Exploration of neuroscience最新文献

{"title":"Colon cancer in a patient with a mosaic monoallelic germline pathogenic <i>NF1</i> gene variant.","authors":"Feras Alsabagh, Karam M Chaaban, Marlene Girardo, Ehab Harahsheh, Misha B Asif, Dusica Babovic-Vuksanovic, Mohamad Bassam Sonbol, Mayowa A Osundiji","doi":"10.37349/en.2026.1006148","DOIUrl":"10.37349/en.2026.1006148","url":null,"abstract":"<p><p>Pathogenic variants in the tumor suppressor gene <i>NF1</i> cause neurofibromatosis type 1 (NF1), one of the most common hereditary cancer predisposition syndromes. Pathogenic <i>NF1</i> variants have been associated with an increased risk of several cancers; however, the relationship between <i>NF1</i> variation and colon cancer remains underreported. We report a 41-year-old woman with a mosaic monoallelic germline pathogenic <i>NF1</i> variant, NM_000267.3:c.1756_1759del (p.Thr586Valfs*18), previously detected on germline multigene panel testing in saliva at a variant allele frequency of approximately 35%. She later presented with fatigue, dyspnea on exertion, and iron-deficiency anemia. Computed tomography, colonoscopy, biopsy, mismatch repair immunohistochemistry, surgical pathology, and tumor next-generation sequencing led to the diagnosis of right-sided colon adenocarcinoma that was mismatch repair deficient (dMMR) and microsatellite instability-high (MSI-H). She underwent right hemicolectomy, recovered postoperatively, and entered standard surveillance; at the time of manuscript development, she was also receiving systemic therapy. This case highlights the co-occurrence of an <i>NF1</i> variant and dMMR colorectal cancer and underscores the need for further studies to determine whether this represents a coincidental finding or a biologically meaningful association.</p>","PeriodicalId":73001,"journal":{"name":"Exploration of neuroscience","volume":"5 ","pages":"1006148"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13647451/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149139436","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":"Two cellular models for analyzing mitochondrial heteroplasmy","authors":"Yaning Hu, Lin Jiang, Wen Liu, Xingbo Zhao","doi":"10.37349/en.2025.100669","DOIUrl":"https://doi.org/10.37349/en.2025.100669","url":null,"abstract":"Aim: Mitochondria are essential for brain development, and the presence of different mitochondrial types is called mitochondrial heteroplasmy. Mitochondrial dysfunction is a central aspect of many people’s neurological diseases. Heteroplasmy is commonly observed in eukaryotes due to mitochondrial genome (mtDNA) mutation, paternal leakage, mitochondria transplantation/mitotherapy, and somatic cell nuclear transfer (SCNT). In this study, we developed two novel approaches to construct mitochondrial heteroplasmy cellular models. Methods: Model 1: the yak cell line (Bos grunniens) was transfected with p-eGFP-neo plasmid while mammary alveolar cell-T (MAC-T) cell line from cattle cells (Bos taurus) was stained with MitoTracker Deep Red FM. The yak cell line was used as recipient cells which fused with enucleated cattle cells. Model 2: The cattle cell line was stained with MitoTracker Green FM while yak cells were stained with MitoTracker Deep Red FM. Cattle cells were used as recipient cells which fused with enucleated yak cells. Following fusions, the single cells exhibiting dual positive fluorescence signals were sorted into 96-well plate by fluorescence-activated cell sorting. Confocal fluorescence examination confirmed that the cells with mitochondrial heteroplasmy were sorted. Results: The two methods can generate a variety of mitochondrial heteroplasmy cells of interest which can aid in understanding the patterns and influencing factors underlying heteroplasmy changes. Conclusions: The mitochondrial heteroplasmy cellular model contributes to managing heteroplasmy mitochondrial changes and preventing the development of mitochondrial declines.","PeriodicalId":73001,"journal":{"name":"Exploration of neuroscience","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-01-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.explorationpub.com/uploads/Article/A100669/100669.