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.

The economic cost of sleep disorders.

Abstract: STUDY OBJECTIVES: To determine the economic cost of sleep disorders in Australia and relate these to likely costs in similar economies. DESIGN AND SETTING: Analysis of direct and indirect costs for 2004 of sleep disorders and the fractions of other health impacts attributable to sleep disorders, using data derived from national databases (including the Australian Institute of Health and Welfare and the Australian Bureau of Statistics). MEASUREMENTS: Direct health costs of sleep disorders (principally, obstructive sleep apnea, insomnia, and periodic limb movement disorder) and of associated conditions; indirect financial costs of associated work-related accidents, motor vehicle accidents, and other productivity losses; and nonfinancial costs of burden of disease. These were expressed in US dollars (dollar). RESULTS: The overall cost of sleep disorders in Australia in 2004 (population: 20.1 million) was dollar 7494 million. This comprised direct health costs of dollar 146 million for sleep disorders and dollar 313 million for associated conditions, dollar 1956 million for work-related injuries associated with sleep disorders (net of health costs), dollar 808 million for private motor vehicle accidents (net of health costs), dollar 1201 million for other productivity losses, dollar 100 million for the real costs associated with raising alternative taxation revenue, and dollar 2970 million for the net cost of suffering. CONCLUSIONS: The direct and indirect costs of sleep disorders are high. The total financial costs (independent of the cost of suffering) of dollar 4524 million represents 0.8% of Australian gross domestic product. The cost of suffering of dollar 2970 million is 1.4% of the total burden of disease in Australia.

Daytime sleepiness and hyperactivity in children with suspected sleep-disordered breathing.

Abstract: Objectives. Excessive daytime sleepiness (EDS) is seen less frequently as a presenting complaint in children with sleep-disordered breathing than in adults. Instead, symptoms of hyperactivity are often described. We hypothesized that children with suspected sleep-disordered breathing (S-SDB) were both sleepier and more hyperactive than control subjects. Furthermore, we hypothesized that overnight polysomnographic parameters correlated with sleepiness and hyperactivity. Methods. A cross-sectional study was conducted at a university-affiliated hospital and a community-based pediatric clinic. A total of 108 patients with S-SDB (mean [standard deviation] age: 7 ± 4 years) and 72 control subjects (8 ± 4 years) were recruited. A modified Epworth Sleepiness Scale (ESS) and the Conners Abbreviated Symptom Questionnaire were administered. Polysomnography was performed in patients with S-SDB. Results. Patients with S-SDB had a higher ESS (8.1 ± 4.9 vs 5.3 ± 3.9) and a higher Conners score (12.8 ± 7.6 vs 9.0 ± 6.2) than control subjects. On the basis of adult criteria, 28% of patients had EDS. There was no difference in the ESS and Conners scores of patients with primary snoring and patients with obstructive sleep apnea. The ESS had weak correlations with polysomnographic parameters. Conclusions. Although the ESS score of children with S-SDB was within the normal range for adults, these children were sleepier and more hyperactive than control subjects. However, these data should be confirmed by a population-based study.

Antidepressants and sleep: a qualitative review of the literature.

