Brain communications最新文献

{"title":"Appetite loss in patients with motor neuron disease: impact on weight loss and neural correlates of visual food cues.","authors":"Jeryn Chang, Thomas B Shaw, Pamela A McCombe, Robert D Henderson, Diana Lucia, Christine C Guo, Jinglei Lv, Kelly Garner, Saskia Bollmann, Shyuan T Ngo, Frederik J Steyn","doi":"10.1093/braincomms/fcaf111","DOIUrl":"10.1093/braincomms/fcaf111","url":null,"abstract":"<p><p>Motor Neuron Disease (MND) is associated with significant non-motor symptoms, including the loss of appetite. Loss of appetite has emerged as a dominant feature of the disease that may contribute to negative energy balance, faster disease progression and earlier death. We examined the prevalence and impact of appetite loss and analysed neural correlates of visual food stimuli with prandial status and appetite in people living with MND (plwMND). 157 plwMND and 120 non-neurodegenerative controls (NND Controls) were assessed for anthropometric, metabolic, appetite and clinical measures. Of these, 35 plwMND and 23 NND Controls underwent further functional MRI assessment of fasting and post-prandial responses to visual food cues. plwMND presented with reduced appetite (<i>P</i> < 0.001), with loss of appetite being more prevalent in plwMND than NND controls [OR = 2.59 (95% CI: = 1.46-4.61)]. Loss of appetite was not associated with hypermetabolism; however, was associated with fat mass loss (<i>P</i> < 0.05). Imaging assessment revealed no overall difference in response between plwMND and NND controls when viewing non-food and food images. In contrast, we found no prandial response in the temporal pole of plwMND compared with NND controls, and decreased activity in the cerebellum relative to appetite in plwMND. Loss of appetite, not hypermetabolism, contributes to negative energy balance in MND. Alterations in the temporal pole and cerebellum could contribute to altered appetite responses in some plwMND-brain regions not widely considered in appetite control-providing additional evidence to support widespread involvement of non-motor areas in the disease.</p>","PeriodicalId":93915,"journal":{"name":"Brain communications","volume":"7 2","pages":"fcaf111"},"PeriodicalIF":4.1,"publicationDate":"2025-03-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11938820/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143722988","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":"Spine plasticity to restore the cortical networks of movement: a therapeutic approach to spinal cord injury.","authors":"Caroline Machado, Edmund Hollis","doi":"10.1093/braincomms/fcaf076","DOIUrl":"10.1093/braincomms/fcaf076","url":null,"abstract":"<p><p>This scientific commentary refers to 'Edonerpic maleate enhances functional recovery from spinal cord injury with cortical reorganization in non-human primates', by Uramaru <i>et al</i>. (https://doi.org/10.1093/braincomms/fcaf036).</p>","PeriodicalId":93915,"journal":{"name":"Brain communications","volume":"7 2","pages":"fcaf076"},"PeriodicalIF":4.1,"publicationDate":"2025-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11903254/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143625846","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":"Mild traumatic brain injury increases cortical iron: evidence from individual susceptibility mapping.","authors":"Christi A Essex, Devon K Overson, Jenna L Merenstein, Trong-Kha Truong, David J Madden, Mayan J Bedggood, Catherine Morgan, Helen C Murray, Samantha J Holdsworth, Ashley W Stewart, Richard L M Faull, Patria Hume, Alice Theadom, Mangor Pedersen","doi":"10.1093/braincomms/fcaf110","DOIUrl":"10.1093/braincomms/fcaf110","url":null,"abstract":"<p><p>Quantitative susceptibility mapping has been applied to map brain iron distribution after mild traumatic brain injury to understand properties of neural tissue which may be related to cellular dyshomeostasis. However, this is a heterogeneous injury associated with microstructural brain changes, and 'traditional' group-wise statistical approaches may lead to a loss of clinically relevant information, as subtle alterations at the individual level can be obscured by averages and confounded by within-group variability. More precise and individualized approaches are needed to characterize mild traumatic brain injury better and elucidate potential cellular mechanisms to improve intervention and rehabilitation. To address this issue, we use quantitative MRI to build individualized profiles of regional positive (iron-related) magnetic susceptibility across 34 bilateral cortical ROIs following mild traumatic brain injury. Healthy population templates were constructed for each cortical area using standardized <i>Z</i>-scores derived from 25 age-matched male controls aged between 16 