scholarly journals Characterization of focal cortical dysplasia with balloon cells by layer-specific markers: Evidence for differential vulnerability of interneurons

Epilepsia ◽  
2017 ◽  
Vol 58 (4) ◽  
pp. 635-645 ◽  
Author(s):  
Julia M. Nakagawa ◽  
Catharina Donkels ◽  
Susanne Fauser ◽  
Andreas Schulze-Bonhage ◽  
Marco Prinz ◽  
...  
Keyword(s):  
Focal Cortical Dysplasia ◽  
Cortical Dysplasia ◽  
Balloon Cells ◽  
Differential Vulnerability

scholarly journals Balloon cells promote immune system activation in focal cortical dysplasia type 2B

2021 ◽  
Author(s):  
Till S. Zimmer ◽  
Diede W.M. Broekaart ◽  
Mark Luinenburg ◽  
Caroline Mijnsbergen ◽  
Jasper J. Anink ◽  
...  
Keyword(s):  
Immune System ◽  
Focal Cortical Dysplasia ◽  
Cortical Dysplasia ◽  
Balloon Cells ◽  
Immune System Activation ◽  
System Activation

Tuberous sclerosis complex and Focal cortical dysplasia with balloon cells: is it the same disorder?

2008 ◽  
Vol 12 ◽  
pp. S7
Author(s):  
K. Kotulska ◽  
W. Grajkowska ◽  
J. Jóźwiak ◽  
E. Jurkiewicz ◽  
D. Chmielewski ◽  
...  
Keyword(s):  
Tuberous Sclerosis ◽  
Tuberous Sclerosis Complex ◽  
Focal Cortical Dysplasia ◽  
Cortical Dysplasia ◽  
Balloon Cells

Mcm2 labelling of balloon cells in focal cortical dysplasia

2005 ◽  
Vol 31 (6) ◽  
pp. 580-588 ◽  
Author(s):  
M. Thom ◽  
L. Martinian ◽  
S. M. Sisodiya ◽  
J. H. Cross ◽  
G. Williams ◽  
...  
Keyword(s):  
Focal Cortical Dysplasia ◽  
Cortical Dysplasia ◽  
Balloon Cells

scholarly journals Histological Characterization of the Irritative Zones in Focal Cortical Dysplasia Using a Preclinical Rat Model

2018 ◽  
Vol 12 ◽  
Author(s):  
Abhay Deshmukh ◽  
Jared Leichner ◽  
Jihye Bae ◽  
Yinchen Song ◽  
Pedro A. Valdés-Hernández ◽  
...  
Keyword(s):  
Rat Model ◽  
Focal Cortical Dysplasia ◽  
Cortical Dysplasia

Molecular Pathogenesis of Focal Cortical Dysplasia and Hemimegalencephaly

2004 ◽  
Vol 19 (3) ◽  
pp. 330-336 ◽  
Author(s):  
Peter B. Crino
Keyword(s):  
Cyclin D1 ◽  
Glycogen Synthase ◽  
Focal Cortical Dysplasia ◽  
Cortical Dysplasia ◽  
Messenger Rnas ◽  
Dna Arrays ◽  
Ribonucleic Acids ◽  
P70s6 Kinase ◽  
Balloon Cells ◽  
Upstream Kinase

My laboratory recently demonstrated that there is selective expression of phosphoribosomal S6 protein in balloon cells in focal cortical dysplasia and hemimegalencephaly but no expression of the upstream kinase, phospho-p70S6 kinase. Two proteins activated by phospho-p70S6 kinase, phospho-STAT3 and phospho-4EBP1, were not detected in balloon cells. Using complementary DNA arrays in hemimegalencephaly specimens, we found increased expression of cyclin D1 and c-myc messenger ribonucleic acids (RNAs). Expression of cyclin D1 and c-myc genes is transcriptionally activated by βcatenin. Western analysis demonstrated increased levels of nonphosphorylated β-catenin in hemimegalencephalic cortex. Reduced levels of Ser33, Ser37, and Thr41 phospho-β-catenin, sites known to be phosphorylated by glycogen synthase kinase 3 and to be essential for β-catenin inactivation, were detected in hemimegalencephaly. Enhanced transcription of cyclin D1 and c-myc messenger RNAs, increased transcriptionally active β-catenin, and decreased Ser33/Ser37/Thr41 phospho-β-catenin suggest activation of the Wnt-1/β-catenin cascade in hemimegalencephaly, which can lead to aberrant cell proliferation and hemispheric enlargement during brain development. Enhanced activation of phospho-S6 and β-catenin suggests two converging cell pathways that can be pivotal in the pathogenesis of focal cortical dysplasia and hemimegalencephaly. ( J Child Neurol 2005;20:330—336).

