Sleep Disorders Center Department of Neurology University of Parma Italy
Epilepsy and Vigilance States Sleep Propensity and Body Temperature Rhythms Sleep Intensity and Slow-Wave Sleep Nonrapid Eye Movement/Rapid Eye Movement Sleep Cycle
Dynamics of Thalamic Neurons during Sleep Low-Frequency (<1 Hz) Oscillations in the Human Sleep Electroencephalogram
Scoring of Cyclic Alternating Pattern Parameters
Cyclic Alternating Pattern and Noncyclic Alternating Pattern
Cyclic Alternating Pattern Rate
Effects of Cyclic Alternating Pattern on Epileptic Events
Primary Generalized Epilepsy
Lesional Epilepsy with Frontotemperal Focus
Epilepsy and Sleep: Physiological and Clinical Relationships
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Benign Epilepsy with Rolandic Spikes
Arousal Mechanisms and Location of Interictal Foci
Modulatory Effects of Phase A Subtypes
Cyclic Alternating Pattern and Nocturnal Motor Seizures
Neurophysiological Bases of Electroencephalographic Synchrony
Circadian Homeostatic Ultradian Microstructural Conclusions References epilepsy and vigilance states
The variations of the arousal level across the 24-h rhythm play an important role in the modulation of epileptic events. The sleep-wake cycle, and particularly the conditions of instability that occur during sleep, affect significantly the appearance of interictal electroencephalography (EEG) discharges and epileptic seizures. This interaction, either in the sense of inhibition or, more frequently, in the direction of activation, relies on the characteristics of the epileptic syndrome (type of attacks, clinical course, and etiology), on the time of the day, and on the structural components of sleep (falling asleep, EEG arousal, nonrapid eye movement (NREM) stages, and rapid eye movement (REM) sleep). In particular, the two neurophysiological states that characterize sleep (NREM and REM) have opposite consequences on interictal abnormalities and on critical manifestations. A pioneering contribution published 60 years ago on the incidence of epileptic attacks over the 24-h period indicated a clear circadian variation (Griffiths and Fox, 1938). During sleep, the number of seizures showed a gradual increase from midnight to dawn. The early morning peak was followed by a sharp reduction until noon. There was a small postmeal peak, while a considerable increase in seizure incidence was found again in the early evening hours.
Other 24-h studies have investigated the influence of the vigilance states on the occurrence of epileptic manifestations, showing that epileptic manifestations are more likely to appear when the level of vigilance is low (relaxation, drowsiness, or sleep) and unstable (arousal fluctuations) and that frequency and morphology of epileptiform EEG patterns may depend on sleep stages. According to most studies, generalized discharges and clinical seizures mostly occur in NREM sleep, which may be globally considered a natural "convulsive agent" (Passouant, 1991). The large majority of EEG paroxysms are found in stage 2 of sleep, although there are reports of a maximum of discharges during stages 3 and 4. In contrast, there is general agreement on the fact that the number of EEG abnormalities, especially generalized bursts, is lowest during REM sleep (Shouse et al., 1996). These findings clearly indicate that the epileptic event is extremely sensitive to the ongoing arousal condition. Because the vigilance states vary across the diurnal and nocturnal periods and because the changing functional states of the brain seem to have important modulatory effects on most epilepsies, a survey of the basic mechanisms underlying the sleep-wake continuum is outlined.
sleep propensity and body temperature rhythms
An important modulation of the sleep-wake rhythm is mediated by the endogenous circadian system. Both human and animal studies have demonstrated that the mammalian circadian oscillator is located in the suprachiasmatic nuclei of the antierior hypothalamus and serves as a topical source for the timing boundaries of sleep and wakefulness in the 24-h cycle. Independent of other factors, the circadian clock potentiates wakefulness at one phase of the diurnal cycle and facilitates sleep at the opposite phase (Fig. 8.1). This autonomous pacemaker determines the sleep propensity in relation to other biological functions and, in particular, to the rhythmicity of deep body temperature. The sleep regulation process homeostatic swa ultradian
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