Generalized spike-and-wave (SW) discharges are often associated with periods of impaired consciousness (i.e., withabsence seizures) and reflect thalamocortical oscillations similar to those involved in sleep spindles, but at a lowerfrequency. Both cortical and thalamic neuronal networks contribute to SWdischarge. Moreover, according to recentevidence obtained from rodent models, discrete cortical networks initiate these seizures by producing enhancedcorticothalamic output activity that initiates the following sequence: (i) corticothalamic activity makes thalamicreticular γ-aminobutyric acid (GABA)-ergic cells fire intense action potential bursts; (ii) these bursts cause extended inhibitory postsynaptic potentials (IPSPs) in thalamic relaycells, which results in (iii) a slowing of relay cell pacing frequency and (iv) a recruitment of a larger number of corticaland thalamic neurons – which leads to SW activity. The changes that cause the initiating cortical hyperexcitabilityinclude both intrinsic and synaptic mechanisms.