Weak association between sleep bruxism and obstructive sleep apnea. A sleep laboratory study

Purpose

No definitive associations or causal relationships have been determined between obstructive sleep apnea-hypopnea (OSAH) and sleep bruxism (SB). The purpose of this study was to investigate, in a population reporting awareness of both OSAH and SB, the associations between each specific breathing and jaw muscle event.

Methods

Polysomnography and audio–video data of 59 patients reporting concomitant OSAH and SB history were analyzed. Masseteric bursts after sleep onset were scored and classified into three categories: (1) sleep rhythmic masticatory muscle activity with SB (RMMA/SB), (2) sleep oromotor activity other than RMMA/SB (Sleep-OMA), and (3) wake oromotor activity after sleep onset (Wake-OMA).

Spearman’s rank correlation coefficient analyses were performed. Dependent variables were the number of RMMA/SB episodes, RMMA/SB bursts, Sleep-OMA, and Wake-OMA; independent variables were apnea-hypopnea index (AHI), arousal index(AI), body mass index(BMI), gender, and age.

Results

Although all subjects had a history of both SB and OSAH, sleep laboratory results confirmed that these conditions were concomitant in only 50.8 % of subjects. Moderate correlations were found in the following combinations (p?<?0.05); RMMA/SB episode with AI, RMMA/SB burst with AI and age, Sleep-OMA burst with AHI, and Wake-OMA burst with BMI.

Conclusions

The results suggest that (1) sleep arousals in patients with concomitant SB and OSAH are not strongly associated with onset of RMMA/SB and (2) apnea-hypopnea events appear to be related to higher occurrence of other types of sleep oromotor activity, and not SB activity. SB genesis and OSAH activity during sleep are probably influenced by different mechanisms.

     

Actimetry in sleep medicine

Actigraphy is more and more used in the longterm record of sleep of patients with insomnia. The correlation with data from polysomnography is reasonable for parameters like total sleep period (TSP) with r = 0,95-0,97 in healthy controls and r = 0,77-0,91 in patients. However for parameters, which inform about sleep fragmentation like wake after sleep onset (WASO) the correlation is not satisfieing with r = 0,87 in healthy controls and r = 0,49-0,63 in patients with fragmented sleep. The question is therefore, if actigraphs are really more useful in the record of sleep in patients with insomnia and fragmented sleep than sleep calenders.     

Effect of sleep position on sleep apnea and parafunctional activity

Parafunctional activity (toothgrinding, toothclenching and bruxism) is a common problem which may lead to masticatory muscle and temporomandibular joint pain, and may result from sleep arousal or disturbances. Sleep apnea is another common sleep disorder which results in disrupted sleep architecture and frequent arousals. Because sleep apnea leads to sleep arousals, and because sleep arousals are thought to result in increased parafunctional activity, we undertook the present study to determine the relationship between sleep apnea and parafunctional activity. We were also interested in assessing the effects of sleep posture on sleep disordered breathing and parafunctional activity. We prospectively studied 24 patients who were referred to the clinical sleep apnea laboratory for study. They underwent standard nocturnal polysomnographic examination; in addition, masticatory activity was measured with a masseter electromyogram. Patients slept in the supine and lateral decubitus positions. Nocturnal clenching was slightly higher in patients with sleep apnea than those without (12.2 vs 7.6 clenches/hr, p = 0.18), and there was a correlation between the clench index (CI) and apnea plus hypopnea index (A + HI) by linear regression (r = 0.49, p less than 0.05). There were significant falls in both the A + HI (64.4 +/- 28.8 vs 36.5 +/- 36.7, p = 0.02) and CI (12.5 +/- 12.1 vs 7.0 +/- 8.6, p = 0.04) in the lateral decubitus vs supine sleeping positions. We conclude that there is an association between obstructive sleep apnea and parafunctional activity, that sleep position affects the incidence of both sleep disordered breathing and parafunctional activity, and that analysis of apneas and hypopneas in both supine and lateral decubitus sleeping positions may be helpful.     

