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PubMed2005

The role of behavioral sleep medicine in the assessment and treatment of sleep disordered breathing.

With the dramatic rise in obesity in the United States, comorbid medical issues, such as sleep apnea and other forms of sleep disordered breathing (SDB), are becoming increasingly prevalent. Individuals with SDB have impairments in social, cognitive, and emotional functioning and an overall reduction in quality of life. Continuous positive airway pressure (CPAP) is the first-line treatment for SDB. CPAP use is associated with improvements in psychosocial functioning when individuals use the machine regularly. Unfortunately, CPAP adherence rates are often low. Patients sometimes discontinue CPAP therapy due to undesirable side effects, such as anxiety, insomnia, and nasal discomfort, or inconvenience. The goal of this review is to highlight the growing role of behavioral sleep medicine in the assessment and treatment of SDB and psychosocial impairments comorbid with SDB. More than any other health specialty, psychologists with behavioral sleep medicine experience are in the best position to treat psychiatric symptoms exacerbated by SDB-related sleep disturbances. Behavioral sleep medicine specialists also possess the expertise to address psychological obstacles to CPAP use. The assimilation of behavioral sleep medicine specialists into sleep clinics is likely to improve the overall quality of care for patients with SDB.

Behavior Therapy↗
PubMed2006

Sleep and sleep disorders in adults with attention deficit/hyperactivity disorder.

Attention deficit/hyperactivity disorder (ADHD) is a frequent disorder that often persists in adulthood. Persistent ADHD is known to be a serious risk factor for other disorders in adulthood, and adults with ADHD often report on sleep disorders. Despite this, only few studies have investigated the subjective and objective quality of sleep in adults suffering from ADHD. Previous studies have revealed seriously impaired subjective sleep quality and increased nocturnal motor activity in spite of essentially normal standard polysomnographic parameters in this patient group. However, primary sleep disorders such as sleep apnea syndrome or restless legs syndrome (RLS) may be misdiagnosed as ADHD. Moreover, ADHD and primary sleep disorders may occur as comorbidities. In particular, RLS was suggested to be highly associated with ADHD, indicating a probable common central nervous dopaminergic dysfunction. To date, larger studies with adequate sample sizes that compare sleep in adult patients with ADHD, healthy control groups and patients with other primary sleep disorders are still lacking.

Adult↗
PubMed2000

Post-trial sleep sequences including transition sleep are involved in avoidance learning of adult rats.

High resolution computerized EEG analyses, and behavioral observations were used to identify slow wave sleep (SS), paradoxical sleep (PS) and transition sleep (TS) in adult male Wistar rats exposed to a session of two-way active avoidance training. Of the four sleep sequences that could be identified, two included TS (SS-->TS-->W and SS-->TS-->PS), while the other two did not (SS-->W and SS-->PS). Comparison of post-trial sleep variables between fast learning rats (FL, reaching criterion in the training session), slow learning rats (SL, reaching criterion in the retention session the following day), and non learning rats (NL, failing to reach criterion) indicated that the total amounts of SS, TS and PS of the SS-->TS-->PS sequence was markedly higher in FL rats than in SL rats. In addition, in comparison with the corresponding baseline period, the average duration and total amount of SS and TS episodes of the SS-->TS-->PS sequence increased in FL rats, while the number of SS-->TS-->W sequences decreased. On the other hand, the average duration of SS episodes increased in the SS-->TS-->W and SS-->W sequences of SL rats, and in the SS-->W and SS-->TS-->PS sequences of NL rats. Correlative analyses between number of avoidances and post-trial sleep variables demonstrated that avoidances were directly correlated with the duration of SS episodes of the SS-->TS-->PS sequence and with the duration of TS episodes of the SS-->TS-->W sequence, but inversely correlated with the number and amount of SS episodes of the SS-->W sequence and with the duration and amount of SS episodes of the SS-->PS sequence. On the whole, the data supported the view that TS-containing sleep sequences are involved in long-term storage of novel adaptive behavior, while sleep sequences lacking TS are involved in the maintenance of innate behavioral responses.

Animals↗
PubMed2000

Sleep onset REM period appearance rate is affected by REM propensity in circadian rhythm in normal nocturnal sleep.

