BMC Neurology最新文献

Background: Epilepsy is a common condition that affects the brain and causes frequent seizures. Impaired brain biology is the world's fastest-growing brain disorder, and exposure to environmental pollutants is the leading cause of mental health impairment. The growing literature suggests that air pollution is an emerging cause of neurological diseases. However, the existing evidence on air pollution and epilepsy is inadequate. This study aimed to investigate the effect of environmental pollutants particulate matter (PM_2.5, PM₁₀), nitrogen dioxide (NO₂), sulfur dioxide (SO₂), carbon monoxide (NO) and ground-level ozone (O₃) on epilepsy.

Methods: This study recorded data on air pollutants and epilepsy using the electronic platforms Pub Med, Web of Science, Scopus, and Google Scholar. The keywords included for the literature search were based on two main aspects: exposure (air pollutants) and outcome (epilepsy). Initially, 78 articles and reports were identified, and after revising the abstracts and full articles, 06 studies were selected for a detailed analysis and discussion. The Odds Ratio (OR) and 95% confidence intervals (CIs) were extracted to investigate the impact between air pollutants and epilepsy. The effect of air pollution on epilepsy has been investigated through a compilation of six studies encompassing 371,515 individuals. The Cochrane chi-squared test (Chi²), fixed-effects design was used when I² < 50% and P > 0.05; otherwise, a random-effects model was adopted.

Results: The results revealed that exposure to PM_2.5 and NO₂ were positively and significantly associated with epilepsy (RR = 1.00; 95% CI: 1.00-1.01; p = 0.03), NO₂ (RR = 1.03; 95% CI: 1.02-1.03; p < 0.01). However, no association was identified between PM₁₀, SO₂, CO, and O₃ with epilepsy. The results suggest a potential association between air pollution exposure and epilepsy.

Conclusions: Air pollutants PM_2.5 and NO₂ increase the risk of epilepsy. The findings suggest that reducing levels of these pollutants could be a strategic approach to mitigate neurological health risks in populations worldwide. Further research is warranted to elucidate the mechanisms and causal relationships between air pollutants and epilepsy. Public health initiatives aimed at reducing air pollution levels and targeted interventions to protect vulnerable populations hold promise for alleviating the burden of epilepsy associated with environmental exposures.

Background: Growth-associated protein 43 (GAP-43) is a key protein involved in neuronal growth and synaptic plasticity. Alterations in GAP-43 levels have been associated with Alzheimer's Disease (AD), potentially reflecting synaptic dysfunction. We evaluated the potential of GAP-43 as a biomarker for AD and explored its association with amyloid-beta (Aβ) levels, as well as its correlation with Aβ plaque burden in the brain.

Methods: We screened 1,639 participants from the Alzheimer's Disease Neuroimaging Initiative (ADNI) cohort. A total of 226 individuals met the eligibility criteria and were enrolled. Participants were classified into three groups: 77 cognitively normal (CN) individuals, 111 with mild cognitive impairment (MCI), and 38 with a diagnosis of AD. The associations between cerebrospinal fluid (CSF) GAP-43 levels with other biomarkers as well as [¹⁸F] AV-45 (Florbetapir) PET Standardized Uptake Value Ratios (SUVR) were investigated.

Results: Our findings revealed significantly elevated CSF GAP-43 levels in individuals with AD compared to CN and MCI groups. Furthermore, GAP-43 levels showed a significant positive correlation with tau pathology. Notably, we observed a significant association between GAP-43 and [¹⁸F] Florbetapir PET SUVR in the MCI group, suggesting that GAP-43 may serve as a reliable biomarker in the early stages of AD.

Conclusion: This study provides evidence supporting the role of GAP-43 as a potential biomarker for AD, particularly in relation to predicting the amyloid pathology pattern in the brain in the MCI stage.

Objective: Choosing migraine prevention medications often involves trial and error. Operations research methodologies, however, allow us to derive a mathematically optimum way to conduct such trial and error processes.

Background: Given probability of success (defined as 50% reduction in headache days) and adverse events as a function of time, we seek to develop and solve an operations research model, applicable to any arbitrary patient, minimizing time until discovery of an effective migraine prevention medication. We then seek to apply our model to real life data for chronic migraine prevention.

