Background: Complaints of fatigue and poor sleep quality are common in patients with epilepsy. Fatigue may precipitate seizures, and patients with poor sleep quality have higher frequency of seizures and are more likely to have symptoms of depression. Objectives: This study aims to determine the association of baseline fatigue and sleep quality with antiseizure medication (ASM) resistance in patients with newly diagnosed epilepsy (PWNDE). We also evaluate whether the association is mediated by depression symptoms. Methods: We performed a prospective cohort study of PWNDE at comprehensive epilepsy center in Northeast China between June 2020 and May 2024. Fatigue, sleep quality, and depression symptoms were assessed at baseline. All patients were followed for 24 months for ASM-resistant epilepsy. Cox proportional hazard regression models were used to estimate the hazard ratios (HRs) of ASM resistance. Models fitted with restricted cubic spline were performed to test for linear and nonlinear shapes of each association. Mediation analysis was used to estimate the mediating effects of depression severity on association between fatigue, sleep quality, and ASM resistance. Results: A total of 189 patients (59 ASM-resistant cases and 130 ASM-responsive controls) were included in the final analysis. Baseline fatigue (HR, 1.98; 95% confidence interval (CI), 1.094–3.583, p = 0.024) and poor sleep quality (HR, 2.193; 95% CI, 1.29–3.729, p = 0.004) were associated with an increased hazard of ASM resistance in PWNDE after full adjustments. There exists a nonlinear association between Fatigue Severity Scale score and the hazard of ASM resistance ( P for nonlinear = 0.012). Depression severity partly mediated the effect of fatigue and sleep quality on ASM resistance, with mediated proportions of 18.5% for the fatigue and 23.7% for the sleep quality. Conclusion: Baseline fatigue and poor sleep quality were associated with an increased risk of ASM resistance. The association between fatigue, sleep quality, and ASM resistance were partly mediated by depression severity. These findings emphasize that patients with ASM-resistant epilepsy are more likely to have fatigue, depression, and poor sleep quality at baseline and this may be unrelated to ASM intake.

OBJECTIVE:Although sleep duration and sleep quality are considered to be significant factors associated with epilepsy and seizure risk, findings are inconsistent, and their joint association remains uncertain. This study aimed to determine independent and joint associations of these two modifiable sleep features with seizure recurrence risk in newly treated patients with epilepsy (PWE). METHODS:This is a prospective cohort study of newly treated PWE at a comprehensive epilepsy center in northeast China between June 2020 and December 2023. Self-reported sleep duration and sleep quality were collected at baseline. All patients were followed for 12 months for recurrent seizures. Cox proportional hazard regression models were used to estimate the hazard ratios (HRs) of seizure recurrence. Models fitted with restricted cubic spline were conducted to test for linear and nonlinear shapes of each association. RESULTS:A total of 209 patients were included, and 103 experienced seizure recurrence during follow-up. Baseline short sleep was significantly associated with greater risk of seizure recurrence (adjusted HR = 2.282, 95% confidence interval [CI] = 1.436-3.628, p < .001). Sleep duration (h/day) and recurrent seizure risk showed a significant nonlinear U-shaped association, with a nadir at 8 h/day. Baseline poor sleep quality was significantly associated with greater risk of seizure recurrence (adjusted HR = 1.985, 95% CI = 1.321-2.984, p < .001). Pittsburgh Sleep Quality Index score and seizure recurrence risk exhibited a positive linear association. Participants with a combination of poor quality-short sleep showed the highest risk of seizure recurrence (adjusted HR = 3.13, 95% CI = 1.779-5.507, p < .001) compared to the referent good quality-intermediate sleep group. SIGNIFICANCE:Baseline sleep duration and sleep quality were independently and jointly associated with risk of seizure recurrence in newly treated PWE. Our results point to an important potential role of baseline sleep duration and sleep quality in shaping seizure risk.

