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Focal Cortical Dysplasias: MR Imaging, Histopathologic, and Clinical Correlations in Surgically Treated Patients with Epilepsy

Nadia Colomboa, Laura Tassic, Carlo Gallib, Alberto Citterioa, Giorgio Lo Russoc, Giuseppe Scialfaa and Roberto Spreaficod

a Department of Neuroradiology, Ospedale Cà Granda Niguarda, Milano, Italy
b Department of Pathology, Ospedale Cà Granda Niguarda, Milano, Italy
c Claudio Munari Epileptic Surgery Center, Ospedale Cà Granda Niguarda, Milano, Italy
d Department of Experimental Neurophysiology and Epileptology, Istituto Nazionale Neurologico "C. Besta", Milano, Italy



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FIG 1. Photomicrographs show the histologic characteristics of the FCD subtypes.

A, Architectural dysplasia characterized by moderate derangement of cortical lamination, with neurons of the same shape and size scattered throughout the cortex (Kluver-Barrera stain; original magnification, x250).

B, Cytoarchitectural dysplasia. Note the cluster of cytomegalic neurons with satellitosis (arrows) (Kluver-Barrera stain; original magnification, x250).

C, Taylor’s FCD with balloon cells. Note large balloon cell characterized by homogeneous eosinophilic cytoplasm and peripheral nucleus with prominent nucleolus (arrow) (hematoxylin-eosin stain; original magnification, x250).

D, Taylor’s FCD with balloon cells. Note large dysmorphic neurons containing abundant cytoplasmic neurofilaments (arrows) (Bielchowsky stain; original magnification, x250).



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FIG 2. MR images of Taylor’s FCD with balloon cells.

A, Coronal turbo SE IR T1-weighted image (3000/20/400/2) demonstrates thickening of the right frontal cortex with loss of demarcation between gray and white matter and decreased white matter signal intensity (arrow) tapering toward the ventricle.

B, Coronal turbo SE T2-weighted image (2300/100/4) and C, coronal turbo SE FLAIR T2-weighted image (6000/100/2000/3), obtained at the same level as A, show increased signal intensity (arrow) of the subcortical white matter extending to the ventricle as a radial band. No mass effect is present.



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FIG 3. MR images of Taylor’s FCD without balloon cells.

A, Transverse SE T2-weighted image (2300/90/1) shows extensive hyperintense lesion in the left temporo-occipitobasal region, with no mass effect on adjacent structures.

B, Coronal turbo SE IR T1-weighted image (3000/20/400/2) better demonstrates thickening of the cortex (arrows) with blurring of the gray-white matter junction and subcortical white matter hypointensity.

C, Coronal turbo SE FLAIR T2-weighted image (6000/100/2000/3) reveals that the hyperintensity of the lesion mainly involves the subcortical white matter (arrows). The ventricular trigone is enlarged on the left.



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FIG 4. MR images of cytoarchitectural dysplasia.

A, Coronal turbo SE IR T1-weighted image (3000/20/400/2), B, coronal turbo SE T2-weighted image (2300/100/4), and C, sagittal turbo SE T2-weighted image of a 3D volume acquisition (2100/130/1). Note reduced demarcation of the gray-white matter boundary in the right temporal lobe, with marked signal intensity alterations of subcortical white matter, which is hypointense on the T1-weighted image in A and hyperintense on the T2-weighted images in B and C. These alterations induced us to diagnose Taylor’s FCD. Note, however, that the thickening of the cortex (arrows in A and B), is only mild. This is a case of histologic cytoarchitectural dysplasia resembling Taylor’s FCD.



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FIG 5. MR images of architectural dysplasia and ipsilateral hippocampal sclerosis (dual abnormality).

A, Coronal turbo SE T2-weighted image (2300/100/4) reveals hypoplasia of right temporal pole with white matter hyperintensity.

B, Transverse SE T2-weighted image (2300/90/1) confirms reduced volume of right temporal pole compared with the contralateral side, with enlargement of the overlying subarachnoid space.

C, Coronal turbo SE T2-weighted image (2300/100/4) shows right hippocampal head (arrow), characterized by atrophy and signal hyperintensity, suggesting hippocampal sclerosis.