Dynamic changes in local cerebral glucose utilization following cerebral concussion in rats: evidence of a hyper- and subsequent hypometabolic state

Yoshino, Atsuo; Hovda, David A.; Kawamata, Tatsuro; Katayama, Yoichi; Becker, Donald P.

doi:10.1016/0006-8993(91)90755-k

Cited by 544 publications

(389 citation statements)

References 35 publications

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“…This distinguishes the present studies from other investigations of brain injury, where acute insults to the brain were shown to result in widespread metabolic deficits that improved with time [4,11,30,46]. In brain lesion models, the period of post-injury metabolic depression has been shown to correlate with the duration of behavioral deficits [11,20,45].…”

Section: Discussionmentioning

confidence: 51%

“…Studies of brain energy metabolism after human and rodent brain injury demonstrate dynamic changes occurring during the acute period after injury, such that a hypermetabolic state lasting only 30 minutes (in rats) to a few hours (in humans) is followed by a profound depression lasting 5-10 to 30 days in rats and humans, respectively [27,30,46]. Along the same time course, we have recently shown that NMDA glutamate receptors in mice subjected to closed head injury undergo dynamic changes in activation and availability [5], with a transient activation (less than 1 hour) followed by long lasting decrease (over seven days) in receptor function and availability.…”

Section: Discussionmentioning

confidence: 99%

“…In experimental animals, surgical procedures such as cannulation, electrode placement and microdialysis probe implants are performed routinely in studies of brain organization and function. Studies in our laboratory and others have shown that following these routine surgical procedures, animals undergo dramatic short-term and long-term neurochemical and metabolic changes [5,34,39,41,46].…”

Section: Introductionmentioning

confidence: 94%

“…Specifically, brain energy metabolism after injury fluctuates such that immediately after injury, a hyperactivated state lasting only 30 minutes (in rats) to a few hours (in humans) is followed by a metabolic depression lasting from 5-10 or 30 days in rats or humans, respectively [4,27,30,46]. We have recently used serial small animal PET imaging to show a profound, persistent metabolic decline following microdialysis cannula implant that began as early as 2.0 hrs after the surgery, was at its lowest point 48 hrs after the surgery and persisted for the duration of the experiment, 25 days [39].…”

Section: Introductionmentioning

confidence: 99%

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Metabolic and behavioral deficits following a routine surgical procedure in rats

et al. 2007

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To test the hypothesis that functional metabolic deficits observed following surgical brain injury are associated with changes in cognitive performance in rodents, we performed serial imaging studies in parallel with behavioral measures in control animals and in animals with surgical implants. Memory function was assessed using the novel object recognition (NOR) test, administered 3 days prior to and 3, 7, 14, and 56 days after surgery. At each time point, general locomotion was also measured. Metabolic imaging with 18 F-fluorodeoxyglucose ([ 18 F]FDG) occurred 28 and 58 days after surgery. Animals with surgical implants performed significantly worse on tests of object recognition, while general locomotion was unaffected by the implant. There was a significant decrease in glucose uptake after surgery in most of the hemisphere ipsilateral to the implant relative to the contralateral hemisphere. At both time points, the most significant metabolic deficits occurred in the primary motor cortex (-25%; p<0.001), sensory cortex (-15%, p<0.001) and frontal cortex (-12%; p<0.001). Ipsilateral areas further from the site of insertion became progressively worse, including the sensory cortex, dorsal striatum and thalamus. This data was supported by a voxel-based analysis of the PET data, which revealed again a unilateral decrease in [ 18 F]FDG uptake that extended throughout the ipsilateral cortex and persisted for the duration of the 58-day study. Probe implantation in the striatum results in a widespread and long lasting decline in cortical glucose metabolism together with a persistent, injury-related deficit in the performance of a cognitive (object recognition) task in rats.

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Section: Discussionmentioning

confidence: 51%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 94%

Section: Introductionmentioning

confidence: 99%

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Metabolic and behavioral deficits following a routine surgical procedure in rats

et al. 2007

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“…Indeed, increased lactate production in the injured brain seems to be independent of oxygen availability, and therefore cannot be considered as a direct ischemic and hypoxic metabolic marker30. Instead, experimental and clinical studies highlight the existence of an acute hyperglycolysis after severe TBI followed by subacute decrease in glucose metabolism 31, 32. The early hyperglycolytic phase seems to reflect the energy demands for reversal of ionic imbalances caused by massive release of glutamate33, while in subacute phase, the decrease in glucose utilization may indicate impaired mitochondrial function 33, 34…”

Section: Discussionmentioning

confidence: 99%

Elevated glutamate and lactate predict brain death after severe head trauma

Stefani

Modkovski

Hansel

et al. 2017

Ann Clin Transl Neurol

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ObjectiveClinical neurological assessment is challenging for severe traumatic brain injury (TBI) patients in the acute setting. Waves of neurochemical abnormalities that follow TBI may serve as fluid biomarkers of neurological status. We assessed the cerebrospinal fluid (CSF) levels of glutamate, lactate, BDNF, and GDNF, to identify potential prognostic biomarkers of neurological outcome.MethodsThis cross‐sectional study was carried out in a total of 20 consecutive patients (mean [SD] age, 29 [13] years; M/F, 9:1) with severe TBI Glasgow Coma Scale ≤ 8 and abnormal computed tomography scan on admission. Patients were submitted to ventricular drainage and had CSF collected between 2 and 4 h after hospital admission. Patients were then stratified according to two clinical outcomes: deterioration to brain death (nonsurvival, n = 6) or survival (survival, n = 14), within 3 days after hospital admission. CSF levels of brain‐derived substances were compared between nonsurvival and survival groups. Clinical and neurological parameters were also assessed.ResultsGlutamate and lactate are significantly increased in nonsurvival relative to survival patients. We tested the accuracy of both biomarkers to discriminate patient outcome. Setting a cutoff of >57.75, glutamate provides 80.0% of sensitivity and 84.62% of specificity (AUC: 0.8214, 95% CL: 54.55–98.08%; and a cutoff of >4.65, lactate has 100% of sensitivity and 85.71% of specificity (AUC: 0.8810, 95% CL: 54.55–98.08%). BDNF and GDNF did not discriminate poor outcome.InterpretationThis early study suggests that glutamate and lactate concentrations at hospital admission accurately predict death within 3 days after severe TBI.

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The effects of early relational trauma on right brain development, affect regulation, and infant mental health

Schore

2001

Infant Ment. Health J.

814

478

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Dynamic changes in local cerebral glucose utilization following cerebral concussion in rats: evidence of a hyper- and subsequent hypometabolic state

Cited by 544 publications

References 35 publications

Metabolic and behavioral deficits following a routine surgical procedure in rats

Metabolic and behavioral deficits following a routine surgical procedure in rats

Elevated glutamate and lactate predict brain death after severe head trauma

The effects of early relational trauma on right brain development, affect regulation, and infant mental health

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