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Sleep deprivation activates epileptiform discharges independent of the activating effects of sleep.

An electroencephalogram (EEG) recorded after sleep deprivation (SDEEG) in epilepsy patients often discloses epileptiform discharges (ED) when routine EEG (REEG) does not, but since sleep alone activates ED, activation during SDEEG may result merely from the induction of sleep. We retrospectively investigated whether SDEEG is useful when REEG containing wakefulness and sleep fails to show ED. Subjects were patients with definite or highly probable epilepsy whose REEG lacked ED and who later underwent SDEEG. All had wakefulness and at least stage II sleep during both REEG and SDEEG. Patients with ED on REEG were specifically excluded to avoid including patients with activation due merely to the occurrence of sleep. Patient and EEG characteristics were studied, including duration of wakefulness and each sleep stage and timing and characteristics of ED. Fifteen of 29 patients (52%) had activation on SDEEG; exclusively during wakefulness in 1, exclusively during sleep in 6 and in both wakefulness and sleep in 8. Activation rates were not significantly different between wakefulness (9, 60%), stage I (11, 74%) and stage II (11, 74%). EEG characteristics were similar for REEG and SDEEG, except that total EEG duration and stage II sleep were longer in SDEEG than in REEG, which did not influence activation by a logistic regression model (p > 0.05). We conclude that sleep deprivation activates ED independent of the activating effects of sleep and therefore is useful in evaluation of suspected epilepsy even when REEG contains sleep.

Adolescent↗

A multicenter, double-blind comparison of the effects of nefazodone and fluoxetine on sleep architecture and quality of sleep in depressed outpatients.

This study was an 8-week, randomized, double-blind, parallel-group investigation that compared the effects of nefazodone and fluoxetine on sleep architecture and on clinician- and patient-rated sleep measures in 43 outpatients with moderate to severe, nonpsychotic major depressive disorder and insomnia. Twenty-two patients received nefazodone 200 mg daily for 1 week, followed by 400 mg daily for 7 weeks. Twenty-one patients received fluoxetine 20 mg daily. Dosage increases (to 500 mg/day for nefazodone and 40 mg/day for fluoxetine) were available after day 29, depending on clinician judgement. Sleep parameters were measured during baseline phase, while patients were unmeasured and symptomatic, and at weeks 2, 4, and 8 of treatment. Nefazodone and fluoxetine were equally effective as antidepressants. However, compared with baseline, nefazodone increased sleep efficiency and reduced the number of awakenings and percent awake and movement time, whereas fluoxetine increased the number of awakenings and did not significantly alter sleep efficiency or percent awake and movement time. Although fluoxetine increased stage 1 sleep and rapid eye movement (REM) latency and reduced total percent REM sleep, nefazodone increased REM sleep, decreased REM latency, and did not alter stage 1 sleep. Differences between treatment groups, based on change from baseline, revealed greater sleep efficiency, fewer awakenings, less percent awake and movement time, less percent stage 1 and more REM sleep, and shorter REM latency for nefazodone compared with fluoxetine. Significantly greater improvement in clinician- and patient-rated sleep disturbance was found with nefazodone compared with fluoxetine. Nefazodone was associated with better sleep quality.

Adult↗

Subjective sleep complaints in pediatric depression: a controlled study and comparison with EEG measures of sleep and waking.

OBJECTIVE: Children with major depressive disorder (MDD) often complain of sleep disturbances; however, polysomnographic studies have failed to find objective evidence of these disturbances. This article examines subjective sleep reports of children with MDD and healthy controls focusing on comparing subjective and objective sleep measures. METHOD: Fifty-one subjects with MDD and 42 healthy subjects, 8-17 years old, participated in a comprehensive psychobiologic study including three nights of EEG sleep recording. Each morning, subjects completed a post-sleep form subjectively rating their sleep, which was then compared with their polysomnographic studies. RESULTS: Depressed subjects reported significantly worse sleep on four scales: subjective sleep quality, perceived number of awakenings, estimated minutes awake, and perceived ease of waking. In contrast to these subjective complaints, objective EEG measures indicated no evidence of disturbed sleep in the depressed sample compared to controls. Furthermore, exploratory analyses focusing on the subset of depressed subjects with the greatest subjective sleep disturbance showed, paradoxically, significantly better sleep in terms of the number of EEG awakenings and objective disturbances. CONCLUSIONS: Despite clinical evidence of subjective sleep complaints in depressed children, our EEG measures showed little evidence to indicate an objective basis for these perceptions. These findings raise provocative questions regarding the nature of sleep complaints associated with early-onset depression.

