This chapter examines possible neuronal networks and mechanisms responsible for the switch from waking to non-rapid eye movement (NREM) and REM sleep. The activated cortical state during waking is induced by the activity of multiple waking neurochemical systems. In contrast to the complex and extensive neurochemical network involved in waking, the neurons inducing slow-wave sleep (SWS) are localized in the lateral preoptic area and the adjacent basal forebrain. A cluster of these neurons is localized in a small nucleus called the ventrolateral preoptic nucleus (VLPO), which is situated above the optic chiasm. Neurons specifically active during paradoxical sleep (PS) were recorded in the posterior hypothalamus (PH) of cats or head-restrained rats. One-third of these GABAergic neurons were immunoreactive for the neuropeptide melanin concentrating hormone (MCH). PS onset would be due to the activation of glutamatergic PS-on neurons from the sublaterodorsal tegmental nucleus (SLD).

Although the neurophysiological origin of the functional magnetic resonance imaging (fMRI) blood oxygen level-dependent (BOLD) signal is still poorly understood, spontaneous fMRI signal fluctuations show consistent spatial correlations in functionally related networks. Large-scale functional brain networks as derived from fMRI time-series can be examined by graph theoretical analysis; such analysis has revealed a small-world organization of human functional brain networks during wakefulness, with high local clustering and short path length. A hierarchical cluster analysis indeed illustrated that frontoparietal clusters could be detected in wakefulness but not in deeper non-rapid eye movement (NREM) sleep stages. Functional connectivity of phasic events allows further spatial and temporal refinement of vigilance-state dependent connectivity patterns, and may be of special interest for phasic electroencephalography (EEG) events during sleep. Finally, although functional connectivity appears to overlap to a considerable extent with brain metabolism, these measures seem to represent correlated but different dimensions.

This chapter reviews the functional brain imaging studies, using positron emission tomography (PET) and functional magnetic resonance imaging (fMRI), that have examined neural activity patterns between non-rapid eye movement (NREM) sleep and wakefulness, and within NREM sleep in association with phasic neuronal oscillations. It explores recent fMRI data investigating the relationship between these rhythms and the processing of external stimulation during sleep. In order to further explore this relationship between external stimulation and NREM sleep phasic activity, brain responses to pure tones delivered during NREM sleep were evaluated in a recent event-related fMRI study. In the fMRI study, the relationship between auditory stimulation and slow waves was also explored. It is well known that external stimulation during NREM sleep can trigger a slow wave on electroencephalographic (EEG) recordings: such evoked slow waves, especially during stage N2, are also termed K-complexes.

Extensive electroencephalographic (EEG) sleep studies have demonstrated increases in rapid eye movement (REM) sleep and changes in non-rapid eye movement (NREM) sleep in depression. Preclinical evidence shows that REM sleep is generated in the brainstem. It also shows that NREM sleep is characterized by slower frequency, higher amplitude thalamocortical electrical oscillations. The alterations in NREM sleep in depressed patients may lead to impaired restoration of prefrontal cortex function during NREM sleep. Functional neuroimaging studies of sleep extend the preclinical understanding of the mechanisms of sleep/wake regulation by providing potential links between neural systems involved in emotional behavior and those involved in sleep. The notion of hyperarousal in paralimbic structures in depressed patients has received further support from an extensive literature describing the functional neuroanatomical correlates of the antidepressant response to sleep deprivation in depressed patients. Patients with schizophrenia are known to have severely disturbed subjective sleep.

This chapter discusses the organization of human sleep by the brain mechanisms and specific sleep disorders that lead to disturbances in the brain mechanisms. Non-rapid eye movement (NREM) sleep is controlled by brainstem oscillators whose activation leads to the multiple physiological accompaniments of the NREM state. The dream is the unusual mental content that often accompanies REM sleep. As humans transition from wakefulness to sleep, characteristic physiological changes include decreases in respiratory rate, heart rate, and blood pressure. The domain of the insomnias benefits from thoughtful differential diagnosis, as the causation may be both multiple and obscure. The insomnia complaints that are comorbid with medical disorders include both sleep disturbances caused by medical symptoms, and also those sleep disturbances caused by the pathophysiology underlying the medical condition. Restless leg syndrome (RLS) and periodic limb movements of sleep (PLMS) are considered as sleep disorders.

If the notions of dream and nightmare are centuries old, going back to ancient Egyptian and Jewish civilizations, the distinction between nightmares and parasomnias is recent. As parasomnias became distinguishable from nightmares, a possible link between such episodic nocturnal phenomena and seizure disorders was proposed. In 1999, Ohayon et al. in their epidemiological studies on sleepwalking and sleep terrors found that obstructive sleep apnea syndrome was the most common sleep disorder associated with parasomnias between the ages of 15 and 24 years. Epileptic disorders were shown to be rarely involved in abnormal behavior during non-rapid eye movement (NREM) sleep, but when sleep-related seizure disorders are present, specific seizure entities are implicated. Nocturnal polysomnography has allowed the dissociation of NREM from REM sleep abnormal behavior. The initial description of what is now known as REM sleep behavior disorder (RBD) came from Japanese researchers.

During Rhazes' time, research shows that mater puerorum have been used to describe both epileptic attacks and night terrors. In a case report published in 1953, Sullivan described night terrors as an indication of an emotional problem arising out of certain stages in a child's development. Classically, night terrors arise during the first sleep cycle, usually within 1-3 hours of sleep. Parents identified the following as precipitants: overtiredness, fever, separation, loss, moving, divorce, change of school, death in the family, return to school from vacation, or change of school. The prevalence of sleepwalking and night terrors in first-degree relatives was estimated as being ten times greater than in the general population. Treatment of night terrors can be divided into two categories: behavioral and medical strategies. Night terrors are fascinating entities that share many of the same characteristics of the other parasomnias occurring as arousals from non-rapid eye movement (NREM) sleep.

Arousal parasomnias occur mainly during non-rapid eye movement (NREM) sleep. This group consists of confusional arousals, sleepwalking and sleep terrors. Sleepwalking and sleep terrors can be triggered by stress, sleep deprivation, alcohol ingestion, and almost all sedative medications. This group of parasomnias is composed of three disorders occurring essentially during rapid eye movement (REM) sleep. Sleep paralysis is one of the main symptoms associated with narcolepsy, but it can also occur individually. REM sleep behavior disorder is characterized by a loss of generalized skeletal muscle REM-related atonia and the presence of physical dreamenactment. Polysomnographic recordings of individuals with RBD showed a reduction of the tonic phenomena of REM sleep and the activation of the phasic phenomena. Parasomnias are frequent in the general population; more than 30% of individuals experiences at least one type of parasomnia. At the genetic level, there is growing evidence that many parasomnias have a genetic component.