Methods: An operations research model is developed and then solved for the optimum solution, taking into account the likelihood of reaching 50% headache day reduction as a function of time. We then estimate key variables using FORWARD study by Rothrock et al. as well as erenumab data published by Barbanti et al. at International Headache Congress 2019.

Results: The solution for our model is to order the medications in decreasing order by probability of efficacy per unit time. This result can be generalized through calculation of Gittins index. In the case of chronic migraine the optimum sequence of chronic migraine prevention medication is a trial of erenumab for 12 weeks, followed by a trial of onabotulinumtoxinA for 32 weeks, followed by a trial of topiramate for 32 weeks.

Conclusions: We propose an optimal sequence for preventive medication trial for patients with chronic migraine. Since our model makes limited assumptions on the characteristics of disease, it can be readily applied also to episodic migraine, given the appropriate data as input. Indeed, our model can be applied to other scenarios so long as probability of success/adverse event as a function of time can be estimated. As such, we believe our model may have implications beyond our sub-specialty.

Background: Previous results on the association between HDL (high-density lipoprotein cholesterol) levels and intracranial aneurysm (IA) rupture were controversial. We aimed to investigate the association between HDL levels and the risk of IA rupture.

Methods: Medical records of patients with solitary IA diagnosed at West China Hospital of Sichuan University were reviewed and analyzed between December 2008 and March 2023. Univariable and multivariable logistic regression analyses were performed to determine the effects of HDL levels on IA rupture risk. A three-piece-wise logistic regression model with smoothing was used to analyze different association thresholds between HDL and the risk of IA rupture after adjusting for confounding factors.

Results: Univariable and multivariable logistic regression analysis showed the independent association between HDL and IA rupture. After being adjusted for confounders, different U-shaped relationships were found between HDL levels and the risk of IA in males, females, and all patients. Compared to HDL in the range of 0.9 ~ 1.3 mmol/L, patients had 79% [OR (95%CI):1.79(1.16 ~ 2.78), p = 0.009] increase of rupture when lower than 0.9 mmol/L, 60% [OR (95%CI):1.6(1.19 ~ 2.17), p = 0.002] increase when higher than 1.3 mmol/L before or after adjusted confounders. We found gender differences in the HDL range of IA rupture; the lowest range of HDL was 1.1 ~ 1.4 mmol/L in females and 0.8 ~ 1.1 mmol/L in males.

Conclusions: There was a U-shaped relationship between HDL levels and the risk of IA rupture. People with HDL levels between 0.9 and 1.3 mmol/L are least likely to experience IA rupture in the Chinese population.

Background: Social cognitive impairments often occur in patients with various neurological disorders that involve brain damage, such as traumatic brain injury, stroke, brain tumours, and multiple sclerosis. Patients with social cognitive impairments experience difficulties in perceiving and understanding social information and show social inadequate behaviour. Recently, the first multi-faceted treatment, T-ScEmo (Treatment for Social Cognition and Emotion Regulation) has been developed and evaluated for patients with TBI. T-ScEmo showed to be effective in improving social cognitive functioning, participation, relationships, and quality of life. Up to now, no evidence-based treatment has been available for social cognitive impairments in neurological patients other than traumatic brain injury. Therefore, the main aims of the current study are to investigate the efficacy of T-ScEmo in various neurological patient groups such as stroke (including subarachnoid haemorrhage), brain tumours, and multiple sclerosis and to study factors that might influence this, potential, efficacy.

Methods: In this multi-centre, assessor-blind randomized controlled trial, 84 patients with mixed aetiology will be randomly divided over a treatment condition and a waiting list condition. Patients in treatment condition will follow twenty T-ScEmo sessions, of which five are online. Neuropsychological assessment and questionnaires directly after treatment (T1) and follow-up (T2, three to five months after treatment) will be compared to baseline assessment (T0). Ten TBI patients who receive T-ScEmo as regular rehabilitation care will be included as an extra control group. The main outcome measure will be the comparison of proxy rated behaviour between T0 and T2 on the Dysexecutive Questionnaire Social scales proxy version. Moreover, a compact barrier analysis is performed to facilitate the implementation of the treatment and to provide input for a process evaluation in the current study protocol.

