SUMMARY Wrist actigraphy is employed increasingly in sleep research and clinical sleep medicine.Critical evaluation of the performance of new actigraphs and software is needed. Actigraphic sleep-wake estimation was compared with polysomnographic (PSG) scoring as the standard in a clinical sleep laboratory. A convenience sample of 116 patients undergoing clinical sleep recordings volunteered to participate. Actiwatch-L recordings were obtained from 98 participants, along with 18 recordings using the newer Spectrum model (Philips Electronics), but some of the actigraphic recordings could not be adequately aligned with the simultaneous PSGs. Of satisfactory alignments, 40 Actiwatch recordings were used as a training set to empirically develop a new Scripps Clinic algorithm for sleep-wake scoring. The Scripps Clinic algorithm was then prospectively evaluated in 39 Actiwatch recordings and 16 Spectrum recordings, producing epoch-by-epoch sleep-wake agreements of 85-87% and kappa statistics averaging 0.52 (indicating moderate agreement). Wake was underestimated by the scoring algorithm. The correlations of PSG versus actigraphic wake percentage estimates were r = 0.6690 for the Actiwatch and r = 0.2197 for the Spectrum. In general, using a different weighting of activity counts from previous and subsequent epochs, the Scripps Clinic algorithm discriminated sleep-wake more successfully than the manufacturerÕs Actiware algorithms. Neither algorithm had fully satisfactory agreement with PSG. Further evaluations of algorithms for these actigraphs are needed, along with controlled comparisons of different actigraphic designs and software.

SciEnTific invESTigATiOnSBackground: Type 2 diabetes and obstructive sleep apnea (OSA) are frequently comorbid conditions. OSA is associated with increased insulin resistance, but studies of continuous positive airway pressure (CPAP) have shown inconsistent effects on glycemic control. However, endpoints such as hemoglobin A1c and insulin sensitivity might not reflect short-term changes in glycemic control during sleep. Methods: We used a continuous glucose-monitoring system to measure interstitial glucose every 5 minutes during polysomnography in 20 patients with type 2 diabetes and newly diagnosed OSA. The measurements were repeated after an average of 41 days of CPAP (range 26-96 days). All patients were on a stable diet and medications. Each 30-second epoch of the polysomnogram was matched with a continu-second epoch of the polysomnogram was matched with a continu-epoch of the polysomnogram was matched with a continuous glucose-monitoring system reading, and the sleeping glucose level was calculated as the average for all epochs scored as sleeping. Results: The mean sleeping glucose decreased from untreated (122.0 ± 61.7 mg/dL) to treated (102.9 ± 39.4 mg/dL; p = 0.03 by Wilcoxon paired rank test). The sleeping glucose was more stable after treatment, with the median SD decreasing from 20.0 to 13.0 mg/dL (p = 0.005) and the mean difference between maximum and minimum values decreasing from 88 to 57 mg/dL (p = 0.003). The change in the mean hemoglobin A1c from 7.1% to 7.2% was not significant. conclusions: Our study is limited by the lack of a control group, but the results suggest that sleeping glucose levels decrease and are more stable after patients with type 2 diabetes and OSA are treated with CPAP.

Background: The incidence of insomnia and depression in the elder population is significant. It is hoped that use of light treatment for this group could provide safe, economic, and effective rapid recovery.

We estimated diurnal and nocturnal levels of ocular perfusion pressure at rest in both young and older adults in a clinical sleep laboratory. Measurements of blood pressure and intraocular pressure (IOP) were obtained every 2 hours for 24 consecutive hours in 16 healthy young adults (ages 18-25 years) and 16 older adults (ages 47-74 years). In the 16-hour diurnal wake period, blood pressure and IOP were measured after a 5-minute sitting rest. In the 8-hour nocturnal period, measurements were taken with subjects in the supine position. Sitting and supine ocular perfusion pressures in the diurnal and nocturnal periods were calculated respectively based upon the blood pressure and IOP. Ocular perfusion pressure was found to be higher in the older group than in the younger group throughout the 24 hours. The peak of ocular perfusion pressure was in the nocturnal period for both groups. Within each subject group, the average nocturnal ocular perfusion pressure in the supine position was higher than the average diurnal ocular perfusion pressure in the sitting position. The diurnal-to-nocturnal increase of ocular perfusion pressure was larger in the older group than in the younger group.

Recent meta-analyses raising concern about risks of hypnotics suggest a need for more clarification of these risks. Methods: Because of preliminary suggestions that eszopiclone causes infections, we studied US Food and Drug Administration files on the 4 most-recently approved hypnotics, combined with published studies, to compile the risk ratios of infections for groups randomly assigned to receive hypnotics versus those assigned to receive placebos in controlled trials. Parallel controlled clinical trials of eszopiclone, ramelteon, zaleplon, and zolpidem were included when data on subjects, duration of exposure, and adverse effects were available. Results of trials were combined by meta-analyses. Results: Of 8828 participants assigned to the 4 hypnotics and 4383 participants who randomly received placebos, 606 in the hypnotics groups and 200 in the placebo groups were reported to develop some kind of infection (risk ratio = 1.44, 95% confidence interval 1.25-1.64, p < 0.00001). Most infections were apparently mild and did not lead to dropouts. Subanalyses for individual drugs indicated that eszopiclone and zolpidem individually were associated with reported infections. There were insufficient data concerning individual studies of zaleplon and ramelteon for valid secondary meta-analyses of zaleplon or ramelteon by themselves. Conclusions: Research is needed to objectively determine whether the use of hypnotics increases the risk of infections. Immune compromise or esophageal reflux and aspiration should be studied as possible mechanisms.