Movement Disorders最新文献

{"title":"Comment on “Neuropsychological Tests of Memory, Visuospatial, and Language Function in Parkinson's Disease: Review, Critique, and Recommendations”","authors":"Joshua P. Woller MSc, Alireza Gharabaghi MD","doi":"10.1002/mds.70148","DOIUrl":"10.1002/mds.70148","url":null,"abstract":"<p>We commend Bezdicek and colleagues for a rigorous, consensus-based evaluation of neuropsychological tests for memory, language, visuospatial function, and premorbid intelligence in Parkinson's disease (PD).<span><sup>1</sup></span> Their tiered recommendations provide practical guidance for level-II assessment across Parkinson's Disease Mild Cognitive Impairment (PD-MCI) and PD dementia (PDD) and for outcome selection in trials.</p><p>The panel's core messages are clear. Word-list and story-recall measures show acceptable validity, reliability, and sensitivity to change in PD. The Boston Naming Test is a practical reference for language, matrix reasoning is the current visuospatial choice, and National adult reading test (NART) or NAART improves adjudication through premorbid-ability estimates. These points, including the stated limitations for early-stage sensitivity and motor confounds, provide a strong foundation for standardized workflows.</p><p>We suggest three additions that support the authors' framework.</p><p>First, reliability should also be treated as a design constraint of subsequent analyses. The maximum observable association between two variables is limited by their reliabilities. When studies compare or pool correlations across outcomes with unequal reliability, attenuation biases estimate toward zero and can be mistaken for weak construct associations.<span><sup>2</sup></span> Explicit reporting of reliability for each selected measure, and correction for attenuation in secondary analyses where justified, would reduce interpretive variability and improve cross-cohort comparability.</p><p>Second, sensitivity to change should use complementary thresholds. Minimal detectable change quantifies the smallest difference beyond measurement error, and minimal clinically important difference reflects patient-perceived benefit.<span><sup>3</sup></span> The latter is, therefore, often used when assessing outcomes of clinical trials.<span><sup>4</sup></span> If responder classification is applied, minimally detectable change (MDC) and minimal clinically important difference (MCID) should shape that split. When MCID is smaller than MDC, individual change scores that exceed MCID but fall below MDC remain indeterminate and should not be interpreted as true change. This differentiation is especially relevant given the substantial day-to-day variability of PD symptoms, which may surpass MCID values.<span><sup>5</sup></span></p><p>Third, measurement invariance should be established before comparing groups, subtypes, therapy states, or time points.<span><sup>6</sup></span> Without item-level invariance, observed score differences may be driven by a subset of items that function differentially, which decouples scores from the intended construct. Given the paper's critique about uneven domain sensitivity and executive contamination of visuospatial measures, routine checks for differential item functioning and factorial stability would strengthen in","PeriodicalId":213,"journal":{"name":"Movement Disorders","volume":"41 1","pages":"281-282"},"PeriodicalIF":7.6,"publicationDate":"2025-12-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://movementdisorders.onlinelibrary.wiley.com/doi/epdf/10.1002/mds.70148","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145759727","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":"LRRK2 as a Potential Disease‐Modifying Target in Sporadic Parkinson's Disease","authors":"Anthony E. Lang, Robert A. Hauser, Lorraine V. Kalia, Bonnie Hersh, Zdenek Berger, Roy Llorens Arenas, Coro Paisan‐Ruiz, Kyle Fraser, Danna Jennings, Jillian H. Kluss, Sarah Huntwork‐Rodriguez, Anastasia G. Henry, J. Timothy Greenamyre","doi":"10.1002/mds.70100","DOIUrl":"https://doi.org/10.1002/mds.70100","url":null,"abstract":"A growing understanding of the role that leucine‐rich repeat kinase 2 (LRRK2) plays in Parkinson's disease (PD) supports continued focus on this enzyme as a therapeutic target for PD. Accumulating evidence suggests that there