Cause Of Daytime Sleepiness Research Articles

Behavioral KSA Intervention Class to Boost Positive Airway Pressure Adherence Among Active Duty Military Personnel With Obstructive Sleep Apnea.

Obstructive sleep apnea (OSA) is a treatable cause of daytime sleepiness and associated medical problems that can negatively impact soldier readiness and performance. This study examined adherence to positive airway pressure (PAP) by soldiers who were newly diagnosed with OSA and prescribed PAP therapy and participated in a Knowledge, Skills, and Attitudes (KSA) behavioral intervention class. The KSA was a one-time, interactive 90-minute class attended by up to 10 patients per class. PAP adherence was examined using Medicare standard at 30-, 60-, 90-, and 180 days post class. The analytic sample comprised 379 active duty patients (93% men; mean age 40.21 ± 8.06) categorized into 3 groups: KSA (n = 235), did not show (DNS; n = 61), and mandatory education class (MEC; n = 83). The MEC group comprised patients from an education class in a previous year. Baseline scores on the apnea hypopnea index, body mass index, sleepiness, insomnia severity, and age were non-significant among the 3 groups. At 30 days, significantly more patients in KSA (48%) and MEC (51%) were adherent than the DNS group (16%). At 60 days, the adherence rates for the KSA, DNS, and MEC were significantly different at 39%, 22%, and 27%, respectively. At 90- and 180 days, the adherence rates among the KSA, DNS, and MEC groups did not differ significantly at 34%, 17%, and 26% (90 days) and 34%, 27%, and 25% (180 days), respectively. Consistently, more patients in KSA were adherent than those in DNS and MEC, except at 30 days. Additionally, adherence rates for KSA intervention declined more gradually over the 6 month period. The mean PAP usage on nights used was 4.6 hours that computed to a 34% non-use rate based on an optimal 7-hour/night sleep time. KSA could be a behavioral intervention that enhances PAP adherence with a booster session implemented at the 90 days mark.

Comorbidities and Laryngeal Cancer in Patients with Obstructive Sleep Apnea: A Review.

Introductions: The global prevalence of obstructive sleep apnea shows that this disease appears in 1 billion people, with the prevalence exceeding 50% in some countries. Treatment is necessary to minimize negative health impacts. Obstructive sleep apnea (OSA) is defined as a cause of daytime sleepiness, as well as a clinical manifestation of sleep-disordered breathing. In the literature, there are numerous controversial studies regarding the etiology of this condition, but it is universally accepted that reduced activity in the upper airway muscles plays a significant role in its onset. Additionally, OSA has been associated with a series of comorbidities, such as type II diabetes, metabolic syndrome, and cardiovascular and pulmonary conditions, as well as head and neck tumors, especially oropharyngeal and laryngeal tumors. This is a review of the subject of OSA that considers several aspects: an analysis of the comorbidities associated with OSA, the involvement of tumor pathology in the onset of OSA, and the association of OSA with various types of laryngeal cancers. Additionally, it includes an evaluation of postoperative and medical outcomes for patients with OSA and laryngeal tumors treated surgically and medically, including chemotherapy. Relevant Sections: By taking into consideration the stated objective, a systematic analysis of the available literature was conducted, encompassing the PubMed, Medline, and Scopus databases. The evaluation was based on several keywords, including head and neck cancer, diabetes, diabetic, overlap syndrome, cardiovascular conditions, laryngeal neoplasm, radiotherapy, and chemotherapy, as well as the concept of quality of life in laryngectomized patients and patients with OSA. Discussions: The review evaluates the involvement of OSA in the presence of comorbidities, as well as the increased incidence of OSA in patients with laryngeal cancer. It is important to note that surgical and post-surgical treatment can play a significant role in triggering OSA in these patients. Conclusions: The studies regarding the correlations between OSA, comorbidities, and head and neck tumors indicate a significantly increased risk of OSA in association with conditions such as diabetes, metabolic syndrome, cardiovascular diseases, and head and neck tumors, particularly laryngeal tumors. This association has a physio-pathological basis. The various surgical methods followed by radiation and chemotherapy for tumor treatment do not exclude an increased risk of developing OSA after treatment. This significantly influences the quality of life of patients who survive these types of tumors. Future directions: Due to the multiple comorbidities associated with OSA, the extension of polysomnography associated with investigations during sleep, such as drug-induced sleep endoscopy, represents a tendency for the early diagnosis of this pathology, which affects the quality of life of these patients. Patients with head and neck cancer are at high risk of developing obstructive sleep apnea; this is why it is necessary to expand the polysomnographic investigation of these patients after surgical procedures or after radiotherapy and chemotherapy.

