Annals of Neurology最新文献

{"title":"Mapping Postictal Aphasia through Signal Complexity: A Stereo-Electroencephalography Study.","authors":"Ionuț-Flavius Bratu, Christian G Bénar, Samuel Medina Villalon, Lison Ciavatti, Fantine Mazel, Fabrice Bartolomei, Agnès Trébuchon","doi":"10.1002/ana.27307","DOIUrl":"https://doi.org/10.1002/ana.27307","url":null,"abstract":"<p><strong>Objective: </strong>The postictal period provides an opportunity to investigate the pathophysiology underlying aphasia and recovery following epileptic seizures. This study examines postictal aphasia in stereo-electroencephalography (SEEG)-explored patients to identify brain regions associated with task-specific language deficits using signal complexity analysis.</p><p><strong>Methods: </strong>We evaluated video-SEEG-recorded focal seizures with and without postictal aphasia in patients with SEEG-confirmed hemispheric language dominance. SEEG traces were analyzed using permutation entropy (PE), with the postictal period quantified by a PE-based metric, the Postictal Alteration Time (PAT). Brain region PAT was correlated with language function recovery (eg, repetition). Electro-clinical recuperation was also assessed within the dorsal-ventral language stream framework. Additionally, a bedside testing battery was developed to evaluate postictal aphasia severity and task-specific deficits.</p><p><strong>Results: </strong>A total of 322 seizures from 98 patients were analyzed. Seizures with postictal aphasia had longer PAT than those without. Task-specific language recovery correlated with regional PAT (eg, naming - middle temporal gyrus). Moreover, the dorsal stream recovered faster than the ventral stream. Additionally, the Postictal Aphasia Scale (PAS) was developed, evaluating naming, reading, repetition, and comprehension (verbal and written) and automatic speech. Higher PAS scores (indicating milder deficits) correlated with faster regional complexity recovery. At 5 and 10 minutes postictally, PAS revealed a global aphasia pattern, with comprehension deficits gradually resolving. By 15 minutes, aphasia was primarily production-related, particularly affecting naming.</p><p><strong>Interpretation: </strong>This study provides new insights into the pathophysiology of postictal aphasia and introduces PAS as a tool for assessing postictal aphasia severity and domain-specific deficits, aiding surgical planning and rehabilitation. ANN NEUROL 2025.</p>","PeriodicalId":127,"journal":{"name":"Annals of Neurology","volume":" ","pages":""},"PeriodicalIF":8.1,"publicationDate":"2025-07-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144615591","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":"Cognitive Performance in Early Neuronal Synuclein Disease with Hyposmia but without Motor Disability: Association with Dopamine Deficiency and Isolated Rapid Eye Movement Sleep Behavior Disorder","authors":"Daniel Weintraub MD,&nbsp;Anuprita R. Nair MPH,&nbsp;Ryan Kurth MS,&nbsp;Michael C. Brumm MS,&nbsp;Christine Kohnen PhD,&nbsp;Michele K. York PhD,&nbsp;Roseanne D. Dobkin PhD,&nbsp;Kenneth Marek MD,&nbsp;Caroline Tanner MD, PhD,&nbsp;Tanya Simuni MD,&nbsp;Andrew Siderowf MD, MSCE,&nbsp;Douglas Galasko MD,&nbsp;Lana M. Chahine MD,&nbsp;Christopher Coffey PhD,&nbsp;Kalpana Merchant PhD,&nbsp;Kathleen L. Poston MD, MS,&nbsp;Tatiana Foroud PhD,&nbsp;Brit Mollenhauer MD,&nbsp;Ethan G. Brown MD,&nbsp;Karl Kieburtz MD, MPH,&nbsp;Mark Frasier PhD,&nbsp;Sohini Chowdhury MA,&nbsp;Roy N. Alcalay MD, MS,&nbsp;Aleksandar Videnovic MD,&nbsp;The Parkinson's Progression Markers Initiative","doi":"10.1002/ana.27263","DOIUrl":"10.1002/ana.27263","url":null,"abstract":"<div>\u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>To determine the impact of dopamine deficiency and isolated rapid eye movement (REM) sleep behavior disorder (iRBD) on cognitive performance in early neuronal α-synuclein disease (NSD) with hyposmia but without motor disability.