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147908627","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":"Most prominent challenges in translational neuroscience and strategic solutions to bridge the gaps: Perspectives from an editorial board interrogation.","authors":"Dirk M Hermann, Marco Bacigaluppi, Claudio L Bassetti, Gabrio Bassotti, Johannes Boltze, Andrew Chan, Turgay Dalkara, Adam Denes, Exuperio Diez-Tejedor, Richard Dodel, Thorsten R Doeppner, Egor Dzyubenko, Ayman ElAli, Tamas Fulop, Alexander Gerhard, Bernd Giebel, Janine Gronewold, Matthias Gunzer, Thomas Heinbockel, Kaibin Huang, Marcello Iriti, Hans-Otto Karnath, Kasteleijn-Nolst Trenite, Ertugrul Kilic, Giuseppe Lanza, Arthur Liesz, Tim Ullrich Magnus, Jessica Mandrioli, Ayan Mohamud-Yusuf, Thomas Müller, Suyue Pan, Luca Peruzzotti-Jametti, Stefano Pluchino, Ryszard Pluta, Aurel Popa-Wagner, Ameneh Rezayof, Mohamed L Seghier, Xinhua Shu, Vikram Singh, Jussi Sipilä, Mark Slevin, Yamei Tang, Georgios Tsivgoulis, Giustino Varrassi, Chen Wang, Bayram Yilmaz, Maha S Zaki, Jinwei Zhang","doi":"10.37349/en.2025.1006106","DOIUrl":"10.37349/en.2025.1006106","url":null,"abstract":"<p><p>Recent progress in translational neuroscience has significantly advanced our understanding of neurological diseases. Research progress closely went in line with innovations in research methods, which have expanded our insights considerably beyond previous limits. However, despite the development of disease-modifying treatments, therapeutic options in brain diseases still lag behind fundamental discoveries in basic neuroscience. This perspective examines the factors that hinder clinical progress in translational neuroscience and provides solutions on how to overcome them. Editorial board members of <i>Exploration of Neuroscience</i> were interrogated about the most prominent challenges they see in translational neuroscience and about possible ways to overcome these issues. Key challenges were seen at the interface between experimental research and clinical studies by several members, both from the basic and applied neuroscience fields, which include the selection of appropriate study readouts and endpoints. The establishment of refined study endpoints, combined with biomarkers capable of predicting treatment responses in human patients, will be crucial for the successful clinical implementation of new therapies. Further obstacles were found in the standardization of experimental models, interventions, and assessments both in animals and humans, as well as in the development of personalized treatment strategies. These challenges can be addressed through more clearly defined experimental procedures that closely match clinical conditions and precision-based approaches that ensure efficient therapeutic responses. As a great opportunity, treatment options targeting pathophysiological processes in multiple brain diseases and disease processes in different organ systems were noted. Significant barriers remain in the funding of investigator-driven clinical trials through public research programs, as well as the education of translational and clinician scientists dedicated to clinical translation. Enhanced communication between experimental neuroscientists and clinicians, with a shared understanding and common language, will be essential for the success of future research endeavors.</p>","PeriodicalId":73001,"journal":{"name":"Exploration of neuroscience","volume":"4 ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12373390/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144980998","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":"Neurostimulation devices to treat Alzheimer's disease.","authors":"Felipe P Perez, Brett Walker, Jorge Morisaki, Haitham Kanakri, Maher Rizkalla","doi":"10.37349/en.2025.100674","DOIUrl":"10.37349/en.2025.100674","url":null,"abstract":"<p><p>The use of neurostimulation devices for the treatment of Alzheimer's disease (AD) is a growing field. In this review, we examine the mechanism of action and therapeutic indications of these neurostimulation devices in the AD process. Rapid advancements in neurostimulation technologies are providing non-pharmacological relief to patients affected by AD pathology. Neurostimulation therapies include electrical stimulation that targets the circuitry-level connection in important brain areas such as the hippocampus to induce therapeutic neuromodulation of dysfunctional neural circuitry and electromagnetic field (EMF) stimulation that targets anti-amyloid molecular pathways to promote the degradation of beta-amyloid (Aβ). These devices target specific or diffuse cortical and subcortical brain areas to modulate neuronal activity at the electrophysiological or molecular pathway level, providing therapeutic effects for AD. This review attempts to determine the most effective and safe neurostimulation device for AD and provides an overview of