scholarly journals Chronic traumatic encephalopathy (CTE) is absent from a European community-based aging cohort while cortical aging-related tau astrogliopathy (ARTAG) is highly prevalent

2021 ◽  
Vol 48 (s1) ◽  
pp. S5-S5
Author(s):  
SL Forrest ◽  
JJ Kril ◽  
S Wagner ◽  
S Hönigschnabl ◽  
A Reiner ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
European Community ◽  
Chronic Traumatic Encephalopathy ◽  
Case Series ◽  
List Type ◽  
Community Based ◽  
High Prevalence ◽  
History Of ◽  
Cortical Involvement

Chronic traumatic encephalopathy (CTE) and aging-related tau astrogliopathy (ARTAG) are characterised by tau-immunopositive neuronal and/or astrocytic inclusions, with overlapping cortical involvement and astrocytic inclusion morphology. This study determined the prevalence of CTE and cortical ARTAG in a European community-based population (n=310) and explored overlap of both pathological entities. Frontal, parietal and temporal cortices were assessed. No case fulfilling CTE criteria was found. However, isolated astroglial or neuronal tau pathologies were recognized in sulcal depths (<2%). One case without history of traumatic brain injury showed combined tau-immunoreactive features confined to frontal sulci without perivascular accumulation. Another 24 cases had single tau pathologies in cortical sulci. ARTAG was identified in 117 cases (38%), with a similar regional prevalence. Grey matter ARTAG was the most common followed by subpial, white matter and perivascular. The presence of any type of ARTAG was associated with having another type of ARTAG in the same region (P<0.05). In summary, cortical ARTAG in this population is common and contrasts the high prevalence of CTE in individuals with repeated mild traumatic brain injury.LEARNING OBJECTIVESThis presentation will enable the learner to:Classify tau-immunopositive astrocytic inclusions characteristic of ARTAG1.Describe neuropathological components of CTE2.Identify CTE and cortical ARTAG in a case series

scholarly journals The Delayed Neuropathological Consequences of Traumatic Brain Injury in a Community-Based Sample

2021 ◽  
Vol 12 ◽  
Author(s):  
Nadia Postupna ◽  
Shannon E. Rose ◽  
Laura E. Gibbons ◽  
Natalie M. Coleman ◽  
Leanne L. Hellstern ◽  
...  
Keyword(s):  
Gene Expression ◽  
Traumatic Brain Injury ◽  
Free Radical ◽  
Brain Injury ◽  
Rna Sequencing ◽  
Chronic Traumatic Encephalopathy ◽  
Mass Spectrometry Analysis ◽  
Community Based ◽  
Amyloid A ◽  
History Of

The late neuropathological effects of traumatic brain injury have yet to be fully elucidated, particularly with respect to community-based cohorts. To contribute to this critical gap in knowledge, we designed a multimodal neuropathological study, integrating traditional and quantitative approaches to detect pathologic changes in 532 consecutive brain autopsies from participants in the Adult Changes in Thought (ACT) study. Diagnostic evaluation including assessment for chronic traumatic encephalopathy (CTE) and quantitative immunoassay-based methods were deployed to examine levels of pathological (hyperphosphorylated) tau (pTau) and amyloid (A) β in brains from ACT participants with (n = 107) and without (n = 425) history of remote TBI with loss of consciousness (w/LOC). Further neuropathological assessments included immunohistochemistry for α-synuclein and phospho-TDP-43 pathology and astro- (GFAP) and micro- (Iba1) gliosis, mass spectrometry analysis of free radical injury, and gene expression evaluation (RNA sequencing) in a smaller sub-cohort of matched samples (49 cases with TBI and 49 non-exposed matched controls). Out of 532 cases, only 3 (0.6%–none with TBI w/LOC history) showed evidence of the neuropathologic signature of chronic traumatic encephalopathy (CTE). Across the entire cohort, the levels of pTau and Aβ showed expected differences for brain region (higher levels in temporal cortex), neuropathological diagnosis (higher in participants with Alzheimer's disease), and APOE genotype (higher in participants with one or more APOE ε4 allele). However, no differences in PHF-tau or Aβ1−42 were identified by Histelide with respect to the history of TBI w/LOC. In a subset of TBI cases with more carefully matched control samples and more extensive analysis, those with TBI w/LOC history had higher levels of hippocampal pTau but no significant differences in Aβ, α-synuclein, pTDP-43, GFAP, Iba1, or free radical injury. RNA-sequencing also did not reveal significant gene expression associated with any measure of TBI exposure. Combined, these findings suggest long term neuropathological changes associated with TBI w/LOC may be subtle, involve non-traditional pathways of neurotoxicity and neurodegeneration, and/or differ from those in autopsy cohorts specifically selected for neurotrauma exposure.

