Distant Organ Damage in Acute Brain Injury

Acute brain injuries pose a great threat to global health, having significant impact on mortality and disability. Patients with acute brain injury may develop distant organ failure, even if no systemic diseases or infection is present. The severity of non-neurologic organs’ dysfunction depends on the extremity of the insult to the brain. In this comprehensive review we sought to describe the organ-related consequences of acute brain injuries. The clinician should always be aware of the interplay between central nervous system and non-neurological organs, that is constantly present. Cerebral injury is not only a brain disease, but also affects the body as whole, and thus requires holistic therapeutical approach.

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Study of Traumatic Brain Injury Due To Recent Earthquake in Manipal Teaching Hospital

Nepal Journal of Neuroscience ◽

10.3126/njn.v12i2.15895 ◽

2016 ◽

Vol 12 (2) ◽

pp. 63-66

Author(s):

Bal G Karmacharya ◽

Brijesh Sathian

Keyword(s):

Traumatic Brain Injury ◽

Brain Injury ◽

Head Injury ◽

Teaching Hospital ◽

Brain Injuries ◽

Injury Severity ◽

Traumatic Brain Injuries ◽

The Body ◽

Mild Head Injury ◽

Associated Injuries

The objective of this study was to review the demographics, causes injury, severity, treatment and outcome of traumatic brain injuries in victims of the April 2015 earthquake who were admitted in Manipal Teaching Hospital, Pokhara. A total of 37 patients was admitted under Neurosurgery Services. Collapse of buildings was the commonest cause of head injury. The majority of them had mild head injury. Associated injuries to other parts of the body were present in 40.54% patients.Nepal Journal of Neuroscience 12:63-66, 2015

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MR and CT imaging in the Dyke-Davidoff-Masson syndrome: report of three cases and contribution to pathogenesis and differential diagnosis

Arquivos de Neuro-Psiquiatria ◽

10.1590/s0004-282x1998000500016 ◽

1998 ◽

Vol 56 (4) ◽

pp. 803-807 ◽

Cited By ~ 21

Author(s):

PAULO HENRIQUE AGUIAR ◽

WEI LIU CHING ◽

HELIO LEITÃO ◽

F. ISSA ◽

GUILHERME LEPSKI ◽

...

Keyword(s):

Differential Diagnosis ◽

Mental Retardation ◽

Brain Injury ◽

Paranasal Sinuses ◽

Facial Asymmetry ◽

Cerebral Injury ◽

Radiological Features ◽

Cerebral Hemiatrophy ◽

The Brain ◽

Syndrome Report

Cerebral hemiatrophy or Dyke-Davidoff-Masson syndrome is a condition characterized by seizures, facial asymmetry, contralateral hemiplegia or hemiparesis, and mental retardation. These findings are due to cerebral injury that may occur early in life or in utero. The radiological features are unilateral loss of cerebral volume and associated compensatory bone alterations in the calvarium, like thickening, hyperpneumatization of the paranasal sinuses and mastoid cells and elevation of the petrous ridge. The authors describe three cases. Classical findings of the syndrome are present in variable degrees according to the extent of the brain injury. Pathogenesis is commented.

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A Model of Metabolic Supply-Demand Mismatch Leading to Secondary Brain Injury

Journal of Neurophysiology ◽

10.1152/jn.00674.2020 ◽

2021 ◽

Author(s):

Jiangling Song ◽

Jennifer A. Kim ◽

Aaron Frank Struck ◽

Rui Zhang ◽

M. Brandon Westover

Keyword(s):