Adolescent↗

Symptomatic gastro-oesophageal reflux, arousals and sleep quality in patients undergoing polysomnography for possible obstructive sleep apnoea.

INTRODUCTION: Nocturnal acid reflux is common and could disturb sleep by causing arousals that fragment sleep. AIM: To determine the prevalence of gastro-oesophageal reflux symptoms and their association with arousals, stages of sleep and quality of life in patients undergoing evaluation for excessive daytime sleepiness and obstructive sleep apnoea. METHODS: Ninety-four consecutive patients with excessive daytime sleepiness were prospectively studied. Patients completed the gastrointestinal symptom rating scale, a validated symptom questionnaire for reflux disease and a disease-specific quality of life questionnaire, the sleep apnoea quality of life index and then underwent overnight polysomnography, which was read in a blinded manner. RESULTS: There were 40 males and 54 females with a mean age of 47 +/- 13 years. Reflux symptoms were present in 63 of the 94 (67%) patients. Patients with reflux symptoms had significantly more arousals from sleep 43 +/- 70/h than those without (20 +/- 24/h; P = 0.03). The sleep duration during the second stage of sleep was shorter (44 +/- 21%) for those with reflux symptoms than those without (52 +/- 12%; P = 0.03). Patients with reflux spent significantly shorter periods in stage II sleep (44 +/- 21%) than those without (52 +/- 12%; P = 0.03). The sleep-related quality of life score in patients with gastro-oesophageal reflux (3.1 +/- 1.1) was significantly lower than in patients without reflux (3.7 +/- 1.0; P = 0.02). Regression analysis demonstrated a significant inverse correlation between quality of life and reflux symptom score (P =0.002) and total spontaneous arousals (P = 0.04). CONCLUSIONS: Gastro-oesophageal reflux is common in patients with sleep disorders, is associated with increased arousal, decreased durations spent in the deeper stages of sleep and poorer sleep-related quality of life.

Arousal↗

REM sleep motor dysfunction in multiple system atrophy: with special emphasis on sleep talk as its early clinical manifestation.

Various neurodegenerative diseases involving brainstem structures as one of the main pathological lesions are reported to be associated with REM sleep behaviour disorder. Full blown REM sleep behaviour disorder can be diagnosed clinically, but REM sleep motor dysfunction, a pathophysiological basis of REM sleep behaviour disorder, is difficult to detect without all night polysomnography. Twenty one consecutive patients with multiple system atrophy with no complaints of nocturnal abnormal behaviours were clinically evaluated to determine the presence of sleep related symptoms. All night polysomnography with video monitoring was performed to investigate REM sleep characteristics and patients' behaviours. In 85.7% (18 of 21) of the patients' sleep talk started or increased around or after the clinical onset of the primary diseases. REM sleep without atonia occupied more than 15% (16.2%-100%) of the REM sleep time in all but one patient. In 90.5% (19 of 21) of patients, motor events such as sleep talk and various combinations of craniofacial, orofacial, or limb movements occurred at various frequencies mostly during REM sleep without atonia. In patients with multiple system atrophy, REM sleep motor dysfunction is a common polysomnographic finding which is otherwise overlooked, and sleep talk may be its early clinical manifestation.

Aged↗

Light treatment for sleep disorders: consensus report. II. Basic properties of circadian physiology and sleep regulation.

