Current Opinion in Neurology最新文献

{"title":"The role of brain MRI in autoimmune encephalitis.","authors":"Tim J Hartung, Joseph Kuchling, Carsten Finke","doi":"10.1097/WCO.0000000000001484","DOIUrl":"10.1097/WCO.0000000000001484","url":null,"abstract":"<p><strong>Purpose of review: </strong>Brain MRI is central to the diagnostic work-up of autoimmune encephalitis (AE). This review summarizes established patterns on routine MRI sequences across antibody-defined AE types and highlights emerging quantitative and network-based approaches aimed at improving sensitivity, phenotypic stratification, and prognostication.</p><p><strong>Recent findings: </strong>Conventional MRI reveals syndrome-associated patterns that can support diagnosis in several AE types, including medial temporal involvement in LGI1, CASPR2, and GABA(B) receptor encephalitis; multifocal cortico-subcortical lesions in GABA(A) receptor encephalitis, and radial perivascular enhancement in GFAP astrocytopathy. Longitudinal studies show that regional and global atrophy better reflect cumulative injury and clinical outcome than acute lesions in entities such as NMDA receptor encephalitis or IgLON5 antibody-mediated disease. Basic quantitative measures derived from routine sequences can detect microstructural abnormalities in normal-appearing tissue. Advanced techniques including quantitative MRI, diffusion tensor imaging, and resting-state functional MRI demonstrate widespread structural and functional network disruption beyond visible lesions. Translational animal studies further link imaging changes to antibody-mediated synaptic dysfunction.</p><p><strong>Summary: </strong>Conventional MRI remains indispensable for differential diagnosis and pattern recognition in AE. Pragmatic approaches such as volumetry and basic quantitative metrics are closest to clinical implementation, whereas advanced techniques require further standardization and validation. Together, these developments position MRI to evolve from a primarily diagnostic tool toward precision phenotyping, prognosis, and longitudinal monitoring in AE.</p>","PeriodicalId":11059,"journal":{"name":"Current Opinion in Neurology","volume":" ","pages":"332-340"},"PeriodicalIF":4.4,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13152077/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147632792","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"PET imaging of microglial pathology in multiple sclerosis.","authors":"Olli Hartiala, Joel Tuomaala, Laura Airas","doi":"10.1097/WCO.0000000000001490","DOIUrl":"10.1097/WCO.0000000000001490","url":null,"abstract":"<p><strong>Purpose of review: </strong>This review evaluates recent advances in the development of translocator protein (TSPO) - and purinergic receptor-binding PET tracers and highlights the capacity of TSPO-PET-imaging to capture microglial activation across multiple regions of interest in multiple sclerosis brain. We discuss the added value of integrating PET-derived measures with fluid and metabolic biomarkers, as well as their successful application in recent clinical trials.</p><p><strong>Recent findings: </strong>Recent research highlights PET as a robust molecular imaging tool for detecting microglial activation and implicates dysregulated microglial activity as a key driver of smouldering multiple sclerosis pathology. PET-detectable microglial activation appears not merely as a secondary response to neuroaxonal injury but is increasingly recognized as an integral inflammatory component of ongoing pathological processes that lead to future brain atrophy and clinical deterioration.</p><p><strong>Summary: </strong>Recent advances establish PET as an essential research tool for evaluating the presence of smouldering inflammation in MS brain not detectable using MRI. Furthermore, PET-based methods have proven suitable for measuring glial responses to potentially neuroprotective therapies currently under development.</p>","PeriodicalId":11059,"journal":{"name":"Current Opinion in Neurology","volume":" ","pages":"240-246"},"PeriodicalIF":4.4,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13152060/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147632824","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Chronobiology and cluster headache: insights into a hypothalamic disorder.","authors":"Caroline Ran, Stefan Spulber, Andrea Carmine Belin","doi":"10.1097/WCO.0000000000001466","DOIUrl":"10.1097/WCO.0000000000001466","url":null,"abstract":"<p><strong>Purpose of review: </strong>Cluster headache is a disorder which has been shown to have both a circadian and a circannual pattern. This review gives an overview of the chronobiology of cluster headache summarizing recent findings on structural variations with a focus on the hypothalamus and the implication of the molecular clock and circadian and circannual variations in gene expression.