potential and current clinical indications. Several EMF devices have shown a beneficial or harmful effect in cell cultures and animal models but not in AD human studies. These contradictory results may be related to the stimulation parameters of these devices, such as frequency, penetration depth, power deposition measured by specific absorption rate, time of exposure, type of cell, and tissue dielectric properties. Based on this, determining the optimal stimulation parameters for EMF devices in AD and understanding their mechanism of action is essential to promote their clinical application, our review suggests that repeated EMF stimulation (REMFS) is the most appropriate device for human AD treatments. Before its clinical application, it is necessary to consider the complicated and interconnected genetic and epigenetic effects of REMFS-biological system interaction. This will move forward the urgently needed therapy of EMF in human AD.</p>","PeriodicalId":73001,"journal":{"name":"Exploration of neuroscience","volume":"4 ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11904933/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143626953","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":"Molecular and cellular processes underlying Unverricht-Lundborg disease—prospects for early interventions and a cure","authors":"E. Žerovnik","doi":"10.37349/en.2024.00051","DOIUrl":"https://doi.org/10.37349/en.2024.00051","url":null,"abstract":"A short overview of the main features of progressive myoclonus epilepsies (PMEs), such as Lafora disease (LD), neuronal ceroid lipofuscinoses (NCLs), and myoclonus epilepsy with ragged-red fibers (MERRF) is given. The stress of this review paper is put on one of the PME’s, the Unverricht-Lundborg disease (ULD)—EPM1, which is caused by mutations in the human cystatin B gene (stefin B is an alternative protein’s name). However, different other genes/proteins were found mutated in patients presenting with EPM1-like symptoms. By understanding their function and pathophysiological roles, further insights into the underlying processes of EPM1 can be obtained. On a broader scale, common pathophysiological mechanisms exist between ULD, LD and NCLs, such as, reactive glia, synaptic remodeling, neuronal hyperexcitability, impairements in the lysosomal/endocytosis system, cytoskeletal functions, and mitochondria. Oxidative stress is also in common. By understanding the underlying molecular and cellular processes, early interventions, better therapies and eventually, by using modern stem cell, gene editing or replacement methods, a cure can be expected.","PeriodicalId":73001,"journal":{"name":"Exploration of neuroscience","volume":" 16","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-07-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141826841","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The role of inflammation and oxidative stress in the pathophysiology of depressions: time to consider vitamin C deficiency","authors":"C. Vollbracht, Marc Werner","doi":"10.37349/en.2024.00050","DOIUrl":"https://doi.org/10.37349/en.2024.00050","url":null,"abstract":"Depression is on the rise and medication does not always provide satisfactory relief. This raises the question of a treatment gap that has not yet been (sufficiently) addressed. Inflammation and oxidative stress play an important pathophysiological role, which also leads to a deficiency of antioxidants such as vitamin C. This perspective mini-review reflects the results of a PubMed search combining the search terms depression with inflammation, oxidative stress and vitamin C. Vitamin C is an important antioxidant and co-factor for many neuronal metabolic and epigenetic pathways, and a deficiency is associated with depression and cognitive disorders. Inadequate vitamin C blood levels that do not yet result in somatic symptoms may induce neuropsychiatric scurvy, which is associated with increased neuroinflammation and characterized by depression and cognitive impairment. Experimental studies show that vitamin C has multifactorial effects on metabolic pathways relevant to depression. Treatment of vitamin C deficiency, which is more common than appreciated, should be considered in the management of depressed patients. Further studies should investigate whether the pharmacological administration of vitamin C has additional effects beyond the correction of deficiency.","PeriodicalId":73001,"journal":{"name":"Exploration of neuroscience","volume":"48 