IntroductionN-methyl-D-aspartate receptor (NMDAR) is one of the main receptor of the excitatory neurotransmitter glutamate in the brain, which is the key determinant of the excitatory/inhibitory balance of neural network. GluN2A/GRIN2A is one of the subunits of NMDAR and plays an important role in epilepsy. Approximately 78% of patients with GluN2A/Grin2a mutations have epilepsy, and the underlying mechanism of this association is not well characterized.MethodsWe constructed a mouse model of hyperthermic seizure, and conducted in vitro and in vivo electrophysiological and behavioral studies to clarify the pathogenic characteristics and mechanism of GluN2A/GRIN2A-V685G mutation. In addition, the drug efavirenz (EFV), which is used to treat HIV infection, was administrated to mutant animals to assess whether it can restore the loss of function.ResultsMutant mice showed no significant change in the mRNA or protein expressions of NMDAR compared with wild type (WT) mice. Mice with GluN2A/GRIN2A-V685G mutation exhibited shorter latency to seizure, increased frequency of seizure-like events, decreased peak current and current area of NMDAR excitatory postsynaptic current, and decreased event frequency of micro-inhibitory postsynaptic current, compared to WT mice. They also exhibited decreased threshold, increased amplitude, increased input resistance, and increased root number of action potential. EFV administration reversed these changes. The loss-of-function (LoF) mutation of NMDAR changed the excitatory/inhibitory balance of neural network, rendering animal more prone to seizures.DiscussionEFV was indicated to hold its potential in the treatment of inherited epilepsy.

BACKGROUND:Investigations have revealed the association between inflammation and post-stroke depression (PSD). However, whether the C-reactive protein (CRP) level, a biomarker of inflammation, would affect the development of PSD is still controversial. METHODS:A systematic search of databases was performed for eligible studies. Standardized Mean Difference (SMD) with 95 % Confidence Interval (CI) was used to assess the association between the CRP level in the acute phase of stroke and the risk of PSD. RESULTS:13 cohort studies that involved 3536 participants were included. Combined results showed that compared with non-PSD patients, the CRP level of PSD patients was significantly higher on admission (SMD = 0.19, 95 % CI: 0.12-0.27). A subgroup analysis by classifying the assessment time of depression showed obvious differences of the CRP levels between the PSD patients who were diagnosed more than 1 month after stroke and the non-PSD (1-3 months: SMD = 0.16, 95 % CI: 0.06-0.25; >3months: SMD = 0.34, 95 % CI: 0.18-0.51). CONCLUSION:A higher level of CRP in the acute phase of stroke suggests an increased risk for PSD.

To assess the efficacy and safety of pregabalin during short-term treatment in adults with neuropathic pain. We searched the PubMed, Embase, Web of Science, Cochrane Central Register of Controlled Trials, and Clinical Trials databases. Twelve eligible articles were finally selected. Efficacy outcomes included change in Daily Pain Rating Scale score (DPRS; 0 = 'no pain' to 10 = 'worst possible pain') and sleep interference score (0 = 'pain does not interfere with sleep' to 10 = 'completely interferes'). Safety was based on adverse events, serious adverse events (SAEs) and the incidence of treatment emergent adverse events (TEAEs).The authors used the Cochrane Collaboration's Risk of Bias Tool to assess the risk of bias in included trials. Review Manager 5.3 was used for all statistical analyses. Data from 12 articles including 3,169 patients (pregabalin, n = 1,677; placebo, n = 1,492) were analyzed. Mean changes in the daily pain rating scale score [MD = -0.65, 95%CI(-0.88,-0.41), P<0.001] and daily sleep interference score in patients that received pregabalin were compared to those that received placebo [MD = -0.81, 95%CI(-1.16,-0.46), P < 0.001]. The incidence of any TEAE was significantly increased in patients that received pregabalin [OR = 1.70, 95%CI (1.44,2.01), P<0.001]. Serious adverse events (SAEs) rate in the pregabalin group was higher than the placebo group [OR=2.09, 95%CI (1.49,2.93), P<0.001], while there was no significant difference in the incidence rate of discontinuation [OR=1.29, 95%CI (0.79,2.11), P = 0.31]. Comparative results revealed pregabalin (150-600 mg/day) significantly reduced the symptoms of neuropathic pain in adults and its safety was acceptable.

