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Delineation of seizure onset regions using intracranial electroencephalography (icEEG) is vital in the surgical workup of drug-resistant epilepsy cases. However, it is unknown whether the complete resection of these regions is necessary for seizure freedom, or whether postsurgical seizure recurrence can be attributed to the incomplete removal of seizure onset regions. To address this gap, we retrospectively analyzed icEEG recordings from 63 subjects, identifying seizure onset regions visually and algorithmically. We assessed onset region resection and correlated this with postsurgical seizure control. The majority of subjects had more than half of their onset regions resected (82.46% and 80.65% of subjects using visual and algorithmic methods, respectively). There was no association between the proportion of the seizure onset zone (SOZ) that was subsequently resected and better surgical outcomes (area under the receiver operating characteristic curve [AUC] < .7). Investigating the spatial extent of onset regions, we found no substantial evidence of an association with postsurgical seizure control (all AUC < .7). Although seizure onset regions are typically resected completely or in large part, incomplete resection is not associated with worse postsurgical outcomes. We conclude that postsurgical seizure recurrence cannot be attributed to an incomplete resection of the icEEG SOZ alone. Other network mechanisms beyond icEEG seizure onset likely contribute.
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http://dx.doi.org/10.1111/epi.18061 | DOI Listing |
Mol Cell Neurosci
September 2025
Department of Personalized & Molecular Medicine, Era University, Lucknow, India.
Epilepsy is a neurological disorder that shows strong genetic control on the timing and onset of symptoms and drug response variability. Some epilepsy syndromes have clear monogenic mutations but genes with control on the phenotype and severity of the disorder and drug sensitivity are present in the whole genetic profile. Genetic modifiers are not the cause of epilepsy but control significant networks such as synaptic plasticity and ion channels and neurodevelopment and neuroinflammation and therefore the reason why two individuals with the same primary mutations have different clinical courses.
View Article and Find Full Text PDFEpilepsia
September 2025
Department of Neurosurgery, Beijing Tiantan Hospital, Capital Medical University, Beijing, China.
Objective: This study aims to determine whether the anatomically heterogeneous lesions that cause hyperkinetic seizures (HKS) are connected to a common functional network.
Methods: We identified patients from the Beijing Tiantan-Fengtai Epilepsy Center with HKs as the primary ictal semiology. These included patients had focal seizure-onset zone, here referred to as a "lesion.
bioRxiv
August 2025
Department of Neuroscience and Physiology.
Cannabidiol (CBD) decreases seizures in patients with severe pediatric-onset epilepsies including Dravet, Lennox-Gastaut, and Tuberous Sclerosis syndromes. However, the effects of CBD on neuronal activity and circuits remain obscure. In the mouse hippocampus, we found that CBD causes a GPR55-independent decrease in CA1 pyramidal neuron firing frequency and a GPR55-dependent reduction in CA3 to CA1 hippocampal activity propagation.
View Article and Find Full Text PDFClin Toxicol (Phila)
September 2025
Rocky Mountain Poison and Drug Safety, Denver Health and Hospital Authority, Denver, CO, USA.
Introduction: The clinical presentations associated with spp. (true morel) and spp. (false morel) mushroom ingestions are incompletely characterized.
View Article and Find Full Text PDFNeurotherapeutics
September 2025
Department of Biomedical and Neuromotor Sciences, University of Bologna, Italy. Electronic address:
CDKL5 Deficiency Disorder (CDD) is a severe neurodevelopmental disorder caused by mutations in the X-linked CDKL5 gene, resulting in early-onset seizures, developmental delays, and cognitive and sensorimotor impairments. While emerging therapies show promise, substantial challenges remain in developing a cure for CDD. In our prior work, we developed an innovative gene therapy strategy based on an Igk-TATk-CDKL5 fusion protein, which enhances brain distribution of the therapeutic protein, significantly improving treatment efficacy in a Cdkl5 knockout male mouse model.
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