and 32 years (<i>M</i> = 21.10, SD = 4.35), serving as a reference against which <i>Z</i>-scores of 35 males with acute (<14 days) sports-related mild traumatic brain injury were compared [<i>M</i> = 21.60 years (range: 16-33), SD = 4.98]. Secondary analyses sensitive to cortical depth and curvature were also generated to approximate the location of iron accumulation in the cortical laminae and the effect of gyrification. Primary analyses indicated that approximately one-third (11/35; 31%) of injured participants exhibited elevated positive susceptibility indicative of abnormal iron profiles relative to the healthy population, a finding that was mainly concentrated in regions within the temporal lobe. Injury severity was significantly higher (<i>P</i> = 0.02) for these participants than their iron-normal counterparts, suggesting a link between injury severity, symptom burden, and elevated cortical iron. Secondary exploratory analyses of cortical depth and curvature profiles revealed abnormal iron accumulation in 83% (29/35) of mild traumatic brain injury participants, enabling better localization of injury-related changes in iron content to specific loci within each region and identifying effects that may be more subtle and lost in region-wise averaging. Our findings suggest that individualized approaches can further elucidate the clinical relevance of iron in mild head injury. Differences in injury severity between iron-normal and iron-abnormal mild traumatic brain injury participants identified in our primary analysis highlight not only why precise investigation is required to understand the link between objective changes in the brain and subjective symptomatology, but also identify iron as a candidate biomarker for tissue pathology after mild traumatic brain injury.</p>","PeriodicalId":93915,"journal":{"name":"Brain communications","volume":"7 2","pages":"fcaf110"},"PeriodicalIF":4.1,"publicationDate":"2025-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11954555/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143756433","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":"Brain structural alterations in vestibular schwannoma beyond tinnitus and hearing loss.","authors":"Abraham A Adegboro, Ziyan Chen, Jens J Peters, Cyrille D Dantio, Siyi Wanggou, Chubei Teng, Xuejun Li","doi":"10.1093/braincomms/fcaf107","DOIUrl":"10.1093/braincomms/fcaf107","url":null,"abstract":"<p><p>Brain tumours alter brain structures and functions. However, morphometric alterations induced by unilateral vestibular schwannoma, a benign tumour of the vestibulocochlear nerve, have not been extensively explored. Recent studies have suggested that the tumour does not grow bigger following diagnosis in several patients, suggesting an avenue for conservative therapy. This study aims to comprehensively investigate brain structural re-organizations in vestibular schwannoma patients taking into account the effects of hearing loss and tinnitus-the most common symptoms. To this end, preoperative data from 48 vestibular schwannoma pathology-confirmed patients and a healthy control group of 30 volunteers were retrospectively included in this study. The clinical and imaging data from these participants were processed. General linear models were designed to identify tumour-related brain alterations in grey matter volume and cortical thickness, alongside three other surface measures: sulcal depth, gyrification index and fractal dimension. The differences obtained were further analysed for correlation with tumour size and pure tone audiometry. Interestingly, grey matter volume, cortical thickness and for the first time, fractal dimension measures were increased in vestibular schwannoma patients across key frontal regions (<i>P_FWE</i> < 0.05). The precuneus, superior and inferior frontal gyrus had increased grey matter volumes and cortical thickening in patients compared to controls, among other changes (<i>P _FWE</i> < 0.05). Meanwhile, the sulcal depth and gyrification index measures demonstrated no significant alterations. Furthermore, grey matter volume changes at the paracentral lobule and precuneus were positively correlated to the tumour size, while the fractal dimension at the superior frontal sulcus was negatively correlated. Finally, grey matter volume increase at the inferior frontal gyrus and cortical thickening at the supramarginal gyrus were negatively correlated to pure tone audiometry. These findings suggest that factors beyond hearing loss and tinnitus contribute to brain structural alterations in this tumour, a better understanding of which might pave the way for non-surgical symptomatic therapies.