Abstracts

To define amygdala onset seizures in relation with the clinical, electrophysiological, neuroimaging and pathological changes. Clinical, extracranial EEG, MRI, and pathological findings, as well as surgical outcome were retrospectively analyzed in 13 patients with intractable temporal lobe epilepsy and focal AOS defined by depth electrode studies (D-EEG). All underwent temporal lobectomies with amygdalohippocampectomy. The amygdala and the hippocampus were removed en bloc in seven. A presumed etiology was present in 8 patients, and included meningoencephalitis with or without febrile convulsion (FC), isolated FC, and parasitic infectionSeizures were complex partial only in 6 (46%) and complex partial with secondary generalization the other 7 (54%). Extracranial EEGs failed to lateralize the ictal onset zone. Low voltage fast activity was the most common electrographic pattern at ictal onset on D-EEG ( 9 patients, 69%). [italic]Ictal discharges propagated first to the contralateral temporal lobe in 2 (15%).[/italic] MRI abnormalities were seen in 10 patients, and suggested simultaneous sclerosis of amygdala and hippocampus in 6 (46%), isolated hippocampal sclerosis in 3 (23%), and parahippocampal gliosis in one (8%). The imaging abnormality was always concordant with the side of resection. Amygdaloid sclerosis was present in all patients on histopathology, being mild in 9 (71%), moderate in 2 (14%) and severe in the other 2 (14%). Ten patients are seizure free, one is almost seizure free, and the other two had a worthwhile improvement after operation, after mean follow-up of 59 months. AOS are arise from sclerotic amygdala of varying severity, can only be confirmed through D-EEG studies, and may first propagate to the contralateral temporal lobe, potentially leading to mislateralization of ictal onset on scalp-sphenoidal EEGs. Surgical outcome was excellent in the majority of patients.