Purpose Our aims were to determine (1) whether the marriage rate was different between the sexes and (2) whether the influencing factors of marital status varied by sexes. Methods A cross-sectional study was performed among 475 people with epilepsy (PWE) in Northeast China. The demographic information and clinical data were gathered and recorded. Sex differences in the marriage rate of PWE and the related influencing factors were analyzed. Multivariate logistic regression analyses were used to investigate the independent factors influencing marital status in men and women, respectively. Results Among 475 participants, 219 (79.6%) men with epilepsy (MWE) were married, and 140 (70%) women with epilepsy (WWE) were married. In MWE, age, educational level, age at seizure onset, and disease duration were significantly different between the married men and the single men. In WWE, age, educational level, occupation and age at seizure onset showed significant differences between the married women and the single women. In the multiple logistic regression model, age and age at first seizure onset had an independent effect on the marital status in men with epilepsy. Multiple logistic regression analysis also revealed that age and age at first seizure onset were independent factors that influenced marital status in WWE. Conclusion Men with epilepsy were more likely to marry than WWE. Age and the age of seizure onset independently affected the marital status of men and women.

Immunoglobulin G4 (IgG4)-related disease is a systemic disease characterized by sclerosing lesions and an increased serum IgG4 level. This condition can involve any organ, but IgG4-related spinal pachymeningitis is relatively rare. In the current study, we report a case of spinal cord compression caused by IgG4-related spinal pachymeningitis. A 39-year-old man presented to us with a 15-day history of back pain and a 3-day history of dysuresia, exacerbated by weakness in the lower extremities for 2 days. Cervical magnetic resonance imaging (MRI) showed strip-shaped abnormal signals along the anterior and posterior borders of the spinal cord at the C5-T4 levels. The IgG level in cerebrospinal fluid was 718.0 mg/L. Thoracic MRI revealed strip-shaped abnormal signals with remarkable enhancement along the anterior and posterior borders of the dural sac at the T1-T6 levels. Histopathological examination confirmed IgG4-related spinal pachymeningitis. The symptoms worsened rapidly, and surgical resection of the space-occupying lesion in the vertebral canal was performed for spinal decompression. Corticosteroid therapy was administered, and the patient's motor functions were mildly improved. IgG4-related disease can manifest as spinal pachymeningitis and cause spinal cord compression. Clinicians should be aware of this rare condition, and early diagnosis, timely surgical decompression, and appropriate corticosteroid therapy should be highlighted.

RATIONALE:Anti-GQ1b antibody syndrome refers to a distinct variant of Guillain- Barré syndrome. Involvement of the optic nerve in anti-GQ1b antibody syndrome is extremely rare. PATIENT CONCERNS:Here, we report a case of anti-GQ1b antibody syndrome presenting with visual deterioration as the initial symptom. A 73-year-old man presented with a 5-day history of bilateral blurred vision and ptosis. He had a previous history of diarrhea starting 10 days before admission. Physical examination showed visual deterioration, ophthalmoplegia, and peripheral facial paralysis. Testing of both serum and cerebrospinal fluid was positive for anti-GQ1b immunoglobulin G antibodies and negative for anti-aquaporin 4antibodies. DIAGNOSIS:Anti-GQ1b antibody syndrome. INTERVENTIONS:The patient was treated with intravenous methylprednisolone and human immunoglobulin. OUTCOMES:After a 20-day follow-up, the patient's condition took a favorable turn. LESSONS:This case reminds us that anti-GQ1b antibody syndrome should be suspected in patients with visual deterioration and preceding infection.

Objective: Atorvastatin and aspirin have been used in treating different forms of epilepsy. However, their effect on post-stroke epilepsy (PSE) still needs to be validated by large-scale clinical studies. In addition, their impact on the use of the antiepileptic drug levetiracetam for post-stroke epilepsy remains to be explored. Thus, the aim of this study was to further evaluate the effect of atorvastatin and aspirin on PSE and their effect on the usage of the antiepileptic drug levetiracetam in PSE patients. Methods: Patients, aged 65 to 85 years, with newly diagnosed post-ischemic stroke epilepsy from August 30, 2014 to August 30, 2018 were included in the study, with the exclusion of those with coexisting conditions. Results: Initially, 1321 patients were included, and 780 remained in the study at the 1-year follow-up. During the study, atorvastatin treatment with or without aspirin reduced the number of clinical epileptic episodes in PSE patients. It also reduced the dosage of levetiracetam and achieved better control of epilepsy compared to levetiracetam mono-treatment. Aspirin co-treatment with levetiracetam did not result in a significant improvement. However, the combination of aspirin with atorvastatin significantly reduced the number of seizures compared to atorvastatin treatment alone. Conclusion: Atorvastatin and aspirin co-treatment with levetiracetam can reduce epilepsy in PSE patients and reduce the dosage of levetiracetam required for effective control of PSE.