</p>","PeriodicalId":93915,"journal":{"name":"Brain communications","volume":"7 2","pages":"fcaf107"},"PeriodicalIF":4.1,"publicationDate":"2025-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11937892/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143722990","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":"Unravelling pathological ageing with brain age gap estimation in Alzheimer's disease, diabetes and schizophrenia.","authors":"Maria Fátima Dias, João Valente Duarte, Paulo de Carvalho, Miguel Castelo-Branco","doi":"10.1093/braincomms/fcaf109","DOIUrl":"10.1093/braincomms/fcaf109","url":null,"abstract":"<p><p>Brain age gap estimation (BrainAGE), the difference between predicted brain age and chronological age, might be a putative biomarker aiming to detect the transition from healthy to pathological brain ageing. The biomarker primarily models healthy ageing with machine learning models trained with structural magnetic resonance imaging (MRI) data. BrainAGE is expected to translate the deviations in neural ageing trajectory and has been shown to be increased in multiple pathologies, such as Alzheimer's disease (AD), schizophrenia and Type 2 diabetes (T2D). Thus, accelerated ageing seems to be a general feature of neuropathological processes. However, neurobiological constraints remain to be identified to provide specificity to this biomarker. Explainability might be the key to uncovering age predictions and understanding which brain regions lead to an elevated predicted age on a given pathology compared to healthy controls. This is highly relevant to understanding the similarities and differences in neurodegeneration in AD and T2D, which remains an outstanding biological question. Sensitivity maps explain models by computing the importance of each voxel on the final prediction, thereby contributing to the interpretability of deep learning approaches. This paper assesses whether sensitivity maps yield different results across three conditions related to pathological neural ageing: AD, schizophrenia and T2D. Five deep learning models were considered, each model trained with different MRI data types: minimally processed T₁-weighted brain scans, and corresponding grey matter, white matter, cerebrospinal fluid tissue segmentation and deformation fields (after spatial normalization). Our results revealed an increased BrainAGE in all pathologies, with a different mean, which is the smallest in schizophrenia; this is in line with the observation that neural loss is secondary in this early-onset condition. Importantly, our findings suggest that the sensitivity, indexing regional weights, for all models varies with age. A set of regions were shown to yield statistical differences across conditions. These sensitivity results suggest that mechanisms of neurodegeneration are quite distinct in AD and T2D. For further validation, the sensitivity and the morphometric maps were compared. The findings outlined a high congruence between the sensitivity and morphometry maps for age and clinical group conditions. Our evidence outlines that the biological explanation of model predictions is vital in adding specificity to the BrainAGE and understanding the pathophysiology of chronic conditions affecting the brain.</p>","PeriodicalId":93915,"journal":{"name":"Brain communications","volume":"7 2","pages":"fcaf109"},"PeriodicalIF":4.1,"publicationDate":"2025-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11950532/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143756458","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":"Higher plasma neurofilament-light chain concentration in drug-resistant epilepsy.","authors":"Sarah Akel, Markus Axelsson, Fredrik Asztely, Henrik Zetterberg, Johan Zelano","doi":"10.1093/braincomms/fcaf108","DOIUrl":"10.1093/braincomms/fcaf108","url":null,"abstract":"<p><p>Drug-resistant epilepsy is the most severe form of epilepsy and is frequently associated with cognitive decline. Whether drug-resistant epilepsy results in neurodegeneration or other types of brain injury is not known, and early detection of detrimental clinical trajectories would be clinically very useful. Blood biomarkers of brain injury reflect neurodegeneration or brain injury in several brain diseases but have not been extensively studied in epilepsy. We investigated a panel of such markers in a large epilepsy cohort with an emphasis on assessing differences between drug-resistant and monotherapy-controlled epilepsy. Blood neurofilament light, glial fibrillary acidic protein, total tau, S100 calcium-binding protein B and neuron-specific enolase concentrations were measured in 444 patients (aged ≥ 18 years) with epilepsy participating in a prospective regional Biobank study in Västra Götaland (Sweden). Multiple linear regression assessed associations between clinical variables and marker levels. Levels were then compared between patients with drug-resistant