The Feasibility and Utility of Continuous Sleep Monitoring in Critically Ill Patients Using a Portable Electroencephalography Monitor.

BACKGROUND: Sleep disruption in critically ill adults can result in acute decrements in cognitive function, including delirium, but it is underdiagnosed in the setting of the intensive care unit (ICU). Although sleep stages can be assessed by polysomnography (PSG), acquisition and interpretation of PSG is costly, is labor intensive, is difficult to do over an extended period of time with critically ill patients (multiple days of continuous recording), and may interfere with patient care. In this pilot study, we investigated the feasibility and utility of monitoring sleep in the ICU setting using a portable electroencephalography (EEG) monitor, the SedLine brain monitor. METHODS: We first performed a baseline comparison study of the SedLine brain monitor by comparing its recordings to PSG recorded in a sleep laboratory (n = 3). In a separate patient cohort, we enrolled patients in the ICU who were monitored continuously with the SedLine monitor for sleep disruption (n = 23). In all enrolled patients, we continuously monitored their EEG. The raw EEG was retrieved and sleep stages and arousals were analyzed by a board-certified technologist. Delirium was measured by a trained research nurse using the Confusion Assessment Method developed for the ICU. RESULTS: For all enrolled patients, we continuously monitored their EEGs and were able to retrieve the raw EEGs for analysis of sleep stages. Overall, the SedLine brain monitor was able to differentiate sleep stages, as well as capture arousals and transitions between sleep stages compared with the PSG performed in the sleep laboratory. The percentage agreement was 67% for the wake stage, 77% for the non-rapid eye movement (REM) stage (N1 = 29%, N2 = 88%, and N3 = 6%), and 89% for the REM stage. The overall agreement was measured with the use of weighted kappa, which was 0.61, 95% confidence interval, 0.58 to 0.64. In the ICU study, the mean recording time for the 23 enrolled patients was 19.10 hours. There were several signs indicative of poor-quality sleep, where sleep was distributed throughout the day, with reduced time spent in REM (1.38% ± 2.74% of total sleep time), and stage N3 (2.17% ± 5.53% of total sleep time) coupled with a high arousal index (34.63 ± 19.04 arousals per hour). The occurrence of ICU delirium was not significantly different between patients with and without sleep disruption. CONCLUSIONS: Our results suggest the utility of a portable EEG monitor to measure different sleep stages, transitions, and arousals; however, the accuracy in measuring different sleep stages by the SedLine monitor varies compared with PSG. Our results also support previous findings that sleep is fragmented in critically ill patients. Further research is necessary to develop portable EEG monitors that have higher agreement with PSG.

Cognitive-behavioral therapy for insomnia in knee osteoarthritis: a randomized, double-blind, active placebo-controlled clinical trial.

OBJECTIVE: Insomnia is prevalent among patients with knee osteoarthritis (OA). Research indicates that sleep disruption may amplify clinical pain by altering central pain modulation, suggesting that treatment of insomnia may improve pain. The aims of this study were to evaluate the efficacy of cognitive-behavioral therapy for insomnia (CBT-I) in patients with knee OA, to determine whether improvements in sleep predict reduced pain, and to determine whether alterations in pain modulation mediate improvements in clinical pain. METHODS: We conducted a randomized, double-blind, active placebo-controlled clinical trial of CBT-I in 100 patients with knee OA and insomnia (mean ± SD age 59.4 ± 9.5 years). Patients were randomized (1:1) to receive either 8 sessions of CBT-I or behavioral desensitization (placebo). We conducted in-home polysomnography (PSG), diary assessment, and sensory tests of pain modulation at baseline, posttreatment, 3 months, and 6 months. RESULTS: Intent-to-treat analyses demonstrated substantial improvement in sleep in both groups of patients. Patients in the CBT-I group had significantly greater reductions in wake after sleep onset (WASO), as measured by patient diary and PSG. Patients in both groups reported significant and comparable reductions in pain over 6 months, with one-third reporting a 30% reduction in pain severity. Baseline-to-posttreatment reductions in WASO as measured by diary and PSG predicted subsequent decreases in clinical pain. This effect was significantly greater for CBT-I compared with behavioral desensitization. No significant changes in laboratory measures of pain modulation were observed. CONCLUSION: Compared with active placebo, CBT-I was efficacious in reducing sleep maintenance insomnia. CBT-I decreased clinical pain, but not pain modulation, suggesting that it has the potential to augment pain management in knee OA. Future work is needed to identify the mechanisms by which improved sleep reduces clinical pain.