Topic: Interictal epileptiform discharges

Interictal epileptiform discharges (IEDs) are brief, sporadic, pathologic electrical bursts in the brains of patients with epilepsy. IEDs represent an important disease biomarker for tracking seizure risk and they also convey direct pathophysiological impacts including on cognitive function. While most work in human IED mechanisms has targeted the population-level neural activity using macro-electrode recordings, the single-neuron mechanisms of IEDs across the depth of human cortical lamina in vivo are largely unknown. We leveraged high-density Neuropixels probes to evaluate single-neuron acti

Network hyperexcitability in Alzheimer’s Disease (AD) is claimed to be an important and potentially treatable pathophysiological mechanism. Empirical and modeling studies suggest that functional connectivity (FC) are promising quantitative neurophysiological markers for network hyperexcitability. This study examines how robust FC measures differ between AD patients with and without interictal epileptiform discharges (IEDs). We obtained eyes closed source-level magnetoencephalography recordings from demographically matched biomarker confirmed AD patients in the mild cognitive impairment and dem

Interictal Epileptiform Discharges (IEDs) are essential biomarkers of epilepsy in patients’ electroencephalograms (EEGs).The correct detection of IEDs helps the diagnosis, the localization of the epileptogenic zone and the monitoring of treatment. The gold standard to detect IEDs is the visual inspection of EEGs, performed by clinical experts. However, this task is time-consuming, prone to human error and subjectivity, and suffers from intra and inter-observer variability.This motivates the development of automated IED detectors. Researchers have explored various methods, from classical signal

Epileptogenesis, arising from alterations in synaptic strength, shares mechanistic and phenotypic parallels with memory formation. However, direct evidence supporting the existence of seizure memory remains scarce. We developed a novel conditioned seizure memory (CSM) paradigm, in which seizures and specific cues were paired. The CSM could be reliably retrieved, demonstrating a robust association. We also found that activation of cue-responding engram cells in hippocampus DG could create artificial CSM. After seizure memory retrieval, a protein synthesis-dependent reconsolidation process invol