Reduced cellular discharge and chemical release in reticulothalamic pathways promote IID generation during NREM in primary generalized epilepsies (e.g., Gloor and Testa, 1974; Gloor, 1979; Steriade et al., 1993), probably by en hancing the thalamocortical EEG synchronization patterns with which spike-wave and polyspike-wave complexes are associated. Synchronized sleep transients such as sleep spindles and possibly even delta waves are contingent on sequenced hyperpolarizing GABAergic input from the thalamic reticular nucleus to the thalamocortical relay cells (e.g., McCormick, 1992; Steriade et al, 1993; Steriade, 1994). Increased GABA release from thalamic and cortical neurons is considered critical to generation of slow components of these IlDs (e.g., Gloor and Fariello, 1988; von Krosigk et al, 1993).
The peak in GABA release that occurs during NREM, although promoting IlDs, seems to discourage clinically evident seizures such as generalized myoclonic and tonic-clonic convulsions. The moderate levels of reticular activation, chemical release, and synchronous thalamocortical discharge patterns during drowsiness are conducive to generalized epileptic EEG discharge propagation with clinical accompaniment (e.g., Gloor and Testa, 1974). In contrast to NREM and drowsiness, extreme activation of ascending brain stem afferents, particularly cholinergic cells, occurs during alert waking and REM sleep (e.g., Jones, 1994; Siegel, 1994), abolishes GABA-mediated synchronous thalamocortical discharge oscillations (Steriade, 1994), and is thought to suppress both ictal and interictal events in PGE (e.g., Guberman and Gloor, 1982; Shouse et al, 1989).
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