Prevalence and consequences of sleep disorders in traumatic brain injury

Division of Pulmonary, Critical Care and Sleep Medicine, University of Texas Health Science Center at Houston, TX 77030, USA.
Journal of clinical sleep medicine: JCSM: official publication of the American Academy of Sleep Medicine (Impact Factor: 3.05). 06/2007; 3(4):349-56.
Source: PubMed


Determine prevalence and consequences of sleepiness and sleep disorders after traumatic brain injury (TBI).
Prospective evaluation with polysomnography (PSG), multiple sleep latency test (MSLT), Epworth Sleepiness Scale (ESS) and neuropsychological testing including Psychomotor Vigilance Test (PVT), Profile of Mood States (POMS), and Functional Outcome of Sleep Questionnaire (FOSQ).
Three academic medical centers with level I trauma centers, accredited sleep disorders centers, and rehabilitative medicine programs. Participants; Eighty-seven (87) adults at least 3 months post TBI. Measurements And Results: Abnormal sleep studies were found in 40 subjects (46%), including 20 (23%) with obstructive sleep apnea (OSA), 10 (11%) with posttraumatic hypersomnia (PTH), 5 (6%) with narcolepsy, and 6 (7%) with periodic limb movements in sleep (PLMS). Among all subjects, 22 (25%) were found to have objective excessive daytime sleepiness with MSLT score <10 minutes. There was no correlation between ESS score and MSLT (r = 0.10). There were no differences in age, race, sex, or education between the sleepy and non-sleepy subjects. Likewise, there were no differences in severity of injury or time after injury between sleepy and non-sleepy subjects. Sleepy subjects had a greater body mass index (BMI) than those who were not sleepy (p = 0.01). OSA was more common in obese subjects (BMI > or =30, p < 0.001). Sleepy subjects demonstrated poorer PVT scores (p < 0.05), better self-reported sleep related quality of life (FOSQ scores [p < 0.05]), and no differences in POMS.
There is a high prevalence of sleep disorders (46%) and of excessive daytime sleepiness (25%) in subjects with TBI. Sleepy subjects may be more impaired than comparable non-sleepy TBI subjects, yet be unaware of problems. Given the high prevalence of OSA (23%), PTH (11%), and narcolepsy (7%) in this population, there is a clinical indication for NPSG and MSLT.

