Cerebral Lactate Metabolism After Traumatic Brain Injury.
Level 5 - mechanism / opinion, no new human data
Narrative review synthesizing preclinical mechanisms and pilot clinical studies without systematic review methodology.
PubMed 26898683 · doi:10.1007/s11910-016-0638-5
What was done
This narrative review summarizes clinical and experimental literature investigating cerebral energy dysfunction and lactate metabolism following traumatic brain injury (TBI). It examines mechanistic monitoring methods (cerebral microdialysis, positron emission tomography, jugular bulb oximetry), the astrocyte-neuron lactate shuttle model, animal injury models, and pilot human interventional studies evaluating exogenous hypertonic lactate infusions.
What was found
The abstract reports no numerical values or effect sizes. Qualitatively, studies show that TBI causes severe cerebral glucose deficits, prompting metabolic adaptation to alternative substrates like lactate. In animal injury models, exogenous lactate supplementation demonstrated neuroprotection. In human pilot interventional studies, hypertonic lactate infusions reduced brain edema, increased cerebral blood flow, and improved neuroenergetics via a cerebral glucose-sparing effect.
Why it matters
It highlights lactate as an active metabolic fuel and signaling molecule rather than merely a waste product in acute brain injury, supporting further investigation into hypertonic lactate as a metabolic therapy.
Limits
The paper is a non-systematic narrative review with no defined search protocol or quantitative data synthesis. Clinical evidence is limited to pilot interventional studies with unspecified sample sizes, and the impact of hypertonic lactate on functional neurological outcomes remains unproven in large randomized trials.
Cited by
- context Following traumatic brain injury, cerebral glycolysis is impaired, leaving neurons starving for preferred lactate fuel.