Brain Injury ◽

Mechanistic Model ◽

Acute Brain Injury ◽

Extracellular Potassium ◽

Secondary Brain Injury ◽

Proposed Model ◽

The Common ◽

High Level ◽

The Brain ◽

Common Association

Secondary brain injury (SBI) is defined as new or worsening injury to the brain after an initial neurologic insult, such as hemorrhage, trauma, ischemic stroke, or infection. It is a common and potentially preventable complication following many types of primary brain injury (PBI). However, mechanistic details about how PBI leads to additional brain injury and evolves into SBI are poorly characterized. In this work, we propose a mechanistic model for the metabolic supply demand mismatch hypothesis (MSDMH) of SBI. Our model, based on the Hodgkin-Huxley model, supplemented with additional dynamics for extracellular potassium, oxygen concentration and excitotoxity, provides a high-level unified explanation for why patients with acute brain injury frequently develop SBI. We investigate how decreased oxygen, increased extracellular potassium, excitotoxicity, and seizures can induce SBI, and suggest three underlying paths for how events following PBI may lead to SBI. The proposed model also helps explain several important empirical observations, including the common association of acute brain injury with seizures, the association of seizures with tissue hypoxia and so on. In contrast to current practices which assume that ischemia plays the predominant role in SBI, our model suggests that metabolic crisis involved in SBI can also be non-ischemic. Our findings offer a more comprehensive understanding of the complex interrelationship among potassium, oxygen, excitotoxicity, seizures and SBI.

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Lack of mitochondrial ferritin aggravated neurological deficits via enhancing oxidative stress in a traumatic brain injury murine model

Bioscience Reports ◽

10.1042/bsr20170942 ◽

2017 ◽

Vol 37 (6) ◽

Cited By ~ 9

Author(s):

Ligang Wang ◽

Libo Wang ◽

Zhibo Dai ◽

Pei Wu ◽

Huaizhang Shi ◽

...

Keyword(s):

Oxidative Stress ◽

Traumatic Brain Injury ◽

Brain Injury ◽

Knockout Mice ◽

Brain Injuries ◽

Brain Infarction ◽

Neurological Deficits ◽

Important Correlation ◽

The Brain ◽

And Oxidative Stress

Oxidative stress has been strongly implicated in the pathogenesis of traumatic brain injury (TBI). Mitochondrial ferritin (Ftmt) is reported to be closely related to oxidative stress. However, whether Ftmt is involved in TBI-induced oxidative stress and neurological deficits remains unknown. In the present study, the controlled cortical impact model was established in wild-type and Ftmt knockout mice as a TBI model. The Ftmt expression, oxidative stress, neurological deficits, and brain injury were measured. We found that Ftmt expression was gradually decreased from 3 to 14 days post-TBI, while oxidative stress was gradually increased, as evidenced by reduced GSH and superoxide dismutase levels and elevated malondialdehyde and nitric oxide levels. Interestingly, the extent of reduced Ftmt expression in the brain was linearly correlated with oxidative stress. Knockout of Ftmt significantly exacerbated TBI-induced oxidative stress, intracerebral hemorrhage, brain infarction, edema, neurological severity score, memory impairment, and neurological deficits. However, all these effects in Ftmt knockout mice were markedly mitigated by pharmacological inhibition of oxidative stress using an antioxidant, N-acetylcysteine. Taken together, these results reveal an important correlation between Ftmt and oxidative stress after TBI. Ftmt deficiency aggravates TBI-induced brain injuries and neurological deficits, which at least partially through increasing oxidative stress levels. Our data suggest that Ftmt may be a promising molecular target for the treatment of TBI.

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Analysis of the brain bioavailability of peripherally administered magnesium sulfate: A study in humans with acute brain injury undergoing prolonged induced hypermagnesemia*

Critical Care Medicine ◽

10.1097/01.ccm.0000156293.35868.b2 ◽

2005 ◽

Vol 33 (3) ◽

pp. 661-666 ◽

Cited By ~ 59

Author(s):

J Andrew McKee ◽

Randall P. Brewer ◽

Gary E. Macy ◽

Barbara Phillips-Bute ◽

Kurt A. Campbell ◽

...

Keyword(s):

Brain Injury ◽

Magnesium Sulfate ◽

Acute Brain Injury ◽

The Brain

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Traumatic Injury to the Developing Brain: Emerging Relationship to Early Life Stress

Frontiers in Neurology ◽

10.3389/fneur.2021.708800 ◽

2021 ◽

Vol 12 ◽

Author(s):

Kaila N. Parker ◽

Michael H. Donovan ◽

Kylee Smith ◽

Linda J. Noble-Haeusslein

Keyword(s):

Brain Injury ◽

Life Stress ◽

Early Life ◽

Brain Injuries ◽

Traumatic Injury ◽

Early Life Stress ◽

Early Age ◽

Functional Impairments ◽

The Brain

Despite the high incidence of brain injuries in children, we have yet to fully understand the unique vulnerability of a young brain to an injury and key determinants of long-term recovery. Here we consider how early life stress may influence recovery after an early age brain injury. Studies of early life stress alone reveal persistent structural and functional impairments at adulthood. We consider the interacting pathologies imposed by early life stress and subsequent brain injuries during early brain development as well as at adulthood. This review outlines how early life stress primes the immune cells of the brain and periphery to elicit a heightened response to injury. While the focus of this review is on early age traumatic brain injuries, there is also a consideration of preclinical models of neonatal hypoxia and stroke, as each further speaks to the vulnerability of the brain and reinforces those characteristics that are common across each of these injuries. Lastly, we identify a common mechanistic trend; namely, early life stress worsens outcomes independent of its temporal proximity to a brain injury.

