Subtle pathological changes in neocortical temporal lobe epilepsy

- Subtle parahippocampal cortical abnormalities are associated with non-lesional mesial temporal epilepsy.
- EEG source imaging provides fairly good localization but not enough to differentiate hippocampal vs parahippocampal onset.
- Intracranial ictal HFO accurately correlated with seizure onset and histopathology.
- Histopathology of FCD in the parahippocampal gyrus is not commonly reported in routine pathology testing.
- Accurate localization of nTLE may allow less invasive treatments.

This was a prospective observational study to correlate the clinical symptoms, electrophysiology, imaging, and surgical pathology of patients with temporal lobe epilepsy (TLE) without hippocampal sclerosis. We selected consecutive patients with TLE and normal MRI undergoing temporal lobe resection between April and September 2015. Clinical features, imaging, and functional data were reviewed. Intracranial monitoring and language mapping were performed when it was required according to our team recommendation. Prior to hippocampal resection, intraoperative electrocorticography was performed using depth electrodes in the amygdala and the hippocampus. The resected hippocampus was sent for pathological analysis. Results: Five patients with diagnosis with non-lesional TLE were included. We did not find distinctive clinical features that could be a characteristic of non-lesional TLE. The mean follow-up was 13.2 months (11-15 months); 80% of patients achieved Engel Class I outcome. There was no distinctive electrographic findings in these patients. Histopathologic analysis was negative for mesial temporal sclerosis. A second blinded independent neuropathologist with expertise in epilepsy found ILAE type I focal cortical dysplasia in the parahippocampal gyrus in all patients. A third independent neuropathologist reported changes in layer 2 with larger pyramidal neurons in 4 cases but concluded that none of these cases met the diagnostic criteria of FCD.Subtle pathological changes could be associated with a parahippocampal epileptic zone and should be investigated in patients with MRI-negative TLE. This study also highlights the lack of interobserver reliability for the diagnosis of mild cortical dysplasia. Finally, selective amygdalo-hippocampectomy or laser ablation of the hippocampus may not control intractable epilepsy in this specific population.