An Investigation of Spontaneous Cortical Slow Oscillations Using 256-channel EEG in Normal and Epileptic Patients
Abstract number :
3.350
Submission category :
13. Neuropathology of Epilepsy
Year :
2010
Submission ID :
13362
Source :
www.aesnet.org
Presentation date :
12/3/2010 12:00:00 AM
Published date :
Dec 2, 2010, 06:00 AM
Authors :
Tara Gilbert, P. Luu, M. Holmes and D. Tucker
Rationale: Cortical slow oscillations (CSO) (<1Hz) are generated by the neocortex during non-REM sleep. CSO exist within in-vivo cortical slices and after thalamectomy. These cortical oscillations affect the excitability of neocortical networks with a down and up state. The down state reflects a hyperpolarization and neuronal quiescence of the neocortical cells while the up state reflects depolarization and a heightened activity of the neocortical cells. Spike-wave nocturnal seizures have been shown to emerge from CSO (Tucker et. al., 2009). Using dense-array EEG, we attempt to identify the cortical sources for spontaneously generated CSO during slow-wave sleep (SWS) for both normal and epileptic patients. Methods: We acquired sleep EEG from 14 participants using a 256-channel sensor array (7 normal and 7 epileptic). Sleep stages were identified and CSO were scored during SWS from the first sleep cycle. CSO were evaluated in source space using a 4-shell spherical model that represents the scalp, skull, cerebrospinal fluid, and the cortex with standardized low-resolution brain electromagnetic tomography method (sLORETA). Statistical analyses were performed on the CSO source waveforms. Results: We found considerable variability between subjects related to CSO source analysis. However, there are shared regions of cortical source activity within medial temporal and medial frontal areas. Evaluation of the cortical source activity within subjects indicated that there are stable regions of activity for different types of CSO. Conclusions: From these results, we can conclude that the cortex is utilizing the synchronous nature of the CSO up and down states to regulate different cortical regions during sleep. This may be a way to coordinate neuronal activity such as synaptic plasticity or strengthening during sleep. A better understanding of the modulation of neural excitability in sleep may lead to new options for treatment of nocturnal seizure pathology.
Neuropathology of Epilepsy