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Fulltext Parasomnias during trans-meridian and long-distance travel: Critical literature review and clinical practice recommendations

Walsh SM, Forward CL, Flaherty GT

J Sleep Res, 2022 Dec;31(6):e13672.
PMID: 35726362 DOI: 10.1111/jsr.13672

Parasomnias are undesirable events that occur during sleep. They can be classified into rapid eye movement parasomnias and non-rapid eye movement parasomnias. Those who experience parasomnias may be anxious about travel for many reasons, including the occurrence of unwanted events during the trip, increased exposure to environmental trigger factors, and the propensity for harm to occur due to unfamiliar surroundings while travelling. There is a paucity of literature examining this area. This review summarizes the relevant literature and the clinical experience of the authors to compile clinical practice recommendations. The clinical features of parasomnias and how they relate to trans-meridian and long-distance travel are described. Triggers for non-rapid eye movement parasomnias, particularly the use of sedative hypnotic drugs, alcohol, drug withdrawal, sleep deprivation, emotional stress and environmental stimulations, are described. Management of parasomnias whilst travelling is reviewed, with a particular focus on trigger minimalization. The role for clonazepam and melatonin is outlined. At the pre-travel health consultation, the physician is strongly advised to screen the traveller for co-morbid sleep conditions, which exacerbate parasomnias. Areas for further research are explored, including the extent to which these sleep disorders impact on the travel experience.

Matched MeSH terms: Sleep, REM
Paradoxical sleep characteristics and cultural environment. Preliminary results

Petre-Quadens O, Hussain H, Balaratnan C

Acta Neurol Belg, 1975 Mar;75(2):85-92.
PMID: 168717

The Temiars are a tribe of negroid pygmies of basically Proto-Malaysian affinities. Field-work in the Malaysian jungle provided some observations on the sleep-wakefulness cycle of two young Temiar adults. This cycle was monophasic circumstances permitting. Their rest-activity cycle at night was similar in the jungle and in the laboratory. Polygraphic total night-sleep recordings were made with both of them in the EEG laboratory in the Hospital Besar in Kuala Lumpur. The eye-movement frequencies of PS were compared with those from young adults of the West. Although the differences were not statistically significant, the Rem-densities of the Temiars were constantly at the low side. The significance of the results are being discussed.

Matched MeSH terms: Sleep, REM*
Fulltext Nicotine-prevented learning and memory impairment in REM sleep-deprived rat is modulated by DREAM protein in the hippocampus

Abd Rashid N, Hapidin H, Abdullah H, Ismail Z, Long I

Brain Behav, 2017 06;7(6):e00704.
PMID: 28638710 DOI: 10.1002/brb3.704

INTRODUCTION: REM sleep deprivation is associated with impairment in learning and memory, and nicotine treatment has been shown to attenuate this effect. Recent studies have demonstrated the importance of DREAM protein in learning and memory processes. This study investigates the association of DREAM protein in REM sleep-deprived rats hippocampus upon nicotine treatment.
METHODS: Male Sprague Dawley rats were subjected to normal condition, REM sleep deprivation and control wide platform condition for 72 hr. During this procedure, saline or nicotine (1 mg/kg) was given subcutaneously twice a day. Then, Morris water maze (MWM) test was used to assess learning and memory performance of the rats. The rats were sacrificed and the brain was harvested for immunohistochemistry and Western blot analysis.
RESULTS: MWM test found that REM sleep deprivation significantly impaired learning and memory performance without defect in locomotor function associated with a significant increase in hippocampus DREAM protein expression in CA1, CA2, CA3, and DG regions and the mean relative level of DREAM protein compared to other experimental groups. Treatment with acute nicotine significantly prevented these effects and decreased expression of DREAM protein in all the hippocampus regions but only slightly reduce the mean relative level of DREAM protein.
CONCLUSION: This study suggests that changes in DREAM protein expression in CA1, CA2, CA3, and DG regions of rat's hippocampus and mean relative level of DREAM protein may involve in the mechanism of nicotine treatment-prevented REM sleep deprivation-induced learning and memory impairment in rats.

