Traumatic brain injury and hyperglycemia

Oliveira, Daniel; Amorim, Robson Luís Oliveira de; Vieira, Rodrigo Barreiros; Paiva, Wellingson Silva

doi:10.18632/oncotarget.15740

Cited by 7 publications

(3 citation statements)

References 4 publications

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“…A progressive degeneration of dopaminergic neurons occurs along with microglia activation in TBI [21]. Likewise, mice exposed to closed head TBI showed a higher vulnerability to 6-hydroxydopamine injection [39]. Experimental TBI is also associated with accumulation of α-synuclein in activated microglial cells, resulting in injury to dopaminergic neurons [20].…”

Section: Discussionmentioning

confidence: 99%

Interleukin-1 Beta Neutralization Attenuates Traumatic Brain Injury-Induced Microglia Activation and Neuronal Changes in the Globus Pallidus

Özen

Ruscher

Nilsson

et al. 2020

IJMS

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Traumatic brain injury (TBI) increases the risk of delayed neurodegenerative processes, including Parkinson’s disease (PD). Interleukin-1beta (IL-1β), a key pro-inflammatory cytokine, may promote secondary injury development after TBI. Conversely, neutralizing IL-1β was found to improve functional recovery following experimental TBI. However, the mechanisms underlying the behavioral improvements observed by IL-1β neutralization are still poorly understood. The present study investigated the role of IL-1β on the microglia response and neuronal changes in the globus pallidus in response to diffuse TBI. Mice were subjected to sham injury or the central fluid percussion injury (cFPI) (a model of traumatic axonal injury), and were randomly administered an IL-1β neutralizing or a control antibody at 30 min post-injury. The animals were analyzed at 2, 7, or 14 days post-injury. When compared to controls, mice subjected to cFPI TBI had increased microglia activation and dopaminergic innervation in the globus pallidus, and a decreased number of parvalbumin (PV) positive interneurons in the globus pallidus. Neutralization of IL-1β attenuated the microglia activation, prevented the loss of PV+ interneurons and normalized dopaminergic fiber density in the globus pallidus of brain-injured animals. These findings argue for an important role for neuro-inflammation in the PD-like pathology observed in TBI.

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Section: Discussionmentioning

confidence: 99%

Interleukin-1 Beta Neutralization Attenuates Traumatic Brain Injury-Induced Microglia Activation and Neuronal Changes in the Globus Pallidus

Özen

Ruscher

Nilsson

et al. 2020

IJMS

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“…Hypernatremia and hyperglycemia were associated with poor outcome after severe TBI 49 , 60 - 64 . The main point is that stress response activates the hypothalamic-pituitary-adrenal axis and sympathetic nervous system, leading to elevated levels of neurohormones and insulin resistance 65 . Intensive insulin therapy was considered as a therapeutic strategy to treat cerebral metabolic distress in a previous study 66 .…”

Section: Discussionmentioning

confidence: 99%

Clinical predictors of prognosis in patients with traumatic brain injury combined with extracranial trauma

Liu¹,

Xie²,

Xiao³

et al. 2021

Int. J. Med. Sci.

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Objective: The purpose of this study was to investigate whether routine blood tests on admission and clinical characteristics can predict prognosis in patients with traumatic brain injury (TBI) combined with extracranial trauma. Methods: Clinical data of 182 patients with TBI combined with extracranial trauma from April 2018 to December 2019 were retrospectively collected and analyzed. Based on GOSE score one month after discharge, the patients were divided into a favorable group (GOSE 1-4) and unfavorable group (GOSE 5-8). Routine blood tests on admission and clinical characteristics were recorded. Results: Overall, there were 48 (26.4%) patients with unfavorable outcome and 134 (73.6%) patients with favorable outcome. Based on multivariate analysis, independent risk factors associated with unfavorable outcome were age (odds ratio [OR], 1.070; 95% confidence interval [CI], 1.018-1.124; p< 0.01), admission Glasgow Coma Scale (GCS) score (OR, 0.807; 95% CI, 0.675-0.965; p< 0.05), heart rate (OR, 1.035; 95% CI, 1.004-1.067; p< 0.05), platelets count (OR, 0.982; 95% CI, 0.967-0.997; p< 0.05), and tracheotomy (OR, 15.201; 95% CI, 4.121-56.078; p< 0.001). Areas under the curve (AUC) of age, admission GCS, heart rate, tracheotomy, and platelets count were 0.678 (95% CI, 0.584-0.771), 0.799 (95% CI, 0.723-0.875), 0.652 (95% CI, 0.553-0.751), 0.776 (95% CI, 0.692-0.859), and 0.688 (95% CI, 0.606-0.770), respectively. Conclusions: Age, admission GCS score, heart rate, tracheotomy, and platelets count can be recognized as independent predictors of clinical prognosis in patients with severe TBI combined with extracranial trauma.

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“…Therefore, a systematic review and quantitative analysis of currently available evidence may provide useful information to guide clinical practice and the design of future clinical trials. [ 11 ]…”

Section: Introductionmentioning

confidence: 99%

Effect of hyperglycemia on all-cause mortality from pediatric brain injury

Chen

Liu

2020

Medicine

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Background: This study aimed to assess the effect of hyperglycemia on all-cause mortality in pediatric patients with brain injury, based on currently available evidence. Methods: We systematically searched the PubMed, Embase, and Cochrane Library databases with the keywords “hyperglycemia”, “brain injury”, and “pediatrics”. The retrieved records were screened by title, abstract, and full-text to include original articles assessing the effects of hyperglycemia on pediatric brain injury. The extracted data were assessed by a fixed-effects model. The risk of bias in the eligible studies was evaluated with the Newcastle-Ottawa Scale. Publication bias was visually examined with a funnel plot. Begg and Egger tests, respectively, were used to identify small-study effects. Sensitivity analysis was performed to evaluate the robustness of the original effect size. Results: Nine observational studies were identified from 1439 primary hits. A total of 970 pediatric patients, including 304 with hyperglycemia and brain injury, were included for meta-analysis. Hyperglycemia was strongly associated with a higher risk of all-cause mortality in pediatric patients (odds ratio = 11.60, 95% confidence interval [CI] 7.88–17.08; I 2 = 0%). The overall quality of eligible studies was low, but the funnel plot indicated no publication bias. Conclusions: Hyperglycemia is significantly associated with high all-cause mortality in pediatric patients with brain injury. However, the relationship should be confirmed by larger-scale observational studies and randomized controlled trials.

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Traumatic brain injury and hyperglycemia

Cited by 7 publications

References 4 publications

Interleukin-1 Beta Neutralization Attenuates Traumatic Brain Injury-Induced Microglia Activation and Neuronal Changes in the Globus Pallidus

Interleukin-1 Beta Neutralization Attenuates Traumatic Brain Injury-Induced Microglia Activation and Neuronal Changes in the Globus Pallidus

Clinical predictors of prognosis in patients with traumatic brain injury combined with extracranial trauma

Effect of hyperglycemia on all-cause mortality from pediatric brain injury

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