European Neurology最新文献

Introduction: Migraine is a neurovascular disorder and is clinically characterized by episodic attacks of mild to severe headaches. Due to the involvement of multiple environmental and genetic factors, it has become a much more complex neurological condition to understand. Apart from the environmental variables, a plethora of genes have been implicated, and one such example is ESR1. The present study was focused to find out the association of two important polymorphisms, namely, PvuII and XbaI of the ESR1 with migraine in the population of Jammu and Kashmir (UT).

Methods: The PCR-RFLP genotyping method was utilized to detect PvuII and XbaI polymorphism, and the result was confirmed by statistical analysis.

Results: Although we did not find a signification association of ESR-PvuII polymorphism with migraine susceptibility {OR: 1.14 at 95% CI [0.76-1.71] (p value 0.5)}, a strong association was found with the clinical subtype of migraine; migraine with aura (MA) {OR: 2.014 at 95% CI [1.069-3.792] (p value 0.028)}. Furthermore, a significant association of ESR-XbaI polymorphism was observed with migraine {OR: 1.908 at 95% CI [1.252-2.907] (p value 0.002) and its both clinical subtypes; migraine without aura (MO) {OR: 1.870 at 95% CI [1.186-2.950] (p value 0.006)} and MA {OR: 2.014 at 95% CI [1.069-3.792] (p value 0.028)}.

Conclusion: In conclusion, ESR1-XbaI polymorphism is significantly associated with migraine risk including both subtypes (MA and MO) in the North Indian population of Jammu.

A solitary pontine lesion (SPL) is a single brainstem lesion on the trigeminal nerve pathway without any other central nervous system lesion. This research aimed to investigate the demographic and clinical features of nonpainful TNO patients with SPL and identify the most frequently affected anatomical areas using lesion mapping techniques. Demographic and clinical features were retrospectively reviewed from the patients' charts. Brain lesions were mapped using MRIcroGL software. The study included 6 patients (three females and three males) with an SPL. The median age of the patients was 57 (range: 46-68) years. Cranial MRI displayed lesions in the dorsolateral pons and the cerebellar peduncle. The lesion mapping revealed that the lesions were on the trigeminal nerve pathway. SPL is an uncommon cause of TNO. Nonpainful SPL patients have demographic, clinical, and radiological features similar to those of painful SPL patients. The lesion mapping showed that the same brainstem areas are affected in painful and nonpainful SPL patients.

Introduction: Many clinical studies reported the coexistence of Alzheimer's disease (AD) and multiple sclerosis (MS), but the common molecular signature between AD and MS remains elusive. The purpose of our study was to explore the genetic linkage between AD and MS through bioinformatic analysis, providing new insights into the shared signatures and possible pathogenesis of two diseases.

Methods: The common differentially expressed genes (DEGs) were determined between AD and MS from datasets obtained from Gene Expression Omnibus (GEO) database. Further, functional and pathway enrichment analysis, protein-protein interaction network construction, and identification of hub genes were carried out. The expression level of hub genes was validated in two other external AD and MS datasets. Transcription factor (TF)-gene interactions and gene-miRNA interactions were performed in NetworkAnalyst. Finally, receiver operating characteristic (ROC) curve analysis was applied to evaluate the predictive value of hub genes.

Results: A total of 75 common DEGs were identified between AD and MS. Functional and pathway enrichment analysis emphasized the importance of exocytosis and synaptic vesicle cycle, respectively. Six significant hub genes, including CCL2, CD44, GFAP, NEFM, STXBP1, and TCEAL6, were identified and verified as common hub genes shared by AD and MS. FOXC1 and hsa-mir-16-5p are the most common TF and miRNA in regulating hub genes, respectively. In the ROC curve analysis, all hub genes showed good efficiency in helping distinguish patients from controls.

Conclusion: Our study first identified a common genetic signature between AD and MS, paving the road for investigating shared mechanism of AD and MS.

Introduction: The aim of this study was to systematically explore progressive resistance training (PRT) effects in Parkinson's disease (PD).

