Modeling absence seizure dynamics: implications for basic mechanisms and measurement of thalamocortical and corticothalamic latencies.
A successful physiologically based continuum model of the corticothalamic system is applied to determine the relative contributions of axonal and intrinsic cellular delays to the waveforms of absence seizures. The predicted period of the absence seizure depends linearly on model parameters describing thalamocortical, corticothalamic, intracortical, and synaptodendritic delays, and these dependences are linked to the seizure mechanism by showing how time intervals between peaks in the waveforms depend on the parameters. Counterintuitively, it is found that a peak in the local field potential recorded in the thalamic relay nuclei can precede the peak in the cortical field that drove it, without violating causality, but rendering naive interpretation of time intervals between peaks invalid. We argue that a thalamocortical loop mechanism for absence seizures is consistent with intrathalamic cellular properties being the leading determinant of the frequency of spike-wave discharges in rat genetic models, with the combination of network and cellular properties providing a natural explanation for the lower frequency of human absence seizures. Finally, our results imply that the seizure frequency is not determined by the fastest thalamocortical and corticothalamic fibers, but rather depends on an effective weighted conduction velocity of all pathways present.
Roberts
James A
JA
School of Physics, University of Sydney, New South Wales 2006, Australia. jamesr@physics.usyd.edu.au
Robinson
Peter A
PA
D002540:Cerebral Cortex / Q000503:physiopathology*; D003198:Computer Simulation; D004569:Electroencephalography; D004832:Epilepsy, Absence / Q000503:physiopathology*; D006801:Humans; D008959:Models, Neurological; D009434:Neural Pathways; D013788:Thalamus / Q000503:physiopathology*