Abstracts

Rationale: The mechanism of altered glucose metabolism seen on positron emission tomography (PET) in focal epilepsy is not fully understood. We determined the association between interictal glucose metabolism and interictal neuronal activity, using PET and electrocorticography (ECoG) measures.Methods: A total of 11 children with focal epilepsy associated with tuberous sclerosis complex (TSC) (age: 0.5 – 16 years) who underwent epilepsy surgery were studied. All patients underwent preoperative MRI, extraoperative electrocorticography recording and PET. PET and electrocorticography (ECoG) measures were derived from 865 intracranial electrode sites. A multiple linear regression analysis was applied to each patient, to determine whether the glucose uptake at each electrode site on interictal PET was predicted by ECoG amplitude powers and interictal spike-frequency measured in the given electrode site. The regression slopes as well as R-square values (an indicator of fitness of the regression models) were finally averaged across the 11 patients. Results: The mean regression slope for delta amplitude power was -0.0025 (95%CI: -0.0045 to -0.0004; p=0.02 based on one-sample t-test) and that for spike frequency was -0.023 (95%CI: -0.042 to -0.0038; p=0.02). On the other hand, the mean regression slopes for the remaining ECoG amplitude powers (theta, alpha, sigma, beta and gamma activities) were not significantly different from zero. The mean R-square value was 0.39. Conclusions: These results suggest that increased delta-slowing and frequent spike activity were independently and additively associated with glucose hypometabolism in children with focal epilepsy associated with TSC. Association between frequent interictal spike activity and low glucose metabolism may be attributed to slow-wave components following spike discharges on ECoG recording, and a substantial proportion of the variance in regional glucose metabolism on PET could be explained by electrophysiological traits derived from conventional subdural ECoG recording. Supported by NIH NS47550 (E.A.)