The slow oscillation during non-REM (NREM) sleep is a traveling wave that propagates across the cerebral cortex. This study used high-density EEG recordings in humans to show that each slow oscillation cycle originates at a specific site and travels across the scalp at a speed of 1.2–7.0 m/sec. The waves originate more frequently in prefrontal–orbitofrontal regions and propagate in an anteroposterior direction. The rate of occurrence increases as sleep deepens, reaching nearly once per second in deep sleep. The pattern of origin and propagation is reproducible across nights and subjects, indicating a consistent cortical excitability and connectivity. The orderly propagation of correlated activity may play a role in spike timing-dependent synaptic plasticity during sleep. The slow oscillation is a fundamental cellular phenomenon underlying NREM sleep, involving a hyperpolarization phase (down state) followed by a depolarization phase (up state). During the up state, neurons fire at high rates, and the entire thalamocortical system is active. The slow oscillation is generated and sustained by the cerebral cortex and is disrupted by disconnection of intracortical pathways. The study found that each slow oscillation is a traveling wave with a definite origin and direction of propagation. The speed of propagation was measured as 2.7 m/sec on average, with variations depending on the direction. The slow oscillation originates more frequently in anterior regions and propagates in an anteroposterior direction. The general pattern of origin and propagation is reproducible across nights and subjects, suggesting a consistent cortical excitability and connectivity. The slow oscillation may play a functional role in synaptic plasticity during sleep, as the orderly propagation of correlated activity along connected pathways may contribute to synaptic consolidation or downscaling. The study also suggests that the sites of origin of slow oscillation cycles are not uniformly distributed over the cortical surface but are more concentrated in certain regions, such as the transition between dorsolateral and orbitofrontal cortex. This region appears to have a stronger need for sleep, as evidenced by lower cerebral blood flow during NREM sleep and increased slow wave activity in anterior prefrontal regions after sleep deprivation. These findings suggest that traveling waves may serve a physiological function in sleep.The slow oscillation during non-REM (NREM) sleep is a traveling wave that propagates across the cerebral cortex. This study used high-density EEG recordings in humans to show that each slow oscillation cycle originates at a specific site and travels across the scalp at a speed of 1.2–7.0 m/sec. The waves originate more frequently in prefrontal–orbitofrontal regions and propagate in an anteroposterior direction. The rate of occurrence increases as sleep deepens, reaching nearly once per second in deep sleep. The pattern of origin and propagation is reproducible across nights and subjects, indicating a consistent cortical excitability and connectivity. The orderly propagation of correlated activity may play a role in spike timing-dependent synaptic plasticity during sleep. The slow oscillation is a fundamental cellular phenomenon underlying NREM sleep, involving a hyperpolarization phase (down state) followed by a depolarization phase (up state). During the up state, neurons fire at high rates, and the entire thalamocortical system is active. The slow oscillation is generated and sustained by the cerebral cortex and is disrupted by disconnection of intracortical pathways. The study found that each slow oscillation is a traveling wave with a definite origin and direction of propagation. The speed of propagation was measured as 2.7 m/sec on average, with variations depending on the direction. The slow oscillation originates more frequently in anterior regions and propagates in an anteroposterior direction. The general pattern of origin and propagation is reproducible across nights and subjects, suggesting a consistent cortical excitability and connectivity. The slow oscillation may play a functional role in synaptic plasticity during sleep, as the orderly propagation of correlated activity along connected pathways may contribute to synaptic consolidation or downscaling. The study also suggests that the sites of origin of slow oscillation cycles are not uniformly distributed over the cortical surface but are more concentrated in certain regions, such as the transition between dorsolateral and orbitofrontal cortex. This region appears to have a stronger need for sleep, as evidenced by lower cerebral blood flow during NREM sleep and increased slow wave activity in anterior prefrontal regions after sleep deprivation. These findings suggest that traveling waves may serve a physiological function in sleep.