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Using Parkinson's Progression Markers Initiative baseline data, cognitive performance was assessed with a cognitive summary score (CSS) derived from robust healthy control (HC) norms. Performance was examined for participants with hyposmia in early NSD-Integrated Staging System (NSD-ISS), either stage 2A (cerebrospinal fluid α-synuclein seed amplification assay [SAA]+, dopamine transporter scan [DaTscan]−) or 2B (SAA+, DaTscan+).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Participants were stage 2A (n = 101), stage 2B (N = 227), and HCs (n = 158). Although stage 2 had intact Montreal Cognitive Assessment scores (mean [SD] = 27.0 [2.3]), stage 2A had a numerically worse CSS (z-score mean difference = 0.05, <i>p =</i> NS; effect size = 0.09) and stage 2B a statistically worse CSS (z-score mean difference = 0.23, <i>p</i> &lt; 0.05; effect size = 0.40) compared with HCs. In stage 2A, hyposmia alone was associated with normal cognition, but those with comorbid iRBD had significantly worse cognition (z-score mean difference = 0.33, <i>p</i> &lt; 0.05, effect size =0.50). In stage 2B, hyposmia alone had abnormal cognition (z-score mean difference = 0.18, <i>p</i> = 0.0078, effect size = 0.29), and superimposed iRBD had a statistically significant additive effect.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Interpretation</h3>\u0000 \u0000 <p>Using a novel CSS, we demonstrated that hyposmia is associated with cognitive deficits in prodromal NSD without motor disability, particularly when comorbid dopamine system impairment or comorbid iRBD is present. Therefore, it is critical to include and assess cognition at all stages when studying synuclein disease, even in the absence of motor disability. ANN NEUROL 2025;98:482–491</p>\u0000 </section>\u0000 </div>","PeriodicalId":127,"journal":{"name":"Annals of Neurology","volume":"98 3","pages":"482-491"},"PeriodicalIF":7.7,"publicationDate":"2025-07-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/ana.27263","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144606932","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":"Chronic Striatal Cholinergic Interneuron Excitation Causes Cerebral Palsy-Related Dystonic Behavior in Mice.","authors":"Kat Gemperli, Xinguo Lu, Keerthana Chintalapati, Alyssa Rust, Rishabh Bajpai, Nathan Suh, Joanna Blackburn, Rose Gelineau-Morel, Michael C Kruer, Dararat Mingbunjerdsuk, Jennifer O'Malley, Laura Tochen, Jeff L Waugh, Steve Wu, Timothy Feyma, Joel Perlmutter, Steven Mennerick, Jordan G McCall, Bhooma R Aravamuthan","doi":"10.1002/ana.27299","DOIUrl":"10.1002/ana.27299","url":null,"abstract":"<p><strong>Objective: </strong>Mouse models of genetic dystonias have demonstrated abnormal striatal cholinergic interneuron excitability, but do not consistently demonstrate subjective dystonic features. To determine whether striatal cholinergic interneuron excitation can cause potentially dystonic motor behaviors, we first determined features correlated specifically with dystonia severity in people and then determined whether these features emerged in mice following striatal cholinergic interneuron excitation.</p><p><strong>Methods: </strong>Eight movement disorders experts rated dystonia severity in 193 videos of people with cerebral palsy doing a seated task. Leg adduction variability metrics, which are known to correlate with leg dystonia severity during gait, were quantified in these videos of seated tasks. Metrics significantly associated with leg dystonia severity during seated tasks in people were then quantified in mice and compared between mice who underwent chemogenetic striatal cholinergic interneuron excitation (n = 17) and mice who did not (n = 17).</p><p><strong>Results: </strong>Leg adduction variability correlated well with experts' leg dystonia severity scores in people. Leg adduction variability was also significantly increased in mice that underwent striatal cholinergic interneuron excitation compared to mice that did not (p < 0.05). This difference was not present with acute excitation and emerged only after 14 days of ongoing excitation.