Current Neurology and Neuroscience Reports最新文献

{"title":"Pulsed Radiofrequency for Post-Stroke Complications: From Neuromodulation to Functional Recovery.","authors":"Rujuan Liu, Huali Gu, Xingyu Kang, Wei Chen, Chengfei Gao, Xiao Han, Lijun Meng, Ting Zhu, Zhengyu Gao","doi":"10.1007/s11910-026-01509-y","DOIUrl":"10.1007/s11910-026-01509-y","url":null,"abstract":"<p><strong>Purpose of review: </strong>This review synthesizes the mechanisms, applications, and evidence gaps regarding pulsed radiofrequency (PRF) in the rehabilitation of post-stroke complications to guide its standardized integration.</p><p><strong>Recent findings: </strong>PRF, a minimally invasive neuromodulation technique, modulates neuronal excitability without thermal damage. Emerging evidence highlights multi-target effects, including improved microcirculation, suppressed neuroinflammation, and regulated neurotrophic factors. Clinically, PRF effectively alleviates refractory post-stroke pain and may indirectly ameliorate post-stroke depression while facilitating motor recovery. Image-guided procedures targeting specific nerves demonstrate favorable safety profiles. Despite promising outcomes for stroke rehabilitation, current evidence relies primarily on small case series and preclinical studies. Significant gaps remain in standardized protocols and high-quality randomized controlled trials. Further validation of long-term efficacy and safety is essential to establish PRF's definitive role in comprehensive post-stroke management.</p>","PeriodicalId":10831,"journal":{"name":"Current Neurology and Neuroscience Reports","volume":"26 1","pages":""},"PeriodicalIF":7.4,"publicationDate":"2026-08-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148697121","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 Neurology of Menopause.","authors":"Hannah J Roeder, Enrique C Leira","doi":"10.1007/s11910-026-01506-1","DOIUrl":"10.1007/s11910-026-01506-1","url":null,"abstract":"<p><strong>Purpose of review: </strong>Menopause is a neuroendocrine process with important implications for neurological health. This review examines the complex, multidirectional relationships between menopause and major central nervous system conditions, including stroke, migraine, epilepsy, multiple sclerosis, Parkinson's disease, and Alzheimer's disease.</p><p><strong>Recent findings: </strong>Menopause may mark an inflection point for vascular injury, neurodegeneration, and disability accumulation in several neurological conditions. Perimenopausal hormonal fluctuations may exacerbate migraines and seizures in susceptible women. Research increasingly supports the critical window hypothesis for estrogen therapy and highlights the importance of distinguishing reproductive and chronological aging when interpreting neurologic trajectories. Menopause represents an important transition for many conditions. Hormone therapy has heterogenous effects with cognitive benefit in premature ovarian insufficiency, harm related to stroke risk in older women, and greater uncertainty in other conditions. Therefore, individualized risk-benefit assessment is essential. Research gaps remain significant, and menopause should be a priority area for neurologic research.</p>","PeriodicalId":10831,"journal":{"name":"Current Neurology and Neuroscience Reports","volume":"26 1","pages":""},"PeriodicalIF":7.4,"publicationDate":"2026-07-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13400467/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148577335","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":"Post-Stroke Dysphagia: Moving Toward Evidence-Based, Recovery-Oriented Systems of Care.","authors":"Heather Shaw Bonilha, Brittany N Krekeler, Janina Wilmskoetter, Sandeep Kumar, Erin L Reedy, Wuwei Feng, Salman Ikramuddin, Fadi Nahab","doi":"10.1007/s11910-026-01507-0","DOIUrl":"10.1007/s11910-026-01507-0","url":null,"abstract":"<p><strong>Purpose of review: </strong>This review examines challenges in post-stroke dysphagia management, including access to swallowing imaging, enteral feeding decisions, and barriers to reassessment and rehabilitation. It evaluates how healthcare systems and practice patterns influence swallowing outcomes and stroke recovery.</p><p><strong>Recent findings: </strong>Recent literature emphasizes that post-stroke dysphagia is a dynamic condition requiring longitudinal management rather than a temporary acute complication. Evidence supports validated dysphagia screening followed by clinical swallowing evaluation and swallowing imaging for accurate diagnosis and treatment planning. Studies highlight variability in gastrostomy tube practices, post-acute access to swallowing imaging, continuity of care, and the psychosocial burden of oral restriction and feeding decisions after stroke. Dysphagia management systems remain fragmented, contributing to inconsistent diagnosis, reassessment, access to intervention, and prolonged unnecessary oral intake restrictions. Future efforts should prioritize rehabilitation pathways that support recovery-oriented dysphagia management.</p>","PeriodicalId":10831,"journal":{"name":"Current Neurology and Neuroscience Reports","volume":"26 1","pages":""},"PeriodicalIF":7.4,"publicationDate":"2026-07-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13400586/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148577261","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":"Considerations in Alzheimer's Disease in Women.","authors":"Caroline Just, Kaitlin Seibert, Carol Chan, Carolina Maldonado-Correa, Danita Jones","doi":"10.1007/s11910-026-01504-3","DOIUrl":"10.1007/s11910-026-01504-3","url":null,"abstract":"<p><strong>Purpose of review: </strong>To examine sex differences in Alzheimer's disease and cognition with a focus on hormonal transitions, biomarker trajectory, and implications for diagnosis and treatment.