Movement Disorders最新文献

{"title":"March Infographic","authors":"","doi":"10.1002/mds.29845","DOIUrl":"10.1002/mds.29845","url":null,"abstract":"<p>\u0000 \u0000 <figure>\u0000 <div><picture>\u0000 <source></source></picture><p></p>\u0000 </div>\u0000 </figure>\u0000 Unraveling Isoform Complexity: The Roles of M1- and M87-Spastin in Spastic Paraplegia 4 (SPG4)</p>","PeriodicalId":213,"journal":{"name":"Movement Disorders","volume":"40 3","pages":""},"PeriodicalIF":7.4,"publicationDate":"2025-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/10.1002/mds.29845","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143675216","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Movement Disorders: Volume 40, Number 3, March 2025","authors":"","doi":"10.1002/mds.30177","DOIUrl":"10.1002/mds.30177","url":null,"abstract":"","PeriodicalId":213,"journal":{"name":"Movement Disorders","volume":"40 3","pages":""},"PeriodicalIF":7.4,"publicationDate":"2025-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mds.30177","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143675198","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Conversion between NMSS and MDS-NMS in Parkinson's Disease","authors":"Michela Garon MSc,&nbsp;José-Manuel Rojo-Albuin,&nbsp;K. Ray Chaudhuri DSc, FRCP, MD,&nbsp;Alexandra Rizos MSc,&nbsp;Carmen Rodriguez-Blazquez PhD,&nbsp;Eugenia Mamikonyan MS,&nbsp;Roberta Biundo PsyD, PhD,&nbsp;Anette Schrag FRCP, PhD,&nbsp;Daniel Weintraub MD,&nbsp;Angelo Antonini MD, PhD,&nbsp;Per Odin MD, PhD,&nbsp;Pablo Martinez-Martin MD, PhD","doi":"10.1002/mds.30172","DOIUrl":"10.1002/mds.30172","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>The burden of non-motor symptoms in Parkinson's disease (PD) can be measured with the Non-Motor Symptoms Scale (NMSS) and the International Parkinson and Movement Disorder Society Non-Motor Rating Scale (MDS-NMS), for which scoring systems, structure and clinical coverage differ.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Objectives</h3>\u0000 \u0000 <p>The goal was to develop conversion formulas between the NMSS and the MDS-NMS scores.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Data from 402 patients with PD participating in the primary MDS-NMS validation study were used. The association between domain and total scores of both scales was assessed by the Spearman rank correlation coefficient and Kendall's <i>W</i> concordance coefficient. Equations for between-scale transformation of total score were constructed from weighted linear regression models.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Spearman rank correlations showed that MDS-NMS domains correlated 0.39 to 0.88 with the corresponding NMSS domains. The equation for transforming the NMSS total score to MDS-NMS total score is: MDS-NMS = 11.629 + 1.624 × NMSS (<i>P</i> &lt; 0.001, <i>R</i>² = 0.748). For converting the MDS-NMS total score to NMSS total score, the formula is NMSS = 2.475 + 0.495 × MDS-NMS (<i>P</i> &lt; 0.001, <i>R</i>² = 0.771).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Our conversion equations enable direct comparison of the NMSS and MDS-NMS instruments, facilitating data comparability across studies. © 2025 International Parkinson and Movement Disorder Society.</p>\u0000 </section>\u0000 </div>","PeriodicalId":213,"journal":{"name":"Movement Disorders","volume":"40 5","pages":"813-820"},"PeriodicalIF":7.4,"publicationDate":"2025-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143661426","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":"Is Parkinson Disease Better Defined Solely by Biology or as a Clinical–Biological Entity? Lessons to be Learned from Alzheimer's Disease on Biological Definition and Staging","authors":"Tiago A. Mestre MD, PhD,&nbsp;Cristina Sampaio MD, PhD","doi":"10.1002/mds.30173","DOIUrl":"10.1002/mds.30173","url":null,"abstract":"","PeriodicalId":213,"journal":{"name":"Movement Disorders","volume":"40 