Current Neurology and Neuroscience Reports最新文献

{"title":"Gastrointestinal Dysfunction in Critically Ill Patients With Traumatic Brain Injury: Clinical Implications and Putative Mechanisms: a Narrative Review.","authors":"Ori J Lieberman, Luisa Rojas-Valencia, Edilberto Amorim, Adam R Ferguson, H E Hinson","doi":"10.1007/s11910-026-01500-7","DOIUrl":"10.1007/s11910-026-01500-7","url":null,"abstract":"<p><strong>Purpose of the review: </strong>Moderate to severe traumatic brain injury (TBI) requiring intensive care is associated with high morbidity, mortality and long-term disability. In addition to neurologic sequelae, TBI causes a systemic disease with associated injury to other organ systems, including the gastrointestinal (GI) tract. Here, we review the evidence that GI tract dysfunction occurs after TBI and discuss the clinical implications of GI tract dysfunction on the clinical care of TBI patients, including inadequate nutritional support, elevated risk of pneumonia, and a hyperactive inflammatory response.</p><p><strong>Recent findings: </strong>We highlight recent findings that highlight putative mechanisms through which GI tract pathology may arise after TBI, including vagal nerve and enteric nervous system dysfunction, gut microbiome dysbiosis, sympathetic hyperactivity and iatrogenic injury. Finally, we highlight future approaches to target the GI tract that could improve outcomes in this critically ill patient population. In summary, we review the evidence supporting a role for GI tract dysfunction in the pathophysiology of critically ill TBI patients and highlight potential mechanisms through which GI tract dysfunction may worsen outcomes in this population.</p>","PeriodicalId":10831,"journal":{"name":"Current Neurology and Neuroscience Reports","volume":"26 1","pages":""},"PeriodicalIF":7.4,"publicationDate":"2026-07-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13332980/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148387190","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":"The Potential of Rehabilitation to Amplify Experience-Induced Myelin Plasticity and Remyelination in Multiple Sclerosis: A Narrative Review.","authors":"Michelle Ploughman, Davide Cattaneo, Francesca Marazzini, Nick W Bray, Nora E Fritz","doi":"10.1007/s11910-026-01501-6","DOIUrl":"10.1007/s11910-026-01501-6","url":null,"abstract":"<p><strong>Purpose of review: </strong>This narrative review synthesizes emerging evidence on experience-dependent myelin plasticity and its relevance for neurorehabilitation in persons with multiple sclerosis (MS). Building on foundational work demonstrating motor learning-induced neuroplasticity, we highlight growing recognition that myelination remains adaptable across the lifespan and may be harnessed to support motor relearning, neuroprotection, and remyelination in MS.</p><p><strong>Recent findings: </strong>Preclinical and human studies demonstrate that neuronal activity, especially that induced by motor learning, regulates oligodendrocyte behavior and myelin remodeling. Rodent models show that skilled training enhances oligodendrocyte precursor cell proliferation and myelin thickness, while human neuroimaging confirms training-related increases in myelin-sensitive metrics within task-relevant systems. In MS, early evidence from exercise and motor training studies suggests task-specific white matter plasticity, though sample sizes remain small and imaging outcomes heterogeneous. Additional work points to synergistic potential between behavioral training, neuromodulation, and pharmacologic remyelinating agents. Notably, the combination of exercise and clemastine produces robust remyelination in preclinical models. With MS patients now living longer, aging introduces additional vulnerabilities-including inflammation, microglial dysfunction, and reduced regenerative capacity-but myelin retains responsiveness to behavioral and environmental enrichment. Experience-dependent myelin plasticity represents a promising but underexplored mechanism for enhancing neurorehabilitation outcomes. Motor learning, physical exercise, and multimodal interventions may support adaptive myelination, though optimized dosing, timing, and biomarkers remain undefined. Future research should employ targeted, multimodal imaging approaches and integrate behavioral, neuromodulatory, and pharmacologic strategies, in addition to following patients longitudinally post-intervention, to clarify the therapeutic potential of activity-driven remyelination.