Brain最新文献

{"title":"Neurotransmitter-informed connectivity maps and their application for outcome inference after stroke.","authors":"Philipp J Koch,Benedikt M Frey,Winifried Backhaus,Nora Petersen,Gabriel Girard,Pawel P Wróbel,Hanna Braaß,Marlene Bönstrup,Lisa Kunkel Genannt Bode,Bastian Cheng,Götz Thomalla,Christian Gerloff,Hannes Schacht,Peter Schramm,Georg Royl,Fanny Quandt,Robert Schulz","doi":"10.1093/brain/awaf185","DOIUrl":"https://doi.org/10.1093/brain/awaf185","url":null,"abstract":"Neuroscience has evolved by framing numerous neuropsychiatric conditions as network diseases. Alterations within neurotransmitter (NT) systems are central to the development of these diseases. Recently, normative data on whole-brain NT fingerprints derived from PET tracer data has become accessible; limited data related such information to sequelae after stroke. This work aims to explore (1) the integration of NT data into whole-brain structural connectivity analyses and (2) its potential contribution to understanding outcome variability following stroke. Normative maps of NT receptor and transporter densities were integrated with a normative structural connectome to generate NT-specific connectivity maps for serotonin, dopamine, GABA, glutamate, and acetylcholine receptors and transporters. Stroke lesion data from two independent, matched cohorts comprising a total of 126 severely impaired acute stroke patients were used to assess NT-related network damage on a patient-specific basis across each receptor and transporter distribution. Multivariable logistic regression models were applied to evaluate the relationship between NT-informed network disconnections and functional outcomes three to six months post-stroke, operationalised by the modified Rankin scale (mRS). Analyses were adjusted for lesion-induced global network damage, age, sex, lesion volume, and baseline neurological symptom burden. We present an innovative method to incorporate PET tracer data of various NT systems into normative structural connectome data. The resulting NT-informed connectivity maps revealed distinct spatial distributions consistent with the established literature. In both cohorts of severely impaired stroke patients, incorporating lesion-induced disruptions within specific NT systems provided more insights into variability in stroke outcomes than structural disconnection alone. Notably, greater damage to networks with high dopamine transporter (DAT) density was associated with poorer functional recovery. Based on NT-informed structural connectivity maps with distinct topographical features for individual receptors and transporters, we show that lesion-induced disruptions in large-scale dopaminergic brain networks, beyond global structural network damage, may play a key role in stroke recovery. These insights hold significant translational potential for advancing personalised medicine in stroke care, such as those achieved by targeted pharmacologic interventions.","PeriodicalId":9063,"journal":{"name":"Brain","volume":"63 1","pages":""},"PeriodicalIF":14.5,"publicationDate":"2025-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144103701","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Are brain arteriovenous malformations congenital or developmental? Evidence from paediatric age data.","authors":"Sivaram S Emani,Ari D Kappel,Shivani D Rangwala,Paulina Piwowarczyk,Nikita Singh,Joon Hyeok Choi,Alfred P See,Darren B Orbach","doi":"10.1093/brain/awaf190","DOIUrl":"https://doi.org/10.1093/brain/awaf190","url":null,"abstract":"The natural history of pediatric brain arteriovenous malformations (AVMs) remains uncertain, particularly regarding their origin (congenital versus postnatal) and risk of rupture. This study analyzes age-related patterns in AVM presentation from a single quaternary referral center. A retrospective review of 275 pediatric AVM cases from 2009-2022, was conducted using radiological, surgical, and hospital records to identify age at first hemorrhage and associated AVM characteristics. Two mathematical models were developed: (i) a congenital model with a variable age-dependent rupture risk, and (ii) a postnatal model of AVM development, assuming age-dependent variable incidence and a constant rupture rate. Data were normalized to institutional age-based presentation rates. Hemorrhagic presentation peaked between ages 7 and 14, before declining sharply, a trend which remained after normalization. A congenital model with age-dependent rupture rate accounted well for the empirical distribution, while the postnatal model overpredicted adolescent hemorrhage and could not account for the observed decline. However, the rising distribution of