ReviewCurrent neurology and neuroscience reports2016
Cerebral Lactate Metabolism After Traumatic Brain Injury.
Review in Current neurology and neuroscience reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers, 3 of them syntheses that pooled it.
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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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
53 citing papers in PubMed, 3 syntheses or guidelines pooled it, 94 citations in OpenAlex.
- Comparison of half-molar sodium lactate and mannitol to treat brain edema in severe traumatic brain injury: A systematic review.Chinese journal of traumatology = Zhonghua chuang shang za zhi · 2021Pooled it
- The diagnosis and prognostic value of plasma copeptin in traumatic brain injury: a systematic review and meta-analysis.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2021Pooled it
- A Systematic Review of Neuroprotective Strategies in the Management of Hypoglycemia.International journal of molecular sciences · 2019Pooled it
- Trial
- The effect of an adenosine AFluids and barriers of the CNS · 2018Trial
- Effects of Hypertonic Lactate Solutions on Intracranial Dynamics, Cerebral Oxygenation, and Metabolism in Patients with Acute Brain Injury: A Scoping Review.Neurocritical care · 2026Review
- Molecular vehicles for therapeutic delivery of lactate in exercise and medicine.Sports medicine and health science · 2026Review
- Exogenous lactate administration alleviates post-cardiac arrest brain injury by coordinating metabolic reprogramming and pathological mitophagy suppression.Cellular and molecular life sciences : CMLS · 2026Article
- Advances in cellular and molecular mechanisms of trauma-induced organ inflammation and dysfunction.Burns & trauma · 2026Review
- Effects of astrocytic PKM2 gene deletion on neuronal death following traumatic brain injury.Cell death discovery · 2025Article
- Preferential lactate metabolism in the human brain during exogenous and endogenous hyperlactataemia.The Journal of physiology · 2025Article
- Unlocking the metabolic and anti-inflammatory therapeutic potential of lactate in critically ill patients.Critical care (London, England) · 2025Review
- Article
- Imaging a concussion and the ensuing immune response at the blood-brain barrier.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Lactate dehydrogenase to albumin ratio and poor prognosis after thrombolysis in ischemic stroke patients: developing a novel nomogram.BMC medical informatics and decision making · 2025Article
- Brain energy homeostasis: the evolution of the astrocyte-neuron lactate shuttle hypothesis.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2025Review
- From Physiology to Pathology of Astrocytes: Highlighting Their Potential as Therapeutic Targets for CNS Injury.Neuroscience bulletin · 2025Review
- Metabolomic and lipidomic pathways in aneurysmal subarachnoid hemorrhage.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025Review
- Article
- Cerebral net uptake of lactate contributes to neurological injury after experimental cardiac arrest in rabbits.Scientific reports · 2024Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cerebral energy dysfunction has emerged as an important determinant of prognosis following traumatic brain injury (TBI). A number of studies using cerebral microdialysis, positron emission tomography, and jugular bulb oximetry to explore cerebral metabolism in patients with TBI have demonstrated a critical decrease in the availability of the main energy substrate of brain cells (i.e., glucose). Energy dysfunction induces adaptations of cerebral metabolism that include the utilization of alternative energy resources that the brain constitutively has, such as lactate. Two decades of experimental and human investigations have convincingly shown that lactate stands as a major actor of cerebral metabolism. Glutamate-induced activation of glycolysis stimulates lactate production from glucose in astrocytes, with subsequent lactate transfer to neurons (astrocyte-neuron lactate shuttle). Lactate is not only used as an extra energy substrate but also acts as a signaling molecule and regulator of systemic and brain glucose use in the cerebral circulation. In animal models of brain injury (e.g., TBI, stroke), supplementation with exogenous lactate exerts significant neuroprotection. Here, we summarize the main clinical studies showing the pivotal role of lactate and cerebral lactate metabolism after TBI. We also review pilot interventional studies that examined exogenous lactate supplementation in patients with TBI and found hypertonic lactate infusions had several beneficial properties on the injured brain, including decrease of brain edema, improvement of neuroenergetics via a "cerebral glucose-sparing effect," and increase of cerebral blood flow. Hypertonic lactate represents a promising area of therapeutic investigation; however, larger studies are needed to further examine mechanisms of action and impact on outcome.
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