{"title":"Lyme Disease and Other Tick-Borne Infections.","authors":"John J Halperin, Gary P Wormser","doi":"10.1007/s11910-026-01530-1","DOIUrl":"https://doi.org/10.1007/s11910-026-01530-1","url":null,"abstract":"<p><strong>Purpose of review: </strong>The neurologic manifestations of selected tick-transmitted infections in North America and Eurasia were reviewed.</p><p><strong>Recent findings: </strong>Both Powassan virus in North America, and Tick-Borne Encephalitis (TBE) virus in Eurasia can cause encephalitis, often with significant neurologic morbidity. Lyme disease, Ehrlichia chaffeensis (the cause of human monocytic ehrlichiosis [HME]), and Borrelia miyamotoi infections can cause meningitis (the third primarily in immunocompromised individuals). Patients with Lyme disease may also develop cranial neuropathy, and/or radiculoneuropathy. Tick-borne infections are being increasingly recognized in North America and Eurasia. While many tick-borne infections can cause headaches, lethargy or other non-specific symptoms, these are generally not evidence of nervous system infection - i.e., neuroinvasive disease. The latter is less common but may occur in infections due to Powassan and TBE viruses, in HME and in Lyme disease. Patients with symptomatic nervous system infection due to Powassan or TBE virus are at high risk of developing significant neurologic impairment and sequelae.</p>","PeriodicalId":10831,"journal":{"name":"Current Neurology and Neuroscience Reports","volume":"26 1","pages":""},"PeriodicalIF":7.4,"publicationDate":"2026-10-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149227432","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":"Sleep Spindles and Slow Oscillations as Potential Biomarkers and Therapeutic Targets in Mild-to-Moderate Alzheimer's Disease.","authors":"Arsenio Páez, Gerard Piñol-Ripoll, Farida Dakterzada, Thien Thanh Dang-Vu","doi":"10.1007/s11910-026-01528-9","DOIUrl":"https://doi.org/10.1007/s11910-026-01528-9","url":null,"abstract":"<p><strong>Purpose of review: </strong>This review critically evaluates evidence on sleep spindles (SP), slow oscillations (SOs), and their coordination in mild-to-moderate Alzheimer's disease (AD), focusing on their relationships with cognition, AD biomarkers, and their therapeutic potential.</p><p><strong>Recent findings: </strong>Longitudinal studies associate greater SP and/or SO activity with better cognition and favourable amyloid and tau profiles after clinical onset. Spindle and SO coupling may index network integrity. Preserved NREM sleep oscillations are associated with lower orexin concentrations and weaker adverse relationships between orexin and cognitive and neuropsychiatric outcomes. Closed-loop acoustic stimulation and slow-oscillatory transcranial direct-current stimulation can modify SO activity, spindle activity, and coupling, although cognitive and biomarker benefits remain uncertain. Spindle-SO activity, including their temporal coupling, are associated with cognition and AD biomarkers across the disease continuum. Closed-loop acoustic and electrical stimulation can modify these oscillations, but biomarker-characterized trials in MCI and AD are needed to determine whether treatment produces durable cognitive and biomarker benefits.</p>","PeriodicalId":10831,"journal":{"name":"Current Neurology and Neuroscience Reports","volume":"26 1","pages":""},"PeriodicalIF":7.4,"publicationDate":"2026-10-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149227454","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":"Network-guided Thalamic Neuromodulation for Epilepsy.","authors":"Sihyeong Park, Nicholas M Gregg","doi":"10.1007/s11910-026-01526-x","DOIUrl":"https://doi.org/10.1007/s11910-026-01526-x","url":null,"abstract":"<p><strong>Purpose of review: </strong>This review takes a network-based perspective on thalamic neuromodulation for epilepsy, examining how each target (e.g., anterior (ANT), centromedian (CM), and pulvinar (PUL) thalamic nuclei) engage distinct seizure networks, what evidence supports each, and how stimulation/electrophysiologic mapping can guide individualized targeting rather than a fixed, syndrome-based approach.</p><p><strong>Recent findings: </strong>Randomized and prospective trials have expanded the evidence for ANT and CM stimulation, while emerging data support the pulvinar as a target for posterior quadrant and temporal lobe epilepsies. Syndrome-specific sweet-spot analyses reveal distinct optimal sites within the CM for LGS and IGE. Thalamic sEEG with single-pulse stimulation and trials of DBS-style stimulation now enables characterization of seizure network engagement and identification of acute biomarkers that may inform target and parameter selection. Multi-target strategies combining thalamic nuclei, or thalamic and cortical leads, show preliminary promise for broadly distributed seizure networks. No single thalamic target is uniformly effective across epilepsy types; optimal targeting requires individualized, network-informed characterization. This supports a shift toward connectomic and individualized approaches, with future work needed to refine target selection, stimulation paradigms, and individualized optimization using clinical outcomes and electrophysiological biomarkers.