Brain communications最新文献

{"title":"Neural tracking of natural speech: an effective marker for post-stroke aphasia.","authors":"Pieter De Clercq, Jill Kries, Ramtin Mehraram, Jonas Vanthornhout, Tom Francart, Maaike Vandermosten","doi":"10.1093/braincomms/fcaf095","DOIUrl":"10.1093/braincomms/fcaf095","url":null,"abstract":"<p><p>After a stroke, approximately one-third of patients suffer from aphasia, a language disorder that impairs communication ability. Behavioural tests are the current standard to detect aphasia, but they are time-consuming, have limited ecological validity and require active patient cooperation. To address these limitations, we tested the potential of EEG-based neural envelope tracking of natural speech. The technique investigates the neural response to the temporal envelope of speech, which is critical for speech understanding by encompassing cues for detecting and segmenting linguistic units (e.g. phrases, words and phonemes). We recorded EEG from 26 individuals with aphasia in the chronic phase after stroke (>6 months post-stroke) and 22 healthy controls while they listened to a 25-min story. We quantified neural envelope tracking in a broadband frequency range as well as in the delta, theta, alpha, beta and gamma frequency bands using mutual information analyses. Besides group differences in neural tracking measures, we also tested its suitability for detecting aphasia at the individual level using a support vector machine classifier. We further investigated the reliability of neural envelope tracking and the required recording length for accurate aphasia detection. Our results showed that individuals with aphasia had decreased encoding of the envelope compared to controls in the broad, delta, theta and gamma bands, which aligns with the assumed role of these bands in auditory and linguistic processing of speech. Neural tracking in these frequency bands effectively captured aphasia at the individual level, with a classification accuracy of 83.33% and an area under the curve of 89.16%. Moreover, we demonstrated that high-accuracy detection of aphasia can be achieved in a time-efficient (5-7 min) and highly reliable manner (split-half reliability correlations between <i>R</i> = 0.61 and <i>R</i> = 0.96 across frequency bands). In this study, we identified specific neural response characteristics to natural speech that are impaired in individuals with aphasia, holding promise as a potential biomarker for the condition. Furthermore, we demonstrate that the neural tracking technique can discriminate aphasia from healthy controls at the individual level with high accuracy, and in a reliable and time-efficient manner. Our findings represent a significant advance towards more automated, objective and ecologically valid assessments of language impairments in aphasia.</p>","PeriodicalId":93915,"journal":{"name":"Brain communications","volume":"7 2","pages":"fcaf095"},"PeriodicalIF":4.1,"publicationDate":"2025-03-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11891514/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143598602","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Phantom limb experience after brachial plexus anaesthesia.","authors":"Apolline Savarit, Violeta Pellicer Morata, Daniel Ma, Maribel Lopez, Kassondra L Collins, Katherine E Robinson-Freeman, Nicole K Weber, Margaret Cooper Knack, Frederick Martin Azar, Thomas W Throckmorton, Robert S Waters, Jack W Tsao","doi":"10.1093/braincomms/fcaf025","DOIUrl":"10.1093/braincomms/fcaf025","url":null,"abstract":"<p><p>There are more than two million amputees in the USA, and almost all will experience phantom limb sensations (PLS), describing the missing limb as still present. They may also experience intense pain, known as phantom limb pain (PLP), a considerable factor in poor quality of life. In some upper extremity amputees and following brachial plexus avulsion injury (BPAI), hand digits can be detected and mapped to distinct facial skin areas, termed hand-to-face remapping. In this study, we analysed PLS following brachial plexus anaesthesia (BPA) administered prior to upper limb surgeries. Our 39 participants had planned shoulder, wrist or hand surgery. We sought to determine the time course for the emergence of phantom limb experiences after BPA up to the following 24 hours in participants with intact limbs. We also investigated whether there was hand-to-face remapping, suggesting potential cortical reorganization, or changes in proprioception before and after the induction of BPA. Twenty (54%) participants reported PLS immediately after the onset of BPA (T2), and 28 (72%) participants altered proprioception (AP) after surgery (T3). However, neither PLP nor hand mapping onto the face was reported or evoked. PLS were seen earlier than AP. We conclude that PLS arise rapidly after BPA-induced temporary deafferentation of the upper limb and might serve as a model for the permanent deafferentation experienced in individuals with a major upper limb amputation or BPAI. These results contribute to defining a time course for changes after BPA and increase our understanding of how phantom limb phenomena might arise following limb amputation or BPAI.