Penicillin Epilepsy Amygdala Kindling Discussion
Primary Generalized Epilepsy Localization-Related Epilepsies Conclusions References introduction
The two main sleep states, nonrapid eye movement (NREM) sleep and rapid eye movement (REM) sleep, have different physiological components and contrasting effects on generalized ictal and interictal discharges (IIDs). Epileptiform discharges are likely to propagate during NREM sleep, including its synchronized electroencephalographic (EEG) transients, such as K-com-
Epilepsy and Sleep: Physiological and Clinical Relationships
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plexes and sleep spindles, and its transitional "drowsy" EEG arousal periods. In contrast, REM sleep, with its asynchonous cellular discharge patterns and skeletal motor paralysis, is resistant to propagation of epileptic EEG potentials and to clinical motor accompaniment even though focal IID persists at this time.
The contrasting effects of NREM and REM on IIDs and clinically evident seizures are to some extent nonspecific with respect to epileptic syndrome (Shouse et al., 1996), defined by seizure type, etiology, and clinical course (Commission Report, 1989). On the other hand, clinically evident seizures, particularly generalized tonic-clonic or myoclonic convulsions, occur mainly during NREM sleep, mainly during drowsy wakefulness, or randomly in the sleep-wake cycle depending on epileptic syndrome (e.g., Janz, 1962). Interictal discharges are less likely to propagate and to lead to a clinically evident seizure during intact REM sleep than in any other state regardless of epileptic syndrome (e.g., Sammaritano et al., 1991; Shouse et al., 1989, 1996).
The clinical observations raise three questions that this chapter addresses:
(1) Which characteristics of NREM account for the activation of IIDs?
(2) Which characteristics of REM sleep suppress them? (3) How do the physiological mechanisms of specific sleep-waking state components interact with epileptic seizure pathology to provoke clinically evident seizures at different times?
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