Apnea duration and hypoxemia during REM sleep in patients with obstructive sleep apnea

Nocturnal sleep studies of 12 patients with obstructive sleep apnea and a matched control group of 12 subjects without the sleep apnea syndrome were analyzed to compare arterial oxyhemoglobin saturation (SaO2) during REM and non-REM sleep. Mean percentage of total sleep time spent in REM sleep was not significantly different in patients with obstructive sleep apnea and in subjects without significant apnea (14.2 +/- SEM 2.2 percent in patients vs 12.0 +/- 2.2 percent in nonapnea subjects). Apneas were longer during REM than non-REM sleep in all 12 patients (p less than 0.01). Oxyhemoglobin desaturations were more frequent during REM than non-REM sleep in both apnea patients and the control subjects. In addition, there was a greater mean fall in SaO2 per desaturation episode in both the apnea patients and non-apnea subjects. We conclude: 1) sleep apneas are longer during REM sleep than non-REM sleep in patients with obstructive sleep apnea; 2) hypoxemia is greater during REM sleep than non-REM sleep in subjects with and without the sleep apnea syndrome.     

Fibromyalgia and sleep

Chronic pain in fibromyalgia patients, together with its associated symptoms and co-morbidities, is now considered a result of dysregulated mechanisms in the central nervous system (CNS). As fibromyalgia patients often report sleep problems, the physiological processes that normally regulate sleep may be disturbed and overlap with other CNS dysfunctions. Although the mechanisms potentially linking chronic widespread pain, sleep alterations and mood disorders have not yet been proven, polysomnography findings in patients with fibromyalgia and non-restorative sleep and their relationships with clinical symptoms support the hypothesis of a conceptual common mechanism called 'central sensitisation'. Food and Drug Administration (FDA)-approved drugs for the treatment of fibromyalgia may benefit sleep, but their label does not include the treatment of fibromyalgia-associated sleep disorders. Non-pharmacological therapies (including a thorough sleep assessment) can be considered in the first-line treatment of non-restorative sleep, although they have not yet been fully investigated in patients with fibromyalgia. Both pharmacological and non-pharmacological treatments should be used cautiously in patients with fibromyalgia, bearing in mind the patients' underlying disorders and the potential interactions of the therapies.     

Optogenetically induced sleep spindle rhythms alter sleep architectures in mice

Sleep spindles are rhythmic patterns of neuronal activity generated within the thalamocortical circuit. Although spindles have been hypothesized to protect sleep by reducing the influence of external stimuli, it remains to be confirmed experimentally whether there is a direct relationship between sleep spindles and the stability of sleep. We have addressed this issue by using in vivo photostimulation of the thalamic reticular nucleus of mice to generate spindle oscillations that are structurally and functionally similar to spontaneous sleep spindles. Such optogenetic generation of sleep spindles increased the duration of non-rapid eye movement (NREM) sleep. Furthermore, the density of sleep spindles was correlated with the amount of NREM sleep. These findings establish a causal relationship between sleep spindles and the stability of NREM sleep, strongly supporting a role for the thalamocortical circuit in sleep regulation.     

Effects of treatment by laser-assisted uvuloplasty on sleep energy expenditure in obstructive sleep apnea patients

The purpose of this study was to evaluate the effect of successful laser-assisted uvulopalatoplasty (LAUP) on sleep energy expenditure (EE) in obstructive sleep apnea syndrome (OSAS) patients. Fifteen healthy subjects (group I) and 25 patients with moderately severe or severe OSAS (group II) proven by overnight sleep study and who wanted LAUP were enrolled. During the night of the sleep studies, EE was measured with a metabolic cart (indirect calorimetry with canopy), including basal metabolic rate (BMR), mean sleep EE, lowest sleep EE, ratios of mean sleep EE/BMR, and lowest sleep EE/BMR. For the OSAS patients, a second sleep study with EE measurement was performed 3 months after LAUP. Based on this assessment of their sleep architecture, they were divided into 2 groups: responders (group IIa) and nonresponders (group IIb). The mean sleep EE, the ratio of mean sleep EE/BMR and lowest EE/BMR were significantly higher in group II than group I. After LAUP in group II, 6 patients were found to be responders (group IIa) and 19 patients were nonresponders (group IIb). Group IIa had decreased mean sleep EE, ratios of mean sleep EE/BMR, and lowest sleeping EE/BMR after LAUP than before LAUP compared with no significant changes in group IIb after LAUP. In conclusion, there is increased sleep EE in moderately severe OSAS patients when compared with normal controls. LAUP, when effective in reversing the sleep abnormalities, also normalizes the sleep EE. If it does not adequately treat the OSAS, however, the sleep EE remains abnormal.     