</p>","PeriodicalId":93915,"journal":{"name":"Brain communications","volume":"7 2","pages":"fcaf025"},"PeriodicalIF":4.1,"publicationDate":"2025-03-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11882501/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143574941","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Phase 2 study of palmitoylethanolamide combined with luteoline in frontotemporal dementia patients.","authors":"Martina Assogna, Francesco Di Lorenzo, Sonia Bonnì, Ilaria Borghi, Emanuele Cerulli Irelli, Lucia Mencarelli, Michele Maiella, Marilena Minei, Romina Esposito, Elias P Casula, Valentina Pezzopane, Alessia D'Acunto, Francesco Porrazzini, Francesca Candeo, Matteo Ferraresi, Caterina Motta, Clarissa Ferrari, Carlo Caltagirone, Alessandro Martorana, Giacomo Koch","doi":"10.1093/braincomms/fcaf080","DOIUrl":"10.1093/braincomms/fcaf080","url":null,"abstract":"&lt;p&gt;&lt;p&gt;Frontotemporal dementia is a devastating neurodegenerative disorder for which no pharmacological treatments have been approved. Neuroinflammation plays a central role in driving the pathogenic mechanisms underlying frontotemporal dementia. In the last few years, co-ultramicronized palmitoylethanolamide combined with luteoline has emerged as a potential therapeutic molecule in neurodegenerative disorders pathogenically related to frontotemporal dementia, for its demonstrated strong anti-inflammatory and neuroprotective properties. Here we wanted to determine whether treatment with co-ultramicronized palmitoylethanolamide combined with luteoline may have a clinical impact in frontotemporal dementia patients. We performed a Phase 2, monocentric, randomized, double-blind, placebo-controlled trial to evaluate the safety and efficacy of co-ultramicronized palmitoylethanolamide combined with luteoline in frontotemporal dementia patients. Forty eight patients with a diagnosis of probable frontotemporal dementia were randomly assign in a 1:1 ratio to receive co-ultramicronized palmitoylethanolamide combined with luteoline oral suspension at the dosage of 700 mg + 70 mg twice/day (&lt;i&gt;n&lt;/i&gt; = 25) or placebo twice/day (&lt;i&gt;n&lt;/i&gt; = 23) for 24 weeks. The primary efficacy outcome measure was the change at 24-weeks in the Clinical Dementia Rating Dementia Staging Instrument from the National Alzheimer's Coordinating Center and frontotemporal lobar degeneration modules-sum of boxes (CDR plus NACC FTLD-SoB). Secondary outcome measures included the Frontal Assessment Battery, Screening for Aphasia in Neurodegeneration, Alzheimer's Disease Cooperative Study-Activities of Daily Living, Neuropsychiatric Inventory, Mini-Mental State Examination and Addenbrooke's Cognitive Examination Revised. Among 48 patients randomized [mean (SD) age 63.2 (8.4), 23 (47.9%) female], 45 (93%) completed the study. Patients in the co-ultramicronized palmitoylethanolamide combined with luteoline group showed less decline for the primary outcome measure (CDR plus NACC FTLD) as compared with patients treated with placebo. The estimated mean change (W0-W24) in CDR plus NACC FTLD score was 0.53 for the co-ultramicronized palmitoylethanolamide combined with luteoline group [95% confidence interval (0.12-0.94)] and 1.39 for the placebo group [95% confidence interval (0.96-1.82)], with an estimated mean difference between of 0.86 [95% confidence interval (0.28-1.45), &lt;i&gt;P&lt;/i&gt; = 0.005]. Estimated mean change in Alzheimer's Disease Cooperative Study-Activities of Daily Living score was -1.8 for co-ultramicronized palmitoylethanolamide combined with luteoline (95% confidence interval, -3.67 to 0.06) and -7.39 for placebo (95% confidence interval -9.34 to -5.45). Estimated mean change in screening for Aphasia in neurodegeneration scores was -3.987 for co-ultramicronized palmitoylethanolamide combined with luteoline (95% confidence interval, -7.75 to -0.22) and -10.35 for placebo (95% confidence","PeriodicalId":93915,"journal":{"name":"Brain communications","volume":"7 2","pages":"fcaf080"},"PeriodicalIF":4.1,"publicationDate":"2025-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11881584/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143568990","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sleep on it!","authors":"Laurent Sheybani","doi":"10.1093/braincomms/fcaf072","DOIUrl":"10.1093/braincomms/fcaf072","url":null,"abstract":"<p><p>Our Associate Editor, Laurent Sheybani, discusses some very old and very recent findings on sleep physiology and function, hoping to raise further interest and publications in the field.