ReviewFrontiers in neuroscience2014
Cerebral metabolism following traumatic brain injury: new discoveries with implications for treatment.
Review in Frontiers in neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
66 citing papers in PubMed, 1 synthesis or guideline pooled it, 104 citations in OpenAlex.
- Effectiveness of controlled decompression against conventional decompression methods for the management of severe traumatic brain injury patients: a meta-analysis.European journal of medical research · 2025Pooled it
- Effects of probiotics combined with early enteral nutrition on endothelin-1 and C-reactive protein levels and prognosis in patients with severe traumatic brain injury.The Journal of international medical research · 2020Trial
- Aerobic Exercise for Adolescents With Prolonged Symptoms After Mild Traumatic Brain Injury: An Exploratory Randomized Clinical Trial.The Journal of head trauma rehabilitationTrial
- Thiol-Based Neuroprotective Copolymers Acutely Restore Redox Metabolism and Mediate Vasogenic Edema in a Mouse Model of Traumatic Brain Injury.Macromolecular bioscience · 2026Article
- SIRT3/AARS2 regulates SOD2 lactylation to determine neuronal fate in TBI.Molecular neurobiology · 2026Article
- Molecular vehicles for therapeutic delivery of lactate in exercise and medicine.Sports medicine and health science · 2026Review
- Mirror Effect of Parvalbumin and Connexin 43 Expression in the Acute and Subacute Phases After Penetrating Traumatic Brain Injury Reveals a Non-Canonical Interaction.Molecules (Basel, Switzerland) · 2026Article
- Investigation of the Expression, Localization, and Acidosis-Associated Conformational Changes in Connexin 43 in Traumatic Brain Injury with the Development of a Neural Network Model for Assessing Systemic Inflammation.International journal of molecular sciences · 2025Article
- The Neurological Metabolic Phenotype in Prolonged/Chronic Critical Illness: Propensity Score Matched Analysis of Nutrition and Outcomes.Nutrients · 2025Article
- Cerebral Metabolic Rate of Oxygen and Accelerometry-Based Fatigability in Community-Dwelling Older Adults.Aging cell · 2025Article
- A low-cost open-source 3D-printed mouse cradle suspension system for awake or anaesthetisedHardwareX · 2025Article
- Article
- Review
- Astrocyte-mediated inflammatory responses in traumatic brain injury: mechanisms and potential interventions.Frontiers in immunology · 2025Review
- Metabolic Pathophysiology of Cortical Spreading Depression: A Review.Brain sciences · 2024Review
- Modern Perspective of Lactate Metabolism.Physiological research · 2024Review
- Tracing the path of disruption:CNS neuroscience & therapeutics · 2024Review
- Cerebral Glucose Metabolism following TBI: Changes in Plasma Glucose, Glucose Transport and Alternative Pathways of Glycolysis-A Translational Narrative Review.International journal of molecular sciences · 2024Review
- Metabolomics in severe traumatic brain injury: a scoping review.BMC neuroscience · 2023Article
- Using metabolomics to predict severe traumatic brain injury outcome (GOSE) at 3 and 12 months.Critical care (London, England) · 2023Article
6 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Because it is the product of glycolysis and main substrate for mitochondrial respiration, lactate is the central metabolic intermediate in cerebral energy substrate delivery. Our recent studies on healthy controls and patients following traumatic brain injury (TBI) using [6,6-(2)H2]glucose and [3-(13)C]lactate, along with cerebral blood flow (CBF) and arterial-venous (jugular bulb) difference measurements for oxygen, metabolite levels, isotopic enrichments and (13)CO2 show a massive and previously unrecognized mobilization of lactate from corporeal (muscle, skin, and other) glycogen reserves in TBI patients who were studied 5.7 ± 2.2 days after injury at which time brain oxygen consumption and glucose uptake (CMRO2 and CMRgluc, respectively) were depressed. By tracking the incorporation of the (13)C from lactate tracer we found that gluconeogenesis (GNG) from lactate accounted for 67.1 ± 6.9%, of whole-body glucose appearance rate (Ra) in TBI, which was compared to 15.2 ± 2.8% (mean ± SD, respectively) in healthy, well-nourished controls. Standard of care treatment of TBI patients in state-of-the-art facilities by talented and dedicated heath care professionals reveals presence of a catabolic Body Energy State (BES). Results are interpreted to mean that additional nutritive support is required to fuel the body and brain following TBI. Use of a diagnostic to monitor BES to provide health care professionals with actionable data in providing nutritive formulations to fuel the body and brain and achieve exquisite glycemic control are discussed. In particular, the advantages of using inorganic and organic lactate salts, esters and other compounds are examined. To date, several investigations on brain-injured patients with intact hepatic and renal functions show that compared to dextrose + insulin treatment, exogenous lactate infusion results in normal glycemia.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.