Discussion: When T-ScEmo is proven effective based on the current study, this will be the first effectual evidence-based multi-faceted treatment for patients with social cognitive impairments caused by various neurological disorders. Implementation of this treatment is expected to contribute to better participation and better quality of life for patients and their significant others.

Trial registration: This study is prospectively registered in the database PaNaMa under number 202000479. Furthermore the study is registered in the database of clinicaltrials.gov (Study Details | Improving Social Cognition and Social Behaviour in Various Brain Disorders | ClinicalTrials.gov) under identifier NCT06330298.

Background: Ischemic stroke is a common chronic disease worldwide and is correlated with a high disability rate. Sarcopenia is considered a key factor in the disablement process. Limited evidence of sarcopenia in acute ischemic stroke is available. The aim of this study was to investigate the effect of sarcopenia on the prognosis of patients with acute ischemic stroke.

Methods: A prospective cohort study was conducted and included patients who were diagnosed with acute ischemic stroke between August 2020 and May 2021. A modified Poisson regression was applied to determine the relative risk (RR) for the change in modified Rankin Scale (mRS) score and allow adjustment for confounders. The modified Poisson regression was used to identify associations between sarcopenia, and multiple linear regression analyses were used to assess the effect of sarcopenia on the Barthel Index (BI) and stroke-specific quality of life (SSQOL). The generalized linear mixed model was used to investigate the effect of sarcopenia on prognosis at 1, 3 and 6 months. Cox regression proportional risk model was used to analyze the effect of sarcopenia on readmission in patients with acute ischemic stroke.

Results: The prevalence of sarcopenia was 39.83% among the 118 enrolled acute ischemic stroke patients (aged 64.98 ± 11.053 years; 72.88% males). Modified Poisson regression showed that a poor prognostic outcome occurred in sarcopenia patients (relative risk [RR] = 3.021, 95% CI: 1.621-5.633; P = 0.001). Even after adjusting for confounders, sarcopenia still was a risk predictor of the increase of mRS (RR = 2.149, 95% CI: 1.045-4.420; P = 0.038). And sarcopenia was positively correlated with BI and SSQOL with or without adjustment for confounding factors (P < 0.01). Patients with sarcopenia in mild acute ischemic stroke exhibit worse prognoses compared to those without sarcopenia. (t = 3.128, P = 0.002). Cox regression risk ratio model showed that sarcopenia was a predictor of readmission within 6 months after mild ischemic stroke (hazard ratio [HR] = 3.361, 95% CI: 1.277-8.848; P = 0.014). Sarcopenia remained an independent risk factor for mild acute ischemic stroke readmission after adjusting for confounders.

Conclusions: Sarcopenia has a high prevalence in mild acute ischemic stroke patients. Sarcopenia is an independent risk factor for poor outcomes following mild acute ischemic stroke and contributes to high rates of readmission. These findings may be useful for selecting therapeutic strategies for mild acute ischemic stroke patients with sarcopenia.

Background: Leigh syndrome (LS) is an inherited form of mitochondrial encephalopathy associated with various gene mutations of the oxidative phosphorylation system, typically occurring in infancy or early childhood and resulting in disability or even death. However, few late-onset cases have been reported.

Objective: The objective of this case report was to investigate the radiological and clinical characteristics of an adult patient diagnosed with Leigh syndrome.

Case presentation: This article describes a patient who presented with recurrent generalized seizures, peripheral neuropathy and hypertension and was ultimately diagnosed with Leigh syndrome with a mitochondrial gene variant, c.9176T > C (p.Leu217Pro), in 20,315 of the MT-ATP6 gene. Here, we discuss the possible pathogenesis of its clinical manifestations according to the related literature and review the current therapeutic approaches and prognosis of LS.

Conclusion: A possible diagnosis of LS should be taken into consideration when patients with characteristic neuroimaging findings of LS demonstrate recurrent seizures, peripheral neuropathy, or hypertension, and genetic analysis should be carried out for differential diagnosis.

