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Query: UMLS:C0037315 (sleep apnea)
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Obesity has epidemic proportions in Western societies and, because of its significant association with morbidity and mortality, is a major public health issue. Excessive daytime sleepiness (EDS) and fatigue (tiredness without increased sleep propensity)--which have been associated with obesity--have a significant impact on individual well-being and public safety. In this article, we review data that challenge the belief that sleep apnea and sleep disruption per se are the primary determinants of obesity-related daytime sleepiness and fatigue. Specifically, it appears that obesity per se is associated with objective and subjective daytime sleepiness compared to normal-weight controls regardless of sleep apnea and sleep loss. Indeed, obese patients without sleep apnea are sleepier compared to nonobese controls whereas within the morbidly obese, those who have high sleep efficiency at night are sleepier than those who have low sleep efficiency. In addition, in recent studies based on large random samples of the general population, the primary determinants of subjective EDS were depression and metabolic disturbances, that is, obesity/diabetes, and not sleep apnea or objective sleep disruption. Furthermore, sleepiness and fatigue are very prevalent in conditions associated with insulin resistance, for instance, the polycystic ovary syndrome (PCOS), independently of sleep apnea or obesity, or in conditions of insufficient physical activity. On the basis of these data, we propose that obesity-related objective daytime sleepiness and fatigue are associated primarily with metabolic and psychological factors and less with sleep apnea and sleep disruption per se. Furthermore, we suggest that objective sleepiness is primarily related to metabolic factors, whereas fatigue appears to be related to psychological distress. Finally, based on data from studies in normal controls and patients with sleep disorders, we propose that the interaction of the hypothalamic-pituitary-adrenal (HPA) axis and proinflammatory cytokines determines the level of sleep/arousal within the 24-h cycle, that is, "hypercortisolemia" plus hypercytokinemia is associated with low sleep efficiency and fatigue, whereas "eucortisolemia" or "hypocortisolemia" plus hypercytokinemia is associated with high sleep efficiency and objective sleepiness.
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PMID:Obesity-related sleepiness and fatigue: the role of the stress system and cytokines. 1714 48

Excessive daytime sleepiness (EDS) is not invariably present in patients with obstructive sleep apnoea syndrome (OSAS). The aim of the present study was to investigate polysomnographic determinants of EDS in patients with OSAS. EDS was assessed using the Epworth Sleepiness Scale (ESS) and the multiple sleep latency test (MSLT). Patients showed EDS whenever the ESS score was >10 and the MSLT score <5 min. Absence of EDS was defined as having an ESS score of <10 and an MSLT score of >10 min. In total, 23 male patients with EDS (mean+/-sd ESS and MSLT score 17+/-3 and 4+/-1 min, respectively) and 17 without EDS (ESS and MSLT score 5+/-2 and 16+/-3 min, respectively), were studied. Both groups exhibited a similar apnoea/hypopnoea index (62+/-18 versus 60+/-20 events.h(-1)). Patients with EDS exhibited shorter sleep latency (11+/-16 versus 18+/-18 min) and greater sleep efficiency (90+/-7 versus 82+/-13%) than those without EDS. Patients with EDS showed lower oxygenation (lowest arterial oxygen saturation 69+/-12 versus 79+/-8%; mean arterial oxygen saturation 87+/-6 versus 90+/-5%). Sleep stage distribution and arousal index did not differ between the groups. Patients with obstructive sleep apnoea syndrome and excessive daytime sleepiness are characterised by shorter sleep latency, increased sleep efficiency and worse nocturnal oxygenation than those without excessive daytime sleepiness. Nocturnal hypoxaemia can be a major determinant of excessive daytime sleepiness in patients with obstructive sleep apnoea syndrome.
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PMID:Daytime sleepiness and polysomnographic variables in sleep apnoea patients. 1866 96