</p><p><strong>Interpretation: </strong>We demonstrate that leg adduction variability correlates with leg dystonia severity in people with cerebral palsy and that chronic, but not acute, striatal cholinergic interneuron excitation can cause leg adduction variability in mice. These results support targeting striatal cholinergic interneurons for dystonia drug development and demonstrate the potential value of using quantifiable leg adduction metrics to study dystonia pathophysiology. ANN NEUROL 2025.</p>","PeriodicalId":127,"journal":{"name":"Annals of Neurology","volume":" ","pages":""},"PeriodicalIF":8.1,"publicationDate":"2025-07-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144551498","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 Spectrum of Neurologic Phenotypes Associated With NUS1 Pathogenic Variants: A Comprehensive Case Series","authors":"Sarah M. Brooker MD, PhD,&nbsp;Maria Novelli MD,&nbsp;Robert Coukos PhD,&nbsp;Neha Prakash MBBS,&nbsp;Walaa A. Kamel MD,&nbsp;Marta Amengual-Gual MD,&nbsp;Mathieu Anheim MD, PhD,&nbsp;Giulia Barcia MD, PhD,&nbsp;Tanya Bardakjian MS,&nbsp;Franciska Baur MD,&nbsp;Steffen Berweck MD,&nbsp;Bigna K. Bölsterli MD,&nbsp;Melanie Brugger MD,&nbsp;Thomas Cassini MD,&nbsp;Nicolas Chatron MD,&nbsp;Brian Corner MS,&nbsp;Hormos Salimi Dafsari MD,&nbsp;Jean-Madeleine de Sainte Agathe MD,&nbsp;Colin A. Ellis MD,&nbsp;Kimberly M. Ezell APRN, FNP,&nbsp;Cendrine Foucard MD,&nbsp;Steven J. Frucht MD,&nbsp;Maria C. Garcia MBBS,&nbsp;Deepak Gill MBBS, FRACP,&nbsp;Anne Guimier MD,&nbsp;Rizwan Hamid MD, PhD,&nbsp;Damià Heine-Suñer PhD,&nbsp;Peter Herkenrath MD,&nbsp;Marie Hully MD,&nbsp;Ioannis U. Isaias MD, PhD,&nbsp;Louis Januel MD,&nbsp;Chloe Laurencin MD,&nbsp;Taylor Laut MS,&nbsp;Alinoe Lavillaureix MD,&nbsp;Gaetan Lesca MD, PhD,&nbsp;Marion Lesieur-Sebellin MD,&nbsp;Luca Magistrelli MD, PhD,&nbsp;Cecilia Marelli MD, PhD,&nbsp;Heather C. Mefford MD, PhD,&nbsp;Bryce A. Mendelsohn MD,&nbsp;Saadet Mercimek-Andrews MD, PhD,&nbsp;Claire Miller MD, PhD,&nbsp;Shekeeb S. Mohammad MBBS, PhD, FRACP,&nbsp;Francesca Morgante MD, PhD,&nbsp;Sirisha Nandipati MD,&nbsp;Thomas Opladen MD,&nbsp;Mahesh Padmanaban MD,&nbsp;Micaela Pauni MD,&nbsp;Gianni Pezzoli MD,&nbsp;Amelie Piton PhD,&nbsp;Francis Ramond MD, PhD,&nbsp;Giulietta M. Riboldi MD, PhD,&nbsp;Christelle Rougeot-Jung MD,&nbsp;Fernando Santos-Simarro MD, PhD,&nbsp;Ingrid E. Scheffer MBBS, PhD,&nbsp;Naoual Serari M2,&nbsp;Christine M. Stahl MD,&nbsp;Ann Stembridge Kung MS,&nbsp;Susana Tarongí Sanchez MD,&nbsp;Christel Thauvin-Robinet MD, PhD,&nbsp;Marianne Till MD,&nbsp;Christine Tranchant MD, PhD,&nbsp;Christopher Troedson MBBS, FRACP,&nbsp;Thomas F. Tropea DO, MPH,&nbsp;Olivier Vanakker MD, PhD,&nbsp;Patricia Vega MD,&nbsp;Maxi Leona Wiese MD,&nbsp;Udo Wieshmann MD, PhD, FRCP,&nbsp;Laura J. Williams MB BCh BAO, MD,&nbsp;Thomas Wirth MD,&nbsp;Michael Zech MD,&nbsp;Hans Zempel MD, PhD,&nbsp;Emmanuel Roze MD, PhD,&nbsp;Vincenzo Leuzzi MD,&nbsp;Serena Galosi MD, PhD,&nbsp;Victor S. C. Fung PhD, FRACP,&nbsp;Gemma Carvill PhD,&nbsp;Dimitri Krainc MD, PhD,&nbsp;Elizabeth Gerard MD,&nbsp;Niccolò E. Mencacci MD, PhD","doi":"10.1002/ana.27272","DOIUrl":"10.1002/ana.27272","url":null,"abstract":"<div>\u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>A growing body of evidence indicates a strong genetic overlap between developmental and epileptic encephalopathies (DEEs) and movement disorders. De novo loss-of-function variants in <i>NUS1</i> have been recently identified in DEE cases. Herein, we report a large cohort of cases with pathogenic <i>NUS1</i> variants and describe their clinical presentation and the details of the associated epilepsy and movement disorders.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Cases with <i>NUS1</i>-related disorders were identified through a multicentric international collaboration made possible by the GeneMatcher platform. Clinical data were acquired through retrospective case-note review.