Abstracts

The pathogenesis of partial epilepsy is poorly understood. We have reviewed our adult epilepsy surgical cases for potential perinatal and childhood contributors to the development of epilepsy. Retrospective review of surgical cases since 2000 included age of seizure onset, age at surgery, seizure type and frequency, lobe(s) resected, pathology, MRI/PET, neuropsychology, and surgical outcome. Patients, and when possible their mothers, were called for childhood history. Birth records were requested from outside hospitals. Queries included survey of risk factors in the mother, fetus, neonate, infant, and child. Forty-six epilepsy surgery cases, excluding malignant tumors, were reviewed. The median age in years at surgery was 45 (range 16-74). The median duration of intractable epilepsy was 15 years with a range of several months to 60 years. Average full scale IQ was 95 (SD=15.2). Resections were of the temporal lobe in 33 (29 standard, 4 neocortical), frontal lobe in 5, parietal lobe in 3, and multilobar in 5. Pathology revealed dysplastic etiologies in 20 patients: focal cortical dysplasia (FCD) in 12 (Palmini classification Ia n=4, Ib n= 3, IIa n= 5), DNET in 6 and ganglioglioma in 2. Other lesions identified were: vascular malformations (7), pilocytic astrocytoma (1), meningioangiomatosis (1), osteoma (1), and pathogen-free granuloma (1). Mesial temporal sclerosis was co-identified in 7 cases of FCD (Type I, IIa) and 9 cases in isolation. MTS was associated with febrile seizures, status epilepticus and/or meningitis in 9 of 17 cases (as infants in 6). Infantile spasms was associated with one case of Type IIa FCD. Significant maternal risk factors were not identified though a maternal history of neurofibramatosis (NF1) was identified in one case of MTS. Isolated MTS was associated with low birth weight (1800 g) in one and with high birth weight (above 4000 g) in 4 patients. Presumed congenital structural abnormalities of the brain were identified in 60% of our adult surgical series: 26% FCD (15% Type I and 11% Type IIa), 17% [quot]extreme FCD[quot] (DNET/ganglioglioma), 15% vascular malformations, and 2% meningioangiomatosis. Isolated MTS or non-specific gliosis occurred in 34%. These data suggest that developmental dysgenesis of cerebral cortex may be a major cause of adult epilepsy. The timing of microdysgenesis in development as well as genetic and environmental factors in FCD need to be identified.