asymptomatic AVMs with age suggests that a purely congenital model is implausible. The study supports a model where pediatric brain AVMs are largely postnatally acquired, though likely very early, with age-dependent varying annual risk of rupture peaking at age 13, before declining to an adult risk rate.","PeriodicalId":9063,"journal":{"name":"Brain","volume":"37 1","pages":""},"PeriodicalIF":14.5,"publicationDate":"2025-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144103742","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ventriculitis characteristics and outcomes (VELCRO): an international retrospective cohort study.","authors":"David Luque Paz, Beatriz Díaz-Pollán, Marielle Boyer-Besseyre, Flora Djanikian, Anne-Lise Munier, Flávia Cunha, Lélia Escaut, Guillaume Martin-Blondel, Benjamine Sarton, Pierre Jaquet, François Arrivé, Rémi Wolf, Vincent Legros, Mathieu Willig, Oguz Resat Sipahi, Laure Flurin, Antoine Bianchi, Baptiste Balança, Alejandro Díez-Vidal, Joshua Puel, Benjamin Soyer, Rita Lino, Thibaut Leveque, Alexis Salomon, Alexandra Serris, Romaric Larcher, Fabrice Bruneel, Nicolas Mongardon, Martin Martinot, Aurélien Mazeraud, Michel Wolff, Romain Sonneville, Florent Valour, Pierre Tattevin","doi":"10.1093/brain/awaf178","DOIUrl":"https://doi.org/10.1093/brain/awaf178","url":null,"abstract":"<p><p>Ventriculitis is a dreaded complication of central nervous system infections, which has been scarcely described in the literature. We aimed to present a contemporary picture of ventriculitis, describing its characteristics and outcomes across the spectrum of aetiologies that may lead to ventriculitis. VELCRO is an international retrospective multicentre cohort study conducted at 34 hospitals in six countries. Adult patients fulfilling clinical, microbiological and imaging criteria of ventriculitis between 2010 and 2021 were included. Survival analyses were performed using a multivariable Cox proportional hazards regression model to identify risk factors for 1-year all-cause mortality. Overall, 436 patients with ventriculitis were included: 274 (62.8%) males, median age 58 years [interquartile range 48-68], 68 (15.6%) had diabetes mellitus and 62 (14.2%) were immunocompromised. The most common neuroimaging features of ventriculitis were ependymal enhancement (n=310/436, 71.1%), intraventricular pus (n=286/436, 65.6%) and intraventricular septations (n=85/436, 19.5%). To describe the cohort, patients were divided into three groups: ventriculitis with brain abscess(es) (V-BA, n=181), community-acquired ventriculitis without brain abscess (CA-V, n=88), and healthcare-associated ventriculitis without brain abscess (HCA-V, n=167). Intensive care unit admission was required for 351 patients (80.5%) and the median hospital length of stay was 45 days [26-74]. One-year mortality rate was 33.7% (n=147/436), with a lower rate in patients with V-BA (n=50/181, 27.6%) than in patients with CA-V (n=30/88, 34.1%) and HCA-V (n=67/167, 40.1%). On multivariable analysis, the predictive factors for 1-year mortality were: age > 60 years, immunosuppression, diabetes mellitus, Glasgow Coma Scale score < 13 at presentation, infection involving Enterobacterales or fungi, acute hydrocephalus, cerebral ischemia and intraventricular septations. Staphylococcal ventriculitis was associated with a lower 1-year mortality. Long-term unfavourable outcome (modified Rankin score (mRS) > 2 after 6 months of follow-up) occurred in 43.3% (n=91/210), considering that 26.7% (n=56) had a mRS > 2 before the onset of ventriculitis. Ventriculitis is associated with high mortality and neurological morbidity. Further large prospective studies are needed in this area of research.</p>","PeriodicalId":9063,"journal":{"name":"Brain","volume":" ","pages":""},"PeriodicalIF":10.6,"publicationDate":"2025-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144207636","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Direct electrical stimulation maps white matter anatomy to function.","authors":"Davide Giampiccolo,Guillaume Herbet,Hugues Duffau","doi":"10.1093/brain/awaf188","DOIUrl":"https://doi.org/10.1093/brain/awaf188","url":null,"abstract":"","PeriodicalId":9063,"journal":{"name":"Brain","volume":"9 1","pages":""},"PeriodicalIF":14.5,"publicationDate":"2025-05-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144087647","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"FGF14 repeat length and mosaic interruptions: modifiers of spinocerebellar ataxia 27B?","authors":"Joshua Laß, Mirja Thomsen, Max Borsche, Theresa Lüth, Julia C Prietzsche, Susen Schaake, Andona Milovanović, Hannah Macpherson, Emil K Gustavsson, Paula Saffie Awad, Nataša