Superficial 'neocortical' EEG and deep 'paleocortical' SEEG exhibit equal sleep stages equally, i.e. All we can add is that the start of an attack depends not only on the amplitude and frequency of the spikes but also on the regularity of spike intervals. Similar findings were reported by Lieb et al. If prolonged discharges remain localized there is subclinical paroxysm (patient IRL). The time parameter is of no consequence, the inconspicuous motion of the hand is due to a second-lasting discharge of polyspike and wave (patient BRY in sleep). Epileptic activity generalized in all the superficial and deep-implanted leads is mostly accompanied by clinical manifestations (absences, twitching, motor automatisms), or to put it the other way round: if a clinical paroxysms is in progress, there is evidence of generalized epileptic activity in all the leads. FEA intensity tends to drop or even disappear in active vigilance during mental activity or paradoxical sleep. FEA intensity rises in relaxed vigilance and in superficial sleep while tending to decrease in deep synchronous sleep.

Unilateral FEA is hardly ever propagated to the superficial EEG electrodes, bilateral FEA only very rarely (patients BRY and DUS), in some patients solely in deep synchronous sleep (patient LOB).

Focal epileptic activity (FEA) in amygdalohippocampal complexes (AHC) is mostly highly intensive (except in patient BUK where it is nearly missing).

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