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.

Cognitive Behavioral Therapy for Insomnia Improves Sleep and Decreases Pain in Older Adults with Co-Morbid Insomnia and Osteoarthritis

Abstract: Osteoarthritis is a common cause of pain and disability among older adults, affecting 20 million Americans. The prevalence of osteoarthritis is rapidly increasing with the accelerating growth of the older portion of the US population.1 Osteoarthritis is characterized by joint degeneration, pain, and dysfunction, with 80% of patients with osteoarthritis experiencing limitations of movement.1 Osteoarthritis demonstrates a broad spectrum of symptom severity, ranging from intermittent aching and joint stiffness to loss of motion and severe chronic pain.2 Severity and disability tend to increase with age, although severity can fluctuate markedly over short periods of time. Sleep quality is a major concern among persons with osteoarthritis, with 60% of people with osteoarthritis reporting pain during the night.3 In fact, pain secondary to arthritis is the most common factor predicting sleep disturbance in the population at large.4 It is well established that pain interferes with sleep5 and, more recently, that disturbed sleep lowers the pain threshold.6–8 Whether sleep disturbance precedes or follows pain onset is unclear, but reciprocal effects are likely.5 Patients with osteoarthritis who report having pain and stiffness in the morning have more sleep-related muscle spasms and objectively assessed sleep disturbance.9 Even after treatment with anti-inflammatory medications, patients with osteoarthritis show significantly greater objective sleep disturbance, as compared with age-matched control subjects.10 Chronic sleep disturbance, so common among older patients with osteoarthritis, is itself associated with impaired daytime function, daytime sleepiness and fatigue, reduced quality of life, and increased health care utilization.11–12 Given the likely reciprocal effects between pain and sleep disturbance, teasing apart unique causal pathways is difficult. Chronic pain initiates and exacerbates sleep disturbance; disturbed sleep in turn maintains and exacerbates chronic pain and related dysfunction.5,13–14 Sleep disruption, fragmentation, or restriction produces hyperalgesia6–8 and can interfere with analgesic treatments involving opioidergic and serotonergic mechanisms of action.13 The basis for this reciprocal relationship may be the modulation of pain during sleep and waking by reciprocally active neurons in the raphe magnus of the brainstem, providing a potential neural substrate for the reciprocal relationship of chronic pain and sleep disruption.14 Given this reciprocal relationship between sleep and pain, a question with major clinical implications is whether an intervention that improves sleep, per se, in individuals with disturbed sleep and a co-morbid pain state, such as osteoarthritis, might reduce pain as well. A recent randomized controlled trial of cognitive behavioral therapy for insomnia (CBT-I) versus an attention control in a group of older adults with co-morbid illnesses—osteoarthritis, coronary artery disease, or chronic obstructive pulmonary disease—reported clinically significant improvements in sleep quality.15 Although CBT-I has been shown to achieve high levels of efficacy when treating insomnia in otherwise healthy populations,16 prior to the study of Rybarczyk et al.,15 CBT-I was not tested in a well-controlled study of individuals with insomnia and co-morbid chronic medical illnesses. Until recently, the assumption has been that such insomnias usually had medical causes and that the best approach to correcting the insomnia was to treat the medical condition.17 Rybarczyk and colleagues' CBT-I treatment protocol did not specifically address pain management. However, the study investigated the hypothesis that improvements in sleep would result in improvements in daytime functioning, so a broad array of measures were included in their analyses. The CBT-I–treated group showed no reductions in pain report on the McGill Pain Questionnaire (MPQ) across the 3 co-morbid medical illnesses, or for the osteoarthritis group alone, relative to an attention-control group.15 However, Rybarczyk and colleagues analyzed neither a second available pain measure (ie, SF-36 pain subscale) nor the within-group effects. Given the possibility that the attention-control group might have received some pain benefits, examining within-group effects is an important analytic consideration. To better explore the potential impact of improved sleep on osteoarthritis pain, we reanalyzed the Rybarczyk et al. data, using within-group analyses to examine both available measures of pain, as well as previously unavailable 1-year follow-up sleep and pain data, for osteoarthritis participants only. We also examined effects among participants who crossed over from the control group to the CBT-I treatment.