</p><p><strong>Recent findings: </strong>Recent imaging studies using high-resolution structural and functional MRI have highlighted subtle hypothalamic alterations in cluster headache, specifically at the microstructural and connectivity level rather than clear macrostructural changes. Diffusion-based measures reveal altered fractional anisotropy and diffusivity in the hypothalamus, suggesting modified neuronal connectivity that may relate to attack frequency. In parallel, experimental data suggest significant differences in pain perception between day and night, which correlate to circadian oscillations of gene expression, and several drugs used for cluster headache have been reported to alter the molecular clock.</p><p><strong>Summary: </strong>The striking circadian and circannual phenotype of cluster headache opens for the possibility of clock-modulating therapy. The potential to pharmacologically target the molecular clock mechanism is supported by experimental data from mice demonstrating substantial effects of standard cluster headache treatments on the molecular clock.</p>","PeriodicalId":11059,"journal":{"name":"Current Opinion in Neurology","volume":" ","pages":"326-331"},"PeriodicalIF":4.4,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146218945","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The genetics of multiple sclerosis: an updated perspective.","authors":"Gianmarco Bellucci, Sergio E Baranzini","doi":"10.1097/WCO.0000000000001478","DOIUrl":"10.1097/WCO.0000000000001478","url":null,"abstract":"<p><strong>Purpose of review: </strong>This review highlights the latest advances in the genetics of multiple sclerosis (MS). While earlier research defined the polygenic architecture of disease susceptibility, recent efforts have focused on unraveling the genetics of disease progression and dissecting the interplay between host genetics and environmental triggers.</p><p><strong>Recent findings: </strong>The discovery of the first locus associated with MS severity ( DYSF-ZNF638 ) revealed central nervous system (CNS)-intrinsic mechanisms of progression distinct from immune-mediated susceptibility. Recently, a multi-ancestry genome-wide association studies confirmed most of the previously identified susceptibility loci (most of which are involved in immune biology) and identified 4 additional associations. Mounting evidence on EBV-host genetic convergence highlights critical gene-environment interactions in disease etiopathogenesis.</p><p><strong>Summary: </strong>Advances in genetics are broadening the conceptual framework of MS pathogenesis, separating the immunological triggers of disease susceptibility from distinct, CNS-specific drivers of disease progression. Future efforts leveraging longitudinal, deeply phenotyped cohorts and functional validations will empower translational applications for prevention, prognostication, and treatment.</p>","PeriodicalId":11059,"journal":{"name":"Current Opinion in Neurology","volume":" ","pages":"217-223"},"PeriodicalIF":4.4,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147503361","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Progress in the mechanism of neuronal surface P antigen modulating hippocampal function and implications for autoimmune brain disease: Erratum.","authors":"","doi":"10.1097/WCO.0000000000001499","DOIUrl":"10.1097/WCO.0000000000001499","url":null,"abstract":"","PeriodicalId":11059,"journal":{"name":"Current Opinion in Neurology","volume":"39 3","pages":"385"},"PeriodicalIF":4.4,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147765310","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Headache care around the world: a review of access, equity, and system-level solutions.","authors":"Aynur Özge, Amr Hassan, Marcio Nattan Portes Souza","doi":"10.1097/WCO.0000000000001460","DOIUrl":"10.1097/WCO.0000000000001460","url":null,"abstract":"<p><strong>Purpose of review: </strong>Headache disorders are the leading cause of neurological disability globally, yet their management remains marked by profound inequities in access to diagnosis, evidence-based treatment, specialist care, and policy prioritization. This review examines current regional disparities in headache care delivery and highlights emerging system-level approaches aimed at reducing the global treatment gap.</p><p><strong>Recent findings: </strong>High-income regions in Western and Northern Europe, East Asia, and North America have developed advanced care models but continue to face inequities related to socioeconomic gradients, insurance coverage, and fragmented care pathways. In contrast, Eastern Europe, South and Central Asia, Latin America, and much of Africa experience substantial limitations in workforce capacity, diagnostic infrastructure, and medication availability, with population-based surveys indicating high prevalence but minimal health-system readiness. Transitional health systems, including Türkiye and the MENA region, demonstrate increasing awareness and partial integration of structured headache pathways, though coverage remains insufficient. Across regions, telemedicine, digital health tools, community-based initiatives, and workplace programs have shown promise in expanding access, reducing stigma, and improving continuity of care, while reinforcing the central role of primary care.