Polysomnogram

Abstract: Three hundred six consecutively treated surgical patients with obstructive sleep apnea syndrome were evaluated from a group of 415 patients. One hundred nine patients were excluded because they failed to obtain a postoperative polysomnogram or were lost to followup. All patients received a physical examination, cephalometric analysis, fiberoptic examination, and polysomnography before treatment to document OSAS and determine the areas of obstruction. A two-phase surgical protocol was used for the reconstruction of the upper airway. Phase I surgery consisted of a uvulopalatopharyngoplasty (UPPP) for palatal obstruction and genioglossus advancement with hyoid myotomy-suspension for base of tongue obstruction. Failures of phase I were offered phase 2 reconstruction, which consisted of maxillary-mandibular advancement osteotomy. One hundred twenty-one patients were treated with nasal continuous positive airway pressure (CPAP) before surgery and this was the primary method of evaluating surgical success. Results were reported on the polysomnogram performed a minimum of 6 months after surgery and compared to the preoperative polysomnogram and the second night nasal CPAP study. The polysomnographic results included respiratory disturbance index (RDI), lowest oxyhemoglobin saturation (LSAT), and sleep architecture parameters. Surgery was considered a success if it was equivalent to nasal CPAP or the postoperative RDI was less than 20 with normal oxygenation. The overall success rate, which included patients that dropped from the protocol, was 76.5%, with a mean followup of 9.3 months (SD, 6.7). The preoperative RDI, nasal CPAP RDI, and postoperative RDI were 55.8 (SD, 26.7), 7.2 (SD, 5.4), and 9.2 (SD, 7.5), respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Abstract: See Mander et al. (doi:10.1093/awx174) for a scientific commentary on this article.Sleep deprivation increases amyloid-beta, suggesting that chronically disrupted sleep may promote amyloid plaques and other downstream Alzheimer's disease pathologies including tauopathy or inflammation. To date, studies have not examined which aspect of sleep modulates amyloid-beta or other Alzheimer's disease biomarkers. Seventeen healthy adults (age 35-65 years) without sleep disorders underwent 5-14 days of actigraphy, followed by slow wave activity disruption during polysomnogram, and cerebrospinal fluid collection the following morning for measurement of amyloid-beta, tau, total protein, YKL-40, and hypocretin. Data were compared to an identical protocol, with a sham condition during polysomnogram. Specific disruption of slow wave activity correlated with an increase in amyloid-beta40 (r = 0.610, P = 0.009). This effect was specific for slow wave activity, and not for sleep duration or efficiency. This effect was also specific to amyloid-beta, and not total protein, tau, YKL-40, or hypocretin. Additionally, worse home sleep quality, as measured by sleep efficiency by actigraphy in the six nights preceding lumbar punctures, was associated with higher tau (r = 0.543, P = 0.045). Slow wave activity disruption increases amyloid-beta levels acutely, and poorer sleep quality over several days increases tau. These effects are specific to neuronally-derived proteins, which suggests they are likely driven by changes in neuronal activity during disrupted sleep.

Abstract: Epidemiological studies have shown that playing a computer game at night delays bedtime and shortens sleeping hours, but the effects on sleep architecture and quality have remained unclear. In the present study, the effects of playing a computer game and using a bright display on nocturnal sleep were examined in a laboratory. Seven male adults (24.7+/-5.6 years old) played exciting computer games with a bright display (game-BD) and a dark display (game-DD) and performed simple tasks with low mental load as a control condition in front of a BD (control-BD) and DD (control-DD) between 23:00 and 1:45 hours in randomized order and then went to bed at 2:00 hours and slept until 8:00 hours. Rectal temperature, electroencephalogram (EEG), heart rate and subjective sleepiness were recorded before sleep and a polysomnogram was recorded during sleep. Heart rate was significantly higher after playing games than after the control conditions, and it was also significantly higher after using the BD than after using the DD. Subjective sleepiness and relative theta power of EEG were significantly lower after playing games than after the control conditions. Sleep latency was significantly longer after playing games than after the control conditions. REM sleep was significantly shorter after the playing games than after the control conditions. No significant effects of either computer games or BD were found on slow-wave sleep. These results suggest that playing an exciting computer game affects sleep latency and REM sleep but that a bright display does not affect sleep variables.