Polysomnography

About: Polysomnography is a research topic. Over the lifetime, 19527 publications have been published within this topic receiving 858718 citations. The topic is also known as: PSG & polysomnogram.

Patient-ventilator interaction and sleep in mechanically ventilated patients: pressure support versus proportional assist ventilation.

Abstract: Objectives: To understand the role of patient-ventilator asynchrony in the etiology of sleep disruption and determine whether optimizing patient-ventilator interactions by using proportional assist ventilation improves sleep. Design: Randomized crossover clinical trial. Setting: A tertiary university medical-surgical intensive care unit. Patients: Thirteen patients during weaning from mechanical ventilation. Interventions: Patients were randomized to receive pressure support ventilation or proportional assist ventilation on the first night and then crossed over to the alternative mode for the second night. Polysomnography and measurement of light, noise, esophageal pressure, airway pressure, and flow were performed from 10 pm to 8 am. Ventilator settings (pressure level during pressure support ventilation and resistive and elastic proportionality factors during proportional assist ventilation) were set to obtain a 50% reduction of the inspiratory work (pressure time product per minute) performed during a spontaneous breathing trial. Measurements and Main Results: Arousals per hour of sleep time during pressure support ventilation were 16 (range 2‐74) and

A validation study of Fitbit Charge 2™ compared with polysomnography in adults.

Abstract: We evaluated the performance of a consumer multi-sensory wristband (Fitbit Charge 2™), against polysomnography (PSG) in measuring sleep/wake state and sleep stage composition in healthy adults.In-l...

Obstructive Sleep Apnea: Should All Children With Down Syndrome Be Tested?

Abstract: Objectives To determine the incidence of obstructive sleep apnea syndrome in children aged 2 to 4 years with Down syndrome and to determine parents' ability to predict sleep abnormalities in this patient population. Design Prospective cohort study. Setting Tertiary care pediatric referral center. Patients Sixty-five children participating in a 5-year longitudinal study in which the otolaryngologic problems seen in Down syndrome were evaluated. Fifty-six completed overnight polysomnography (PSG) between 4 and 63 months of age (mean age, 42 months). Interventions Overnight PSG was performed. Parents also completed a questionnaire regarding their impressions of their child's sleep patterns before PSG. Main Outcome Measures Polysomnograms were classified as abnormal if the obstructive index was greater than 1, if the carbon dioxide level was greater than 45 mm Hg for more than two thirds of the study or greater than 50 mm Hg for more than 10% of the study, and/or if there was unexpected hypoxemia less than 92% during sleep or repeated intermittent desaturations less than 90%. We also identified a group of children whose PSGs findings were normal except for an arousal index greater than 10 and were associated with increased work of breathing. Results The PSGs revealed that 57% of the children had abnormal results and evidence of obstructive sleep apnea syndrome. If we also include an elevated arousal index, 80% of the PSGs had abnormal results. Sixty-nine percent of parents reported no sleep problems in their children, but in this group, 54% of PSGs had abnormal results. Of the parents who reported sleep problems in their children, only 36% had abnormal sleep study results. Conclusion Because of the high incidence of obstructive sleep apnea syndrome in young children with Down syndrome, and the poor correlation between parental impressions of sleep problems and PSG results, baseline PSG is recommended in all children with Down syndrome at age 3 to 4 years.

Practice Parameters for Using Polysomnography to Evaluate Insomnia: An Update

Abstract: Insomnia is a common and clinically important problem. It may arise directly from a sleep-wake regulatory dysfunction and/or indirectly result from comorbid psychiatric, behavioral, medical, or neurological conditions. As an important public-health problem, insomnia requires accurate diagnosis and effective treatment. Insomnia is primarily diagnosed clinically with a detailed medical, psychiatric, and sleep history. Polysomnography is indicated when a sleep-related breathing disorder or periodic limb movement disorder is suspected, initial diagnosis is uncertain, treatment fails, or precipitous arousals occur with violent or injurious behavior. However, polysomnography is not indicated for the routine evaluation of transient insomnia, chronic insomnia, or insomnia associated with psychiatric disorders.

