Citation

Prins M, Alexander D, Giza CC, Hovda DA. J. Neurotrauma 2013; 30(1): 30-38.

Affiliation

UCLA School of Medicine, Neurosurgery, NPI 18-228, Los Angeles, California, United States, 90095, 310-825-8646; mprins@mednet.ucla.edu.

Copyright

(Copyright © 2013, Mary Ann Liebert Publishers)

DOI

10.1089/neu.2012.2399

PMID

23025820

Abstract

Among the 3.5 million annual new head injury cases is a sub-population of children and young adults who experience repeat traumatic brain injury (RTBI). The duration of vulnerability after a single TBI remains unknown and biomarkers have yet to be determined. Decreases in glucose metabolism (CMRglc) are consistently observed after experimental and human TBI. In the current study it is hypothesized that the duration of vulnerability is related to the duration of decreased CMRglc and that a single mTBI increases the brain's vulnerability to a second insult for a period of time, during which a subsequent mTBI will worsen the outcome. Postnatal day 35 rats were given sham, single mTBI or two mTBI at 24hr or 120hr intervals. 14C-2-deoxy-D-glucose autoradiography was conducted at 1 or 3 days post injury to calculate CMRglc. At 24hrs after a single mTBI, CMRglc is decreased by 19% in both the parietal cortex and hippocampus, but approached sham levels by 3 days post injury. When a second mTBI is introduced during the CMRglc depression of the first injury, the consequent CMRglc is depressed (36.5%) at 24hr and remains depressed (25%) at 3 days. In contrast, when the second mTBI is introduced after the metabolic recovery of the first injury, the consequent CMRglc depression is similar to that seen with a single injury. Results suggest that the duration of metabolic depression reflects the time-course of vulnerability to second injury in the juvenile brain and could serve as a valuable biomarker in establishing window of vulnerability guidelines.

Language: en