Alpha sleep characteristics in fibromyalgia

OBJECTIVE: To characterize the patterns of alpha electroencephalographic sleep and their associations with pain and sleep in patients with fibromyalgia. METHODS: Pain and sleep symptoms of 40 female patients with fibromyalgia and 43 healthy control subjects were studied before and after overnight polysomnography. Blinded analyses of alpha activity in non-rapid eye movement (non-REM) sleep were performed using time domain, frequency domain, and visual analysis techniques. RESULTS: Three distinct patterns of alpha sleep activity were detected in fibromyalgia: phasic alpha (simultaneous with delta activity) in 50% of patients, tonic alpha (continuous throughout non-REM sleep) in 20% of patients, and low alpha activity in the remaining 30% of patients. Low alpha activity was exhibited by 83.7% of control subjects (P < 0.01). All fibromyalgia patients who displayed phasic alpha sleep, activity reported worsening of pain after sleep, compared with 58.3% of patients with low alpha activity (P < 0.01) and 25.0% of patients with tonic alpha activity (P < 0.01). Postsleep increase in the number of tender points occurred in 90.0% of patients with phasic alpha activity, 41.7% of patients with low alpha activity, and 25.0% of patients with tonic alpha activity (P < 0.01). Self ratings of poor sleep were reported by all patients with phasic alpha activity, 58.3% of patients with low alpha activity (P < 0.01), and 12.5% of patients with tonic alpha activity (P < 0.01). Patients with phasic alpha activity reported longer duration of pain than patients in other subgroups (P < 0.01). Additionally, patients with phasic alpha sleep activity exhibited less total sleep time than patients in other subgroups (P < 0.05), as well as lower sleep efficiency (P < 0.05) and less slow wave sleep (P < 0.05) than patients with a tonic alpha sleep pattern. CONCLUSION: Alpha intrusion during sleep can be of different patterns. Phasic alpha sleep activity was the pattern that correlated better with clinical manifestations of fibromyalgia.     

The accuracy of subjective sleep time in sleep apnoea recordings

Total sleep time is important in investigations of obstructive sleep apnoea, since the diagnosis is usually based on the average number of apnoeas per hour of sleep. Sleep estimates instead of exact EEG-recorded total sleep time is often used in the clinical setting. However, an overestimated sleep time would underestimate the degree of the disease and vice versa. The purpose of this study was to investigate the accuracy of subjective sleep time and time-in-bed as sleep estimates. One hundred patients undergoing diagnostic polysomnography for suspected obstructive sleep apnoea were asked to estimate their sleep time in a questionnaire. Seventy-five patients were diagnosed as suffering from obstructive sleep apnoea syndrome. The mean difference between self-scored and EEG-recorded total sleep time was 4 +/- 74 min. However, 30% scored with a difference greater than 1 h. The intra-class correlation coefficient was fair (0.58, CI: 0.43-0.70). Fifty-three patients overestimated their sleep time and 47 patients underestimated it. All but four patients underestimated their number of awakenings (P<0.001). The mean difference between time-in-bed and EEG-recorded total sleep time was 110 +/- 63 min. This difference was significantly larger than the difference between subjective sleep time and EEG-recorded total sleep time (P<0.001). The intra-class correlation coefficient was poor (0.38, CI: 0.20-0.54). Mean AHI was 27 +/- 27 using subjective sleep time and did not change significantly compared with the mean AHI of 25 +/- 21 based on EEG-recorded total sleep time. Mean AHI decreased significantly to 20 +/- 17 (P<0.001) when time-in-bed was used. In conclusion, 'time-in-bed' time is a poor predictor of total sleep time and should not be used when calculating the apnoea-hypopnoea index. Subjective sleep time is better as an approximation, but the individual differences are large.     

