Authors :
Presenting Author: Patrick Hartnett, MD – University of Virginia
Naseem Zomorodi, MD – Resident, Neurology, University of Virginia; Howard Goodkin, MD, PhD – Chair, Neurology, University of Virginia; Ifrah Zawar, MD – Faculty, Neurology, University of Virginia
Rationale: Non-lesional drug resistant (DRE) parietal lobe epilepsies (PLEs) often imitate other epilepsies and can be difficult to localize. Understanding epilepsy as a network disease through white matter corridors has become increasingly important in accurate localization of PLEs because of extensive connectivity of the parietal lobe. DTI and functional MRI are often helpful in understanding the brain connectivity. However, the utility of interictal epileptiform discharges (IEDs) in understanding the brain connectivity and rapid propagation of epileptogenicity through white matter tracts is under-studied.
Methods: We report a unique case of non-lesional DRE that highlights the significance of IEDs in providing evidence of rapid white matter propagation via superior longitudinal fasciculus which led to accurate localization in a non-lesional PLE which was initially falsely localized to the frontal lobe. Additionally, comprehensive multi-modality approach using semiology, EEG, MEG and PET also supported parietal lobe onset with rapid propagation to frontal lobe. Later, voxel-based morphometry (VBM) analysis of the non-lesional 3-Testa MRI identified a lesion in the right superior parietal lobule (SPL).
Results: An 18-year-old male was admitted with DRE for presurgical evaluation. His seizures were characterized by behavioral arrest, left head turning, left gaze deviation with secondary generalization. Prior EEGs had noted IEDs and ictal discharges arising from right frontal lobe. MRI was non-lesional. Based on semiology and EEG, he was presumed to have frontal lobe epilepsy.
Ictal EEG was difficult to localize but IEDs showed a consistent phase reversal at the right frontal (F4) region (Fig 1). However, a detailed IED analysis demonstrated a posterior to anterior time lag with an initial spike component over the right parieto-occipital (P4/O2) (Fig 1) followed by frontal lobe. This slight delay between parietal and frontal involvement is likely due to rapid white matter propagation. Analysis of his recorded seizure semiology also showed a subtle nystagmus prior to left gaze deviation and generalization.
Further, a VBM analysis of his non-lesional brain MRI identified a lesion in the right SPL (Fig 2). PET (Fig 2) showed an area of hypometabolism corresponding to VBM lesion. MEG also showed dipoles over the right parietal lobe (Fig 2) concordant with VBM lesion. Stereo-EEG implantation confirmed epileptogenic zone (EZ) in the right SPL with rapid spread to frontal lobe. Right SPL EZ underwent successful laser ablation.
Conclusions: IEDs in our case provide evidence of rapid propagation of epileptogenicity from parietal to frontal lobe likely via superior longitudinal fasciculus, a white matter bundle connecting SPL to frontal lobe. This highlights how IED lag demonstrates brain connectivity. This case also highlights the utility of VBM in identifying epileptogenic lesions on a non-lesional MRI and the significance of multi-modality approach including MRI, PET, EEG, semiology, MEG and VBM in accurately localizing epilepsies. Understanding epilepsy as a network disease in this fashion can help accurate localization especially in difficult to localize and deceptive non-lesional PLEs.
Funding: None.