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Cited by 380Sleep and related disordersSleep and Wakefulness ResearchTraumatic Brain Injury Research

Sleep-wake disturbances 6 months after traumatic brain injury: a prospective study

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Baumann, C. R., Werth, E., Stocker, R., Ludwig, S., Bassetti, C. L.·2007·Brain
DOI 10.1093/brain/awm109
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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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  • Patients with mild TBI still experience sleep disorders and show decreased orexin in the CSF.

    “Patients with mild TBI still experience sleep disorders,59,60 and show decreased orexin in the CSF,56,57”

    From Effects of Traumatic Brain Injury on the Orexin/Hypocretin System (2025) · cites this paper as [57]

    The sleep-studies section (Table 2, page not provided) documents sleep disturbances six months after mild TBI, including objective excessive daytime sleepiness in 9 of 26 patients. The Conclusion reports low CSF hypocretin-1 (orexin) in most patients during acute TBI, but the clinical-characteristics section says levels were normal in 17 of 21 patients tested six months later. The paper therefore does not establish persistently decreased CSF orexin in patients with mild TBI as a group. (LLM, conf=0.85)

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  • Injury to ascending arousal pathways from the brainstem may contribute to chronic sleepiness after head trauma.

    “Injury to ascending arousal pathways from the brainstem may contribute, but recent findings suggest a key role for the neuropeptides hypocretin-1 and -2 (also known as orexin-A and -B).2,4,5”

    From Loss of hypocretin (orexin) neurons with traumatic brain injury (2009) · cites this paper as [2]

    The section on clinical characteristics and potential causes proposes that TBI may damage hypocretin neurons or their axons, contributing to post-traumatic sleepiness. It does not identify injury to ascending arousal pathways from the brainstem as that mechanism. The risk-factors section reports no association between lesion location and sleep-wake disturbances; outcomes in patients with visible brainstem or hypothalamic lesions did not differ from those of other patients. Page numbers were not available in our copy. (LLM, conf=0.84)

    Experimental — accuracy not yet measured

  • Even after 6 months recovery, many TBI patients with EDS have persistently low hypocretin-1 levels.

    “Even after 6 months recovery, many TBI patients with EDS have persistently low hypocretin-1 levels.2”

    From Loss of hypocretin (orexin) neurons with traumatic brain injury (2009) · cites this paper as [2]

    The Laboratory studies section reports that hypocretin-1 remained low in 4 of 21 patients at six months, while it was normal in 17. The Clinical characteristics section says levels were lower in patients with EDS, but does not establish that many patients with EDS had persistently low levels. The claim overstates the prevalence of persistent deficiency. (LLM, conf=0.88)

    Experimental — accuracy not yet measured

  • Even after 6 months recovery, 43% of patients have symptoms of sleep disorders.

    “Coma and obtundation are common during the acute period, but even after 6 months recovery, 43% of patients have symptoms of sleep disorders.2,3”

    From Loss of hypocretin (orexin) neurons with traumatic brain injury (2009) · cites this paper as [2]

    The Fig. 3 caption (Single patient reports; page unavailable) reports that 28 of 65 patients (43%) had sleep–wake disturbances for which no cause other than traumatic brain injury was identified. But it reports sleep–wake disturbances in 47 of 65 patients overall, so 43% is the rate for a narrower group, not the overall rate implied by the claim. (LLM, conf=0.88)

    Experimental — accuracy not yet measured

  • In Baumann et al. 2007, 25/27 patients had low CSF hypocretin after acute injury (1-4 days post-injury).

    “25/27 patients had low levels of CSF hypocretin after acute injury (1–4 days post-injury).”

    From Effects of Traumatic Brain Injury on the Orexin/Hypocretin System (2025) · cites this paper as [57]

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Research works printed but not linked: 1

  1. Danker-Hopfe H, Schaefer M, Dorn H, Anderer P, Saletu B, Gruber G, et al. Percentile reference charts for selected sleep parameters for 20-to 80-year-old healthy subjects from the SIESTA database. Somnologie 2005; 9: 3-14.

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Authors
Baumann, C. R., Werth, E., Stocker, R., Ludwig, S., & Bassetti, C. L.
Affiliations
University Hospital Zurich (CH)
ORCID
Venue
Brain
Publisher
Oxford University Press (OUP)
Published
2007-05-29
Volume
130
Issue
7
Pages
1873-1883
ISSN
  • 0006-8950 (ISSN-L)
  • 1460-2156
DOI
10.1093/brain/awm109
OpenAlex
W2145062984
Cited by
380
References
53
Citations by year
2026: 8 · 2025: 11 · 2024: 12 · 2023: 9 · 2022: 21 · 2021: 15 · 2020: 19 · 2019: 24 · 2018: 34 · 2017: 20 · 2016: 30 · 2015: 32 · 2014: 26 · 2013: 35 · 2012: 22
FWCI
17.55
Type
journal article
Language
en
Open access
Locations
  • Brain (publishedVersion)
  • PubMed (publishedVersion)
  • Zurich Open Repository and Archive (University of Zurich) (acceptedVersion, other-oa)
  • reroDoc Digital Library (submittedVersion)
  • Zurich Open Repository and Archive (University of Zurich) (submittedVersion, other-oa)
  • Zurich Open Repository and Archive (University of Zurich)
Topics
  • Social Sciences › Psychology › Experimental and Cognitive Psychology › Sleep and related disorders
  • Life Sciences › Neuroscience › Cognitive Neuroscience › Sleep and Wakefulness Research
  • Health Sciences › Medicine › Epidemiology › Traumatic Brain Injury Research
Keywords
traumatic brain injury, sleep-wake disturbances, orexin-A, cerebrospinal fluid, excessive daytime sleepiness, insomnia, fatigue, risk factors, HLA typing, multiple sleep latency test, actigraphy, polysomnography, HLA-DR
MeSH terms
Orexins, Adolescent, Adult, Aged, Brain Injuries, Female, Humans, Male, Middle Aged, Neuropeptides, Prognosis, Prospective Studies, Quality of Life, Risk Factors, Polysomnography, Sleep Disorders, Circadian Rhythm, Glasgow Outcome Scale, Intracellular Signaling Peptides and Proteins

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