Prevalence of sleep disturbances: Sleep disordered breathing,short sleep duration,and non-restorative sleep

Recently, interest in sleep disturbances, such as sleep disordered breathing (SDB), short sleep duration, and non-restorative sleep (NRS), has been increasing. The potentially large public health implications of sleep disturbances indicate a need to determine their prevalence in a general population. This review describes the characteristics of population-based sleep cohorts from past to present. Unavoidable methodological and baseline characteristic heterogeneity was found between studies. The prevalence of SDB (apnea hypopnea index (AHI), respiratory disturbance index (RDI), or oxygen desaturation index (ODI) ≥5/h) was 24.0–83.8% in men and 9.0–76.6% in women, and that of moderate-to-severe SDB (AHI, RDI, or ODI ≥15/h) was 7.2–67.2% in men and 4.0–50.9% in women. Additionally, the prevalence of SDB in post-menopausal women was 3–6 times higher than in pre-menopausal women. The prevalence of subjective short sleep duration (<6 h) was 7.5–9.6%, while that of objective short sleep duration (<6 h) was 22.1–53.3%. The prevalence of NRS was 19.2–31.0% in men and 26.3–42.1% in women, as determined from studies using a yes-no questionnaire, while a multi-national survey using a telephone-based expert system showed a wide range of prevalence between countries, from 2.4% to 16.1%. An association between SDB, short sleep duration, and NRS has recently been suggested. To gain a better understanding of the burden of sleep disturbances, a consensus on the definition of several sleep disturbances is needed, as methodological heterogeneity exists, including SDB scoring rules, subjective versus objective data collection for short sleep duration, and the definition of NRS itself.     

Effects of alcohol on sleep and the sleep electroencephalogram in healthy young women

BACKGROUND: Although the association between sleep and alcohol has been of interest to scientists for decades, the effects of alcohol on sleep and sleep electroencephalogram (EEG) have not been extensively studied in women. Our specific aim was to determine whether sleep stage variables and/or spectral characteristics of the sleep EEG are altered by alcohol administration in women. METHODS: Changes of sleep and the sleep EEG were investigated after administration of a moderate dose of alcohol (0.49 g/kg) in the hour before bedtime compared with placebo in young healthy women. After approximately 2 weeks at home on a fixed 8.5- or 9-hour stabilization sleep schedule, sleep was continuously recorded by polysomnography for 3 consecutive nights [adaptation, placebo, alcohol (mean breath alcohol concentration 0.043 g/% before bedtime)] in the laboratory in 7 women (ages 22-25, mean=23.5, SD=1 year). Sleep stages were scored according to conventional criteria. Electroencephalogram power spectra of the bipolar derivations Fz/Cz (anterior) and Pz/Oz (posterior) were calculated using a fast Fourier transform routine. RESULTS: Only few changes in sleep and the sleep EEG were observed. Across the entire night rapid eye movement (REM) sleep decreased, while minutes of stage 4 sleep were increased in the first 2-hour interval on alcohol nights compared with placebo nights. Spectral analysis of the EEG showed increased power in the alpha range (9-11 Hz) during all-night non-REM (NREM) sleep in anterior derivations after alcohol compared with placebo. Differences in spectral EEG power were also present in 2-hour intervals of NREM sleep; in particular, EEG power was increased on the alcohol night for frequency bins within the alpha range in anterior derivations and within the delta range (3-4 Hz) in posterior derivations during the initial part of the night. CONCLUSIONS: A moderate dose of alcohol just before bedtime resulted in a short-lived increase in sleep intensity. A limitation of the study, however, was that only a single dose of alcohol was used to examine the effects of alcohol on sleep.     

Regulation of respiration during sleep in congenital central sleep apnea

We report on 2 children aged 13 and 14 months with congenital central alveolar sleep apnea which showed depression of respiratory drive during sleep resulting from dysfunction of central chemoreceptors. Hypoventilation was found to be more severe during NREM sleep (minimum of alveolar ventilation in stages 3/4) than during REM sleep. During NREM sleep arousal responses to hypoxia proved to be an important factor in influencing the level of alveolar ventilation and in preventing fatal asphyxia.     

