Authors :
Presenting Author: Keza Motlana, HBSc – University of Western Ontario
Ali Khan, Ph.D., B. Sc. – Assistant Professor, Medical Biophysics, Medical Imaging, University of Western Ontario; Seyed Mirsattari, MD, PhD. FRCPC – Associate Professor of Neurology, Medical Biophysics, University of Western Ontario; Mohamed Yousif, BMSc – Masters Student, Medical Biophysics, University of Western Ontario; Elma Paredes Aragón, M.D. – Epilepsy and EEG Clinical Fellow, Clinical Neurological Sciences, University of Western Ontario
Rationale:
An epilepsy diagnosis after a First Time Unprovoked Seizure (FUS) could help to alleviate epilepsy uncertainty anxiety and allow for quicker medical intervention, reducing subsequent seizure occurrence. Establishing an additional epilepsy diagnosis method could identify cases missed by current methods like EEG and lesion detection. This research aims to determine if cortical thickness changes can be a biomarker for epilepsy in FUS patients.
Methods:
This study compared 7T MRI scans of FUS patients with age and sex-matched healthy controls. The London Health Sciences Centre referred adult patients to this study after they experienced their first unprovoked seizure and underwent a clinical 1.5T or 3T MRI scan. Those who endured a second seizure or epilepsy diagnosis before the scan were excluded and all accepted subjects underwent a 7T MRI scan; 16 healthy controls and 16 FUS subjects, six FUS were diagnosed with epilepsy (DE) after the scan. Schafer 200 parcel and 17 networks map were used for parcellation, FreeSurfer software was used to measure cortical thickness.
Results:
The cortical thicknesses of two subject groups were compared using a two-tail t-test; no significant differences were identified between the participant groups and healthy controls after applying false discover rate (FDR) correction. However, the data indicated cortical thickening and thinning trends in FUS subjects. In the FUS subjects, there was cortical thinning in the left extrastriate, motor and retrosplenial cortices, while cortical thickening was observed in the right extrastriate, motor, auditory, prefrontal (PF), insula, intraparietal sulcus and cingulate cortices. In a sex-based analysis, females exhibited cortical thickening in the right temporal cortex and cortical thinning in the bilateral motor cortices, left postcentral gyrus, and right striate calcarine cortex. Males displayed cortical thinning in the left striate calcarine and intraparietal sulcus cortices, bilateral thickening in the insula, as well as the right extrastriate, motor, auditory, PF, intraparietal sulcus, and cingulate cortices. When analyzing only the DE subjects, left motor cortical thinning was observed. With further bilateral thickening in secondary somatosensory, PF and temporal cortices, with more substantial thickening in the right hemisphere and additional thickening in the right parietal cortices. Females DE subjects bilateral thinning and right hemisphere thickening in the motor cortex. Additional thickening occurred in the bilateral PF, the right parietal, temporoparietal, cingulate cortices, the left extrastriate, secondary somatosensory, frontal operculum and temporal cortices. Males exhibited cortical thickening in the left motor, extrastriate, and temporoparietal cortices and right auditory, PF, orbitofrontal, and precuneus cortices.
Conclusions: After applying FDR correction, the trend of cortical thickness differences between FUS subjects and healthy controls is not significant. This lack of significance, potentially due to the small sample size, disallows any conclusion that cortical thickness changes are a reliable bioindicator of epilepsy.
Funding:
LHSF, NSERC CRSNG, Canada Research Chairs, CIHR, OBI, EPLINK