Hyper-synchrony in focal cortical dysplasia

Taylor's focal dysplasia presents a localized anomalous cortical lamination, associated with the presence of large aberrant neurons. Dysplastic cortex can generate epileptiform discharges, which then use the connectivity retained by the abnormal tissue to propagate. We studied pieces of cortex, dysplastic or not, obtained during the surgical resection of the epileptigenic zone in patients suffering from intractable epilepsy. In slices of cortical tissue maintained in vitro, we analyzed the properties of the dysplastic cortex, which could explain its ability to generate abnormal discharges. In this brief review of our results we show that: 1) cortical tissue from the epileptogenic zone, dysplastic or not, challenged with the convulsing drug 4-aminopyridine, generates synchronous potentials that are mainly contributed by gaba-A receptor-mediated conductances; 2) slices from dysplastic cortex have an intrinsic ability to generate, either spontaneously or when challenged with 4-aminopyridine, ictal-like epileptiform events; 3) ictal-like discharges are not observed in slices obtained from cortex with no dysplastic anomaly, even when challenged with 4-aminopyridine; 4) ictal-like discharges results from the activation of glutamate receptors and notably those of the N-methyl-D aspartate type; 5) ictal-like discharges need the involvement of gap junctions.