Subjective and objective sleep quality and aging in the sleep heart health study

OBJECTIVES: To examine the extent to which subjective and objective sleep quality are related to age independent of chronic health conditions.
DESIGN: Cross-sectional study.
SETTING: The Sleep Heart Health Study (SHHS) is a multicenter study designed to determine the cardiovascular consequences and the natural history of sleep disordered breathing.
PARTICIPANTS: Five thousand four hundred seven community-dwelling adults who participated in the SHHS (mean age 63, range 45–99; 52% women).
MEASUREMENTS: Unattended home polysomnography (PSG) and sleep questionnaires.
RESULTS: Older age was associated with shorter sleep time, diminished sleep efficiency, and more arousals in men and women. In men, age was independently associated with more Stage 1 and Stage 2 sleep and less slow-wave (Stage 3 to 4) and rapid eye movement sleep. In women, older age was less strongly associated according to linear trend with sleep stage. Conversely, poor subjective sleep quality was not associated with older age in men, but older women had more trouble falling asleep, and there was a trend toward older women having more problems with waking up during the night and waking up too early. Associations between self-report and directly measured sleep time and sleep latency were low to moderate across age groups (correlation coefficient=0.06–0.32).
CONCLUSION: Older age was more strongly associated with poorer sleep according to PSG in men than women, yet the subjective report of poor sleep with older age was stronger in women. The higher prevalence of chronic health conditions, including sleep apnea, in older adults did not explain changes of sleep parameters with aging and age–sex differences in these relationships.     

经皮电刺激对阻塞性睡眠呼吸暂停的影响

目的研究经皮颏下电刺激对睡眠期阻塞性睡眠呼吸暂停综合征的影响。方法１６例阻塞性睡眠呼吸暂停患者在接受经皮颏下电刺激（ＴＥＳ）治疗前后进行了全夜多导睡眠图监测。结果１６例中的１４例ＴＥＳ治疗成功，睡眠呼吸暂停指数（ＡＩ）下降＞５０％，平均ＡＩ下降了２９次／小时（Ｐ＜０．００１），平均呼吸暂停时间从２２秒降至７秒（Ｐ＜０．００１）呼吸暂停时间／总睡眠时间（ＴＳＴ）下降了２０％。最低血氧饱和度从７１％升至８７％（Ｐ＜０．００１）。ＴＥＳ未引起觉醒。慢波睡眠（Ⅲ＋Ⅳ）期，快动眼期（ＲＥＭ）睡眠及睡眠效率增加。结论ＴＥＳ是一种非手术的、有效的治疗阻塞性睡眠呼吸暂停综合征的方法，但对中枢性睡眠呼吸暂停无效     

Cystic fibrosis patients have poor sleep quality despite normal sleep latency and efficiency

STUDY OBJECTIVES: Cystic fibrosis (CF) patients may be predisposed to poor sleep quality due to upper and lower airway abnormalities and impaired gas exchange. Previous sleep investigations of CF patients using single-night polysomnography have reported conflicting results. We hypothesized that sampling sleep for a prolonged period in a patient's normal environment may give a more representative assessment of sleep quality than a single-night polysomnogram, and that impaired sleep quality would correlate with pulmonary disease severity and self-assessed sleep quality. DESIGN: Using wrist actigraphy, we measured sleep quality in clinically stable CF patients and age-matched control subjects. In addition, each CF patient and control subject completed the following three questionnaires: the Epworth sleepiness scale; the Pittsburgh sleep quality index (PSQI); and the Medical Outcomes Study 36-item short form. RESULTS: Twenty CF patients and control subjects were enrolled in the study, and were well-matched for age, sex, and body mass index. The mean (+/- SD) FEV(1) for CF patients was 61.0 +/- 20.1% predicted. CF patients and control subjects had similar sleep duration, sleep latency, and sleep efficiency. However, CF patients had higher PSQI scores (6.45 vs 4.55, respectively; p = .04), a higher fragmentation index (FI) [31.72 vs 18.02, respectively; p < 0.001], and less immobile time (88.87 vs 91.89, respectively; p = 0.02). There was a significant correlation of FI with FEV(1) and PSQI scores. CONCLUSIONS: Stable CF patients have disrupted sleep, and sleep disruption may in part be related to the severity of pulmonary disease. In addition, the PSQI may be useful in detecting CF patients with poor sleep quality.     

Accuracy of respiratory inductive plethysmography during wakefulness and sleep in patients with obstructive sleep apnea.