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Circulating Tight-Junction Proteins Are Potential Biomarkers for Blood-Brain Barrier Function in a Model of Neonatal Hypoxic/Ischemic Brain Injury

10.21203/rs.3.rs-90299/v1 ◽

2020 ◽

Author(s):

Axel Erik Andersson ◽

Carina Mallard ◽

Carl Joakim Ek

Keyword(s):

Brain Injury ◽

Blood Brain Barrier ◽

Brain Injuries ◽

Brain Barrier ◽

Neonatal Brain ◽

Ischemic Brain ◽

Blood Brain ◽

Hypoxia Ischemia ◽

The Brain ◽

Junction Proteins

Abstract BackgroundNeonatal hypoxia-ischemia often leads to lifelong disabilities with limited treatments currently available. The brain vasculature is an important factor in many neonatal brain pathologies but there is a lack of diagnostic tools to evaluate the brain vascular health of neonates in a clinical setting. Measurement of blood-brain barrier tight-junction proteins have shown promise as biomarkers for brain injury in the adult. Here we tested the biomarker potential of tight-junctions in the context of neonatal brain injury.MethodsThe levels of TJ-proteins (occluding, claudin-5, and zonula occludens-1) in both blood plasma and cerebrospinal fluid (CSF) as well as blood-brain barrier function were measured in a clinically relevant hypoxia/ischemia model in neonatal rats.ResultsTemporally acute elevated levels of occludin and claudin-5 could be measured in blood and CSF after hypoxia/ischemia with males generally having higher levels than females. The levels of claudin-5 in CSF correlated with the severity of the brain injury at 24h post- hypoxia/ischemia. Simultaneously, we detected early increase in blood-brain barrier-permeability at 6 and 24h after hypoxia/ischemia.ConclusionsLevels of circulating claudin-5 and occludin are increased after hypoxic/ischemic brain injuries and blood-brain barrier-impairment and have promise as early biomarkers for cerebral vascular health and as a tool for risk assessment of neonatal brain injuries.

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P015: Efficacy of the Brain Injury Guidelines for complicated mild traumatic brain injuries

CJEM ◽

10.1017/cem.2020.223 ◽

2020 ◽

Vol 22 (S1) ◽

pp. S69-S70

Author(s):

J. Tourigny ◽

C. Malo ◽

V. Boucher ◽

P. Blanchard ◽

J. Chauny ◽

...

Keyword(s):