</p>","PeriodicalId":93915,"journal":{"name":"Brain communications","volume":"7 2","pages":"fcaf072"},"PeriodicalIF":4.1,"publicationDate":"2025-03-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11879451/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143569137","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction to: The role of brain white matter in depression resilience and response to sleep interventions.","authors":"","doi":"10.1093/braincomms/fcaf064","DOIUrl":"https://doi.org/10.1093/braincomms/fcaf064","url":null,"abstract":"<p><p>[This corrects the article DOI: 10.1093/braincomms/fcad210.].</p>","PeriodicalId":93915,"journal":{"name":"Brain communications","volume":"7 1","pages":"fcaf064"},"PeriodicalIF":4.1,"publicationDate":"2025-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11879035/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143560388","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Longitudinal alterations in brain networks and thalamocortical connectivity in paediatric focal epilepsy: a structural connectomics pilot study.","authors":"Aswin Chari, Rory J Piper, Rachel Wilson-Jeffers, Michelle Ruiz-Perez, Kiran Seunarine, M Zubair Tahir, Chris A Clark, Richard Rosch, Rod C Scott, Torsten Baldeweg, Martin M Tisdall","doi":"10.1093/braincomms/fcaf081","DOIUrl":"10.1093/braincomms/fcaf081","url":null,"abstract":"<p><p>Epilepsy is an archetypal brain network disorder characterized by recurrent seizures and associated psychological, cognitive and behavioural sequelae. Progressive brain network dysfunction may contribute to poorer outcomes following treatment, but this has never been tested in humans. In this structural connectomics pilot study, we assess whether there is progressive brain network dysfunction in a cohort of 23 children undergoing repeated multi-shell diffusion tensor imaging as part of their pre-surgical evaluation of focal epilepsy prior to epilepsy surgery. We analyse global and nodal graph metrics and thalamocortical connectivity, comparing the longitudinal changes to a cross-sectional cohort of 57 healthy controls. We identify no robust longitudinal changes in global or nodal network properties over a median of 1.15 years between scans. We also do not identify robust longitudinal changes in thalamic connectivity between scans. On sensitivity analyses, we identify increases in weighted degree at higher scales of brain parcellation and a decrease in the proportion of nodes with a low participation coefficient, suggesting progressive increases in intermodular connections. These findings of no or subtle structural longitudinal brain network changes over a relatively short timeframe indicate that either there are no progressive structural brain network changes over time in epilepsy or the changes appear over longer timescales. Larger studies with longer timeframes between scans may help clarify these findings.</p>","PeriodicalId":93915,"journal":{"name":"Brain communications","volume":"7 1","pages":"fcaf081"},"PeriodicalIF":4.1,"publicationDate":"2025-02-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11878571/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143560391","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neural correlates of fatigue after traumatic brain injury.","authors":"Annina E Anliker, Léa A S Chauvigné, Leslie Allaman, Adrian G Guggisberg","doi":"10.1093/braincomms/fcaf082","DOIUrl":"10.1093/braincomms/fcaf082","url":null,"abstract":"<p><p>Fatigue is the main cause of disability after traumatic brain injury and has negative impact on social, physical and cognitive functions, participation in daily activities, and ability to work. Since the neural underpinnings are largely unknown, few causal treatments are currently available. This study therefore aimed to investigate the neural correlates of subjective fatigue after traumatic brain injury, controlling for differences in cognitive performance, motor performance and subjective psychological covariates such as depression, anxiety and apathy. Seventeen chronic traumatic brain injury patients (10 with and seven without fatigue) and 11 age, sex, and education-matched healthy controls participated in the study. The dependent variable, overall fatigue, was quantified as the sum of the subscales of the multivariate fatigue inventory. Subjective psychological covariates were extracted from appropriate questionnaires. Brain activation during a two-back task and functional connectivity at rest were reconstructed from