are phenotypic, neuropathologic, and biological similarities between sporadic PD (sPD) and familial forms in which <jats:italic>LRRK2</jats:italic> variants are inherited in an autosomal‐dominant pattern with variable penetrance (LRRK2‐PD). Further, genome‐wide association studies have found specific non‐coding variants that are risk factors for sPD. In this review, we describe the current state of knowledge as it relates to LRRK2's role in sPD, with a focus on comparing the physiology and pathology of sPD with LRRK2‐PD. As in LRRK2‐PD, LRRK2 activity may also be increased in sPD, possibly through interactions between genetics and the environment. Increased activity of LRRK2 and associated endolysosomal dysfunction have been observed in sPD patients, including evidence from postmortem brains of patients with sPD and animal models showing increased LRRK2 activity. Additionally, beneficial effects of LRRK2 inhibitors, such as improved lysosomal function, reduced α‐synuclein accumulation, and amelioration of neurodegeneration, have been demonstrated in animal models of sPD. Therefore, inhibition of LRRK2 kinase activity may be a promising approach to disease modification for sPD and LRRK2‐PD. Ongoing and future clinical studies examining LRRK2 kinase inhibitors will aim to elucidate their clinical efficacy in PD and to assess their potential effects on lysosomal function. © 2025 The Author(s). <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":"11 1","pages":""},"PeriodicalIF":8.6,"publicationDate":"2025-12-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145730690","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":"It Is Personal: What People with Parkinson's Disease Say Matters Most for Quality of Life","authors":"Samantha Dorrance, Richa Patel, Glenn T. Stebbins, Jamie Adams, Allison M. Allen, Tara Hastings, Soania Mathur, Onanong Phokaewvarangkul, Gary Rafaloff, Rajasumi Rajalingam, Anette Schrag, Christine Sun, Jennifer Mammen, Connie Marras","doi":"10.1002/mds.70134","DOIUrl":"https://doi.org/10.1002/mds.70134","url":null,"abstract":"Background Little is known about what matters most for quality of life in people with Parkinson's disease and how much it varies between individuals. Objective The goal was to define the relative impact of quality of life determinants in people with Parkinson's disease, including variation across individuals and by disease severity, gender, age, and ethnicity. Methods Sixty‐one factors potentially associated with quality of life in people with Parkinson's disease were identified from the literature and nominated by participants with Parkinson's disease. Forty‐four participants then rated their degree of impact on quality of life from “a lot” to “not at all,” and identified their “top 3 most important” factors. Results At the individual level, determinants of utmost importance varied greatly, with 39 of 61 factors being reported at least once in the “top 3.” There were 17 factors that at least 50% of the sample agreed affected quality of life “a lot,” and only two were symptoms of the disease. Twelve (all positive experiences) retained at least 50% agreement across subgroups defined by disease severity, age, gender and ethnicity. Symptom‐related factors of high importance varied markedly in mild disease subgroup in particular. Conclusions Factors that are not direct consequences of the disease, but may be highly personal and interfere with what one finds meaningful, emerged as highly relevant. Symptoms also greatly impacted quality of life for most individuals, but specific symptoms varied across individuals. Quality of life determinants in people with Parkinson's disease appear highly individualized, and currently used measurement tools with fixed items may not be optimal. © 2025 The Author(s). <jats:italic>Movement Disorders</jats:italic> published by Wiley Periodicals LLC on behalf of International Parkinson and Movement Disorder Society. © 2025 The Author(s). <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":"35 1","pages":""},"PeriodicalIF":8.6,"publicationDate":"2025-12-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145730689","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 Impact of Calcitriol on Frataxin Levels in Friedreich's Ataxia Patients: Insights and Future Directions","authors":"Nie Zhang, Yahui