Combat-related blast exposure and traumatic brain injury influence brain glucose metabolism during REM sleep in military veterans

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 underpinn...

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Veröffentlicht in:NeuroImage (Orlando, Fla.) Fla.), 2014-10, Vol.99, p.207-214
Hauptverfasser: Stocker, Ryan P.J., Cieply, Marissa A., Paul, Benjamin, Khan, Hassen, Henry, Luke, Kontos, Anthony P., Germain, Anne
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container_title NeuroImage (Orlando, Fla.)
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Cieply, Marissa A.
Paul, Benjamin
Khan, Hassen
Henry, Luke
Kontos, Anthony P.
Germain, Anne
description 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, [18F]-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 28.1±4.3) 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 that 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. •Results showed decreased rCMRglc during wakefulness and REM sleep in blast and/or mTBI exposure.•Hypometabolism in right basal ganglia and limbic system.•Hypometabolism in culmen, associative visual cortices, and frontal cortices.•These effects are beyond concurrent PTSD symptoms, combat, and sleep quality.•Hypometabolic profile may reflect long-term neural effects of blast/TBI exposure.
doi_str_mv 10.1016/j.neuroimage.2014.05.067
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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, [18F]-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 28.1±4.3) 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 that 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. •Results showed decreased rCMRglc during wakefulness and REM sleep in blast and/or mTBI exposure.•Hypometabolism in right basal ganglia and limbic system.•Hypometabolism in culmen, associative visual cortices, and frontal cortices.•These effects are beyond concurrent PTSD symptoms, combat, and sleep quality.•Hypometabolic profile may reflect long-term neural effects of blast/TBI exposure.</description><identifier>ISSN: 1053-8119</identifier><identifier>EISSN: 1095-9572</identifier><identifier>DOI: 10.1016/j.neuroimage.2014.05.067</identifier><identifier>PMID: 24893322</identifier><language>eng</language><publisher>Amsterdam: Elsevier Inc</publisher><subject>Adult ; Biological and medical sciences ; Blast exposure ; Blast Injuries - diagnostic imaging ; Blast Injuries - metabolism ; Brain Chemistry ; Brain damage ; Brain Injuries - diagnostic imaging ; Brain Injuries - metabolism ; Brain research ; Cerebral glucose metabolism ; Combat Disorders - diagnostic imaging ; Combat Disorders - metabolism ; Consciousness ; Female ; Fluorodeoxyglucose F18 ; Fundamental and applied biological sciences. Psychology ; Glucose - metabolism ; Head injuries ; Humans ; Injuries of the nervous system and the skull. Diseases due to physical agents ; Insomnia ; Male ; Medical sciences ; Metabolism ; Military veterans ; mTBI ; Polysomnography ; Positron-Emission Tomography ; Rapid eye movement sleep ; Sleep, REM ; Sleep. Vigilance ; Stress Disorders, Post-Traumatic - diagnostic imaging ; Stress Disorders, Post-Traumatic - metabolism ; Studies ; Traumas. Diseases due to physical agents ; Vertebrates: nervous system and sense organs ; Veterans</subject><ispartof>NeuroImage (Orlando, Fla.), 2014-10, Vol.99, p.207-214</ispartof><rights>2014 Elsevier Inc.</rights><rights>2015 INIST-CNRS</rights><rights>Copyright © 2014 Elsevier Inc. All rights reserved.</rights><rights>Copyright Elsevier Limited Oct 1, 2014</rights><rights>2014 Elsevier Inc. 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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, [18F]-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 28.1±4.3) completed FDG PET studies during wakefulness, REM sleep, and NREM sleep. Whole-brain analyses were conducted using Statistical Parametric Mapping (SPM8). 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subjects Adult
Biological and medical sciences
Blast exposure
Blast Injuries - diagnostic imaging
Blast Injuries - metabolism
Brain Chemistry
Brain damage
Brain Injuries - diagnostic imaging
Brain Injuries - metabolism
Brain research
Cerebral glucose metabolism
Combat Disorders - diagnostic imaging
Combat Disorders - metabolism
Consciousness
Female
Fluorodeoxyglucose F18
Fundamental and applied biological sciences. Psychology
Glucose - metabolism
Head injuries
Humans
Injuries of the nervous system and the skull. Diseases due to physical agents
Insomnia
Male
Medical sciences
Metabolism
Military veterans
mTBI
Polysomnography
Positron-Emission Tomography
Rapid eye movement sleep
Sleep, REM
Sleep. Vigilance
Stress Disorders, Post-Traumatic - diagnostic imaging
Stress Disorders, Post-Traumatic - metabolism
Studies
Traumas. Diseases due to physical agents
Vertebrates: nervous system and sense organs
Veterans
title Combat-related blast exposure and traumatic brain injury influence brain glucose metabolism during REM sleep in military veterans
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