptoms completely disappeared, and the myodynamia of the left limbs improved to grade 4. Her platelet count rose to 199×109/L. The second brain MRV and MRI demonstrated partial reopening of the right superior sagittal sinus, transverse sinus, and sigmoid sinus, and the improvement of bilaterally SDH, which revealed that the treatment with an anticoagulant, pulse methylprednisolone therapy, and intravenous gamma globulin was effective. We summarized possible mechanisms in this case, which can improve our understanding of CVST and SDH in SLE. And we consider that such patients should be treated as soon as possible, and the outcome can be good.

Colchicine poisoning complicated by medulla oblongata myelinolysis: a case report.

Medulla oblongata myelinolysis is an extremely rare manifestation of extrapontine myelinolysis (EPM). Herein, we report a case of a 34-year-old man with a history of gout who presented repeated vomiting and diarrhea after ingesting 15 colchicine pills. A hyponatremia diagnosis was given and after an intensive treatment, his serum sodium level increased from 118 to 129 mmol/L within 24 hours. Brain magnetic resonance imaging (MRI) revealed a lesion in the medulla oblongata that appeared as a hypointense area in T1-weighted images and a hyperintense area in T2-weighted images. A diagnosis of medulla oblongata myelinolysis and colchicine poisoning was then given, and methylprednisolone therapy was initiated. Seventeen days later, the patient achieved a good outcome with methylprednisolone therapy. However, his medulla oblongata lesion remained detectable with MRI. Medulla oblongata myelinolysis is an extremely rare manifestation of EPM, and unique for being colchicine-induced. This case shows that colchicine poisoning can lead to hyponatremia, which in turn can induce myelinolysis if not treated correctly. As exemplified by our patient's case, desirable treatment outcomes are possible in such cases, although these outcomes may not be associated with a visible reduction of the brain lesions in MRI scans.

Disseminated histoplasmosis in primary Sjögren syndrome: A case report.

BACKGROUND: Sjögren syndrome (SS) is a chronic and systemic autoimmune disease characterized by lymphocytic infiltration of the exocrine glands. And histoplasmosis is an invasive mycosis caused by the saprophytic dimorphic fungus H. capsulatum. In patients with primary SS (PSS), disseminated histoplasmosis (DH) is extremely rare. CASE SUMMARY: We report a 37-year-old female patient admitted to our hospital with exacerbating fatigue, somnolence, and pancytopenia as the main symptoms. She was eventually diagnosed with DH based on pancytopenia, splenomegaly, and findings of bone marrow smears. The atypical clinical symptoms made the diagnosis process more tortuous. Unfortunately, she died of respiratory failure on the day the diagnosis was confirmed. CONCLUSION: We present a rare and interesting case of DH in a PSS patient. This case updates the geographic distribution of histoplasmosis in China, and expands the clinical manifestations of DH in PSS, highlighting the significance of constantly improving the understanding of PSS with DH.

Recurrent Cerebral Infarctions in Primary Sjögren Syndrome: A Case Report and Literature Review.

Recurrent cerebral infarctions are extremely rare in patients with primary Sjögren syndrome. We report a 66-year-old woman who was admitted to our hospital due to acute cerebral infarction with exacerbation of dysphagia and right-sided hemiplegia as the main symptoms. In the past 3 months, she had developed cerebral infarction twice, even though she had no risk factors for atherosclerosis. She was eventually diagnosed with primary Sjögren syndrome based on a long history of dryness of the eyes and mouth, positive anti-Ro(SSA) antibodies, and the findings of a labial salivary gland biopsy. The response to pulse methylprednisolone therapy after recurrent cerebral infarctions was poor. Thus we consider primary Sjögren syndrome patients with central nervous system involvement should be treated as soon as possible.

The c-Jun N-terminal kinase signaling pathway in epilepsy: activation, regulation, and therapeutics.

Epilepsy affects approximately 50-70 million people worldwide and 30-40% of patients do not benefit from medication. Therefore, it is necessary to identify novel targets for epileptic treatments. c-Jun N-terminal kinase (JNK) is a member of the mitogen-activated protein kinase (MAPK) family that activates diverse substrates, such as transcriptional factors, adaptor proteins, and signaling proteins, and has a wide variety of functions in both physiological and pathological conditions. The excessive activation of JNK is found not only in the acute phase of epilepsy, but also in the chronic phase, which potentiates it as a promising target in epilepsy control. In this review, we discuss the activation of the JNK pathway in epilepsy and its role in neuronal death, astrocyte activation, and mossy fiber sprouting (MFS) based on recent updates. Finally, we briefly introduce the current agents that target JNK signaling to control epilepsy.