Clinical and instrumental features in 82 patients with insufficient sleep syndrome.

Insufficient sleep syndrome possibly represents the worldwide leading cause of daytime sleepiness, but remains poorly recognised and studied. The aim of this case series is to comprehensively describe a cohort of patients with insufficient sleep syndrome. Eighty-two patients were studied concerning demographic and socio-economic features, medical, psychiatric and sleep comorbidities, substance use, sleep symptoms, actigraphy, video-polysomnography, multiple sleep latency tests and treatment. The typical patient with insufficient sleep syndrome is a middle-aged adult (with no difference of gender), employed, who has a family, often carrying psychiatric and neurological comorbidities, in particular headache, anxiety and depression. Other sleep disorders, especially mild sleep apnea and bruxism, were common as well. Actigraphy was a valuable tool in the characterisation of insufficient sleep syndrome, showing a sleep restriction during weekdays, associated with a recovery rebound of night sleep during weekends and a high amount of daytime sleep. An over- or underestimation of sleeping was common, concerning both the duration of night sleep and daytime napping. The average daily sleep considering both daytime and night-time, weekdays and weekends corresponds to the recommended minimal normal duration, meaning that the burden of insufficient sleep syndrome could mainly depend on sleep fragmentation and low quality. Sleep efficiency was elevated both in actigraphy and video-polysomnography. Multiple sleep latency tests evidenced a tendency toward sleep-onset rapid eye movement periods. Our study offers a comprehensive characterisation of patients with insufficient sleep syndrome, and clarifies their sleeping pattern, opening avenues for management and treatment of the disorder. Current options seem not adapted, and in our opinion a cognitive-behavioural psychotherapy protocol should be developed.

Whoop there it is: decoding sleep, cirrhosis, and HE.

Sleep abnormalities in cirrhosis and HE have long been an area of interest.1 Sleep disturbances are highly prevalent in patients with cirrhosis, and HE is often characterized as a reversal of the sleep-wake cycle.2 As assessed by validated questionnaires, such as the Pittsburgh Sleep Quality Index, studies have reported over 80% of patients with cirrhosis suffer from poor sleep and associated low quality of life scores.3 Patients with cirrhosis have impaired hepatic clearance of melatonin, a major regulator of the sleep-wake cycle. Higher daytime serum melatonin and peak levels later in the day contribute to daytime sleepiness, and nighttime arousal observed in many patients with HE.4 Not only do patients with cirrhosis suffer from disrupted sleep timing, but conventional methods of monitoring sleep, that is, polysomnography (PSG), have also demonstrated disrupted sleep architecture resulting in less restorative sleep.5,6 Patients with cirrhosis have been found to have decreased sleep efficiency, decreased rapid eye movement (REM) sleep, and increased sleep latency compared with healthy controls.7 These disturbances appear to increase in severity along with more advanced cirrhosis.7 Abnormal sleep architecture, including decreased REM and slow wave sleep on PSG, has also been observed in patients with covert HE (CHE) compared with controls.8 In this issue of Hepatology Communications, Buckholz and colleagues remotely monitored sleep in 25 patients with cirrhosis for almost 3000 nights of data, using the Whoop fitness tracker. They found that patients with CHE were more likely to experience decreased restorative sleep, especially lowered REM sleep. The team provided insight into sleep characteristics and cycle changes over almost 6 months. Furthermore, the authors discovered that these disturbances, such as the percent of time spent in REM sleep, vary from night to night. These are clear advantages of using this technique over traditional PSG, and this unique study furthers the trend of extending the patient-clinician relationship beyond the clinic into their homes.9 Although the study excluded patients with current treatment of overt HE, there remains a major overlap in patients with obstructive sleep apnea (OSA), HE, and those with disordered sleep due to altered melatonin metabolism secondary to cirrhosis (Fig. 1).10 As obesity rates rise, NAFLD represents an increasing proportion of the population with cirrhosis, and OSA as an etiology of sleep disturbances is likely concordantly increasing in prevalence.7 Symptoms such as daytime sleepiness, fatigue, and nighttime arousal are nonspecific, making diagnosis challenging based on the interview alone.10 Adding to the challenge of making the appropriate diagnosis, sleep architecture is disrupted in both OSA and cirrhosis. When using PSG to compare patients with OSA alone to patients with both OSA and cirrhosis, patients had similar sleep architecture with no significant differences in time spent in restorative sleep, such as REM sleep or slow wave sleep.8 In addition, patients with OSA without cirrhosis may have abnormal results on common tests for CHE, including inhibitory control, number connection, and digit symbol tests.11FIGURE 1: Sleep apnea and disordered sleep secondary to melatonin dysregulation share greater symptom overlap than with covert HE (CHE). Not all daytime sleepiness, fatigue, nighttime arousal, and disrupted sleep architecture in patients with cirrhosis can be attributed to CHE alone.Although appropriate identification of the cause of daytime sleepiness in patients with cirrhosis is challenging, it is critical in determining the next steps in management. Patients with OSA and cirrhosis treated with continuous positive airway pressure have demonstrated improvement in PSQI and improvement in executive function on inhibitory control testing.11 In patients with overt and CHE, there is mixed evidence that traditional HE therapies affect sleep parameters or architecture.5,12 Given the relative overlap in symptoms among OSA, disordered sleep secondary to melatonin dysregulation, and CHE, as well as the lack of specificity of current tests for CHE, clinicians should consider testing at-risk patients for sleep apnea and employing multiple modalities for appropriate CHE diagnosis. Although more work is needed, encouraging monitoring of sleep architecture remotely to gauge response to therapy, as outlined in by Buckholz and colleagues, may be an important first step.