The rationale for the treatment of sleep disorders by scheduled exposure to bright light in seasonal affective disorder, jet lag, shift work, delayed sleep phase syndrome, and the elderly is, in part, based on a conceptual framework developed by nonclinical circadian rhythm researchers working with humans and other species. Some of the behavioral and physiological data that contributed to these concepts are reviewed, and some pitfalls related to their application to bright light treatment of sleep disorders are discussed. In humans and other mammals the daily light-dark (LD) cycle is a major synchronizer responsible for entrainment of circadian rhythms to the 24-h day, and phase response curves (PRCs) to light have been obtained. In humans, phase delays can be induced by light exposure scheduled before the minimum of the endogenous circadian rhythm of core body temperature (CBT), whereas phase advances are induced when light exposure is scheduled after the minimum of CBT. Since in healthy young subjects the minimum of CBT is located approximately 1 to 2 h before the habitual time of awakening, the most sensitive phase of the PRC to light coincides with sleep, and the timing of the monophasic sleep-wake cycle itself is a major determinant of light input to the pacemaker. The effects of light are mediated by the retinohypothalamic tract, and excitatory amino acids play a key role in the transduction of light information to the suprachiasmatic nuclei. LD cycles have direct "masking" effects on many variables, including sleep, which complicates the assessment of endogenous circadian phase and the interpretation of the effects of light treatment on sleep disorders. In some rodents motor activity has been shown to affect circadian phase, but in humans the evidence for such a feedback of activity on the pacemaker is still preliminary. The endogenous circadian pacemaker is a major determinant of sleep propensity and sleep structure; these, however, are also strongly influenced by the prior history of sleep and wakefulness. In healthy young subjects, light exposure schedules that do not curtail sleep but induce moderate shifts of endogenous circadian phase have been shown to influence the timing of sleep and wakefulness without markedly affecting sleep structure.

Body Temperature↗

A model of human sleep-related growth hormone secretion in dogs: effects of 3, 6, and 12 hours of forced wakefulness on plasma growth hormone, cortisol, and sleep stages.

Twenty-four canine GH (cGH) and cortisol secretion patterns associated with sleep stages were studied in 10 male adult dogs. Plasma samples were obtained at 30- or 15-min intervals via an indwelling catheter. Under baseline conditions, all dogs showed irregular polyphasic sleep, and the episodic cGH secretion had no apparent relationship with sleep or the light-dark cycle. Five dogs were subjected to regular sleep-wake cycles; 3, 6, and 12 h of forced wakefulness (FW) were repeated at 3-, 6-, and 12-h intervals (recovery sleep periods), respectively. Peak cGH secretion (mean +/- SD, 6.4 ng/ml +/- 2.4) occurred soon after recovery sleep onset in 25 of 40 total recovery periods. The incidence of sleep-onset cGH peaks and cGH secretion during the first hour of recovery sleep significantly increased with the length of the preceding FW, but were not affected by the time of day. Delta wave sleep increased during this hour, suggesting a possible correlation with the sleep-onset cGH peak. During the first 3 h of recovery after 6 and 12 h of FW, cGH secretion was significantly enhanced, but cortisol was not. Considering the characteristics of human sleep-related GH secretion, we suggest that this peak cGH secretion represents a model of human GH secretion. Possibly, a close association of cGH secretion with sleep is concealed under the baseline condition and uncovered by inducing longer sleep-wake cycles in dogs. No circadian cortisol variation was detected under the baseline or the experimental conditions.

Animals↗

Sleep and the sleep electroencephalogram across the menstrual cycle in young healthy women.

Cyclic changes in hormones, body temperature, and metabolic rate characterize the menstrual cycle. To investigate whether these changes are associated with changes in sleep and the sleep electroencephalogram (EEG), a total of 138 sleep episodes from 9 women with no premenstrual syndrome symptoms were recorded every second night throughout one ovulatory menstrual cycle and analyzed in relation to menstrual phase. Ovulation and menstrual cycle stage were confirmed by measurements of temperature, urinary LH, and midluteal plasma levels of estrogen and progesterone. No significant variation across the menstrual cycle was observed for subjective ratings of sleep quality and mood as well as for objective measures of total sleep time, sleep efficiency, sleep latency, rapid eye movement sleep latency, and slow wave sleep. In nonrapid eye movement sleep, EEG power density in the 14.25-15.0 hertz band, which corresponds to the upper frequency range of the sleep spindles, exhibited a large variation across the menstrual cycle, with a maximum in the luteal phase. The data show that in healthy young women, sleep spindle frequency activity varies in parallel with core body temperature, whereas homeostatic sleep regulatory mechanisms, as indexed by the time course of EEG slow wave activity are not substantially affected by the menstrual cycle.

