Population-based epidemiologic studies have uncovered the high prevalence and wide severity spectrum of undiagnosed obstructive sleep apnea, and have consistently found that even mild obstructive sleep apnea is associated with significant morbidity. Evidence from methodologically strong cohort studies indicates that undiagnosed obstructive sleep apnea, with or without symptoms, is independently associated with increased likelihood of hypertension, cardiovascular disease, stroke, daytime sleepiness, motor vehicle accidents, and diminished quality of life. Strategies to decrease the high prevalence and associated morbidity of obstructive sleep apnea are critically needed. The reduction or elimination of risk factors through public health initiatives with clinical support holds promise. Potentially modifiable risk factors considered in this review include overweight and obesity, alcohol, smoking, nasal congestion, and estrogen depletion in menopause. Data suggest that obstructive sleep apnea is associated with all these factors, but at present the only intervention strategy supported with adequate evidence is weight loss. A focus on weight control is especially important given the expanding epidemic of overweight and obesity in the United States. Primary care providers will be central to clinical approaches for addressing the burden and the development of cost-effective case-finding strategies and feasible treatment for mild obstructive sleep apnea warrants high priority.

Epidemiology of obstructive sleep apnea: a population health perspective.

The American Academy of Sleep Medicine (AASM) Sleep Apnea Definitions Task Force reviewed the current rules for scoring respiratory events in the 2007 AASM Manual for the Scoring and Sleep and Associated Events to determine if revision was indicated. The goals of the task force were (1) to clarify and simplify the current scoring rules, (2) to review evidence for new monitoring technologies relevant to the scoring rules, and (3) to strive for greater concordance between adult and pediatric rules. The task force reviewed the evidence cited by the AASM systematic review of the reliability and validity of scoring respiratory events published in 2007 and relevant studies that have appeared in the literature since that publication. Given the limitations of the published evidence, a consensus process was used to formulate the majority of the task force recommendations concerning revisions.The task force made recommendations concerning recommended and alternative sensors for the detection of apnea and hypopnea to be used during diagnostic and positive airway pressure (PAP) titration polysomnography. An alternative sensor is used if the recommended sensor fails or the signal is inaccurate. The PAP device flow signal is the recommended sensor for the detection of apnea, hypopnea, and respiratory effort related arousals (RERAs) during PAP titration studies. Appropriate filter settings for recording (display) of the nasal pressure signal to facilitate visualization of inspiratory flattening are also specified. The respiratory inductance plethysmography (RIP) signals to be used as alternative sensors for apnea and hypopnea detection are specified. The task force reached consensus on use of the same sensors for adult and pediatric patients except for the following: (1) the end-tidal PCO(2) signal can be used as an alternative sensor for apnea detection in children only, and (2) polyvinylidene fluoride (PVDF) belts can be used to monitor respiratory effort (thoracoabdominal belts) and as an alternative sensor for detection of apnea and hypopnea (PVDFsum) only in adults.The task force recommends the following changes to the 2007 respiratory scoring rules. Apnea in adults is scored when there is a drop in the peak signal excursion by ≥ 90% of pre-event baseline using an oronasal thermal sensor (diagnostic study), PAP device flow (titration study), or an alternative apnea sensor, for ≥ 10 seconds. Hypopnea in adults is scored when the peak signal excursions drop by ≥ 30% of pre-event baseline using nasal pressure (diagnostic study), PAP device flow (titration study), or an alternative sensor, for ≥ 10 seconds in association with either ≥ 3% arterial oxygen desaturation or an arousal. Scoring a hypopnea as either obstructive or central is now listed as optional, and the recommended scoring rules are presented. In children an apnea is scored when peak signal excursions drop by ≥ 90% of pre-event baseline using an oronasal thermal sensor (diagnostic study), PAP device flow (titration study), or an alternative sensor; and the event meets duration and respiratory effort criteria for an obstructive, mixed, or central apnea. A central apnea is scored in children when the event meets criteria for an apnea, there is an absence of inspiratory effort throughout the event, and at least one of the following is met: (1) the event is ≥ 20 seconds in duration, (2) the event is associated with an arousal or ≥ 3% oxygen desaturation, (3) (infants under 1 year of age only) the event is associated with a decrease in heart rate to less than 50 beats per minute for at least 5 seconds or less than 60 beats per minute for 15 seconds. A hypopnea is scored in children when the peak signal excursions drop is ≥ 30% of pre-event baseline using nasal pressure (diagnostic study), PAP device flow (titration study), or an alternative sensor, for ≥ the duration of 2 breaths in association with either ≥ 3% oxygen desaturation or an arousal. In children and adults, surrogates of the arterial PCO(2) are the end-tidal PCO(2) or transcutaneous PCO(2) (diagnostic study) or transcutaneous PCO(2) (titration study). For adults, sleep hypoventilation is scored when the arterial PCO(2) (or surrogate) is > 55 mm Hg for ≥ 10 minutes or there is an increase in the arterial PCO(2) (or surrogate) ≥ 10 mm Hg (in comparison to an awake supine value) to a value exceeding 50 mm Hg for ≥ 10 minutes. For pediatric patients hypoventilation is scored when the arterial PCO(2) (or surrogate) is > 50 mm Hg for > 25% of total sleep time. In adults Cheyne-Stokes breathing is scored when both of the following are met: (1) there are episodes of ≥ 3 consecutive central apneas and/or central hypopneas separated by a crescendo and decrescendo change in breathing amplitude with a cycle length of at least 40 seconds (typically 45 to 90 seconds), and (2) there are five or more central apneas and/or central hypopneas per hour associated with the crescendo/decrescendo breathing pattern recorded over a minimum of 2 hours of monitoring.

