Military- and Sports-Related Mild Traumatic Brain Injury: Clinical Presentation, Management, and Long-Term Consequences

Introduction. Mild traumatic brain injury (mTBI) was reported to be the most frequent among other types of brain injuries and is the main reason for the disability in mid-life and middleaged people. It’s known that antioxidants can reduce oxidative stress, so, to prevent secondary brain injury modulating maintaining of long-term consequences after mTBI. Purpose of the study. This work was to study the serum vitamin E, C and A levels in the patients with long-term consequences after mTBI to explore their potential pathogenetic influence. Materials and methods. Sixty-seven patients with long-term consequences after mTBI were investigated with the mean age of 43,61 ± 8,24 years (18 women, 26,86% and 49 men, 73,14%) where the vitamin E, C and A contents were measured in sera by spectrophotometer method using standard protocols and reagents (Sigma, USA). Results. In this work, it was found descending serum levels of all investigated vitaminantioxidants in almost all patients with longterm consequences after mTBI where the content of vitamins A (M ± s: 1,63 ± 1,56 mkM/l) and E (25,41 ± 0,93 mkM/l) had a tendency to decreasing without significant differences compare to controls. It was found the statistically significant decreased of vitamin C levels in the serum samples of our investigated patients when compared to controls (p < 0,05, t = 4,59, 95% CI 98,81 to 55,68) where in the main patient group, the medians of total vitamin C level was 30,57 ± 5,38 mkM/l vs 36,91 ± 5,22 mkM/l in controls. It was shown that the patients with long-term consequences after mild contusion in anamnesis (64,18%) had the prominent changes in the vitamin C content. Conclusion. The maintaining of long-term consequences of mTBI was accompanied by the vitamin-antioxidant dyshomeostasis such as decreasing of vitamin C serum level associated with a tendency to decreasing of vitamins A and E levels that may play the certain role in the pathogenesis. All these data are needed to be accounted into the consideration during the treatment of this patient category. Keywords: long-term consequences of mild traumatic brain injury, vitamin-antioxidant homeostasis.

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SOME METABOLIC PROCESSES IN THE PATIENTS WITH LONG-TERM CONSEQUENCES OF MILD TRAUMATIC BRAIN INJURY

International Journal of Medicine and Medical Research ◽

10.11603/ijmmr.2413-6077.2019.2.10459 ◽

2020 ◽

Vol 5 (2) ◽

pp. 25-31

Author(s):

Ye. Lekomtseva

Keyword(s):

Traumatic Brain Injury ◽

Alkaline Phosphatase ◽

Brain Injury ◽

Mild Traumatic Brain Injury ◽

Disease Duration ◽

Metabolic Processes ◽

Gamma Glutamyl Transpeptidase ◽

Positive Dependence ◽

Long Term Consequences

Background. Mild traumatic brain injury (mTBI) leads to disturbance of various metabolic processes significant in pathogenesis of the maintaining of long-term consequences after it. The objective of the research was to analyse changes in the activity of some membrane-associated enzyme markers, which are involved in different redox reactions, reflecting main metabolic processes. Methods. Forty-seven patients with long-term consequences of mTBI, thirty controls were enrolled. The levels of aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, lactate dehydrogenase (LDH), gamma-glutamyl transpeptidase were evaluated in sera by gas-liquid chromatograph and calorimetric methods. Results. The study revealed significant changes in metabolic processes observed for alkaline phosphatase and LDH, which were the indicators of membrane and redox processes disturbances, acidosis severity and impaired energy cell metabolism. The averages of LDH level was 662.7 versus 381.9 U/L, in the controls. The disease progression was followed by directly proportional LDH increase reaching very high values in the patients with disease duration more than 15 years (mean ±SD 144.6±16.3 versus 82.6±8.4 U/L, controls p<0.05). The long-term consequences of mTBI were characterized by statistically significant decrease of alkaline phosphatase and positive dependence (p<0.05) of it (r=+0.48) on the disease duration with the averages of alkaline phosphatase level of 152.5±11.21 versus 212.6±9.63 U/L, controls (p<0.01). The significance of changes in membrane-associated enzymes serum levels correlated with development of oxidative stress and metabolic processes dysfunction. Conclusion. In the patients with long-term consequences of mTBI, dysregulation of enzymes activity was detected that might be a marker of nervous system energy impairment and membranes destruction.