自发性低颅压(spontaneous intracranial hypotension,SIH)又称自发性低脑脊液容量(pontaneous cerebrospinal fluid hypovolemia,SCFH) 是一种少见的神经系统疾患.虽然其典型的临床特点是体位性头痛,在临床上的漏诊和误诊率仍较高.由于国内很多神经诊疗中心一直沿用陈旧的诊疗观念,有些明确诊断的患者得不到规范的治疗.低颅压的病理基础是硬脊膜脑脊液瘘,文献报道瘘口以胸腰段脊柱多发,而颈段特别是高位颈段相对罕见.本文报道 1 例轻微外伤后高颈段脑脊液瘘导致 SIH 的患者.通过文献复习,对其致病机制、 诊断手段和治疗方法进行梳理.

Toxoplasmosis is a worldwide zoonosis caused by an intracellular protozoan parasite, Toxoplasma gondii. We report here a diabetic patient who was diagnosed as toxoplasmosis with multiple cranial nerve palsies and cavernous sinusitis. A 37-year-old male presented with an 11-day history of gingival pain, one day history of ptosis and diplopia. He has been having diabetes mellitus for 6 years, and has a history of contact with cats. After admission, his symptoms worsened with right 3rd to 7th cranial nerve palsies. The brain magnetic resonance imaging (MRI) showed cavernous sinusitis in the right sellar region. Serology for toxoplasma was positive for IgM and negative IgG. The patient was treated with oral clindamycin (900 mg/day) and dexamethasone (15 mg/day). The right visual acuity and lid-conjunctival swelling improved after 3 days. At follow-up after a month, the movement of the right eye significantly improved. This case demonstrate the rare occurrence of multiple cranial nerve (3rd to 7th) palsies from toxoplasmosis cavernous sinusitis, which is a potentially treatable condition.

RATIONALE:Neuroacanthocytosis (NA) is a heterogeneous group of inherited neurodegenerative disorders characterized by misshapen spiculated erythorcytes and symptoms that resemble Huntington's disease.PATIENT CONCERNS:A 59-year-old female who developed hyperkinetic involuntary movements that became progressively more obvious during the course of a year.DIAGNOSES:Acanthocytes were observed in a peripheral blood smear. The patient had elevated levels of serum creatine kinase (CK). Gene sequencing did not reveal a genetic mutation.INTERVENTIONS:The patient was administered oral tiapride, alprazolam, B1 and B12 Vitamins.OUTCOMES:After 2 months of treatment the patient's symptoms were obviously alleviated. At the 6 month follow-up, the patient could feed herself and walk without assistance.LESSONS:The NA syndrome is extremely rare. It may be identified in the clinic based on abnormal orofacial movement, chorea, cognitive decline, elevated CK levels, and acanthocytosis. If available, protein- or genetic-based testing may provide a confirmatory diagnosis.

BACKGROUND This study investigated the clinical effect of interventional therapy in ischemic cerebrovascular disease (ICD). MATERIAL AND METHODS A retrospective analysis was performed on 260 ICD patients who were divided into a control group (122 patients, conventional drug treatment) and an observation group (138 patients, interventional therapy plus conventional drug treatment). Enzyme-linked immunosorbent assay was used to examine the expression of IL-1β, IL-6, and NLR. Furthermore, neurological deficit scores and Barthel index scores as well as the correlation of IL-1β, IL-6 and NLR were examined in these 2 groups. RESULTS The expression of IL-1β, IL-6, and NLR significantly decreased in both groups after 1 week or 4 weeks of treatment compared with before treatment (P<0.05). Significant differences in neurological impairment scores were detected between these 2 groups after 4 weeks of treatment (P<0.05), and the control group showed higher neurological deficit scores than did the observation group (P<0.05). Barthel index scores were significantly higher after treatment than before treatment in the control and observation group (P<0.05), and the control group had lower Barthel index scores than did the observation group (P<0.05). Pearson correlation analysis showed that IL-1β, IL-6, and NLR expression were positively correlated in ICD patients (P<0.05). CONCLUSIONS Interventional surgery combined with conventional drug therapy can reduce serum IL-1β and IL-6 levels, decrease neurological impairment, and improve the quality of life of patients. The combined treatment group showed better outcomes than did the group that received the drug alone; therefore, combined therapy is suitable for promoting better clinical outcomes.