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>We identified 41 subjects carrying 38 different pathogenic or likely pathogenic heterozygous <i>NUS1</i> variants. The majority of cases displayed developmental delays and intellectual disability of variable severity. Epilepsy was present in 68.3% of cases (28/41) with onset typically in early childhood. Strikingly, 87.8% of cases (36/41) presented with movement disorders and for 13 of these cases the movement disorder was not accompanied by epilepsy. The phenomenology of the movement disorders was complex with myoclonus observed in 68.3% of cases (28/41), either in isolation or in combination with dystonia, ataxia, and/or parkinsonism. Seven cases that otherwise did not have prominent movement disorders had mild incoordination and intention tremor, suggestive of cerebellar dysfunction. There was no observed genotype–phenotype correlation, suggesting that other genetic or acquired factors impact the clinical presentation.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Interpretation</h3>\u0000 \u0000 <p>Heterozygous <i>NUS1</i> pathogenic variants cause a complex neurological disorder, variably featuring developmental and epileptic encephalopathies and a broad spectrum of movement disorders, which represent the major source of neurological disability for most cases. ANN NEUROL 2025;98:561–572</p>\u0000 </section>\u0000 </div>","PeriodicalId":127,"journal":{"name":"Annals of Neurology","volume":"98 3","pages":"561-572"},"PeriodicalIF":7.7,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12221205/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144537544","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":"Toward Natural Limb Function: A New Era in Prosthetic Innovation.","authors":"Yucheng Tian, Dylan M Wallace, Paul S Cederna, Cynthia A Chestek, Stephen W P Kemp","doi":"10.1002/ana.27287","DOIUrl":"https://doi.org/10.1002/ana.27287","url":null,"abstract":"<p><p>The past decade has witnessed groundbreaking clinical implementation of neuroprosthetic limbs driven by signals from peripheral targets (eg, nerves and muscle) and the brain to restore limb function for individuals with limb loss or impairment. In this review, we highlight recent key clinical trials in peripheral neuroprosthetic interfaces directly with nerve, residual muscle, and reinnervated muscle. We then highlight the key advances in brain interfaces, including clinical trials using electroencephalography, electrocorticography, and intracortical electrodes to control neuroprosthetics. Finally, we explore the future of neuroprosthetic control where both peripheral and brain interfaces can be combined to improve neuroprosthetic performance. ANN NEUROL 2025.</p>","PeriodicalId":127,"journal":{"name":"Annals of Neurology","volume":" ","pages":""},"PeriodicalIF":8.1,"publicationDate":"2025-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144525672","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":"Clonal Hematopoiesis of Indeterminate Potential Associated with Covert Cerebral Changes.","authors":"Yijuan Li, Dingding Zhang, Fei Han, Lixin Zhou, Jun Ni, Ming Yao, Zhengyu Jin, Shuyang Zhang, Liying Cui, Xinzhuang Yang, Yi-Cheng Zhu","doi":"10.1002/ana.27304","DOIUrl":"https://doi.org/10.1002/ana.27304","url":null,"abstract":"<p><strong>Objective: </strong>Clonal hematopoiesis of indeterminate potential (CHIP) is an emerging risk factor for cardio-cerebrovascular diseases. This study aimed to investigate CHIP's association with cerebrovascular or glymphatic changes in a community-based population.