high-density EEG. Cortical excitability was quantified from motor evoked potentials induced by transcranial magnetic stimulation over the primary motor cortex. Cognitive performance was assessed with a two-back task as well as with a comprehensive neuropsychological test battery. Motor performance was quantified with Jamar dynamometer. Beside the between-group differences in most fatigue subscales resulting from the group attribution, participants also differed in subjective memory functions, depression, anxiety and apathy. Conversely, objective neuropsychological performance was similar across groups in most domains, except for alertness and divided attention (<i>P</i> ≤ 0.039). At the neural level, we observed no difference in corticospinal excitability, but a significant disruption of global resting-state alpha-band functional connectivity between cortical midline structures and the rest of the brain in patients with fatigue (<i>P</i> = 0.006). Furthermore, individuals with fatigue exhibited reduced signs of overall brain activation compared with healthy controls throughout the cognitive task (<i>P</i> = 0.032) without time-on-task effect. In a multivariate regression model, resting-state functional connectivity (<i>P</i> = 0.013) and subjective psychological questionnaire scores (<i>P</i> < 0.0001) were independent predictors of fatigue. In conclusion, our results suggest that disrupted network interactions are the primary independent neural predictor of fatigue. This may serve as a new target for therapy.</p>","PeriodicalId":93915,"journal":{"name":"Brain communications","volume":"7 2","pages":"fcaf082"},"PeriodicalIF":4.1,"publicationDate":"2025-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11891517/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143598601","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Plasma biomarkers for diagnosis and differentiation and their cognitive correlations in patients with Alzheimer's disease.","authors":"Wenhao Sun, Shuwei Ye, Yu Wang, Huifeng Chen, Ping Che, Jingshan Chen, Nan Zhang","doi":"10.1093/braincomms/fcaf094","DOIUrl":"10.1093/braincomms/fcaf094","url":null,"abstract":"<p><p>Increasing evidence has shown the potential value of plasma biomarkers in Alzheimer's disease diagnosis. This study aimed to determine the diagnostic and differential values of emerging plasma biomarkers for different types of dementia in a Chinese population and to explore their cognitive correlations. One hundred twenty patients with dementia, including 51 Alzheimer's disease patients, 54 subcortical ischaemic vascular dementia (SIVD) patients and 15 frontotemporal lobar degeneration (FTLD) patients were recruited alongside 27 cognitively unimpaired (CU) control subjects. Global and domain-specific cognition was assessed in all participants by a battery of neuropsychological tests. Plasma amyloid-beta (Αβ)42, Aβ40 and total tau (in CU controls and Alzheimer's disease patients) and phosphorylated tau at threonine-181 (<i>P</i>-tau181), neurofilament light (NfL) and glial fibrillar acidic protein (GFAP) levels (in all participants) were measured using the single-molecule array platform. The levels of all biomarkers differed between Alzheimer's disease patients and CU controls, with <i>P</i>-tau181 and GFAP levels and the Aβ42/P-tau181 ratio best differentiating the two groups [area under the curve (AUC) = 0.966, 0.932 and 0.927, respectively]. P-tau181 and GFAP levels were greater in the Alzheimer's disease group than in the other two patient groups and showed the best performance in distinguishing Alzheimer's disease patients from SIVD (AUC = 0.922) and FTLD patients (AUC = 0.894), respectively. Moreover, compared with that in the CU group, the GFAP level was elevated in the SIVD group, and the NfL level was elevated in all patient groups. Compared with other single biomarkers, the plasma Aβ42/P-tau181 ratio correlated with broader cognitive domains, including global cognition [Mini-Mental Status Examination (MMSE), <i>r</i> = 0.314, <i>P</i> = 0.027; Montreal Cognitive Assessment (MoCA), <i>r</i> = 0.313, <i>P</i> = 0.043], memory (<i>r</i> = 0.339, <i>P</i> = 0.016), language (<i>r</i> = 0.333, <i>P</i> = 0.020), attention and information processing speed (<i>r</i> = 0.369, <i>P</i> = 0.008), executive function (<i>r</i> = 0.305, <i>P</i> = 0.031) and visuospatial function memory (<i>r</i> = 0.453, <i>P</i> = 0.001). P-tau181 was an optimal plasma biomarker for identifying Alzheimer's disease patients and differentiating Alzheimer's disease patients from SIVD and FTLD patients. Moreover, the GFAP level and the Aβ42/P-tau181 ratio showed potential diagnostic and progression monitoring value, respectively, for Alzheimer's disease patients.