Methods: Eligible literature was systematically searched from five electronic databases (PubMed, Web of Science, Ovid, Wanfang, and China National Knowledge Infrastructure) from their inception to February 2022. Included studies were selected based on strict eligibility criteria. RevMan 5.3 software was used for statistical analysis.

Results: A total of 14 studies with 761 PD patients were selected for eligibility in this systematic review and meta-analysis. A total of 383 performed trunk or upper or lower extremity PRT and 378 underwent balance training, modified fitness counts, or did not change their lifestyle. The results demonstrated positive PRT effect on freezing of gait (standardized mean difference [SMD] = -0.55, 95% CI = -0.95 to -0.16, p = 0.006), muscular strength (SMD = 1.9, 95% CI = 0.55-3.24, p = 0.006), and quality of life (SMD = -0.86, 95% CI = -1.66 to -0.06, p = 0.04) in adults with PD compared with other training programmes but not for gait velocity, stride length, timed up and go test, and Berg Balance Scale.

Conclusions: This meta-analysis revealed that PRT had positive effects on freezing of gait, muscle strength, and improved quality of life during rehabilitation in PD patients.

Introduction: The purpose of this study was to analyze IL-33 maybe as a biomarker especially with respect to intrathecal immunoglobulin G (IgG) synthesis which was involved in the immune-mediated process in the demyelinating disease of the central nervous system.

Methods: We aimed to determine the risk association of the serum and CSF levels of IL-33 in aquaporin-4 (AQP4)+neuromyelitis optica spectrum disorder (NMOSD) patients and myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) patients compared with the control group. Levels of inflammatory (IL-2, IL-4, IL-6, and IL-10) markers and QAlb, the IgG index, and 24-h IgG synthesis rate were assessed in 28 AQP4+NMOSD patients and 11 MOGAD patients. Disease severity was assessed using the Expanded Disability Status Scale (EDSS).

Results: The level of IL-33 in serum decreased first but then increased gradually in AQP4+NMOSD and MOGAD. The serum level of IL-2, IL-4, and IL-10 increased more significantly and decreased more rapidly after methylprednisolone treatment. The level of IL-33 in CSF increased progressively in AQP4+NMOSD and MOGAD, especially in MOGAD. The QAlb levels were increased significantly in the CSF of MOGAD patients and AQP4+NMOSD patients on the acute stage of the disease. The IgG index and 24-h IgG synthesis rate were also increased significantly in the CSF of two groups similarly.

Conclusions: Thus, we concluded that IL-33 may induce dysfunction of the blood-brain barrier and lead to intrathecal synthesis of immunoglobulin in the AQP4+NMOSD and MOGAD, especially in MOGAD. It maybe as a biomarker, at least in part, was involved in the demyelinating diseases of the central nervous system.

Introduction: Subarachnoid hemorrhage (SAH) is a severe cerebrovascular event with high mortality and disability rate. Neuroinflammation is involved in the brain injury after SAH, but the exact association between SAH progression and peripheral blood inflammatory factors is unknown. Therefore, to determine the relationship between inflammatory factors and the prognosis of SAH, we performed a meta-analysis.

Method: A systematic literature review was conducted in PubMed, Embase, and the Cochrane Library. Studies comparing the relationship between inflammatory factors (C-reactive protein [CRP], interleukin-6 [IL-6], interleukin-10 [IL-10], and tumor necrosis factor [TNF-α]) and prognosis of SAH were included in the study. A random-effects meta-analysis was conducted based on mRS, GOS, and the occurrence of cerebral vasospasm, delayed cerebral ischemia, and delayed ischemic neurologic deficits. Sensitivity analysis was performed using the leave-one-out method. The Newcastle-Ottawa Scale (NOS) for case-control studies was used to assess the quality of included studies. For continuous variables, we calculated the mean difference with a 95% confidence interval (CI).