</p><p><strong>Methods: </strong>This study examined Chinese community cohort participants. CHIP mutations were identified through whole-exome sequencing. Intracranial arterial stenosis, silent brain infarcts, cerebral small vessel disease markers, and diffusion along the perivascular space index were identified by magnetic resonance imaging. The correlation between CHIP and neuroimaging outcomes was investigated through univariate and multivariate logistic/linear regression. The multivariate regression model was adjusted for cerebrovascular disease risk factors, including age, sex, body mass index, smoking status, hypertension, diabetes, and hyperlipidemia.</p><p><strong>Results: </strong>In total, 18.2% (224 out of 1,229) participants were identified as carriers of CHIP mutations. The prevalence of CHIP generally increases with age (p = 0.009). After adjusting for vascular risk factors using multivariate regression, CHIP mutations were found to be significantly associated with increased odds of large magnetic resonance imaging-defined infarcts (>15 mm; OR 3.20; 95% CI 1.18 to 8.43; p = 0.018), inversely associated with diffusion along the perivascular space (β = -0.02; 95% CI -0.04 to 0; p = 0.034), and showed a borderline association with intracranial arterial stenosis (OR 1.52; 95% CI 0.99 to 2.30; p = 0.053). Notably, no statistically significant correlations were observed between CHIP and cerebral small vessel disease markers or brain atrophy measures.</p><p><strong>Interpretation: </strong>CHIP was significantly associated with glymphatic dysfunction and large infarcts, and marginally associated with intracranial arterial stenosis. Further research is needed to elucidate the pathophysiology linking CHIP to cerebral covert changes. ANN NEUROL 2025.</p>","PeriodicalId":127,"journal":{"name":"Annals of Neurology","volume":" ","pages":""},"PeriodicalIF":8.1,"publicationDate":"2025-06-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144504315","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 Role of Electroencephalography in Predicting Post-Stroke Seizures and an Updated Prognostic Model (SeLECT-EEG).","authors":"Kai Michael Schubert, Vijaya Dasari, Ana Lúcia Oliveira, Chiara Tatillo, Gilles Naeije, Adam Strzelczyk, Giovanni Merlino, Mariarosaria Valente, Nicolas Gaspard, Vineet Punia, Marian Galovic, Carla Bentes","doi":"10.1002/ana.27301","DOIUrl":"https://doi.org/10.1002/ana.27301","url":null,"abstract":"<p><strong>Objective: </strong>Seizures negatively impact stroke outcomes, highlighting the need for reliable predictors of post-stroke epilepsy. Although acute symptomatic seizures are a known risk factor, most stroke survivors who develop epilepsy do not experience them. Early electroencephalography (EEG) findings may enhance risk prediction, particularly in patients without acute symptomatic seizures, aiding in patient management and counseling.</p><p><strong>Methods: </strong>We conducted a multicenter cohort study using data from 1,105 stroke survivors (mean age 71 years, 54% male) with neuroimaging-confirmed ischemic stroke who underwent EEG within 7 days post-stroke. Electrographic biomarkers, including epileptiform activity and regional slowing, were analyzed for their association with post-stroke epilepsy using Cox proportional hazards regression and Fine-Gray subdistribution hazard models, adjusted for differences in EEG timing and patient characteristics.</p><p><strong>Results: </strong>Post-stroke epilepsy developed in 119 patients (11%), whereas 233 (21%) had acute symptomatic seizures. The 5-year epilepsy risk was 42% (95% confidence interval [CI]: 30-49%) in patients with epileptiform activity versus 13% (95% CI: 9-16%) in those without. Regional slowing doubled the 5-year epilepsy risk (23%, 95% CI: 17-30% vs 11%, 95% CI: 7-16%). Epileptiform activity (subdistribution hazard ratio: 2.3, 95% CI: 1.5-3.4, p < 0.001) and regional slowing (subdistribution hazard ratio: 1.7, 95% CI: 1.1-2.7, p = 0.02) were independently associated with post-stroke epilepsy. A novel prognostic model, SeLECT-EEG (concordance statistic: 0.75, 95% CI: 0.71-0.80), outperformed the previous standard (SeLECT_2.0; 0.71, 95% CI: 0.65-0.76, p < 0.001).