Objectives: To determine the profile of late epileptic seizures following cerebral infarcts and the predictive clinical and radiological factors associated with their development.
Methods: We compared 86 patients who developed late seizures after cerebral infarction with 285 similar patients who did not develop seizures for at least 1 year after their stroke. Patients who had seizures only at the onset of the stroke were excluded. Odds' ratios were used for statistical analysis.
Results: Simple partial, and mainly motor seizures, with or without secondary generalization, accounted for 80% of the classifiable seizures but it was not possible to determine the seizure type in half of the cases. Factors that appeared to be predictive of seizure development were the presence of large cortical infarcts and the presence of apparently preserved cerebral tissue within the infarcted area. Seizures were rare in patients with lacunar infarction but the presence of associated leukoaraiosis increased the risk. The risk was also increased in patients with other medical problems known to lower seizure threshold, such as renal failure.
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http://dx.doi.org/10.1111/j.1600-0404.1999.tb00674.x | DOI Listing |
Ann Vasc Surg
January 2025
Vascular and Endovascular Surgery, University of Miami School of Medicine, Miami, Florida. Electronic address:
Background: Cerebral hyperperfusion syndrome (CHS) is a rare but serious complication after carotid artery revascularization. This study aims to determine the impact of carotid artery stenting (CAS) modality on the incidence, severity and overall outcomes of CHS after carotid revascularization.
Methods: Data from patients who underwent CAS with either distal embolic protection (CAS+DEP) or transcarotid artery revascularization (TCAR) were obtained from the Vascular Quality Initiative (VQI) database 2016-2023.
J Neurosci
January 2025
Department of Neuroscience, Brown University, Providence RI, USA.
Voltage-gated potassium conductances [Formula: see text] play a critical role not only in normal neural function, but also in many neurological disorders and related therapeutic interventions. In particular, in an important animal model of epileptic seizures, 4-aminopyridine (4-AP) administration is thought to induce seizures by reducing [Formula: see text] in cortex and other brain areas. Interestingly, 4-AP has also been useful in the treatment of neurological disorders such as multiple sclerosis (MS) and spinal cord injury, where it is thought to improve action potential propagation in axonal fibers.
View Article and Find Full Text PDFMol Biol Cell
January 2025
Department of Cell Biology, Emory University, 615 Michael St, Atlanta, GA, USA, 30322.
Rare inherited diseases caused by mutations in the copper transporters (CTR1) or induce copper deficiency in the brain, causing seizures and neurodegeneration in infancy through poorly understood mechanisms. Here, we used multiple model systems to characterize the molecular mechanisms by which neuronal cells respond to copper deficiency. Targeted deletion of CTR1 in neuroblastoma cells produced copper deficiency that produced a metabolic shift favoring glycolysis over oxidative phosphorylation.
View Article and Find Full Text PDFNeurosurgery
January 2025
Service de Neurochirurgie, GHU-Paris Psychiatrie et Neurosciences, Paris, France.
Background And Objectives: The risk-to-benefit ratio of transopercular awake resection for recurrent insular diffuse gliomas is poorly studied. We assessed feasibility, safety, and efficacy of awake surgical resection of recurrent insular diffuse gliomas in patients with previous treatments (resection and/or radiotherapy and/or chemotherapy and/or combination).
Methods: Observational, retrospective, single-institution cohort analysis (2010-2023) of 123 consecutive adult patients operated on for an insular diffuse glioma (2021 World Health Organization classification) under awake conditions.
Hum Mol Genet
January 2025
Department of Cell & Developmental Biology, Vanderbilt University School of Medicine, 1161 21st Ave S, Nashville, Tennessee, 37232, United States of America.
Tuberous Sclerosis Complex (TSC) is a debilitating developmental disorder characterized by a variety of clinical manifestations. While benign tumors in the heart, lungs, kidney, and brain are all hallmarks of the disease, the most severe symptoms of TSC are often neurological, including seizures, autism, psychiatric disorders, and intellectual disabilities. TSC is caused by loss of function mutations in the TSC1 or TSC2 genes and consequent dysregulation of signaling via mechanistic Target of Rapamycin Complex 1 (mTORC1).
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