Use of actigraphy for monitoring agitation and rest-activity cycles in patients with acute traumatic brain injury in the ICU.

BACKGROUND: In traumatic brain injury patients (TBI) admitted to the intensive care unit (ICU), agitation can lead to accidental removal of catheters, devices as well as self-extubation and falls. Actigraphy could be a potential tool to continuously monitor agitation. The objectives of this study were to assess the feasibility of monitoring agitation with actigraphs and to compare activity levels in agitated and non-agitated critically ill TBI patients. METHODS: Actigraphs were placed on patients' wrists; 24-hour monitoring was continued until ICU discharge or limitation of therapeutic efforts. Feasibility was assessed by actigraphy recording duration and missing activity count per day. RESULTS: Data from 25 patients were analyzed. The mean number of completed day of actigraphy per patient was 6.5 ± 5.1. The mean missing activity count was 20.3 minutes (±81.7) per day. The mean level of activity measured by raw actigraphy counts per minute over 24 hours was higher in participants with agitation than without agitation. CONCLUSIONS: This study supports the feasibility of actigraphy use in TBI patients in the ICU. In the acute phase of TBI, agitated patients have higher levels of activity, confirming the potential of actigraphy to monitor agitation.

Sleep from acute to chronic traumatic brain injury and cognitive outcomes.

STUDY OBJECTIVES: Traumatic brain injuries (TBIs) cause persistent cerebral damage and cognitive deficits. Because sleep may be a critical factor for brain recovery, we characterized the sleep of patients with TBI from early hospitalization to years post-injury and explored the hypothesis that better sleep during hospitalization predicts more favorable long-term cognitive outcomes. METHODS: We tested patients with moderate-to-severe TBI in the hospitalized (n = 11) and chronic (n = 43) stages using full-night polysomnography, with 82% of the hospitalized group being retested years post-injury. Hospitalized patients with severe orthopedic and/or spinal cord injury (n = 14) and healthy participants (n = 36) were tested as controls for the hospitalized and chronic TBI groups, respectively. Groups had similar age and sex and were compared for sleep characteristics, including slow waves and spindles. For patients with TBI, associations between sleep during hospitalization and long-term memory and executive function were assessed. RESULTS: Hospitalized patients with TBI or orthopedic injuries had lower sleep efficiency, higher wake after sleep onset, and lower spindle density than the chronic TBI and healthy control groups, but only hospitalized patients with brain injury had an increased proportion of slow-wave sleep. During hospitalization for TBI, less fragmented sleep, more slow-wave sleep, and higher spindle density were associated to more favorable cognitive outcomes years post-injury, while injury severity markers were not associated with these outcomes. CONCLUSION: These findings highlight the importance of sleep following TBI, as it could be a strong predictor of neurological recovery, either as a promoter or an early marker of cognitive outcomes.

Slow wave activity moderates the association between new learning and traumatic brain injury severity.

STUDY OBJECTIVES: Sleep-wake complaints and difficulties in making new learning are among the most persistent and challenging long-term sequelea following moderate to severe traumatic brain injury (TBI). Yet, it is unclear whether, and to what extent, sleep characteristics during the chronic stage of TBI contribute to sleep-wake and cognitive complaints. We aimed to characterize sleep architecture in chronic moderate to severe TBI adults and assess whether non-rapid eye movement slow wave activity (SWA) is associated to next day performance in episodic memory tasks according to TBI severity. METHODS: Forty-two moderate to severe TBI participants, 12-47 months post-injury, and 38 healthy controls were tested with one night of in-laboratory polysomnography, followed the next morning by questionnaires (sleep quality, fatigue, and sleepiness) and neuropsychological assessment. We used multiple regression analyses to assess the moderator effect of SWA power on TBI severity and next-day memory performance. RESULTS: We found that TBI participants reported worse sleep quality and fatigue, and had worse cognitive performance than controls. No between group differences were found on macro- and micro-architecture of sleep. However, SWA significantly interacted with TBI severity to explain next-day memory performance: higher SWA was more strongly associated to better memory performance in more severe TBI compared to milder TBI. CONCLUSIONS: This study provides evidence that the injured brain is able to produce macro- and micro-architecture of sleep comparable to what is seen in healthy controls. However, with increasing TBI severity, lower non-rapid eye movement SWA power is associated with reduced ability to learn and memorise new information the following day.