</p>","PeriodicalId":10831,"journal":{"name":"Current Neurology and Neuroscience Reports","volume":"26 1","pages":""},"PeriodicalIF":7.4,"publicationDate":"2026-07-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148387336","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":"Update on Genetic Chorea.","authors":"Miriam Ostrozovicova, Matej Skorvanek","doi":"10.1007/s11910-026-01502-5","DOIUrl":"10.1007/s11910-026-01502-5","url":null,"abstract":"<p><strong>Purpose of review: </strong>Chorea is a symptom of numerous pathophysiologically and clinically heterogeneous genetic conditions. A number of developments have been made in this field over the last years linked to improved genomic testing, large cohort collaborations and improved understanding of the molecular mechanisms. This review aims to provide an update on the new genetic conditions and phenotypes linked to chorea disorders, their modification factors and pathophysiological background.</p><p><strong>Recent findings: </strong>Several novel genetic conditions have been linked to chorea over the last 3 years, including mutations in FTH1, NAA60, ACBD6 or TOR1AIP2. Also, novel phenotypes have been established and linked to chorea, such as Adult-onset Neurodegeneration in Nucleotide Excision Repair Disorder (NERD-ND). Major advances have been made in understanding of the pathophysiological role of somatic instability in HD. Striatal pallidal neurons (SPNs) with 150-500 + CAG repeats seem to lose positive and then negative features of neuronal identity, de-repress senescence/apoptosis genes, ultimately leading to cell death. Improved recognition of the genetic background of chorea leads to more effective diagnostic processes, better prognostication and improved personalized treatment. The findings on somatic instability in HD suggest that neurodegeneration in HD is an asynchronous DNA process for >95% of a neuron's life, with majority of neurons in all disease stages having a HTT gene which is not biologically harmful. This has potential major therapeutic implications not only in HD but also in other neurological repeat expansion disorders.</p>","PeriodicalId":10831,"journal":{"name":"Current Neurology and Neuroscience Reports","volume":"26 1","pages":""},"PeriodicalIF":7.4,"publicationDate":"2026-07-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13332979/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148387312","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":"The Noradrenergic Brain in Parkinson's Disease.","authors":"Jacopo Pasquini, Giovanni Palermo, Nicola Pavese, Roberto Ceravolo","doi":"10.1007/s11910-026-01499-x","DOIUrl":"10.1007/s11910-026-01499-x","url":null,"abstract":"<p><strong>Purpose of review: </strong>Cerebral noradrenergic activity modulates physiological functions of behaviour, cognition, movement, arousal and sleep. This review aims to provide an accurate summary of the current knowledge on the involvement of the noradrenergic system in Parkinson's Disease (PD) and its clinical correlations based on neuroimaging studies.</p><p><strong>Recent findings: </strong>Studies in PD highlight neuromelanin MRI signal loss in the locus coeruleus (LC), and positron emission tomography shows noradrenergic denervation across subcortical and cortical areas. More severe phenotypes of PD, manifesting with cognitive decline, apathy, REM sleep behaviour disorder and autonomic dysfunction, are associated with more severe noradrenergic dysfunction. Conversely more preserved noradrenergic transmission is common in tremulous PD. Furthermore, noradrenergic dysfunction, is also involved in transient motor manifestations such as tremor and freezing of gait. Recent neuroimaging advances greatly expanded the knowledge about noradrenergic dysfunction pathophysiology in PD. However, pharmacological treatment of its several associated manifestations is still lacking and needs further investigation.</p>","PeriodicalId":10831,"journal":{"name":"Current Neurology and Neuroscience Reports","volume":"26 1","pages":""},"PeriodicalIF":7.4,"publicationDate":"2026-06-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13272226/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148257719","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":"Mapping the Silent Onset of Parkinson's Disease: Monoamine Imaging in the Era of the Race for Preclinical Intervention.","authors":"Valentina Leta, Valtteri Kaasinen, Bénédicte Ballanger, Roberto Cilia","doi":"10.1007/s11910-026-01498-y","DOIUrl":"10.1007/s11910-026-01498-y","url":null,"abstract":"<p><strong>Purpose of the review: </strong>The main unmet need of Parkinson's disease (PD) is the lack of a therapy able to slow progression. The field is shifting from syndromic diagnosis toward biologically anchored definitions and staging, enabling PD identification before motor onset. In this context, imaging biomarkers provide in vivo measures to identify subtypes, enrich cohorts, and track changes in disease-modifying trials. This review focuses on the role of monoaminergic imaging for preclinical intervention.