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.

REM Sleep Behavior Disorder in Parkinson’s Disease and Dementia with Lewy Bodies:

Abstract: Rapid eye movement (REM) sleep behavior disorder (RBD) is a parasomnia manifested by vivid, often frightening dreams associated with simple or complex motor behavior during REM sleep. Patients appe...

Sleep and breathing in Prader-Willi syndrome.

Abstract: Prader-Willi syndrome (PWS) is a genetic disorder, with hypotonia being the predominant feature in infancy, and developmental delay, obesity, and behavioral problems becoming more prominent in childhood and adolescence. Children with this disorder frequently suffer from excessive daytime sleepiness and have a primary abnormality of the circadian rhythm of rapid eye movement sleep. They also have primary abnormal ventilatory responses to hypoxia and hypercapnia, and these abnormalities may be exacerbated by obesity. Children with PWS are at risk of a variety of abnormalities of breathing during sleep, including obstructive sleep apnea and sleep-related alveolar hypoventilation. Clinical evaluation should include a careful history of sleep-related symptoms and assessment of the upper airway and lung function. Polysomnography should be considered for those with symptoms suggestive of sleep-disordered breathing. Treatment options depend on the underlying problem, but may include behavioral interventions, weight control, adenotonsillectomy, and nocturnal ventilation.

The case against memory consolidation in REM sleep.

Abstract: We present evidence disputing the hypothesis that memories are processed or consolidated in REM sleep. A review of REM deprivation (REMD) studies in animals shows these reports to be about equally divided in showing that REMD does, or does not, disrupt learning/memory. The studies supporting a relationship between REM sleep and memory have been strongly criticized for the confounding effects of very stressful REM deprivation techniques. The three major classes of antidepressant drugs, monoamine oxidase inhibitors (MAOIs), tricyclic antidepressants (TCAs), and selective serotonin reuptake inhibitors (SSRIs), profoundly suppress REM sleep. The MAOIs virtually abolish REM sleep, and the TCAs and SSRIs have been shown to produce immediate (40-85%) and sustained (30-50%) reductions in REM sleep. Despite marked suppression of REM sleep, these classes of antidepressants on the whole do not disrupt learning/memory. There have been a few reports of patients who have survived bilateral lesions of the pons with few lingering complications. Although these lesions essentially abolished REM sleep, the patients reportedly led normal lives. Recent functional imaging studies in humans have revealed patterns of brain activity in REM sleep that are consistent with dream processes but not with memory consolidation. We propose that the primary function of REM sleep is to provide periodic endogenous stimulation to the brain which serves to maintain requisite levels of central nervous system (CNS) activity throughout sleep. REM is the mechanism used by the brain to promote recovery from sleep. We believe that the cumulative evidence indicates that REM sleep serves no role in the processing or consolidation of memory.

Rapid Eye Movement Sleep Behavior Disorder and Neurodegenerative Disease

Abstract: Importance The dream enactment of rapid eye movement sleep behavior disorder (RBD) is often the first indication of an impending α-synuclein disorder, such as Parkinson disease, multiple-system atrophy, or dementia with Lewy bodies. Objective To provide an overview of RBD from the onset of dream enactment through the emergence of a parkinsonian disorder. Evidence Review Peer-reviewed articles, including case reports, case series, retrospective reviews, prospective randomized trials, and basic science investigations, were identified in a PubMed search of articles on RBD from January 1, 1986, through July 31, 2014. Findings Under normal conditions, vivid dream mentation combined with skeletal muscle paralysis characterizes rapid eye movement sleep. In RBD, α-synuclein abnormalities in the brainstem disinhibit rapid eye movement sleep motor activity, leading to dream enactment. The behaviors of RBD are often theatrical, with complexity, aggression, and violence; fighting and fleeing actions can be injurious to patients as well as bed partners. Rapid eye movement sleep behavior disorder is distinguished from other parasomnias by clinical features and the demonstration of rapid eye movement sleep without atonia on polysomnography. Consistent with early neurodegeneration, patients with RBD demonstrate subtle motor, cognitive, and autonomic impairments. Approximately 50% of patients with spontaneous RBD will convert to a parkinsonian disorder within a decade. Ultimately, nearly all (81%-90%) patients with RBD develop a neurodegenerative disorder. Among patients with Parkinson disease, RBD predicts a non–tremor-predominant subtype, gait freezing, and an aggressive clinical course. The most commonly cited RBD treatments include low-dose clonazepam or high-dose melatonin taken orally at bedtime. Conclusions and Relevance Treatment of RBD can prevent injury to patients and bed partners. Because RBD is a prodromal syndrome of Parkinson disease (or related disorder), it represents a unique opportunity for developing and testing disease-modifying therapies.

The Atonia and Myoclonia of Active (REM) Sleep

Abstract: Postsynaptic inhibition is a principal process responsible not only for the atonia of the somatic musculature during active sleep but also for the phasic episodes of decreased motoneuron excitability that accompany bursts of REMs during this state. These postsynaptic processes are dependent upon the presence of active sleep-specific IPSPs, which are apparently mediated by glycine. The phasic excitation of motoneurons during REM periods is due to excitatory postsynaptic potentials that, when present, encounter a motoneuron already subjected to enhanced postsynaptic inhibition. These EPSPs are mediated by a non-NMDA neurotransmitter. Thus, from the perspective of motoneurons, active sleep can be characterized as a state abundant in the availability of strikingly potent patterns of postsynaptic inhibition and, during REM periods, not only by enhanced postsynaptic excitation, but also by enhanced postsynaptic inhibition. The site of origin of these inhibitory and excitatory drives is, at present, less clearly defined. There is a consensus that the structure(s) from which the inhibitory drives emanate are located in the lower brainstem, with a cholinoceptive trigger zone situated in the dorsolateral pontine tegmentum in or in the vicinity of the nucleus pontis oralis. We have suggested that from this cholinoceptive trigger zone there emanates an excitatory drive that directly, or through interneurons, excites a medullary are in or in the vicinity of the nucleus reticularis gigantocellularis. Thus, a cascade of cholinoceptively activated excitatory activity proceeds to eventually activate inhibitory interneurons whose activation results in motoneuron inhibition and muscle atonia during active sleep. Resolution of the precise location and mechanisms of interaction of the supraspinal inhibitory and excitatory motoneuron control mechanism constitutes a major goal of future experiments and the next major challenge for researchers in this field.