Focal cortical dysplasias (FCDs) are estimated to be responsible for half of the drug-resistant epilepsies in the children and 20% in the adult population. Pathologically, FCDs include a wide spectrum of lesions including (a) a cortical dyslamination with heterotopic neurons in the white matter (WM; architectural dysplasia), (b) a cortical dyslamination with heterotopic neurons in the WM and dysmorphic neurons (mostly in layers II–III; cytoarchitectural dysplasia), and (c) a cortical dyslamination with heterotopic neurons in the WM, dysmorphic and giant neurons, and balloon cells (Taylor type 2) or not (Taylor type 1). The pathogenesis of FCDs involves an early disorder of cell proliferation/differentiation related to the presence of neuromegaly and balloon cells, but later developmental processes such as neuronal migration and cortical organization are involved as well (1). In FCD, electroencephalograms (EEGs) usually record interictal rhythmic epileptiform activity that could be related to more continuous epileptiform discharges with electrocorticography (ECoG). It is accepted that the best surgical strategy is to remove not only the visible lesion (magnetic resonance imaging; MRI), but also all the ECoG discharging area.
The aim of this work was to correlate ECoG patterns with immunohistochemical (IHC) findings in six patients with Taylor's type FCD who underwent limited corticectomy for drug-resistant epilepsy.