Sleep slow wave activity (SWA) is thought to reflect sleep need, increasing after wakefulness and decreasing after sleep. We showed recently that a learning task involving a circumscribed brain region produces a local increase in sleep SWA. We hypothesized that increases in cortical SWA reflect synaptic potentiation triggered by learning. To further investigate the link between synaptic plasticity and sleep, we asked whether a procedure leading to synaptic depression would cause instead a decrease in sleep SWA. We show here that if a subject's arm is immobilized during the day, motor performance deteriorates and both somatosensory and motor evoked potentials decrease over contralateral sensorimotor cortex, indicative of local synaptic depression. Notably, during subsequent sleep, SWA over the same cortical area is markedly reduced. Thus, cortical plasticity is linked to local sleep regulation without learning in the classical sense. Moreover, when synaptic strength is reduced, local sleep need is also reduced.

Consciousness never fades during wake. However, if awakened from sleep, sometimes we report dreams and sometimes no experiences. Traditionally, dreaming has been identified with REM sleep, characterized by a wake-like, globally ‘activated’, high-frequency EEG. However, dreaming also occurs in NREM sleep, characterized by prominent low-frequency activity. This challenges our understanding of the neural correlates of conscious experiences in sleep. Using high-density EEG, we contrasted the presence and absence of dreaming within NREM and REM sleep. In both NREM and REM sleep, reports of dream experience were associated with a local decrease in low-frequency activity in posterior cortical regions. High-frequency activity within these regions correlated with specific dream contents. Monitoring this posterior ‘hot zone’ predicted whether an individual reported dreaming or the absence of experiences during NREM sleep in real time, suggesting that it may constitute a core correlate of conscious experiences in sleep.

In the human EEG, the decline of SWA during sleep is accompanied by changes in slow-wave parameters that were predicted by a computer model simulating a homeostatic reduction of cortical synaptic strength.

By employing transcranial magnetic stimulation (TMS) in combination with high-density electroencephalography (EEG), we recently reported that cortical effective connectivity is disrupted during early non-rapid eye movement (NREM) sleep. This is a time when subjects, if awakened, may report little or no conscious content. We hypothesized that a similar breakdown of cortical effective connectivity may underlie loss of consciousness (LOC) induced by pharmacologic agents. Here, we tested this hypothesis by comparing EEG responses to TMS during wakefulness and LOC induced by the benzodiazepine midazolam. Unlike spontaneous sleep states, a subject's level of vigilance can be monitored repeatedly during pharmacological LOC. We found that, unlike during wakefulness, wherein TMS triggered responses in multiple cortical areas lasting for >300 ms, during midazolam-induced LOC, TMS-evoked activity was local and of shorter duration. Furthermore, a measure of the propagation of evoked cortical currents (significant current scattering, SCS) could reliably discriminate between consciousness and LOC. These results resemble those observed in early NREM sleep and suggest that a breakdown of cortical effective connectivity may be a common feature of conditions characterized by LOC. Moreover, these results suggest that it might be possible to use TMS-EEG to assess consciousness during anesthesia and in pathological conditions, such as coma, vegetative state, and minimally conscious state.anesthesia | high-density electroencephalography | transcranial magnetic stimulation T heoretical considerations suggest that consciousness depends on the brain's ability to integrate information, and that if information integration is impaired within a complex of cortical areas, consciousness should fade (1). The most common situation in which the level of consciousness changes is early non-rapid eye movement (NREM) sleep, when subjects, if awakened, report no or little conscious experience (2), despite the fact that their brain remains highly active (3). To establish whether the brain's ability to integrate information is higher in wakefulness than in early NREM sleep, in a previous study we perturbed one brain area using transcranial magnetic stimulation (TMS) and recorded the responses of other cortical areas using TMScompatible high-density electroencephalography (hd-EEG) (4). We found that during wakefulness, TMS initially evoked a local cortical activation, which then moved to a series of distant cortical areas, whereas during NREM sleep, the initial local response to TMS did not propagate beyond the stimulation site, thus indicating a breakdown of cortical effective connectivity and a loss of cortical integration (5). Moreover, in subsequent TMS/hd-EEG studies, we established that during wakefulness, TMS of different brain regions evoked different, specific EEG patterns (6), whereas during early NREM sleep, TMS yielded EEG responses characterized by a positive wave followed by a negative deflection, suggesting a loss of information capacity ...

Slow waves are the most prominent electroencephalographic (EEG) feature of sleep. These waves arise from the synchronization of slow oscillations in the membrane potentials of millions of neurons. Scalplevel studies have indicated that slow waves are not instantaneous events, but rather they travel across the brain. Previous studies of EEG slow waves were limited by the poor spatial resolution of EEGs and by the difficulty of relating scalp potentials to the activity of the underlying cortex. Here we use high-density EEG (hd-EEG) source modeling to show that individual spontaneous slow waves have distinct cortical origins, propagate uniquely across the cortex, and involve unique subsets of cortical structures. However, when the waves are examined en masse, we find that there are diffuse hot spots of slow wave origins centered on the lateral sulci. Furthermore, slow wave propagation along the anterior؊posterior axis of the brain is largely mediated by a cingulate highway. As a group, slow waves are associated with large currents in the medial frontal gyrus, the middle frontal gyrus, the inferior frontal gyrus, the anterior cingulate, the precuneus, and the posterior cingulate. These areas overlap with the major connectional backbone of the cortex and with many parts of the default network.brain mapping ͉ default network ͉ electroencephalography ͉ slow oscillation ͉ traveling wave