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Journal Article

Citation

Stocker RP, Cieply MA, Paul B, Khan H, Henry L, Kontos AP, Germain A. Neuroimage 2014; 99: 207-214.

Affiliation

Department of Psychiatry, University of Pittsburgh School of Medicine, Pittsburgh, PA. Electronic address: germax@upmc.edu.

Copyright

(Copyright © 2014, Elsevier Publishing)

DOI

10.1016/j.neuroimage.2014.05.067

PMID

24893322

Abstract

Traumatic Brain Injury (TBI), a signature wound of Operations Enduring and Iraqi Freedom, can result from blunt head trauma or exposure to a blast/explosion. While TBI affects sleep, the neurobiological underpinnings between TBI and sleep are largely unknown. To examine the neurobiological underpinnings of this relationship in military veterans, [(18)F]-fluorodeoxyglucose positron emission tomography (FDG PET) was used to compare mTBI-related changes in relative cerebral metabolic rate of glucose (rCMRglc) during wakefulness, Rapid Eye Movement (REM) sleep, and non-REM (NREM) sleep, after adjusting for the effects of posttraumatic stress (PTS). Fourteen Veterans with a history of Blast Exposure and/or mTBI (B/mTBI) (age 27.5±3.9) and eleven Veterans with no history (No B/mTBI) (age 27.7±3.8) completed FDG PET studies during wakefulness, REM sleep, and NREM sleep. Whole-brain analyses were conducted using Statistical Parametric Mapping (SPM8). Between group comparisons revealed that B/mTBI was associated with significantly lower rCMRglc during wakefulness and REM sleep in the amygdala, hippocampus, parahippocampal gyrus, thalamus, insula, uncus, culmen, visual association cortices, and midline medial frontal cortices. These results suggest alterations in neurobiological networks during Wakefulness and REM sleep subsequent to B/mTBI exposure, may contribute to chronic sleep disturbances, and differ in individuals with acute symptoms.


Language: en

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