To assess the accuracy of the respiratory inductive plethysmograph (RIP) during sleep in obese patients with obstructive sleep apnea (OSA), we monitored 13 patients with OSA during wakefulness and nocturnal sleep with simultaneous measurements of tidal volume from RIP and integrated airflow. Patients wore a tightly fitting face mask with pneumotachograph during wakefulness and sleep. Calibrations were performed during wakefulness prior to sleep and compared with subsequent wakeful calibrations at the end of the study. Patients maintained the same posture during sleep (supine, 11; lateral, two) as during calibrations. There were no significant differences in calibrations before sleep and after awakening. The mean error in 13 patients undergoing RIP measurements of tidal volume during wakefulness was -0.7 +/- 3.4 percent while that during sleep was 2.1 +/- 14.9 percent (p < 0.001). The standard deviation (SD) of the differences between individual breaths measured by RIP and integrated airflow was 9.8 +/- 5.5 percent during wakefulness and 25.5 +/- 18.6 percent during sleep (p < 0.001). During both wakefulness and sleep, errors in RIP tidal volume were not significantly correlated with body mass index. In 12 patients with at least 10 percent time in each of stages 1 and 2 sleep, SD was greater in stage 2 sleep compared with wakefulness and stage 1 (p < 0.001). In three patients who manifested all stages of sleep, SD was greater in REM sleep than in wakefulness and all stages of non-REM sleep (p < 0.001). In three patients who manifested all stages of sleep, SD was greater in REM sleep than in wakefulness and all stages of non REM sleep (p < 0.001). This was associated with paradoxic motion of the rib cage in two patients during REM. We conclude that, despite increased errors in individual breath measurements during sleep, more marked during stages 2 and REM sleep, RIP is clinically useful to measure ventilation quantitatively in obese patients with sleep apnea. The criterion of a decrease of 50 percent in tidal volume assessed by RIP is appropriate to define hypopneas in such patients.     

Effect of musculoskeletal pain on sleep architecture in patients with obstructive sleep apnea

Rationale

Obstructive sleep apnea and chronic musculoskeletal pain both affect sleep. Sleep architecture of patients suffering from both is largely unknown.

Objectives

This study seeks to define the sleep architecture of patients with chronic musculoskeletal pain and obstructive sleep apnea.

Methods

Patients with obstructive sleep apnea diagnosed by sleep study during the past 3 years were included. Patients with clinical documentation of chronic musculoskeletal pain constituted cases, while others were classified as controls.

Measurements

Demographics, clinical factors affecting sleep, medications affecting sleep, Epworth sleepiness scores, and polysomnographic parameters; total sleep time, sleep efficiency, sleep stages, rapid eye movement (REM) sleep onset, apnea–hypopnea index, arousal index, and periodic leg movements were recorded.

Results

There were 393 subjects: 200 cases (obstructive sleep apnea and chronic musculoskeletal pain) and 193 controls (obstructive sleep apnea alone). There was significant difference in total sleep time (274.5?±?62.5 vs. 302.2?±?60.1 min, p?=?0.0001), sleep efficiency (73.54?±?15.8 vs. 78.76?±?14.3 %, p?=?0.0003), and REM sleep onset (148.18?±?80.5 vs. 124.8?±?70.9 min, p?=?0.006). Subgroup analysis within the obstructive sleep apnea with chronic musculoskeletal pain group revealed that subjects had better total sleep time and sleep efficiency if they were on REM sleep affecting medications (suppressants and stimulants). Those on REM sleep suppressants slept 25.7 min longer and had 6.4 % more efficient sleep than those not on REM suppressants (p?=?0.0034 and p?=?0.0037).

Conclusion

Patients with obstructive sleep apnea and chronic musculoskeletal pain sleep not only significantly less but also with inferior sleep quality. Their REM sleep is also less in duration and its onset is delayed. Despite low TST and SE, these patients may not exhibit sleepiness.     

