Automated Whole-Brain Focal Cortical Dysplasia Detection Using MR Fingerprinting With Deep Learning.
Authors
Affiliations (7)
Affiliations (7)
- Epilepsy Center, Neurological Institute, Cleveland Clinic, OH.
- Department of Biomedical Engineering, Case Western Reserve University, OH.
- Department of Biomedical Engineering, Yonsei University, Wonju, South Korea.
- Neuropathologisches Institut, Universitätsklinikum Erlangen and Partner of the European Reference Network EpiCare, Friedrich-Alexander Universität Erlangen-Nuremberg, Germany.
- Quantitative Health Science, Cleveland Clinic, OH.
- Imaging Institute, Cleveland Clinic, OH; and.
- Departments of Neurosurgery and Biomedical Engineering, Duke University, Durham, NC.
Abstract
Focal cortical dysplasia (FCD) is a common pathology for pharmacoresistant focal epilepsy, yet detection of FCD on clinical MRI is challenging. Magnetic resonance fingerprinting (MRF) is a novel quantitative imaging technique providing fast and reliable tissue property measurements. The aim of this study was to develop an MRF-based deep-learning (DL) framework for whole-brain FCD detection. We included patients with pharmacoresistant focal epilepsy and pathologically/radiologically diagnosed FCD, as well as age-matched and sex-matched healthy controls (HCs). All participants underwent 3D whole-brain MRF and clinical MRI scans. T1, T2, gray matter (GM), and white matter (WM) tissue fraction maps were reconstructed from a dictionary-matching algorithm based on the MRF acquisition. A 3D ROI was manually created for each lesion. All MRF maps and lesion labels were registered to the Montreal Neurological Institute space. Mean and SD T1 and T2 maps were calculated voxel-wise across using HC data. T1 and T2 <i>z</i>-score maps for each patient were generated by subtracting the mean HC map and dividing by the SD HC map. MRF-based morphometric maps were produced in the same manner as in the morphometric analysis program (MAP), based on MRF GM and WM maps. A no-new U-Net model was trained using various input combinations, with performance evaluated through leave-one-patient-out cross-validation. We compared model performance using various input combinations from clinical MRI and MRF to assess the impact of different input types on model effectiveness. We included 40 patients with FCD (mean age 28.1 years, 47.5% female; 11 with FCD IIa, 14 with IIb, 12 with mMCD, 3 with MOGHE) and 67 HCs. The DL model with optimal performance used all MRF-based inputs, including MRF-synthesized T1w, T1z, and T2z maps; tissue fraction maps; and morphometric maps. The patient-level sensitivity was 80% with an average of 1.7 false positives (FPs) per patient. Sensitivity was consistent across subtypes, lobar locations, and lesional/nonlesional clinical MRI. Models using clinical images showed lower sensitivity and higher FPs. The MRF-DL model also outperformed the established MAP18 pipeline in sensitivity, FPs, and lesion label overlap. The MRF-DL framework demonstrated efficacy for whole-brain FCD detection. Multiparametric MRF features from a single scan offer promising inputs for developing a deep-learning tool capable of detecting subtle epileptic lesions.