Dragašević-Mišković, Björn-Hergen Laabs, Inke R König, Ana Westenberger, Christopher E Pearson, Norbert Brüggemann, Christine Klein, Joanne Trinh","doi":"10.1093/brain/awaf183","DOIUrl":"https://doi.org/10.1093/brain/awaf183","url":null,"abstract":"Deep intronic FGF14 repeat expansions have been identified as a frequent genetic cause of late-onset cerebellar ataxias, explaining up to 30% of patients. Interruptions between repeats have previously been identified to impact the penetrance in other repeat expansion disorders. Repeat interruptions within FGF14 have yet to be characterized in detail. We utilized long-range PCR, Sanger sequencing, repeat-primed PCR, Nanopore, and PacBio sequencing to distinguish the repeat motifs, mosaicism, and number of repeat interruptions present in FGF14-related ataxia patients and unaffected individuals. A total of 304 patients with late-onset ataxia and 190 unaffected individuals were previously screened for repeat expansions in the FGF14 gene by long-range PCR, identifying 37 individuals with expanded repeat lengths (≥250 repeats). These, along with three newly identified expansion carriers were included in the present study, and advanced genetic methods were applied to investigate the repeat composition in 27 patients and 13 unaffected individuals. The expansions, based on Nanopore data, ranged from 236 to 486 repeats (SD = 60), with 20 individuals showing repeat interruptions, including complex motifs such as GAG, GAAGGA, GAAGAAAGAA, GAAAAGAAGAAGGAAGAAGGAA, GAAAAGAAGAAGGAA, and GCAGAAGAAGAAGAA. We calculated the longest pure GAA length from the long-read data for all 40 individuals. When comparing the pure GAA tract between patients and unaffected individuals, clusters were apparent based on greater or less than 200 repeats. Five ataxia patients with interruptions still had a remaining pure GAA expansion &amp;lt;200. We observed an association of the pure GAA length with age at onset (p=0.016, R2=0.256). Somatically-incurred mosaic divergent repeat interruptions were discovered that affect motif length and sequence (mDRILS), which varied in number and mosaicism (frequency: 0.37-0.93). The mDRILS correlated with pure GAA length (p=0.022, R2=0.334), with a higher mosaic frequency of interruptions in unaffected individuals compared to patients (unaffected: 0.90; patients: 0.67; p=0.009). We demonstrate that i) long-read sequencing is required to detect complex repeat interruptions accurately; ii) repeat interruptions in FGF14 are mosaic, have various lengths and start positions in the repeat tract, and can thereby be annotated as mDRILS, which iii) enabled us to establish a categorization based on remaining pure GAA repeats quantifying the impact of mDRILS on pathogenicity or age at onset, dependent on the interruption length and position, with high accuracy. Finally, we iv) provide evidence that mosaicism stabilizes pure GAA repeats in interrupted FGF14 repeat expansions.","PeriodicalId":9063,"journal":{"name":"Brain","volume":"18 1","pages":""},"PeriodicalIF":14.5,"publicationDate":"2025-05-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144066910","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Astrocytic mGluR5-dependent calcium hyperactivity promotes amyloid-β pathology and cognitive impairment.","authors":"Tianqi Yang,Dianjun Zhang,Haiwei Huang,Fangyue Liu,Juanli Wu,Xiaolin Ma,Shuangshuang Liu,Man Huang,Yu-Dong Zhou,Yi Shen","doi":"10.1093/brain/awaf186","DOIUrl":"https://doi.org/10.1093/brain/awaf186","url":null,"abstract":"Astrocytic dysfunction is a crucial factor for the pathogenesis of Alzheimer's disease. Metabotropic glutamate receptor 5 (mGluR5) is ubiquitously expressed in the brain and is a key molecule that regulates synaptic transmission and plasticity. It has been shown that mGluR5 is elevated in astrocytes in Alzheimer's disease. However, it remains elusive how astrocytic mGluR5 contributes to the pathogenesis of Alzheimer's disease. Here, we first quantified a high expression level of astrocytic mGluR5 in the hippocampus of Alzheimer's disease brains and demonstrated that the expression of astrocytic mGluR5 was positively correlated with Alzheimer's disease progression in both humans and mice. Upregulating astrocytic mGluR5 in the CA1 area at an early stage accelerated, whereas downregulating these receptors rescued, Aβ pathology and cognitive impairment in Alzheimer's disease mice. Moreover, the activation of mGluR5 led to calcium hyperactivity in astrocytes, causing Aβ pathology progression due to dysregulated Aβ uptake and degradation in astrocytes. Importantly, attenuating astrocytic calcium hyperactivity in the hippocampal CA1 area in the prodromal phase ameliorated Aβ pathology and cognitive defects in Alzheimer's disease mice. Our findings thus reveal a fundamental contribution of astrocytic mGluR5 in presymptomatic Alzheimer's disease that may serve as a potential diagnostic and therapeutic target for early Alzheimer's disease pathogenesis.","PeriodicalId":9063,"journal":{"name":"Brain","volume":"4 1","pages":""},"PeriodicalIF":14.5,"publicationDate":"2025-05-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144065808","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Structural covariance analysis for neurodegenerative and neuroinflammatory brain disorders.","authors":"Neus Mongay-Ochoa,Gabriel Gonzalez-Escamilla,Vinzenz Fleischer,Deborah Pareto,Àlex Rovira,Jaume Sastre-Garriga,Sergiu Groppa","doi":"10.1093/brain/awaf151","DOIUrl":"https://doi.org/10.1093/brain/awaf151","url":null,"abstract":"Structural MRI can robustly assess brain tissue alterations related to neurological diseases and ageing. Traditional morphological MRI metrics, such as cortical volume and thickness, only partially relate to functional impairment and disease trajectories at the individual level. Emerging research has increasingly focused on reconstructing interregional meso- and macro-structural relationships in the brain by analysing covarying morphometric patterns. These patterns suggest that structural variations in specific brain regions tend to covary with deviations in other regions across individuals, a phenomenon termed structural covariance. This concept reflects the idea that physiological and pathological processes follow an anatomically defined spreading pattern. Advanced computational strategies, particularly those within the graph-theoretical framework, yield quantifiable properties at both the whole-brain and regional levels, which correlate more closely with the clinical state or cognitive performance than classical atrophy patterns. This review highlights cutting-edge methods for evaluating morphometric covariance networks on an individual basis, with a focus on their utility in characterizing ageing, central nervous system inflammation and neurodegeneration. Specifically, these methods hold significant potential for quantifying structural alterations in patients with Alzheimer's disease, Parkinson's disease, frontotemporal dementia, and multiple sclerosis. By capturing the distinctive morphometric organization of each individual's brain, structural covariance network analyses allow for the tracking and prediction of pathology progression and clinically outcomes, information that can be integrated into clinical decision-making and used as variables in clinical trials. Furthermore, by investigating distinct and cross-diagnostic patterns of structural covariance, these approaches offer insights into shared mechanistic processes that are critical to the understanding of severe neurological disorders and their therapeutic implications. Such advancements pave the way for more precise diagnostic tools and targeted therapeutic strategies.","PeriodicalId":9063,"journal":{"name":"Brain","volume":"124 1","pages":""},"PeriodicalIF":14.5,"publicationDate":"2025-05-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144065809","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Linking polygenic risk scores to dopaminergic neuron loss using neuromelanin-sensitive imaging.","authors":"Aymeric Lanore, Rahul Gaurav, François Xavier Lejeune, Aymeric Basset, Christelle Tesson, Gatepe Kodjovi, Sara Sambin, Graziella Mangone, Isabelle Arnulf, Marie Vidailhet, Louise-Laure Mariani, Alexis Brice, Suzanne Lesage, Stéphane Lehericy, Jean-Christophe Corvol","doi":"10.1093/brain/awaf184","DOIUrl":"https://doi.org/10.1093/brain/awaf184","url":null,"abstract":"<p><p>Parkinson's disease is characterized by the degeneration of dopaminergic neurons in the substantia nigra, and neuromelanin-sensitive MRI provides a biomarker to track this neuronal loss. Isolated rapid eye movement sleep behavior disorder, associated with cognitive decline, may represent a distinct subtype of synucleinopathy. Polygenic risk scores for these conditions may be associated with the neuronal degeneration. This study investigates whether genetic risk scores for Parkinson's disease (PGS000903) or isolated rapid eye movement sleep behavior disorder (PGS003414) are associated with neuromelanin signal loss in the substantia nigra in the ICEBERG cohort. The analysis included 123 individuals with Parkinson's disease, 37 with isolated rapid eye movement sleep behavior disorder, and 48 healthy individuals. Neuromelanin signal intensity was analyzed through linear mixed models by status and genetic risk adjusted for age and sex. Compared to healthy