• Neurosurgery · Aug 2015

    111 New Observations in Cerebral Glucose Metabolism Following Traumatic Brain Injury: The Mystery of the Missing Glucose 246 Studies in 74 Patients and Comparison to Normal Controls.

    • Joshua Robert Dusick, Thomas C Glenn, Paul M Vespa, and Neil A Martin.
    • Neurosurgery. 2015 Aug 1;62 Suppl 1:200.

    IntroductionPrevious studies have demonstrated a profound dysfunction of cerebral metabolism following traumatic brain injury (TBI). Despite overall depression of cerebral metabolism, the cerebral metabolic rate (CMR) of oxygen is depressed out of proportion to the mildly reduced CMRglucose. This mismatch has raised the question, where does the missing glucose go if it is not metabolized oxidatively? We have previously demonstrated that an increased proportion of glucose is shunted through the pentose phosphate pathway prompting us to further investigate the total percentage of glucose metabolized by alternative pathways (the "missing glucose") in an attempt to understand the full milieu of altered or dysfunctional metabolism in the injured brain.MethodsTo determine CMR for oxygen, glucose, and lactate by a modified Kety-Schmidt method, daily arterial and jugular venous blood samples and cerebral blood flow measurements were made in 74 moderate and severe TBI patients over the first 6 days postinjury. Data were also collected from 35 healthy subjects. Using molar units, missing glucose utilization was calculated by CMRglucose (missing) = CMRglucose (total) - (CMRO2/6) + (CMRlactate/2) and converted to a percentage as CMRglucose (missing) % = (CMRglucose (missing)/CMRglucose (total)) × 100. Overall trauma-normal differences were compared using a mixed-effects model with random subject effect to account for the repeated measurements in the trauma group.ResultsThe average calculated missing glucose (proportion of alternative glucose metabolism, not accounted for by oxidative metabolism or lactate production) was 34.45% in TBI subjects compared with 12.18% in healthy subjects (P = .004). Overall CMRO2 (0.599 vs 1.391; P < .001), CMRglucose (0.193 vs 0.296; P < .001) and metabolic ratio (3.92 vs 4.93; P = .006) were all depressed in TBI subjects.ConclusionIn addition to an overall depression of cerebral metabolism for oxygen and glucose, the percentage of glucose with alternative metabolic fates (missing glucose) was significantly higher in the posttraumatic brain than in the normal brain, almost a 3-fold elevation. Further study is needed to fully identify the alternative metabolic pathways involved.

      Pubmed     Full text   Copy Citation     Plaintext  

      Add institutional full text...

    Notes

     
    Knowledge, pearl, summary or comment to share?
    300 characters remaining
    help        
    You can also include formatting, links, images and footnotes in your notes
    • Simple formatting can be added to notes, such as *italics*, _underline_ or **bold**.
    • Superscript can be denoted by <sup>text</sup> and subscript <sub>text</sub>.
    • Numbered or bulleted lists can be created using either numbered lines 1. 2. 3., hyphens - or asterisks *.
    • Links can be included with: [my link to pubmed](http://pubmed.com)
    • Images can be included with: ![alt text](https://bestmedicaljournal.com/study_graph.jpg "Image Title Text")
    • For footnotes use [^1](This is a footnote.) inline.
    • Or use an inline reference [^1] to refer to a longer footnote elseweher in the document [^1]: This is a long footnote..

    hide…

Want more great medical articles?

Keep up to date with a free trial of metajournal, personalized for your practice.
1,704,841 articles already indexed!

We guarantee your privacy. Your email address will not be shared.