</p><p><strong>Recent findings: </strong>Monoaminergic imaging captures both the core substrate of motor phenoconversion and extranigral mechanisms underlying early non-motor symptoms. Presynaptic dopaminergic imaging remains the most robust marker of conversion risk in prodromal cohorts, while noradrenergic and serotonergic imaging delineate early brainstem and limbic involvement. Peripheral autonomic imaging further extends biomarker coverage, with cardiac sympathetic imaging detecting early extracerebral denervation in prodromal stages. Together, harmonised monoaminergic imaging provides a unifying framework for staging and clinical trial readiness.</p>","PeriodicalId":10831,"journal":{"name":"Current Neurology and Neuroscience Reports","volume":"26 1","pages":""},"PeriodicalIF":7.4,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148136942","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":"Astrocytopathy in Wernicke Encephalopathy and Neuromyelitis Optica Spectrum Disorder. Pathogenic Differences With Occasional Clinical and Neuroimaging Overlap. A Review.","authors":"Xiaojun Zhang, Jorge C Kattah","doi":"10.1007/s11910-026-01497-z","DOIUrl":"10.1007/s11910-026-01497-z","url":null,"abstract":"<p><p>PURPOSE OF THE REVIEW: There is an increasing number of single case reports describing patients with findings compatible with thiamine deficiency, in whom rapid replacement of thiamine fails to induce improvement. Further work-up identifies positive aquaporin-4 antibodies (AQP-4) leading to a final diagnosis of neuromyelitis optica spectrum disorder (NMOSD). Occasionally, NMOSD is the initial diagnosis, but it turns out that the patient has thiamine deficiency. Similarly, these two diagnoses may overlap, particularly with area postrema lesions and in other cases of protracted vomiting. RECENT FINDINGS: We reviewed the literature to attempt further clarification for this clinical overlap. The common denominator is the astrocyte, as cytotoxic edema due to impaired mitochondrial dysfunction and lactic acidosis in instances of thiamine deficiency causes downregulation of the AQP-4 receptor leading to vasogenic edema and breakdown of the blood-brain-barrier (BBB). Similar dysfunction of the AQP-4 receptor occurs because of IgG binding antibodies in NMOSD. Impaired glutamate transport in the astrocytic podocytes regardless of the AQP4 receptor etiologic mechanism causes excitotoxicity. Awareness of this clinical overlap is critical to initiate timely treatment in thiamine deficiency states and NMOSD</p>","PeriodicalId":10831,"journal":{"name":"Current Neurology and Neuroscience Reports","volume":"26 1","pages":""},"PeriodicalIF":7.4,"publicationDate":"2026-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13110201/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147764927","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":"Functional and Structural Brain Imaging Correlates of Treatment Response in Functional Movement Disorder.","authors":"Christian J Amlang, Alberto J Espay, David L Perez","doi":"10.1007/s11910-026-01496-0","DOIUrl":"10.1007/s11910-026-01496-0","url":null,"abstract":"<p><p>PURPOSE OF REVIEW: Functional movement disorder (FMD) is a biopsychosocially-complex condition with diverse neurologic, physical, and psychiatric manifestations. Converging neuroimaging evidence demonstrates abnormalities in networks supporting self-agency, attention, sensorimotor processing, multimodal integration, salience/threat detection, and interoception. This review summarizes recent work on the prognostic and therapeutic relevance of these findings. RECENT FINDINGS: Baseline functional neuroimaging predictors of outcome implicate cingulo-insular, frontolimbic, and subcortical circuits involved in attention, emotion regulation, and salience processing. Clinical improvement has been associated with activity changes in frontal premotor and regulatory regions, as well as in paralimbic areas. Preliminary studies of transcranial magnetic stimulation, transcranial direct-current stimulation, and neurofeedback suggest that targeted modulation of dysfunctional networks may alleviate symptoms. Neuroimaging features in FMD may inform outcome prediction, elucidate treatment-response mechanisms, and guide neuromodulation strategies. However, the field remains early in development, and larger, longitudinal studies are needed to translate these insights into routine clinical care.