OBJECTIVE: REM latency is usually 60-120 min, but under certain conditions, its latency may be less than 25 min, in which it is known as sleep onset REM period (SOREMP). In order to identify the factors responsible for the appearance of SOREMP, we used the nocturnal sleep interruption method to investigate whether REM propensity in normal nocturnal sleep, (i.e. circadian variations in REM sleep related to body temperature rhythm), could affect the rate of SOREMP appearance (SOREMP%). MATERIALS AND METHODS: After two adaptation and one baseline nights, we interrupted the nocturnal sleep, either in the second or the fourth cycle (early and late conditions, respectively) of 16 subjects and compared SOREMP% at the second sleep onset between these conditions by chi(2) test. Rectal temperature was measured. RESULTS: SOREMP% was found to be 58.1% in the early condition and 87.5% in the late condition - a significant difference. Body temperature dropped at the second sleep onset in both conditions but the drops did not differ significantly. CONCLUSION: We concluded that SOREMP% was affected by circadian variations in REM propensity but SOREMP% and body temperature drop did not show a linear relationship. Further studies to discriminate the influence of circadian rhythm factors and slow wave sleep on SOREMP% are called for.

Adolescent↗
PubMed1997

Avoiding the supine position during sleep lowers 24 h blood pressure in obstructive sleep apnea (OSA) patients.

Obstructive sleep apnea (OSA), is a common clinical condition affecting at least 2-4% of the adult population. Hypertension is found in about half of all OSA patients, and about one-third of all patients with essential hypertension have OSA. There is growing evidence that successful treatment of OSA can reduce systemic blood pressure (BP). Body position appears to have an important influence on the incidence and severity of these sleep-related breathing disturbances. We have investigated the effect of avoiding the supine position during sleep for a 1 month period on systemic BP in 13 OSA patients (six hypertensives and seven normotensives) who by polysomnography (PSG) were found to have their sleep-related breathing disturbances mainly in the supine position. BP monitoring was performed by 24-h ambulatory BP measurements before and after a 1 month intervention period. We used a simple, inexpensive method for avoiding the supine posture during sleep, namely the tennis ball technique. Of the 13 patients, all had a reduction in 24-h mean BP (MBP). The mean 24-h systolic/diastolic (SBP/DBP) fell by 6.4/2.9 mm Hg, the mean awake SBP/DBP fell by 6.6/3.3 mm Hg and the mean sleeping SBP/DBP fell by 6.5/2.7 mm Hg, respectively. All these reductions were significant (at least P < 0.05) except for the sleeping DBP. The magnitude of the fall in SBP was significantly greater in the hypertensive than in the normotensive group for the 24 h period and for the awake hours. In addition, a significant reduction in BP variability and load were found. Since the majority of OSA patients have supine-related breathing abnormalities, and since about a third of all hypertensive patients have OSA, avoiding the supine position during sleep, if confirmed by future studies, could become a new non-pharmacological form of treatment for many hypertensive patients.

Adult↗
PubMed2001

Spatiotemporal changes of slow wave activities before and after 14 Hz/12 Hz sleep spindles during stage 2 sleep.

The present study examined the spatiotemporal changes of slow wave (delta and theta bands) activities before and after 14 Hz/12 Hz sleep spindles during stage 2 sleep, using topographic mapping of electroencephalogram (EEG) power. Both types of sleep spindles appeared after slow wave activities of background EEG decreased. Moreover, the appearance of sleep spindles provided increasing EEG slow wave activities in the subsequent period. Further, the present results showed that an appearance of 14 Hz sleep spindle facilitated slow wave activities at the centro-parietal areas, while an appearance of 12 Hz sleep spindle facilitated slow wave activities at the fronto-central areas. These results suggest that sleep spindles provide cortical de-arousal, and serve to maintain sleep.

Arousal↗
PubMed2005

The relationship of HRV to sleep EEG and sleep rhythm.

