Abstract
PurposeThe loss of synaptic vesicle glycoprotein 2A (SV2A) is well established as the major correlate of epileptogenesis in focal cortical dysplasia type II (FCD II), but this has not been directly tested in vivo. In this positron emission tomography (PET) study with the new tracer 18F-SynVesT-1, we evaluated SV2A abnormalities in patients with FCD II and compared the pattern to 18F-fluorodeoxyglucose (18F-FDG).MethodsSixteen patients with proven FCD II and 16 healthy controls were recruited. All FCD II patients underwent magnetic resonance imaging (MRI) and static PET imaging with both 18F-SynVesT-1 and 18F-FDG, while the controls underwent MRI and PET with only 18F-SynVesT-1. Visual assessment of PET images was undertaken. The standardized uptake values (SUVs) of 18F-SynVesT-1 were computed for regions of interest (ROIs), along with SUV ratio (SUVr) between ROI and centrum semiovale (white matter). Asymmetry indices (AIs) were analyzed between the lesion and the contralateral hemisphere for intersubject comparisons.ResultsLesions in the brains of FCD II patients had significantly reduced 18F-SynVesT-1 uptake compared with contralateral regions, and brains of the controls. 18F-SynVesT-1 PET indicated low lesion uptake in 14 patients (87.5%), corresponding to hypometabolism detected by 18F-FDG PET, with higher accuracy for lesion localization than MRI (43.8%) (P < 0.05). AI analyses demonstrated that in the lesions, SUVr for each of the radiotracers were not significantly different (P > 0.05), and 18F-SynVesT-1 SUVr correlated with that of 18F-FDG across subjects (R2 = 0.41, P = 0.008). Subsequent visual ratings indicated that 18F-SynVesT-1 uptake had a more restricted pattern of reduction than 18F-FDG uptake in FCD II lesions (P < 0.05).ConclusionSV2A PET with 18F-SynVesT-1 shows a higher accuracy for the localization of FCD II lesions than MRI and a more restricted pattern of abnormality than 18F-FDG PET.
Highlights
Focal cortical dysplasia type II (FCD II) constitutes the most common cause of seizures in patients who undergo surgery before the age of 18 years [1]
We found an Asymmetry indices (AIs) based on lesion standardized uptake value (SUV) ratio (SUVr) of 27.14% ± 10.15% in patients with FCD II, which was much higher than that in the controls
One study in temporal lobe epilepsy found that hippocampal 18F-FDG uptake was correlated with 11C-UCB-J binding potential [10]. These findings suggest that the hypometabolism in FCD II lesions may be related to the decrease in synaptic vesicle glycoprotein 2A (SV2A), and SV2A positron emission tomography (PET) provides a complementary measure of the epileptogenic substrate
Summary
Focal cortical dysplasia type II (FCD II) constitutes the most common cause of seizures in patients who undergo surgery before the age of 18 years [1]. Epilepsy in FCD II is commonly pharmacoresistant and challenging for antiepileptic treatment [2]. Surgical resection of FCD II lesions may prevent seizures and improve quality of life [3]. It has been well established that the main predictor of favorable surgical outcomes is the complete removal of the dysplastic cortex. FCD II is predominantly located in extratemporal areas, in particular the eloquent cortex [3]. Magnetic resonance imaging (MRI) features in FCD II have been widely
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