Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0037315 (sleep apnea)
 8,000 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Restless legs syndrome (RLS) is a common sensorimotor disorder with an estimated prevalence of between 1% and 5%. The symptomatology is characterized by unpleasant sensations experienced predominantly in the legs and rarely in the arms. The symptoms occur only at rest and become more pronounced in the evening or at night. In addition, the patients suffer from a strong urge to move the limbs, typically manifest as walking around, which leads to complete but only temporary relief of the symptoms. Most of the patients with RLS have periodic leg movements (PLMS) during sleep and relaxed wakefulness that are characterized by repetitive flexions of the extremities. PLMS can occur as an isolated phenomenon, but often they occur together with other sleep disorders including RLS, narcolepsy, sleep apnoea syndrome or REM sleep behaviour disorder. In all these disorders, PLMS, contribute considerably to disturbed sleep, as the movements may lead to brief arousals or repeated full awakenings. The aetiology of RLS and PLMS is unknown. It is hypothesized that periodic leg movements result from a suprasegmental disinhibition of descending inhibitory pathways. Based on the efficacy of the drugs listed below, the dopaminergic, adrenergic and opiate systems are thought to play a major role in the pathogenesis of RLS/PLMS. Since the cause is unclear, therapy of RLS and PLMS remains symptomatic except for some secondary forms. Studies on the pharmacological treatment of RLS have shown the efficacy of levodopa, dopamine agonists, benzodiazepines, opioids, clonidine and carbamazepine. With regard to the drug treatment of PLMS in other sleep disorders including their isolated occurrence, indications and efficacy have been poorly defined until now.
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PMID:Restless legs and periodic leg movements in sleep syndromes. 911 88

Post-traumatic stress disorder (PTSD) overlaps major depression (MD) clinically, but differs with respect to treatment response and some biological markers. Sleep disturbances represent core features of PTSD and are also common in MD. Rapid eye movement sleep (REM) has been postulated to be involved in the pathophysiology of PTSD, and REM abnormalities occur in MD. Twenty-five patients with combat-related PTSD, 16 men with a principal diagnosis of MD, and 10 asymptomatic male controls were compared by polysomnography (PSG) under medication and substance-free conditions. Data were obtained from recordings made after an accommodation night. One subject from each group was excluded for significant apnea or limb movements. Sleep efficiency was decreased in the PTSD group compared to the MD and control groups. REM density was comparably increased in PTSD and MD groups, while the amount of REM sleep was reduced in PTSD compared to MD groups. These sleep measures were not significantly associated with co-morbid depression, substance-use disorder histories, or subclinical sleep apnea or limb movements within the PTSD group. These findings support sleep maintenance being impaired in chronic PTSD patients. Increased REM density in PTSD patients was replicated and was comparable to increases in the MD group. Divergence of REM time between these clinical groups suggests the possibility of different underlying mechanisms.
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PMID:A polysomnographic comparison of veterans with combat-related PTSD, depressed men, and non-ill controls. 913 Mar 34

Twenty patients of interstitial lung disease (ILD) and same number of healthy adults were selected to monitor arterial hemoglobin oxygen saturation (SaO2) breathing pattern and arrhythmias during sleep. The maximum fall in SaO2 during sleep was 13.1% (10-16%) in ILD patients as compared to 4.8% (3-6%) in controls and the difference was significant (p < 0.005). The ILD patients spent 16.9% of mean total sleep time (TST) below 85% SaO2 and 0.7% of mean TST below 80% SaO2 whereas none of the healthy subjects had SaO2 below 90% during sleep. These patients had more disturbed sleep than controls. Abnormally high breathing frequency demonstrated by ILD patients while awake, was not altered during sleep. Both tidal volume (VT) and minute ventilation (Vmin) decreased by 6.6% and 11.5%, respectively in ILD patients during sleep though it was not significant (p > 0.25) statistically. The respiratory drive was declined during sleep in ILD patients. The percent of tidal volume contributed by rib cage (% RC) lessened during sleep in all the subjects. The ratio of the total excursion of the rib cage and abdomen during inspiration without considering the direction of movement, divided by tidal volume (TCD/VT) revealed asynchronous breathing in ILD patients during sleep. Arrhythmias were found in 6 (30%) of ILD patients and 4 (20%) of control subjects. Observed apnea-hypopnea did not qualify for sleep apnea syndrome in any case.
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PMID:Study of oxygen saturation, breathing pattern and arrhythmias in patients of interstitial lung disease during sleep. 935 49

