Abstracts

RATIONALE: The purpose of this study was to explore the potential utility of flumazenil PET (FMZ-PET) in the surgical evaluation of extratemporal or neocortical temporal epilepsy vs. mesial temporal epilepsy patients using intracranial monitoring as the gold-standard for localization of the epileptogenic zone. At the end of this activity, the participants should be able to discuss the use of flumazenil PET in the presurgical evaluation of epilepsy patients.
METHODS: Only patients who were already scheduled for (or previously underwent) intracranial monitoring were included in this study. Sixty-minute dynamic FMZ-PET images were acquired in all patients using a Siemens (Iselin, NJ) CTI ECAT EXACT HR tomograph after injection of 20 to 30 mCi of [11C] Flumazenil. Decisions for placement of intracranial EEG recording electrodes and any subsequent surgical resection (n=3) were blinded to FMZ-PET results. 3-D gradient echo high resolution MRI of whole brain was also acquired for anatomical coregistration of FMZ-PET images. A summed FMZ-PET image using the data 16 to 60 minutes after injection was used for visual evaluation of focal areas of decreased FMZ uptake and measurement of an asymmetry index of FMZ binding between the area of decreased binding and the mirror area of the normal contralateral side. FMZ-PET interpretation was blinded to all clinical and electrical data. This research was performed under a protocol approved by the Washington University Institutional Review Board with informed consent from all subjects.
RESULTS: Eight patients were studied, four with mesial temporal epilespy and four with neocortical epilepsy.Clear, focal decreased flumazenil binding was detected three of the four of the neocortical patients and the fourth may have had some subtle decrease. These were located in the right frontal lobe, right posterior temporal lobe, the right parietal and temporal lobes. The asymmetry indicies were 46%, 21%, and 85%, respectively. In these three patients, the locations of the abnormal binding of flumazenil corresponded to the focus of epileptogenicity found by intracranial EEG recordings. In the fourth patient, there were multiple epileptogenic zones within the region of subtley decreased flumazenil binding. Three of these four patients had normal MRI. Three had surgical resection, including two with normal MRI, with pathological diagnosis as microdysgenesis in white matter, cortical gliosis, and neuronal dysplastic/dysmorphic changes in subcortical white matter, respectively. Intracranial monitoring revealed bitemporal onset of seizures in the remaining four patients. No localized abnormal flumazenil binding was detected although a subtle bitemporal decrease could not be excluded in all four patients.
CONCLUSIONS: In this small sample FMZ-PET appears be able to localize the focus of epileptogenicity in patients with intractable neocortical epilepsy. FMZ-PET may have a role in surgical planning of patients with inconsistent results in MRI, FDG-PET and extracranial EEG recordings
[Supported by: This work was supported by the Charles A. Dana Foundation with additional support from NIH Training grant NS07205-20 (LNE) and NINDS grant NS41272 (JGO).]