Cerebrospinal fluid monoamine levels in central disorders of hypersomnolence.

Whether the cause of daytime sleepiness in narcolepsy type 1 (NT1) is a direct consequence of the loss of orexin (ORX) neurons or whether low orexin reduces the efficacy of the monoaminergic systems to promote wakefulness is unclear. The neurobiology underlying sleepiness in other central hypersomnolence disorders, narcolepsy type 2 (NT2), and idiopathic hypersomnia (IH), is currently unknown. Eleven biogenic amines including the monoaminergic neurotransmitters and their metabolites and five trace amines were measured in the cerebrospinal fluid (CSF) of 94 drug-free subjects evaluated at the French National Reference Center for Narcolepsy: 39 NT1(orexin-deficient) patients, 31 patients with objective sleepiness non orexin-deficient (NT2 and IH), and 24 patients without objective sleepiness. Three trace amines were undetectable in the sample: tryptamine, octopamine, and 3-iodothyronamine. No significant differences were found among the three groups for quantified monoamines and their metabolites in crude and adjusted models; however, CSF 5-hydroxyindoleacetic acid (5-HIAA) levels tended to increase in NT1 compared to other patients after adjustment. Most of the biomarkers were not associated with ORX-A levels, clinical or neurophysiological parameters, but a few biomarkers (e.g. 3-methoxy-4-hydroxyphenylglycol and norepinephrine) correlated with daytime sleepiness and high rapid eye movement (REM) sleep propensity. We found no striking differences among CSF monoamines, their metabolites and trace amine levels, and few associations between them and key clinical or neurophysiological parameters in NT1, NT2/IH, and patients without objective sleepiness. Although mostly negative, these findings are a significant contribution to our understanding of the neurobiology of hypersomnolence in these disorders that remain mysterious and deserve further exploration.

Hypersomnolence in Children and Adolescents: Causes, Assessment, and Management

Hypersomnolence is common in children and adolescents and its etiology is multifactorial. Developmental changes in melatonin release and slower accumulation of sleep pressure lead to a preference for later sleep times, which conflicts with early school start times leading to increased daytime sleepiness. Although the most common cause of daytime sleepiness in children and adolescents is insufficient sleep, central disorders of hypersomnolence can also manifest in these age groups. Excessive sleepiness could also result from other disorders such as sleep apnea, psychiatric illnesses, and medication use. Hypersomnolence should be evaluated by careful history taking, and when necessary additional tests including actigraphy, polysomnography, and multiple sleep latency test may need to be performed. In this review, we discuss the prevalence of hypersomnolence in children and adolescents, common etiological factors, and assessment of excessive sleepiness. We also discuss management strategies for hypersomnolence. [ Psychiatr Ann. 2019;49(12):529–534.]

