Global and regional techniques for monitoring cerebral oxidative metabolism after severe traumatic brain injury

The disturbance of normal mechanisms of oxygen delivery and metabolism is a hallmark of severe traumatic brain injury (TBI). In the past, investigations into the status of cerebral oxygen metabolism depended on changes in the differences in oxygen content between arterial and jugular venous blood. The development of jugular venous oximetry permitted continuous monitoring of jugular venous oxygen saturation, thereby overcoming earlier limitations caused by intermittent sampling. Neuromonitoring techniques that utilize only jugular vein sampling provide information only about global cerebral metabolism, but direct measurement of brain tissue oxygen tension via intraparenchymal probes makes possible the assessment of regional cerebral oxygen metabolism. Regional and global neuromonitoring techniques are not competitive or mutually exclusive. Rather, they are best regarded as complementary, with each providing valuable information that has a direct bearing on patient outcomes. The authors review the currently available techniques used in the monitoring of cerebral oxidative metabolism in patients who have sustained severe TBI.

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Effects of ulinastatin on cerebral oxygen metabolism and CRP levels in patients with severe traumatic brain injury

Experimental and Therapeutic Medicine ◽

10.3892/etm.2014.1666 ◽

2014 ◽

Vol 7 (6) ◽

pp. 1683-1686 ◽

Cited By ~ 5

Author(s):

LEI HUI ◽

FAZHENG SHEN ◽

HAIGANG CHANG ◽

XIANGSHENG LI ◽

GUOJUN GAO ◽

...

Keyword(s):

Traumatic Brain Injury ◽

Brain Injury ◽

Severe Traumatic Brain Injury ◽

Oxygen Metabolism ◽

Cerebral Oxygen ◽

Cerebral Oxygen Metabolism

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Monitoring of cerebral metabolism: non-ischemic impairment of oxidative metabolism following severe traumatic brain injury

Neurological Research ◽

10.1179/016164107x240017 ◽

2007 ◽

Vol 29 (7) ◽

pp. 654-660 ◽

Cited By ~ 32

Author(s):

Jean F. Soustiel ◽

Gill E. Sviri

Keyword(s):

Traumatic Brain Injury ◽

Brain Injury ◽

Severe Traumatic Brain Injury ◽

Oxidative Metabolism ◽

Cerebral Metabolism

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Faculty Opinions recommendation of Differential influence of arterial blood glucose on cerebral metabolism following severe traumatic brain injury.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.1158503.618678 ◽

2009 ◽

Author(s):

Arun Gupta

Keyword(s):

Traumatic Brain Injury ◽

Blood Glucose ◽

Brain Injury ◽

Severe Traumatic Brain Injury ◽

Cerebral Metabolism ◽

Arterial Blood ◽

Arterial Blood Glucose

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Abstract TMP57: Cerebral Oxygen Metabolism as a Biomarker to Stratify Stroke Risk in Young Adults with Sickle Cell Disease

Stroke ◽

10.1161/str.48.suppl_1.tmp57 ◽

2017 ◽

Vol 48 (suppl_1) ◽

Author(s):

Andria L Ford ◽

Kristin P Guilliams ◽

Melanie E Fields ◽

Dustin K Ragan ◽

Cihat Eldeniz ◽

...

Keyword(s):