Previous studies have shown that there exists a cycle of NREM (non-rapid eye movement)-REM (rapid eye movement) during normal human sleep, and heart rate variability (HRV) has a close relationship to sleep stages and sleep cycle. This article reports the relationship between the electroencephalographic activity and the HRV spectral power in several specific frequency bands. The authors discovered that relationships do exist between HRV and electroencephalogram (EEG) during sleep. In particular, it was found that, prior to the changes of EEG, the changes of HRV usually indicate the shift of sleep stages. HRV frequency analysis indicates that the very-low-frequency components of HRV are closely related to sleep EEG. Results show that the rhythm of the spectral power oscillations in some specific frequency bands of HRV is almost the same as the sleep cycle, which reflects the rhythm of sleep to a certain extent.

Adolescent↗
PubMed2002

Pre- and post-natal protein malnutrition alters the effect of rapid eye movements sleep-deprivation by the platform-technique upon the electrocorticogram of the circadian sleep-wake cycle and its frequency bands in the rat.

Selective deprivation of paradoxical (or rapid eye movements) sleep (REMS) in protein malnourished young male rats, results in circadian and homeostatic alterations. By means of electrocorticographic recordings, we have examined the sleep-wake cycle as a functional maturity index, and its circadian and homeostatic mechanisms in prenatal (PM) and chronically (CM) protein malnourished young male rats. The effects of rapid eye movements sleep-deprivation (REMS-D), by the platform technique in a "conflict experiment" (i.e. recovery from REMS-D begun during the circadian phase of activity), revealed that in PM animals, wake (WAK) was increased significantly during recovery days 1 and 2 (RD1, RD2); and slow wave sleep (SWS) was reduced significantly during these days. Prenatal protein-malnutrition altered the phase of WAK and REMS rhythms, and the amplitude of SWS rhythm was decreased. The REMS compensatory increase after REMS-D (REMS rebound) was confined to the first 4-h block of the activity phase in all experimental groups and 24 h later another REMS rebound was displayed in PM animals. The paradoxical sleep-rebound in CM animals was significantly higher than control and PM rats and it was only shown at the first 4-h block after REMS-D. Before and after REMS-D the circadian distribution of both sleep states, and the electrocortical frequency bands showed different circadian phases at the same day-time in control, PM and CM rats. The aforementioned indicates that protein malnutrition exerts important effects on the circadian and homeostatic mechanisms driving sleep. Therefore, the temporal structure of the malnourished rats may not allow proper synchronization of some sleep parameters, particularly REMS, to the environmental time cues.

Animals↗
PubMed2002

Sleep studies for sleep apnoea.

Sleep studies have grown to encompass a broad range of technologies employed to study and diagnose a variety of sleep disorders. From their inception in neurophysiology laboratories interested in investigating primary disorders of sleep architecture from psychiatric illness, their remit has widened such that their most common role is currently to diagnose secondary sleep disruption from respiratory, cardiovascular or other systemic causes. This review outlines the pathophysiology of obstructive sleep apnoea in particular and how sleep studies have improved our understanding of the complex dynamic changes in blood gas tensions, cardiovascular control and cerebral arousal that occur with these repetitive events. We review the historical development of standard laboratory-based sleep studies and discuss their limitations in staging sleep, reflecting the episodes of increased upper airway resistance that underlie these disorders and their ability to predict individuals' symptoms or response to medical or surgical therapies. We then describe some alternative signals that have been employed to monitor the physiological changes in upper airway resistance and arousal with a discussion of some of the evidence that these 'limited' studies may provide diagnostic information that can guide clinical decision making and may predict the outcome without the need, in some cases, for more complex and costly laboratory-based studies.

Humans↗
PubMed1991

Sleep laboratory studies on the single-dose effects of serotonin reuptake inhibitors paroxetine and fluoxetine on human sleep and awakening qualities.