Matched MeSH terms: Sleep, REM/drug effects; Sleep, REM/physiology
REM sleep deprivation induces changes of down regulatory antagonist modulator (DREAM) expression in the ventrobasal thalamic nuclei of sprague-dawley rats

Siran R, Ahmad AH, Abdul Aziz CB, Ismail Z

J Physiol Biochem, 2014 Dec;70(4):877-89.
PMID: 25218926 DOI: 10.1007/s13105-014-0356-x

REM sleep is a crucial component of sleep. Animal studies indicate that rapid eye movement (REM) sleep deprivation elicits changes in gene expression. Down regulatory antagonist modulator (DREAM) is a protein which downregulates other gene transcriptions by binding to the downstream response element site. The aim of this study is to examine the effect of REM sleep deprivation on DREAM expression in ventrobasal thalamic nuclei (VB) of rats. Seventy-two male Sprague-Dawley rats were divided into four major groups consisting of free-moving control rats (FMC) (n = 18), 72-h REM sleep-deprived rats (REMsd) (n = 18), 72-h REM sleep-deprived rats with 72-h sleep recovery (RG) (n = 18), and tank control rats (TC) (n = 18). REM sleep deprivation was elicited using the inverted flower pot technique. DREAM expression was examined in VB by immunohistochemical, Western blot, and quantitative real-time polymerase chain reaction (qRT-PCR) studies. The DREAM-positive neuronal cells (DPN) were decreased bilaterally in the VB of rats deprived of REM sleep as well as after sleep recovery. The nuclear DREAM extractions were increased bilaterally in animals deprived of REM sleep. The DREAM messenger RNA (mRNA) levels were decreased after sleep recovery. The results demonstrated a link between DREAM expression and REM sleep deprivation as well as sleep recovery which may indicate potential involvement of DREAM in REM sleep-induced changes in gene expression, specifically in nociceptive processing.

Matched MeSH terms: Sleep, REM*
Lipid peroxidation in the descending thoracic aorta of rats deprived of REM sleep using the inverted flowerpot technique

Nawi A, Eu KL, Faris ANA, Wan Ahmad WAN, Noordin L

Exp Physiol, 2020 08;105(8):1223-1231.
PMID: 32539237 DOI: 10.1113/EP088667

NEW FINDINGS: What is the central question of this study? Deprivation of rapid eye movement (REM) sleep is associated with increased oxidative stress, but its effects on the blood vessels are poorly documented. We investigated whether REM sleep deprivation induces oxidative stress and causes lipid peroxidation in the aorta. What is the main finding and its important? We demonstrate that REM sleep deprivation induces oxidative stress and mediates lipid peroxidation in the aorta. This can cause endothelial changes and increased blood pressure. These findings will contribute to the growing body of literature on the mechanism underlying the effects of sleep deprivation on cardiovascular disease.
ABSTRACT: Oxidative stress-mediated lipid peroxidation is a known cause of endothelial injury or dysfunction. Deprivation of rapid eye movement (REM) sleep is associated with oxidative stress. To date, the pathogenesis of increased blood pressure after sleep deprivation remains poorly understood, particularly in the REM sleep phase. Our aim was to investigate the effects of REM sleep deprivation on blood vessels in the REM sleep-deprived rat model. Twenty-eight male Sprague-Dawley rats were divided into four equal groups: free-moving control rats, rats deprived of REM sleep for 72 h (REMsd), tank control rats and 72 h sleep-recovered rats after 72 h of REM sleep deprivation. The rats were deprived of REM sleep using the inverted flowerpot technique. Food consumption, body weight gain and systolic blood pressure were monitored. At the end of the experiment, the descending thoracic aorta was isolated for the measurement of oxidative stress markers. Despite a significant increase in food consumption in the REMsd group compared with the other groups, there was a significant reduction in body weight gain. Systolic blood pressure also showed a significant increase in the REMsd group compared with the other groups. Superoxide dismutase activity was significantly lower and malondialdehyde concentrations significantly higher in the REMsd group compared with the other groups. Increased levels of malondialdehyde are suggestive of lipid peroxidation in the blood vessels, and oxidative stress may be attributed to the initiation of the process. The changes after REM sleep deprivation revert during sleep recovery. In conclusion, the findings of the present study provide convincing evidence that REM sleep deprivation induced lipid peroxidation, leading to endothelial damage.

Matched MeSH terms: Sleep, REM