Sickle Cell ◽

Stroke Risk ◽

Cerebral Metabolism ◽

Infarct Volume ◽

Oxygen Metabolism ◽

Imaging Biomarkers ◽

Cerebral Oxygen ◽

Cerebral Oxygen Metabolism ◽

Imminent Risk ◽

Hemispheric Infarct

Background: While imaging biomarkers guide stroke prevention strategies in children with sickle cell (SC) disease, none have been adequately studied in adults. High oxygen extraction (OEF) predicts stroke in non-SC adults with carotid occlusion, while low oxygen metabolism (CMRO 2 ) predicts tissue at imminent risk in acute ischemic stroke. We hypothesized that metrics of cerebral metabolism: (1) differ between SC adults with and without stroke and (2) correlate with infarct burden. Methods: A prospective MRI study enrolled 37 adults (28 ± 8 yr) from SC clinic into 4 groups: (1) 9 age/race matched healthy controls, (2) 6 SC adults without infarcts, (3) 15 SC adults with infarcts (infarct volume 7.4 ± 17.5 ml), and (4) 7 SC adults on chronic transfusions (Tx) (infarct volume 3.6 ± 6.6 ml). Arterial spin labelling and asymmetric spin echo measured voxel-wise cerebral blood flow (CBF) and OEF. CMRO 2 = CBF x OEF x blood oxygen content. Infarcts were delineated on FLAIR. OEF, CBF, and CMRO 2 (excluding infarcted tissue) were compared: between groups 1-3 (Kruskal-Wallis) and in group 4 between pre- and post-tx scans (Signed Rank). An ROI defined by high OEF within the deep white matter (a region at high stroke risk in SC) was applied to group 3. OEF, CBF, and CMRO 2 within the ROI were correlated with hemispheric infarct volume (IV) (Spearman’s ρ ). Results: Whole brain OEF showed a stepwise increase from controls, to SC adults without stroke, to SC adults with stroke (P<.001). SC adults on chronic Tx had intermediate OEF, with lowering of OEF post-Tx (Fig A). CBF and CMRO 2 were similar for SC adults with and without stroke (Fig B, C). High OEF and low CBF/CMRO 2 in the ROI correlated with hemispheric infarct burden: IV vs. OEF ( ρ =.40, P=.043); IV vs. CBF ( ρ =-.61, P=.002); and IV vs. CMRO 2 ( ρ =-.50, P=.016). Conclusion: Global OEF holds promise to stratify stroke risk in SC disease. Regional metrics of cerebral oxygen metabolism may indicate tissue-specific metabolic stress at imminent risk of infarction.

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Glucose and Oxygen Metabolism after Penetrating Ballistic-Like Brain Injury

Journal of Cerebral Blood Flow & Metabolism ◽

10.1038/jcbfm.2014.243 ◽

2015 ◽

Vol 35 (5) ◽

pp. 773-780 ◽

Cited By ~ 15

Author(s):

Shyam Gajavelli ◽

Shimoda Kentaro ◽

Julio Diaz ◽

Shoji Yokobori ◽

Markus Spurlock ◽

...

Keyword(s):

Brain Injury ◽

Brain Injuries ◽

Cerebral Metabolism ◽

Age Groups ◽

Oxygen Metabolism ◽

Control Group ◽

Cerebral Oxygen ◽

Ischemic Penumbra ◽

Primary Injury ◽

Time Point

Traumatic brain injury (TBI) is a major cause of death and disability in all age groups. Among TBI, penetrating traumatic brain injuries (PTBI) have the worst prognosis and represent the leading cause of TBI-related morbidity and death. However, there are no specific drugs/interventions due to unclear pathophysiology. To gain insights we looked at cerebral metabolism in a PTBI rat model: penetrating ballistic-like brain injury (PBBI). Early after injury, regional cerebral oxygen tension and consumption significantly decreased in the ipsilateral cortex in the PBBI group compared with the control group. At the same time point, glucose uptake was significantly reduced globally in the PBBI group compared with the control group. Examination of Fluorojade B-stained brain sections at 24 hours after PBBI revealed an incomplete overlap of metabolic impairment and neurodegeneration. As expected, the injury core had the most severe metabolic impairment and highest neurodegeneration. However, in the peri-lesional area, despite similar metabolic impairment, there was lesser neurodegeneration. Given our findings, the data suggest the presence of two distinct zones of primary injury, of which only one recovers. We anticipate the peri-lesional area encompassing the PBBI ischemic penumbra, could be salvaged by acute therapies.

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