Paroxetine is a novel antidepressant drug with selective serotonin (5-HT) reuptake inhibitory properties. In a double-blind placebo-controlled crossover sleep laboratory study the single-dose effects on objective and subjective sleep and awakening qualities were investigated after paroxetine 20, 30 and 40 mg morning doses (PX 20, 30, 40), paroxetine 30 mg evening dose, fluoxetine 40 mg morning dose (FX 40) and placebo in 18 healthy young volunteers. The drugs were orally administered in 2-wk intervals. In addition to each drug night, the adaptation night and washout night were recorded. Polysomnographic investigations (10:30 p.m. to 6:00 a.m.) showed a delayed sleep onset only after the morning intake of paroxetine, PX 40 being statistically different from placebo. Total sleep time and sleep efficiency deteriorated under morning PX 30, PX 40 and evening PX 30 as compared to placebo. The nocturnal wake time and sleep stage 1 increased under the paroxetine. Rapid eye movement (REM) reduction (min and %) occurred dose dependently after all paroxetine doses, but the REM latency was lengthened only after the morning intake. The suppressant effect on REM sleep is characteristic for antidepressants and was still significant in the washout nights following PX 40 and evening PX 30. The only statistically relevant finding under 40 mg fluoxetine referred to the increase of REM latency in both drug and washout nights. In contrast to objective results, subjective sleep quality remained generally unchanged. Attention, concentration and reaction performance improved under paroxetine as compared to baseline. The deterioration of well-being under PX 40 might be related to the appearance of drowsiness and nausea. Blood pressure and pulse rate were unaffected.

Adult↗
PubMed1996

Delayed phase jumps of sleep onset in a patient with non-24-hour sleep-wake syndrome.

We studied a 30-year-old man with non-24-hour sleep-wake syndrome. To investigate the relationship between environmental light-dark cycles and his sleep-wake rhythm, we documented his sleep log and rectal temperature data without any therapeutic interventions. We found that 1) the patient's sleep-wake pattern consisted of two different components, appearing alternatively, with a period of 27.2 days: regular free-run (R free-run), consisting of a daily 30- to 60-minute regular delay of sleep onset; and jumping free-run (J free-run), with clusters of delayed (> 4 hours) phase jumps in sleep onset (DP jump): 2) the frequency of sleep onset was higher during late evening hours to midnight hours than in the daytime; 3) DP jumps occurred exclusively when the prior sleep onset was delayed into the daytime; and 4) a cluster of DP jumps was likely to start when the patient's low temperature zone (a period in which rectal temperature was below average) at subjective night was illuminated by sunlight. These results suggest that DP jumps in the patient may occur due to illumination of the delay portion of the phase-response curve.

Adult↗
PubMed1997

A finger-tapping task and a reaction time task as behavioral measures of the transition from wakefulness to sleep: which task interferes less with the sleep onset process.

The aim of this study was to assess whether a finger-tapping task (FTT), in which normal subjects repeatedly tap on a button while falling asleep, could be less disturbing and provide comparable information on the sleep onset period (SOP) with respect to a reaction-time task (RTT) to acoustic stimuli, in which the onset of sleep can be delayed by the arousing effect of the acoustic stimuli. Twelve subjects slept at their homes and six slept in a sleep laboratory for four consecutive nights. After one adaptation night and one baseline night, subjects were required to fall asleep in the third and fourth nights, bimanually performing either a RTT or a FTT. The results indicate that the FTT interfaces less with the SOP compared to the RTT and suggest that the FTT provides further advantages as a behavioral measure of the transition from wakefulness to sleep. In fact, the tapping task is associated with significantly shorter behavioral and polysomnographic sleep onset latencies and with a greater proportion of slow-wave sleep (SWS) during the transition from wakefulness to sleep compared with the RTT. Furthermore, correlations among subjective, behavioral, and electroencephalograph (EEG) latencies confirm the validity of the finger-tapping task as a behavioral measure of sleep onset.

Acoustic Stimulation↗
PubMed1998

Sleep position and sleep stages: evidence of their independence.

Recently we conducted a first ontogenetic study of sleep positions in the human, which involved five groups of 10 subjects (5 males, 5 females) from each of the following age categories: 3-5 years, 8-12 years, 18-24 years, 35-45 years, 65-80 years. They slept for 4 consecutive nights in the laboratory. Sleep positions were recorded during 2 nights with super-8 time-lapse photography. In a first report we presented results showing developmental trends in sleep position shifts, position durations and in the use of prone, supine and side positions. In the current report we present results showing that there was no significant relationship between sleep stages and sleep positions in any group. Furthermore, time-series analyses revealed no consistent pattern of position sequences in any of the age groups. It is concluded that, while there are ontogenetic trends in sleep position preferences, sleep positions are independent of sleep stages and do not show consistent rhythmicity.

