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.

Analysis of polysomnographic events surrounding 252 slow-wave sleep arousals in thirty-eight adults with injurious sleepwalking and sleep terrors

Abstract: A systematic study of electrophysiologic events [eight-channel EEG, electrocardiogram, electromyogram (EMGs)] surrounding 252 arousals from slow-wave sleep (SWS) in adults with sleepwalking (SW) and sleep terrors (ST) is reported. Hospital-based, overnight polysomnographic monitoring was conducted in 38 adults presenting to a sleep disorders center with injurious SW, ST (21 males, 17 females; mean age 29 years, range 17-69 years). Before nonbehavioral or behavioral arousals from SWS, neither EEG "delta wave buildup," nor heart rate (HR) acceleration, nor tonic/phasic EMG activation was identified. The postarousal EEG demonstrated three patterns: (a) diffuse, rhythmic, delta activity with a typical frequency of 2.2 Hz, a typical amplitude of 85 microV, and a typical duration of 20 s; (b) diffuse delta and theta activity intermixed with alpha and beta activity; and (c) prominent alpha and beta activity. Multichannel, high-voltage, delta activity was observed in <2% of all prearousal periods. HR acceleration emerged abruptly with SWS arousals, with significant changes in mean pre- versus postarousal HR (p < .001). Macrostructural sleep parameters ("sleep architecture") were intact. Therefore, our findings in adults with SW, ST strongly support the classification of SW/ST as disorders of (abrupt) arousal.

Nocturia: A Rarely Recognized Symptom of Sleep Apnea and Other Occult Sleep Disorders

Abstract: Background: Nocturia, awakening from sleep to urinate, is a common symptom in a variety of medical disorders and in the elderly. Awakening from sleep as a result of nocturia is thought to be secondary to a sensation of urinary urgency resulting from an overextended bladder. Nocturia-related awakenings cause significant sleep disruption and fatigue in elderly patients and are correlated with an increased number of falls at night. Sleep disorders such as sleep apnea are also common in the elderly and are frequently the source of awakenings from sleep. The high incidence of both nocturia and sleep disorders in the elderly and other groups of patients suggests that sleep disorders may be the source of some awakenings from sleep usually attributed by patients to nocturia. Nocturia secondary to sleep disorders would be causatively different from nocturia secondary to pressure to urinate in common medical disorders and would require different diagnostic procedures and treatment. Objective: To determine the frequency of nocturia as a symptom of primary sleep disorders. Methods: Eighty consecutive patients, 27 women and 53 men with a mean (±SD) age of 58.7±±14.1 years, undergoing polysomnography (sleep study or PSG) for the evaluation of a suspected sleep disorder and who met the sole criteria of awakening from sleep at least once and urinating voluntarily. Each patient had either a standard PSG recording or a PSG with administration of nasal continuous positive airway pressure. Immediately after each episode of nocturia during the PSG, patients were questioned about the reason they believed they had awakened. The PSG record immediately before awakening from sleep was then reviewed for potential causes of awakening. Patients were also asked on final morning awakening to fill in a questionnaire regarding their awakenings during the prior night. Patient reports were compared with the PSG to determine the accuracy of subjective reports. Results: Patients awakened from sleep and voluntarily urinated a mean (±SD) of 1.5±0.75 times per night for a total of 121 awakenings for the group. The majority (79.3%) of these awakenings from sleep were found to be directly secondary to sleep apnea, snoring, or periodic leg movements in sleep. Patients correctly identified the source of their awakening from sleep on only five (4.9%) occasions and only once was sleep apnea correctly cited by a patient as a source of awakening during the night. Conclusions: Most awakenings from sleep attributed by our patients to pressure to urinate were instead a result of sleep disorders, particularly sleep apnea. The fact that patients do urinate once awake likely contributed to faulty post hoc reasoning and might have limited further inquiry by patients and their physicians in clinical settings into the actual sources of awakening from sleep. Even in those patients with well-known medical reasons for nocturia, sleep disorders were still found to be the source of almost all awakenings from sleep. Patients were extremely poor judges of the reasons they awoke from sleep. The diagnosis of a sleep disorder should be seriously considered whenever a patient reports frequent awakenings from sleep to urinate. (Arch Intern Med. 1996;156:545-550)

Sleep and circadian rhythm dysregulation in schizophrenia.

Abstract: Sleep-onset and maintenance insomnia is a common symptom in schizophrenic patients regardless of either their medication status (drug-naive or previously treated) or the phase of the clinical course (acute or chronic). Regarding sleep architecture, the majority of studies indicate that non-rapid eye movement (NREM), N3 sleep and REM sleep onset latency are reduced in schizophrenia, whereas REM sleep duration tends to remain unchanged. Many of these sleep disturbances in schizophrenia appear to be caused by abnormalities of the circadian system as indicated by misalignments of the endogenous circadian cycle and the sleep-wake cycle. Circadian disruption, sleep onset insomnia and difficulties in maintaining sleep in schizophrenic patients could be partly related to a presumed hyperactivity of the dopaminergic system and dysfunction of the GABAergic system, both associated with core features of schizophrenia and with signaling in sleep and wake promoting brain regions. Since multiple neurotransmitter systems within the CNS can be implicated in sleep disturbances in schizophrenia, the characterization of the neurotransmitter systems involved remains a challenging dilemma.

Glycinergic and GABAA-Mediated Inhibition of Somatic Motoneurons Does Not Mediate Rapid Eye Movement Sleep Motor Atonia

Abstract: A hallmark of rapid eye movement (REM) sleep is a potent suppression of postural muscle tone. Motor control in REM sleep is unique because it is characterized by flurries of intermittent muscle twitches that punctuate muscle atonia. Because somatic motoneurons are bombarded by strychnine-sensitive IPSPs during REM sleep, it is assumed that glycinergic inhibition underlies REM atonia. However, it has never been determined whether glycinergic inhibition of motoneurons is indeed responsible for triggering the loss of postural muscle tone during REM sleep. Therefore, we used reverse microdialysis, electrophysiology, and pharmacological and histological methods to determine whether glycinergic and/or GABAA-mediated neurotransmission at the trigeminal motor pool mediates masseter muscle atonia during REM sleep in rats. By antagonizing glycine and GABAA receptors on trigeminal motoneurons, we unmasked a tonic glycinergic/GABAergic drive at the trigeminal motor pool during waking and non-rapid eye movement (NREM) sleep. Blockade of this drive potently increased masseter muscle tone during both waking and NREM sleep. This glycinergic/GABAergic drive was immediately switched-off and converted into a phasic glycinergic drive during REM sleep. Blockade of this phasic drive potently provoked muscle twitch activity in REM sleep; however, it did not prevent or reverse REM atonia. Muscle atonia in REM even persisted when glycine and GABAA receptors were simultaneously antagonized and trigeminal motoneurons were directly activated by glutamatergic excitation, indicating that a powerful, yet unidentified, inhibitory mechanism overrides motoneuron excitation during REM sleep. Our data refute the prevailing hypothesis that REM atonia is caused by glycinergic inhibition. The inhibitory mechanism mediating REM atonia therefore requires reevaluation.