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.

Sleep Slow-Wave Activity Regulates Cerebral Glycolytic Metabolism

Abstract: Non-rapid eye movement sleep (NREMS) onset is characterized by a reduction in cerebral metabolism and an increase in slow waves, 1–4-Hz oscillations between relatively depolarized and hyperpolarized states in the cerebral cortex. The metabolic consequences of slow-wave activity (SWA) at the cellular level remain uncertain. We sought to determine whether SWA modulates the rate of glycolysis within the cerebral cortex. The real-time measurement of lactate concentration in the mouse cerebral cortex demonstrates that it increases during enforced wakefulness. In spontaneous sleep/wake cycles, lactate concentration builds during wakefulness and rapid eye movement sleep and declines during NREMS. The rate at which lactate concentration declines during NREMS is proportional to the magnitude of electroencephalographic (EEG) activity at frequencies of <10 Hz. The induction of 1-Hz oscillations, but not 10-Hz oscillations, in the electroencephalogram by optogenetic stimulation of cortical pyramidal cells during wakefulness triggers a decline in lactate concentration. We conclude that cerebral SWA promotes a decline in the rate of glycolysis in the cerebral cortex. These results demonstrate a cellular energetic function for sleep SWA, which may contribute to its restorative effects on brain function.

Positron emission tomography studies of sleep and sleep disorders

Abstract: Using positron emission tomography (PET) it is possible to perform an in vivo study of cerebral physiological and biochemical processes in man. Employing this technique in sleep studies, decreased cerebral metabolic rates for glucose during slow wave sleep compared with those seen during wakefulness were first demonstrated, whereas similar rates of cerebral glucose metabolism were observed during paradoxical sleep and wakefulness. More recently, regional modifications of cerebral blood flow during sleep have also been demonstrated. During slow wave sleep, cerebral blood flow is decreased particularly in the prefrontal cortex. Rapid eye movement sleep is characterized by activation of the pons, thalami, amygdaloid complexes and a number of cortical areas (e.g. the anterior cingulate cortex). Although data remain incomplete, a variety of sleep disorders, including narcolepsy, fatal familial insomnia and continuous spike-and-wave discharges during slow sleep have been investigated. These results are briefly reviewed.

Study of image findings in rapid eye movement sleep behavioural disorder.

Abstract: To elucidate the cause of idiopathic rapid eye movement (REM) sleep behavior disorder (RBD), magnetic resonance imaging and single-photon emission computed tomography of the brain were conducted on 20 patients with RBD. Blood flow in the upper portion of both sides of the frontal lobe and pons was significantly lower in patients with RBD than in the normal elderly group. Among the patients with RBD, decreased blood flow in the frontal lobe showed no correlation with the extent of frontal lobe atrophy. Decreased blood flow in the upper portion of the frontal lobe and pons might be associated with the pathogenesis of idiopathic RBD.

REM sleep behavioral disorders.

Abstract: REM sleep behaviors were recently described as wild, dream-enacting behaviors during REM sleep with loss of usual atonia on submental muscles. We examined 6 patients (5 M, 1F) with characteristic episodes of behavioral manifestations during REM sleep. Polysomnographic data indicate a decrease in first REM latency, an absence of stage 4 NREM, altered phasic motor activity and behavioral episodes during REM sleep even with normal chin muscle atonia. Three patients had Shy-Drager syndrome, 1 olivopontocerebellar atrophy and 2 patients had no neurological disease. The crucial importance of a disinhibited locomotor system during sleep appears to be responsible for this REM parasomnia.