</p>","PeriodicalId":10831,"journal":{"name":"Current Neurology and Neuroscience Reports","volume":"26 1","pages":""},"PeriodicalIF":7.4,"publicationDate":"2026-10-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149215250","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":"Neuropathic Mechanisms in Phantom Pain: A Review of Pain Pathways and Peripheral Localization.","authors":"Sarah Nisthar, Sumaya Omar","doi":"10.1007/s11910-026-01525-y","DOIUrl":"10.1007/s11910-026-01525-y","url":null,"abstract":"<p><strong>Purpose of review: </strong>Phantom limb pain (PLP), the perception of pain in a limb no longer present, is a phenomenon affecting over 80% of amputees. Its prevalence induces severe pain and psychological distress causing a significant decline in the quality of life of amputees. PLP's complex interplay of peripheral and central mechanisms remains the leading cause for limited understanding and management of the condition. This article aims to examine PLP within the framework of pain localization by reviewing previous studies and investigating underexplored dimensions of PLP.</p><p><strong>Recent findings: </strong>With the current fragmentation of the clinical landscape, a pattern of research inefficiencies and procedures remains implemented, leading to poorer interpretation and less effective treatment options. This review presents an update on the literature regarding the neuropathic mechanisms of phantom pain, with a focus on its manifestation as a failure of general pain localization within the body. Additionally, we examine the limitations that lead to poor understanding of phantom pain, what factors can be implemented to push towards a better comprehension of PLP, as well as underline the necessity of interdisciplinary approaches and individualized patient care in managing this challenging condition.</p>","PeriodicalId":10831,"journal":{"name":"Current Neurology and Neuroscience Reports","volume":"26 1","pages":""},"PeriodicalIF":7.4,"publicationDate":"2026-10-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149180064","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}
Alvaro Andres Gaitan, Annelise Velasco de Azevedo Pereira, Javier Romero, Alfredo Lopez-Yunez
{"title":"Neuroinflammation as a Final Common Pathway in Systemic Disease - How Systemic Disease Becomes Brain Disease.","authors":"Alvaro Andres Gaitan, Annelise Velasco de Azevedo Pereira, Javier Romero, Alfredo Lopez-Yunez","doi":"10.1007/s11910-026-01512-3","DOIUrl":"10.1007/s11910-026-01512-3","url":null,"abstract":"<p><strong>Purpose of review: </strong>This chapter reviews evidence that neuroinflammation constitutes a final common pathway linking systemic disease of diverse origin to a shared spectrum of CNS injury, and synthesizes its mechanistic, biomarker, and therapeutic implications.</p><p><strong>Recent findings: </strong>Autoimmune, infectious, metabolic, malignant, and age-related diseases converge on five shared CNS mechanisms-blood-brain barrier disruption, microglial priming, complement-mediated synaptic injury, microvascular and thromboinflammatory injury, and autoantibody-mediated neuronal targeting-that interact as a self-perpetuating loop rather than a linear cascade, with meningeal lymphatic and glymphatic clearance governing whether the cycle resolves or persists. These processes are increasingly measurable with non-disease-specific fluid biomarkers (IL-6, IL-1β, neurofilament light chain, GFAP) and imaging biomarkers (TSPO PET, vessel-wall and permeability MRI), and several are now targets of mechanism-directed therapy-IL-1 inhibition, complement blockade, blood-brain barrier stabilization, microglial modulation, and precision immunotherapy timed to disease stage. Recognizing neuroinflammation as this final common pathway reframes diagnosis around shared biomarkers rather than disease labels, predicts cross-disease therapeutic benefit, and relocates the therapeutic window earlier-toward protecting a brain vulnerable long before overt neurological disease declares itself.</p>","PeriodicalId":10831,"journal":{"name":"Current Neurology and Neuroscience Reports","volume":"26 1","pages":""},"PeriodicalIF":7.4,"publicationDate":"2026-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149105391","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":"Neuropsychiatric Symptoms in Primary Progressive Aphasia: Phenomenology, Circuits, and Clinical Management.","authors":"Davide Vilella, Alessandra Vitulli, Eleonora Rollo, Giancarlo Logroscino, Daniele Urso","doi":"10.1007/s11910-026-01523-0","DOIUrl":"10.1007/s11910-026-01523-0","url":null,"abstract":"<p><strong>Purpose of review: </strong>This review synthesizes evidence on the phenomenology, neurobiology, assessment, and treatment of neuropsychiatric symptoms in primary progressive aphasia (PPA), with emphasis on variant-specific patterns and consequences.