The clinico-pathological characterisation of focal cortical dysplasia type IIb genetically defined by MTOR mosaicism

Neuropathol Appl Neurobiol. 2023 Feb;49(1):e12874. doi: 10.1111/nan.12874.

Abstract

Aims: Focal cortical dysplasia (FCD) is a major cause of drug-resistant paediatric epilepsy and is amenable to successful neurosurgical resection. FCD ILAE Type IIb is the most common FCD subtype, and brain somatic mutations affecting the mTOR pathway play a major pathogenic role. The aim of this study was to comprehensively describe the genotype-phenotype association of 20 patients with histopathologically confirmed FCDIIb using next generation sequencing (NGS) of paired blood-brain samples.

Methods: Clinical and neuropathological data were retrospectively reviewed from the hospital archive. The NGS panel included 11 mTOR-pathway-related genes with maximum coverage of 2000×. The detected variants were validated by digital droplet PCR.

Results: Pathogenic MTOR variants were identified in 10 patients (50%). Further comparison with MTOR-wildtype FCDIIb suggested a profound genotype-phenotype association characterised by (1) a non-temporal lobe lesion on MRI, (2) a larger lesion volume occupying grey and white matter (3.032 ± 1.859 cm3 vs 1.110 ± 0.856 cm3 , p = 0.014), (3) more balloon cells (50.20 ± 14.40 BC/mm2 vs 31.64 ± 30.56 BC/mm2 , p = 0.099) and dysmorphic neurons (48.72 ± 19.47DN/mm2 vs 15.28 ± 13.95DN/mm2 , p = 0.000) and (4) a positive correlation between VAF and the lesion volume (r = 0.802, p = 0.017).

Conclusions: Our study identified frequent MTOR mutations in the cell-rich FCDIIb phenotype, clinically characterised by a non-temporal location and large lesion volume. Comprehensive genotype-phenotype associations will help us further explore and define the broad spectrum of FCD lesions to make more targeted therapies available in the realm of epileptology.

Keywords: brain; brain somatic variants; epilepsy; neuropathology; seizure.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Epilepsy* / pathology
  • Focal Cortical Dysplasia*
  • Humans
  • Malformations of Cortical Development* / genetics
  • Mosaicism
  • Retrospective Studies
  • TOR Serine-Threonine Kinases / metabolism

Substances

  • TOR Serine-Threonine Kinases
  • MTOR protein, human

Supplementary concepts

  • Focal cortical dysplasia of Taylor