Prevalence of concomitant sleep disorders in patients with obstructive sleep apnea

We determined the prevalence of concomitant sleep disorders in patients with a primary diagnosis of obstructive sleep apnea (OSA). We retrospectively analyzed 643 patients, aged 18, with a primary diagnosis of OSA, evaluated by sleep specialists, in whom clinical and polysomnographic data were derived using standardized techniques by reviewing data from a standardized database and clinical charts. Concomitant sleep disorders were listed according to the International Classification of Sleep Disorders (American Academy of Sleep Medicine, 2000). The mean age was 48.5±13.5 years and 55% were male. Racial distributions were African–Americans 51.8% and Caucasian 47%. Indices of disordered breathing were respiratory disturbance index 32.4±30.4/h sleep and time <90% O₂ saturation 44.5±81.6 min. Thirty-one percent of patients had a concomitant sleep disorder. The most common were inadequate sleep hygiene (14.5%) and periodic limb movement disorder (PLMD, 8.1%). Of patients with other sleep disorders, 66.8% had treatment initiated for these disorders. Predictors of inadequate sleep hygiene (logistic regression) were: age (each decade OR=0.678, P=0.000000), gender (for M, OR=0.536), and the presence of at least one other major system disorder (OR=2.123, P=0.0015). Predictors of PLMD were: age (each decade OR=0.794, P=0.0005), gender (for M, OR=0.433, P=0.004), and total sleep time (for each 10 min, OR=0.972, P=0.0013). We conclude that approximately one third of patients with sleep apnea have another identifiable sleep disorder, usually requiring treatment. This suggests that practitioners evaluating and treating sleep apnea ought to be prepared to deal with other sleep disorders as well.     

Erythropoietin and obstructive sleep apnea

OBJECTIVE: We tested the hypothesis that repetitive severe hypoxemia resulting from obstructive sleep apnea would increase serum erythropoietin, and that this increase would be attenuated by effective treatment of obstructive sleep apnea. METHODS: We studied healthy untreated patients with obstructive sleep apnea (18 severe and 10 very mild) before and after acute treatment with continuous positive airway pressure, and 12 healthy control subjects free of obstructive sleep apnea. RESULTS: Baseline erythropoietin levels before sleep were similar in the obstructive sleep apnea and control groups. However, erythropoietin levels increased (by 20%, P =.037) in patients with severe obstructive sleep apnea after 3.5 hours untreated (lowest O2, 77% +/- 3%), and decreased after 4 hours of continuous positive airway pressure treatment (P =.001). Erythropoietin responses in patients with severe obstructive sleep apnea were different (F = 4.0, P =.03) from controls, in whom erythropoietin levels remained stable throughout the night (P =.94). Erythropoietin responses were similar in very mild obstructive sleep apnea and controls (P =.58). CONCLUSIONS: Our results indicate that untreated severe obstructive sleep apnea results in increased erythropoietin, which decreases after continuous positive airway pressure treatment. Increased erythropoietin may be a potential reversible mechanism to explain the association between obstructive sleep apnea and cardiovascular disease.     

Effects of sleep and sleep deprivation on catecholamine and interleukin-2 levels in humans: clinical implications.

The objective of this study was to evaluate the effects of nocturnal sleep, partial night sleep deprivation, and sleep stages on catecholamine and interleukin-2 (IL-2) levels in humans. Circulating levels of catecholamines and IL-2 were sampled every 30 min during 2 nights: undisturbed, baseline sleep and partial sleep deprivation-late night (PSD-L; awake from 0300-0600 h) in 17 healthy male volunteers. Sleep was monitored somnopolygraphically. Sleep onset was associated with a significant (P < 0.05) decline of circulating concentrations of norepinephrine and epinephrine, with a nocturnal nadir that occurred 1 h after nocturnal sleep. On the PSD-L night, levels of norepinephrine and epinephrine significantly (P < 0.05) increased in association with nocturnal awakening. During stage 3-4 sleep, levels of norepinephrine, but not epinephrine, were significantly lower (P < 0.05) compared to average levels during the awake period, stages 1-2 sleep, and rapid eye movement sleep. Nocturnal levels of circulating IL-2 did not change with sleep onset or in relation to PSD-L or the various sleep stages. We conclude that sleep onset is associated with changes in levels of circulating catecholamines. Loss of sleep and disordered sleep with decreases in slow wave sleep may serve to elevate nocturnal catecholamine levels and contribute to cardiovascular disease.