Epileptiform synchronization in the human dysplastic cortex

Taylor's focal cortical dysplasia corresponds to a localized disruption of the normal cortical lamination with an excess of large, aberrant cells. Sustained epileptic discharges originate from the dysplastic neocortex and this tissue retains sufficient connectivity for expressing seizure abnormalities. In this brief review, we summarize the findings obtained by analyzing surgically-resected human tissue with focal cortical dysplasia that was maintained in vitro in a brain slice preparation. These data have been compared with those obtained from human cortex with normal structural organization; such tissue was available from patients undergoing surgery for a variety of neurological disorders, most often for mesial temporal lobe epilepsy. These studies have shown that: (i) slices obtained from focal cortical dysplastic tissue have an intrinsic ability to generate ictal-like epileptiform events when challenged with the convulsant drug 4-aminopyridine; (ii) 4-aminopyridine-induced ictal discharges are not seen in neocortical slices obtained from neocortical samples with no or minimal structural lesion; (iii) these ictal discharges are caused bythe activation of excitatory amino acid receptors, and in particular those of the N-methyl-D aspartate type; (iv) focal cortical dysplastic tissue also generates synchronous potentials that are mainly contributed by GABAA receptor-mediated conductances.