8","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141659977","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Novel treatments of depression: bridging the gap in current therapeutic approaches","authors":"Amit Jagtiani","doi":"10.37349/en.2024.00049","DOIUrl":"https://doi.org/10.37349/en.2024.00049","url":null,"abstract":"Depression poses a significant global health burden, yet current therapeutic approaches focusing on monoaminergic neurotransmission often fall short of achieving full remission and managing acute episodes effectively. This article explores novel treatment avenues beyond conventional monoaminergic approaches, focusing on emerging strategies targeting glutamatergic modulation, electrophysiological/magnetic brain stimulation techniques, anti-inflammatory agents, gut-brain axis interventions, gamma-aminobutyric acid (GABA) modulation, and psychedelic-assisted therapy. Through a narrative review of recent literature, this paper elucidates the mechanisms, clinical efficacy, safety profiles, and future directions of these innovative treatments. These insights offer valuable perspectives for advancing depression management and bridging existing therapeutic gaps.","PeriodicalId":73001,"journal":{"name":"Exploration of neuroscience","volume":"122 18","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-07-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141666329","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Validation and cultural adaption of the neuropathic pain screening questionnaire painDETECT in Chinese","authors":"Howan Leung, Josephine W.Y. Ip, J. Lam, Gavin K.W. Lee, Carina C.F. Li, Richard Li, Vincent Mok, Tak H. Tsoi, Chun P. Wong, Steven H.S. Wong, Chun M. Chang, Rainer Freynhagen","doi":"10.37349/en.2024.00046","DOIUrl":"https://doi.org/10.37349/en.2024.00046","url":null,"abstract":"Aim: The aim of this study was to validate a Chinese version of the painDETECT questionnaire (PD-Q) for the screening and assessment of neuropathic pain (NeP) in a Hong Kong Chinese population. Methods: The PD-Q was translated and cross-culturally adapted from the original German PD-Q, with forward and backward translation according to standard guidelines followed by cognitive debriefing, and finalized by an expert panel. A multicenter (6-site) observational study was conducted to evaluate the validity of the PD-Q. Patients aged 18 or above with medical conditions giving rise to either neuropathic or nociceptive pain (NoP) provided informed consent to participate in this study. Each patient was evaluated by at least two healthcare professionals for causes of pain, the visual analogue scale (VAS), numeric rating scale (NRS) and the PD-Q. Results: Hong Kong Chinese adults (n = 151) were given the clinical description of NeP (n = 93), NoP (n = 41), or mixed pain (n = 17). The mean age of study subjects was 58.5 years (age range: 26–90 years); 94 subjects (62.3%) were female. The mixed pain group was only analysed qualitatively, with validation based on the remaining 134 patients. Mean PD-Q scores for patients diagnosed with NeP and NoP were 19.9 [standard deviation (SD) = 6.4] and 12.5 (SD = 6.2) respectively. Receiver operating characteristic (ROC) curves were plotted for the upper/lower boundaries. The upper boundary was calculated on the basis of a neuropathic diagnosis and a nociceptive diagnosis. The cut-off point was > 18 (80% sensitivity, 60% specificity), and area under the ROC curve (AUC) was 0.67 (P < 0.001). The lower boundary was calculated on the basis of a nociceptive and a neuropathic diagnosis. The cut-off point was < 13 (90% sensitivity, 50% specificity), and AUC was 0.79 (P < 0.001). Conclusions: The PD-Q is a reliable and valid scale to determine neuropathic components of chronic pain in the Hong Kong Chinese population. Validation in a larger Chinese-speaking population worldwide is necessary.","PeriodicalId":73001,"journal":{"name":"Exploration of neuroscience","volume":"17 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-06-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141343312","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Extracellular vesicles derived from mesenchymal stem cells ameliorate cognitive impairment caused by neuroinflammation in young but not aged mice","authors":"O. Lykhmus, O. Kalashnyk, M. Skok, O. Deryabina, Olena Toporova, I. Pokholenko, Oksana Gorbatiuk, Vitalii Kordium","doi":"10.37349/en.2024.00045","DOIUrl":"https://doi.org/10.37349/en.2024.00045","url":null,"abstract":"Aim: The aim of this work was to study the effects of extracellular vesicles (EVs) derived from mesenchymal stem cells (MSCs) on inflammation-impaired cognitive functions and the brain of mice.