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Jorge A. González-Martínez, Zhong Ying, Richard Prayson, William Bingaman and Imad Najm

studied patients: architectural disorganization (Type 1A), architectural disorganization with the presence of dysmorphic (dysplastic) neurons (Type 1B), architectural disorganization with cytomegalic neurons (Type 2A), presence of balloon cell (Type 2B), 29 and regions with normal architecture and normal-looking neurons. As previously described, BCs were defined on cresyl echt violet staining according to the following criteria: 1) cells with diameter that is at least double the size of surrounding neurons with eccentric nuclear component, and 2) cells with

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Aaron A. Cohen-Gadol, Korey Özduman, Richard A. Bronen, Jung H. Kim and Dennis D. Spencer

epilepsy may harbor cortical dysplasia as the cause of their disease. 51 Focal cortical dysplasia is the most commonly reported subtype of cortical dysplasia causing epilepsy. 91 Interest has centered on focal cortical dysplasia because of its unique electroclinical, radiographic, and neuropathological features. 8, 10, 23, 29, 66, 94 It is recognized by its histological attributes, which include blurring of the gray—white matter junction, cortical dyslamination, and the presence of abnormal balloon cells in cortical and subcortical regions. In most patients with

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Friederike Knerlich-Lukoschus, Mary B. Connolly, Glenda Hendson, Paul Steinbok and Christopher Dunham

cytoarchitectural/cellular dysplasia (FCD Types I and II) and, in the new classification system, FCD associated with principal pathologies (FCD Type III). According to the recent clinicopathological spectrum of FCD, FCD Type II is presently considered the most severe form of FCD. 38 This histopathological subgroup is defined by the presence of dysmorphic neurons (FCD Types IIA and IIB). The additional presence of balloon cells is the neuropathological hallmark of FCD Type IIB. 6 , 7 , 33 Although these cytological varieties indicate biological differences between these 2 FCD

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Venita Jay, Laurence E. Becker, Hiroshi Otsubo, Paul Hwang, Harold J. Hoffman and Derek C. Armstrong

aspirator, up to 15 ml in total. Extensive cortical abnormalities were seen in multiple microscopic sections, with shallow and indistinct sulci and focal polymicrogyria. There was extensive disorganization of neuronal layering, with clusters of maloriented neurons. A scattering of abnormal neurons and large cells with eosinophilic pale glassy cytoplasm with eccentric nuclei (“balloon cells”) was seen throughout the cortex. The latter cells were somewhat reminiscent of cells seen in cortical tubers. Clusters of reactive astrocytes were encountered throughout the cortex

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Vincent Y. Wang, Edward F. Chang and Nicholas M. Barbaro

Focal cortical dysplasia (FCD) is found in approximately one-half of patients with medically refractory epilepsy. These lesions may involve only mild disorganization of the cortex, but they may also contain abnormal neuronal elements such as balloon cells. Advances in neuroimaging have allowed better identification of these lesions, and thus more patients have become surgical candidates. Molecular biology techniques have been used to explore the genetics and pathophysiological characteristics of FCD. Data from surgical series have shown that surgery often results in significant reduction or cessation of seizures, especially if the entire lesion is resected.

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Walter J. Hader, Mark Mackay, Hiroshi Otsubo, Shiro Chitoku, Shelly Weiss, Lawrence Becker, O. Carter Snead III and James T. Rutka

on neuroimaging studies prior to surgical intervention;8 however, the diagnosis may not be established until the time of pathological examination in up to 34% of cases. 27, 39 An inability to identify FCD preoperatively may reflect the spectrum of the disease, which varies from mild microdysgenesis to severe focal dysplastic lesions with significant cortical disorganization and bizarre balloon cells. 3, 4, 10, 18, 27, 32, 40, 42, 43 The authors of studies involving outcome after surgery for cortical dysplasia have reported that the completeness of resection is a

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Doris D. Wang, Abby E. Deans, A. James Barkovich, Tarik Tihan, Nicholas M. Barbaro, Paul A. Garcia and Edward F. Chang

formalin, embedded in paraffin, and sectioned. Multiple sections were stained using H & E, Nissl stain, Bielschowsky stain, and glial fibrillary acidic protein. The pathological features of the specimens were all reviewed, including the presence of reactive astrogliosis, heterotopias, dyslamination, cytomegaly, dysmorphic neurons, hypercellularity, balloon cells, bizarre cells, and mesial temporal sclerosis. All specimens were also classified according to the new ILAE classification system for FCD: 5 Type I, dyslamination of cerebral cortex; Type IA, abnormal radial

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Joshua J. Chern, Akash J. Patel, Andrew Jea, Daniel J. Curry and Youssef G. Comair

T aylor et al. provided the first histological characterization of FCD, in which they noted cytoarchitectural disarray caused by large, disoriented neurons and balloon cells in both the subcortical white matter and the cortex. 2 It is now accepted that FCD is a common cause of epilepsy in both children and adults. Furthermore, resection has emerged as an important treatment modality in cases of FCD that are medically refractory. A summary of the surgical series in FCD published from 1971 to 2000 showed that the outcome was poor in comparison with surgery

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Doris D. Wang, Barlas Benkli, Kurtis I. Auguste, Paul A. Garcia, Joseph Sullivan, A. James Barkovich, Edward F. Chang and Tarik Tihan

, heterotopia, microglial nodules, balloon cells, satellitosis, neuronophagia, vascular proliferation, immature cells, and dystrophic calcification. The assessment of the severity of each parameter was defined as the presence of that particular parameter in quartiles of the submitted material. The parameter was defined as mild if it was seen in one-quarter of the tissue, moderate if it was seen in 2 of the 4 quadrants, and severe if it was seen in more than half of the submitted tissue. Hypercellularity was defined as a greater than 50% increase in the cell density of the

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Pathology of temporal lobectomy for refractory seizures in children

Review of 20 cases including some unique malformative lesions

Venita Jay, Laurence E. Becker, Hiroshi Otsubo, Paul A. Hwang, Harold J. Hoffman and Derek Harwood-Nash

, astrocytic, & ganglionic cell components); multifocal distribution, with hippocampus infiltrated by  tumor merging with disorganized cortex; extensive calcification tumor 14 microdysgenesis with some large neurons, clustering of neurons, & scattered heterotopic neurons in white hippocampus NA  matter 15 focal cortical dysplasia with abnormal architecture & arrangement of neurons, binucleate neurons, large hippocampus NA  bizarre neurons, numerous “ballooncells with glassy eosinophilic cytoplasm in cortex & white matter