Xu","doi":"10.1002/mds.29933","DOIUrl":"https://doi.org/10.1002/mds.29933","url":null,"abstract":"","PeriodicalId":213,"journal":{"name":"Movement Disorders","volume":"1 1","pages":""},"PeriodicalIF":8.6,"publicationDate":"2025-12-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145730691","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":"Longitudinal Dynamics of Plasma Neurofilament Light Chain in Hereditary Spastic Paraplegia Type 11 (HSP-SPG11) and Type 15 (HSP-ZFYVE26).","authors":"Habibah A P Agianda,Julian E Alecu,Amy Tam,Hyo-Min Kim,Joshua Rong,Nicole Battaglia,Kaitlyn Warren,Rebekah Mannix,Nunzio Setola,Melissa Barghigiani,Grace Yoon,Yoshihisa Takiyama,Jangsup Moon,Katerina Bernardi,Kathryn Yang,Luca Schierbaum,Filippo Maria Santorelli,Darius Ebrahimi-Fakhari","doi":"10.1002/mds.70142","DOIUrl":"https://doi.org/10.1002/mds.70142","url":null,"abstract":"BACKGROUNDHSP-SPG11 and HSP-ZFYVE26 are autosomal-recessive forms of hereditary spastic paraplegias (HSPs). As therapeutic trials emerge, validated biomarkers are critically needed.OBJECTIVESTo evaluate plasma neurofilament light chain (pNfL) as a biomarker for neurodegeneration and disease progression.METHODSWe analyzed pNfL levels in 57 patients (36 HSP-SPG11, 21 HSP-ZFYVE26) and matched controls using single-molecule array technology. Longitudinal clinical and biomarker data were collected over 5 years.RESULTSBaseline pNfL levels were significantly elevated in patients: 33.85 pg/mL (IQR 25.15-47.38) in HSP-SPG11, 46.70 pg/mL (IQR 29.95-54.84) in HSP-ZFYVE26, and 4.90 pg/mL (IQR 3.48-6.90) in controls (P < 0.001). No significant difference was observed between HSP-SPG11 and HSP-ZFYVE26. In matched pair analysis, pNfL showed inverse correlation with age (ρ = -0.463, P < 0.001). Baseline pNfL did not predict future clinical progression.CONCLUSIONSElevated pNfL reflects early neuroaxonal injury in HSP-SPG11 and HSP-ZFYVE26; however, it could not be used as a surrogate for disease progression. © 2025 International Parkinson and Movement Disorder Society.","PeriodicalId":213,"journal":{"name":"Movement Disorders","volume":"5 1","pages":""},"PeriodicalIF":8.6,"publicationDate":"2025-12-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145710871","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":"Oligodendrocyte Inclusion Pathology in Fragile X‐Associated Tremor/Ataxia Syndrome","authors":"Yingratana McLennan, Hassan Aliashrafzadeh, Faith Zirkelbach‐Ngai, Forrest McKenzie, Brett D. Dufour, Lina V. Becerra‐Hernández, Adolfo Sanchez Escobar, Flora Tassone, Paul Hagerman, Randi Hagerman, Veronica Martínez‐Cerdeño","doi":"10.1002/mds.70145","DOIUrl":"https://doi.org/10.1002/mds.70145","url":null,"abstract":"Background Fragile X‐associated tremor/ataxia syndrome (FXTAS) is a neurodegenerative disorder marked by white matter degeneration and intranuclear inclusions. While astrocytic and neuronal inclusions are well‐documented, oligodendrocytes were previously thought to lack such pathology. Objective To demonstrate that oligodendrocytes in the prefrontal cortex of FXTAS patients do harbor intranuclear inclusions, with significantly higher burden in white matter than gray matter. Methods Ubiquitin and p62 immunofluorescence and enzymatic staining were employed to confirm the presence of intranuclear inclusions in oligodendrocytes across multiple brain regions. Results Oligodendrocytes contain inclusions and inclusion burden is correlated with <jats:italic>FMR1</jats:italic> CGG repeat length ( <jats:italic>ρ</jats:italic> = 0.97, <jats:italic>P</jats:italic> &lt; 0.001) in white matter. Conclusions These findings implicate oligodendrocyte dysfunction in FXTAS pathogenesis which may contribute to demyelination and white matter degeneration. Our data emphasize the need to consider cell type‐specific mechanisms in FXTAS and support future therapeutic efforts aimed at restoring glial proteostasis. © 2025 International Parkinson and Movement Disorder Society.","PeriodicalId":213,"journal":{"name":"Movement Disorders","volume":"127 1","pages":""},"PeriodicalIF":8.6,"publicationDate":"2025-12-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145680154","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":"Primary Brain Calcification: An International Consensus on Nomenclature, Diagnosis, Evaluation, and