Neurobehavioral Dynamics Following Chronic Sleep Restriction: Dose-Response Effects of One Night for Recovery

Abstract: RECOVERY OF NEUROBEHAVIORAL FUNCTIONS FROM CHRONIC CURTAILMENT OF SLEEP DURATION AS A RESULT OF WORK, MEDICAL CONDITIONS, OR lifestyle1 is not well understood. It has been rarely studied, despite the fact that a common sleep pattern for millions of people involves sleep restriction for 5 weekdays/workdays, followed by sleep extension on at least one weekend night (or day off from work).2–4 Much of what is known about recovery from sleep loss has been based on total sleep deprivation experiments, where robust NREM EEG slow wave activity (SWA, 0.5-4.5Hz) responses are the norm.5–9 Experiments in chronically sleep-restricted rats revealed increased recovery sleep duration, NREM and REM sleep durations, and elevated SWA, while only a small portion of the chronically lost sleep was actually recovered.10,11 Experiments in healthy humans have confirmed that chronic reduction of sleep can result in waking neurobehavioral deficits that become progressively worse over days;12–15 that the rate of accumulation of waking deficits is a function of the magnitude of the sleep restriction;12,15,16 and that measures of sleepiness, performance lapsing, and cognitive slowing can accumulate to deficit levels found for total sleep deprivation.15 These findings indicate that waking brain impairment from chronic sleep loss is sleep dose-dependent, that it can be as severe as that resulting from total sleep deprivation, and that the “sleep debt” is a result of prior sleep-wake history extending back in time more than a day. Thus, chronic sleep restriction appears to induce slow changes (spanning days to weeks) in neural processes mediating alertness, attention and other aspects of cognitive functioning, including learning and memory.17 How these slow (cumulative) changes are reversed via the dynamics of recovery sleep is not known. Kleitman suggested “sleep debts” are “liquidated” by extending recovery sleep duration (p. 317).18 However, the primary model of human sleep homeostasis, the two-process model,19,20 posits that the intensity and temporal dynamics of NREM EEG SWA, more so than sleep duration, reflect the recovery process. For example, the two-process model predicts only an initial modest (∼10%-20%) elevation in SWA over the first few days of sleep restricted to 4 h per night, which has been experimentally confirmed,15,21 although increases of 50% have been reported for a broader EEG frequency band (1.25-7.75 Hz).22 The relatively modest increment in SWA during and following sleep restriction is not congruent with the large cumulative neurobehavioral deficits that develop across days of sleep restriction.15 The apparent uncoupling during chronic sleep restriction of the putative marker of homeostatic sleep drive (SWA) and waking neurobehavioral functions suggests that sleep duration and/or other aspects of sleep (e.g., REM sleep) may also have a critical role in recovery of neurobehavioral capability following chronic sleep restriction. On the other hand, the high degree of colinearity among SWA, TST and the duration of sleep stages may prevent attributing recovery from chronic sleep restriction to a specific physiological feature of sleep. The dynamics of recovery of human waking alertness and neurobehavioral functions following chronic sleep restriction have not been systematically investigated. Experiments in healthy adults scheduled to 7 nights of sleep restricted to 3 h-7 h TIB12 or 5 nights of sleep restricted to 4 h TIB22 yielded data suggesting that some neurobehavioral functions may not return to baseline following up to 3 recovery sleep periods limited to 8 h TIB.12,23 Studying the dynamics of recovery from cumulative sleep loss is critical to a range of behavioral guidelines (e.g., days off duty for recovery from work schedules),24 biological questions (e.g., mechanisms and rates of homeostatic sleep drive build-up and dissipation),25 and theoretical issues (e.g., processes to instantiate into mathematical models predicting sleep and alertness).26–28The present experiment was designed to provide the first systematic, randomized, sleep dose-response data on the dynamic recovery of neurobehavioral functions when a single recovery sleep opportunity follows 5 days of nocturnal sleep restriction to 4 h TIB. The study tested the hypothesis that following sleep restriction, recovery of primary measures of neurobehavioral alertness would increase monotonically in relation to the duration of time allowed for recovery sleep. We also sought to determine the features of sleep that parallel this recovery.