Mapping slow waves by EEG topography and source localization: effects of sleep deprivation

Slow waves are a salient feature of the electroencephalogram (EEG) during non-rapid eye movement (non-REM) sleep. The aim of this study was to assess the topography of EEG power and the activation of brain structures during slow wave sleep under normal conditions and after sleep deprivation. Sleep EEG recordings during baseline and recovery sleep after 40 h of sustained wakefulness were analyzed (eight healthy young men, 27 channel EEG). Power maps were computed for the first non-REM sleep episode (where sleep pressure is highest) in baseline and recovery sleep, at frequencies between 0.5 and 2 Hz. Power maps had a frontal predominance at all frequencies between 0.5 and 2 Hz. An additional occipital focus of activity was observed below 1 Hz. Power maps ≤ 1 Hz were not affected by sleep deprivation, whereas an increase in power was observed in the maps ≥ 1.25 Hz. Based on the response to sleep deprivation, low-delta (0.5-1 Hz) and mid-delta activity (1.25-2 Hz) were dissociated. Electrical sources within the cortex of low- and mid-delta activity were estimated using eLORETA. Source localization revealed a predominantly frontal distribution of activity for low-delta and mid-delta activity. Sleep deprivation resulted in an increase in source strength only for mid-delta activity, mainly in parietal and frontal regions. Low-delta activity dominated in occipital and temporal regions and mid-delta activity in limbic and frontal regions independent of the level of sleep pressure. Both, power maps and electrical sources exhibited trait-like aspects

Dopaminergic role in regulating neurophysiological markers of sleep homeostasis in humans

While dopamine affects fundamental brain processes such as movement control, emotional responses, addiction, and pain, the roles for this neurotransmitter in regulating wakefulness and sleep are incompletely understood. Genetically modified animal models with reduced dopamine clearance exhibit hypersensitivity to caffeine, reduced-responsiveness to modafinil, and increased homeostatic response to prolonged wakefulness when compared with wild-type animals. Here we studied sleep-wake regulation in humans and combined pharmacogenetic and neurophysiologic methods to analyze the effects of the 3'-UTR variable-number-tandem-repeat polymorphism of the gene (DAT1, SLC6A3) encoding dopamine transporter (DAT). Previous research demonstrated that healthy homozygous 10-repeat (10R/10R) allele carriers of this genetic variant have reduced striatal DAT protein expression when compared with 9-repeat (9R) allele carriers. Objective and subjective estimates of caffeine sensitivity were higher in 10R allele homozygotes than in carriers of the 9R allele. Moreover, caffeine and modafinil affected wakefulness-induced changes in functional bands (delta, sigma, beta) of rhythmic brain activity in wakefulness and sleep in a DAT1 genotype-dependent manner. Finally, the sleep deprivation-induced increase in well established neurophysiologic markers of sleep homeostasis, including slow-wave sleep, electroencephalographic slow-wave activity (0.5-4.5 Hz), and number of low-frequency (0.5-2.0 Hz) oscillations in non-rapid-eye-movement sleep, was significantly larger in the 10R/10R genotype than in the 9R allele carriers of DAT1. Together, the data suggest that the dopamine transporter contributes to homeostatic sleep-wake regulation in humans

Spindle frequency activity may provide lateralizing information in drug-resistant nocturnal mesial frontal lobe epilepsy: A pilot study on the contribution of sleep recordings

PURPOSE: Nocturnal frontal lobe epilepsy (NFLE) is characterized by sleep-related paroxysmal motor attacks occurring almost exclusively during non-REM sleep. Surgical treatment may relieve symptoms in drug-resistant patients. However, the identification of the epileptogenic zone, the region to be resected, is frequently challenging because of the absence of lateralizing and localizing information and the lack of informative EEG correlates. The aim of this study was to find asymmetries in the ictal activity that could provide information on the lateralization of the epileptogenic zone. METHOD: We retrospectively analyzed the sleep EEG of four patients recorded prior to surgical intervention. The epileptogenic zone was known, as these patients had subsequently undergone successful surgery after bilateral intracerebral stereo-EEG investigation. Sleep EEG during the ictal phase was compared with sleep EEG during the pre-ictal phase. RESULTS: In all patients, electrical sources of sigma activity (12-16Hz) exhibited increased activity during the ictal phase which was higher in the epileptogenic hemisphere. Conversely, increased delta activity (1-4Hz) was predominant contralateral to the epileptogenic focus in three of four patients. CONCLUSION: Sigma activity may have a predictive role in the lateralization of the epileptogenic zone and be useful during the pre-surgical evaluation of patients with NFLE