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\"With the burden of brain disorders increasing worldwide, there has been a resurgence of interest in techniques to control the brain and thereby improve its function. Yet how realistic are these expectations and what are the ethical implications? This book reviews the main techniques that can enable patients to use their brains for communication and control and doctors to modify brain function. It explains how paralysed patients may be helped through brain reading, how brain stimulation can help to improve Parkinson's disease and certain mental disorders and how patients can be trained to regulate their own brain activity through neurofeedback. Brain Control situates the application of these techniques within ethical and legal debates on the principles of autonomy and fairness, and suggests ethical standards for their future development\"-- Provided by publisher.

Background Parkinson’s disease (PD) is a progressive neurodegenerative disorder characterised by both motor and nonmotor symptoms. Galectin-3, a protein involved in the regulation of inflammatory responses, has emerged as a potential contributor to neurodegenerative processes. This study aimed to measure serum and urinary galectin-3 levels in patients with PD and to evaluate the associations of this biomarker with disease stages and clinical symptoms. Methods The present cross-sectional study included 30 PD patients and 29 healthy controls. Galectin-3 levels in serum and urine samples were measured via Enzyme-Linked Immunosorbent Assay (ELISA). The clinical data recorded included demographic information, Hoehn and Yahr (H&Y) stage, Unified Parkinson’s Disease Rating Scale (UPDRS) motor score, nonmotor symptom score (NMS), and total dopaminergic treatment dose parameters. Multivariate analyses were adjusted for age and sex due to demographic differences between groups. Results Serum galectin-3 optical density (OD) levels (0.2 [0.1–1.4]) and urinary galectin-3 OD levels (0.2 [0.1–0.6]) were significantly higher in PD patients than in controls ( p  < 0.050). Serum and urinary galectin-3 concentration (C) values were also elevated in the PD group. A moderate negative correlation was observed between serum galectin-3 levels and both the H&Y stage ( r = − 0.418, p  = 0.021) and the UPDRS motor score ( r = − 0.541, p  = 0.002). After adjusting for age and sex, serum galectin-3 C remained independently associated with motor severity. ROC analysis revealed that serum galectin-3 levels demonstrated promising diagnostic performance, with high specificity and sensitivity in distinguishing patients with PD from healthy controls (AUC = 0.716, p  = 0.001). The serum/urine galectin-3 concentration ratio also showed significant discriminative value (AUC = 0.722, p  = 0.035). Conclusion Our findings suggest that elevated levels of galectin-3 in serum and urine are associated with Parkinson’s disease and may reflect underlying neuroinflammatory mechanisms contributing to its pathophysiology. The diagnostic performance of galectin-3 markers remained robust even after adjusting for age and sex. However, the strict exclusion criteria and the age imbalance between groups may limit the generalizability of these results to broader clinical populations. Therefore, these findings should be considered exploratory and require confirmation through larger, longitudinal studies to determine their diagnostic and prognostic utility.

Background With advancements in acute stroke treatments, more patients receive timely interventions and survive. However, during the recovery phase, stroke patients often experience a range of coexisting symptoms, which contribute to significant physical and psychological distress and hinder rehabilitation outcomes, thereby exacerbating their symptom burden. Addressing the symptom burden and implementing precise management strategies are therefore essential to improve the quality of life and rehabilitation outcomes of convalescent stroke patients. This study aimed to identify the symptom burden profiles of convalescent stroke patients and explore the factors influencing these profiles. Methods This was a cross-sectional study. A total of 330 convalescent stroke patients who were hospitalized in a tertiary hospital in Guangdong Province were selected as survey subjects. A demographic and clinical characteristics questionnaire, the Symptom Experience Scale for Stroke Survivors, the Fear of Progression Questionnaire-Short Form, and the Acceptance of Illness Scale were used for the investigation. Latent profile analysis of symptom burden in convalescent stroke patients was conducted, and the factors influencing the latent profiles were explored by unordered logistic regression analysis. Results The symptoms of convalescent stroke patients are complex, with the top five common symptoms being: fatigue (88.2%), moodiness (79.4%), unilateral limb weakness (79.1%), slower response (70.0%), and uncoordinated movement (68.8%). Symptom burden of convalescent stroke patients was divided into three categories: low symptom burden group (40.7%), moderate symptom burden group (36.8%), and high symptom burden - somatic discomfort group (22.5%). The unordered logistic regression analysis indicated that age, daily caregiver status, self-care ability, fear of disease progression, and illness acceptance were influential factors across different potential categories. Conclusion There was heterogeneity in symptom burden among convalescent stroke patients. Clinicians should tailor interventions to the distinct symptom profiles and influencing factors of stroke patients in the recovery period. Targeted interventions should focus on elderly patients and those who experience fear of disease progression, as this may be an effective approach to alleviate symptoms in the moderate symptom burden group and the high symptom burden - somatic discomfort group.