\u0000Methods: Young mice (~3-month-old) and aged mice (~18-month-old) were injected with bacterial lipopolysaccharide (LPS) and obtained intravenously donor 106 human umbilical cord MSCs, EVs isolated from a similar amount of MSCs or conditioned medium (CM) of MSCs. Subsequently, the mice were examined in behavioral tests and the mouse brains were analyzed for the levels of pro-inflammatory cytokines, α7 nicotinic acetylcholine receptors (α7 nAChRs) and amyloid beta 1-42 (Aβ1-42).\u0000Results: EVs prevented LPS-induced memory impairment in mice, whereas CM provided a weaker and temporal effect. Both EVs and MSCs injected once after regular injections of LPS stably improved memory of young mice. In contrast, both cells and EVs provided only transient effect in aged mice injected with LPS. The brains of aged LPS-treated mice contained elevated amounts of IL-1β and IL-6; both MSCs and EVs decreased them significantly. The brains of non-treated aged mice contained decreased levels of α7 nAChRs and increased levels of Aβ1-42 and α7-bound Aβ1-42 compared to the brains of young mice. LPS treatment decreased α7 nAChRs in both young and aged mice, while both MSCs and EVs restored them up to the control level. In young mice, LPS treatment increased the level of Aβ1-42 and α7-bound Aβ1-42, whereas MSCs and EVs decreased it. In contrast, neither LPS nor MSCs/EVs influenced the elevated level of Aβ1-42 but increased α7-bound Aβ1-42 in the brains of aged mice.\u0000Conclusions: Regenerative potential of MSCs and MSC-derived EVs is sufficient to support cognitive functions of LPS-treated young mice but is quite poor for aged animals, possibly, due to decreased levels of α7 nAChRs and accumulated Aβ1-42 in their brains.","PeriodicalId":73001,"journal":{"name":"Exploration of neuroscience","volume":"27 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-06-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141349978","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Using magnetic resonance-guided laser interstitial thermal therapy corpus callosotomy to lateralize a seizure focus for staged surgical approach","authors":"Kabir Sheikh, Derryl Miller, Robert Blake, Lisa Smith, Susan Conrad, Deborah Sokol, M. Obeid, Rupa Radhakrishnan, Anna Schultheis, Jeffrey Raskin","doi":"10.37349/en.2024.00044","DOIUrl":"https://doi.org/10.37349/en.2024.00044","url":null,"abstract":"New onset refractory status epilepticus (NORSE) is an etiologically heterogeneous condition that is associated with high morbidity and mortality. NORSE is often refractory to medical management prompting a workup for epilepsy surgery. Because NORSE remains etiologically elusive in most cases, surgical evaluations are challenging, especially when the epileptogenic zone (EZ) is not easy to lateralize as can be seen in frontal lobe seizures. Lateralizing a frontal lobe EZ may be challenging due to bilateral synchrony from commissural connections through the corpus callosum and low spatiotemporal resolution of the scalp electroencephalography (EEG). We report a pediatric patient with NORSE presenting with focal impaired awareness seizures clustering into super refractory status epilepticus (SRSE). She required surgical intervention for the treatment of her seizures after failing therapeutic doses of antiseizure medications, anesthetic drips, immunomodulation with methylprednisolone, intravenous immunoglobulin and anakinra, and the ketogenic diet. Despite her semiology being focal, the seizures were not well lateralized on scalp EEG and during phase 2 stereo-EEG (sEEG). Anterior magnetic resonance-guided laser interstitial thermal therapy corpus callosotomy (MRgLITT CC) was performed in a multistage surgical approach to successfully lateralize the EZ with a left-lateralized ictal pattern seen after reimplantation of sEEG electrodes. Our case suggests that minimally invasive MRgLITT CC can be successfully used to lateralize an EZ in frontal lobe epilepsy and that epilepsy surgery should be considered in patients with NORSE with SRSE. We also demonstrate that laser interstitial thermal therapy (LITT), while not always resulting in seizure freedom, can sufficiently disrupt a network to abort status epilepticus and lead to seizure improvements.","PeriodicalId":73001,"journal":{"name":"Exploration of neuroscience","volume":"6 3","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141271446","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}