scholarly journals Prevalence of Traumatic Brain Injury in a Male Adult Prison Population and Its Association with the Offence Type

2017 ◽  
Vol 48 (3-4) ◽  
pp. 164-170 ◽  
Author(s):  
Tracey Mitchell ◽  
Alice Theadom ◽  
Elizabeth du Preez
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Prison Population ◽  
Binary Logistic Regression ◽  
Sentence Length ◽  
Male Adult ◽  
High Prevalence ◽  
History Of ◽  
Prison Populations ◽  
Male Prisoners

Background: The prevalence of traumatic brain injury (TBI) in prison populations has been found to vary considerably. This study aimed to determine the prevalence of TBI in a prison population in New Zealand and to identify whether age, ethnicity, offence type, security classification and sentence length were linked to TBI prevalence. Methods: All offenders admitted to a new Corrections Facility over a 6-month period (May-November 2015) were screened to understand their history of TBI. Data was merged with demographic information, details of the offence type, sentence length and security classification from the prison database. Binary logistic regression was used to identify the contribution of predictors on TBI history. Results: Of the 1,061 eligible male prisoners, 1,054 (99.3%) completed a TBI history screen. Out of the 672 (63.7%) who had sustained at least one TBI in their lifetime, 343 (32.5%) had experienced multiple injuries. One in 5 participants experienced their first TBI injury before the age of 15 years. A regression model was able to correctly classify 66.9% of cases and revealed that belonging to Māori ethnicity or being imprisoned for violent, sexual or burglary offences were independently predictive of TBI (χ2 = 9.86, p = 0.28). Conclusions: The high prevalence of TBI within male prisoners and a high proportion of injuries sustained in childhood suggest the need for routine screening for TBI to identify prisoners at risk of persistent difficulties. Interventions to support those experiencing persistent difficulties post-TBI are needed to optimise functioning and prevent reoffending.

scholarly journals Seizures are a druggable mechanistic link between TBI and subsequent tauopathy

2020 ◽  
Author(s):  
Hadeel Alyenbaawi ◽  
Richard Kanyo ◽  
Laszlo F. Locskai ◽  
Razieh Kamali-Jamil ◽  
Michèle G. DuVal ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Cell Death ◽  
Brain Injury ◽  
Chronic Traumatic Encephalopathy ◽  
Brain Activity ◽  
Brain Regions ◽  
List Type ◽  
Larval Zebrafish ◽  
Post Traumatic

SummaryTraumatic brain injury (TBI) is a prominent risk factor for neurodegenerative diseases and dementias including chronic traumatic encephalopathy (CTE). TBI and CTE, like all tauopathies, are characterized by accumulation of Tau into aggregates that progressively spread to other brain regions in a prion-like manner. The mechanisms that promote spreading and cellular uptake of tau seeds after TBI are not fully understood, in part due to lack of tractable animal models. Here, we test the putative roles for excess neuronal activity and dynamin-dependent endocytosis in promoting the in vivo spread of tauopathy. We introduce ‘tauopathy reporter’ zebrafish expressing a genetically-encoded fluorescent Tau biosensor that reliably reports accumulation of human tau species when seeded via intra-ventricular brain injections. Subjecting zebrafish larvae to a novel TBI paradigm produced various TBI symptoms including cell death, hemorrhage, blood flow abnormalities, post–traumatic seizures, and Tau inclusions. Bath application of anticonvulsant drugs rescued TBI-induced tauopathy and cell death; these benefits were attributable to inhibition of post-traumatic seizures because co-application of convulsants reversed these beneficial effects. However, one convulsant drug, 4-Aminopyridine, unexpectedly abrogated TBI-induced tauopathy - this was due to its inhibitory action on endocytosis as confirmed via additional dynamin inhibitors. These data suggest a role for seizure activity and dynamin-dependent endocytosis in the prion-like seeding and spreading of tauopathy following TBI. Further work is warranted regarding anti-convulsants that dampen post-traumatic seizures as a route to moderating subsequent tauopathy. Moreover, the data highlight the utility of deploying in vivo Tau biosensor and TBI methods in larval zebrafish, especially regarding drug screening and intervention.Graphical AbstractHighlightsIntroduces first Traumatic Brain Injury (TBI) model in larval zebrafish, and its easyTBI induces clinically relevant cell death, haemorrhage & post-traumatic seizuresCa2+ imaging during TBI reveals spike in brain activity concomitant with seizuresTau-GFP Biosensor allows repeated in vivo measures of prion-like tau aggregationpost-TBI, anticonvulsants stop tauopathies akin to Chronic Traumatic Encephalopathy

