Article

Effect of traumatic brain injury on the timing of sleep

School of Psychology, Psychiatry and Psychological Medicine, Building 17, Clayton Campus, Monash University, Melbourne, Victoria, Australia.
Chronobiology International (Impact Factor: 2.88). 02/2005; 22(1):89-105. DOI: 10.1081/CBI-200042428
Source: PubMed

ABSTRACT While there have been single case reports of the development of circadian rhythm sleep disorders, most commonly delayed sleep phase syndrome following traumatic brain injury (TBI), to our knowledge there have been no group investigations of changes to sleep timing in this population. The aim of the present study was to investigate sleep timing following TBI using the dim light melatonin onset (DLMO) as a marker of circadian phase and the Morningness-Eveningness Questionnaire (MEQ) as a measure of sleep-wake behavior. A sleep-wake diary was also completed. It was hypothesized that the timing of DLMO would be delayed and that there would be a greater tendency toward eveningness on the MEQ in a post-acute TBI group (n=10) compared to a gender and age matched control group. Participants were recruited at routine outpatient review appointments (TBI) and from the general population (control) as part of a larger study. They attended the sleep laboratory where questionnaires were completed, some retrospectively, and saliva melatonin samples were collected half-hourly according to a standard protocol. The results show that the TBI and control groups reported similar habitual sleep times and this was reflected on the MEQ. There was, however, significant variability in the TBI group's change from the pre-injury to the current MEQ score. The timing of melatonin onset was not different between the groups. While subtle changes (advances or delays) in this small sample may have cancelled each other out,. the present study does not provide conclusive objective evidence of shift in circadian timing of sleep following TBI. Furthermore, although participants did report sleep timing changes, it is concluded that the MEQ may not be suitable for use with this cognitively impaired clinical group.

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    • ". Many of these disorders are sufficiently burdensome after TBI [19]. Specifically, this applies to insomnias [20] [21], sleep-related breathing disorders (SRBD) [22], hypersomnia not due to breathing disorders [3] [23], circadian rhythm sleep disorders (CRSD) [24] [25] [26], sleep-related movement disorders [27], and other sleep disorders [28] "
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    ABSTRACT: Numerous studies on the high prevalence of sleep disorders in individuals with traumatic brain injury (TBI) have been conducted in the past few decades. These disorders can accentuate other consequences of TBI, negatively impacting mood, exacerbating pain, heightening irritability, and diminishing cognitive abilities and the potential for recovery. Nevertheless, sleep is not routinely assessed in this population. In our review, we examined the selective screening criteria and the scientific evidence regarding screening for post-TBI sleep disorders to identify gaps in our knowledge that are in need of resolution. We retrieved papers written in the English-language literature before June 2012 pertinent to the discussion on sleep after TBI found through a PubMed search. Within our research, we found that sleep dysfunction is highly burdensome after TBI, treatment interventions for some sleep disorders result in favorable outcomes, sensitive and specific tests to detect sleep disorders are available, and the cost-effectiveness and sustainability of screening have been determined from other populations. The evidence we reviewed supports screening for post-TBI sleep dysfunction. This approach could improve the outcomes and reduce the risks for post-TBI adverse health and nonhealth effects (e.g., secondary injuries). A joint sleep and brain injury collaboration focusing on outcomes is needed to improve our knowledge.
    Sleep Medicine 09/2013; 14(12). DOI:10.1016/j.sleep.2013.07.009 · 3.10 Impact Factor
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    • "The findings pertaining to circadian sleep–wake disorders are also rather inconclusive. Anecdotal reports on a posttraumatic delayed sleep phase syndrome have been published, but a recent study of 10 patients failed to provide evidence of any shift in circadian timing of sleep subsequent to TBI (Quinto et al., 2000; Steele et al., 2005). The neurobiological bases for post-traumatic SWD are unknown. "
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    ABSTRACT: Sleep-wake disturbances (SWD) are common after traumatic brain injury (TBI). In acute TBI, we recently found decreased CSF levels of hypocretin-1, a wake-promoting neurotransmitter. In the present study, we aimed to delineate the frequency and clinical characteristics of post-traumatic SWD, to assess CSF hypocretin-1 levels 6 months after TBI, and to identify risk factors for posttraumatic SWD. A total of 96 consecutive patients were enrolled within the first 4 days after TBI. Six months later, out of 76 TBI patients, who did not die and who did not move to foreign countries, we included 65 patients (86%, 53 males, mean age 39 years) in our study. Patients were examined using interviews, questionnaires, clinical examinations, computed tomography of the brain, laboratory tests (including CSF hypocretin-1 levels, and HLA typing), conventional polysomnography, maintenance of wakefulness and multiple sleep latency tests (MSLT) and actigraphy. Potential causes of post-traumatic SWD were assessed according to international criteria. New-onset sleep-wake disturbances following TBI were found in 47 patients (72%): subjective excessive daytime sleepiness (EDS; defined by the Epworth Sleepiness Scale > or = 10) was found in 18 (28%), objective EDS (as defined by mean sleep latency < 5 min on MSLT) in 16 (25%), fatigue (daytime tiredness without signs of subjective or objective EDS) in 11 (17%), post-traumatic hypersomnia 'sensu strictu' (increased sleep need of > or = 2 h per 24 h compared to pre-TBI) in 14 (22%) patients and insomnia in 3 patients (5%). In 28 patients (43% of the study population), we could not identify a specific cause of the post-traumatic SWD other than TBI. Low CSF hypocretin-1 levels were found in 4 of 21 patients 6 months after TBI, as compared to 25 of 27 patients in the first days after TBI. Hypocretin levels 6 months after TBI were significantly lower in patients with post-traumatic EDS. There were no associations between post-traumatic SWD and severity or localization of TBI, general clinical outcome, gender, pathological neurological findings and HLA typing. However, post-traumatic SWD correlated with impaired quality of life. These results suggest that sleep-wake disturbances, particularly EDS, fatigue and hypersomnia are common after TBI, and significantly impair quality of life. In almost one out of two patients, post-traumatic SWD appear to be directly related to the TBI. An involvement of the hypocretin system in the pathophysiology of post-traumatic SWD appears possible. Other risk factors predisposing towards the development of post-traumatic SWD were not identified.
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    ABSTRACT: To explore subjective sleep reports from people in the chronic stages of traumatic brain injury (TBI) and to examine the extent and nature of sleep complaints in this population. Survey. All participants were community based at the time of data collection. Sixty-three subjects with TBI consecutively recruited after discharge from rehabilitation and 63 age- and sex-matched controls from the general community. Not applicable. A 7-day self-reported sleep-wake diary assessing sleep and wake times, sleep onset latency, frequency, and duration of nocturnal awakenings and daytime naps; a general sleep questionnaire used to evaluate sleep changes and quality; and the Epworth Sleepiness Scale to measure daytime sleepiness. Group-wise comparisons showed a significantly higher frequency of reported sleep changes after TBI (80%) relative to the control group (23%), supporting previous findings. The TBI group reported more nighttime awakenings and longer sleep onset latency; these changes were more frequently reported by participants with TBI with milder injuries. Increased levels of anxiety and depression were associated with increased reporting of sleep changes. These findings confirm the experience of changes to sleep after TBI and may at least in part account for the reported increased daytime sleepiness in this population. Sleep disturbance should be addressed during rehabilitation. Treatments need to focus on correcting the underlying cause of the sleep problem and to address patients' subjective experiences of their sleep, possibly through education and mood stabilization.
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