Rapid Eye Movement Sleep Behavior Disorder: A Treatable Parasomnia Affecting Older Adults

Abstract: Rapid eye movement (REM) sleep behavior disorder (RBD) is a parasomnia defined by intermittent loss of electromyographic atonia during REM sleep with emergence of complex and vigorous behaviors. Punching, kicking, and leaping from bed during attempted dream enactment caused repeated injury in nine of our first ten adult patients. Mean age at onset was 62 years; nine of the patients were male. All patients underwent standard polysomnographic studies with videotaping of behaviors and extensive neurologic and psychiatric evaluations. The RBD was unrelated to psychopathologic conditions but in five cases was closely linked with major neuropathologic disorders: dementia (two), olivopontocerebellar degeneration, subarachnoid hemorrhage, and the Guillain-Barre syndrome. Other common polysomnographic abnormalities were high REM density, increased stage 3/4 (slow-wave) sleep, and both periodic and aperiodic limb twitching in non-REM sleep. Eight patients had dream changes involving motor overactivity and violent confrontations of dream characters. Clonazepam induced rapid and sustained improvement of dream and sleep behavior problems in seven patients, as did desipramine hydrochloride in one patient. ( JAMA 1987;257:1786-1789)

Changes in Mood, Craving, and Sleep During Short-term Abstinence Reported by Male Cocaine Addicts: A Controlled, Residential Study

Abstract: • We examined changes over 28 days in mood states, craving for cocaine, and sleep during short-term abstinence reported by 12 male, predominantly intravenous-using, cocaine-addicted subjects residing in a research facility. For comparison, we examined 10 nonaddicted control subjects. There were no significant differences between cocaine addicts and controls regarding demographics and selected DSM-III-R diagnoses other than psychoactive substance use disorder and antisocial personality disorder. There were significantly higher scores of psychiatric symptoms reported by cocaine addicts 1 week before admission. Mood-distress and depression scores recorded at admission and during short-term abstinence were significantly greater than those reported by controls. Addicts' mood-distress scores and craving for cocaine were greatest at admission and decreased gradually and steadily during the 28-day study. There were no significant differences between groups regarding reports of sleep other than difficulty falling asleep and clearheadedness on arising. Although there were significant differences in resting heart rate at admission and over time, there were no significant differences in weight gain or blood pressure. Given the absence of a classic "withdrawal" pattern, "short-term abstinence" may be a more appropriate classification of psychological and physical phenomena experienced by cocaine addicts who initiate abstinence in a controlled environment.

Inflammatory markers and sleep disturbance in major depression.

Abstract: OBJECTIVE: This study was conducted to determine whether immune activation occurs in major depression, and to evaluate the associations between disordered sleep and markers of inflammation in patients with major depressive disorder. METHODS: All-night polysomnography was obtained in patients with acute Diagnostic and Statistical Manual of Mental Disorders, 4th edition major depressive disorder (n = 22) and age-, gender-, and body weight-matched comparison controls (n = 18). After the onset of sleep, nocturnal serum levels of interleukin-6 (IL-6), soluble intercellular adhesion molecule (sICAM), monocyte chemotactic protein (MCP-1), and IL-6 soluble receptor (IL-6sR) were sampled. RESULTS: As compared with matched controls, depressed patients showed significant (p or = 0.30). Backward regression analyses indicated that sleep latency (beta = 0.34, p <.05) and REM density (beta = 0.27, p = .09) were better predictors of IL-6 than depressive status. Similarly, sleep latency (beta = 0.27, p = .06) and REM density (beta = 0.32, p = .02) were also better predictors of sICAM. CONCLUSION: These findings support the hypothesis that sleep disturbance is associated with elevated levels of the inflammatory markers IL-6 and sICAM. This relationship was not accounted for by other confounding factors such as age and body weight. These findings suggest that the elevations in inflammatory markers found in depressive subjects may be partially the result of disturbances of sleep initiation found in this population.