Cerebral microdialysis in TBI—limitations and possibilities

Nordström, Carl‐Henrik

doi:10.1007/s00701-017-3339-1

Cited by 9 publications

(10 citation statements)

References 6 publications

(6 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Advances in CMD use and interpretation have allowed CMD to become a routine neuromonitoring tool to help guide individualized treatment in neurointensive care TBI patients ( 114 , 115 ). However, CMD is limited because metabolites can only be measured in a very narrow zone surrounding the CMD probe ( 116 ). While this narrow measurement zone can help understand the metabolism of specific areas in the brain, CMD does not provide a complete metabolic picture of the entire brain.…”

Section: Limitations and Unknownsmentioning

confidence: 99%

The Therapeutic Potential and Limitations of Ketones in Traumatic Brain Injury

Daines

2021

Front. Neurol.

View full text Add to dashboard Cite

Traumatic brain injury (TBI) represents a significant health crisis. To date, no FDA approved pharmacotherapies are available to prevent the neurological deficits caused by TBI. As an alternative to pharmacotherapy treatment of TBI, ketones could be used as a metabolically based therapeutic strategy. Ketones can help combat post-traumatic cerebral energy deficits while also reducing inflammation, oxidative stress, and neurodegeneration. Experimental models of TBI suggest that administering ketones to TBI patients may provide significant benefits to improve recovery. However, studies evaluating the effectiveness of ketones in human TBI are limited. Unanswered questions remain about age- and sex-dependent factors, the optimal timing and duration of ketone supplementation, and the optimal levels of circulating and cerebral ketones. Further research and improvements in metabolic monitoring technology are also needed to determine if ketone supplementation can improve TBI recovery outcomes in humans.

show abstract

Section: Limitations and Unknownsmentioning

confidence: 99%

The Therapeutic Potential and Limitations of Ketones in Traumatic Brain Injury

Daines

2021

Front. Neurol.

View full text Add to dashboard Cite

show abstract

“…A high-cost and technically complex diagnostic method such as cerebral microdialysis, helps to measure the metabolites in the microenvironment of the injured brain tissue; however, due to its high cost and technical complexity, this system is only accessible to research centers in very high income countries. 5 There has been a recent growing search for biomarkers that enable the identification of the evolution of tissue injury and that may even foresee the magnitude of the brain damage before the identification of the primary injury using imaging. The objective of this review is to discuss some considerations around the most representative biomarkers in determining the magnitude of the TBI and their practical application in therapeutic decisionmaking protocols.…”

Section: Introductionmentioning

confidence: 99%

Utility of biomarkers in traumatic brain injury: a narrative review

Mendoza

Lopez

Echeverri

et al. 2020

Colomb. J. Anesthesiol.

View full text Add to dashboard Cite

Introduction: With the evolution of diagnostic techniques in traumatic brain injury (TBI), the study of neurological injury has made progress based on the concepts of primary and secondary injury, leading to the era of proteomics to understand the complex molecular events involved in the process. Objectives: This narrative review is intended to discuss the state of the art of the most frequently used biomarkers in TBI, their clinical utility, and the implications for therapeutic decisionmaking protocols. Materials and methods: In order to fulfill the objective of this paper, a literature review was conducted of the most important databases. Results: Several biomarkers have been studied as prognostic factors in patients with TBI. Learning about their sensitivity and specificity in neurological injury, and its post-trauma evolution over time, has been the goal of various papers in the past few years. Conclusion: Breakthroughs in the study of protein degradation make it necessary to broaden the spectrumand knowledge of new diagnostic methods in TBI. Further studies are needed to define the role of biomarkers and to promote protocols integrating specific values.

show abstract

“…Cerebral microdialysis (CMD) is used in neuro-intensive care to monitor cerebral metabolism for the prevention of secondary injury in patients with traumatic brain injury and aneurysmal subarachnoid hemorrhage (aSAH) [1]. It has also been a valuable tool in cerebrovascular research for many years.…”

Section: Introductionmentioning

confidence: 99%

Ethyl Pyruvate Increases Post-Ischemic Levels of Mitochondrial Energy Metabolites: A 13C-Labeled Cerebral Microdialysis Study

et al. 2020

Self Cite

View full text Add to dashboard Cite

Mitochondrial dysfunction after transient cerebral ischemia can be monitored by cerebral microdialysis (CMD) using changes in the lactate and pyruvate concentrations and ratio. Other metabolites associated with mitochondrial (dys)function are, e.g., tricyclic acid (TCA) and purine metabolites. Ethyl pyruvate (EP) is a putative neuroprotectant, supposedly targeting mitochondrial energy metabolism, but its effect on cerebral energy metabolism has never been described using microdialysis. In this study we monitored the metabolic effects of EP in the endothelin-1 (ET-1) rat model using perfusion with 13C-succinate and analysis of endogenous and 13C-labeled metabolites in the dialysates by liquid chromatography-mass spectrometry (LC-MS). Adult Sprague Dawley rats (n = 27 of which n = 11 were included in the study) were subjected to the microdialysis experiments. Microdialysis probes were perfused with 13C-labeled succinate (1 mM), and striatal dialysates were collected at 30 min intervals before induction of the insult, during intracerebral application of ET-1, and during intravenous treatment with either EP (40 mg/kg) or placebo, which was administered immediately after the insult. The rats were subjected to transient cerebral ischemia by unilateral microinjection of ET-1 in the piriform cortex, causing vasoconstriction of the medial cerebral artery. Monitoring was continued for 5 h after reperfusion, and levels of endogenous and 13C-labeled energy metabolites before and after ischemia-reperfusion were compared in EP-treated and control groups. Infarct volumes were assessed after 24 h. In both the EP-treated and placebo groups, ET-1-induced vasoconstriction resulted in a transient depression of interstitial glucose and elevation of lactate in the ipsilateral striatum. In the reperfusion phase, the concentrations of labeled malate, isocitrate, and lactate as well as endogenous xanthine were significantly higher in the EP-group than in the placebo-group: (mean ± SEM) labeled malate: 39.5% ± 14.9, p = 0.008; labeled isocitrate: 134.8% ± 67.9, p = 0.047; labeled lactate: 61% ± 22.0, p = 0.007; and endogenous xanthine: 93.9% ± 28.3, p = 0.0009. In the placebo group, significantly elevated levels of uridine were observed (mean ± SEM) 32.5% ± 12.7, p = 0.01. Infarct volumes were not significantly different between EP-treated and placebo groups, p = 0.4679. CMD labeled with 13C-succinate enabled detection of ischemic induction and EP treatment effects in the ET-1 rat model of transient focal cerebral ischemia. EP administered as a single intravenous bolus in the reperfusion-phase after transient cerebral ischemia increased de novo synthesis of several key intermediate energy metabolites (13C-malate, 13C-isocitrate, and endogenous xanthine). In summary, mitochondria process 13C-succinate more effectively after EP treatment.

show abstract

Cerebral microdialysis in TBI—limitations and possibilities

Cited by 9 publications

References 6 publications

The Therapeutic Potential and Limitations of Ketones in Traumatic Brain Injury

The Therapeutic Potential and Limitations of Ketones in Traumatic Brain Injury

Utility of biomarkers in traumatic brain injury: a narrative review

Ethyl Pyruvate Increases Post-Ischemic Levels of Mitochondrial Energy Metabolites: A 13C-Labeled Cerebral Microdialysis Study

Contact Info

Product

Resources

About