Adolescent↗
PubMed1999

Practice parameters for the use of light therapy in the treatment of sleep disorders. Standards of Practice Committee, American Academy of Sleep Medicine.

These clinical guidelines were developed by the Standards of Practice Committee and reviewed and approved by the Board of Directors of the American Academy of Sleep Medicine. The guidelines provide recommendations for the practice of sleep medicine in North America regarding the use of light therapy for treatment of various sleep disorders. This paper is based on a series of articles in the Journal of Biological Rhythms and also includes evidence tables from an updated Medline review covering the period January 1994 to December 1997. Evidence is presented by grade and level. Recommendations are identified as standards, guidelines, or options. Recommendations are provided for delayed sleep phase syndrome (DSPS), advanced sleep phase syndrome (ASPS), non-24-hour sleep-wake syndrome, jet lag, shift work, dementia, and sleep complaints in the healthy elderly. Light therapy appears generally safe if used within recommended intensity and time limits. Light therapy can be useful in treatment of DSPS and ASPS. Benefits of light therapy are less clear and treatment is an option in jet lag, shift work, and non-24-hour sleep-wake syndrome in some blind patients.

Humans↗
PubMed2002

Larger phase angle between sleep propensity and melatonin rhythms in sighted humans with non-24-hour sleep-wake syndrome.

STUDY OBJECTIVES: This study was aimed to clarify phase angle between sleep propensity and the circadian pacemaker in patients with non-24-hour sleep-wake syndrome (Non-24). DESIGN AND SETTING: A case-control study was underaken. PARTICIPANTS: Sighted patient with Non-24 (4 males and 1 female, aged 16 to 39 y), and sex- and age-matched healthy controls (12 males and 3 females, aged 19 to 35 y) participated the study. MEASUREMENT AND INTERVENTION: Following an actigraphic assessment of the sleep-wake cycle in their homes, the participants entered an ultra-short sleep-wake schedule together with simultaneous measurement of dim light melatonin rhythm after 24-hour sleep deprivation. RESULTS: The period of the sleep-wake cycle observed at home was longer in the Non-24 patients (25.12 hours) than in the controls (24.02 hours, p<0.0001). The interval from sleep propensity (SP) onset to the melatonin midpoint (MLmid) was significantly shorter in the Non-24 patients than in the controls. The interval from the MLmid to the SP offset was significantly longer in the Non-24 patients than in the controls. CONCLUSIONS: It was postulated that Non-24 sufferers' delayed SP onset relative to the circadian pacemaker may accelerate the light-induced phase-delay, leading to sleep-wake cycle that is longer than 24 hours.

Adolescent↗
PubMed2002

Effects of age and sleeping position on arousal from sleep in preterm infants.

STUDY OBJECTIVES: Preterm infants are at increased risk of sudden infant death syndrome (SIDS). We investigated whether the prone sleeping position impaired arousal from sleep in healthy preterm infants and whether this impairment was related to cardiorespiratory variables, temperature or postnatal age. DESIGN: Longitudinal SETTING/PARTICIPANTS: 14 healthy preterm infants (mean 32 +/- 0.4 weeks) were studied using daytime polysomnography on 4 occasions: 36-38 weeks postconception age, 2 to 3 weeks postterm, 2 to 3 months postterm, and 5 to 6 months postterm. INTERVENTIONS: N/A. MEASUREMENTS: Multiple measurements of arousal threshold (cm H2O) in response to air-jet stimulation applied alternately to the nares were made in both active sleep and quiet sleep when infants slept both prone and supine. RESULTS: Arousal thresholds were significantly higher in both AS and QS when infants slept prone at 36 to 38 weeks postconception age and 2 to 3 months postterm but not at 2 to 3 weeks or 5 to 6 months postterm. These increases were independent of any sleep position-related changes in either rectal or abdominal skin temperature, respiratory rate, oxygen saturation or heart rate. CONCLUSIONS: At the age when the risk of SIDS is highest, the prone position significantly impairs arousal from both active sleep and quiet sleep in healthy infants born prematurely. This impairment in arousability occurred with no clinically significant changes in cardiorespiratory parameters or body temperature. Decreased arousability from sleep in the prone position may explain its role as a risk factor for SIDS.