The relation between snoring and obstructive sleep apnea as well as hypothyroidism is the object of interest of many authors. The respiratory disturbances during sleep are often observed in patients suffering from hypothyroidism. The relation of snoring to overweight in those patients has not been taken into account. The aim of the study was to evaluate the relations between hypothyroidism and quantitative and qualitative respiratory disturbances during sleep. Additional aim was to establish the relations of sleep apnea syndrome, snoring, hypothyroidism and overweight. The subjects included 15 patients (11 females and 4 males) aged from 28 to 73 (mean 50.3) suffering from hypothyroidism. All of them underwent thyroid testing before and after the hormonal treatment. TSH and fT4 concentrations were determined. At the same time the sleep assessment (PolyMESAM) was performed twice. Data were obtained from sleep studies and questionnaires (Epworth sleepiness scale). After the thyroid hormones stabilization significant decrease of snoring severity was observed. On the contrary, the respiratory disturbance index (RDI), desaturation index (DI), the lowest saturation (LSAT) did not change significantly, however, the Epworth scale score showed significant improvement. The correlations showed the strong relation between loud snoring and TSH (r=0.73, p<0.01) and fT4 (r=-0.66, p<0.003) concentrations before the treatment. The analysis showed no correlation between body mass (BMI) and snoring. The hormonal stabilization in patients suffering from hypothyroidism causes improvement in snoring severity. Based on our investigation the relationship between hypothyroidism and severity of snoring and excessive daytime somnolence was confirmed. It indicates a possible connection between hypothyroidism and upper airway resistance syndrome.
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PMID:Sleep apnea syndrome and snoring in patients with hypothyroidism with relation to overweight. 1744 29

Several studies indicate an association between obstructive sleep apnea syndrome (OSAS) and diabetic autonomic neuropathy (DAN). Observed frequency of OSAS in diabetic patients with DAN varies between 26% and 30%. Excessive daytime sleepiness is one of the major clinical symptoms of sleep disordered breathing. Diabetics with autonomic neuropathy might have abnormal control of respiration during sleep, probably resulting in a reduced daytime sleepiness. We investigated the impact of autonomic diabetic neuropathy on clinical symptoms (e.g., daytime sleepiness, measured by Epworth Sleepiness Scale, ESS) in patients with suspected OSAS. We examined 196 patients suspected of sleep apnea (52 female, 144 male, mean age 58.7 yrs, mean BMI 30.57 kg/m2). All patients underwent overnight polysomnography and were tested for autonomic neuropathy by a method of measuring heart rate variabilty and heart rate response to the Valsalva maneuver, standing and deep breathing using a computerized data analysis system. Eighty diabetic subjects: 52 DAN-, 28 DAN+; 116 subjects without diabetes: 101 without autonomic neuropathy (AN), 15 AN+. The group of diabetics with DAN+ had a mean apnoea/hypopnea index (AHI) of 38.6/h, mean oxygen desaturation: 77.5%, mean ESS-Score: 9.86. Diabetic patients DAN-: mean AHI:30.4/h, mean oxygen desaturation: 79.3%, mean ESS-Score 9.73. Defining OSAS as AHI>5/h and ESS-Score>9, 46% of the diabetic patients DAN+ were positive, whereas in the DAN- group 61% met the criteria (non-diabetic patients without AN 50.5%; with AN: 60%). Although the group of diabetic patients with autonomic neuropathy had the lowest percentage of OSAS, statistical analysis showed no significance in comparisons between DAN-/DAN+ or diabetic/non-diabetic. In conclusion, although this study did not give statistical evidence, there is reason to assume that patients with diabetic autonomic neuropathy show fewer clinical symptoms of OSAS than those without it. The examination for OSAS might be indicated even without excessive daytime sleepiness because of elevated cardiovascular risk.
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PMID:Obstructive sleep apnea syndrome: the effect of diabetes and autonomic neuropathy. 1820 41