4","pages":"625-626"},"PeriodicalIF":7.4,"publicationDate":"2025-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143646657","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":"The Heart of the Matter: Cardiac Denervation Casts Doubt on the Brain-First Versus Body-First Hypothesis of Parkinson's Disease","authors":"Tomoko Totsune MD, PhD,&nbsp;Toru Baba MD, PhD,&nbsp;Takafumi Hasegawa MD, PhD,&nbsp;Atsushi Takeda MD, PhD","doi":"10.1002/mds.30174","DOIUrl":"10.1002/mds.30174","url":null,"abstract":"&lt;p&gt;Parkinson's disease (PD) is an increasingly common neurodegenerative disease that is pathologically characterized by preferential dopaminergic cell loss in the substantia nigra (SN) and the appearance of Lewy bodies (LBs) in other neurons. Braak and colleagues&lt;span&gt;&lt;sup&gt;1&lt;/sup&gt;&lt;/span&gt; have shown that the dorsal motor nucleus of the vagal nerve (DMV) in the medulla oblongata and the olfactory bulb (OB) are the two major sites of early LB formation. Further, the DMV has a higher burden of LB pathology than the upper brainstem, including the locus coeruleus and the SN in PD. Due to the caudorostral gradient of brainstem LBs, it has been hypothesized that the pathological process in PD begins in the lower brainstem and subsequently progresses in an ascending fashion. This is referred to as the Braak hypothesis.&lt;span&gt;&lt;sup&gt;1, 2&lt;/sup&gt;&lt;/span&gt; Thereafter, Hawkes et al&lt;span&gt;&lt;sup&gt;3&lt;/sup&gt;&lt;/span&gt; refined this concept by incorporating the peripheral autonomic nervous system (PNS) and the OB, and they have proposed an in-depth hypothesis that neurotoxic pathogens (eg, viruses, pesticides, and air pollutants) enter the brain via two routes in the enteric nervous system (ENS) and the OB. This is referred to as the dual-hit hypothesis. Then, some experimental findings (eg, α-synuclein [aS] aggregates propagating from one cell to another) were integrated,&lt;span&gt;&lt;sup&gt;4&lt;/sup&gt;&lt;/span&gt; leading to a compelling hypothesis, in particular, that the pathophysiology of PD is governed unitarily by prion-like transmission of misfolded aS either from the brain or the gut (the brain-first vs. body-first PD hypothesis).&lt;span&gt;&lt;sup&gt;5, 6&lt;/sup&gt;&lt;/span&gt; This conceptual framework has attracted significant attention with the expectation that transmissible aS species could be novel targets of neuroprotective therapies such as immunotherapy.&lt;span&gt;&lt;sup&gt;7&lt;/sup&gt;&lt;/span&gt; However, the notion that PD pathology can be explained solely by the spread of noxious aS remains a matter of debate&lt;span&gt;&lt;sup&gt;8-10&lt;/sup&gt;&lt;/span&gt; and has been mainly criticized for its oversimplification as an explanation for the complexity of actual PD pathology.&lt;span&gt;&lt;sup&gt;11&lt;/sup&gt;&lt;/span&gt; Recently, we reported that cardiac sympathetic denervation was associated with widespread cortical atrophy, but not with nigrostriatal neurodegeneration in PD.&lt;span&gt;&lt;sup&gt;12&lt;/sup&gt;&lt;/span&gt; The finding that neurodegeneration in PD occurs in both the PNS and central nervous system (CNS) independent of a midbrain lesion may support the idea of multifocal or diffuse pathological initiation rather than one-way propagation from a single origin. To address these issues, we discuss limitations of the brain-first versus body-first hypothesis in PD by focusing on the unique feature of cardiac sympathetic involvement.