Abstracts

Rationale: Recently, TLE with amygdala enlargement (TLE-AE) has been particularly attracted attention as a subtype of drug resistant TLE without hippocampal sclerosis. However, there have been few reports regarding the relationship between seizure semiology and electrophysiological findings in this category. Therefore, we investigated retrospectively seizure characteristics and the seizure onset zone from the scalp EEG and electrocorticography (ECoG) in this study. Methods: Six patients of drug-resistant dominant side TLE-AE were enrolled in this study. We confirmed the amygdala enlargement without hippocampal sclerosis on 3T-MRI by two independent epileptologists. We reviewed their seizure semiology especially for the following symptoms; fears, de javu, epigastric sensation, automatism, and tonic-clonic seizures. We examined their memory functions using WMS-R, and averaged their verbal memory index, visual memory index, and delayed recall index. We evaluated the distribution of interictal and ictal epileptiform discharges (IEDs) from prolonged video-scalp EEG. All the patient underwent video ECoG using subdural electrodes on amygdala, hippocampus, and cortex of lateral temporal lobe. We detected the seizure onset zone by visual evaluation, and categorized them into the following three regions; amygdala, hippocampus, and lateral temporal cortex. Results: All patients had focal impaired conscious seizure with oral or hand automatisms. Three patients showed the focal onset bilateral tonic-clonic seizure. No patients presented fear, deja vu or epigastric sensation as an initial seizure symptom. Seizure frequency was at least once per month in all patients. Average of verbal memory, visual memory, and delayed recall indexes through WMS-R were 109, 108, and 99, respectively. In video-scalp EEG, all subjects had IEDs at mesial temporal lobe (T1,F7) as ipsilateral to AE. Additionally, seven ictal discharges were detected from the same area as IEDs. In ECoG data, IEDs were detected from both of the amygdala and hippocampus in five patients, and from amygdala and lateral temporal lobe in a patient. We obtained the ictal recordings from all patient, and the seizure onset was only the hippocampus in three, both of the amygdala and hippocampus in two, and only the amygdala in one, respectively. Conclusions: We found that the semiology of patients with TLE-AE was compatible with mesial temporal lobe epilepsy but it is not linked to a seizure focus in the amygdala. TLE-AE patients did not manifest memory disturbance, in spite of the high seizure frequency. Seizure onset zone was confirmed from hippocampus rather than amygdala in our six patients, however, MRI negative and memory intact hippocampus required the treatment of multiple subpial transection for seizure control. The epileptogenic zone is suspected in the hippocampus rather than the enlarged amygdala. Funding: none