</p><p><strong>Recent findings: </strong>Neuropsychiatric symptoms are pervasive across PPA and extend beyond language impairment. Contemporary studies identify affective, active behavioural, passive behavioural, and psychotic dimensions, with the greatest behavioural burden observed in semantic variant PPA and apathy prominent across non-fluent/agrammatic and logopenic phenotypes. Converging structural, functional, and molecular evidence implicates distributed language, salience, limbic, and frontostriatal networks, alongside serotonergic and dopaminergic dysfunction. Emerging manifestations, including Problematic Internet Use, broaden the recognised behavioural spectrum. Neuropsychiatric symptoms are integral determinants of disability, caregiver burden, and clinical complexity in PPA. Routine, caregiver-informed assessment and multidisciplinary, non-pharmacological-first management are warranted. Future studies should validate PPA-specific measures, clarify longitudinal trajectories, test targeted interventions, and determine whether neuropsychiatric features should be incorporated into revised PPA diagnostic criteria.</p>","PeriodicalId":10831,"journal":{"name":"Current Neurology and Neuroscience Reports","volume":"26 1","pages":""},"PeriodicalIF":7.4,"publicationDate":"2026-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149073850","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":"Potential Roles of Neuroimaging in Motor Neuron Disease.","authors":"Jan Kassubek, Hans-Peter Müller","doi":"10.1007/s11910-026-01524-z","DOIUrl":"10.1007/s11910-026-01524-z","url":null,"abstract":"<p><strong>Purpose of review: </strong>The review is intended to summarize and discuss the increasing roles and perspectives of neuroimaging in the clinical and scientific work-up of amyotrophic lateral sclerosis (ALS) and other motor neuron diseases (MND).</p><p><strong>Recent findings: </strong>The applications of magnetic resonance imaging (MRI) and positron emission tomography (PET) identify characteristic disease-specific patterns especially for ALS including its clinical subtypes. Guided by neuroanatomical pattern stratification, these MND-associated alterations could be detected by dedicated analysis parameters from MRI, including T1-weighted structural imaging and microstructural diffusion tensor imaging, in combination with additional MR techniques, to act as diagnostic and monitoring biomarkers. Imaging in MND increasingly makes use of machine learning-based analysis methods. The conceptualization of (neuro-)imaging in ALS and other MND encompasses multiparametric technical approaches, also of regions outside the central nervous system, together with aspects of disease-specific pathophysiology which will further advance the field in future applications.</p>","PeriodicalId":10831,"journal":{"name":"Current Neurology and Neuroscience Reports","volume":"26 1","pages":""},"PeriodicalIF":7.4,"publicationDate":"2026-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13616006/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149058739","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":"Cognition in Cardiovascular Disease.","authors":"Arash Salardini, Sayena Azarbar","doi":"10.1007/s11910-026-01519-w","DOIUrl":"10.1007/s11910-026-01519-w","url":null,"abstract":"<p><strong>Purpose of review: </strong>Acute cerebrovascular events once dominated efforts to protect the brain from cardiovascular disease. As stroke prevention and treatment have advanced, attention has broadened to the more continuous vascular processes that contribute to cognitive decline across later life. This review organizes cardiovascular brain injury by route, direct structural injury versus indirect mediated pathways, and tempo, acute events versus chronic processes, with vessel caliber determining lesion topography.</p><p><strong>Recent findings: </strong>Vascular and Alzheimer pathology commonly coexist in older adults with cognitive impairment, and their relationship appears bidirectional but asymmetric: Alzheimer pathology can directly injure the cerebral vasculature, while vascular dysfunction may facilitate Alzheimer pathology and, more clearly, accumulated vascular injury lowers the threshold at which Alzheimer pathology becomes clinically expressed. Covert infarction, microbleeds, white matter disease, and blood-brain barrier disruption accumulate into a cumulative vascular substrate that erodes cognition over decades without requiring a recognized clinical event, and the clinical syndrome follows the lesion, with the subcortical dysexecutive phenotype the modal presentation. Evidence from SPRINT MIND, FINGER, US POINTER, BRAIN-AF, LACI-2, CREST-2, and Mendelian randomization identifies blood pressure control as the best-established intervention, uses discordant and null findings to refine presumed mechanisms, and frames the emerging dilemma of anti-amyloid therapy in patients with substantial vascular disease. In the mixed vascular and Alzheimer disease that dominates late-life dementia, the vascular component is often the more modifiable, and cardiovascular risk management remains among the most actionable strategies for preserving cognition.