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Introduction: Calcified parenchymal neurocysticercosis (NCC) lesions are commonly detected in many individuals with refractory epilepsy. However, the relationship between these lesions and epilepsy is not fully determined. We sought to determine if calcified parenchymal NCC demonstrated topographic congruence with epileptiform activity in refractory epilepsy patients. Additional patients with other structural brain lesions were included for comparison.
Subjects And Methods: Retrospective cross-sectional analysis of all patients treated at a community-based neurology clinic for refractory epilepsy during a 3-month period and with structural brain lesions detected by neuroimaging studies.
Results: A total of 105 patients were included in the study, including 63 with calcified parenchymal NCC lesions and 42 with other structural brain lesions. No significant relationship was detected between hemispheric localization of calcified parenchymal NCC lesions and epileptiform activity. For those with other structural brain lesions, the hemispheric localization was significantly related to the side of epileptiform activity (Chi-square = 11.13, P = 0.025). In addition, logistic regression models showed that those with right-sided non-NCC lesions were more likely to have right-sided epileptiform activity (odds ratio = 4.36, 95% confidence interval [CI] =1.16-16.31, P = 0.029), and those with left-sided non-NCC lesions were more likely to have left-sided epileptiform activity (odds ratio = 7.60, 95% CI = 1.89-30.49, P = 0.004).
Conclusion: The lack of correlation between the side of calcified parenchymal NCC lesions and the side of the epileptiform activity suggests that these lesions may be incidental findings in many patients.
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http://dx.doi.org/10.4103/2229-5070.175093 | DOI Listing |
Cogn Affect Behav Neurosci
December 2024
Department of Psychology, University of Utah, 380 S 1530 E BEH S 502, Salt Lake City, UT, 84112, USA.
Amygdala activation by emotional arousal during memory formation can prioritize events for long-term memory. Building upon our prior demonstration that brief electrical stimulation to the human amygdala reliably improved long-term recognition memory for images of neutral objects without eliciting an emotional response, our study aims to explore and describe individual differences and stimulation-related factors in amygdala-mediated memory modulation. Thirty-one patients undergoing intracranial monitoring for intractable epilepsy were shown neutral object images paired with direct amygdala stimulation during encoding with recognition memory tested immediately and one day later.
View Article and Find Full Text PDFBMC Neurol
December 2024
Laboratory for Epilepsy Research, KU Leuven, Belgium.
Background: Neuronal hyperexcitability has been proposed to play a key role in Alzheimer's disease (AD). Understanding the relation between this enhanced excitability and AD pathology could provide a window for therapeutic interventions. However epileptiform activity is often subclinical, hidden on scalp EEG and very challenging to assess with current diagnostic modalities.
View Article and Find Full Text PDFSci Data
December 2024
Sagol School of Neuroscience, Tel Aviv University, Tel Aviv, Israel.
Interictal epileptiform discharges (IEDs) such as spikes and sharp waves represent pathological electrophysiological activities occurring in epilepsy patients between seizures. IEDs occur preferentially during non-rapid eye movement (NREM) sleep and are associated with impaired memory and cognition. Despite growing interest, most studies involving IED detections rely on visual annotations or employ simple amplitude threshold approaches.
View Article and Find Full Text PDFEpilepsy Behav
December 2024
Tufts University School of Medicine, Neuroscience Department, Boston, MA, USA. Electronic address:
Stress is a common seizure trigger that has been implicated in worsening epilepsy outcomes, which encompasses psychiatric and cognitive comorbidities and sudden unexpected death in epilepsy (SUDEP) risk. The neuroendocrine response to stress is mediated by the hypothalamic-pituitary-adrenal (HPA) axis and HPA axis dysfunction worsens epilepsy outcomes, increasing seizure burden, behavioral comorbidities, and risk for SUDEP in mice. Early life stress (ELS) reprograms the HPA axis into adulthood, impacting both the basal and stress-induced activity.
View Article and Find Full Text PDFbioRxiv
December 2024
Department of Neurology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104.
Pathological tau spreads throughout the brain along neuronal connections in Alzheimer's disease (AD), but the mechanisms that underlie this process are poorly understood. Given the high incidence and deleterious consequences of epileptiform activity in AD, we hypothesized neuronal hyperactivity and seizures are key factors in tau spread. To examine these interactions, we created a novel mouse model involving the cross of targeted recombination in active populations (TRAP) mice and the 5 times familial AD (5XFAD; 5X-TRAP) model allowing for the permanent fluorescent labelling of neuronal activity.
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