</p>","PeriodicalId":93915,"journal":{"name":"Brain communications","volume":"7 2","pages":"fcaf094"},"PeriodicalIF":4.1,"publicationDate":"2025-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11881799/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143569124","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The role of microglia in the prion-like transmission of protein aggregates in neurodegeneration.","authors":"Muhammet M Öztürk, Jakob Emgård, Juan García-Revilla, Rosalía Fernández-Calle, Yiyi Yang, Tomas Deierborg, Tomas T Roos","doi":"10.1093/braincomms/fcaf087","DOIUrl":"10.1093/braincomms/fcaf087","url":null,"abstract":"<p><p>Numerous neurodegenerative diseases such as Alzheimer's disease, Parkinson's disease and amyotrophic lateral sclerosis share a neuropathological hallmark: aberrant protein aggregation in the CNS. Microglia, the brain's innate immune cells, also play a pivotal role in the pathogenesis of these disorders. Multiple studies indicate that these pathological aggregates can propagate throughout the brain in a prion-like manner. A protein/peptide that adopts a prion-like conformation can induce homologous proteins to misfold into a prion-like conformation through templated seeding, enabling cell-to-cell spread and accelerating protein aggregation throughout the brain. Two important questions in the prion-like paradigm are where the prion-like misfolding occurs and how the prion-like aggregates are spread throughout the CNS. Here, we review the role of microglia and associated inflammation in the prion-like spread of pathologically aggregated proteins/peptides in Alzheimer's disease, Parkinson's disease and amyotrophic lateral sclerosis. A growing body of evidence suggests that microglia can internalize prion-like proteins and transport them to neighbouring neurons and other glial cells. Microglia may also influence the potential seeding of proteins in neurons and induce inflammatory pathways in their microenvironment. This review aims to broaden the understanding of the role of microglia in the prion-like spread of protein aggregation.</p>","PeriodicalId":93915,"journal":{"name":"Brain communications","volume":"7 2","pages":"fcaf087"},"PeriodicalIF":4.1,"publicationDate":"2025-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11879441/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143569177","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Anti-seizure medication tapering correlates with daytime delta band power reduction in the cortex.","authors":"Guillermo M Besné, Nathan Evans, Mariella Panagiotopoulou, Billy Smith, Fahmida A Chowdhury, Beate Diehl, John S Duncan, Andrew W McEvoy, Anna Miserocchi, Jane de Tisi, Matthew C Walker, Peter N Taylor, Chris Thornton, Yujiang Wang","doi":"10.1093/braincomms/fcaf020","DOIUrl":"10.1093/braincomms/fcaf020","url":null,"abstract":"<p><p>Anti-seizure medications are the primary treatment for epilepsy; yet medication tapering effects have not been investigated in a dose, region and time-dependent manner, despite their potential impact on research and clinical practice. We examined over 3000 h of intracranial EEG recordings in 32 subjects during long-term monitoring, of which 22 underwent concurrent anti-seizure medication tapering. We estimated anti-seizure medication plasma levels based on known pharmaco-kinetics of all the major anti-seizure medication types. We found an overall decrease in the power of delta band (<i>δ</i>) activity around the period of maximum medication withdrawal in most (80%) subjects, independent of their epilepsy type or medication combination. The degree of withdrawal correlated positively with the magnitude of <i>δ</i> power decrease. This dose-dependent effect was evident across all recorded cortical regions during daytime; but not in subcortical regions, or during night time. We found no evidence of a differential effect in seizure onset, spiking, or pathological brain regions. The finding of decreased <i>δ</i> band power during anti-seizure medication tapering agrees with previous literature. Our observed dose-dependent effect indicates that monitoring anti-seizure medication levels in cortical regions may be feasible for applications such as medication reminder systems, or closed-loop anti-seizure medication delivery systems. Anti-seizure medications are also used in other neurological and psychiatric conditions, making our findings relevant to a general neuroscience and neurology audience.</p>","PeriodicalId":93915,"journal":{"name":"Brain communications","volume":"7 1","pages":"fcaf020"},"PeriodicalIF":4.1,"publicationDate":"2025-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11851006/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143506057","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}