Acquired brain injury and violent offending: prevalence and risk factors

2011 ◽  
Vol 26 (S2) ◽  
pp. 775-775 ◽  
Author(s):  
R. Faruqui
Keyword(s):  
Risk Factors ◽  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Head Injury ◽  
Mental Disorder ◽  
Acquired Brain Injury ◽  
List Type ◽  
Violent Offending ◽  
History Of ◽  
Associated Risk Factors

IntroductionAcquired brain injury has been reported to be associated with violence.ObjectivesTo determine whether an association exists between acquired brain injury and violent offendingAimsStudy an association between brain injury and crime and identify associated risk factors.MethodsSystematic search of Medline, Embase, PsychInfo, CINAHL, TRIP, using terms, Acquired brain injury, traumatic brain injury (TBI), head injury, frontal lobe, crime, offending, violent offending, sexual offending, prison.ResultsA:Multiple studies reported higher life time history of head injury in prison or offender populations in comparison to control groups. Sampling bias and case definition problems have influenced reported prevalence of head injury in offender population ranging from 3.3% to 82%. Reports from secure psychiatric services identify that patients with history of head injury may be more difficult to discharge. Community based studies report cognitive damage as significant risk factor for domestic violence.B:Large scale population and military cohorts have reported a higher relative risk for criminal conviction in mild traumatic brain injury (TBI) group. TBI increases the risk of mental disorder by two-folds but also that TBI is significantly related to mental disorder with co-existing criminality.C:Childhood conduct problems, loss of a parent, substance misuse, maternal drug use in pregnancy, impaired executive cognitive functioning, structural damage to orbito-frontal and ventromedial areas, amygdala, and hippocampus are reported as risk factors for violent offending in this population group.ConclusionsThe review provides evidence for an association between brain injury and violent offending and also identifies associated risk factors.

scholarly journals The Natural History of Acute Recovery of Blast-Induced Mild Traumatic Brain Injury: A Case Series During War

2016 ◽  
Vol 181 (5S) ◽  
pp. 23-27 ◽  
Author(s):  
David T. Larres ◽  
Walter Carr ◽  
Elizandro G. Gonzales ◽  
Jason S. Hawley
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Natural History ◽  
Mild Traumatic Brain Injury ◽  
Case Series ◽  
History Of

scholarly journals Prevalence of anemia in pediatric patients of traumatic brain injury and problems associated with management in a developing country: Unfolding of an underrated comorbidity

2021 ◽  
Vol 12 ◽  
pp. 75
Author(s):  
Mohammad Ashraf ◽  
Usman Ahmad Kamboh ◽  
Mohammad Zubair ◽  
Kashif Ali Sultan ◽  
Muhammad Asif Raza ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Common Knowledge ◽  
Demographic Data ◽  
Hospital Setting ◽  
Case Series ◽  
Tertiary Hospital ◽  
High Prevalence ◽  
Prevalence Of Anemia

Background: Pediatric anemia has a high prevalence in developing countries such as Pakistan. It is common knowledge among hospital specialties but little is done to manage this condition by hospitalists. The issue is compounded with a poor primary care infrastructure nationally. The aim of this study is to bring to light the high prevalence of anemic children in neurosurgery and to describe the difficulties in managing their anemia in a tertiary hospital setting. A literature review is presented highlighting the socioeconomic difficulties that contribute to this widespread comorbidity and the difficulty in managing it from a hospital specialty point of view. Methods: A prospective descriptive case series was carried out between March 2020 and September 2020. All patients under the age of 13 who presented to our department for traumatic brain injury (TBI) meeting our inclusion and exclusion criteria were enrolled and assessed for the presence and severity of anemia. Demographic data were collected. Following discharge, patients were referred to our hospital’s pediatrics’ anemia clinic which was before their first neurosurgery follow-up 2 weeks following discharge and attendance to follow up was documented. Results: The prevalence of anemia was 78.9%. Over 95% of patients attended their neurosurgery follow-up but only 28% of patients attended their referral to the anemia clinic. Conclusion: Anemia is highly prevalent in children presenting to neurosurgery for TBI and its longitudinal management has difficulties with lost to follow up in a tertiary hospital setting. There is a need for national initiatives to reduce the prevalence of anemia but concurrently better strategies need to be devised to manage anemic children in a hospital setting.