Management","authors":"Wei Luo, Zhidong Cen, Huiberdina Koek, Miryam Carecchio, Isao Hozumi, Wan‐Jin Chen, Amit Batla, Alexander Balck, Francesca Magrinelli, Dehao Yang, Xuewen Cheng, Ana Westenberger, Akiyoshi Kakita, Liam Chen, Christian Lambert, Jing‐Yu Liu, Annika Keller, João Ricardo Mendes de Oliveira, Zhi‐Qi Xiong, Henry Houlden, Kailash P. Bhatia, Christine Klein, Gaël Nicolas","doi":"10.1002/mds.70140","DOIUrl":"https://doi.org/10.1002/mds.70140","url":null,"abstract":"Our understanding of primary brain calcification (PBC) has accelerated with the identification of seven causative genes over the past 13 years, vastly expanding knowledge of the molecular underpinnings of this disorder. Despite this progress, a lack of standardized clinical definitions, variable presentations, and heterogeneous calcification patterns has perpetuated inconsistencies in diagnosis and patient care. To address these challenges, an international expert panel undertook a comprehensive process—combining systematic literature review, virtual and in‐person expert discussions, and iterative Delphi consensus questionnaires—to develop unified recommendations. These consensus guidelines encompass terminology, diagnostic criteria, neuroimaging protocols, clinical evaluation standards, genetic testing approaches, and management strategies. Notably, PBC is recommended as the clinical standard, with new diagnostic criteria, including the use of a computed tomography–based total calcification score and a three‐tiered diagnostic algorithm (possible, probable, definite PBC). A systematic review of 27 symptoms and signs identified 19 as most closely linked with PBC, guiding more focused clinical assessment. Recommendations strongly support comprehensive next‐generation sequencing for genetic testing, favoring whole genome over exome or targeted panels to maximize diagnostic yield. Multidisciplinary management priorities are outlined in four key principles centering on individualized care, symptom relief, genetic counseling, and ongoing monitoring. Widespread adoption of these unified guidelines will facilitate consistent diagnosis, enable comparative international data collection, and lay the groundwork for large‐scale collaborative research—including future randomized controlled trials of symptomatic and disease‐modifying PBC therapies. This consensus fosters clarity and consistency, creating a framework for improved patient care and scientific discovery. © 2025 International Parkinson and Movement Disorder Society.","PeriodicalId":213,"journal":{"name":"Movement Disorders","volume":"367 1","pages":""},"PeriodicalIF":8.6,"publicationDate":"2025-12-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145673571","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":"Delayed Disease Onset Report in UK Biobank: Implications for Prodromal Studies in Parkinson's Disease","authors":"Sheida Zolfaghari, Trycia Kouchache, Aline Delva, Sarah Bouhadoun, Mirja Kuhlencord, Amélie Pelletier, Alastair J. Noyce, Sheena Waters, Daniel Belete, Tim Wilkinson, Kathryn Bush, Filip Morys, Andrew Vo, Kristiina Rannikmae, Alain Dagher, Ronald B. Postuma","doi":"10.1002/mds.70147","DOIUrl":"https://doi.org/10.1002/mds.70147","url":null,"abstract":"Background <jats:styled-content style=\"fixed-case\">UK</jats:styled-content> Biobank ( <jats:styled-content style=\"fixed-case\">UKBB</jats:styled-content> ) provides extensive genetic, imaging, and health data for ~500,000 participants, enabling studies of prodromal phases of diseases like Parkinson's disease ( <jats:styled-content style=\"fixed-case\">PD</jats:styled-content> ). However, during analysis, we became concerned about the accuracy of diagnosis timing. Objective To evaluate the accuracy of PD diagnosis timing in UKBB. Methods We examined <jats:styled-content style=\"fixed-case\">PD</jats:styled-content> diagnosis timing using hospital, primary care, death records, and self‐reported data. We assessed discrepancies between sources and identified co‐occurring diagnoses recorded on the same date as <jats:styled-content style=\"fixed-case\">PD</jats:styled-content> . Results Among 3979 <jats:styled-content style=\"fixed-case\">PD</jats:styled-content> cases, 97% of the 786 participants with both self‐reported and electronic health records ( <jats:styled-content