Results: 1,469 patients from 18 case-control studies met the inclusion criteria. The results found that patients in the good outcome group had significantly lower CRP levels than those in the poor outcome group (SMD: -1.15, 95% CI: -1.64 to -0.66, p < 0.00001, I2 = 87%), and peripheral IL-6 levels were significantly lower in SAH patients with the good functional outcome than those with the poor functional outcome (SMD: -0.99, 95% CI: -1.48 to -0.51, p < 0.0001, I2 = 88%). As for IL-10 (SMD: -0.28, 95% CI: -0.97 to 0.42, p = 0.43, I2 = 88%) and TNF-α (SMD: -0.40, 95% CI: -0.98 to 0.19, p = 0.18, I2 = 79%), due to the small number of studies, heterogeneity, and uncontrollable factors, robust conclusions cannot be drawn.

Conclusion: SAH patients with good prognoses have significantly lower peripheral CRP and IL-6 levels. In addition, due to the small number of studies, heterogeneity, and uncontrollable factors, robust conclusions cannot be drawn for IL-10 and TNF-α. More high-quality studies are needed in the future to provide more specific recommendations for the clinical practice of inflammatory factors.

Introduction: Sleep disorders are common in Parkinson's disease (PD) and significantly impact quality of life. Herein, we surveyed the incidence and severity of sleep disorders in Chinese PD patients and observed their relationship with dopaminergic drugs.

Methods: We collected the demographic and disease information of 232 PD patients. The incidence and severity of sleep disorders were surveyed with the Parkinson's disease sleep scale (PDSS) Chinese version. Data on dopaminergic drug intake were collected and converted to levodopa equivalent doses (LED).

Results: The average total score of PDSS in 232 patients was 119.3 ± 19.7. There was a significant difference in PDSS scores between groups classified by the Hoehn-Yahr (H&Y) stage, but not between the groups classified by the type of dopaminergic drugs. Stepwise regression analysis revealed that the LED of dopaminergic drugs taken before bedtime (p < 0.00), LED of dopaminergic drugs taken over a 24-h period (p < 0.00), and scores of the Hamilton Rating Scale for Depression (HAMD) (p = 0.01) were determinants of PDSS.

Conclusion: Sleep disorders in PD patients may be multifactorial. High dosage of dopaminergic drugs taken prior to sleep, daily total high dosage of dopaminergic drugs, and depression exert negative effects on subjective sleep. The timing and dosage of dopaminergic drugs taken before bedtime should be considered in PD management.

Background: Futile reperfusion (FR) is becoming an urgent issue for acute ischemic stroke patients who underwent endovascular treatment (EVT). Although the recanalization rate has improved after EVT, it is far from translating to increased tissue reperfusion and functional independence.

Summary: Many underlying mechanisms including the "no-reflow" phenomenon, poor collateral flow, venous dysfunction, and inflammation were proposed, but the pathophysiology of FR is still unclear. Clinically, reliable predictors are still yet to be identified, and ongoing trials on shortening the time delay and cytoprotection may provide novel ideas for interventions of FR.

Key messages: This review will summarize the latest advances in FR and hopefully shed light on potential interventions.

Background: The no-reflow phenomenon refers to a failure to restore normal cerebral microcirculation despite brain large artery recanalization after acute ischemic stroke, which was observed over 50 years ago.

Summary: Different mechanisms contributing to no-reflow extend across the endovascular, vascular wall, and extravascular factors. There are some clinical tools to evaluate cerebral microvascular hemodynamics and represent biomarkers of the no-reflow phenomenon. As substantial experimental and clinical data showed that clinical outcome was better correlated with reperfusion status rather than recanalization in patients with ischemic stroke, how to address the no-reflow phenomenon is critical. But effective treatments for restoring cerebral microcirculation have not been well established until now, so there is an urgent need for novel therapeutic perspectives to improve outcomes after recanalization therapies.

Conclusion: Here, we review the occurrence of the no-reflow phenomenon after ischemic stroke and discuss its impact, detection method, and therapeutic strategies on the course of ischemic stroke, from basic science to clinical findings.