Citation

Selwyn RG, Cooney SJ, Khayrullina G, Hokenbury N, Wilson CM, Jaiswal S, Bermudez S, Armstrong RC, Byrnes K. J. Neurotrauma 2015; 33(16): 1479-1491.

Affiliation

Uniformed Services University, Anatomy, Physiology and Genetics , 4301 Jones Bridge Road , Room B2048 , Bethesda, Maryland, United States , 20814 , 301-295-3217 ; kimberly.byrnes@usuhs.edu.

Copyright

(Copyright © 2015, Mary Ann Liebert Publishers)

DOI

10.1089/neu.2015.4129

PMID

26650903

Abstract

Repeated mild traumatic brain injury (rmTBI) results in worsened outcomes compared to a single injury, but the mechanism of this phenomenon is unclear. We have previously shown that mild TBI in a rat lateral fluid percussion model results in globally depressed glucose uptake, with a peak depression at 24 hours that resolves by 16 days post-injury. The current study investigated the outcomes of a repeat injury conducted at various times during this period of depressed glucose uptake. Adult male rats were therefore subjected to rmTBI with a latency of 24 hours, 5 days or 15 days between injuries, followed by assessment of motor function, histopathology and glucose uptake using positron emission tomography (PET). Rats that received a 24 hour rmTBI showed significant deficits in motor function tasks as well as significant increases in lesion volume and neuronal damage. The level of microglial and astrocytic activation was also associated with the timing of the second impact. Finally, rmTBI with latencies of 24 hours and 5 days showed significant alterations in FDG uptake in comparison to baseline scans. Therefore, we conclude that the state of the metabolic environment, as indicated by FDG-PET, at the time of the repeat injury significantly influences neurological outcomes.

Language: en