&lt;/p&gt;&lt;p&gt;The aS origin site and connectome (SOC) model, which was proposed by Borghammer and colleagues,&lt;span&gt;&lt;sup&gt;5, 13&lt;/sup&gt;&lt;/span&gt; is a recent topical hypothesis about prion-like spreading of aS pathologies in PD. In this model, interneuronal","PeriodicalId":213,"journal":{"name":"Movement Disorders","volume":"40 5","pages":"807-812"},"PeriodicalIF":7.4,"publicationDate":"2025-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mds.30174","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143653418","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Antidopaminergic Medications and Clinical Changes in Measures of Huntington's Disease: A Causal Analysis","authors":"Michal Geva PhD,&nbsp;Y. Paul Goldberg MBChB, PhD,&nbsp;Henk Schuring PharmD,&nbsp;Andrew M. Tan PhD,&nbsp;Jeffrey D. Long PhD,&nbsp;Michael R. Hayden MBChB, PhD","doi":"10.1002/mds.30164","DOIUrl":"10.1002/mds.30164","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Antidopaminergic medications (ADM) are often used for symptom management of Huntington's disease (HD). Evidence from past research suggests that ADMs are associated with worse clinical outcomes in HD, but their impact on various domains remains underexplored.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>We used causal inference analysis to understand the impact of ADM use on measures of clinical progression in HD across multiple domains over 2 years.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>We used the Enroll-HD database with a new-user design, which compared a cohort that initiated ADM use after the first visit with an unexposed cohort that remained <i>off</i> ADMs. To control for 27 covariates, we used a doubly robust <i>targeted maximum likelihood estimation</i> and conducted two analyses. First, we analyzed ADM treatment 2 years post-baseline and separately for 12 outcome measures. Second, we examined the association of ADM dose with measures of clinical outcomes.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>The ADM-exposed group exhibited faster change in measures of clinical outcome compared with the <i>off</i>-ADM group, which was statistically reliable in cognitive and functional outcome measures, and the composite Unified Huntington's Disease Rating Scale (cUHDRS). Motor domain analyses showed faster change in bradykinesia in the ADM-exposed group versus <i>off</i>-ADM but no difference in chorea or total motor score (TMS). Higher ADM doses also showed greater differences compared to the <i>off</i>-ADM group.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>ADM use was associated with more rapid change in clinical measures, particularly in cognitive and functional domains. However, assumptions required to establish causation between ADM use and disease progression may not have been fully met, and further research is warranted. © 2025 The Author(s). <i>Movement Disorders</i> published by Wiley Periodicals LLC on behalf of International Parkinson and Movement Disorder Society.</p>\u0000 </section>\u0000 </div>","PeriodicalId":213,"journal":{"name":"Movement Disorders","volume":"40 5","pages":"928-937"},"PeriodicalIF":7.4,"publicationDate":"2025-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mds.30164","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143653427","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Long-Term Stability of Spatial Distribution and Peak Dynamics of Subthalamic Beta Power in Parkinson's Disease Patients.","authors":"Jennifer K Behnke, Robert L Peach, Jeroen G V Habets, Johannes L Busch, Jonathan Kaplan, Jan Roediger, Varvara Mathiopoulou, Lucia K Feldmann, Moritz Gerster, Juliette Vivien, Gerd-Helge Schneider, Katharina Faust, Patricia Krause, Andrea A Kühn","doi":"10.1002/mds.30169","DOIUrl":"https://doi.org/10.1002/mds.30169","url":null,"abstract":"<p><strong>Background: </strong>Subthalamic beta oscillations are a biomarker for bradykinesia and rigidity in Parkinson's disease (PD), incorporated as a feedback signal in adaptive deep brain stimulation with potential for guiding electrode contact selection. Understanding their longitudinal stability is essential for successful clinical implementation.</p><p><strong>Objectives: </strong>We aimed to analyze the long-term dynamics of beta peak parameters and beta power distribution along electrodes.