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. 2018 Sep 27;5(10):1200-1210.
doi: 10.1002/acn3.634. eCollection 2018 Oct.

Multimodal computational neocortical anatomy in pediatric hippocampal sclerosis

Sophie Adler  1   2 , Mallory Blackwood  3 , Gemma B Northam  1 , Roxana Gunny  2 , Seok-Jun Hong  4 , Boris C Bernhardt  5 , Andrea Bernasconi  4 , Neda Bernasconi  4 , Thomas Jacques  6   7 , Martin Tisdall  1   2 , David W Carmichael  1   2 , J Helen Cross  1   2 , Torsten Baldeweg  1   2
Affiliations

Multimodal computational neocortical anatomy in pediatric hippocampal sclerosis

Sophie Adler et al. Ann Clin Transl Neurol. .

Abstract

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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Figures

Figure 1
Figure 1
Hippocampal atrophy and FLAIR signal intensity. Hippocampal segmentations: coronal section of T1‐weighted (A) and FLAIR (B) images; and axial (C) and sagittal (D) T1‐weighted sections in a healthy control subject. E) Reduced ipsilateral but not contralateral hippocampal volume in patients. Increased normalized FLAIR signal of ipsilateral and contralateral hippocampi in patients.
Figure 2
Figure 2
Surface‐based processing pipeline. (A) MRI preprocessing in FreeSurfer to create pial and white matter surfaces. (B) Co‐registration of FLAIR to T1 scans. (C) Feature extraction. Quantification of cortical thickness, gray–white matter boundary intensity contrast and FLAIR signal intensity at 50% cortical depth.
Figure 3
Figure 3
Whole‐brain analysis. FLAIR hyperintensity (A), cortical thinning (B) and gray–white matter boundary blurring (C) in pediatric TLE patients compared to controls. Findings were corrected for multiple comparisons controlling the family‐wise error (FWE) to be below PFWE < 0.05. Difference in FLAIR hyperintensity (D), cortical thickness (E) and gray–white matter intensity contrast (F) in anterior temporal lobe cluster between TLE patients with (yes) and without (no) a history of febrile convulsions.
Figure 4
Figure 4
Topography of neocortical FLAIR hyperintensity. Surface‐based map of the t‐statistic. Unlike Figure 3A, FLAIR hyperintensity in pediatric TLE patients compared to controls has not been corrected for multiple comparisons.
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