Body Temperature↗

Effects of total sleep loss on sleep tendency.

Effects of two nights of sleep loss were assessed in six young adult (18--21 yr.) volunteers (2 women, 4 men). Performance on the Wilkinson Addition Test fell significantly below baseline values during the sleep-loss procedure and recovered after one or two full nights of sleep. Performance on a Serial Alternation Task also declined during sleep loss. Mood and sleepiness, assessed by subjective self-rating scales, showed a significantly less positive mood and a greater degree of sleepiness during sleep loss, with a recovery to baseline levels after one full night of sleep. Sleep tendency, measured at 2-hr. intervals during all waking periods, was assessed using an objective measure of latency to sleep onset, the Sleep Latency Test. The scores fell to about 1 min. at 0600 on the first night of sleep loss and remained at similarly low values throughout the sleep loss period. After one night of recovery sleep the scores remained significantly below baseline levels, which were not achieved until after the second recovery night. The multiple sleep latency test appears to be a valuable operationally defined tool for measuring daytime sleepiness.

Achievement↗

A survey of sleep habits and sleeping difficulties in an elderly Swedish population.

A random sample of 876 subjects aged 65-79 years were investigated by means of a questionnaire concerning sleep and related factors. Sleep problems were reported by 23.8% of females and 13.3% of males. Moderate or major complaints of maintaining sleep were reported by 43.5% of subjects, early morning awakening 33.4% and difficulties falling asleep 31.4%. Daytime sleepiness was more common among males, and a relationship between daytime sleepiness and perceived poor sleep was found. Daytime napping was common, but not related to poor sleep. The prevalence of regular sleeping pill users was 7.6% for females and 3.0% for males and a relationship between sleep problems, sleeping pill usage and psychiatric symptoms was established. Among the regular sleeping pill users 39.1% had possible depression (PD) and 63.0% had possible anxiety disorder (PA). Among respondents with sleep complaints 29.8% had PD and 48.7% had PA. Sleep problems were also related to impaired physical health. Various medical illnesses contributed to sleep complaints among males, and depression affected sleep the most among females.

Aged↗

The effect of snoring and obstructive sleep apnea on the sleep quality of bed partners.

OBJECTIVE: To measure the effect of snoring and obstructive sleep apnea (OSA) on the sleep of snorers' bed partners and to determine whether a bed partner's sleep improves when snoring and OSA are treated. MATERIALS AND METHODS: We studied 10 married couples in which 1 member was undergoing polysomnography to evaluate suspected OSA. The patients and their spouses underwent simultaneous polysomnography. Midway through the 1-night study, the patients received nasal continuous positive airway pressure (CPAP) with the pressure adjusted to eliminate snoring and obstructive breathing events. Apnea-hypopnea index (episodes/hours of sleep time), arousal index (arousals/hours of sleep time), and sleep efficiency (percent time asleep) were calculated to measure sleep quality. RESULTS: The patients (all male) demonstrated a median (range) apnea-hypopnea index of 26 (3-75) that decreased to 7 (0-34) during the trial of nasal CPAP therapy (P < .05). During the CPAP trial, the median (range) arousal index of the spouses decreased from 21 (14-34) to 12 (4-27) (P < .01), and the spouses' median (range) sleep efficiency increased from 74% (56%-80%) to 87% (64%-95%) (P < .01). CONCLUSION: The elimination of snoring and OSA in these patients was associated with an improvement in the quality of their bed partners' sleep, as indicated by improved sleep efficiency and continuity, even when the spouses had been habitually exposed to snoring and OSA. Assuming that 480 minutes were spent in bed for sleep, a 13% improvement in sleep efficiency (i.e., from 74% to 87%) translates to an additional 62 minutes of sleep per night for the spouses of snorers with OSA.

Adult↗

The association between daytime sleepiness and sleep-disordered breathing in NREM and REM sleep.