controls, patients with Parkinson's disease had higher genetic risk scores for both disorders, while patients with isolated rapid eye movement sleep behavior disorder had higher genetic risk scores only for rapid eye movement sleep behavior disorder. Both patient groups showed significant signal loss over time (P<0.001). In Parkinson's disease, higher genetic risk for the condition was associated with greater neuromelanine signal decline (P=0.008), particularly in sensorimotor (P=0.04) and limbic (P=0.02) regions. No significant association was found in isolated rapid eye movement sleep behavior disorder. In Parkinson's disease, genetic susceptibility was linked to neuromelanin signal loss, indicating genetic susceptibility to neuronal degeneration. The absence of significant effect in isolated rapid eye movement sleep behavior disorder may be due to a lack of power. These results should be replicated in independent studies.</p>","PeriodicalId":9063,"journal":{"name":"Brain","volume":" ","pages":""},"PeriodicalIF":10.6,"publicationDate":"2025-05-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144207635","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neurological complications of orthopoxvirus infections: neurotropism and neurovirulence","authors":"Hajar Miranzadeh Mahabadi, Ryan S Noyce, David H Evans, Christopher Power","doi":"10.1093/brain/awaf181","DOIUrl":"https://doi.org/10.1093/brain/awaf181","url":null,"abstract":"With the declaration of monkeypox virus (MPXV) infection as a global health emergency in 2022 by the WHO and its ongoing presence, Orthopoxviruses have garnered increasing attention, including their capacity to cause neurological disease. Indeed, the mpox syndrome caused by MPXV infection is recapitulated in humans for several other Orthopoxviruses including variola (VARV, the cause of smallpox), Vaccinia (VACV), camelpox (CMPX), and cowpox (CPXV) viruses, albeit with variable disease severities. In addition to prototypic signs and symptoms of orthopoxvirus infections, such as fever, swollen lymph nodes, malaise, and skin lesions, MPXV-infected individuals also develop neurological syndromes such as headaches, myalgias, seizures, altered consciousness, and encephalopathy/encephalitis. Magnetic resonance imaging (MRI) of the brains of MPXV-infected persons can display hyperintensities consistent with brain edema. Pleocytosis has also been reported in the cerebrospinal fluid (CSF) from persons with MPXV infections, implying active infection of the central nervous system (CNS). Of note, newborn rodents, or animals with severe combined immune deficiency, were found to be susceptible to MPXV infection with evidence that the virus can cross the blood-brain barrier (BBB). In the present review we highlight the current understanding of Orthopoxvirus neuropathogenesis together with germane diagnostic and therapeutic considerations.","PeriodicalId":9063,"journal":{"name":"Brain","volume":"5 1","pages":""},"PeriodicalIF":14.5,"publicationDate":"2025-05-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143980023","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Classifying neurogenic dysphagia as a movement disorder.","authors":"Corinne A Jones,Maggie-Lee Huckabee,Georgia A Malandraki,David Paydarfar","doi":"10.1093/brain/awaf177","DOIUrl":"https://doi.org/10.1093/brain/awaf177","url":null,"abstract":"Swallowing is a complex sensorimotor task critical for maintaining nutrition, hydration, and quality of life. Given the widespread neural involvement and combined volitional and reflexive control, many neurologic conditions can result in swallowing disorders (dysphagia). There is no classification framework for neurogenic dysphagia according to where dysfunction lies within the sensorimotor hierarchy. Thus, underlying neuropathology is not thoroughly considered during dysphagia assessment and rehabilitation. In this review, we explore neurogenic dysphagia through classical sensorimotor hierarchy and movement disorders terminology. We provide comprehensive evidence of dysphagia signs and symptoms in pure cases of movement disorders and discuss nuances related to assessing signs of neuropathology responsible for disordered oropharyngeal swallowing biomechanics. Appreciation of the complexities of dysphagia and investigations into underlying pathologies will advance clinical management of neurogenic dysphagia and inform investigations of dysphagia identification and treatment.","PeriodicalId":9063,"journal":{"name":"Brain","volume":"116 1","pages":""},"PeriodicalIF":14.5,"publicationDate":"2025-05-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143945552","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}