Metabolomic fingerprinting approach to sleep apnea disorder in human plasma

Obstructive sleep apnea/hypopnea syndrome (OSAHS) is becoming a major cause of morbidity and it is the most common medical cause of daytime sleepiness. Metabolomics fingerprinting is able to achieve through the identification of novel biomarkers the comprehensive characterization of the entire metabolome of a disease, with the final aim to predict response to different therapies and outcomes and increase the knowledge regarding the pathological bases underlying sleep disorders. A non-targeted metabolomic study of plasma from 42 OSAHS patients and 16 healthy subjects was performed. The individual analytical fingerprints obtained by gas chromatography coupled to mass spectrometry (GC-Q-MS) were deconvoluted using AMDIS software and identified by the information compiled in Fiehn’s and NIST libraries. The same set of samples were analysed by liquid chromatography coupled with quadrupole time-of-flight mass spectrometer (LC-QTOF-MS). Profiles were aligned and filtered using Mass Profiler Professional. Univariate and multivariate statistical analysis were applied for screening potential biomarkers. OPLS-DA plots obtained using SIMCA-P+, based on GC-MS and LC-MS data, show clear separation between control and severe patient. Changes in the metabolic profiles of amino acids were found between both groups, showing an increase trend, including some branched-chain amino acid (BCAAs). Different metabolic pathways could be altered under conditions related to insulin resistance, such as metabolic syndrome and obesity causing alterations in branched-chain keto acid dehydrogenase that could be reflected in the increased level of BCAAs. Phosphocholine and compounds related to the glycine and glutamate metabolism were putatively assigned. Glutamate receptors have recently being found present in the lung (NMDA receptors) causing a wide range of damage (lipid peroxidation, DNA bridges broken, activation of the system caspases, loss of energy and cell death). These findings reflect considerable differences in individual metabolite fingerprints of OSAHS patients and open the possibility of identifying novel biomarkers associated to sleep disorders, that can help to uncover the complexity underlyingthe metabolic alterations occurring in OSAHS. The research leading to these results has received funding from the [European Union] Seventh Framework Programme [FP7/2007- 2013] under grant agreement n o 264864”.

A practical guide to the therapy of narcolepsy and hypersomnia syndromes.

SummaryNarcolepsy and other syndromes associated with excessive daytime sleepiness can be challenging to treat. New classifications now distinguish narcolepsy/hypocretin deficiency (also called type 1 narcolepsy), a lifelong disorder with well-established diagnostic procedures and etiology, from other syndromes with hypersomnolence of unknown causes. Klein-Levin Syndrome, a periodic hypersomnia associated with cognitive and behavioral abnormalities, is also considered a separate entity with separate therapeutic protocols. Non hypocretin-related hypersomnia syndromes are diagnoses of exclusion. These diagnoses are only made after eliminating sleep deprivation, sleep apnea, disturbed nocturnal sleep, and psychiatric comorbidities as the primary cause of daytime sleepiness. The treatment of narcolepsy/hypocretin deficiency is well-codified, and involves pharmacotherapies using sodium oxybate, stimulants, and/or antidepressants, plus behavioral modifications. These therapies are almost always needed, and the risk-to-benefit ratio is clear, notably in children. Detailed knowledge of the pharmacological profile of each compound is needed to optimize use. Treatment for other syndromes with hypersomnolence is more challenging and less codified. Preferably, therapy should be conservative (such as modafinil, atomoxetine, behavioral modifications), but it may have to be more aggressive (high-dose stimulants, sodium oxybate, etc.) on a case-by-case, empirical trial basis. As cause and evolution are unknown in these conditions, it is important to challenge diagnosis and therapy over time, keeping in mind the possibility of tolerance and the development of stimulant addiction. Kleine-Levin Syndrome is usually best left untreated, although lithium can be considered in severe cases with frequent episodes. Guidelines are provided based on the literature and personal experience of the author.Electronic supplementary materialThe online version of this article (doi:10.1007/s13311-012-0150-9) contains supplementary material, which is available to authorized users.

What is this thing called somnolence?

