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 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sleep-related complaints have become a highlight for physicians as well as public health administrators. Studies of sleep patterns and sleep-related complaints of shift workers have been useful in minimizing reduction in the quality of life due to the warping of the sleep-wake cycle. The objective of the present study was to assess patterns of sleep, sleep-related complaints as well as physical activity and scoring rates for depression and anxiety in interstate bus drivers. Data were obtained with a sleep questionnaire, with the Beck inventory for depression, and the State-Trait Anxiety Inventory (STAI). A total of 400 interstate bus drivers from the northern, southern, central-western and south-eastern regions of Brazil were interviewed. Sixty percent of the subjects interviewed presented at least one sleep-related complaint, 16% admitted to have dozed at the wheel while on duty, and 41% stated that they exercised on a regular basis. Other sleep disturbance complaints reported were: sleep latency 29'17"; physical fatigue, 59.8%; mental fatigue, 45.4%; sleepiness, 25.8%; irritability, 20.6%; insomnia, 37.5%, respiratory disturbances, 19. 25% and snoring, 20.75%. Scores for anxiety and depression were not in the pathological range. The present data reinforce the view that bus drivers are generally discontent with shift work and its effects on sleep. Consequently, it is very important to establish an appropriate work schedule for drivers, besides implementing photo-therapy and physical activities in order to minimize sleepiness when driving.
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PMID:Sleep patterns and sleep-related complaints of Brazilian interstate bus drivers. 1062 77

Sleep-related breathing disorders, ranging from habitual snoring to the increased upper airway resistance syndrome to sleep apnea, are now recognized as major health problems. The majority of patients have excessive daytime sleepiness and tiredness. Neuropsychological dysfunction results in poor work performance, memory impairment, and even depression. Until recently, the coexistence of cardiovascular and cerebrovascular diseases with sleep-related breathing disorders was thought to be the result of shared risk factors, such as age, sex, and obesity. However, in the past 5 years several epidemiologic studies have demonstrated that sleep-related breathing disorders are an independent risk factor for hypertension, probably resulting from a combination of intermittent hypoxia and hypercapnia, arousals, increased sympathetic tone, and altered baroreflex control during sleep. Sleep apnea may lead to the development of cardiomyopathy and pulmonary hypertension. Early recognition and treatment of sleep-related breathing disorders may improve cardiovascular function.
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PMID:Sleep-related breathing disorders and cardiovascular disease. 1075 96

Based on a case report, we offer brief guidelines on the perioperative management of patients with Sleep-Apnea-Syndrome (SAS) who present with a high incidence of a difficult airway and a high risk of respiratory depression during the perioperative period. A 39 year old male patient with a body mass index of 34.22 kg/m2 and receiving continuous-positive-airway-pressure-(CPAP) therapy for known SAS was scheduled for elective plastic surgery. After induction of anaesthesia and direct laryngoscopy no adequate airway could be established and the patient became hypoxic, hypercapnic and developed hypotension and bradycardia. With the use of a laryngeal mask airway the patient was stabilized and did not show neurologic sequale after immediate awakening. The following fiberoptic intubation of the awake patient, still showing tendency of upper airway obstruction, confirmed the difficult anatomical structures. The subsequent general anesthesia was uneventful. The patient received CPAP therapy and was monitored during the first postoperative night in the Intensive Care Unit. He made an uneventful recovery. He was advised to have regional anaesthesia or planned fiberoptic intubation, where possible, in the case of further anesthetic intervention. SAS has major implications for the anaesthesiologist and whenever patients exhibiting the high risk factors (obesity, male sex, history of intense snoring, impaired daytime performance, nonrefreshing daytime naps) are presented for surgery this condition should be considered. Elective surgery should be postponed until after adequate examination and treatment when necessary. Patients with SAS should always be suspected of having cardiopulmonary dysfunctions such as hypertension, cardiac dysrhythmia or cor pulmonale. It is most important to avoid sedative premedication, to initiate CPAP therapy preoperatively, to encourage regional anaesthesia if possible and to ensure close monitoring over the complete perioperative period. Planned fiberoptic intubation, preferably with surgical personnel available for an emergency airway, is a safe method for the induction of anaesthesia. Postoperatively, patients are at high risk from respiratory depression, even in the awake state. Postoperative opioid analgesia, no matter what route, should only be given under close monitoring. Independently of regional or general anaesthesia there is an increased risk of respiratory depression in the middle of the first postoperative week, suspected to be caused by the catching up on lost REM-sleep, due to shifts in the normal sleep pattern during the first postoperative days.
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PMID:[Induction of anesthesia for a patient with sleep apnea syndrome]. 1084 May 41