BACKGROUND: Daytime sleepiness is common in patients with sleep-disordered breathing. Although respiratory events during sleep are associated with the occurrence of daytime sleepiness, the differential impact of these events during non-rapid eye movement (NREM) and rapid eye movement (REM) sleep on daytime sleepiness has not been well characterized. STUDY OBJECTIVES: To determine the effect of respiratory events during REM sleep and NREM sleep on daytime sleepiness, as assessed by the multiple sleep latency test (MSLT). DESIGN: Cross-sectional study. SETTING: University-based sleep disorders laboratory. PARTICIPANTS: Patients referred for polysomnography and daytime MSLT (n=1,821). INTERVENTIONS: N/A. MEASUREMENTS AND RESULTS: The study sample was initially divided into quartiles based on the level of the apnea-hypopnea index (AHI) during NREM sleep. Within the first NREM-AHI quartile (NREM-AHI < 8.3 events/hr), the association between REM-related respiratory events and daytime sleepiness was examined using the method of Kaplan-Meier analysis and Cox proportional hazards regression. After adjusting for age, gender, body mass index, and the duration of NREM and REM sleep, REM-AHI was not associated with daytime sleepiness (Relative Risk: 1.01; 95%CI: 0.94-1.10). Similarly, no significant association was observed between REM-AHI and the MSLT in patients within the second through fourth NREM-AHI quartiles. In contrast, increasing severity of disordered breathing during NREM sleep was associated with daytime sleepiness. For a 10-point increase in NREM-AHI, the adjusted relative risks for daytime sleepiness in the second through fourth NREM-AHI quartile were 1.21 (95%CI: 1.01-1.46), 1.20 (95%CI: 1.05-1.37), and 1.10 (95%CI: 1.04-1.16), respectively. CONCLUSION: Sleep-disordered breathing during NREM sleep, but not REM sleep, is associated with increased risk of daytime sleepiness.

Adult↗

Sleep and sleep disorders: an overview.

Sleep has been preserved during evolutionary history and is found in all mammalian species and birds. Despite the apparent strong survival advantage of sleep, and the observation in experimental animals that persistent sleep deprivation leads to rapid physical deterioration and death, the function of sleep is poorly understood. Modern neurophysiologic techniques have shown that sleep is not a homogeneous state but rather is divided into rapid eye movement and non-rapid eye movement stages. These two sleep states are as different from one another as sleep is from wakefulness. The advent of polysomnography has led to the recognition of a variety of sleep disorders; some, such as sleep apnoea, have potentially fatal consequences. Bruxism is an example of a parasomnia, viz a disorder which intrudes in normal sleep but does not lead to a primary sleep complaint. Recent improvements in diagnostic and therapeutic approaches to sleep disorders has led to the development of multidisciplinary Sleep Disorders Clinics.

Bruxism↗

[Short-term and long-term influences of nasal continuous positive airway pressure to sleep architecture of obstructive sleep apnea hypopnea syndrome].

OBJECTIVE: To observe the short-term and long-term influences of nasal continuous positive airway pressure (nCPAP) to sleep architecture of obstructive sleep apnea hypopnea syndrome (OSAHS). METHODS: Thirty cases who were diagnosed as OSAHS patients by polysomnography (PSG) were enrolled in the study. They received the nCPAP treatment in hospital at first night and then at home. Seventeen healthy adults were enrolled as control group and experienced PSG monitoring and recording. The sleep architectures of control group and OSAHS group (before nCPAP, first night on the nCPAP and 6 months after continuous nCPAP treatment) were analysed. RESULTS: The sleep shift number, first stage sleep, second stage sleep, stage of slow wave sleep and stage of rapid eye movement (REM) sleep were 34.41 +/- 10.16, (5.95 +/- 3.89)%, (48.13 +/- 7.68)%, (18.30 +/- 4.71)%, and (26.83 +/- 6.65)%, respectively, in control group. These parameters in OSAHS group before nCPAP were 207.30 +/- 149.80, (21.42 +/- 10.17)%, (55.24 +/- 13.28)%, (15.38 +/- 19.57)%, and (10.15 +/- 7.82)%, respectively. At the first night of nCPAP treatment they were 55.77 +/- 25.04, (10.92 +/- 9.62)%, (50.19 +/- 13.34)%, (17.53 +/- 10.06)%, and (21.17 +/- 7.66)%, respectively. There were statistically significant differences between the PSG parameters before and after nCPAP treatment in OSAHS group (P < 0.05). After 6 months of nCPAP treatment, the stage of REM sleep was significantly shorter (P < 0.05), but the other parameters had no significant changes compared with those at the first night on nCPAP (P > 0.05). CONCLUSION: The sleep shift number and first stage sleep in OSAHS group were significantly increased, but the stage of REM sleep was significantly decreased than those in control group. The sleep architecture of OSAHS was significantly improved when the nCPAP treatment was given continuously.