</p><p><strong>Summary: </strong>Collectively, these developments signal a shift toward more coordinated and equity-oriented headache service models. Sustainable progress will require strengthened global collaboration, integration of AI-supported decision tools, expansion of cross-border registries and real-world data platforms, and the systematic inclusion of headache disorders within national noncommunicable disease frameworks to ensure high-quality care across diverse populations.</p>","PeriodicalId":11059,"journal":{"name":"Current Opinion in Neurology","volume":" ","pages":"304-312"},"PeriodicalIF":4.4,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146218888","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Autoimmune encephalitis and paraneoplastic neurologic syndrome: clinical diagnosis.","authors":"Soon-Tae Lee","doi":"10.1097/WCO.0000000000001489","DOIUrl":"10.1097/WCO.0000000000001489","url":null,"abstract":"<p><strong>Purpose of review: </strong>Autoimmune encephalitis (AE) and paraneoplastic neurologic syndromes (PNS) are increasingly identified as causes of rapidly progressive immune-mediated neurologic syndromes. This review outlines diagnostic strategies and identifies key clinical and laboratory features for the accurate differential diagnosis.</p><p><strong>Recent findings: </strong>The diagnostic flow includes taking a detailed history for autoimmune progression, recognizing pattern of antibody-associated symptoms, performing neuroanatomical localization, and application of diagnostic work-up consisting of MRI, CSF analysis, and antibody testing. Specific antibodies correlate with distinct syndromes, while seronegative AE remains a diagnostical challenge. Given the broad differential diagnosis, accurate symptom interpretation and the recognition of red flags are critical to preventing misdiagnosis. Ultimately, the correct application and interpretation of antibody assays are crucial.</p><p><strong>Summary: </strong>AE and PNS represent a heterogeneous group of immune-mediated CNS disorders requiring early diagnosis and timely immunotherapy. Multimodal diagnostic strategies integrating well-balanced clinical, radiological, and serological data are essential to minimize misdiagnosis.</p>","PeriodicalId":11059,"journal":{"name":"Current Opinion in Neurology","volume":" ","pages":"361-369"},"PeriodicalIF":4.4,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147615867","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"T cells in antibody-associated CNS autoimmunity: a mechanistic approach across autoimmune encephalitis and paraneoplastic disorders.","authors":"Frank Leypoldt, Alexander Scheffold, Carina Saggau","doi":"10.1097/WCO.0000000000001492","DOIUrl":"10.1097/WCO.0000000000001492","url":null,"abstract":"<p><strong>Purpose of review: </strong>Autoimmune encephalitis (AE), paraneoplastic neurological syndromes (PNS), and glial antibody-mediated disorders (for example, AQP4-NMOSD) are traditionally classified based on the target antigens of their respective autoantibodies. However, recent insights from immunogenomics, single-cell sequencing, and neuropathology indicate that T cell programs substantially influence disease initiation, localization, and chronicity. This review highlights three emerging dimensions of T-cell involvement - circulating exhausted-like helper T-cell memory, intrathecal T-B cooperation, and parenchymal tissue-resident cytotoxicity - that offer new perspectives on clinical and pathological features across these disorders.</p><p><strong>Recent findings: </strong>In AQP4-NMOSD, circulating exhausted-like CD4 + T cells may constitute a durable autoreactive memory reservoir capable of re-initiating plasmablast responses. In LGI1- and CASPR2-associated encephalitis, systemic and intrathecal CD4 + differentiation appears to support systemic antibody maturation and local plasmablast expansion, with emerging hints of some accompanying CD8 + -mediated tissue injury. In contrast, in PNS and intracellular antigen-associated AE, CD8 + T cell-mediated cytotoxicity dominates and is characterized by parenchymal CD8 + tissue-resident memory (TRM) signatures.</p><p><strong>Summary: </strong>These T-cell dimensions may provide a useful framework for understanding clinical paradoxes - such as relapse despite B-cell depletion, persistent memory dysfunction in IgG4-AE, and therapeutic inefficacy in PNS - and suggest opportunities for therapeutic strategies targeting exhausted T-cell memory, intrathecal cooperation, or TRM stability.