Article

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: 2.83). 06/2007; 3(4):349-56.
Source: PubMed

ABSTRACT 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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    • "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.
    Asian Journal of Psychiatry 04/2014; 8(1). DOI:10.1016/j.ajp.2013.12.017
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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.
    PLoS ONE 01/2014; 9(1):e82507. DOI:10.1371/journal.pone.0082507 · 3.23 Impact Factor
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    • "Some data show that less severe TBI might be associated with greater sleep complaints [3,6,7,11,15], probably because individuals with a milder severity of TBI are prone to struggle to restore their lifestyles and have better insight into the impact of injury. On the contrary, other studies demonstrate that a milder severity of TBI doesn’t contribute significantly to the prediction of the presence of sleep disruption [8,16-19]. Furthermore, only a few data describe whether the location of TBI may be a risk factor for the presence of post-TBI sleep disturbance [14,17]. Currently, a quantity of studies recruits participants from rehabilitation settings rather than hospitals/trauma centers. "
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    ABSTRACT: Sleep disturbance is very common following traumatic brain injury (TBI), which may initiate or exacerbate a variety of co-morbidities and negatively impact rehabilitative treatments. To date, there are paradoxical reports regarding the associations between inherent characteristics of TBI and sleep disturbance in TBI population. The current study was designed to explore the relationship between the presence of sleep disturbance and characteristics of TBI and identify the factors which are closely related to the presence of sleep disturbance in TBI population. 98 TBI patients (72 males, mean age ± SD, 47 ± 13 years, range 18-70) were recruited. Severity of TBI was evaluated based on Glasgow Coma Scale (GCS). All participants performed cranial computed tomography and were examined on self-reported sleep quality, anxiety, and depression. TBI was mild in 69 (70%), moderate in 15 (15%) and severe in 14 (15%) patients. 37 of 98 patients (38%) reported sleep disturbance following TBI. Insomnia was diagnosed in 28 patients (29%) and post-traumatic hypersomnia in 9 patients (9%). In TBI with insomnia group, 5 patients (18%) complained of difficulty falling asleep only, 8 patients (29%) had difficulty maintaining sleep without difficulty in initial sleep and 15 patients (53%) presented both difficulty falling asleep and difficulty maintaining sleep. Risk factors associated with insomnia were headache and/or dizziness and more symptoms of anxiety and depression rather than GCS. In contrast, GCS was independently associated with the presence of hypersomnia following TBI. Furthermore, there was no evidence of an association between locations of brain injury and the presence of sleep disturbance after TBI. Our data support and contribute to a growing body of evidence which indicates that TBI patients with insomnia are prone to suffer from concomitant headache and/or dizziness, report more symptoms of anxiety and depression and severe TBI patients are likely to experience hypersomnia.
    PLoS ONE 10/2013; 8(10):e76087. DOI:10.1371/journal.pone.0076087 · 3.23 Impact Factor
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