Sepsis-associated encephalopathy (SAE) is a common complication of sepsis. It is imperative to recognize, diagnose, and effectively manage SAE at the early stages. The aim of this study was to evaluate the potential of using the serum tau protein level in the diagnosis of SAE and the prediction of SAE outcomes. This was a retrospective and observational study. The patients included in this study were diagnosed with severe sepsis or septic shock. The serum tau protein level was measured using a commercial enzyme-linked immunosorbent assay. The association between the level of serum tau protein and SAE was assessed by multiple logistic regression analysis. One hundred nine patients with severe sepsis were enrolled during a period of two years. Of the 109 enrolled patients, 27 developed SAE. The serum tau protein level was significantly higher in the patients with SAE than that of the non-SAE group. The serum tau protein level and the sequential organ failure assessment (SOFA) score were independent factors that were associated with SAE. The combined use of the serum tau protein level with the SOFA score improved the accuracy in distinguishing SAE from non-SAE patients. A cutoff value serum tau protein level of 75.92 pg/mL had 81.1% sensitivity and 86.1% specificity in predicting the 28-day mortality in patients with severe sepsis. We identified a close association between the serum tau protein level with the appearance of SAE in patients with severe sepsis. The serum tau protein level can be useful in the prediction of poor outcomes in patients with sepsis.

We reported a case of carotid artery stenosis with stroke symptoms detected in a patient with lung cancer after radiotherapy. The patient was a 58-year-old male with a complaint of \"a single episode of temporary amaurosis in the right eye for 10 minutes". The clinical diagnosis at admission, after consideration of the patient's age, medical history, and auxiliary examination results, was as follows: lung cancer; right common carotid artery stenosis; left common carotid artery stenosis; left vertebral artery stenosis; and right subclavian artery occlusion with right subclavian steal syndrome (Grade 3). Carotid angioplasty and stenting (CAS) were subsequently performed. During the 6-month follow-up, we observed no episode of temporary vision loss or other signs of stroke. Clinicians should pay great attention to delayed radiation-induced carotid stenosis. It is recommended that patients with a history of radiotherapy should undergo regular color Doppler ultrasound examination of the cervical region to diagnose, prevent, and treat RICS in an expedient fashion. This approach should improve survival rate and quality of life.

The aim of this study is to investigate the effects of long‐chain noncoding RNA plasmacytoma variant translocation 1 (PVT1) on the activation of astrocytes and the expression of brain‐derived neurotrophic factor (BDNF) in hippocampus tissues of epileptic rats. The epilepsy rat model was induced by intraperitoneal injection of lithium chloride–pilocarpine. Successfully modeled rats were grouped, and their spatial learning and memory, neuronal loss, number of TdT‐mediated dUTP nick labeling (TUNEL)‐positive cells, and the expression of cleaved‐caspase‐3, pro‐caspase‐3, Bax, Bcl‐2, GFAP, BDNF, tumor necrosis factor‐α (TNF‐α), interleukin‐1β (IL‐1β), IL‐6, axin, and cyclin D1 in hippocampus tissues were evaluated. Increased expression of PVT1 was found in hippocampus tissues of epileptic rats. Silencing of PVT1 improved spatial learning and memory, decreased neuronal loss, decreased the number of TUNEL‐positive cell, decreased the expression of cleaved‐caspase‐3 and Bax while increased pro‐caspase‐3 and Bcl‐2 expression, decreased the expression of GFAP, increased the expression of BDNF, decreased the expression of TNF‐α, IL‐1β, and IL‐6, and decreased the expression of axin and cyclin D1 in hippocampus tissues in epileptic rats. Our study provides evidence that the inhibition of PVT1 may decrease the loss of neurons, inhibit the activation of astrocytes, and increase the expression of BDNF in hippocampus by downregulating the Wnt signaling pathway.