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Long-term consequences of mild traumatic brain injury

The British Journal of Psychiatry ◽

10.1192/bjp.bp.112.111492 ◽

2012 ◽

Vol 201 (3) ◽

pp. 172-174 ◽

Cited By ~ 6

Author(s):

Roberto J. Rona

Keyword(s):

Traumatic Brain Injury ◽

Longitudinal Study ◽

Brain Injury ◽

Mild Traumatic Brain Injury ◽

Epidemiological Studies ◽

Objective Tests ◽

Long Term Consequences

SummaryA debate has ensued about the long-term consequences of mild traumatic brain injury, the ‘signature injury’ of the Iraq and Afghanistan Wars. Most epidemiological studies have found that mild traumatic brain injury is unrelated to unspecific post-concussion symptoms based on self-reported symptoms. A longitudinal study, in this issue of the Journal, using objective tests has demonstrated that mild traumatic brain injury has limited lasting neuropsychological consequences.

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Clinical and paraclinical data of the efficacy of metabolic group drugs using in the complex treatment of the patients with long-term consequences after mild closed traumatic brain injury

Shidnoevropejskij zurnal vnutrisnoi ta simejnoi medicini ◽

10.15407/internalmed2020.01.064 ◽

2020 ◽

Vol 2020 (1) ◽

pp. 64-68

Author(s):

Y. Lekomtseva ◽

Keyword(s):

Traumatic Brain Injury ◽

Brain Injury ◽

Complex Treatment ◽

Long Term Consequences

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GPR110 ligands reduce chronic optic tract gliosis and visual deficit following repetitive mild traumatic brain injury in mice

Journal of Neuroinflammation ◽

10.1186/s12974-021-02195-y ◽

2021 ◽

Vol 18 (1) ◽

Author(s):

Huazhen Chen ◽

Karl Kevala ◽

Elma Aflaki ◽

Juan Marugan ◽

Hee-Yong Kim

Keyword(s):

Traumatic Brain Injury ◽

Brain Injury ◽

Mild Traumatic Brain Injury ◽

Visual Evoked Potential ◽

Evoked Potential ◽

Optic Tract ◽

Primary Microglia ◽

Visual Dysfunction ◽

The Brain

Abstract Background Repetitive mild traumatic brain injury (mTBI) can result in chronic visual dysfunction. G-protein receptor 110 (GPR110, ADGRF1) is the target receptor of N-docosahexaenoylethanolamine (synaptamide) mediating the anti-neuroinflammatory function of synaptamide. In this study, we evaluated the effect of an endogenous and a synthetic ligand of GPR110, synaptamide and (4Z,7Z,10Z,13Z,16Z,19Z)-N-(2-hydroxy-2-methylpropyl) docosa-4,7,10,13,16,19-hexaenamide (dimethylsynaptamide, A8), on the mTBI-induced long-term optic tract histopathology and visual dysfunction using Closed-Head Impact Model of Engineered Rotational Acceleration (CHIMERA), a clinically relevant model of mTBI. Methods The brain injury in wild-type (WT) and GPR110 knockout (KO) mice was induced by CHIMERA applied daily for 3 days, and GPR110 ligands were intraperitoneally injected immediately following each impact. The expression of GPR110 and proinflammatory mediator tumor necrosis factor (TNF) in the brain was measured by using real-time quantitative reverse transcription polymerase chain reaction (qRT-PCR) in an acute phase. Chronic inflammatory responses in the optic tract and visual dysfunction were assessed by immunostaining for Iba-1 and GFAP and visual evoked potential (VEP), respectively. The effect of GPR110 ligands in vitro was evaluated by the cyclic adenosine monophosphate (cAMP) production in primary microglia isolated from adult WT or KO mouse brains. Results CHIMERA injury acutely upregulated the GPR110 and TNF gene level in mouse brain. Repetitive CHIMERA (rCHIMERA) increased the GFAP and Iba-1 immunostaining of glia cells and silver staining of degenerating axons in the optic tract with significant reduction of N1 amplitude of visual evoked potential at up to 3.5 months after injury. Both GPR110 ligands dose- and GPR110-dependently increased cAMP in cultured primary microglia with A8, a ligand with improved stability, being more effective than synaptamide. Intraperitoneal injection of A8 at 1 mg/kg or synaptamide at 5 mg/kg significantly reduced the acute expression of TNF mRNA in the brain and ameliorated chronic optic tract microgliosis, astrogliosis, and axonal degeneration as well as visual deficit caused by injury in WT but not in GPR110 KO mice. Conclusion Our data demonstrate that ligand-induced activation of the GPR110/cAMP system upregulated after injury ameliorates the long-term optic tract histopathology and visual impairment caused by rCHIMERA. Based on the anti-inflammatory nature of GPR110 activation, we suggest that GPR110 ligands may have therapeutic potential for chronic visual dysfunction associated with mTBI.

