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Publication Detail
Multimodal computational neocortical anatomy in pediatric hippocampal sclerosis
  • Publication Type:
    Journal article
  • Publication Sub Type:
  • Authors:
    Adler S, Blackwood M, Northam GB, Gunny R, Hong SJ, Bernhardt BC, Bernasconi A, Bernasconi N, Jacques T, Tisdall M, Carmichael DW, Cross JH, Baldeweg T
  • Publication date:
  • Journal:
    Annals of Clinical and Translational Neurology
  • Status:
© 2018 The Authors. Annals of Clinical and Translational Neurology published by Wiley Periodicals, Inc on behalf of American Neurological Association. Objective: In contrast to adult cohorts, neocortical changes in epileptic children with hippocampal damage are not well characterized. Here, we mapped multimodal neocortical markers of epilepsy-related structural compromise in a pediatric cohort of temporal lobe epilepsy and explored how they relate to clinical factors. Methods: We measured cortical thickness, gray–white matter intensity contrast and intracortical FLAIR intensity in 22 patients with hippocampal sclerosis (HS) and 30 controls. Surface-based linear models assessed between-group differences in morphological and MR signal intensity markers. Structural integrity of the hippocampus was measured by quantifying atrophy and FLAIR patterns. Linear models were used to evaluate the relationships between hippocampal and neocortical MRI markers and clinical factors. Results: In the hippocampus, patients demonstrated ipsilateral atrophy and bilateral FLAIR hyperintensity. In the neocortex, patients showed FLAIR signal hyperintensities and gray–white matter boundary blurring in the ipsilesional mesial and lateral temporal neocortex. In contrast, cortical thinning was minimal and restricted to a small area of the ipsilesional temporal pole. Furthermore, patients with a history of febrile convulsions demonstrated more pronounced FLAIR hyperintensity in the ipsilesional temporal neocortex. Interpretation: Pediatric HS patients do not yet demonstrate the widespread cortical thinning present in adult cohorts, which may reflect consequences of a protracted disease process. However, pronounced temporal neocortical FLAIR hyperintensity and blurring of the gray–white matter boundary are already detectable, suggesting that alterations in MR signal intensities may reflect a different underlying pathophysiology that is detectable earlier in the disease and more pervasive in patients with a history of febrile convulsions.
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