The epidemiological study of hypersomnia symptoms is still in its infancy; most epidemiological surveys on this topic were published in the last decade. More than two dozen representative community studies can be found. These studies assessed two aspects of hypersomnia: excessive quantity of sleep and sleep propensity during wakefulness excessive daytime sleepiness. The prevalence of excessive quantity of sleep when referring to the subjective evaluation of sleep duration is around 4% of the population. Excessive daytime sleepiness has been mostly investigated in terms of frequency or severity; duration of the symptom has rarely been investigated. Excessive daytime sleepiness occurring at least 3 days per week has been reported in between 4% and 20.6% of the population, while severe excessive daytime sleepiness was reported at 5%. In most studies, men and women are equally affected. In the International Classification of Sleep Disorders, hypersomnia symptoms are the essential feature of three disorders: insufficient sleep syndrome, hypersomnia (idiopathic, recurrent or posttraumatic) and narcolepsy. Insufficient sleep syndrome and hypersomnia diagnoses are poorly documented. The co-occurrence of insufficient sleep and excessive daytime sleepiness has been explored in some studies and prevalence has been found in around 8% of the general population. However, these subjects often have other conditions such as insomnia, depression or sleep apnea. Therefore, the prevalence of insufficient sleep syndrome is more likely to be between 1% and 4% of the population. Idiopathic hypersomnia would be rare in the general population with prevalence, around 0.3%. Narcolepsy has been more extensively studied, with a prevalence around 0.045% in the general population. Genetic epidemiological studies of narcolepsy have shown that between 1.5% and 20.8% of narcoleptic individuals have at least one family member with the disease. The large variation is mostly due to the method used to collect the information on the family members; systematic investigation of all family members provided higher results. There is still a lot to be done in the epidemiological field of hypersomnia. Inconsistencies in its definition and measurement limit the generalization of the results. The use of a single question fails to capture the complexity of the symptom. The natural evolution of hypersomnia remains to be documented.
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PMID:From wakefulness to excessive sleepiness: what we know and still need to know. 1834 61

Sleep disorders are common in dialysis patients. Insomnia is reported in almost 70% of the dialysed. Old age, presence of common sleep disorders, such as sleep apnea syndrome (SAS) and restless legs syndrome (RLS), comorbid clinical conditions, metabolic parameters and characteristics of dialysis, represent the main risk factors for insomnia. RLS is independently associated with uremia, affecting almost 30% of Caucasians dialysed. Pathophysiology of uremic RLS is still unclear. Although the exact pathogenetic mechanism remains unknown, the efficacy of kidney transplantation on RLS symptoms supports the involvement of renal function in this disturbance. SAS affects 30-80% of dialysis patients. The use of neurophysiological measures is necessary to diagnose SAS. This approach is not applicable in all dialysis patients; consequently, validated questionnaires might be useful to screen patients with a high risk of apnea. Risk of obstructive and central respiratory events are increased by renal failure and dialysis therapy. Excessive daytime sleepiness (EDS) is often reported by the dialysed population. Direct effects of uremic encephalopathy and of somnogenic cytokines have been suggested as the cause of EDS, in addition to the sleep disturbances that increase daytime sleepiness by impairing nocturnal sleep efficiency. Although less frequent, the presence of other sleep disturbances (such as nightmares and narcolepsy) should be carefully evaluated in the uremic population. Several sleep disturbances may potentially be treated but, if left untreated, may impair health status and increase the risk of mortality. However, literature and personal data suggest that undertreatment is common, calling to higher awareness of sleep disturbances among nephrologists.
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PMID:Sleep disturbances in dialysis patients. 1844 35