</p><p><strong>Methods: </strong>We recorded local field potentials from 12 channels per hemisphere of 33 PD patients at rest, in a therapy-off state at two to four sessions (0, 3, 12, 18-44 months) post-surgery. We analyzed bipolar beta power (13-35 Hz) and estimated monopolar beta power in subgroups with consistent recordings.</p><p><strong>Results: </strong>During the initial 3 months, beta peak power increased (P < 0.0001). While detection of high-beta peaks was more consistent, low- and high-beta peak frequencies shifted substantially in some hemispheres during all periods. Spatial distribution of beta power correlated over time. Maximal beta power across segmented contact levels and directions was significantly stable compared with chance and increased in stability over time. Active contacts for therapeutic stimulation showed consistently higher normalized beta power than inactive contacts (P < 0.0001).</p><p><strong>Conclusions: </strong>Our findings indicate that beta power is a stable chronic biomarker usable for beta-guided programming. For adaptive stimulation, high-beta peaks might be more reliable over time. Greater stability of beta power, center frequency, and spatial distribution beyond an initial stabilization period suggests that the microlesional effect significantly impacts neuronal oscillations, which should be considered in routine clinical practice when using beta activity for automated programming algorithms. © 2025 The Author(s). Movement Disorders published by Wiley Periodicals LLC on behalf of International Parkinson and Movement Disorder Society.</p>","PeriodicalId":213,"journal":{"name":"Movement Disorders","volume":" ","pages":""},"PeriodicalIF":7.4,"publicationDate":"2025-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143646659","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":"Treatment for Dyskinesia in Parkinson's Disease: A Network Meta-analysis of Randomized Controlled Trials","authors":"Rui Yan MS,&nbsp;Xiaoqing Zheng MS,&nbsp;Yixuan Yin MS,&nbsp;Junjiao Zhang MS,&nbsp;Yusha Cui MS,&nbsp;Dongning Su MD,&nbsp;Zhirong Wan MD,&nbsp;Tao Feng MD, PhD","doi":"10.1002/mds.30179","DOIUrl":"10.1002/mds.30179","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Dyskinesia is a motor complication of Parkinson's disease (PD) posing therapeutic challenges. The optimal therapy for dyskinesia in PD has not been identified due to the lack of comprehensive evaluation of treatments.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>The aim was to compare the efficacy and safety of interventions for alleviating levodopa-induced dyskinesia in PD.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>We conducted a Bayesian network meta-analysis (NMA) by systematically searching PubMed, Web of Science, Embase, Cochrane Library, ClinicalTrials.gov, and EudraCT databases up to April 1, 2024. The primary efficacy outcome was the change in scores on dyskinesia rating scales from baseline.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>The study included 85 randomized controlled trials (RCT) involving 13,826 PD patients, comprising 39 interventions. Nine treatments were significantly more effective in reducing scores on dyskinesia rating scales than control (placebo, sham surgery, sham repetitive transcranial magnetic stimulation, or best medical treatment). Globus pallidus interna deep brain stimulation (GPi-DBS) had the highest probability to be the most effective (standardized mean difference, 95% credible interval: −1.27, −1.65 to −0.88; surface under the cumulative ranking curve [SUCRA]: 97.4%), followed by levodopa–carbidopa intestinal gel infusion (SUCRA = 89.7%), subthalamic nucleus (STN)-DBS (SUCRA = 89%), immediate-release (IR) amantadine (SUCRA = 86.5%), pallidotomy (SUCRA = 84.9%), ADS-5102 (SUCRA = 82.9%), clozapine (SUCRA = 77.2%), OS320 (SUCRA = 64.8%), and AFQ056 (SUCRA = 54.5%). GPi-DBS was superior to STN-DBS, and pallidotomy ranked higher than subthalamotomy. ADS-5102 and OS320 had higher adverse event (AE) rates compared to control, whereas AFQ056 and ADS-5102 were linked to more serious AEs.