Objective This study aims to investigate the causal relationship between Mitochondrial DNA (mtDNA) copy number and several common neurodegenerative diseases (NDs). Methods We conducted a bidirectional two-sample Mendelian randomization (MR) analysis using data from genome-wide association studies (GWAS) as instrumental variables (IVs). After screening for relevance and potential confounders, we estimated the association between mtDNA copy number and NDs, including Alzheimer’s disease (AD), Parkinson’s disease (PD), Amyotrophic lateral sclerosis (ALS), and Multiple sclerosis (MS). Additionally, we validated our findings using GWAS data on mtDNA copy number from Longchamps et al., sourced from the Genetics Epidemiology Consortium and the UK Biobank (UKB) aging study cohort. Results A GWAS analysis of 395,718 UKB participants found no significant association between mtDNA copy number and the risk of NDs, including AD (OR = 0.956, P  = 0.708), PD (OR = 1.223, P  = 0.179), ALS (OR = 0.972, P  = 0.374), and MS (OR = 0.932, P  = 0.789). Similarly, reverse MR analysis revealed no significant relationship between genetic predictions of NDs and mtDNA copy number: AD (OR = 0.987, P  = 0.062), PD (OR = 0.997, P  = 0.514), ALS (OR = 0.974, P  = 0.706), and MS (OR = 1.003, P  = 0.181). Conclusion Although mitochondrial dysfunction is implicated in the pathogenesis of NDs, no clear evidence supports a causal role for mtDNA copy number. The relationship between mtDNA copy number and NDs is likely mediated by more complex molecular regulatory mechanisms. Further research is required to elucidate these intricate interactions.

Nitromidazole antibiotics, exemplified by metronidazole and ornidazole, have been reported to trigger a spectrum of adverse effects. These encompass ataxia, hearing loss, visual impairment, psychomotor dysfunction, intellectual impairment, and epileptic seizures (Rinsho Shinkeigaku 64:637-641, 2024). Nevertheless, cases of involuntary limb tremors have been scarcely documented. Ornidazole, the most recent derivative within this class, boasts a longer half - life and is infrequently linked to limb tremors. This article reports a 63-year-old female patient who developed progressive limb tremors following long-term, high-dose administration of ornidazole, with symptoms gradually alleviating after discontinuation of the drug.

The COVID-19 pandemic and increased demands for neurologists have inspired the creation of remote, digitalized tests of neurological functions. This study investigates two tests from the Neurological Functional Tests Suite (NeuFun-TS) smartphone application, the “Postural Sway” and “Pronator Drift” tests. These tests capture different domains of postural control and motoric dysfunction in healthy volunteers ( n  = 13) and people with neurological disorders (n = 68 relapsing–remitting multiple sclerosis [MS]; n  = 21 secondary progressive MS; n  = 23 primary progressive MS; n  = 13 other inflammatory neurological diseases; n  = 21 non-inflammatory neurological diseases; n  = 4 clinically isolated syndrome; n  = 1 radiologically isolated syndrome). Smartphone accelerometer data was transformed into digital biomarkers, which were filtered in the training cohort (~ 80% of subjects) for test–retest reproducibility and correlations with subdomains of neurological examinations and validated imaging biomarkers. The independent validation cohort (~ 20%) determined whether biomarker models outperformed the best single digital biomarkers. Postural sway acceleration magnitude in the eyes closed and feet together stance demonstrated the highest reliability (ICC = 0.706), strongest correlations with age (Pearson r <= 0.82) and clinical and imaging outcomes (r <= 0.65, p  < 0.001) and stronger predictive value for sway-relevant neurological disability outcomes than models that aggregated multiple biomarkers (coefficient of determination R 2  = 0.46 vs 0.38). The pronator drift test only captured cerebellar dysfunction, had less reproducible biomarkers, but provided additive value when combined with postural sway biomarkers into models predicting global scales of neurological disability. In conclusion, a simple 1-min postural sway test accurately measures body oscillations that increase with natural aging and differentiates them from abnormally increased body oscillations in people with neurological disabilities.

Background Autoimmune encephalitis associated with anti-GluK2 antibodies is a recently identified condition, typically characterized by cerebellar ataxia. This case report presents a unique clinical manifestation involving involuntary movements and emotional dysregulation, expanding the known phenotype spectrum. Case presentation A 60-year-old woman presented with a two-year history of involuntary movements predominantly affecting her lower limbs and facial muscles, occasionally accompanied by hysterical shouting. Initial investigations revealed coexisting multiple myeloma (MM) and anti-GluK2 antibody positivity. Following MM-specific therapy, including bortezomib, cyclophosphamide, and dexamethasone, the patient's symptoms resolved, and her serum anti-GluK2 antibody titers decreased significantly. Conclusions This case suggests that involuntary movements and psychiatric symptoms may represent novel phenotypes of anti-GluK2 antibody-associated autoimmune encephalitis. The findings underscore the importance of recognizing the diverse clinical presentations of this rare condition and prompt further research into its underlying mechanisms.