</p><p><strong>Recent findings: </strong>Women account for nearly two-thirds of individuals with Alzheimer's disease and demonstrate important biological and clinical differences compared with men. APOE ε4 confers greater risk in women, while menopause, depression, chronic stress, adverse pregnancy outcomes, and metabolic dysfunction may further increase vulnerability. Biomarker studies suggest that amyloid trajectories are broadly similar between sexes, but women exhibit earlier or greater tau accumulation once amyloid pathology is present. Women may maintain verbal memory performance longer than men despite underlying pathology, potentially delaying diagnosis. Emerging plasma biomarkers, particularly p-tau217, may improve early detection, monitoring, and treatment. Alzheimer's disease in women reflects a complex interaction between sex-specific biology, hormonal transitions, psychosocial factors, and neurodegenerative processes. Recognizing these differences has important implications for cognitive assessment, biomarker interpretation, diagnosis, and application of disease-modifying therapies.</p>","PeriodicalId":10831,"journal":{"name":"Current Neurology and Neuroscience Reports","volume":"26 1","pages":""},"PeriodicalIF":7.4,"publicationDate":"2026-07-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13395889/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148561108","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":"Environmental Exposures and Stroke Risk: Converging Pathways, Unequal Burdens, and Prevention Opportunities.","authors":"Muaz Ali, Whitney Mayberry, Rebecca Achey, Jukka Putaala, Amre Nouh","doi":"10.1007/s11910-026-01505-2","DOIUrl":"10.1007/s11910-026-01505-2","url":null,"abstract":"<p><strong>Purpose of review: </strong>To synthesize recent evidence on how environmental exposures influence stroke risk, with emphasis on air pollution, thermal stress, circadian and occupational disruption, built and social environments, and selected toxicants.</p><p><strong>Recent findings: </strong>Long-term and episodic air pollution, especially fine particulate matter with aerodynamic diameter ≤ 2.5 μm (PM₂.₅) and wildfire smoke, remain most consistently associated with stroke risk. Extreme heat combined with heat-humidity metrics is emerging as an important acute stroke trigger. Noise, artificial light at night, shift work, and long working hours show smaller but plausible associations, while greener and more walkable environments may be modestly protective. Social and structural disadvantage clusters, multiple exposures and inequities play an integrated role in risk and prevention. Environmental determinants are increasingly relevant to stroke risk. The strongest current links are realted to pollution, heat, sleep, and work disruption, as well as environmental inequity. Future research should move beyond single-exposure models toward combined-exposure as well as intervention-focused approaches.</p>","PeriodicalId":10831,"journal":{"name":"Current Neurology and Neuroscience Reports","volume":"26 1","pages":""},"PeriodicalIF":7.4,"publicationDate":"2026-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13391753/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148548143","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":"Postoperative Seizure Prophylaxis in Intracranial Tumors: Evaluating the Role of Anti-Seizure Medication in Seizure-Naïve Patients.","authors":"Nitish Seenarine, Samuel Latzman, Laura Mittelman, Vadim Zhigin, Emily Hirowski, Shoaib Syed, Heustein Sy, Randy S D'Amico","doi":"10.1007/s11910-026-01503-4","DOIUrl":"10.1007/s11910-026-01503-4","url":null,"abstract":"<p><strong>Purpose of review: </strong>Postoperative seizures occur in up to 20% of seizure-naïve adult patients undergoing craniotomy for tumor resection, contributing to morbidity and readmissions. Yet, routine prophylactic use of anti-seizure medications (ASMs) in this population remains unsupported by current evidence-based guidelines. In this review, we synthesize current evidence on seizure incidence, timing, risk factors, and practical perioperative management strategies.</p><p><strong>Recent findings: </strong>Postoperative seizure risk varies by tumor type, cortical involvement, peritumoral edema, hemorrhage, and tumor grade. Across randomized trials and meta-analyses, prophylactic ASM administration has not been shown to consistently reduce postoperative seizure incidence, and older agents can increase toxicity and interaction risk. Some studies suggest a modest reduction of early seizures within the first postoperative week, though this benefit is not sustained long-term. When prophylaxis is employed, second-generation ASMs such as levetiracetam are often favored for their higher tolerability and fewer drug-drug interactions compared to older agents. Emerging evidence has described alternative agents to levetiracetam with greater blood-brain-barrier permeability, but further investigation is required. Routine ASM prophylaxis in seizure-naïve patients undergoing intracranial tumor resection is not supported by current evidence or clinical guidelines. A selective, risk-based approach with short-term prophylaxis may be considered in patients with high-risk features. Future prospective, risk-stratified trials are needed to better define subgroups that may benefit from targeted prophylactic strategies.</p>","PeriodicalId":10831,"journal":{"name":"Current Neurology and Neuroscience Reports","volume":"26 1","pages":""},"PeriodicalIF":7.4,"publicationDate":"2026-07-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148519855","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":"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}