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>This RCT-based NMA identifies and ranks nine efficacious interventions for dyskinesia in PD. GPi-DBS may be the most effective therapy for treating dyskinesia, with IR amantadine ranking highest among oral medications. Novel anti-dyskinetic medications are associated with less-favorable tolerance profiles. © 2025 International Parkinson and Movement Disorder Society.</p>\u0000 </section>\u0000 </div>","PeriodicalId":213,"journal":{"name":"Movement Disorders","volume":"40 5","pages":"869-880"},"PeriodicalIF":7.4,"publicationDate":"2025-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143646661","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":"NLX‐112 Randomized Phase 2A Trial: Safety, Tolerability, Anti‐Dyskinetic, and Anti‐Parkinsonian Efficacy","authors":"Per Svenningsson, Per Odin, Filip Bergquist, Karin Wirdefeldt, Dag Nyholm, Mattias Andréasson, Ioanna Markaki, Anders C. Johansson, Måns Jergil, Christopher Jankosky, Mark A. Varney, Fabienne Herbrecht, Steven A. Johnson, Adrian Newman‐Tancredi","doi":"10.1002/mds.30175","DOIUrl":"https://doi.org/10.1002/mds.30175","url":null,"abstract":"BackgroundLevodopa‐induced dyskinesia (LID) in Parkinson's disease (PD) is associated with ‘false neurotransmitter’ release of dopamine from serotonin (5‐HT) neurons. NLX‐112 is a first‐in‐class, highly selective 5‐HT<jats:sub>1A</jats:sub> receptor agonist which counteracts LIDs in experimental PD models.ObjectivesThe primary objective was to evaluate the safety and tolerability of NLX‐112 compared with placebo in people with PD. The secondary objective was to assess the preliminary efficacy of NLX‐112 in reducing LID and its effects on PD symptoms.MethodsParticipants received NLX‐112 or placebo (2:1 ratio) alongside stable Parkinson's medications, with 22 participants completing the study. Dosing was up‐titrated over 28 days to 2 mg/day (1 mg twice daily), stabilized for 14 days (to day 42), and down‐titrated for 14 days. Efficacy was measured using the Unified Dyskinesia Rating Scale (UDysRS), Unified Parkinson's Disease Rating Scale (UPDRS), and Clinical Global Impression of Change (CGI‐C) following a levodopa challenge (150% of usual dose).ResultsAdverse events (AEs) were mainly central nervous system (CNS)‐related and mostly occurred during up‐titration, with no serious AEs in the NLX‐112 group. There were no treatment‐induced clinically significant changes in vital signs, electrocardiogram, or laboratory parameters. NLX‐112 reduced LID from baseline levels: at day 42, UDysRS total score decreased by 6.3 points, whereas placebo group changes were not significant (−2.4). NLX‐112 also reduced parkinsonism from baseline values: UPDRS Part 3 scores decreased by 3.7 points, whereas placebo group changes were non‐significant (+0.1). In CGI‐C assessment, the NLX‐112 group showed greater improvement than the placebo group (53% vs. 29%).ConclusionThese results support further clinical investigation of NLX‐112 for treatment of PD LID. © 2025 Neurolixis SAS. <jats:italic>Movement Disorders</jats:italic> published by Wiley Periodicals LLC on behalf of International Parkinson and Movement Disorder Society.","PeriodicalId":213,"journal":{"name":"Movement Disorders","volume":"90 1","pages":""},"PeriodicalIF":8.6,"publicationDate":"2025-03-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143641066","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":"Obituary for C. Warren Olanow","authors":"José A. Obeso MD, PhD,&nbsp;Anthony H.V. Schapira MD, DSc, FRCP,&nbsp;Fabrizio Stocchi MD, PhD","doi":"10.1002/mds.30137","DOIUrl":"10.1002/mds.30137","url":null,"abstract":"","PeriodicalId":213,"journal":{"name":"Movement Disorders","volume":"40 3","pages":"398-399"},"PeriodicalIF":7.4,"publicationDate":"2025-03-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143641076","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}