• Mark D Skopin, Shruti V Kabadi, Shaun S Viechweg, Jessica A Mong, and Alan I Faden.
• Department of Anesthesiology, Center for Shock, Trauma and Anesthesiology Research (STAR), University of Maryland School of Medicine , Baltimore, Maryland.
• J. Neurotrauma. 2015 Mar 1; 32 (5): 289-96.

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

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