</p><p><strong>Interpretation: </strong>Electrographic biomarkers improve post-stroke epilepsy prediction beyond clinical risk factors. The SeLECT-EEG model enhances early risk stratification, particularly in patients without acute symptomatic seizures, informing management strategies and patient counseling. ANN NEUROL 2025.</p>","PeriodicalId":127,"journal":{"name":"Annals of Neurology","volume":" ","pages":""},"PeriodicalIF":8.1,"publicationDate":"2025-06-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144493258","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":"Enhancing the Evaluation of IVT in DOAC-Treated Stroke Patients: Addressing Methodological Considerations for Future Research","authors":"Zhengting Duan MD,&nbsp;Li Qi MD","doi":"10.1002/ana.27282","DOIUrl":"10.1002/ana.27282","url":null,"abstract":"","PeriodicalId":127,"journal":{"name":"Annals of Neurology","volume":"98 2","pages":""},"PeriodicalIF":8.1,"publicationDate":"2025-06-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144493256","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 “Enhancing the Evaluation of IVT in DOAC-Treated Stroke Patients: Addressing Methodological Considerations for Future Research”","authors":"Marius Matusevicius MD, PhD,&nbsp;Malin Säflund MD,&nbsp;Niaz Ahmed MD","doi":"10.1002/ana.27283","DOIUrl":"10.1002/ana.27283","url":null,"abstract":"","PeriodicalId":127,"journal":{"name":"Annals of Neurology","volume":"98 2","pages":"421-423"},"PeriodicalIF":8.1,"publicationDate":"2025-06-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144493257","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":"μ-Opioid Receptor Dynamics in the Parameningeal Tissue During Migraine Attacks.","authors":"Dajung J Kim, Manyoel Lim, Thiago D Nascimento, Frank Porreca, Robert A Koeppe, Nouchine Hadjikhani, Alexandre F DaSilva","doi":"10.1002/ana.27289","DOIUrl":"https://doi.org/10.1002/ana.27289","url":null,"abstract":"<p><strong>Objective: </strong>The possible impact of meningeal μ-opioid receptor (μOR) binding in migraine remains unknown. This study investigated μOR availability in the cranial parameninges involved in migraine initiation via nociceptor activation.</p><p><strong>Methods: </strong>We used positron emission tomography with [¹¹C] carfentanil, and measured μOR availability in meninges and adjacent skull bone (parameningeal tissue [PMT]) under resting and sustained thermal pain threshold stress challenge conditions. μOR availability was compared between individuals with migraine in interictal and ictal phases and healthy controls. Furthermore, we examined the relationship between μOR availability and headache intensity, as well as the potential influence of sex on this measure.</p><p><strong>Results: </strong>A total of 36 patients with interictal episodic migraine (8 also assessed ictally), 7 patients with ictal chronic migraine, and 22 healthy controls were included in the analysis. Both the episodic migraine and chronic migraine groups showed lower μOR availability in the parietal PMT than healthy controls during the ictal resting phase. No significant differences were observed during the interictal phase. Exploratory analyses on the effects of sex indicated that both healthy women and migraine patients of both sexes showed lower μOR availability in the frontal PMT compared with healthy men in the ictal sustained thermal pain threshold stress condition. Furthermore, the interictal μOR availability in the frontal PMT was negatively associated with headache intensity in the preceding month.</p><p><strong>Interpretation: </strong>The observed variability in PMT μOR availability across the different cortical regions and migraine episodes, along with its association with pain intensity, underscores the critical role of extracerebral mechanisms in migraine pathophysiology. ANN NEUROL 2025.</p>","PeriodicalId":127,"journal":{"name":"Annals of Neurology","volume":" ","pages":""},"PeriodicalIF":8.1,"publicationDate":"2025-06-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144493259","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}