The relationship between health-related quality of life (HRQOL) and sleep apnea was examined in a sample of elderly African-Americans screened for snoring and daytime sleepiness. Seventy African-Americans over the age of 65 years completed a comprehensive sleep questionnaire, the Quality of Well-Being Scale (QWB), and the Medical Outcomes Study (MOS) Core Measures of HRQOL (116-item Long Version) and had sleep recorded. Those with moderate-severe sleep apnea had significantly lower Physical Component summary scores than those with no sleep apnea (p < 0.05). After controlling for medical conditions, sleep apnea was significantly related to both general physical functioning and general mental health functioning in those with mild apnea (apnea-hypopnea index [AHI] < 15), but not in those with moderate to severe apnea. There was an initial decrease in HRQOL up to an AHI level of 15, at which point HRQOL remained at a lowered level. The QWB scores of our sleep apnea sample were similar to the QWB scores found in patients with depression and chronic obstructive pulmonary disease (COPD), suggesting that sleep disturbances may impact daily living and health as much as other medical conditions.
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PMID:Sleep apnea and health-related quality of life in African-American elderly. 1096 3

A common clinical dilemma faced by sleep physicians is in deciding the level of severity at which patients with obstructive sleep apnea (OSA) should be treated. There is particular uncertainty about the need for, and the effectiveness of, treatment in mild cases. To help define the role of nasal continuous positive airway pressure (CPAP) treatment in mild OSA we undertook a randomized controlled cross-over trial of CPAP in patients with an apnea- hypopnea index (AHI) of 5 - 30 (mean, 12.9 +/- 6.3 SD). Twenty-four-hour blood pressure and neurobehavioral function were measured at baseline, after 8 wk of treatment with CPAP, and after 8 wk of treatment with an oral placebo tablet. Twenty-eight of 42 patients enrolled in the study completed both treatment arms. Baseline characteristics were not different between those who completed the study and those who did not complete the study. Patients used CPAP for a mean (SD) of 3.53 (2.13) h per night and the mean AHI on the night of CPAP implementation was 4.24 (2.9). Nasal CPAP improved self-reported symptoms of OSA, including snoring, restless sleep, daytime sleepiness, and irritability (in-house questionnaire), more than did placebo, but did not improve objective (Multiple Sleep Latency Test) or subjective (Epworth Sleepiness Scale) measures of daytime sleepiness. We found no benefit of CPAP over placebo in any tests of neurobehavioral function, generic SF-36 (36-item Short Form Medical Outcomes Survey) or sleep-specific (Functional Outcomes of Sleep Questionnaire) quality of life questionnaires, mood score (Profile of Moods States and Beck Depression Index), or 24-h blood pressure. However, the placebo tablet resulted in a significant improvement in a wide range of functional variables compared with baseline. This placebo effect may account for some of the treatment responses to CPAP observed previously in patients with mild OSA.
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PMID:A randomized controlled trial of continuous positive airway pressure in mild obstructive sleep apnea. 1189 36

There is still a controversy regarding the relationship between sleep apnoea syndrome and headaches, especially morning headaches. Our objectives were: (i) to compare the prevalence and the clinical data of headaches in sleep apnoea syndrome (SAS) and control (snorers) groups defined by polysomnographic recording; (ii) to analyse the clinical improvement of headaches with appropriate treatment; and (iii) to correlate headaches with mood disorders, and nocturnal respiratory and architectural sleep parameters in order to understand the underlying pathophysiological mechanisms. This is a prospective study of 324 consecutive patients referred to our sleep centre for snoring. Of these, 312 patients who underwent sleep polysomnography were finally included. Patients and controls were interviewed about their medical past, headache history and clinical characteristics, their daytime sleepiness (Epworth's sleepiness scale) and their mood disorders (Zerssen's scale). Follow-up of patients with headaches (SAS and control groups), treated or not, was also assessed. According to our definition of SAS, patients were dissociated in SAS (n=164) and snorers (n=148). Fifty-three SAS patients had headaches, of whom 58.5% (n=30) suffered from morning headaches. However, there was no statistical difference between the two groups concerning the prevalence and the clinical characteristics of headaches. In addition, headaches and morning headaches were not correlated with nocturnal respiratory and architectural sleep parameters, nor with excessive daytime sleepiness, but were strongly correlated with mood disorders. In 36 SAS patients, headaches improved under treatment, but this was not statistically different from what was found among untreated snorers. Headaches and morning headaches are common in patients with SAS but may be considered as a non-specific symptom. The underlying mechanisms are not fully elucidated but depression could play an important role. Despite this absence of specificity, the treatment of SAS, especially nasal continuous positive airway pressure, leads to an improvement in headaches in several cases.
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PMID:Relationship between sleep apnoea syndrome, snoring and headaches. 1211 Jan 8