Nocturnal arousals are the essential cause of disturbed sleep structure in patients with obstructive sleep apnoea syndrome (OSAS). The aim of this study was to analyse the relationship between sleep stages, respiratory (type-R) and movement (type-M) related EEG arousals. Furthermore, the value of these arousals as a criterion for the efficiency of nCPAP treatment was estimated. We examined 38 male patients aged between 30 and 71 (49.1 +/- 20.9 SD) y. All patients suffered from OSAS. The mean respiratory disturbance index (RDI) was 47.3 +/- 27.8 per h. Polysomnographic monitoring was carried out on 4 subsequent nights: baseline night, 2 nights of nCPAP titration and nCPAP control night. Sleep was visually scored and EEG arousals were classified into type R and M, depending on whether changes of respiration or movement caused the arousal. The RDI, the R index (type-R/h), the M index (type-M/h) and the R and M indices in different sleep stages were calculated. During the baseline night a deficit of slow wave sleep (SWS) and REM sleep was found. Furthermore there were more type-R than type-M arousals registered (17.4 h-1 [3.6-43.6] vs. 5.9 h-1 [1.6-11.8]) (P < 0.01). They occurred during stages NREM 1, NREM 2 and REM (P < 0.01). An SWS sleep rebound and a reduction of the SWS and REM latencies were already found during the first CPAP night. The R index was reduced during the first CPAP night in all sleep stages (P < 0.01) and remained approximately the same in the following 2 nights (3. CPAP night: 1.1 h-1 [0.3-5.0]). Type M arousals occurred more in stages 1 and 2 (P < 0.01), and remained unchanged under nCPAP. We concluded that differentiation of nocturnal arousals may provide more detailed information regarding the influence of breathing disturbances on sleep. Respiratory related, not movement related, arousals may be a useful additional tool in judging the efficiency of OSAS.
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PMID:Arousals and sleep stages in patients with obstructive sleep apnoea syndrome: Changes under nCPAP treatment. 937 32

Textbook descriptions of dialysis patients have long included features of insomnia, day-night reversal, and disturbed sleep. Moore recently, a very high prevalence of subjective sleep complaints and specific primary sleep disorders such as sleep apnea syndrome, periodic leg movement disorder, and restless legs syndrome have been documented in the population. These problems may in part be responsible for the low rehabilitation rate seen in ESRD patients. The purpose of this article is to assist dialysis nurses in their efforts to better understand the sleep alterations experienced by their patients by presenting a succinct review of the research literature. The major topics of discussion include: the prevalence and importance of sleep complaints in dialysis patients; subjective features and related factors; polysomnographic features; and contributing factors.
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PMID:Sleep and dialysis: a research-based review of the literature. 944 3

The mechanisms and pathophysiology of sleep disturbances in patients with endocrine diseases are reviewed. Abnormalities in sleep regulations were demonstrated in patients with thyrotoxicosis and hypothyroidism in a use of electroencephalogram during sleep. Mental disorders are one of the causes of sleep disturbance, for example insomnia due to depression in Cushing's syndrome. Metabolic abnormalities such as hyponatremia and hypoglycemia due to adrenal insufficiency could also contribute to sleep disturbance. Obstructive, central and mixed types of sleep apnea syndrome are known to occur in hypothyroidism, acromegaly and diabetic neuropathy with autonomic dysfunction. Thus, multiple factors are involved in sleep disturbance in patients with endocrine disorders.
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PMID:[Sleep disorders in several pathologic states--endocrine diseases]. 950 51