Impact of Mandatory Wake Time on Sleep Timing, Sleep Quality and Rest-Activity Cycle in College and University Students Complaining of a Delayed Sleep Schedule: An Actigraphy Study.

BACKGROUND: Individuals complaining of a delayed sleep schedule are expected to have shorter sleep duration and lower sleep quality when they must comply with morning obligations. The changes in the sleep schedule imposed by morning obligations may in turn decrease the stability and amplitude of their rest-activity cycle. These expectations were only partially supported in previous studies, possibly due to poor differentiation between days with mandatory or free wake times. PARTICIPANTS: Fourteen college/university students (8 women) with a complaint of a late sleep schedule and a bedtime after midnight were compared to fourteen controls with an earlier sleep schedule and no complaint. METHODS: During a week of 24-h activity recording, participants specified in their sleep diary whether their wake time was free or determined by an obligation. RESULTS: The number of nights with mandatory wake times was similar in the two groups. Groups were also similar for sleep duration and sleep quality over the 7 days of recording. Actigraphic sleep efficiency was the same in the two groups for both free and mandatory wake times, but subjective sleep quality decreased on the nights with mandatory wake time in both groups. On the nights with mandatory wake time, delayed participants had shorter sleep episodes and less total sleep time than controls. Rest-activity cycle amplitude was lower in the delayed group whether wake time was free or mandatory. CONCLUSION: Sleep duration and total sleep time differed between the two groups only when wake time was mandatory. Prior to mandatory wake times, delayed participants kept the same bedtime and shortened their sleep; sleep latency and sleep efficiency were preserved but subjective sleep quality and alertness on awakening decreased compared to nights with free wake time. Lower amplitude of the rest-activity cycle in delayed subjects may reflect lifestyle differences compared to control participants.

Home versus laboratory assessments of melatonin production and melatonin onset in young adults complaining of a delayed sleep schedule.

Recent evidence points toward an association between higher non-visual sensitivity to light and a later circadian phase in young adults complaining of a delayed sleep schedule. Light exposure in the evening may therefore induce a larger suppression of melatonin production in these individuals, which might: (a) bias home estimates of melatonin onset; and (b) decrease sleep propensity at bedtime. In this study, we compared home and laboratory melatonin onsets and production in sleep-delayed and control participants, using saliva samples collected in the 3 hr preceding habitual bedtime. The mean light intensity measured during saliva sampling at home was ~10 lux in both groups. Melatonin suppression at home was significant, averaging 31% and 24% in sleep-delayed and control individuals, respectively. Group difference in melatonin suppression was not significant. Estimates of melatonin onset were on average 27 min later at home than in laboratory conditions, with no group difference. Looking specifically at sleep-delayed participants, there was no correlation between non-visual sensitivity to light and home-laboratory differences in melatonin onsets. However, higher light sensitivity was associated with greater melatonin suppression in the hour before habitual bedtime. Greater melatonin suppression before bedtime was also associated with a later circadian phase. These results indicate that the validity of home estimates of melatonin onset is similar in sleep-delayed and in control individuals. Results also suggest that increased non-visual sensitivity to light could impact melatonin secretion in sleep-delayed individuals and contribute to a late bedtime by delaying circadian phase and decreasing sleep propensity.

Sleep-wake disturbances in hospitalized patients with traumatic brain injury: association with brain trauma but not with an abnormal melatonin circadian rhythm.