Objective: To report a case of Corynebacterium striatum meningitis and conduct a comprehensive literature review to determine the clinical presentation, microbiology, and treatment approaches for these patients.

Materials and methods: A 75-year-old male patient presented with headache and fever; however, bacterial cultures of cerebrospinal fluid (CSF) yielded negative results. Metagenomic next-generation sequencing (mNGS) of CSF subsequently identified Corynebacterium striatum meningitis as the causative agent for meningitis. A systematic search was performed across various databases encompassing systematic reviews, cohort studies, case series, and case reports involving patients diagnosed with Corynebacterium striatum meningitis regardless of age. Clinical presentation characteristics and the most frequently employed diagnostic technologies were obtained. A narrative summary of the findings is presented.

Results: Corynebacterium striatum meningitis patients do not exhibit any specific age or sex predisposition or distinctive symptoms or signs. In patients with Corynebacterium striatum meningitis, CSF tests typically reveal an increased number of white blood cells (predominantly polymorphonuclear cells), elevated protein levels, and decreased glucose levels. Notably, the prevalence of antibiotic-resistant strains of Corynebacterium striatum has increased in recent years, leading to a gradual rise in antibiotic treatment failure rates. It is predicted that by 2030, vancomycin may be the sole effective drug available.

Conclusion: The possibility of Corynebacterium striatum infection should be considered during clinical diagnosis and laboratory testing procedures for bacterial meningitis. mNGS can serve as a supplementary gold standard in the diagnosis of bacterial meningitis, effectively enhancing the detection rate of rare pathogens.

Background: This investigation is designed to evaluate the effects of rTMS and its varying stimulation parameters and target sites on the therapeutic outcomes for post-stroke lower limb motor impairment and balance, with the objective of pinpointing stimulation locations and parameters that are both reasonable and applicable in clinical practice.

Materials and methods: An exhaustive search was carried out across the PubMed, MEDLINE, Embase, CENTRAL, and Web of Science databases to identify RCTs that assessed the effectiveness of rTMS in the treatment of lower limb motor impairment following a stroke. Meta-analysis was performed usingR statistical environment (V.4.2.2, www.r-project.org ). The review period encompassed the interval from the databases' origination through to February 18, 2024.

Results: Research reveals that applying rTMS to the unaffected motor cortex markedly enhances gait speed in stroke patients,exhibiting a significant effect (SMD: 1.117, 95% CI:0.40, 1.82, I² = 0.0%). rTMS sessions comprising 1000-1500 pulses (SMD: 0.92, 95% CrI:0.63, 1.21, I² = 42%, six studies), with a total session count ≥ 10 (SMD: 0.85, 95% CrI:0.53, 1.18, I2 = 54.1%, six studies), and high-frequency rTMS (SMD: 0.83, 95% CrI:0.34, 1.09, I² = 46.3%, three studies) exhibit significant efficacyin improving lower limb balance and gait post-stroke.

Conclusions: The research indicates that rTMS has been instrumental in enhancing the post-stroke prognosis for gait and limb balance. Nevertheless, the therapeutic efficacy of rTMS is subject to the diversity in stimulation locations and parameter settings.

Background: Optic neuritis (ON) is an inflammatory optic neuropathy characterized by acute vision loss. Primary anti-PLA2R-positive membranous nephropathy, an autoimmune disease, has been reported to be related to neurological diseases. However, the co-occurrence of ON and primary membranous nephropathy (PMN) has not been reported.

Case presentation: A 57-year-old male presented with acute bilateral vision loss. Laboratory tests indicated proteinuria, hypoalbuminemia, hyperlipidemia, and a significantly increased level of anti-phospholipase A2 receptor antibody (PLA2RAb). Orbital MRI revealed inflammatory changes in the posterior segments of both optic nerves. Following treatments with corticosteroids and immunosuppressants, there was a significant improvement in the patient's vision and proteinuria.

Conclusion: This case suggests that early identification and intervention for multisystem autoimmune damages are crucial for improving patient prognosis.