Rules for Scoring Respiratory Events in Sleep: Update of the 2007 AASM Manual for the Scoring of Sleep and Associated Events

Disordered breathing during sleep is associated with acute, unfavorable effects on cardiovascular physiology, but few studies have examined its postulated association with cardiovascular disease (CVD). We examined the cross-sectional association between sleep- disordered breathing and self-reported CVD in 6,424 free-living individuals who underwent overnight, unattended polysomnography at home. Sleep-disordered breathing was quantified by the apnea-hypopnea index (AHI)-the average number of apneas and hypopneas per hour of sleep. Mild to moderate disordered breathing during sleep was highly prevalent in the sample (median AHI: 4.4; interquartile range: 1.3 to 11.0). A total of 1,023 participants (16%) reported at least one manifestation of CVD (myocardial infarction, angina, coronary revascularization procedure, heart failure, or stroke). The multivariable-adjusted relative odds (95% CI) of prevalent CVD for the second, third, and fourth quartiles of the AHI (versus the first) were 0.98 (0.77-1.24), 1.28 (1.02-1.61), and 1.42 (1.13-1.78), respectively. Sleep-disordered breathing was associated more strongly with self-reported heart failure and stroke than with self-reported coronary heart disease: the relative odds (95% CI) of heart failure, stroke, and coronary heart disease (upper versus lower AHI quartile) were 2.38 (1.22-4.62), 1.58 (1.02- 2.46), and 1.27 (0.99-1.62), respectively. These findings are compatible with modest to moderate effects of sleep-disordered breathing on heterogeneous manifestations of CVD within a range of AHI values that are considered normal or only mildly elevated.

Sleep-disordered breathing and cardiovascular disease: cross-sectional results of the Sleep Heart Health Study.

Restless legs syndrome: diagnostic criteria, special considerations, and epidemiology. A report from the restless legs syndrome diagnosis and epidemiology workshop at the National Institutes of Health.

Caffeine is the most widely consumed behaviorally active substance in the world. Almost all caffeine comes from dietary sources (beverages and food), most of it from coffee and tea. Acute and, especially, chronic caffeine intake appear to have only minor negative consequences on health. For this

Actions of Caffeine in the Brain with Special Reference to Factors That Contribute to Its Widespread Use

EEG arousals: Scoring rules and examples. A preliminary report from the Sleep Disorders Atlas Task Force of the American Sleep Disorder Association

The 1968 Rechtschaffen and Kales (R & K) sleep scoring man- ual was published 15 years after REM sleep was discovered. Advances in the ensuing 28 years warranted a re-look at visual scoring of sleep stages. This paper describes the work of the AASM Visual Scoring Task Force, including methodology, a literature review and the rationale behind the new rules. Reliability studies of R & K scoring were reviewed; reliabil- ity was low for stage one and moderate for slow wave sleep. Evidence indicated that K complexes and slow waves are expressed maximal fron- tally, spindles centrally and alpha rhythm over the occipital region. Three derivations of EEG, two of electro-oculography, and one of chin EMG were recommended. Scoring by 30-second epochs was retained. New terminology for sleep stages was proposed. Attenuation of alpha rhythm was determined to be the most valid electrophysiological marker of sleep onset. Alternative measures were proposed for non-alpha generating subjects. K complexes associated with arousals were determined to be insufficient alone to define the new stage N2. No evidence was found to justify dividing slow wave sleep into two stages. No reasons were found to alter the current slow wave amplitude criteria at any age. The phenomena of REM sleep were defined. The rules for defining onset and termination of REM sleep periods were simplified. Movement time was eliminated and major body movements defined. Studies are needed to test the reliability of the new rules. Future advances in technology may require modification of these rules with time.