style=\"fixed-case\">EHRs</jats:styled-content> ) reported their diagnosis earlier than recorded in the <jats:styled-content style=\"fixed-case\">EHR</jats:styled-content> , with a typical delay of 5 to 7 years. Multiple codiagnoses were often logged on the same date, suggesting retrospective or batch data entry. Conclusions Substantial delays in <jats:styled-content style=\"fixed-case\">PD</jats:styled-content> documentation may misclassify already diagnosed individuals as prodromal. This introduces significant bias into studies of early disease markers and distorts the timing between risk factors and clinical onset. © 2025 The Author(s). <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":"19 1","pages":""},"PeriodicalIF":8.6,"publicationDate":"2025-12-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145673609","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":"Reply to: Deep Learning to Differentiate Parkinsonian Syndromes: From Proof of Concept to Clinical Trust","authors":"Giulia Maria Mattia PhD,&nbsp;Lydia Chougar MD, PhD,&nbsp;Alexandra Foubert-Samier MD, PhD,&nbsp;Wassilios G. Meissner MD, PhD,&nbsp;Margherita Fabbri MD, PhD,&nbsp;Anne Pavy-Le Traon MD, PhD,&nbsp;Olivier Rascol MD, PhD,&nbsp;David Grabli MD, PhD,&nbsp;Bertrand Degos MD, PhD,&nbsp;Nadya Pyatigorskaya MD, PhD,&nbsp;Alice Faucher MD,&nbsp;Marie Vidailhet MD,&nbsp;Jean-Christophe Corvol MD, PhD,&nbsp;Stéphane Lehéricy MD, PhD,&nbsp;Patrice Péran PhD","doi":"10.1002/mds.70136","DOIUrl":"10.1002/mds.70136","url":null,"abstract":"","PeriodicalId":213,"journal":{"name":"Movement Disorders","volume":"41 1","pages":"275-276"},"PeriodicalIF":7.6,"publicationDate":"2025-12-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145673560","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":"Bilateral Deep Brain Stimulation of the Subthalamic Nucleus or Globus Pallidus Internus Improves Gait Impairment in Parkinson's Disease","authors":"Jamal Al Ali, J. Lucas McKay, Joe R. Nocera, Faical Isbaine, Julie T. Tran, Paola Testini, Shirley D. Triche, Christine D. Esper, Pratibha Aia, Laura M. Scorr, Lenora Higginbotham, Richa Tripathi, Nicholas Au Yong, Svjetlana Miocinovic, Cathrin M. Buetefisch","doi":"10.1002/mds.70146","DOIUrl":"https://doi.org/10.1002/mds.70146","url":null,"abstract":"Background The effect of deep brain stimulation (DBS) on gait in patients with Parkinson's disease (PD) remains variable, and prospective, long‐term studies, especially involving globus pallidus interna (GPi) stimulation, are limited. Objectives We tested the hypothesis that subthalamic nucleus (STN) and GPi DBS exert acute and chronic effects on gait in patients with PD. Methods Gait kinematics were collected prospectively on patients with PD with bilateral or unilateral STN or GPi DBS, at baseline before initial DBS activation (n = 104), acutely after activation (n = 102), and chronically at 1 month (n = 75) and 12 months (n = 82) OFF‐medications. Gait speed was the main outcome. Kinematic measures of pace, rhythm, and variability and clinical scales were secondary outcomes. Results Average gait speed at baseline was abnormally slow (80.6 cm/s). DBS activation acutely increased gait speed (97.4 cm/s, <jats:italic>P</jats:italic> &lt; 0.001) which was maintained at 1‐month (93.0 cm/s, <jats:italic>P</jats:italic> &lt; 0.001) and 12‐month follow‐up (91.2 cm/s, <jats:italic>P</jats:italic> &lt; 0.001). Acute changes predicted chronic changes. When DBS targets were analyzed separately, only bilateral STN or GPi DBS improved gait speed along with pace, rhythm, and variability. Presurgical levodopa response on the MDS‐UPDRS axial subscore correlated with the response to DBS while the total score did not. Discussion Bilateral STN or GPi DBS should be considered for treatment of gait as both targets improved gait kinematics acutely and chronically. Acute effects of STN or GPi DBS on gait speed should be considered when programming patients as they predict chronic effects. When determining DBS candidacy, the levodopa response on the MDS‐UPDRS axial subscore should be considered. © 2025 The Author(s). <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":"32 1","pages":""},"PeriodicalIF":8.6,"publicationDate":"2025-12-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145664926","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}