Abstract: Most antidepressants change sleep; in particular, they alter the physiological patterns of sleep stages recorded overnight with EEG and other physiological measures. These effects are greatest and most consistent on rapid eye movement (REM) sleep, and tend to be in the opposite direction to the sleep abnormalities found in major depression, but are usually of greater degree. Reductions in the amount of REM sleep and increases in REM sleep onset latency are seen after taking antidepressants, both in healthy volunteers and in depressed patients. Antidepressants that increase serotonin function by blocking reuptake or by inhibiting metabolism have the greatest effect on REM sleep. The decrease in amount of REM sleep appears to be greatest early in treatment, and gradually diminishes during long-term treatment, except after monoamine oxidase inhibitors when REM sleep is often absent for many months. Sleep initiation and maintenance are also affected by antidepressants, but the effects are much less consistent between drugs. Some antidepressants such as clomipramine and the selective serotonin receptor inhibitors (SSRIs), particularly fluoxetine, are sleep-disturbing early in treatment and some others such as amitriptyline and the newer serotonin 5-HT2-receptor antagonists are sleep promoting. However, these effects are fairly short-lived and there are very few significant differences between drugs after a few weeks of treatment. In general, the objectively measured sleep of depressed patients improves during 3-4 weeks of effective antidepressant treatment with most agents, as does their subjective impression of their sleep. Sleep improvement earlier in treatment may be an important clinical goal in some patients, perhaps when insomnia is particularly distressing, or to ensure compliance. In these patients, the choice of a safely used and effective antidepressant which improves sleep in short term is indicated. Patients with other sleep disorders such as restless legs syndrome and REM sleep behaviour disorder should be identified before choosing a treatment, as some antidepressants worsen these conditions. Conversely, there is evidence that some antidepressants may be useful in the treatment of sleep disorders such as night terrors.

Glymphatic failure as a final common pathway to dementia.

Abstract: Sleep is evolutionarily conserved across all species, and impaired sleep is a common trait of the diseased brain. Sleep quality decreases as we age, and disruption of the regular sleep architecture is a frequent antecedent to the onset of dementia in neurodegenerative diseases. The glymphatic system, which clears the brain of protein waste products, is mostly active during sleep. Yet the glymphatic system degrades with age, suggesting a causal relationship between sleep disturbance and symptomatic progression in the neurodegenerative dementias. The ties that bind sleep, aging, glymphatic clearance, and protein aggregation have shed new light on the pathogenesis of a broad range of neurodegenerative diseases, for which glymphatic failure may constitute a therapeutically targetable final common pathway.

Night terrors, sleepwalking, and confusional arousals in the general population: their frequency and relationship to other sleep and mental disorders.

Abstract: BACKGROUND: Arousal parasomnias (night terrors, sleepwalking, and confusional arousals) have seldom been investigated in the adult general population. Clinical studies of parasomnias, however, show that these disorders may be indicators of underlying mental disorders and may have serious consequences. METHOD: A representative sample of the United Kingdom population (N = 4972) was interviewed by telephone with the Sleep-EVAL system. RESULTS: Night terrors were reported by 2.2% (95% CI = 1.8% to 2.6%) of the sample, sleepwalking by 2.0% (1.6% to 2.4%), and confusional arousals by 4.2% (3.6% to 4.8%). The rate of these 3 parasomnias decreased significantly with age, but no gender difference was observed. Multivariate models identified the following independent factors as associated with confusional arousals (odds ratio [OR]): age of 15-24 years (OR = 4.1), shift work (OR = 2.1), hypnagogic hallucinations (OR = 3.3), deep sleep (OR = 1.6), daytime sleepiness (OR = 1.9), sleep talking (OR = 1.7), daily smoking (OR = 1.7), adjustment disorder (OR = 3.1), and bipolar disorder (OR = 13.0). Factors associated with night terrors were subjective sense of choking or blocked breathing at night (OR = 5.1), obstructive sleep apnea syndrome (OR = 4.1), alcohol consumption at bedtime (OR = 3.9), violent or injury-causing behaviors during sleep (OR = 3.2), hypnagogic hallucinations (OR = 2.2), and nightmares at least 1 night per month (OR = 4.0). Factors associated with sleepwalking were age of 15-24 years (OR = 5.2), subjective sense of choking or blocked breathing at night (OR = 5.1), sleep talking (OR = 5.0), and a road accident in the past year (OR = 3.9) after controlling for possible effects of sleep deprivation, life stress, and mental and sleep disorders. CONCLUSION: Arousal parasomnias, especially night terrors and confusional arousals, are often the expression of a mental disorder. Other life or medical conditions, such as shift work or excessive need of sleep for confusional arousals and stressful events for sleepwalking, may also trigger parasomnias. Prevalence rates are based on self-reported data and, consequently, are likely underestimated. Language: en