scholarly journals Clinical, imaging, and immunohistochemical characteristics of focal cortical dysplasia Type II extratemporal epilepsies in children: analyses of an institutional case series

2017 ◽  
Vol 19 (2) ◽  
pp. 182-195 ◽  
Author(s):  
Friederike Knerlich-Lukoschus ◽  
Mary B. Connolly ◽  
Glenda Hendson ◽  
Paul Steinbok ◽  
Christopher Dunham
Keyword(s):  
Focal Cortical Dysplasia ◽  
Surrogate Marker ◽  
Case Series ◽  
Cortical Dysplasia ◽  
Seizure Type ◽  
Type Ii ◽  
Neurofilament Protein ◽  
Clinical Imaging ◽  
Sample Number ◽  
Balloon Cells

OBJECTIVE Focal cortical dysplasia (FCD) Type II is divided into 2 subgroups based on the absence (IIA) or presence (IIB) of balloon cells. In particular, extratemporal FCD Type IIA and IIB is not completely understood in terms of clinical, imaging, biological, and neuropathological differences. The aim of the authors was to analyze distinctions between these 2 formal entities and address clinical, MRI, and immunohistochemical features of extratemporal epilepsies in children. METHODS Cases formerly classified as Palmini FCD Type II nontemporal epilepsies were identified through the prospectively maintained epilepsy database at the British Columbia Children's Hospital in Vancouver, Canada. Clinical data, including age of seizure onset, age at surgery, seizure type(s) and frequency, affected brain region(s), intraoperative electrocorticographic findings, and outcome defined by Engel's classification were obtained for each patient. Preoperative and postoperative MRI results were reevaluated. H & E–stained tissue sections were reevaluated by using the 2011 International League Against Epilepsy classification system and additional immunostaining for standard cellular markers (neuronal nuclei, neurofilament, glial fibrillary acidic protein, CD68). Two additional established markers of pathology in epilepsy resection, namely, CD34 and α-B crystallin, were applied. RESULTS Seven nontemporal FCD Type IIA and 7 Type B cases were included. Patients with FCD Type IIA presented with an earlier age of epilepsy onset and slightly better Engel outcome. Radiology distinguished FCD Types IIA and IIB, in that Type IIB presented more frequently with characteristic cortical alterations. Nonphosphorylated neurofilament protein staining confirmed dysplastic cells in dyslaminated areas. The white-gray matter junction was focally blurred in patients with FCD Type IIB. α-B crystallin highlighted glial cells in the white matter and subpial layer with either of the 2 FCD Type II subtypes and balloon cells in patients with FCD Type IIB. α-B crystallin positivity proved to be a valuable tool for confirming the histological diagnosis of FCD Type IIB in specimens with rare balloon cells or difficult section orientation. Distinct nonendothelial cellular CD34 staining was found exclusively in tissue from patients with MRI-positive FCD Type IIB. CONCLUSIONS Extratemporal FCD Types IIA and IIB in the pediatric age group exhibited imaging and immunohistochemical characteristics; cellular immunoreactivity to CD34 emerged as an especially potential surrogate marker for lesional FCD Type IIB, providing additional evidence that FCD Types IIA and IIB might differ in their etiology and biology. Although the sample number in this study was small, the results further support the theory that postoperative outcome—defined by Engel's classification—is multifactorial and determined by not only histology but also the extent of the initial lesion, its location in eloquent areas, intraoperative electrocorticographic findings, and achieved resection grade.

Characteristic expression of p57/Kip2 in balloon cells in focal cortical dysplasia

2015 ◽  
Vol 35 (5) ◽  
pp. 401-409
Author(s):  
Tadashi Kimura ◽  
Hiroki Kitaura ◽  
Hiroshi Masuda ◽  
Shigeki Kameyama ◽  
Yuko Saito ◽  
...  
Keyword(s):  
Focal Cortical Dysplasia ◽  
Cortical Dysplasia ◽  
Balloon Cells

scholarly journals Focal cortical dysplasia: a review of pathological features, genetics, and surgical outcome

2006 ◽  
Vol 20 (1) ◽  
pp. 1-7 ◽  
Author(s):  
Vincent Y. Wang ◽  
Edward F. Chang ◽  
Nicholas M. Barbaro
Keyword(s):  
Molecular Biology ◽  
Surgical Outcome ◽  
Refractory Epilepsy ◽  
Focal Cortical Dysplasia ◽  
Cortical Dysplasia ◽  
Pathological Features ◽  
Balloon Cells ◽  
Medically Refractory Epilepsy

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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