Citation

Lucke-Wold BP, Smith KE, Nguyen L, Turner RC, Logsdon AF, Jackson GJ, Huber JD, Rosen CL, Miller DB. Neurosci. Biobehav. Rev. 2015; 55: 68-77.

Affiliation

The Center for Neuroscience, West Virginia University School of Medicine, Morgantown, WV 26506, USA; Centers for Disease Control and Prevention-National Institute for Occupational Safety and Health, Morgantown, WV, USA. Electronic address: dum6@cdc.gov.

Copyright

(Copyright © 2015, Elsevier Publishing)

DOI

10.1016/j.neubiorev.2015.04.010

PMID

25956251

Abstract

Sleep disruption, which includes a loss of sleep as well as poor quality fragmented sleep, frequently follows traumatic brain injury (TBI) impacting a large number of patients each year in the United States. Fragmented and/or disrupted sleep can worsen neuropsychiatric, behavioral, and physical symptoms of TBI. Additionally, sleep disruption impairs recovery and can lead to cognitive decline. The most common sleep disruption following TBI is insomnia. The consequences of disrupted sleep following injury range from deranged metabolomics and blood brain barrier compromise to altered neuroplasticity and degeneration. There are several theories for why sleep is necessary (e.g., glymphatic clearance and metabolic regulation) and these may help explain how sleep disruption contributes to degeneration within the brain. Experimental data indicate disrupted sleep allows hyperphosphorylated tau and amyloid β plaques to accumulate. As sleep disruption may act as a cellular stressor, target areas warranting further scientific investigation include the increase in endoplasmic reticulum and oxidative stress following acute periods of sleep deprivation. Potential treatment options for restoring the normal sleep cycle include melatonin derivatives and cognitive behavioral therapy.

Language: en