In 1929, Cole Porter composed, for a musical comedy, a song called “What Is This Thing Called Love?”, which became a great classic in jazz music [1]. The musical comedy had a suggestive title, very appealing for modern pneumologists: Wake Up and Dream . For many people suffering from obstructive sleep apnoea, we are able nowadays to help them to wake up refreshed, out of dreams or nightmares, and able to face the new day fully awake, fit to burst [2]. This is the usual result of sleeping with a mask connected to a continuous positive pressure device [3]. However, a small number of patients compliant to continuous positive airway pressure (CPAP) therapy, using it every night and all night, remain abnormally sleepy. They declare persistent severe somnolence and fatigue [4, 5]. In this issue of the European Respiratory Journal , Vernet et al. [6] present the results of an extraordinary effort to dissect, define and identify what causes somnolence in these patients. They studied 20 patients with CPAP-treated obstructive sleep apnoea and persistent complains of daytime sleepiness and fatigue, and compared them with 20 other well-matched patients that had no residual sleepiness, and to 20 matched normal subjects. They made every possible effort to exclude other known causes of daytime sleepiness and fatigue, from narcolepsy to restless leg syndrome, depression, behavioural sleep restriction, chronic use of sedative drugs, alcoholism, night shift work, and neurological and psychiatric diseases. Once they were sure that these patients had only …

Identification of Electroencephalographic Arousals in Multichannel Sleep Recordings

Electroencephalographic arousals are defined as abrupt shifts in electroencephalogram (EEG) frequency during sleep. Occurrence of arousals results in fragmented sleep, being one of the most important causes of daytime sleepiness among sleep disorders. Detection of arousals requires a polysomnographic (PSG) recording to be made during the patient's sleep. The resulting PSG is then analyzed offline by the physician. This is a time-consuming task, hence, automation of this process is pursued. The analysis, which involves the correlation of various events in time occurring among the different channels, in conjunction with the complexity of the related biomedical signals, makes this task also difficult to achieve in the computer algorithm. In this paper, we present a method for the detection of EEG arousals working on multichannel PSGs. The algorithm detects arousals using the information available through two EEG channels and the electromyography. A signal-processing technique is first proposed for the analysis of biomedical signals and extraction of relevant information. Individual events are detected from the signals and subsequently are related in time. Finally, a classification phase carries out the final decision on the presence of the event. Classifiers based on Fisher's linear and quadratic discriminants, support vector machines and artificial neural networks are compared at this phase. Experiments conducted on 20 patients reported a sensitivity and specificity respectively of 0.86 and 0.76 in the detection of the arousal events.

Data mining techniques for detection of sleep arousals

Arousals are considered one of the main causes of daytime sleepiness. They impede the proper flow of sleep cycles and cause weariness. Manual scoring of arousals is time-consuming, requires expert knowledge, and has high inter-scorer variability. A major difficulty in detecting arousals automatically is the existing variance across patients. Based on data mining techniques, we present a different approach to the automatic detection of arousals that overcomes the hurdle of differences in signal characteristics across patients. Offline we used a training-set of adult patients to define a set of general rules to detect arousals (termed meta-rules). This was done by analyzing the correlations between occurrences of arousals and the EEG, EMG, pulse and SaO2 signals as follows: (1) each signal was mathematically projected into several spaces (termed projected-signals); (2) from each such projected-signal, the algorithm extracted time points that indicated meaningful changes (termed critical-points); (3) data mining techniques were applied to all the critical-points to discover patterns of repeating behavior; (4) classes of patterns which were highly correlated with manually scored arousals were formalized as meta-rules. Online we used a test-set of adult patients from two other different sleep laboratories. Using the meta-rules, the algorithm extracted individual rules for each patient (termed actual-rules), and used them to automatically detect the patients’ arousals. These arousals were significantly correlated ( R = 0.88, p < 0.0001; sensitivity = 75.2%, positive predictive value = 76.5%) with those detected manually by experts. Since the total number of arousals is a measure of sleep quality, this algorithm constitutes a novel approach to automatically estimate sleep quality.

Gender differences in obstructive sleep apnea and treatment implications

Obstructive sleep apnea (OSA) is a common cause of daytime sleepiness for millions of Americans. It is also a disease associated with an increased likelihood of hypertension, cardiovascular disease, stroke, daytime sleepiness, motor vehicle accidents, and diminished quality of life. A number of population-based studies have shown that OSA is more common in men than in women and this discrepancy is often evident in the clinical setting. There are a number of pathophysiological differences to suggest why men are more prone to the disease than women. Although the exact mechanisms are unknown, differences in obesity, upper airway anatomy, breathing control, hormones, and aging are all thought to play a role. The purpose of this review was to examine the literature on gender differences in OSA and to analyze whether or not these differences in pathogenic mechanisms affect diagnosis or treatment.

