A Thalamocortical Loop Mechanism For Absence Seizures
The mechanism proposed for absence seizures can be summarized as follows. During sleep spindles, the oscillation is generated by intrathalamic interactions (TC-RE loops) and is reinforced by thalamocortical loops, as suggested in a previous model (Destexhe et al., 1998a). The combined action of intrathalamic and thalamocortical loops provides RE cells with moderate excitation, which evokes GABAA-mediated IPSPs in TC cells and sets the frequency to ~10Hz. During spike-and-wave seizures, due to increased cortical excitability, corticothalamic feedback becomes strong enough to force prolonged burst discharges in RE cells which, in turn, evoke IPSPs in TC cells dominated by the GABAb component. In this case, the prolonged inhibition sets the frequency to Hz and the oscillation is generated by a thalamocortical loop in which the thalamus is intact (see details in Destexhe, 1998). Therefore, if the cortex is inactivated during spike-and-wave, this model predicts that the thalamus should resume generating spindle oscillations, as observed experimentally in cats treated with penicillin (Gloor et al., 1979).
Figure 13.18 shows the phase relations between the different cell types in this corticothalamic model of spike-and-wave seizures. High-frequency discharges generated 'spike' components in the field potentials, whereas 'wave' components
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