Brain Injury ◽

Brain Injuries ◽

Penetrating Trauma ◽

Historical Cohort ◽

Radiological Data ◽

Level 1 ◽

Head Computed Tomography ◽

The Brain ◽

Significant Health ◽

Neurosurgical Intervention

Introduction: The Brain Injury Guidelines (BIG) stratifies complicated mild traumatic brain injury (mTBI) patients into 3 groups to guide hospitalization, neurosurgical consultation and repeat head-CT. BIG-1 patients could be managed safely without neurosurgical consultation or transfer. Systematic transfer to neurotrauma centers provide few benefits to this subgroup leading to overtriage. Similarly, unnecessary clinical and radiological follow-ups utilize significant health-care resources. Objective: to validate the safety and efficacy of the BIG for complicated mTBIs. Methods: We performed a multicenter historical cohort study in 3 level-1 trauma centers in Quebec. Patients ≥16 years old assessed in the Emergency Department (ED) with complicated mTBI between 2014 and 2017 were included. Patients with penetrating trauma, cerebral aneurysm or tumor were excluded. Clinical, demographic and radiological data, BIG variables, TBI-related death and neurosurgical intervention were collected using a standardized form. A second reviewer assessed all ambiguous files. Descriptive statistics, over- and under-triage were calculated. Results: A total of 342 patients’ records were assessed. Mean age was 63 ± 20,7 and 236 (69 %) were male. Thirty-five patients were classified under BIG-1 (10.2%), 110 under BIG-2 (32.2%) and 197 under BIG-3 (57.6%). Twenty-six patients (7%) required neurosurgical intervention, all were BIG-3. 90% of TBI-related deaths occurred in BIG-3 and none were classified BIG-1. Among the 192 transfers (51%), 14 were classified under BIG-1 (7.3%) and should not have been transferred according to the guidelines and 50 under BIG-2 (26%). In addition, 40% of BIG-1 received a repeat head computed tomography, although not indicated. Similarly, 7 % of all patients had a neurosurgical consult even if not required. Projected implementation of BIG would lead to 47% of overtriage and 0.3% of undertriage. Conclusion: Our results suggest that the Brain Injury Guidelines could safely identify patients with negative outcomes and could lead to a safe and effective management of complicated mTBI. Applying these guidelines to our cohort could have resulted in significantly fewer repeat head CTs, neurosurgical consults and transfers to level 1 neurotrauma centers.

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Young plasma ameliorates aging-related acute brain injury after intracerebral hemorrhage

Bioscience Reports ◽

10.1042/bsr20190537 ◽

2019 ◽

Vol 39 (5) ◽

Cited By ~ 4

Author(s):

Jun-Jie Yuan ◽

Qin Zhang ◽

Chang-Xiong Gong ◽

Fa-Xiang Wang ◽

Jia-Cheng Huang ◽

...

Keyword(s):

Brain Injury ◽

Intracerebral Hemorrhage ◽

Brain Damage ◽

Mrna Level ◽

Acute Brain Injury ◽

Aging Brain ◽

Neural Cells ◽

Neuroprotective Effects ◽

The Brain ◽

Brain Tissues

Abstract Aging has been shown to contribute to both the declined biofunctions of aging brain and aggravation of acute brain damage, and the former could be reversed by young plasma. These results suggest that young plasma treatment may also reduce the acute brain damage induced by intracerebral hemorrhage (ICH). In the present study, we first found that the administration of young plasma significantly reduced the mortality and neurological deficit score in aging ICH rodents, which might be due to the decreased brain water content, damaged neural cells, and increased survival neurons around the perihematomal brain tissues. Then, proteomics analysis was used to screen out the potential neuroprotective circulating factors and the results showed that many factors were changed in health human plasma among young, adult, and old population. Among these significantly changed factors, the plasma insulin-like growth factor 1 (IGF-1) level was significantly decreased with age, which was further confirmed both in human and rats detected by ELISA. Additionally, the brain IGF-1 protein level in aging ICH rats was markedly decreased when compared with young rats. Interestingly, the relative decreased brain IGF-1 level was reversed by the treatment of young plasma in aging ICH rats, while the mRNA level was non-significantly changed. Furthermore, the IGF-1 administration significantly ameliorated the acute brain injury in aging ICH rats. These results indicated that young circulating factors, like IGF-1, may enter brain tissues to exert neuroprotective effects, and young plasma may be considered as a novel therapeutic approach for the clinical treatment of aging-related acute brain injury.

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Predicting Family Adaptation from Brain Injury-Related Family Stress

Journal of Applied Rehabilitation Counseling ◽

10.1891/0047-2220.29.1.8 ◽

1998 ◽

Vol 29 (1) ◽

pp. 8-12 ◽

Cited By ~ 7

Author(s):

John F. Kosciulek ◽

Daniel C. Lustig

Keyword(s):

Brain Injury ◽

Brain Injuries ◽

Family Stress ◽

Primary Caregivers ◽

Family Intervention ◽

Stepwise Multiple Regression ◽

Family Adaptation ◽

Related Family ◽

The Relationship ◽

The Brain

The purpose of this study was to investigate the relationship between brain injury-related family stress and family adaptation. Participants were 92 primary caregivers of persons with brain injuries recruited through the Head Injury Foundation of Alabama. Stepwise multiple regression of variables measuring family stress on family adaptation indicated that the affective and behavioral functioning of the member with the brain injury was predictive of family adaptation. The hypothesis that family adaptation can be predicted from variables measuring brain injury-related family stress was thus supported. Family intervention and rehabilitation practice implications are discussed.

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