OBJECTIVE: Cerebral small vessel diseases (CSVDs) are common causes of cognitive impairments and mood disorders. In recent years, event-related potential P300 has received increasing attention as a biomarker of cognitive impairments or mood disorders. Previous studies on P300 mainly focused on anxiety, depression or cognitive impairments, and few results have been reported on P300 in CSVD patients. The present study aimed to explore the relationship between neuropsychological test scores and P300 in patients with CSVDs. METHODS: The clinical data of 52 patients with CSVDs admitted to the Neurology ward of the First Hospital of Jilin University from June 2016 to October 2017 were collected. All patients who met the inclusion criteria were assessed by both cognitive tests and mood scales within 1 week after enrollment, followed by measurement of P300. Accordingly, patients were assigned to the following four groups: cognitive impairment, non-cognitive impairment, mood disorder, and non-mood disorder.The amplitude and latency values of P300 were measured from the Pz, Fz, Fpz, C3, C4 and Cz electrode sites. In addition, correlations of P300 responses and neuropsychological test scores were analyzed. RESULTS: Significant differences were found in the P300 latency values between the cognitive impairment group and non-cognitive impairment group (P<0.05). P300 latency values were more significantly prolonged in the mood disorder group at the Fz, C3 and Cz electrode sites than in the non-mood disorder group. Positive correlations were found between Hamilton Depression Scale scores and C3, Fz and Cz latencies. Females tended to have a statistically higher risk of emotional impairment than did males (p<0.05). CONCLUSION: P300 latency values can be used as a objective indicator of cognitive impairments and mood disorders in CSVD patients.

Objective: This research aimed to validate the therapeutic effect of losmapimod and explore the underlying mechanism in its treatment of epilepsy.Methods: A rat model of epilepsy was constructed with an injection of pilocarpine. Microarray analysis was performed to screen aberrantly expressed mRNAs and activated signaling pathways between epileptic rats and normal controls. A TdT-mediated dUTP nick-end labeling (TUNEL) assay was used to identify cell apoptosis. Hippocampal cytoarchitecture was visualized with Nissl staining. The secretion of inflammatory factors as well as the marker proteins in the mitogen-activated protein kinase (MAPK) pathway were detected by Western blot. A Morris water maze navigation test evaluated the rats’ cognitive functions.Results: Activation of the MAPK signaling pathway was observed in epilepsy rats. A decrease in the MAPK phosphorylation level by application of losmapimod protected against epilepsy by reducing neuron loss. Losmapimod effectively improved memory, reduced the frequency of seizures, protected the neuron from damage, and limited the apoptosis of neurons in epilepsy rats.Conclusion: The application of losmapimod could partly reverse the development of epilepsy.

In this report, we describe a woman patient who presented with general fatigue and gradual weakness of the limbs. Her husband was diagnosed with syphilis. We performed a serological examination for syphilis and muscle biopsy. Her serological examination was TPPA (treponema pallidum particle agglutination assay)-positive and RPR (rapid plasma reagin)-positive with a titer of 1:16. Muscle biopsy showed abnormal lipid accumulation in myofibers. The genetic test revealed homozygous mutation at c. 770A > G (p.Y257C) of the ETFDH (electron transferring-flavoprotein dehydrogenase) gene. We conclude that this woman was infected with syphilis from her husband, and because she was a c.770A > G ETFDH mutant, multiple acyl-CoA dehydrogenase deficiency (MADD) was triggered.

BACKGROUNDCVST is an important cause of stroke during late pregnancy and in the puerperium, but it is seldom encountered during early pregnancy. We report a case of a 34-year-old woman presenting with convulsive status epilepticus in early pregnancy.METHODSIn this case, the cranial computed tomography detected hemorrhage. Magnetic resonance imaging revealed a bilateral hypointense signal involving the frontal lobes and a hyperintense lesion on the right temporal lobe on T1-weighted imaging, and a large bilateral hyperintense area involving the frontal lobes on T2-weighted and fluid-attenuated inversion recovery imaging. Magnetic resonance venography showed occlusion of the right transverse sagittal and sigmoid sinus.RESULTSThe patient received a diagnosis of cerebral venous sinus thrombosis (CVST) with cerebral hemorrhage. The patient was given anticoagulant therapy for one month and made a good recovery.CONCLUSIONSThis case report should raise awareness of the diagnosis and treatment of CVST with cerebral hemorrhage in early pregnancy.