scholarly journals Clinical and epidemiological analysis of severe traumatic brain injury: the role of nutritional support to the injured with a prolonged state of impaired consciousness

2020 ◽  
pp. 32-43
Author(s):  
M. V. Nikiforov ◽  
A. A. Korolev
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Nutritional Support ◽  
The Body ◽  
Medical Rehabilitation ◽  
Impaired Consciousness ◽  
Epidemiological Analysis ◽  
The Brain

Relevance. Patients with prolonged impaired consciousness due to traumatic brain injury are the most difficult category of patients in inpatient medical rehabilitation units. Despite the experience gained in managing this complex category of patients, the problem of nutrition status and trophological insufficiency, as well as practical issues regarding the organization of optimal nutrition at this stage of medical rehabilitation remain unresolved.Intention. To study the role of nutritional support for patients with long-term impaired consciousness on the basis of a clinical and epidemiological analysis of severe traumatic brain injury.Methodology. The data of an epidemiological analysis of traumatic brain injuries and features of ongoing nutritional support in patients with long-term impaired consciousness are presented, based on a study of domestic and foreign publications from 2005 to 2019.Results and Discussion. Timely and adequate nutritional support optimizes the structural-functional and metabolic systems of the body, adaptive reserves interfere with rapidly progressive depletion and chronic catabolic processes, contribute to positive changes in the functional state of the brain, reduce infectious complications, and increase the effectiveness of rehabilitation measures and the rate of recovery of consciousness.Conclusion. The analysis revealed the ambiguity of the interpreted data on clinical recommendations and approaches to the use of nutritional support in patients with long-term impaired consciousness due to traumatic brain injury. Considering the fact that in most cases such patients need continuous long-term comprehensive rehabilitation measures, accompanied by significant energy costs of the body, an essential component of the rehabilitation process, in our opinion, is the inclusion of adequate nutritional support that prevents fast-progressing exhaustion and chronic catabolic processes. In this regard, such an urgent task is to optimize the algorithms of nutritional support in patients with long-term impaired consciousness after a traumatic brain injury, the solution of which will improve the functional state of the brain and, therefore, the rehabilitation prognosis and quality of their life.

Potential Role of Adult Hippocampal Neurogenesis in Traumatic Brain Injury

2021 ◽  
Vol 28 ◽  
Author(s):  
Lucas Alexandre Santos Marzano ◽  
Fabyolla Lúcia Macedo de Castro ◽  
Caroline Amaral Machado ◽  
João Luís Vieira Monteiro de Barros ◽  
Thiago Macedo e Cordeiro ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Clinical Studies ◽  
Molecular Mechanisms ◽  
Hippocampal Neurogenesis ◽  
Cognitive Outcomes ◽  
Adult Hippocampal Neurogenesis ◽  
The Brain

: Traumatic brain injury (TBI) is a serious cause of disability and death among young and adult individuals, displaying complex pathophysiology including cellular and molecular mechanisms that are not fully elucidated. Many experimental and clinical studies investigated the potential relationship between TBI and the process by which neurons are formed in the brain, known as neurogenesis. Currently, there are no available treatments for TBI’s long-term consequences being the search for novel therapeutic targets, a goal of highest scientific and clinical priority. Some studies evaluated the benefits of treatments aimed at improving neurogenesis in TBI. In this scenario, herein, we reviewed current pre-clinical studies that evaluated different approaches to improving neurogenesis after TBI while achieving better cognitive outcomes, which may consist in interesting approaches for future treatments.

Sa2015 Traumatic Brain Injury and Intestinal Dysfunction: Investigating a Putative Role of the Brain-Gut Axis in Long-Term Consequences of Injury

2015 ◽  
Vol 148 (4) ◽  
pp. S-384
Author(s):  
Elise L. Ma ◽  
Allen Smith ◽  
Neemesh Desai ◽  
Alan Faden ◽  
Terez Shea-Donohue
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Putative Role ◽  
Long Term Consequences ◽  
The Brain

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

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.

scholarly journals Annexin A2 Deficiency Exacerbates Neuroinflammation and Long-Term Neurological Deficits after Traumatic Brain Injury in Mice

2019 ◽  
Vol 20 (24) ◽  
pp. 6125 ◽  
Author(s):  
Ning Liu ◽  
Yinghua Jiang ◽  
Joon Yong Chung ◽  
Yadan Li ◽  
Zhanyang Yu ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Inflammatory Response ◽  
Neurovascular Unit ◽  
Annexin A2 ◽  
Tissue Loss ◽  
Neurological Deficits ◽  
Endogenous Factors ◽  
The Brain

Our laboratory and others previously showed that Annexin A2 knockout (A2KO) mice had impaired blood–brain barrier (BBB) development and elevated pro-inflammatory response in macrophages, implying that Annexin A2 (AnxA2) might be one of the key endogenous factors for maintaining homeostasis of the neurovascular unit in the brain. Traumatic brain injury (TBI) is an important cause of disability and mortality worldwide, and neurovascular inflammation plays an important role in the TBI pathophysiology. In the present study, we aimed to test the hypothesis that A2KO promotes pro-inflammatory response in the brain and worsens neurobehavioral outcomes after TBI. TBI was conducted by a controlled cortical impact (CCI) device in mice. Our experimental results showed AnxA2 expression was significantly up-regulated in response to TBI at day three post-TBI. We also found more production of pro-inflammatory cytokines in the A2KO mouse brain, while there was a significant increase of inflammatory adhesion molecules mRNA expression in isolated cerebral micro-vessels of A2KO mice compared with wild-type (WT) mice. Consistently, the A2KO mice brains had a significant increase in leukocyte brain infiltration at two days after TBI. Importantly, A2KO mice had significantly worse sensorimotor and cognitive function deficits up to 28 days after TBI and significantly larger brain tissue loss. Therefore, these results suggested that AnxA2 deficiency results in exacerbated early neurovascular pro-inflammation, which leads to a worse long-term neurologic outcome after TBI.

