title: Cortical glucose metabolism correlates negatively with delta-slowing and spike-frequency in epilepsy associated with tuberous sclerosis.
abstract: 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 derived from 865 intracranial electrode sites in 11 children with focal epilepsy associated with tuberous sclerosis complex (TSC) (age: 0.5-16 years) undergoing epilepsy surgery. 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. 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. 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.
authors.affiliation: Department of Pediatrics, Children's Hospital of Michigan, Wayne State University, Detroit, Michigan 48201, USA.
authors.forename: Masaaki
authors.initials: M
authors.lastname: Nishida
authors.forename: Eishi
authors.initials: E
authors.lastname: Asano
authors.forename: Csaba
authors.initials: C
authors.lastname: Juhász
authors.forename: Otto
authors.initials: O
authors.lastname: Muzik
authors.forename: Sandeep
authors.initials: S
authors.lastname: Sood
authors.forename: Harry T
authors.initials: HT
authors.lastname: Chugani
mesh_terms: D000293:Adolescent; D001921:Brain / Q000502:physiology*; D002648:Child; D004569:Electroencephalography; D004827:Epilepsy / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology*; D005260:Female; D005947:Glucose / Q000378:metabolism*; D006801:Humans; D007223:Infant; D008279:Magnetic Resonance Imaging; D008297:Male; D049268:Positron-Emission Tomography; D014402:Tuberous Sclerosis / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology*
chemical_list: D005947:Glucose