Ts; Xiao-li DING produced the model and carried out measurements of vascular reactivity; Liang-ming LIU conceived the study and participated in its design and coordination. All authors approved the final manuscript.
Epilepsia, 54(5):898?08, 2013 doi: ten.1111/epi.FULL-LENGTH ORIGINAL RESEARCHA quantitative study of white matter hypomyelination and oligodendroglial maturation in focal cortical dysplasia form II*Caterina Shepherd, *Joan Liu, *Joanna Goc, *Lillian Martinian, Thomas S. Jacques, *Sanjay M. Sisodiya, and *Maria Thom*Department of Clinical and Experimental Epilepsy, UCL, Institute of Neurology and National Hospital for Neurology and Neurosurgery, London, United kingdom; and UCL-Institute of Child Health and Good Ormond Street Hospital NHS Trust, London, United KingdomSUMMARYPurpose: A diagnostic feature of focal cortical dysplasia (FCD) type II on magnetic resonance imaging (MRI) is increased subcortical white matter (WM) signal on T2 sequences corresponding to hypomyelination, the cause of which is unknown. We aimed to quantify WM pathology in FCD sort II and any deficiency within the numbers and differentiation of oligodendroglial (OL) cell varieties inside the dysplasia. Methods: In 19 cases we defined four regions of interests (ROIs): ROI1 = abnormal WM beneath dysplasia, ROI2 = dysplastic cortex, ROI3 = normal WM, and ROI4 = normal cortex. We quantified axonal and myelin density using immunohistochemistry for neurofilament, myelin basic protein and quantified mature OL with NogoA, cyclic nucleotide 3-phosphodiesterase (CNPase) and OL precursor cell (OPC) densities with platelet derived development factor receptor (PDGFR)a, b and NG-2 in each region. Key Findings: We observed a substantial reduction in myelin and axons within the WM beneath dysplasia relative tonormal WM and there was a correlation between relative reduction of myelin and neurofilament in each case. OL and OPC have been present within the WM beneath dysplasia and despite the fact that present in reduced numbers with most markers, were not significantly distinctive from typical WM.Price of 5-Chloropyrimidin-2(1H)-one Neurofilament and myelin labeling highlighted disorganized orientation of fibers in dysplastic cortex but there had been no important quantitative differences when compared with normal cortex.3-Aminobenzenesulfonyl fluoride Chemical name Clinical correlations showed an association amongst the severity of reduction of myelin and axons inside the WM of FCD and duration of epilepsy.PMID:23290930 Significance: These findings indicate a reduction of myelinated axons inside the WM of FCD kind II as opposed to dysmyelination as the main pathologic course of action underlying WM abnormalities, possibly influenced by duration of seizures. The selection of OPC to OL present in FCD variety II doesn’t implicate a key failure of cell recruitment and differentiation of these cell varieties in this pathology. Key WORDS: Focal cortical dysplasia kind II, White matter, Myelination, Oligodendroglia.In the 1st descriptions of the neuropathology now referred to as focal cortical dysplasia kind II (FCD II), Corsellis and Bruton noted that the adjacent white matter (WM) was poorly myelinated (Taylor et al., 1971). Regardless of many subsequent histopathologic research depending on epilepsy surgical series, this element from the pathology, in particular with regard towards the origin with the lowered myelin, has remained somewhat unexplored. (Blumcke et al., 2011). Diagnostic magnetic resonance imaging (MRI) characteristics of FCD II take into account WM abnormalities, visualized as blurring on the gray-white interface or enhanced subcortical signal on T2.
