Acute glucose and lactate metabolism are associated with cognitive recovery following traumatic brain injury. Issue 4 (13th June 2017)

• Record Type: Journal Article
• Authors: Mannino, Christina; Glenn, Thomas C.; Hovda, David A.; Vespa, Paul M.; McArthur, David L.; Van Horn, John D.; Wright, Matthew J.
• Other Names: Juliano Sharon L. guestEditor.; Perez‐Polo J. Regino guestEditor.
• Is Part Of: Journal of neuroscience research. Volume 96:Issue 4(2018)
• Page Start: 696
• Page End: 701
• Publication Date: 2017-06-13
• Subjects: traumatic brain injury -- brain metabolism -- cognition -- neuropsychology -- glucose -- lactate; Neurobiology -- Periodicals; 612
• DOI: 10.1002/jnr.24097
• Languages: English
• ISSNs: 0360-4012

Abstract

Abstract: Traumatic brain injury (TBI) is associated with acute cerebral metabolic crisis (ACMC). ACMC‐related atrophy appears to be prominent in frontal and temporal lobes following moderate‐to‐severe TBI. This atrophy is correlated with poorer cognitive outcomes in TBI. The current study investigated ability of acute glucose and lactate metabolism to predict long‐term recovery of frontal‐temporal cognitive function in participants with moderate‐to‐severe TBI. Cerebral metabolic rate of glucose and lactate were measured by the Kety‐Schmidt method on days 0–7 post‐injury. Indices of frontal‐temporal cognitive processing were calculated for six months post‐injury; 12 months post‐injury; and recovery (the difference between the six‐ and 12‐month scores). Glucose and lactate metabolism were included in separate regression models, as they were highly intercorrelated. Also, glucose and lactate values were centered and averaged and included in a final regression model. Models for the prediction frontal‐temporal cognition at six and 12 months post‐injury were not significant. However, average glucose and lactate metabolism predicted recovery of frontal‐temporal cognition, accounting for 23% and 22% of the variance, respectively. Also, maximum glucose metabolism, but not maximum lactate metabolism, was an inverse predictor in the recovery of frontal‐temporal cognition, accounting for 23% of the variance. Finally, the average of glucose and lactate metabolism predicted frontal‐temporal cognitive recovery, accounting for 22% of the variance. These data indicate that acute glucose and lactate metabolism both support cognitive recovery from TBI. Also, our data suggest that control of endogenous fuels and/or supplementation with exogenous fuels may have therapeutic potential for cognitive recovery from TBI. Abstract : Traumatic brain injury (TBI) results in neuropathology via primary and secondary mechanisms. One important secondary injury mechanism, acute cerebral metabolic crisis, has been associated with neuropathology, cognitive deficits, and functional decline. The current study demonstrates that greater glucose and lactate metabolism days after injury are related to improved cognitive recovery from TBI. These findings support the potential therapeutic benefit of controlling and/or supplementing fuel sources during acute recovery from TBI.