</p>","PeriodicalId":10831,"journal":{"name":"Current Neurology and Neuroscience Reports","volume":"26 1","pages":""},"PeriodicalIF":7.4,"publicationDate":"2026-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13612708/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149036785","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}
Elizabeth L Broom, Joelle Hanson-Baiden, Lauren M Byrne
{"title":"Fluid and Imaging Biomarkers in Huntington's Disease.","authors":"Elizabeth L Broom, Joelle Hanson-Baiden, Lauren M Byrne","doi":"10.1007/s11910-026-01522-1","DOIUrl":"10.1007/s11910-026-01522-1","url":null,"abstract":"<p><strong>Purpose of review: </strong>Growing interest in earlier and mechanism-targeted interventions for Huntington's disease (HD) has brought focus on biomarkers capable of informing trial design and regulatory pathways. This review discusses recent advances in fluid and neuroimaging biomarkers since the introduction of the HD-Integrated Staging System (HD-ISS), focusing on candidates with the most relevant evidence for regulatory applications.</p><p><strong>Recent findings: </strong>Neurofilament light (NfL) has become a versatile biomarker for prognostic enrichment and safety monitoring. Mutant huntingtin (mHTT) and somatic expansion ratio (SER) provide mechanistic evidence of target engagement. HD-YAS showed SER predicts striatal atrophy over multi-year intervals, but its short-term sensitivity remains uncertain. Structural MRI remains the most sensitive imaging marker of progression, whilst PET and diffusion imaging offer mechanistic insight but limited temporal sensitivity. The most advanced biomarkers now span neuronal injury, target engagement and neurodegeneration. Moving toward qualified endpoints will require harmonised methods, improved analytical validation and stronger evidence linking biomarker change to clinical benefit.</p>","PeriodicalId":10831,"journal":{"name":"Current Neurology and Neuroscience Reports","volume":"26 1","pages":""},"PeriodicalIF":7.4,"publicationDate":"2026-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13612603/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149036840","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":"Electroencephalography Monitoring for Seizure Risk Stratification in the Critically III.","authors":"Marshall Harris, Faris Almubaslat, Clio Rubinos","doi":"10.1007/s11910-026-01517-y","DOIUrl":"10.1007/s11910-026-01517-y","url":null,"abstract":"<p><strong>Purpose of review: </strong>Seizures and epileptiform abnormalities (EAs) are common in critically ill patients, are frequently clinically silent, and are associated with worse outcomes. Continuous electroencephalography (cEEG) remains an essential tool in the diagnosis and management of electrographic seizures (ESz) and EAs in this population, leading to its increased use in critical settings. However, cEEG is resource-intensive, and prolonged monitoring for all patients may not be feasible or necessary in many practice environments.</p><p><strong>Recent findings: </strong>The growing demand for cEEG in critically ill patients has created a need for strategies that optimize its use and prioritize monitoring for patients at highest seizure risk. This need has supported the development of seizure forecasting and cEEG duration-guided risk-stratification approaches. The 2HELPS2B score incorporates early EEG and clinical features to estimate seizure risk, guide monitoring duration, and supports more efficient use of cEEG resources. It has been validated and clinically implemented in critical care settings. This review outlines the evolution and importance of cEEG in critical care, beginning with the recognition that many seizures in this population are electrographic, followed by the identification of rhythmic or periodic patterns and their clinical significance, the expanding use of cEEG, the clinical characterization of patients at highest seizure risk, and the development of the 2HELPS2B score to guide efficient cEEG utilization.</p>","PeriodicalId":10831,"journal":{"name":"Current Neurology and Neuroscience Reports","volume":"26 1","pages":""},"PeriodicalIF":7.4,"publicationDate":"2026-09-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149015683","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}