Our results confirm and extent findings of previous researchers who used unlocalized in vivo manipulations to show that norepinephrine (NE) is a highly antiepileptic agent in the amygdala kindling preparation. With further investigation, the results may ultimately lead to development of microinfusion techniques as an alternative treatment option for limbic epilepsy.
Amygdala-kindled kittens exhibit frequent epileptiform EEG transients, often in conjunction with phasic arousal events of sleep [k-complexes, pontogeniculo-occipital (PGO) waves, and/or sleep spindles]. In this study, paroxysmal microarousals occurred throughout the sleep-wake cycle after kindling, but were most frequent during seizure-prone states of slow-wave sleep (SWS) and the transition into rapid-eye-movement sleep (REM). Their incidence correlated with interictal sleep fragmentation as well as onset of spontaneous convulsions. Results could reflect transsynaptic kindling effects on brainstem and forebrain arousal mechanisms with which amygdala is reciprocally connected. Increased discharge rates of neural generators for normal EEG and behavioral arousal could disrupt sleep at some times and recruit epileptic neurons in the kindled focus to precipitate seizures at others. Alternatively, epileptiform EEG paroxysms were accompanied by subtle behavioral stereotypes (a head nod, limb elevation, eye twitch, lip smack, or a combination of these). Behavioral correlates were elements of partial kindled seizures, suggesting that paroxysmal microarousals may be subclinical seizures. Whether or not the microarousals are true seizures, our findings may link ictal onset and interictal sleep disorders to a subclinical paroxysmal arousal disorder and suggest a common epileptic mechanism.
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