epilepsy (<i>n</i> = 101) and patients with monotherapy-controlled epilepsy (<i>n</i> = 164). We also performed logistic regression analysis to evaluate the significance of the markers as predictors of epilepsy status (drug-resistant epilepsy or monotherapy-controlled epilepsy) while controlling for clinical variables: age, sex, epilepsy duration, epilepsy type and lesions. All markers correlated with age. In younger patients (≤50 years), cases of drug-resistant epilepsy had higher levels of neurofilament light (<i>P</i> = 0.002) and glial fibrillary acidic protein (<i>P</i> = 0.006) compared with monotherapy-controlled epilepsy. After excluding patients with known structural lesions, neurofilament light levels remained significantly elevated in drug-resistant epilepsy versus monotherapy-controlled epilepsy (<i>P</i> = 0.029). Neurofilament light also emerged as a significant predictor of drug-resistant status in a logistic regression model following adjustments for clinical variables. Future studies should explore if neurofilament light can be used for surveillance of disease course and whether it reflects brain injury in drug-resistant epilepsy.</p>","PeriodicalId":93915,"journal":{"name":"Brain communications","volume":"7 2","pages":"fcaf108"},"PeriodicalIF":4.1,"publicationDate":"2025-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11925020/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143671999","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 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":"Abnormalities of iron homeostasis and the dopaminergic system in Tourette syndrome revealed by 7T MRI and PET.","authors":"Dimitrios G Gkotsoulias, Michael Rullmann, Simon Schmitt, Anna Bujanow, Franziska Zientek, Konstantin Messerschmidt, André Pampel, Amira-Philine Büttner, Andreas Schildan, Osama Sabri, Kirsten Müller-Vahl, Henryk Barthel, Harald E Möller","doi":"10.1093/braincomms/fcaf104","DOIUrl":"10.1093/braincomms/fcaf104","url":null,"abstract":"<p><p>While the implication of a dysfunctional dopaminergic system in Tourette syndrome (TS) is well established, the underlying pathophysiological mechanisms remain unclear. Apart from neurotransmitters, disturbed iron homeostasis and iron regulatory mechanisms are also suspected. Iron is a trace element of fundamental biological importance and is involved in the synthesis and metabolism of dopamine and its receptors and transporters. The goal of the current pre-registered, multi-modal, cross-sectional study was to investigate the relationship between potential iron homeostasis imbalances and dopaminergic system disturbances in patients with TS. Susceptibility-sensitive MRI at 7 Tesla was used to obtain surrogate measures for local brain iron in 25 patients with TS (age 30 ± 9 years, 6 female) and 40 matched control subjects. Additionally, dopamine D₁ receptor availability was investigated with [¹¹C]SCH23390 PET in a subgroup of 20 patients and 20 controls. Significantly reduced sub-cortical magnetic susceptibility, indicating reduced iron levels, was observed in TS patients in the caudate, pallidum, sub-thalamic nucleus, thalamus, red nucleus and substantia nigra. These reductions were accompanied by significant reductions of the [¹¹C]SCH23390 binding potential indicating reduced availability of D₁ receptors in the dorsal striatum. The D₁ receptor abnormality correlated with tic severity. These results point to alterations of intra-synaptic dopamine release and reduced striatal D₁ receptor binding, supporting the notion of disruption in multiple functional elements of the dopaminergic system. Such dopaminergic abnormalities appear to be associated with disturbances in iron homeostasis.</p>","PeriodicalId":93915,"journal":{"name":"Brain communications","volume":"7 2","pages":"fcaf104"},"PeriodicalIF":4.1,"publicationDate":"2025-03-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11961303/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143775176","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":"Fatigue in multiple sclerosis: still elusive after all these years.","authors":"Lauren B Krupp, Kimberly A O'Neill","doi":"10.1093/braincomms/fcaf105","DOIUrl":"10.1093/braincomms/fcaf105","url":null,"abstract":"<p><p>This scientific commentary refers to 'Fatigue in early multiple sclerosis: MRI metrics of neuroinflammation, relapse and neurodegeneration', by Meijboom <i>et al.</i> (https://doi.org/10.1093/braincomms/fcae278).</p>","PeriodicalId":93915,"journal":{"name":"Brain communications","volume":"7 2","pages":"fcaf105"},"PeriodicalIF":4.1,"publicationDate":"2025-03-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11961358/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143775165","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}