An Obese Female with Prader-Willi Syndrome and Daytime Sleepiness

An Obese Female with Prader-Willi Syndrome and Daytime Sleepiness

Polysomnographic and Clinical Correlates of Behaviorally Observed Daytime Sleep in Nursing Home Residents

The causes of daytime sleepiness among nursing home residents have not been well recognized. This study examines clinical and polysomnographic factors that are associated with daytime sleepiness among nursing home residents. One hundred seventy-four nursing home residents from eight nursing homes in Atlanta, Georgia, participated in the study. Demographic and clinical data were obtained from medical records and assessment of participants obtained by trained research staff. Daytime sleepiness was determined by behavioral sleep-wake observation performed every 15 minutes. Overnight polysomnography was performed in a subgroup of the sample. The mean +/- standard deviation age was 83.4 +/- 8.8 years, and 136 participants were women (78%). The mean percentage +/- standard deviation of behavioral observations with sleep (BOS%) was 19.5 +/- 13.3%. Participants who were able to ambulate independently had significantly lower BOS% (14.2 +/- 9.6 vs 21.2 +/- 6.0, p =.001). Mini-Mental State Examination score was negatively correlated with BOS% (rho = -.279, p =.001). Among 48 participants who had polysomnography, sleep latency, total sleep time, wake after sleep onset, and sleep efficiency were not associated with BOS%. There was a significant negative correlation between BOS% and percentage of time spent in rapid eye movement sleep (rho = -.367, p =.010). Linear regression analyses, with BOS% as the dependent variable, showed that percentage of time spent in rapid eye movement sleep was the only variable independently predicting BOS%. Absence of association between BOS% and nocturnal sleep suggests that the causes of daytime sleepiness and nocturnal sleep problems may not be related. This finding may have important implications for interventions that aim to reduce daytime sleepiness among nursing home residents.

Risk of traffic accidents in patients with sleep-disordered breathing: reduction with nasal CPAP.

Sleepiness whilst driving constitutes a road safety risk. Sleep-related breathing disorders are the most frequent medical cause of daytime sleepiness, and untreated patients with this condition have been shown to be at a higher risk of having accidents while driving. This study addressed the question of the extent to which treatment of sleep-disordered breathing by nasal continuous positive airway pressure (nCPAP) is related to changes in patient's accident risk. Seventy eight male patients requiring treatment of sleep-related breathing disorders with nCPAP were enrolled in the study. The protocol included a questionnaire dealing with alertness-related problems while driving, an 80 min vigilance test, and the Multiple Sleep Latency Test. These baseline evaluations were repeated after 1 year of treatment with nCPAP. Fifty nine patients completed the study. The accident rate was significantly decreased from 0.8 per 100,000 km (untreated) to 0.15 per 100,000 km with nCPAP treatment. Variables that were considered to be likely to increase accident risk (sleeping spells, fatigue, vigilance test reaction time, daytime sleep latency) also improved with treatment. We conclude that treatment of sleep-disordered breathing by nasal continuous positive airway pressure is related to reduction in patient motor vehicle accident rates, probably due to the reversal of excessive daytime sleepiness.

The sleep apnoea syndrome in obesity: risk of sudden death

A total of 34 severely obese men with a history of heavy snoring and excessive daytime sleepiness indicative of obstructive sleep apnoea syndrome (OSAS) were studied prospectively. Their mean age was 46 years, and mean body mass index was 41.6 kg m-2. During a 4-year follow-up, 15% (5/34) of these subjects died (three cases of acute myocardial infarction and two cases of pulmonary oedema), all of them suddenly and unexpectedly, outside hospital. On autopsy the degree of atherosclerosis was found to be moderate in all cases. In 68% (15/22) of the men a pathological apnoea index (mean value 46 +/- 20) confirmed the OSAS diagnosis. Exercise tests and neurological examinations did not reveal any other causes of daytime sleepiness. Mean blood pressure at rest and during exercise was normal, and mean serum lipid and blood glucose levels were normal. Spirometry revealed intrapulmonary restrictive changes that could not be attributed to the heavy thoracic wall. Compliance was reduced to about 50% of reference values, and the mean pCO2 level (5.8 kPa) was close to the upper reference limit. Blood tests suggested that high alcohol consumption may be an important factor contributing to OSAS. These results demonstrate that morbidly obese men with a history of OSAS have a high risk of sudden cardiovascular death, despite the absence of other conventional risk factors.