Disorders of excessive daytime sleepiness (EDS) constitute a major health hazard, since impaired alertness may lead to accidents and poor quality of life, and some of them are associated with increased cardiovascular morbidity and mortality. Many disorders of EDS are neurological diseases (e.g. narcolepsy and periodic limb movements in sleep, PLMS). The largest group of disorders causing EDS consists of sleep-related disturbances of breathing, where neuroregulatory mechanisms play a major role in pathophysiology. Many patients with neurodegenerative and neuromuscular diseases suffer from sleep disturbances associated with EDS. Therefore, neurologists must be acquainted with the differential diagnosis of EDS and the major categories of sleep disorders causing it. The present update focuses on major sleep disorders causing EDS, and approaches the topic from the neurologist's perspective. Rather than being an extensive review, this update includes recent data on epidemiology, pathophysiology, diagnosis and treatment of obstructive sleep apnea and related conditions (increased upper airway resistance syndrome, central sleep apnea), as well as of narcolepsy and PLMS. Also included are recent data concerning EDS in neurodegenerative (Alzheimer's disease, Parkinson's disease, multiple system atrophy) and neuromuscular disorders.
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PMID:Disorders of excessive daytime sleepiness--an update. 951 78

In many cross-sectional studies an association has been found between snoring and hypertension. However, differing results have been obtained when confounding factors have been taken into account. To establish whether snoring is a risk factor for developing hypertension, a population-based, prospective survey was performed. In 1984 and 1994, 2,668 males, aged 30-69 yrs at baseline, answered questionnaires concerning sleep disturbances and somatic disease. Of the habitual snorers in 1984, 12.5% reported that they had developed hypertension during the period, compared with 7.4% of the remaining subjects (p<0.001). In a multiple logistic regression model persistent snoring, i.e., reported habitual snoring in both 1984 and 1994, was found to be an independent predictor for the development of hypertension among males aged 30-49 yrs (odds ratio 2.6, 95% confidence interval 1.5-4.5) after adjustments for age, body mass index (BMI), weight gain, smoking, alcohol dependence, and physical inactivity. Among the subjects aged 50-69 yrs in 1984, no association between snoring and development of hypertension was found. Although based only on reported data, the results indicate that persistent snoring is an independent risk factor for the development of hypertension among males aged <50 yrs. Prospective surveys, including whole-night sleep recordings, are needed to establish whether this is due to a higher prevalence of obstructive sleep apnoea syndrome among snorers or whether nonapnoeic snorers with increased upper airway resistance also have an increased risk of developing hypertension.
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PMID:Snoring and hypertension: a 10 year follow-up. 962 92

Fibromyalgia (FM) patients report early morning awakenings, awakening feeling tired or unrefreshed, insomnia, as well as mood and cognitive disturbances; they may also experience primary sleep disorders including sleep apnea. Longitudinal studies have demonstrated the chronic nature of these disturbances in patients with FM. A distinct relationship exists between poor sleep quality and pain intensity. Polysomnographic findings during sleep in these patients include an alpha frequency rhythm, termed alpha-delta sleep anomaly, which is also seen in normal controls during stage 4 sleep deprivation; deep pain induced during sleep in normal controls also causes this anomaly. Sleep architecture is altered in FM patients showing an increase in stage 1, a reduction in delta sleep, and an increased number of arousals. Before prescribing pharmacologic compounds aimed at modifying sleep, adequate pain control and sleep habits should be achieved; tricyclic antidepressants, trazadone, zopiclone, and selective serotonin reuptake inhibitors, however, may be required. More research is needed to elucidate the cellular and molecular mechanisms involved in the sleep disturbances occurring in patients with FM.
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PMID:Sleep in fibromyalgia patients: subjective and objective findings. 963 93

1. The upper airway not only provides a passage for air to be breathed in and out of the lungs, but it also heats, humidifies and filters the air and is involved in cough, swallowing and speech. 2. The complex muscle structure of the upper airway that produces speech and swallowing in humans also modulates respiratory airflow throughout the respiratory cycle, but is vulnerable to functional problems that may compromise respiration. 3. Even in normals, there is some collapse of the upper airway and increased upper airway resistance during sleep. 4. A substantial proportion of people suffer from obstructive sleep apnoea, in which the collapse of the upper airway is so great that respiration is compromised to the extent that arousal from sleep is required to restore adequate ventilation; the resulting disturbed sleep and hypoxia produce daytime sleepiness and neuropsychological and cardiorespiratory morbidity. 5. Functional abnormalities of the larynx can also occur, including prolonged inspiratory laryngeal dysfunction, brief upper airway dysfunction and expiratory laryngeal dysfunction or factitious asthma.
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PMID:Upper airway function and dysfunction in respiration. 1002 63


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