Background and aim Using a network meta-analysis, this study evaluates the clinical efficacy and safety of different types of stem cell therapy in regard to the recovery of neurological function, motor function, and daily living ability in ischemic stroke patients. Methods A computerized search of the Cochrane Library, PubMed, Web of Science, Google Scholar, CNKI, and Wanfang Database was performed to collect randomized controlled clinical studies published from the time of library construction to December 2024, on the use of stem cells to improve function in patients with ischemic stroke. Results A total of 19 studies and 1055 patients were included, comprising five stem cell types: bone marrow mononuclear cells (BMMNC), bone marrow mesenchymal stem cells (BMSC), progenitor cells (PC), peripheral blood stem cells (PBSC), and umbilical cord blood mesenchymal stem cells (UBMSC). A network meta-analysis showed that, in terms of National Institute of Health Stroke Scale (NIHSS) scores, the ranked results of different stem cell transplants were: UBMSC [69.4%] > PBSC 29.2%] > BMSC [0.8%] > PC [0.6%] > BMMNC [0.0%] > CRT [0.0%]. In terms of Modified Rankin Scale (mRS) scores, the ranked results of different stem cell transplants were: BMMNC [66.8%] > PBSC [31.7%] > PC [1.3%] > BMSC [0.2%] > CRT [0%]. In terms of Modified Barthel Index (MBI) scores, the ranked results of different stem cell transplants were: BMMNC [56.3%] > PC [34.2%] > BMSC [9.5%] > CRT [0%]. In terms of Fugl-Meyer Assessment (FMA) scores, the results of the ranking of different stem cell transplants were: BMMNC [79.3%] > BMSC [17.3%] > UBMSC [3.4%] > CRT [0%]. Conclusion UBMSC had the best efficacy in repairing neurological function in patients with ischemic stroke. BMMNC had the best efficacy in improving motor function and daily living ability in patients with ischemic stroke. BMMNC had a superior overall effect.

Behçet’s disease (BD) is a multi-system recurrent inflammatory disease. Neuro-Behçet’s disease (NBD), as a severe and rare manifestation of BD, is frequently misdiagnosed in its early stages. Pediatric NBD poses diagnostic challenges due to its insidious onset, highlighting the critical role of neuroimaging. This report describes a pediatric patient with atypical early clinical manifestations and magnetic resonance imaging (MRI) findings. The patient initially presented without mucocutaneous lesions despite persistently elevated inflammatory markers. MRI revealed prolonged T1/T2 signals in the posterior horns of the lateral ventricles. During years of follow-up, the patient gradually developed characteristic BD manifestations while MRI showed progressive intracranial lesions, eventually presenting typical NBD imaging features concurrently with cerebral venous thrombosis. This atypical case highlights the necessity of early multimodal MRI and close clinical monitoring of focal lesions in the posterior horns of the lateral ventricles. When infectious causes are excluded, NBD should be considered. The rarity of this case improves clinicians’ ability to diagnose early NBD through MRI interpretation. Clinical trial This case report did not involve a clinical trial.

Background Parkinson’s disease (PD), a prevalent neurodegenerative disorder in the aging population, poses significant challenges in unraveling its pathogenesis and progression. A key area of investigation is the disruption of oncological metabolic networks in PD, where diseased cells display distinct metabolic profiles compared to healthy counterparts. Of particular interest are Purine Metabolism Genes (PMGs), which play a pivotal role in nucleic acid synthesis. Methods In this study, bioinformatics analyses were employed to identify and validate PMGs associated with PD. A set of 20 candidate PMGs underwent differential expression analysis. GSEA and GSVA were conducted to explore the biological roles and pathways of these PMGs. Lasso regression and SVM-RFE methods were applied to identify hub genes and assess the diagnostic efficacy of the nine PMGs in distinguishing PD. The correlation between these hub PMGs and clinical characteristics was also explored. Validation of the expression levels of the nine identified PMGs was performed using the GSE6613 and GSE7621 datasets. Results The study identified nine PMGs related to PD: NME7, PKM, RRM2, POLR3 C, POLA1, PDE6 C, PDE9 A, PDE11 A, and AMPD1. Biological function analysis highlighted their involvement in processes like neutrophil activation and immune response. The diagnostic potential of these nine PMGs in differentiating PD was found to be substantial. Conclusions This investigation successfully identified nine PMGs associated with PD, providing valuable insights into potential novel biomarkers for this condition. These findings contribute to a deeper understanding of PD’s pathogenesis and may aid in monitoring its progression, offering a new perspective in the study of neurodegenerative diseases.