scholarly journals Role of Thalamus in Recovery of Traumatic Brain Injury

2016 ◽  
Vol 07 (S 01) ◽  
pp. S076-S079 ◽  
Author(s):  
Ashok Munivenkatappa ◽  
Amit Agrawal
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Brain Structures ◽  
Thalamic Nuclei ◽  
Posttraumatic Symptoms ◽  
Injured Brain ◽  
Recovery Mechanisms ◽  
The Brain ◽  
Degree Of Recovery

ABSTRACTDegree of recovery after traumatic brain injury is highly variable that lasts for many weeks to months. The evidence of brain structures involved in recovery mechanisms is limited. This review highlights evidence of the brain structure particularly thalamus in neuroplasticity mechanism. Thalamus with its complex global networking has potential role in refining the cortical and other brain structures. Thalamic nuclei activation both naturally or by neurorehabilitation in injured brain can enhance and facilitate the improvement of posttraumatic symptoms. This review provides evidence from literature that thalamus plays a key role in recovery mechanism after injury. The study also emphasize that thalamus should be specifically targeted in neurorehabilitation following brain injury.

Practical Challenges in Collecting Head Impact Biomechanics Data in Real-World Scenarios via a Helmet-Based Accelerometer System

2013 ◽  
Author(s):  
Mari A. Allison ◽  
Yun Seok Kang ◽  
Matthew R. Maltese ◽  
John H. Bolte ◽  
Kristy B. Arbogast
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Mild Traumatic Brain Injury ◽  
Real World ◽  
Head Impact ◽  
Permanent Damage ◽  
Head Impact Biomechanics ◽  
Impact Biomechanics ◽  
The Brain

Recent studies have shown that mild traumatic brain injury (mTBI) can have long-term neurological consequences and may cause permanent damage to the brain [1,2]. Given estimates that millions of these injuries occur each year [3], this knowledge has created a demand for countermeasures to prevent mTBI. In order to create countermeasures, the biomechanical inputs leading to mTBI, which are still a matter of debate, must be better understood in both children and adults.

scholarly journals A Review of MicroRNA Biomarkers in Traumatic Brain Injury

2019 ◽  
Vol 13 ◽  
pp. 117906951983228 ◽  
Author(s):  
Hamna Atif ◽  
Steven D Hicks
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
The Body ◽  
Symptom Duration ◽  
Public Concern ◽  
Regulate Gene Expression ◽  
Injured Brain ◽  
Patient Reported ◽  
Brain Recovery

There is growing public concern surrounding traumatic brain injury (TBI). TBI can cause significant morbidity, and the long-term sequelae are poorly understood. TBI diagnosis and management rely on patient-reported symptoms and subjective clinical assessment. There are no biologic tools to detect mild TBI or to track brain recovery. Emerging evidence suggests that microRNAs (miRNAs) may provide information about the injured brain. These tiny epigenetic molecules are expressed throughout the body. However, they are particularly important in neurons, can cross the blood-brain barrier, and are securely transported from cell to cell, where they regulate gene expression. miRNA levels may identify patients with TBI and predict symptom duration. This review synthesizes miRNA findings from 14 human studies. We distill more than 291 miRNAs to 17 biomarker candidates that overlap across multiple studies and multiple biofluids. The goal of this review is to establish a collective understanding of miRNA biology in TBI and identify clinical priorities for future investigations of this promising biomarker.

scholarly journals A Role for Nanoparticles in Treating Traumatic Brain Injury

Pharmaceutics ◽  
2019 ◽  
Vol 11 (9) ◽  
pp. 473 ◽  
Author(s):  
Badrul Alam Bony ◽  
Forrest M. Kievit
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Treatment Options ◽  
Unmet Need ◽  
Economic Loss ◽  
Phase Iii ◽  
Target Engagement ◽  
Post Injury ◽  
The Brain

Traumatic brain injury (TBI) is one of the main causes of disability in children and young adults, as well as a significant concern for elderly individuals. Depending on the severity, TBI can have a long-term impact on the quality of life for survivors of all ages. The primary brain injury can result in severe disability or fatality, and secondary brain damage can increase the complexities in cellular, inflammatory, neurochemical, and metabolic changes in the brain, which can last decades post-injury. Thus, survival from a TBI is often accompanied by lifelong disabilities. Despite the significant morbidity, mortality, and economic loss, there are still no effective treatment options demonstrating an improved outcome in a large multi-center Phase III trial, which can be partially attributed to poor target engagement of delivered therapeutics. Thus, there is a significant unmet need to develop more effective delivery strategies to overcome the biological barriers that would otherwise inhibit transport of materials into the brain to prevent the secondary long-term damage associated with TBI. The complex pathology of TBI involving the blood-brain barrier (BBB) has limited the development of effective therapeutics and diagnostics. Therefore, it is of great importance to develop novel strategies to target the BBB. The leaky BBB caused by a TBI may provide opportunities for therapeutic delivery via nanoparticles (NP). The focus of this review is to provide a survey of NP-based strategies employed in preclinical models of TBI and to provide insights for improved NP based diagnostic or treatment approaches. Both passive and active delivery of various NPs for TBI are discussed. Finally, potential therapeutic targets where improved NP-mediated delivery could increase target engagement are identified with the overall goal of providing insight into open opportunities for NP researchers to begin research in TBI.

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