STUDY OBJECTIVES: To test whether the sleep-wake cycle disruption in patients hospitalized with traumatic brain injury (TBI) (1) is also found in patients with traumatic injuries other than TBI (non-TBI) and (2) is associated with a weaker or abnormal circadian clock signal. METHODS: Forty-two non-mechanically ventilated and non-sedated patients hospitalized for moderate-to-severe TBI were compared to 34 non-TBI patients. They wore wrist actigraphs for 9.4 ± 4.2 days, starting 19.3 ± 12.6 days post-injury. Of these, 17 TBI and 14 non-TBI patients had their urine collected every hour for 25 hours, starting 18.3 ± 12.3 days post-injury. We calculated urinary 6-sulfatoxymelatonin concentration to obtain total 24-hour excretion, excretion onset, offset, duration, amplitude, and acrophase. Using Student's t-tests, we compared groups on actigraphy (daytime activity ratio, nighttime total sleep time, and fragmentation index) and melatonin variables. We investigated associations between melatonin and actigraphy variables using Pearson's correlations. RESULTS: TBI patients had poorer daytime activity ratio (TBI: 77.5 ± 9.4%; non-TBI: 84.6 ± 6.9%), shorter nighttime total sleep time (TBI: 353.5 ± 96.6 min; non-TBI: 421.2 ± 72.2 min), and higher fragmentation index (TBI: 72.2 ± 30.0; non-TBI: 53.5 ± 23.6) (all p-values < 0.01). A melatonin rhythm was present in both groups, and no group differences were found on melatonin variables. No associations were found between melatonin and actigraphy variables in TBI patients. CONCLUSION: Moderate-to-severe TBI patients have more serious sleep-wake disturbances than non-TBI patients hospitalized in the same environment, suggesting that the brain injury itself alters the sleep-wake cycle. Despite their deregulated 24-hour sleep-wake cycle, TBI patients have a normal circadian clock signal.

Daily Profiles of Light Exposure and Evening Use of Light-emitting Devices in Young Adults Complaining of a Delayed Sleep Schedule.

A number of factors can contribute to a delayed sleep schedule. An important factor could be a daily profile of light exposure favoring a later circadian phase. This study aimed to compare light exposure between 14 young adults complaining of a delayed sleep schedule and 14 matched controls and to identify possible associations between habitual light exposure and circadian phase. Exposure to white and blue light was recorded with ambulatory monitors for 7 consecutive days. Participants also noted their daily use of light-emitting devices before bedtime. Endogenous circadian phase was estimated with the dim light melatonin onset (DLMO) in the laboratory. The amplitude of the light-dark cycle to which the subjects were exposed was smaller in delayed than in control subjects, and smaller amplitude was associated with a later DLMO. Smaller amplitude was due to both decreased exposure in the daytime and increased exposure at night. Total exposure to blue light, but not to white light, was lower in delayed subjects, possibly due to lower exposure to blue-rich outdoor light. Lower daily exposure to blue light was associated with a later DLMO. Timing of relative increases and decreases of light exposure in relation to endogenous circadian phase was also compared between the 2 groups. In delayed subjects, there was a relatively higher exposure to white and blue light 2 h after DLMO, a circadian time with maximal phase-delaying effect. Delayed participants also had higher exposure to light 8 to 10 h after DLMO, which occurred mostly during their sleep episode but may have some phase-advancing effects. Self-reported use of light-emitting devices before bedtime was higher in delayed than in control subjects and was associated with a later DLMO. This study suggests that individuals complaining of a delayed sleep schedule engage in light-related behaviors favoring a later circadian phase and a later bedtime.

Circadian phase, dynamics of subjective sleepiness and sensitivity to blue light in young adults complaining of a delayed sleep schedule.

OBJECTIVE: To assess factors that might contribute to a delayed sleep schedule in young adults with sub-clinical features of delayed sleep phase disorder. METHODS: Two groups of 14 young adults (eight women) were compared: one group complaining of a delayed sleep schedule and a control group with an earlier bedtime and no complaint. For one week, each subject maintained a target bedtime reflecting their habitual sleep schedule. Subjects were then admitted to the laboratory for the assessment of circadian phase (dim light melatonin onset), subjective sleepiness, and non-visual light sensitivity. All measures were timed relative to each participant's target bedtime. Non-visual light sensitivity was evaluated using subjective sleepiness and salivary melatonin during 1.5-h exposure to blue light, starting one hour after target bedtime. RESULTS: Compared to control subjects, delayed subjects had a later circadian phase and a slower increase of subjective sleepiness in the late evening. There was no group difference in non-visual sensitivity to blue light, but we found a positive correlation between melatonin suppression and circadian phase within the delayed group. CONCLUSIONS: Our results suggest that a late circadian phase, a slow build-up of sleep need, and an increased circadian sensitivity to blue light contribute to the complaint of a delayed sleep schedule. These findings provide targets for strategies aiming to decreasing the severity of a sleep delay and the negative consequences on daytime functioning and health.