Non-rapid eye movement sleep

About: Non-rapid eye movement sleep is a research topic. Over the lifetime, 8661 publications have been published within this topic receiving 389465 citations. The topic is also known as: NREM.

The value of sleep deprivation as a diagnostic tool in adult sleepwalkers

Abstract: Objective: Adult somnambulism can result in injury to the sleeper and to others. Attempts to induce sleepwalking episodes in the sleep laboratory have yielded mixed results. 1,2 Having shown that sleepwalkers have lower slow-wave activity power than control subjects, 3 the authors hypothesized that an enhanced pressure of the homeostatic process underlying sleep regulation could affect the disorder’s characteristics even further. Therefore, the effects of 38 hours of sleep deprivation in adult sleepwalkers and control subjects were investigated. Methods: Ten adult somnambulistic patients and 10 sex- and age-matched control subjects were studied in the sleep laboratory. After a screening night, participants were monitored during 1) one night of baseline recording, and 2) one recovery night in which subjects slept ad libitum immediately after the sleep deprivation protocol. Behavioral manifestations were assessed for frequency and complexity using a 3-point scale of increasing complexity. Results: None of the control subjects had any behavioral manifestations on either of the two nights. Conversely, sleepwalkers showed a significant increase in the frequency and complexity of the somnambulistic episodes during the recovery night compared with baseline. Somnambulistic patients had a greater number of awakenings from slow-wave sleep than control subjects on both nights, but there was no significant increase during the recovery night. Conclusion: Sleep deprivation can be an effective tool for inducing somnambulistic episodes in the laboratory, thereby facilitating the diagnosis of sleepwalking.

Physiology of REM sleep, cataplexy, and sleep paralysis.

Abstract: The main neural structures generating muscle atonia and other phenomena characteristic of REM sleep are present in dorsolateral portions of the pons in the brainstem. Occurrence of REM sleep and the NREM-REM sleep cycle are probably determined by a balance or interaction between the cholinergic and cholinoceptive REM sleep-on neuronal populations and the monoaminergic REM sleep-off neuronal population. Neural activities producing generalized muscle atonia in REM sleep originate mainly in dorsolateral portions of the pontine reticular formation, descend through the medulla and spinal cord, and inhibit the motoneurons in the brainstem and spinal cord, bringing about postural atonia. Cataplexy and sleep paralysis are pathological, dissociated manifestations of the generalized muscle atonia characteristic REM sleep. Cataplexy is triggered by emotional stimuli, probably through activation of the neural structure generating the muscle atonia of REM sleep. During long-lasting cataplectic attacks, narcoleptic humans often experience sleep paralysis and vivid hypnagogic hallucinations in the latter sleep state. Sleep paralysis is caused by the marked dissociation between level of alertness and muscle atonia that often occurs in SOREM sleep episodes. Frequent SOREM sleep episodes in narcoleptic humans and dogs may occur when some of the neural mechanisms producing wakefulness and/or NREM sleep that normally inhibit the occurrence of REM sleep are abnormally weak, or when neural mechanisms facilitating the occurrence of REM sleep are hypersensitive or hyperactive, or both. Both abnormalities may contribute to the occurrence of SOREM sleep episodes and sleep paralysis, and also to the emotional triggering of cataplexy. Frequent occurrence of SOREM sleep episodes seems to be prerequisite but not sufficient for the occurrence of cataplexy. Some additional neural activities induced by emotion also contribute by inhibiting and/or activating the disturbed neural mechanisms related to SOREM sleep episodes. These abnormalities in neural mechanisms probably involve hypersensitivity or hyperactivity of muscarinic cholinergic and/or cholinoceptive neuronal populations in the pontine and suprapontine structures, and/or abnormally decreased activity of noradrenergic or serotonergic neuronal populations in the pons and/or other brainstem structures. This last monoaminergic neuronal population probably has a gating or inhibiting effect upon the cholinergic and cholinoceptive neuronal populations related to the generation of generalized muscle atonia and REM sleep. In spite of many studies and published reports on REM sleep, as well as on cataplexy and sleep paralysis, we are still far from a complete understanding of the physiological mechanisms producing muscle atonia in REM sleep and of the pathophysiological mechanisms of cataplexy and sleep paralysis--though it is apparent that these mechanisms are closely related.

Magnetic resonance findings in REM sleep behavior disorder

Abstract: Rapid eye movement (REM) sleep behavior disorder is characterized by bizarre acts during nocturnal sleep that may lead to physical injuries. Dream content suggests that motor overactivity is an attempted dream enactment and polygraphic studies reveal REM stage without atonia, an alteration of REM sleep generation that facilitates excessive motor activity. In 6 patients with REM sleep behavior disorder. MRI of the brain showed multifocal signal intensity lesions suggestive of lacunar infarcts in periventricular regions (5 patients) and in dorsal pontomesencephalic areas (3 patients). REM sleep behavior disorder may be the result of injury to the midrostral tegmentum nuclei, the tegmentoreticular tracts, or both. This condition is easily controlled with clonazepam.