</p>","PeriodicalId":11059,"journal":{"name":"Current Opinion in Neurology","volume":" ","pages":"351-360"},"PeriodicalIF":4.4,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147688818","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cognition in multiple sclerosis.","authors":"Ermelinda De Meo, Emilio Portaccio, Maria Pia Amato","doi":"10.1097/WCO.0000000000001481","DOIUrl":"10.1097/WCO.0000000000001481","url":null,"abstract":"<p><strong>Purpose of review: </strong>Cognitive dysfunction in multiple sclerosis (MS) has gained increasing attention over recent decades, reflecting its substantial effects on day-to-day functioning and the limited availability of targeted therapies. This review addresses contemporary advances in the role of cognition to detect disease progression, examines biological and MRI correlates of cognitive dysfunction, and summarizes the evidence for treatment effects.</p><p><strong>Recent findings: </strong>Cognitive changes can capture both acute relapse-related drops (including isolated cognitive relapses) and gradual decline consistent with progression independent of relapse activity (PIRA). Among fluid markers, serum neurofilament light chains relates to cognition mostly in relapsing disease, whereas glial fibrillary acidic protein seems to track global progression more than cognitive changes. Cerebrospinal fluid (CSF) candidate markers (CHI3L1, parvalbumin) and synaptic proteins (SNAP-25, neurogranin, β-synuclein) may help identifying patients at higher risk of cognitive decline. MRI demonstrates that grey-matter pathology best explains long-term cognitive trajectories while newer readouts (radiomics, quantitative susceptibility mapping of deep-grey nuclei, structural-functional disconnection and multiplex network indices, and choroid-plexus/glymphatic measures) add mechanistic and prognostic specificity beyond lesion burden and bulk atrophy. Data-driven cognitive phenotyping yields reproducible, biologically anchored profiles that outperform dichotomous impaired/preserved labels. Therapeutically, higher-efficacy disease-modifying therapies show the clearest association with preserved processing speed; cognitive rehabilitation, augmented in some settings by transcranial direct-current stimulation, produces additional gains.</p><p><strong>Summary: </strong>Routine assessment and monitoring of cognitive functions should be embedded in MS care to detect relapse-related changes and progressive decline. Identifying fluid and MRI biomarkers of cognitive dysfunction may help individuate novel targets and specific treatments.</p>","PeriodicalId":11059,"journal":{"name":"Current Opinion in Neurology","volume":" ","pages":"247-252"},"PeriodicalIF":4.4,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13152055/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147644567","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Oxidative and nitrosative damage in multiple sclerosis.","authors":"Tim Prozorovski, Sven G Meuth, Hans-Peter Hartung, Carsten Berndt","doi":"10.1097/WCO.0000000000001482","DOIUrl":"10.1097/WCO.0000000000001482","url":null,"abstract":"<p><strong>Purpose of review: </strong>It is increasingly recognized that reactive oxygen and nitrogen species (ROS and RNS) are not only damaging molecules, but also essential signaling molecules regulating functions on organellar, cellular, organ, and organism levels. Nevertheless, damaging capacity of different ROS and RNS are connected to almost all diseases, including (neuro-)inflammation. One of the most frequent neuroinflammatory diseases is multiple sclerosis (MS). In this opinion article, we discuss recent advances in knowledge about oxidative and nitrosative damage, redox regulation, and the related ferroptotic cell death mechanism in initiation and progression of MS.</p><p><strong>Recent findings: </strong>Specific improvement of supportive or inhibition of harmful redox processes in either brain or immune cells showed great impact on disease severity in MS models. Moreover, (circulating) markers of oxidative damage may hold promise as a supplementary diagnostic tool to differentiate different subtypes of MS.</p><p><strong>Summary: </strong>Oxidative damage is well established as driver of MS. Nevertheless, molecular redox mechanisms underlying initiation and progression of MS are not well known. This existing research gaps impedes the establishment of successful antioxidative therapies.</p>","PeriodicalId":11059,"journal":{"name":"Current Opinion in Neurology","volume":" ","pages":"224-231"},"PeriodicalIF":4.4,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13152042/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147638219","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}