The sleep apnea syndrome (SAS), which is defined by more than 5 apneas or hypopneas per hour of sleep (9), is quite a frequent affection which concerns 1.4 to 10% of general population (1.7). The major daytime complaints of the SAS are daytime sleepiness, memory and attention disorders, headaches and asthenia especially in the morning, and sexual impotence (9). The nocturnal manifestations are dominated by sonorous and generally long standing snoring, increased by dorsal decubitus and intake of alcohol, with repeated interruptions by respiratory arrests. These manifestations are always noted but rarely spontaneously reported. The sleep, non refreshing, is agitated and perturbed by numerous awakenings. The findings of the clinical examination are poor: obesity is found in 2/3 of the cases and arterial hypertension in 1/2 of the cases (20). Polygraphic recording during sleep only permits an absolute diagnosis. This frequent affection is a real problem of public health because of its numerous complications (3, 10, 12, 13, 18, 21). Symptoms of depression are often found when a patient with a SAS is examined and conversely, symptoms which evoke a SAS can be found in the clinical examination of depressed patients. We decided so to study the thymic and anxious status of 24 patients investigated for a SAS and submitted to a polygraphic recording during sleep. Four clinical parameters were studied: DSM III-R diagnosis criteria, Montgomery and Asberg Depression Rating Scale (MADRS), Hamilton Anxiety Rating Scale (HARS) and thymasthenia rating scale of Lecrubier, Payan and Puech. We also reported Total Sleep Time (TST = 6.5 +/- 1.5), Apnea Hypopnea Index (AHI = 26.7 +/- 21.6), number (2.1 +/- 2.8/h) and duration (174.2 +/- 150.8 s/h) of hypoxic events. Results showed that among 24 patients, 8 were depressed according to DSM III-R diagnosis criteria and had MADRS > 25, 22 were anxious, 11 had a major anxiety (HARS > 15) and 15 presented thymasthenia (SET > 15). Significative correlations existed between anxiety and depression (r = 0.82; p < 0.0001), depression and thymasthenia (r = 0.77; p < 0.0001) and thymasthenia and anxiety (r = 0.75; p < 0.0001). Among the 8 depressed patients a correlation existed between AHI and depression (r = 0.72; p = 0.04), but no correlation was found between depression and hypoxic events. These results were comparable to those of Guilleminault (10), Reynolds (21), Kales (12), Bliwise (3), Klonoff (13) and Millman (18) who studied relations between SAS and depression. The evaluation of thymasthenia gave a more precise typology of the depressive state associated to SAS: the type of the mood disorder is more "blunted" and "anhedonic" than "sorrowful", particularly characterised by asthenia, lack of energy, reduction of interests (leisures, libido, work), loss of initiative, difficulties to organise tasks, fall of performances and reduction of pleasure usually felt in pleasant events (15). The physic symptomatology dominated the psychic one. The sleep disorganization, more than metabolic consequences of apneas, could be involved in this associated depressive state. Other neuropsychiatric troubles can be associated to the SAS. In fact, cognitive troubles (2, 8, 14, 16, 19, 22, 24) and personality disorders (12, 18) have been described. Our data confirm previous observations suggesting a frequent association between SAS, depression, fatigue and anxiety. Clinicians should consequently be aware that a depression with severe complaints of fatigue should deserve an investigation oriented towards SAS. Conversely, when a SAS is diagnosed, it is necessary to look for a possible depression in order to set up the most appropriate treatment. The frequency of SAS, like depression's one, increases with age. Prescription and consummation of sedative psychotropic drugs increase too with age. Since respiratory depressant effects of these drugs have been clearly demonstrated, it is important to evoke SAS when depressive and/or anxious states are diagnosed and not to aggravate it. An efficacious treatment of SAS can also cure the associated depressive state, but this one can persist. It is necessary, in this case, to select a non sedative antidepressant.
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PMID:[Depressive symptomatology and sleep apnea syndrome]. 1240 78