Aged↗

Caffeine effects on recovery sleep following 27 h total sleep deprivation.

INTRODUCTION: Caffeine is widely used to reverse alertness and performance decrements. However, caffeine's effects on subsequent recovery sleep and post-recovery performance are not well documented and, therefore, were evaluated. METHODS: Six habitually low (LC: < or = 100 mg x d(-1)) and three habitually high (HC: > or = 400 mg x d(-1)) caffeine users completed a randomized crossover design. After 20 h of wakefulness, repeated doses of caffeine gum [0 (placebo) mg, 100 (low dose) mg, or 300 (high dose) mg] were administered at 03:00, 05:00, and 07:00. At 10:00 (27 h sleep deprivation) subjects slept for 8 h, followed by Psychomotor Vigilance Task (PVT) administration at 33 and 65 min post-awakening. RESULTS: Low dose caffeine increased stage 1 minutes only. However, high dose caffeine impaired sleep maintenance (reduced total sleep time/increased wake) and reduced sleep depth (increased stage 1 minutes/percentage and slow-wave sleep (SWS) latency, and reduced SWS minutes during the first third of the sleep period). With high dose caffeine, LC users had less SWS percentage as compared with HC users. The HC users had reduced stage 2 percentage with high dose caffeine as compared with placebo and low dose caffeine. Caffeine dose and habitual caffeine use did not influence post-recovery sleep PVT performance. DISCUSSION: Caffeine exerts mild deleterious dose-response effects on recovery sleep following total sleep deprivation, primarily early in the sleep period, with potential recovery from these effects after sufficient sleep as suggested by lack of post-recovery sleep performance deficits. Habitual caffeine use appears to minimally reduce caffeine effects.

Adolescent↗

Local sweating responses during recovery sleep after sleep deprivation in humans.

Changes in the central control of sweating were investigated in five sleep-deprived subjects (kept awake for 40 h) during their recovery sleep under warm ambient conditions [operative temperature (T(o)) was either 35 or 38 degrees C]. Oesophageal (T(oes)) and mean skin (Tsk) temperatures, chest sweat rate (msw,ch), and concomitant electro-encephalographic data were recorded. Throughout the night at 35 or 38 degrees C T(o), msw,ch changes were measured at a constant local chest skin temperature (Tch) of 35.5 degrees C. The results showed that body temperatures (T(oes) and Tsk) of sleep-deprived subjects were influenced by thermal and hypnogogic conditions. The msw,ch levels correlated positively with T(oes) in the subjects studied during sleep stage 1-2 (light sleep: LS), sleep stage 3-4 (slow wave sleep: SWS) and rapid eye movement (REM) sleep. Contrary to what has been reported in normal sleep, firstly, the T(oes) threshold for sweating onset differed between REM sleep and both LS and SWS, and, secondly, the slopes of the msw,ch versus T(oes) relationships were unchanged between REM and non-REM (i.e. LS or SWS) sleep. The changes observed after sleep deprivation were hypothesized to be due to alterations in the functioning of the central nervous system controller.

Adult↗

Sleep reactivity during acute nasal CPAP in obstructive sleep apnea syndrome.

