Abstracts

RATIONALE: Cortical resection can alleviate seizures in children with intractable epilepsy. However, despite presurgical application of advanced imaging and electrophysiological techniques, seizures recur in at least 30% of such patients. Further resection of remaining epileptic cortex may ultimately lead to seizure freedom, but accurate delineation of the epileptogenic region is often difficult in these patients. The clinical usefulness of glucose metabolism positron emission tomography (PET) is limited in such cases since glucose hypometabolism often occurs in areas of diaschisis and in non-epileptic damaged tissue surrounding the resection. Previous studies have shown that increased cortical uptake of the PET tracer [alpha][¹¹C]methyl-L-tryptophan (AMT; a tracer for tryptophan metabolism via the serotonin or kynurenine pathways) is very specific for epileptogenic cortex, and can even differentiate between epileptogenic and non-epileptogenic lesions (e.g., in tuberous sclerosis). The goal of the present study was to assess whether AMT PET is able to detect residual epileptic cortex after failed cortical resection.
METHODS: AMT PET scans were performed in 30 children (age: 2.1-19 years) from several institutions with intractable epilepsy in whom seizures recurred following focal cortical resection, and further surgical resection was being considered. Five patients had a cortical lesion preoperatively, while the remaining 25 had normal MRI before surgery. All patients underwent further presurgical scalp EEG evaluation, and 11 children had intracranial EEG monitoring using subdural grid electrodes. On the PET scans, focal cortical increases of AMT uptake were identified, and their locations were correlated with electrophysiological findings.
RESULTS: Eleven (36.7%) of the 30 patients had focal cortical increase of AMT uptake, typically close to the margin of the previous resection (locations: 5 frontal, 3 temporal, 2 parietal and 1 parieto-temporal). Increased AMT uptake was seen in 7 of 25 patients (28%) with normal presurgical MRI, and in 4 of 5 patients (80%) with a previous lesion (two of these had dysembryoplastic epithelial tumor which was incompletely resected, one had posterior megalencephaly with cortical dysplasia, and one child from another institution had a lesion of unknown etiology). Six patients with increased AMT uptake had intracranial EEG monitoring, which showed ictal onset consistent with the PET findings in all cases. Resection of this epileptogenic cortex resulted in seizure-free outcome in 5 of these 6 children.
CONCLUSIONS: AMT PET can delineate residual epileptic cortex in patients with intractable epilepsy who continue to have seizures following cortical resection. The sensitivity of AMT PET appears to be particularly high in patients with preoperative lesions, but AMT PET may also identify residual epileptic cortex in more than 1 of 4 children with a normal MRI prior to the first resection. Cortical areas showing increased AMT uptake close to the resection margin show a good correspondence with the seizure focus delineated by intracranial EEG, and resection of these areas results in good outcome in most cases.
[Supported by: This grant was supported in part by NIH Grant NS 34488 and NS/RR 38324]; (Disclosure: Grant - NS 34488, NS/RR 38324)