Arousal↗
PubMed2005

Haptoglobin phenotype, sleep-disordered breathing, and the prevalence of cardiovascular disease: the Sleep Heart Health Study.

BACKGROUND: Diabetes is an independent risk factor for cardiovascular disease, and there is growing evidence that sleep-disordered breathing also may increase the risk of cardiovascular disease. The mechanism responsible for increased susceptibility of people with diabetes to cardiovascular disease is thought to share several features with sleep-disordered breathing, notably increased oxidative stress. We recently demonstrated that a particular haptoglobin phenotype that is associated with differential antioxidant activity is an independent risk factor for cardiovascular disease in individuals with diabetes. We therefore sought to determine whether sleep-disordered breathing and cardiovascular disease are more strongly associated among people with the unfavorable haptoglobin phenotype. METHODS: We tested this hypothesis in 2612 middle-aged and older participants from the Sleep Heart Health Study. Haptoglobin phenotyping was performed by gel electrophoresis. Respiratory disturbance index was assessed by standard methods. Logistic regression analysis was performed to estimate the association between haptoglobin phenotype and cardiovascular disease, adjusting for known cardiovascular risk factors (age, sex, diabetes, smoking, lipid levels, and hypertension). Possible modification by haptoglobin phenotype of the association of sleep-disordered breathing with cardiovascular disease prevalence was explored by examining interaction terms. RESULTS: We found no significant association between haptoglobin phenotype and prevalent cardiovascular disease in this cohort, nor were significant interactions found between haptoglobin phenotype and sleep-disordered breathing on the prevalence of cardiovascular disease. CONCLUSIONS: Sleep-disordered breathing did not appear to interact with haptoglobin phenotype in modifying the association with prevalent cardiovascular disease in the Sleep Heart Health Study. These findings could be due to the absence of association or to survivor bias in these cross-sectional analyses.

Aged↗
PubMed2006

Comparison of CPAP titration at home or the sleep laboratory in the sleep apnea hypopnea syndrome.

STUDY OBJECTIVES: Continuous positive airway pressure (CPAP) for the treatment of obstructive sleep apnea hypopnea syndrome (OSAHS) is conventionally started after in-laboratory overnight titration. This use of sleep laboratory space is both costly and limits access for diagnostic studies. This study aimed to evaluate whether automated CPAP titration in the home produced patient outcomes equal to those following laboratory-based automated CPAP titration. The main outcomes were Epworth Sleepiness Scale score, objective daytime sleepiness (Oxford SLEep Resistance test or OSLER test), and CPAP use; we also performed quality-of-life questionnaires: Functional Outcomes of Sleep Questionnaire and SF-36. DESIGN: Prospective, randomized, single-blind, parallel-group, controlled trial SETTING: Regional sleep center and patients' homes. PATIENTS: Two hundred CPAP-naïve patients with OSAHS requiring CPAP treatment. INTERVENTIONS: One hundred patients were randomly assigned to a standard 1-night in-hospital CPAP titration and 100 to 3 nights' home CPAP titration and then issued with fixed pressure CPAP. Data were analyzed on an intention-to-treat basis. MEASUREMENTS AND RESULTS: The patient groups did not differ at baseline. The CPAP pressures defined at titration (mean+/- SEM: 10.6+/-0.2, 10.4+/-0.2 cm H20, p = .19), number of mask leaks, and initial acceptance rates were similar in the sleep-laboratory and home-titrated groups. At 3-month follow-up, there was no significant difference in CPAP use (mean+/-SEM: 4.39+/-0.25, 4.38+/-0.25 h/night; p > .9), Epworth Sleepiness Scale score (9.5+/-0.5, 8.5+/-0.5, p = .14), OSLER, Functional Outcomes of Sleep Questionnaire, or SF-36 between the sleep-laboratory and home-titrated groups. CONCLUSIONS: Home-based automated CPAP titration is as effective as automatic in-laboratory titrations in initiating treatment for OSAHS.

Calibration↗