Across the years, several authors have focused their attention on the dynamic relationship between epileptic paroxysms and EEG phasic events during sleep. In the feline generalized penicillin epilepsy, spike-and-wave discharges are thought to represent a pathological cortical response to afferent thalamocortical volleys, which under normal conditions are involved in sleep spindling (Gloor, 1984). In the feline amygdala-kindled model, which is generally assimilated to human temporal epilepsy (Shouse, 1987), and in WAG/Rij rats, genetic models of human absence epilepsy (Drinkenburg et al, 1991), both interictal and ictal discharges are influenced by rapid shifts of EEG synchrony (Shouse et al, 1995). Even in human epilepsy, the frequent association between spike-and-wave complexes and K-complexes suggests that common basic mechanisms and transmission circuitry may be shared by both epileptic abnormalities and phasic events during sleep.
More than 25 years ago, Niedermeyer introduced the concept of dyshormia (1972), postulating that nocturnal paroxysmal discharges are an abnormal exaggeration of the physiological arousal-related microfluctuations expressed in human NREM sleep by a K-complex. In the following decades, a number of contributions have suggested that vertex sharp waves in stage 1, K-complexes in stage 2, and delta bursts in stages 3 and 4 represent the same arousal-related phenomenon along a continuum from the light to the deep NREM sleep (for a review, Terzano et al., 1992). The close relation between epileptogenic manifestations and phasic events corroborates the idea of a circular recursive influence between the mechanisms involved in the dynamic organization of sleep and the neurophysiological correlates of epilepsy. In light of this, sleep is a major physiological activator of epileptic manifestations, while the latter represent an important perturbing agent of sleep instability. The arrangement of NREM sleep phasic events into the CAP/NCAP scaffolds not only allows identification of three neurophysiological conditions:
1. Level of transient activation (phase A)
2. Level of inhibition (phase B)
3. Stationary intermediate condition (NCAP)
but also can contribute to shed light on the modulatory factors involved in epileptic phenomena.
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