It is proposed that the generation of bilaterally generalized spike-wave discharges is only possible in an anatomically and functionally intact corticothalamic network, which is in a suitable state to propagate seizures. This state is characterized by light to moderate hyperpolarization of the intrinsically bursting cortical pyramidal cells and of the thalamocortical relay and the reticular thalamic cells, which makes them highly prone to produce high-frequency bursts of action potentials. The initial event is the generation of a normal or epileptic spike at the site of the cortical focus. Through the presence of a massive interconnectivity of excitatory cells, the cortical network is extremely susceptible for the generation of “runaway” excitation, if this network is not sufficiently controlled by inhibition, as is described for WAG/Rij rats.27 In such a runaway condition, the synchronous bursting of a few pyramidal cells may result in a rapid excitation of other excitatory cells, causing a rapid recruitment of neurons, accumulating into the generation of an epileptic spike. The initial leading spike always appears at first in a circumscribed area of the perioral region of the somatosensory cortex. The spike rapidly spreads over the cortex, thus giving the discharges their generalized appearance. This initial event sets a cascade in motion within the intact thalamocortical network, which transforms the spike into spike-wave activity. During the first few cycles the cortical focus drives the thalamus, which becomes entrained into the oscillation, thus providing a resonant circuitry. Subsequently, thalamus and cortex start to drive each other, hereby amplifying and sustaining the discharges. The rapid generalization of the spike-wave activity over the cortex is due to short-range intracortical fibers and to a subpopulation of cells that have long-range association fibers. These run under the cortex in the white matter, making extensive connections with other cortical areas. This allows for the fast widespread intrahemispheric distribution of activity and the interhemispheric transfer through the callosal fibers. From here the activity spreads again through the local network. Thus, the overall pattern of spread is the result of a combination of local and distant spread. Through its impairment in γ-aminobutyric acid–ergic inhibition, the intracortical networks of the WAG/Rij rat are highly susceptible to such spread.27 The perioral part of the somatosensory cortex may experience a more severe local impairment of γ-aminobutyric acid–ergic inhibition, turning it into a weak cortical focus or “hot spot,” with a low threshold for spike generation. This cortical focus is the prime mover of the discharges but, in the later interaction between cortex and thalamus, forms this “cortical focus” theory of generalized absence seizures (see Figure 1), a synthesis between the cortical and the corticoreticular theories.