</p>","PeriodicalId":10831,"journal":{"name":"Current Neurology and Neuroscience Reports","volume":"26 1","pages":""},"PeriodicalIF":7.4,"publicationDate":"2026-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147764937","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":"When is the Radiologically Isolated Syndrome already Multiple Sclerosis According to the 2024 McDonald Criteria?","authors":"Lies Van Horebeek, Aysika Das, Jake Neufeld, Raphael Schneider","doi":"10.1007/s11910-026-01495-1","DOIUrl":"10.1007/s11910-026-01495-1","url":null,"abstract":"<p><p>PURPOSE OF REVIEW: The McDonald criteria assist neurologists in making accurate and timely diagnoses of multiple sclerosis (MS). The 2024 revision of these criteria aims to enable a more timely diagnosis by including additional biomarkers and alternative diagnostic approaches. They also extend to individuals with MRI findings typical of multiple sclerosis that lack classic MS symptoms, as they would previously have been classified as having radiologically isolated syndrome (RIS). This review examines the scientific foundation of the novel biomarkers used and how the revised criteria influence individuals undergoing diagnostic evaluation, clinical practice, and society. RECENT FINDINGS: Most research concentrates on the scientific foundation for the updates rather than their impact. Benefits and potential disadvantages of the revised criteria can be identified for individuals undergoing diagnostic evaluation, clinical practice, and society. Additional guidelines for real-life application to guide management decisions are advisable.</p>","PeriodicalId":10831,"journal":{"name":"Current Neurology and Neuroscience Reports","volume":"26 1","pages":""},"PeriodicalIF":7.4,"publicationDate":"2026-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147764942","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":"Assessment and Management of Post-traumatic Headache.","authors":"Alex S Aguirre, Yasmine Elhefnawy, Alcy R Torres","doi":"10.1007/s11910-026-01494-2","DOIUrl":"10.1007/s11910-026-01494-2","url":null,"abstract":"<p><p>PURPOSE OF REVIEW: The goal of this narrative review is to provide a comprehensive analysis of Post-Traumatic Headache (PTH), addressing its epidemiology, pathophysiology, and multidisciplinary management. The paper seeks to explore the diagnostic controversies surrounding the timing of symptom onset and evaluates current assessment methods and treatment paradigms for this prevalent sequela of traumatic brain injury. RECENT FINDINGS: Recent research highlights that while current diagnostic criteria require headache onset within seven days of injury, delayed-onset symptoms are common, creating a significant diagnostic dilemma. Pathophysiologically, PTH is understood to be multifaceted, driven by neuroinflammation, neurometabolic cascades, and central sensitization. These processes result in clinical phenotypes that often mirror primary migraine or tension-type headaches. Additionally, while clinical history remains the gold standard for assessment, emerging blood biomarkers are showing promise as objective tools for evaluation. The review concludes that PTH management currently requires a multimodal approach, combining non-pharmacological interventions with pharmacological treatments adapted from primary headache protocols. A major takeaway is the lack of high-quality, PTH-specific randomized controlled trials, which currently forces a reliance on expert opinion rather than robust clinical evidence. To improve patient outcomes, future research must shift toward a more multi-disciplinary, patient-centered paradigm and focus on generating high-quality data to move beyond diagnostic controversies and empiric treatment.</p>","PeriodicalId":10831,"journal":{"name":"Current Neurology and Neuroscience Reports","volume":"26 1","pages":""},"PeriodicalIF":7.4,"publicationDate":"2026-04-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147716396","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":"Redefining Stroke Care with Artificial Intelligence: Recent Advances.","authors":"Shivi Mendiratta, Mark Parsons, Carlos Garcia-Esperon, Amit Mehndiratta","doi":"10.1007/s11910-026-01493-3","DOIUrl":"10.1007/s11910-026-01493-3","url":null,"abstract":"<p><p>PURPOSE OF REVIEW: This review aims to provide an overview of how artificial intelligence (AI) is being integrated into stroke care across the full clinical spectrum with emphasis on its applications in diagnosis, management, and rehabilitation. The focus is on recent advances (2020–2025), addressing key questions on clinical utility and implementation challenges. RECENT FINDINGS: AI has shown promise in enhancing stroke diagnosis through imaging analysis, wearable sensors, and remote monitoring. In stroke management, it supports decision-making and therapy optimization. AI-enabled tools are also improving rehabilitation via robotics and computer vision, and aid prevention through risk prediction and community screening. However, challenges remain in model generalizability, acceptance by the community, and ethical concerns. AI is reshaping stroke care by enabling personalized, timely, and data-driven approaches which can significantly improve quality of life. Future progress will depend on transparent multimodal, globally validated models, supported by interdisciplinary collaboration.</p>","PeriodicalId":10831,"journal":{"name":"Current Neurology and Neuroscience Reports","volume":"26 1","pages":""},"PeriodicalIF":7.4,"publicationDate":"2026-04-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147644377","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}