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Long-term outcomes after mild traumatic brain injury

Journal of the American College of Surgeons ◽

10.1016/j.jamcollsurg.2014.07.775 ◽

2014 ◽

Vol 219 (4) ◽

pp. e144-e145

Author(s):

Elizabeth Shinn ◽

Amy Pate ◽

Frederique Pinto ◽

Akella Chendrasekhar

Keyword(s):

Traumatic Brain Injury ◽

Brain Injury ◽

Mild Traumatic Brain Injury ◽

Long Term Outcomes

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Determining long-term symptoms following mild traumatic brain injury: Method of interview affects self-report

Brain Injury ◽

10.1080/02699050601049247 ◽

2006 ◽

Vol 20 (11) ◽

pp. 1147-1154 ◽

Cited By ~ 32

Author(s):

P. Nolin ◽

R. Villemure ◽

L. Heroux

Keyword(s):

Traumatic Brain Injury ◽

Brain Injury ◽

Mild Traumatic Brain Injury ◽

Self Report

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Exosomal MicroRNA Differential Expression in Plasma of Young Adults with Chronic Mild Traumatic Brain Injury and Healthy Control

Biomedicines ◽

10.3390/biomedicines10010036 ◽

2021 ◽

Vol 10 (1) ◽

pp. 36

Author(s):

Rany Vorn ◽

Maiko Suarez ◽

Jacob C. White ◽

Carina A. Martin ◽

Hyung-Suk Kim ◽

...

Keyword(s):

Traumatic Brain Injury ◽

Young Adults ◽

Brain Injury ◽

Mild Traumatic Brain Injury ◽

Pathophysiological Mechanism ◽

Post Injury ◽

Persistent Symptoms ◽

Healthy Control ◽

Underlying Mechanisms

Chronic mild traumatic brain injury (mTBI) has long-term consequences, such as neurological disability, but its pathophysiological mechanism is unknown. Exosomal microRNAs (exomiRNAs) may be important mediators of molecular and cellular changes involved in persistent symptoms after mTBI. We profiled exosomal microRNAs (exomiRNAs) in plasma from young adults with or without a chronic mTBI to decipher the underlying mechanisms of its long-lasting symptoms after mTBI. We identified 25 significantly dysregulated exomiRNAs in the chronic mTBI group (n = 29, with 4.48 mean years since the last injury) compared to controls (n = 11). These miRNAs are associated with pathways of neurological disease, organismal injury and abnormalities, and psychological disease. Dysregulation of these plasma exomiRNAs in chronic mTBI may indicate that neuronal inflammation can last long after the injury and result in enduring and persistent post-injury symptoms. These findings are useful for diagnosing and treating chronic mTBIs.

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