MR modalities and retrospective coregistration of tissue sample with MRI was not feasible. Furthermore, myelin abnormalities are also present histologically in other FCD subtypes (Blumcke et al., 2011), with abnormal superficial cortical myelination noted in FCD IIIa (Thom et al., 2009) and WM hypomyelination in FCD IIIb (Thom et al., 2011), the later which may be misinterpreted as FCD II in traditional MRI (Campos et al., 2009), such as instances inside the present study. Further investigation of differences (or similarities) in myelin abnormalities in between FCD subtypes, with pathologyimaging coregistration, are warranted to improve preoperative recognition and discrimination of those lesions. In regard to patient outcome within this compact series, we showed significantly reduced measures of white matter myelination in the sufferers with seizure-free outcome at final follow-up. It has been reported that completeness of resection in the dysplastic cortex but not the underlying WM is important for seizure freedom (Wagner et al., 2011) implying that the extent of WM pathology is not relevant to outcome. It is actually doable, in the present series, that the presence of white matter pathology permitted much better discrimination of907 Oligodendroglia in Focal Cortical Dysplasia the extent of the lesion on MRI along with a a lot more comprehensive cortical resection, compared to situations without the need of this feature. Nevertheless, that is a study of a smaller quantity of situations plus the prognostic value of white matter pathology would demand verification within a bigger series. In conclusion, within this study quantifying the pathological basis of dysmyelination abnormalities in FCD we confirm mainly a loss of myelinated WM axons but with disorganized patterns of cortical myelination and overall preservation and representation of OL cells and their precursors. Our study has highlighted several future lines of investigation to pursue as towards the trigger and effects of those integral and diagnostic pathological modifications in the context of FCD.Benzbromarone de la Torre-Ubieta L, Bonni A.Eteplirsen (2011) Transcriptional regulation of neuronal polarity and morphogenesis inside the mammalian brain. Neuron 72:220. Diehl B, Tkach J, Piao Z, Ruggieri P, LaPresto E, Liu P, Fisher E, Bingaman W, Najm I.PMID:24318587 (2010) Diffusion tensor imaging in sufferers with focal epilepsy as a result of cortical dysplasia in the temporo-occipital area: electro-clinico-pathological correlations. Epilepsy Res 90:17887. Eriksson SH, Rugg-Gunn FJ, Symms MR, Barker GJ, Duncan JS. (2001) Diffusion tensor imaging in individuals with epilepsy and malformations of cortical improvement. Brain 124:61726. Ess KC. (2010) Tuberous sclerosis complex: a brave new planet Curr Opin Neurol 23:18993. Geha S, Pallud J, Junier MP, Devaux B, Leonard N, Chassoux F, Chneiweiss H, Daumas-Duport C, Varlet P. (2010) NG2+/Olig2+ cells are the main cycle-related cell population from the adult human typical brain. Brain Pathol 20:39911. Gomis-Ruth S, Wierenga CJ, Bradke F. (2008) Plasticity of polarization: changing dendrites into axons in neurons integrated in neuronal circuits. Curr Biol 18:992000. Hadjivassiliou G, Martinian L, Squier W, Blumcke I, Aronica E, Sisodiya SM, Thom M. (2010) The application of cortical layer markers in the evaluation of cortical dysplasias in epilepsy. Acta Neuropathol 120:51728. Hofman PA, Fitt GJ, Harvey AS, Kuzniecky RI, Jackson G. (2011) Bottom-of-sulcus dysplasia: imaging features. AJR Am J Roentgenol 196:88185. Jakovcevski I, Filipovic R, Mo Z, Rakic S, Zecevic N. (2009) Oligodendr.