Sleep disorders in Parkinson's disease (PD) are frequent and have numerous etiologies. Both nighttime sleep disturbances and daytime sleepiness can occur. The key to effective treatment is appropriate diagnosis. A careful interview of the patient and his or her bed partner provides direction for additional evaluations. Referral to a sleep specialist for quantitative studies is necessary to evaluate for rapid eye movement (REM) sleep behavior disorder, sleep apnea, periodic limb movements, and other sleep disorders. Excessive daytime sleepiness may be attributed to interrupted nighttime sleep or daytime medications (particularly the dopamine agonists) or it may be intrinsic to PD. When the diagnosis is established, treatment is directed toward the primary sleep disturbance. Fragmented sleep due to recurrence of PD symptoms may improve with the use of long-acting preparations of carbidopa/levodopa. Sleep apnea is treated using continuous positive airway pressure, and REM sleep behavior disorder may improve using pharmacologic interventions, although controlled trials are lacking. Restless legs syndrome and periodic limb movements during sleep are treated with direct dopaminergic agonists at bedtime. Excessive daytime sleepiness related to the use of direct dopaminergic agonists may improve with dosage reduction or discontinuation. Stimulants such as modafinil may provide modest benefit.
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PMID:Sleep disorders in Parkinson's disease. 1857 25

Although daytime sleepiness is commonly associated with obstructive sleep apnoea (OSA), the relationship between OSA severity and subjective sleepiness has been documented elusive. This study aimed to identify clinical and polysomnographic determinants of subjective sleepiness among patients suspected of having OSA. A sleep clinic-based sample of 915 patients was interviewed with a structured questionnaire and underwent diagnostic overnight polysomnography. Subjective sleepiness was quantified by Epworth Sleepiness Scale (ESS). Excessive daytime sleepiness (defined as ESS score > 10) was present in 38.8% of patients. In multiple linear regression analysis, respiratory disturbance index [RDI; used to define (whenever RDI was >5) and quantify OSA], depression and diabetes were the most important determinants of ESS score accounting for 17%, 11% and 6% of its variability respectively. Chronic obstructive pulmonary disease (COPD), stroke, heart disease, alcohol use and body mass index were less important determinants of ESS score explaining 1-3% of its variability. In conclusion, OSA should not be considered the sole potential cause of increased subjective sleepiness in patients suspected of having OSA. Primarily depression and diabetes, but also COPD, stroke, heart disease, alcohol use and increased body mass index may contribute to increased subjective sleepiness.
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PMID:Determinants of subjective sleepiness in suspected obstructive sleep apnoea. 1876 99

An observational study of cases of obstructive sleep apnoea-hypopnoea syndrome (OSAHS), both suspected and established, presenting to general neurology outpatient clinics over a 5-year period was undertaken. Only eight new cases of OSAHS, confirmed by sleep studies, were identified, most with neurological problems (poor seizure control, blackouts and headache) in addition to excessive daytime somnolence. OSAHS appears to be a rare cause of new symptomatic neurological presentations, although cases may have been overlooked as judgement was based on the index of clinical suspicion alone.
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PMID:Obstructive sleep apnoea-hypopnoea syndrome presenting in the neurology clinic: a prospective 5-year study. 1879 71

Orthognathic surgery has been used regularly to treat dentofacial deformities. The surgical procedures affect both the facial appearance as well as the posterior airway space (PAS). Our current literature indicates that setback procedures produce an inferior repositioning of the hyoid bone and posterior displacement of the tongue and the soft palate. These movements cause anteroposterior and lateral narrowing of the PAS. Most authors agree that these effects are permanent. The PAS changes in turn produce an adaptive posturing, with an increased craniocervical angle to open up the PAS. Even though most patients do not display snoring and obstructive sleep apnoea (OSA) post-surgery, there is certainly an increased possibility in patients with already compromised airways. Therefore, patients who are undergoing orthognathic surgery should be screened for excessive daytime somnolence, snoring, increased body mass index (BMI) and medical conditions related to OSA and sent for an overnight polysomnography (PSG) if OSA is suspected. Then the proposed treatment plan may be modified according to the risk of potential airway compromise or even to improve it. Conversely, advancement of the maxilla and mandible causes widening of the airway in both the anteroposterior and lateral dimensions. This effect would translate to better airflow and decreased airway resistance. This is supported by the evidence showing high success rates when orthognathic surgery, especially maxillomandibular advancement (MMA), is utilised to treat OSA.
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PMID:Effect of orthognathic surgery on the posterior airway space (PAS). 1879 61


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