OBJECTIVE: To measure the readjustments of sleep macro- and microstructure in patients with obstructive sleep apnea syndrome (OSAS) after acute nasal continuous positive airway pressure (NCPAP) treatment. BACKGROUND: The conventional polysomnographic analysis (macrostructure of sleep) does not necessarily provide the best measures of sleep disruption associated with OSAS. In contrast, microstructural methods of analyzing sleep (i.e., arousals and cyclic alternating pattern) may improve evaluation of patients with OSAS. METHOD: - Ten patients with OSAS were monitored polygraphically before and during the first night of NCPAP therapy. The results were compared with those of 10 age- and sex-matched controls without sleep-related breathing disorders. Each nocturnal recording was followed by daytime observation using the multiple sleep latency test and Visual Analogue Scale (VAS). RESULTS: The first night of ventilatory therapy was characterized by a remarkable expansion of stages 3 and 4 and of REM sleep. In addition, NCPAP suppressed the presence of cyclic alternating pattern (CAP) in REM sleep and induced an impressive rebound of arousals and of certain CAP variables-i.e., CAP rate, CAP time, number of CAP cycles-which dropped well below the physiologic values expressed by controls. A normal duration of phases A and B was re-established starting the first treatment night. When we matched sleep variables with the indices of daytime function, a significant correlation emerged only between the variations of CAP rate and VAS scores. In particular, improvement of daytime sleepiness was less evident when the ventilatory-induced drop of CAP rate was more pronounced. CONCLUSIONS: The application of CAP variables to the microstructural analysis of sleep may expand our knowledge regarding sleep and respiration.

Adult↗

Positional vs nonpositional obstructive sleep apnea patients: anthropomorphic, nocturnal polysomnographic, and multiple sleep latency test data.

STUDY OBJECTIVES: To compare anthropomorphic, nocturnal polysomnographic (PSG), and multiple sleep latency test (MSLT) data between positional (PP) and nonpositional (NPP) obstructive sleep apnea (OSA) patients. DESIGN: This is a retrospective analysis of anthropomorphic, PSG, and MSLT data of a large group of OSA patients who underwent a complete PSG evaluation in our sleep disorders unit. The patients were divided in two groups: the PP group, those patients who had a supine respiratory disturbance index (RDI) that was at least two times higher than the lateral RDI, and the NPP group, those patients in whom the RDI in the supine position was less than twice that in the lateral position. SUBJECTS: From a group of 666 consecutive OSA patients whose conditions were diagnosed in our unit from September 1990 to February 1995, 574 patients met the following criteria and were included in the study: RDI > 10; age > 20 years, and body mass index (BMI) > 20. RESULTS: Of all 574 patients, 55.9% were found to be positional. No differences in height were observed but weight and BMI were significantly higher in the NPP group, these patients being on the average 6.5 kg heavier than those in the PP group. The PP group was, on average, 2 years younger than the NPP group. Nocturnal sleep quality was better preserved in the PP group. In this group, sleep efficiency and the percentages of deep sleep (stages 3 and 4) were significantly higher while the percentages of light sleep (stages 1 and 2) were significantly lower than in the NPP group. No differences for rapid eye movement (REM) sleep were found. In addition, wakefulness after sleep onset and the number of short arousals (< 15 s) were significantly lower in the PP group. Apnea index and total RDI were significantly higher and the minimal arterial oxygen saturation in REM and non-REM sleep was significantly lower in the NPP. No differences in periodic limb movements data were found between the two groups. The average MSLT was significantly shorter in the NPP group. Univariate and multivariate stepwise logistic regression analysis showed that the most dominant variable that correlates with positional dependency in OSA patients is RDI, followed by BMI which also adds a significant contribution to the prediction of positional dependency. Age, although significant, adds only a minor improvement to the prediction of this positional dependency phenomenon. A severe, obese, and older OSA patient is significantly less likely to be positional than a mild-moderate, thin, and young OSA patient. In four obese OSA patients who lost weight, a much more pronounced reduction was seen in the lateral RDI than in the supine RDI, and three of these cases who were previously NPP became PP. CONCLUSIONS: In a large population of OSA patients, most were found to have at least twice as many apneas/hypopneas in the supine than in the lateral position. These so-called "positional patients" are on the average thinner and younger than "nonpositional patients." They had fewer and less severe breathing abnormalities than the NPP group. Consequently their nocturnal sleep quality was better preserved and, according to MSLT data, they were less sleepy during daytime hours. RDI was the most dominant factor that could predict the positional dependency followed by BMI and age. RDI showed a threshold effect, the prevalence of PP in those with severe RDI (RDI > or = 40) was significantly lower than in those OSA patients with mild-moderate RDI. BMI showed a major significant inverse relationship with positional dependency, while age had only a minor although significant inverse relationship with it. Body position during sleep has a profound effect on the frequency and severity of breathing abnormalities in OSA patients.

Adult↗