Citation

Skopin MD, Kabadi SV, Viechweg SS, Mong JA, Faden AI. J. Neurotrauma 2014; 32(5): 289-296.

Affiliation

University of Maryland School of Medicine, Anesthesiology, Baltimore, Maryland, United States ; mskopin@gwu.edu.

Copyright

(Copyright © 2014, Mary Ann Liebert Publishers)

DOI

10.1089/neu.2014.3664

PMID

25242371

Abstract

Traumatic brain injury (TBI) can cause sleep-wake disturbances and excessive daytime sleepiness. However, the pathobiology of sleep disorders in TBI is not well understood and animal models have been underutilized in studying such changes and potential underlying mechanisms. Here we used the rat lateral fluid percussion (LFP) model to analyze sleep-wake patterns as a function of time after injury. Rapid-eye movement sleep (REM), non-REM sleep (NREM), and wake bouts during light and dark phases were measured with electroencephalography (EEG) and electromyography (EMG) at an early as well as chronic time points following LFP. Moderate TBI caused disturbances in ability to maintain consolidated wake bouts during the active phase and chronic loss of wakefulness. Furthermore, TBI resulted in cognitive impairments and depressive-like symptoms, and reduced the number of Orexin-A (ORX-A)-positive neurons in the lateral hypothalamus.

Language: en