Early on, it was thought that dreaming was a product of cortical excitation and that fast-wave sleep was produced in the cerebral cortex. In fact, studies nowadays confirm that tissues above the cerebral bridge do not produce fast-wave sleep; fast-wave sleep is produced by the cerebral bridge and the tissues below it. Different parts of the pons maintain different manifestations of fast-wave sleep. The reticular nucleus of the pons mainly maintains the desynchronized brain waves of fast-wave sleep, and the middle part of the blue spot nucleus innervates the rapid eye movements induced by the pons reticularis. The caudal part of the nucleus accumbens has an inhibitory effect on muscle tension through the reticulospinal tract. These activities of the nucleus accumbens are in turn dependent on the triggering of the middle suture nucleus, which can cause excitation of the middle and tail of the nucleus accumbens, thereby triggering the whole of fast-wave sleep. The transition from slow-wave sleep to fast-wave sleep is a continuous and changing process rather than a simple “on and off” transition. In REM sleep, although there is no external visual information coming in, the activation of the coronal firing system makes the person still believe that information is coming in from the outside, which leads to the formation of various perceptions of dreams, and this cognitive integration process can be interrupted by a PGO wave from the pontine brain, which can be recorded in the pontine brain, lateral geniculate body and occipital cortex as periodic high amplitude firing phenomena called PGO waves. PGO waves mark the onset of fast-wave sleep, so dreams are often discontinuous and illogical.