Rapid eye movement sleep

About: Rapid eye movement sleep is a research topic. Over the lifetime, 3740 publications have been published within this topic receiving 183415 citations. The topic is also known as: REM sleep & REMS.

Dose--response effects of ethanol on the sleep of young women

Abstract: In healthy young women, rapid eye movement sleep decreased, slow-wave sleep increased, sleep-onset latency decreased and late-night disturbance of sleep increased with increasing doses of alcohol.

REM Sleep Behavior Disorder: Diagnosis, Clinical Implications, and Future Directions.

Abstract: Rapid eye movement sleep behavior disorder (RBD) is diagnosed by a clinical history of dream enactment accompanied by polysomnographic rapid eye movement sleep atonia loss (rapid eye movement sleep without atonia). Rapid eye movement sleep behavior disorder is strongly associated with neurodegenerative disease, especially synucleinopathies such as Parkinson disease, dementia with Lewy bodies, and multiple system atrophy. A history of RBD may begin several years to decades before onset of any clear daytime symptoms of motor, cognitive, or autonomic impairments, suggesting that RBD is the presenting manifestation of a neurodegenerative process. Evidence that RBD is a synlucleinopathy includes the frequent presence of subtle prodromal neurodegenerative abnormalities including hyposmia, constipation, and orthostatic hypotension, as well as abnormalities on various neuroimaging, neurophysiological, and autonomic tests. Up to 90.9% of patients with idiopathic RBD ultimately develop a defined neurodegenerative disease over longitudinal follow-up, although the prognosis for younger patients and antidepressant-associated RBD is less clear. Patients with RBD should be treated with either melatonin 3 to 12 mg or clonazepam 0.5 to 2.0 mg to reduce injury potential. Prospective outcome and treatment studies of RBD are necessary to enable accurate prognosis and better evidence for symptomatic therapy and future neuroprotective strategies.

Ketogenic Diet Improves Sleep Quality in Children with Therapy-resistant Epilepsy.

Abstract: Summary: Purpose: The study purpose was to evaluate sleep structure during ketogenic diet (KD) treatment in children with therapy-resistant epilepsy and to correlate possible alterations with changes in clinical effects on seizure reduction, seizure severity, quality of life (QOL), and behavior. Methods: Eighteen children were examined with ambulatory polysomnographic recordings initially and after 3 months of KD treatment. Eleven children continued with the KD and were also evaluated after 12 months. Sleep parameters were estimated. Seizure frequency was recorded in a diary and seizure severity in the National Health Seizure Severity Scale (NHS3). QOL was assessed with a visual analogue scale. Child behavior checklist and Ponsford and Kinsella's rating scale of attentional behavior were used. Results: KD induced a significant decrease in total sleep (p = 0.05) and total night sleep (p = 0.006). Slow wave sleep was preserved, rapid eye movement (REM) sleep increased (p = 0.01), sleep stage 2 decreased (p = 0.004), and sleep stage 1 was unchanged. Eleven children continued with the KD and were also evaluated after 12 months. They showed a significant decrease in daytime sleep (p = 0.01) and a further increase in REM sleep (p = 0.06). Seizure frequency (p = 0.001, p = 0.003), seizure severity (p < 0.001, p = 0.005) and QOL (p < 0.001, p = 0.005) were significantly improved at 3 and 12 months. Attentional behavior was also improved, significantly so at 3 months (p = 0.003). There was a significant correlation between increased REM sleep and improvement in QOL (Spearman r = 0.6, p = 0.01) at 3 months. Conclusion: KD decreases sleep and improves sleep quality in children with therapy-resistant epilepsy. The improvement in sleep quality, with increased REM sleep, seems to contribute to the improvement in QOL. (Less)

Altered sleep physiology in chronic alcoholics: reversal with abstinence.

Abstract: Somnograms obtained from recently abstinent chronic alcoholics reveal gross disruption succinctly described as "fractured" sleep. Sleep onset is delayed and the rhythmic properties of the sleep pattern are markedly disturbed with numerous brief arousals and changes of sleep stage. Excessive stage 1 and stage rapid eye movement sleep are present while the high voltage slow wave sleep is markedly reduced or absent. With continued sobriety (9 mo or more) the sleep stage percentages tend to return to normal levels, but the disruption of the sleep pattern persists after as much as 21 mo of abstinence.