Type II focal cortical dysplasia: Ex vivo 7T magnetic resonance imaging abnormalities and histopathological comparisons. Issue 1 (26th November 2015)

• Record Type: Journal Article
• Authors: Zucca, Ileana; Milesi, Gloria; Medici, Valentina; Tassi, Laura; Didato, Giuseppe; Cardinale, Francesco; Tringali, Giovanni; Colombo, Nadia; Bramerio, Manuela; D'Incerti, Ludovico; Freri, Elena; Morbin, Michela; Fugnanesi, Valeria; Figini, Matteo; Spreafico, Roberto; Garbelli, Rita
• Is Part Of: Annals of neurology. Volume 79:Issue 1(2016:Jan.)
• Page Start: 42
• Page End: 58
• Publication Date: 2015-11-26
• Subjects: Neurology -- Periodicals; Pediatric neurology -- Periodicals; Nervous system -- Surgery -- Periodicals; 616.8
• DOI: 10.1002/ana.24541
• Languages: English
• ISSNs: 0364-5134

Abstract

Abstract : Objective: In the present report, the correlations between ex vivo high‐resolution imaging and specific histological and ultrastructural patterns in type II focal cortical dysplasia (FCD) have been studied to explain the differences in the magnetic resonance imaging (MRI) detection of dysplasia and to contribute to the presurgical imaging evaluation of this pathology. Methods: Surgical specimens from 13 patients with FCD IIa/b were submitted to 7T MRI scanning, and then analyzed histologically and ultrastructurally to compare the results with the MRI findings. Region of interest (ROI)‐based measures on T2‐weighted images (T2wi) were quantitatively evaluated in the lesion and in adjacent perilesional gray and white matter. Results: Matched histological sections and 7T T2wi showed that the core of the lesion was characterized by patchy aggregates of abnormal cells and fiber disorganization related to inhomogeneity of intracortical signal intensity. The quantitative approach on T2wi can help to distinguish the lesions and perilesional areas even in a clinical MRI‐negative case. The ultrastructural study showed that the strong signal hyperintensity in the white matter of FCD IIb was related to a dysmyelination process associated with severe fiber loss and abnormal cells. Less severe histopathological features were found in FCD IIa, thus reflecting their less evident MRI alterations. Interpretation: We suggest that white matter abnormalities in type IIb FCD are due to defects of the myelination processes and maturation, impaired by the presence of balloon cells. To reveal the presence and the border of type II cortical dysplasia on MRI, a quantitative ROI‐based analysis (coefficient of variation) is also proposed. ANN NEUROL 2016;79:42–58