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Available from: Mark Wilde, Mar 09, 2015
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    • "Sleep-wake disturbances (SWD) are frequent following acute traumatic brain injury (TBI) and impair quality of life in TBI patients. Several studies highlighted the high prevalence of excessive daytime sleepiness (EDS) and increased sleep need after TBI (Guilleminault et al., 1983; Masel et al., 2001; Ouellet and Morin, 2006; Parcell et al., 2006; Baumann et al., 2007; Castriotta et al., 2007; Chaumet et al., 2008; Schreiber et al., 2008; Ponsford et al., 2013). In a recent meta-analysis of 21 clinical studies, $50% of TBI patients suffered from post-traumatic SWD: increased sleep need per 24 h and EDS were among the most common and disturbing post-traumatic SWD (Mathias and Alvaro, 2012). "
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    ABSTRACT: Post-traumatic sleep-wake disturbances are common after acute traumatic brain injury. Increased sleep need per 24 h and excessive daytime sleepiness are among the most prevalent post-traumatic sleep disorders and impair quality of life of trauma patients. Nevertheless, the relation between traumatic brain injury and sleep outcome, but also the link between post-traumatic sleep problems and clinical measures in the acute phase after traumatic brain injury has so far not been addressed in a controlled and prospective approach. We therefore performed a prospective controlled clinical study to examine (i) sleep-wake outcome after traumatic brain injury; and (ii) to screen for clinical and laboratory predictors of poor sleep-wake outcome after acute traumatic brain injury. Forty-two of 60 included patients with first-ever traumatic brain injury were available for follow-up examinations. Six months after trauma, the average sleep need per 24 h as assessed by actigraphy was markedly increased in patients as compared to controls (8.3 ± 1.1 h versus 7.1 ± 0.8 h, P < 0.0001). Objective daytime sleepiness was found in 57% of trauma patients and 19% of healthy subjects, and the average sleep latency in patients was reduced to 8.7 ± 4.6 min (12.1 ± 4.7 min in controls, P = 0.0009). Patients, but not controls, markedly underestimated both excessive sleep need and excessive daytime sleepiness when assessed only by subjective means, emphasizing the unreliability of self-assessment of increased sleep propensity in traumatic brain injury patients. At polysomnography, slow wave sleep after traumatic brain injury was more consolidated. The most important risk factor for developing increased sleep need after traumatic brain injury was the presence of an intracranial haemorrhage. In conclusion, we provide controlled and objective evidence for a direct relation between sleep-wake disturbances and traumatic brain injury, and for clinically significant underestimation of post-traumatic sleep-wake disturbances by trauma patients. © The Author (2015). Published by Oxford University Press on behalf of the Guarantors of Brain. All rights reserved. For Permissions, please email:
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    • "Similarly some data show that less severe TBI might be associated with greater sleep complaints (Clinchot et al., 1998; Fichtenberg et al., 2000), probably because individuals with a milder severity of TBI are prone to struggle to restore their lifestyle and have better insight into the impact of injury. On the contrary, other studies demonstrate that a milder severity of TBI does not contribute significantly to the prediction of the presence of sleep disruption (Castriotta et al., 2007; Verma et al., 2007). Furthermore, only a few "
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    ABSTRACT: Study of insomnia and associated factors in Traumatic Brain Injury Objectives This study is designed to investigate prevalence and risk factors of insomnia in TBI. This study has also tried to explore the connection between insomnia with neuroanatomical localization of TBI as well as depression Design Prospective study Material and Method All eligible participants were evaluated initially after two week interval for first 4 weeks and monthly interval subsequently till one year. Demographic and injury characteristics of the participants were assessed on a self designed semi structured performa. Interviews focused on assessment of severity of TBI, insomnia and depression using GCS, ISI and PHQ-9 respectively. Results Total 204 patients were included, mean age was 33.34 years. 40.2% participants were found to have insomnia. None of the demographic variables were associated with insomnia except severity and duration of TBI. Moderate TBI patient (70.73%) had significantly higher occurrence of insomnia than the mild cases (19.67%) (P = 0.000, df 1). First three month after TBI witnessed more than half (63.41%) of those patient who had insomnia. This was found statistically significant (P < 0.017). Neuroanatomical localization was also correlated with insomnia. Cerebral contusion was the most common (40.24%) site of impact. Almost half (42.42%) of the patients with insomnia had multiple contusions. 32.84% of the study population had depression. No significant correlation could be established between depression and insomnia. Conclusion Insomnia is a prevalent condition after TBI requiring more clinical and scientific attention as it may have important repercussions on rehabilitation.
    Full-text · Article · Apr 2014 · Asian Journal of Psychiatry
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    • "The present study was designed to examine injury-induced alterations in acute sleep following TBI. Clinical observations indicate that patients report excessive sleepiness immediately following TBI [6]. In view of these observations, we hypothesized that diffuse brain injury would induce acute post-traumatic sleep in the mouse. "
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    ABSTRACT: Clinical observations report excessive sleepiness immediately following traumatic brain injury (TBI); however, there is a lack of experimental evidence to support or refute the benefit of sleep following a brain injury. The aim of this study is to investigate acute post-traumatic sleep. Sham, mild or moderate diffuse TBI was induced by midline fluid percussion injury (mFPI) in male C57BL/6J mice at 9:00 or 21:00 to evaluate injury-induced sleep behavior at sleep and wake onset, respectively. Sleep profiles were measured post-injury using a non-invasive, piezoelectric cage system. In separate cohorts of mice, inflammatory cytokines in the neocortex were quantified by immunoassay, and microglial activation was visualized by immunohistochemistry. Immediately after diffuse TBI, quantitative measures of sleep were characterized by a significant increase in sleep (>50%) for the first 6 hours post-injury, resulting from increases in sleep bout length, compared to sham. Acute post-traumatic sleep increased significantly independent of injury severity and time of injury (9:00 vs 21:00). The pro-inflammatory cytokine IL-1β increased in brain-injured mice compared to sham over the first 9 hours post-injury. Iba-1 positive microglia were evident in brain-injured cortex at 6 hours post-injury. Post-traumatic sleep occurs for up to 6 hours after diffuse brain injury in the mouse regardless of injury severity or time of day. The temporal profile of secondary injury cascades may be driving the significant increase in post-traumatic sleep and contribute to the natural course of recovery through cellular repair.
    Full-text · Article · Jan 2014 · PLoS ONE
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