Abstracts

RATIONALE: In spite of its reputation in temporal lobe epilepsy, amygdaloid epilepsy has not been extensively studied because of its limitation of accessibility, unclear cytoarchitectonic structure, and loss of surgical specimen during operation. We herein present 12 cases of intractable epilepsy arising from amygdala in relation with electrophysiological, pathological findings, and surgical outcome. METHODS: Twelve patients were selected on the basis of depth electrode investigation demonstrating the origin of seizures within the amygdala. All the patients were extensively investigated according to presurgical evaluation protocol. All the patients underwent standard temporal lobectomy and were followed up for more than 12 months. RESULTS: Complex partial seizures were observed in all. Psychic auras were predominant (50%). MRI showed hippocampal sclerosis (67%), neocortical gliosis (8%), and negative (25%). Standard EEGs showed bitemporal spikes (58%), unitemporal spikes (33%), and multilobar spikes (8%). Five patients showed predominant spikes contralateral to lesions on MRI. Depth electrode recordings showed diverse seizure propagation: 1) amygdala?ipsilateral temporal neocortex (n=8), 2) amygdala ?contralateral amygdala?ipsilateral temporal neocortex (n=2), and 3) amygdala ?ipsilateral extratemporal area (n=2). Pathological analysis showed mild to moderate degree of amygdaloid sclerosis in 5 and severe form in 5 among ten available amygdala specimens. Abnormal neurons containing neurofilaments in their cytoplasm were observed in 4 amygdala specimens. Hippocampal sclerosis was also accompanied in 11 patients. Eleven patients become seizure free (92%) and one showed worthwhile improvement (8%) after mean follow-up of 32 months. CONCLUSIONS: This study supports strong evidence for the epileptogenic role of amygdala in the pathogenesis of TLE. However, relationship with hippocampus should be further defined. Surgical outcome was excellent in this series.