Four basic control mechanisms of breathing (brainstem respiratory centre, peripheral and central chemoreceptors, intero- and exteroceptive reflexes and suprapontine influences), as well as their sleep-related disorders are analysed. A decrease in central chemoreceptor sensitivity to CO2 and an increase in upper airway resistance during sleep result in hypoventilation and mild hypoxaemia already in physiological conditions. Compensatory increase in ventilatory effort with synchronous inhibition of pharyngeal dilators during sleep reduces the upper airway lumen manifesting with snoring, upper airway resistance syndrome, and OSA. The resulting hypoxaemia may cause marked cardiovascular, neuro-psychic, endocrine-metabolic and behavioural disorders. The augmented ventilatory effort and hypoxaemia evoke reflex dilation of airways and arousal from sleep, stimulating the sympatho-adrenal system, which provokes autoresuscitation by gasping preventing fatal asphyxia. Failure of this autoresuscitation mechanism seems to cause SIDS. Elimination of voluntary breathing by sleep either in Ondine's curse induced by lesions of respiratory centre, or in congenital central hypoventilation syndrome caused by insufficient central chemoreceptors result in respiratory failure and death. Nocturnal attacks of bronchial and cardiac asthma, lung oedema and other consequences of pulmonary congestion are also discussed. The pathomechanism of extreme daytime sleepiness, chronic fatigue, and disorders of memory, cognitive and other brain functions, are also analysed. Severe cardiovascular consequences of SAS may manifest acutely as angina pectoris, myocardial infarction. dysrhythmias, transient ischaemic attacks and even stroke or sudden cardiac death. OSAS may result also in development of hypertension, central obesity, diabetes mellitus, erectile dysfunction, depression, and various behavioural disorders.
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PMID:[Regulation of respiration and its sleep-related disorders]. 1244 39

Noxious stimuli and painful disorders interfere with sleep, but disturbances in sleep also contribute to the experience of pain.Chronic paroxysmal hemicrania and possibly cluster headaches are related to REM sleep. Whereas headache is associated with snoring and sleep apnea, morning headaches are not specific for any primary sleep disorder. Nevertheless, the management of the sleep disorder ameliorates both morning headache and migraine.Noxious stimuli administered into muscles during slow-wave sleep (SWS) result in decreases in delta and sigma but an increase in alpha and beta EEG frequencies during sleep. Noise stimuli that disrupt SWS result in unrefreshing sleep, diffuse musculoskeletal pain, tenderness, and fatigue in normal healthy subjects. Such symptoms accompany alpha EEG sleep patterns that often occur in patients with fibromyalgia. The alpha EEG patterns include phasic and tonic alpha EEG sleep as well as periodic K alpha EEG sleep or frequent periodic cyclical alternating pattern. Moreover, alpha EEG sleep, as well as sleep-related breathing disorder and periodic limb movement disorder, occur in some patients with fibromyalgia, rheumatoid arthritis and osteoarthritis. Depression and not alpha EEG sleep are features of somatoform pain disorder. Disturbances in sleep, pain behaviour and psychological distress influence return to work in workers who have suffered a soft tissue injury, e.g. low back pain. Patients with irritable bowel disorder have disturbed sleep and have increased REM sleep. In conclusion, there is a reciprocal relationship between sleep quality and pain. The recognition of disturbed or unrefreshing sleep influences the management of painful medical disorders.
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PMID:Sleep and pain. 1253 Oct 4

The anatomical states of the oral cavity and pharynx during mouth breathing in children with adenoid hypertrophy and in adults confirmed the speculation that mouth breathing is disadvantageous compared with nose breathing. In addition, comparison of the anatomical state between wakefulness and sleep in normal adults showed slight depression of the tongue root and slight narrowing of the oropharynx and hypopharynx during sleep. Obstructive sleep-disordered breathing occurs due to a variety of factors, such as paranasal sinus disease, tonsil and adenoid hypertrophy, hypertrophy and morphological abnormalities of the soft palate and palatine uvula, low-set soft palate, micrognathia, macroglossia, obesity and tongue root depression. Narrowing or obstruction of the middle pharynx and hypopharynx is more marked in patients with obstructive sleep-disordered breathing than in normal people and is especially marked during sleep. Therefore, morphological (i.e. anatomical) changes during mouth breathing may provide useful information for evaluating the pathology of snoring and sleep apnea.
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PMID:Anatomy of oral respiration: morphology of the oral cavity and pharynx. 1273 37


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