Sleep disorder

About: Sleep disorder is a research topic. Over the lifetime, 19380 publications have been published within this topic receiving 884281 citations. The topic is also known as: somnipathy & non-organic sleep disorder.

Physical exercise as non-pharmacological treatment of chronic pain: Why and when.

Abstract: Chronic pain broadly encompasses both objectively defined conditions and idiopathic conditions that lack physical findings. Despite variance in origin or pathogenesis, these conditions are similarly characterized by chronic pain, poor physical function, mobility limitations, depression, anxiety, and sleep disturbance, and they are treated alone or in combination by pharmacologic and non-pharmacologic approaches, such as physical activity (aerobic conditioning, muscle strengthening, flexibility training, and movement therapies). Physical activity improves general health, disease risk, and progression of chronic illnesses such as cardiovascular disease, type 2 diabetes, and obesity. When applied to chronic pain conditions within appropriate parameters (frequency, duration, and intensity), physical activity significantly improves pain and related symptoms. For chronic pain, strict guidelines for physical activity are lacking, but frequent movement is preferable to sedentary behavior. This gives considerable freedom in prescribing physical activity treatments, which are most successful when tailored individually, progressed slowly, and account for physical limitations, psychosocial needs, and available resources.

Effects of sleep and sleep deprivation on catecholamine and interleukin-2 levels in humans: clinical implications.

Abstract: The objective of this study was to evaluate the effects of nocturnal sleep, partial night sleep deprivation, and sleep stages on catecholamine and interleukin-2 (IL-2) levels in humans. Circulating levels of catecholamines and IL-2 were sampled every 30 min during 2 nights: undisturbed, baseline sleep and partial sleep deprivation-late night (PSD-L; awake from 0300-0600 h) in 17 healthy male volunteers. Sleep was monitored somnopolygraphically. Sleep onset was associated with a significant (P < 0.05) decline of circulating concentrations of norepinephrine and epinephrine, with a nocturnal nadir that occurred 1 h after nocturnal sleep. On the PSD-L night, levels of norepinephrine and epinephrine significantly (P < 0.05) increased in association with nocturnal awakening. During stage 3-4 sleep, levels of norepinephrine, but not epinephrine, were significantly lower (P < 0.05) compared to average levels during the awake period, stages 1-2 sleep, and rapid eye movement sleep. Nocturnal levels of circulating IL-2 did not change with sleep onset or in relation to PSD-L or the various sleep stages. We conclude that sleep onset is associated with changes in levels of circulating catecholamines. Loss of sleep and disordered sleep with decreases in slow wave sleep may serve to elevate nocturnal catecholamine levels and contribute to cardiovascular disease.