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Changes in Diffusion Kurtosis Imaging and Magnetic Resonance Spectroscopy in a Direct Cranial Blast Traumatic Brain Injury (dc-bTBI) Model.

Zhuo J, Keledjian K, Xu S, Pampori A, Gerzanich V, Simard JM, Gullapalli RP - PLoS ONE (2015)

Bottom Line: Neurofunctional testing on a separate but similarly treated group of rats showed early disturbances in vestibulomotor functions (days 1-14), which were associated with imaging changes in the internal capsule.Delayed impairments in spatial memory and in rapid learning, as assessed by Morris Water Maze paradigms (days 14-19), were associated with delayed changes in the hippocampus.Overall, our findings indicate delayed neurofunctional and pathological abnormalities following dc-bTBI that are silent on conventional T2-weighted imaging, but are detectable using DKI and proton MRS.

View Article: PubMed Central - PubMed

Affiliation: Departments of Diagnostic Radiology and Nuclear Medicine, University of Maryland School of Medicine, Baltimore, MD, 21201, United States of America.

ABSTRACT
Explosive blast-related injuries are one of the hallmark injuries of veterans returning from recent wars, but the effects of a blast overpressure on the brain are poorly understood. In this study, we used in vivo diffusion kurtosis imaging (DKI) and proton magnetic resonance spectroscopy (MRS) to investigate tissue microstructure and metabolic changes in a novel, direct cranial blast traumatic brain injury (dc-bTBI) rat model. Imaging was performed on rats before injury and 1, 7, 14 and 28 days after blast exposure (~517 kPa peak overpressure to the dorsum of the head). No brain parenchyma abnormalities were visible on conventional T2-weighted MRI, but microstructural and metabolic changes were observed with DKI and proton MRS, respectively. Increased mean kurtosis, which peaked at 21 days post injury, was observed in the hippocampus and the internal capsule. Concomitant increases in myo-Inositol (Ins) and Taurine (Tau) were also observed in the hippocampus, while early changes at 1 day in the Glutamine (Gln) were observed in the internal capsule, all indicating glial abnormality in these regions. Neurofunctional testing on a separate but similarly treated group of rats showed early disturbances in vestibulomotor functions (days 1-14), which were associated with imaging changes in the internal capsule. Delayed impairments in spatial memory and in rapid learning, as assessed by Morris Water Maze paradigms (days 14-19), were associated with delayed changes in the hippocampus. Significant microglial activation and neurodegeneration were observed at 28 days in the hippocampus. Overall, our findings indicate delayed neurofunctional and pathological abnormalities following dc-bTBI that are silent on conventional T2-weighted imaging, but are detectable using DKI and proton MRS.

No MeSH data available.


Related in: MedlinePlus

dc-bTBI causes abnormalities incognitive function measured using Morris Water Maze test.Performance during incremental learning (A), memory probe test (B), and rapid learning test (C) during days 14–21, as indicated; n = 10 sham-injury, 10 dc-bTBI; in (C), 25% represents chance alone;*, p< 0.05; **, p<0.01 for comparison between sham and dc-bTBI rats.
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pone.0136151.g006: dc-bTBI causes abnormalities incognitive function measured using Morris Water Maze test.Performance during incremental learning (A), memory probe test (B), and rapid learning test (C) during days 14–21, as indicated; n = 10 sham-injury, 10 dc-bTBI; in (C), 25% represents chance alone;*, p< 0.05; **, p<0.01 for comparison between sham and dc-bTBI rats.

Mentions: Cognitive abnormalities were prominent later after injury (Fig 6). No differences were identified in incremental learning during days 14–18 after dc-bTBI (Fig 6A). However, significant deficits were found on the memory probe on day 19 and on the rapid learning test on day 21 after dc-bTBI (Fig 6B and 6C).


Changes in Diffusion Kurtosis Imaging and Magnetic Resonance Spectroscopy in a Direct Cranial Blast Traumatic Brain Injury (dc-bTBI) Model.

Zhuo J, Keledjian K, Xu S, Pampori A, Gerzanich V, Simard JM, Gullapalli RP - PLoS ONE (2015)

dc-bTBI causes abnormalities incognitive function measured using Morris Water Maze test.Performance during incremental learning (A), memory probe test (B), and rapid learning test (C) during days 14–21, as indicated; n = 10 sham-injury, 10 dc-bTBI; in (C), 25% represents chance alone;*, p< 0.05; **, p<0.01 for comparison between sham and dc-bTBI rats.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4547765&req=5

pone.0136151.g006: dc-bTBI causes abnormalities incognitive function measured using Morris Water Maze test.Performance during incremental learning (A), memory probe test (B), and rapid learning test (C) during days 14–21, as indicated; n = 10 sham-injury, 10 dc-bTBI; in (C), 25% represents chance alone;*, p< 0.05; **, p<0.01 for comparison between sham and dc-bTBI rats.
Mentions: Cognitive abnormalities were prominent later after injury (Fig 6). No differences were identified in incremental learning during days 14–18 after dc-bTBI (Fig 6A). However, significant deficits were found on the memory probe on day 19 and on the rapid learning test on day 21 after dc-bTBI (Fig 6B and 6C).

Bottom Line: Neurofunctional testing on a separate but similarly treated group of rats showed early disturbances in vestibulomotor functions (days 1-14), which were associated with imaging changes in the internal capsule.Delayed impairments in spatial memory and in rapid learning, as assessed by Morris Water Maze paradigms (days 14-19), were associated with delayed changes in the hippocampus.Overall, our findings indicate delayed neurofunctional and pathological abnormalities following dc-bTBI that are silent on conventional T2-weighted imaging, but are detectable using DKI and proton MRS.

View Article: PubMed Central - PubMed

Affiliation: Departments of Diagnostic Radiology and Nuclear Medicine, University of Maryland School of Medicine, Baltimore, MD, 21201, United States of America.

ABSTRACT
Explosive blast-related injuries are one of the hallmark injuries of veterans returning from recent wars, but the effects of a blast overpressure on the brain are poorly understood. In this study, we used in vivo diffusion kurtosis imaging (DKI) and proton magnetic resonance spectroscopy (MRS) to investigate tissue microstructure and metabolic changes in a novel, direct cranial blast traumatic brain injury (dc-bTBI) rat model. Imaging was performed on rats before injury and 1, 7, 14 and 28 days after blast exposure (~517 kPa peak overpressure to the dorsum of the head). No brain parenchyma abnormalities were visible on conventional T2-weighted MRI, but microstructural and metabolic changes were observed with DKI and proton MRS, respectively. Increased mean kurtosis, which peaked at 21 days post injury, was observed in the hippocampus and the internal capsule. Concomitant increases in myo-Inositol (Ins) and Taurine (Tau) were also observed in the hippocampus, while early changes at 1 day in the Glutamine (Gln) were observed in the internal capsule, all indicating glial abnormality in these regions. Neurofunctional testing on a separate but similarly treated group of rats showed early disturbances in vestibulomotor functions (days 1-14), which were associated with imaging changes in the internal capsule. Delayed impairments in spatial memory and in rapid learning, as assessed by Morris Water Maze paradigms (days 14-19), were associated with delayed changes in the hippocampus. Significant microglial activation and neurodegeneration were observed at 28 days in the hippocampus. Overall, our findings indicate delayed neurofunctional and pathological abnormalities following dc-bTBI that are silent on conventional T2-weighted imaging, but are detectable using DKI and proton MRS.

No MeSH data available.


Related in: MedlinePlus