Topic
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.
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29 May 2015
TL;DR: It is suggested that optimizing sleep quality following trauma, and even strategically timing sleep to strengthen extinction memories therapeutically instantiated during exposure therapy, may allow sleep itself to be recruited in the treatment of PTSD and other trauma and stress-related disorders.
Abstract: Post-traumatic stress disorder (PTSD) is accompanied by disturbed sleep and an impaired ability to learn and remember extinction of conditioned fear. Following a traumatic event, the full spectrum of PTSD symptoms typically requires several months to develop. During this time, sleep disturbances such as insomnia, nightmares, and fragmented rapid eye movement sleep predict later development of PTSD symptoms. Only a minority of individuals exposed to trauma go on to develop PTSD. We hypothesize that sleep disturbance resulting from an acute trauma, or predating the traumatic experience, may contribute to the etiology of PTSD. Because symptoms can worsen over time, we suggest that continued sleep disturbances can also maintain and exacerbate PTSD. Sleep disturbance may result in failure of extinction memory to persist and generalize, and we suggest that this constitutes one, non-exclusive mechanism by which poor sleep contributes to the development and perpetuation of PTSD. Also reviewed are neuroendocrine systems that show abnormalities in PTSD, and in which stress responses and sleep disturbance potentially produce synergistic effects that interfere with extinction learning and memory. Preliminary evidence that insomnia alone can disrupt sleep-dependent emotional processes including consolidation of extinction memory is also discussed. We suggest that optimizing sleep quality following trauma, and even strategically timing sleep to strengthen extinction memories therapeutically instantiated during exposure therapy, may allow sleep itself to be recruited in the treatment of PTSD and other trauma and stress-related disorders.
158 citations
TL;DR: Cholinergic regulation of sleep and wakefulness was studied in freely moving rats locally infused with various doses of carbachol into the pontine reticular formation, indicating that REM sleep induction resulted from the stimulation of pontine muscarinic receptors.
Abstract: Cholinergic regulation of sleep and wakefulness was studied in freely moving rats locally infused with various doses of carbachol into the pontine reticular formation. Induction of REM sleep occurred when carbachol was infused specifically into the posterior oral pontine reticular nucleus (PnO). This effect was observed with 1-10 ng of carbachol, and lasted for at least 6 h. It was antagonized by atropine (100-200 ng) infused into the same site 15 min before carbachol (10 ng), indicating that REM sleep induction resulted from the stimulation of pontine muscarinic receptors. High doses of carbachol (500 ng) did not affect REM sleep but enhanced wakefulness. Cholinergic mechanisms within the PnO may play a critical role in the regulation of REM sleep in the rat.
157 citations
TL;DR: When compared to a group of normal ovulating women, however, REM sleep time decreased during the last two months of pregnancy and, although there was no change in sleep onset latency, the time spent awake during the first six hours of sleep was increased.
Abstract: We conducted a longitudinal polysomnographic study in five healthy primiparous subjects, whose sleep was first recorded between 8 and 16 weeks of gestation, then every 2 months until parturition and at 1 month postpartum. The first 6 hours of sleep were used for statistical analysis. In contrast to previous studies, we found no reduction in stage 4 sleep with pregnancy. Slow-wave sleep (comprising stages 3 and 4), was significantly higher at 27-39 weeks of gestation than at 8-16 weeks, as predicted by the restorative theory of sleep. There was no significant difference in rapid eye movement (REM) sleep time. When compared to a group of normal ovulating women, however, REM sleep time decreased during the last two months of pregnancy and, although there was no change in sleep onset latency, the time spent awake during the first six hours of sleep was increased. Future research into the effects of cortisol and progesterone is indicated.
157 citations
TL;DR: Three patients with REM behavior disorder whose nocturnal symptoms were markedly improved by treatment with the acetylcholinesterase inhibitor donepezil are reported.
Abstract: Three patients with REM behavior disorder whose nocturnal symptoms were markedly improved by treatment with the acetylcholinesterase inhibitor donepezil are reported. Donepezil may have a role in the treatment of REM behavior disorder, possibly through its actions on cholinergic pathways in the brainstem.
155 citations
TL;DR: Three patients are presented here whose RBD preceded the onset of PD by several years, and both the symptoms of PD and RBD improved with levodopa treatment, and it remains to be seen whetherlevodopa can be an alternative to clonazepam in idiopathic RBD without PD.
Abstract: Rapid eye movement (REM) sleep behavior disorder (RBD) involves complex behavior and a loss of muscle atonia occurring during REM sleep. Half of these patients with RBD have an underlying neurologic disorder including dementia, olivopontocerebellar atrophy, subarachnoid hemorrhage, and cerebrovascular disease. Clonazepam is the drug of choice for RBD. RBD has been rarely reported to precede the onset of Parkinson's disease (PD). Three patients are presented here whose RBD preceded the onset of PD by several years, and both the symptoms of PD and RBD improved with levodopa treatment. It is postulated that levodopa ameliorates RBD by suppressing REM sleep, and it remains to be seen whether levodopa can be an alternative to clonazepam in idiopathic RBD without PD.
155 citations