Glucose and oxygen metabolism after penetrating ballistic-like brain injury

Shyam Gajavelli, Shimoda Kentaro, Julio Diaz, Shoji Yokobori, Markus Spurlock, Daniel Diaz, Clayton Jackson, Alexandra Wick, Weizhao Zhao, Lai Y. Leung, Deborah Shear, Frank Tortella, M. Ross Bullock*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

22 Scopus citations


Traumatic brain injury (TBI) is a major cause of death and disability in all age groups. Among TBI, penetrating traumatic brain injuries (PTBI) have the worst prognosis and represent the leading cause of TBI-related morbidity and death. However, there are no specific drugs/interventions due to unclear pathophysiology. To gain insights we looked at cerebral metabolism in a PTBI rat model: penetrating ballistic-like brain injury (PBBI). Early after injury, regional cerebral oxygen tension and consumption significantly decreased in the ipsilateral cortex in the PBBI group compared with the control group. At the same time point, glucose uptake was significantly reduced globally in the PBBI group compared with the control group. Examination of Fluorojade B-stained brain sections at 24 hours after PBBI revealed an incomplete overlap of metabolic impairment and neurodegeneration. As expected, the injury core had the most severe metabolic impairment and highest neurodegeneration. However, in the peri-lesional area, despite similar metabolic impairment, there was lesser neurodegeneration. Given our findings, the data suggest the presence of two distinct zones of primary injury, of which only one recovers. We anticipate the peri-lesional area encompassing the PBBI ischemic penumbra, could be salvaged by acute therapies.

Original languageEnglish
Pages (from-to)773-780
Number of pages8
JournalJournal of Cerebral Blood Flow and Metabolism
Issue number5
StatePublished - 5 May 2015
Externally publishedYes


  • 2-deoxy glucose
  • Fluorojade B
  • cerebral metabolism
  • glucose
  • neurodegeneration
  • oxygen


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