The visual scoring of sleep in adults

Hyperarousal and insomnia: state of the science.

Groups of 10 objectively defined insomniacs and age-, sex- and weight-matched normal sleepers were evaluated on sleep, performance, mood, personality and metabolic measures over a 36-hour sleep laboratory stay. Insomniacs were defined to have increased wake time during the night but also had decreased stage 2 and rapid eye movement sleep. As expected insomniacs reported increased confusion, tension and depression and decreased vigor on the profile of mood states mood scale throughout the evaluation period as compared to the normals. Insomniacs also had decreased memory ability on the short-term memory test and the MAST. These performance and mood differences were not secondary to sleepiness because the insomniacs also had significantly increased multiple sleep latency test (MSLT) values throughout the evaluation period. In conjunction with the consistent mood, performance and MSLT differences during the day and the sleep differences at night, whole body VO2, measured at intervals across the day and throughout one night of sleep, was consistently elevated at all measurement points in the insomniacs as compared to the normals. The nocturnal increase in metabolic rate remained even after metabolic values from periods during the night containing wake time or arousals were eliminated from the data set. It was concluded that patients who report chronic insomnia may suffer from a more general disorder of hyperarousal (as measured here by a 24-hour increase in metabolic rate) that may be responsible for both the daytime symptoms and the nocturnal poor sleep. Future studies need to explore 24-hour insomnia treatment strategies that decrease hyperarousal.

/pdf/24-hour-metabolic-rate-in-insomniacs-and-matched-normal-37fb2e8jxy.pdf

24-Hour metabolic rate in insomniacs and matched normal sleepers.

Summary: Data from recent laboratory studies indicate that nocturnal sleep periods reduced by as little as 1.3 to 1.5 hours for 1 night result in reduction of daytime alertness by as much as 32% as measured by the Multiple Sleep Latency Test (MSLT). Other data document that 1) 170/0--57% of normal young adults have MSLT latencies of ::;5.5 minutes, whereas ::;50% have MSLT values of ~ 10 minutes and 2) 28°/0--29% of young adults reported normally sleeping ::;6.5 hours on each weeknight. More extensive reduction of daily sleep amount is seen in night­ shift workers. A minimum of 2%-4% of middle-aged adults have hypersomnolence associated with sleep apnea. Together, these data show that significant sleep loss exists in one-third or more of normal adults, that the effects are large and replicable and that similar effects can be produced in just I night in the laboratory. In light of the magnitude of this sleep debt, it is not surprising that fatigue is a factor in 57% of accidents leading to the death of a truck driver and in 10% of fatal car accidents and results in costs of up to 56 billion dollars per year. A recent sleep extension study suggests that the average underlying sleep tendency in young adults is about 8.5 hours per night. By comparison, the average reported sleep length of 7.2-7.4 hours is deficient, and common sleep lengths of ::;6.5 hours can be disastrous. We must recognize the alertness function of sleep and the increasing consequences of sleepiness with the same vigor that we have come to recognize the societal impact of alcohol. Key Words: Sleep deprivation-Sleepiness-Sleep disorders- Work schedule tolerance. Weare in the midst of a golden age of discovery of the intricate interrelationship between our nocturnal sleep process and our level of daytime function. Fueled by the discovery of the tremendous incidence of sleep apnea and periodic leg movements in the population, the relationship between fragmented sleep and residual sleepiness, as well as the increased ability to measure the level of objective sleepiness with an objective test [the Multiple Sleep Latency Test (MSLT)] and in am­ bulatory environments, the pervasive role of excessive sleepiness in our society is becoming apparent. Much literature documents the negative effects of sleep deprivation on a wide range of psychomotor per­ formance tasks and mood variables. For the sake of simplicity, the primary outcome measure reported in this paper will be MSL T. However, the MSL T findings reported are consistent with similar changes in a broad range of abilities, including reaction time, short-term memory, vigilance and mood (1). Many empirical and applied studies have provided evidence for our national sleep debt. The degree of our

Michael H. Bonnet

Papers

EEG arousals: Scoring rules and examples. A preliminary report from the Sleep Disorders Atlas Task Force of the American Sleep Disorder Association

The visual scoring of sleep in adults

Hyperarousal and insomnia: state of the science.

24-Hour metabolic rate in insomniacs and matched normal sleepers.

We are chronically sleep deprived