Cortical glucose metabolism correlates negatively with delta‐slowing and spike‐frequency in epilepsy associated with tuberous sclerosis

Abstract

SUMMARY 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.

Differential visually-induced gamma-oscillations in human cerebral cortex

“…In order to animate ‘when’, ‘where’ and ‘how many fold’ gamma-oscillations were increased or decreased, ‘gamma-range amplitude’ (defined as the spectral amplitude averaged across 50- to 150-Hz frequency bands and normalized to that of the reference period) was sequentially delineated on the individual three-dimensional MRI (Figures 1 and 2; Videos S1–S4), using a method previously described (Brown et al, 2008). ‘Gamma-range amplitude’ was calculated without a frequency band at 60Hz if visual inspection revealed a 60-Hz artifact peak on the amplitude spectral curve for all subdural electrodes (Nishida et al, 2007). ‘Gamma-range amplitude’ for each electrode channel at each 10-msec epoch was registered into the SurGe Interpolation Software 1.2 (Web site: http://mujweb.cz/www/SurGe/surgemain.htm), and interpolated topography map of ‘gamma-range amplitude’ at each 10-msec epoch was accurately superimposed to the individual three-dimensional MRI.…”

Spatial–temporal patterns of electrocorticographic spectral changes during midazolam sedation

“…Electrophysiological correlates of benzodiazepine sedation have been studied in human brain primarily using scalp EEG recording, and the common observations include amplitude augmentation of beta (16–31.5 Hz), sigma (12–15.5 Hz) and delta (<3.5 Hz) activities (Schulte am Esch et al, 1990; Veselis et al, 1991; Hering et al, 1994; Liu et al, 1996; Schnider et al, 1996). Beta-sigma oscillations have been considered to comprise idling rhythms signaling the status quo to the underlying cortex (Neuper and Pfurtscheller, 2001; Engel and Fries, 2010), whereas delta oscillations reflect inhibited neuronal states (Steriade and Timofeev, 2003; Nishida et al, 2008; Vyazovskiy et al, 2011). Unanswered questions still exist regarding sedation-induced electrographic changes, partly because scalp EEG recording has a poor spatial resolution.…”

Cortical glucose metabolism positively correlates with gamma-oscillations in nonlesional focal epilepsy

“…Previous studies using PET and functional magnetic resonance imaging (MRI), for example, suggested that frequent interictal epileptiform discharges may induce metabolic and hemodynamic activation in some population with focal epilepsy (Chugani et al, 1993; Maquet et al, 1995; De Tiege et al, 2004; Gotman et al, 2006; Kobayashi et al, 2006a). Yet, our recent study of children with lesional epilepsy associated with tuberous sclerosis complex showed that frequent interictal epileptiform discharges were rather associated with glucose hypometabolism (Nishida et al, 2007), and other functional MRI studies demonstrated that interictal epileptiform discharges were associated with hemodynamic deactivation in some patients with focal epilepsy (Federico et al, 2005; Kobayashi et al, 2006b). Association between frequent interictal spike activity and glucose hypometabolism as well as cortical deactivation was attributed to slow-wave components following spike discharges in these studies (Kobayashi et al, 2006b; Nishida et al, 2007).…”