scholarly journals Dual Vulnerability of TDP-43 to Calpain and Caspase-3 Proteolysis after Neurotoxic Conditions and Traumatic Brain Injury

2014 ◽  
Vol 34 (9) ◽  
pp. 1444-1452 ◽  
Author(s):  
Zhihui Yang ◽  
Fan Lin ◽  
Claudia S Robertson ◽  
Kevin KW Wang
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Caspase 3 ◽  
Chronic Traumatic Encephalopathy ◽  
Prior History ◽  
Mouse Cortex ◽  
History Of ◽  
Fragmentation Patterns ◽  
Wave Induced

Transactivation response DNA-binding protein 43 (TDP-43) proteinopathy has recently been reported in chronic traumatic encephalopathy, a neurodegenerative condition linked to prior history of traumatic brain injury (TBI). While TDP-43 appears to be vulnerable to proteolytic modifications under neurodegenerative conditions, the mechanism underlying the contribution of TDP-43 to the pathogenesis of TBI remains unknown. In this study, we first mapped out the calpain or caspase-3 TDP-43 fragmentation patterns by in vitro protease digestion. Concurrently, in cultured cerebrocortical neurons subjected to cell death challenges, we identified distinct TDP-43 breakdown products (BDPs) of 35, 33, and 12kDa that were indicative of dual calpain/caspase attack. Cerebrocortical culture incubated with calpain and caspase-fragmented TDP-43 resulted in neuronal injury. Furthermore, increased TDP-43 BDPs as well as redistributed TDP-43 from the nucleus to the cytoplasm were observed in the mouse cortex in two TBI models: controlled cortical impact injury and overpressure blast-wave-induced brain injury. Finally, TDP-43 and its 35 kDa fragment levels were also elevated in the cerebrospinal fluid (CSF) of severe TBI patients. This is the first evidence that TDP-43 might be involved in acute neuroinjury and TBI pathology, and that TDP-43 and its fragments may have biomarker utilities in TBI patients.

scholarly journals Apolipoprotein E Epsilon 4 Genotype, Mild Traumatic Brain Injury, and the Development of Chronic Traumatic Encephalopathy

2018 ◽  
Vol 6 (3) ◽  
pp. 78 ◽  
Author(s):  
Hansen Deng ◽  
Angel Ordaz ◽  
Pavan Upadhyayula ◽  
Eva Gillis-Buck ◽  
Catherine Suen ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Mild Traumatic Brain Injury ◽  
Chronic Traumatic Encephalopathy ◽  
Clinical Manifestations ◽  
Case Series ◽  
Population Based ◽  
Postmortem Diagnosis ◽  
Apoe Ε4 ◽  
The Usa

The annual incidence of mild traumatic brain injury (MTBI) is 3.8 million in the USA with 10–15% experiencing persistent morbidity beyond one year. Chronic traumatic encephalopathy (CTE), a neurodegenerative disease characterized by accumulation of hyperphosphorylated tau, can occur with repetitive MTBI. Risk factors for CTE are challenging to identify because injury mechanisms of MTBI are heterogeneous, clinical manifestations and management vary, and CTE is a postmortem diagnosis, making prospective studies difficult. There is growing interest in the genetic influence on head trauma and development of CTE. Apolipoprotein epsilon 4 (APOE-ε4) associates with many neurologic diseases, and consensus on the ε4 allele as a risk factor is lacking. This review investigates the influence of APOE-ε4 on MTBI and CTE. A comprehensive PubMed literature search (1966 to 12 June 2018) identified 24 unique reports on the topic (19 MTBI studies: 8 athletic, 5 military, 6 population-based; 5 CTE studies: 4 athletic and military, 1 leucotomy group). APOE-ε4 genotype is found to associate with outcomes in 4/8 athletic reports, 3/5 military reports, and 5/6 population-based reports following MTBI. Evidence on the association between APOE-ε4 and CTE from case series is equivocal. Refining modalities to aid CTE diagnosis in larger samples is needed in MTBI.

scholarly journals The Immune System's Role in the Consequences of Mild Traumatic Brain Injury (Concussion)

2021 ◽  
Vol 12 ◽  
Author(s):  
Laura N. Verboon ◽  
Hiren C. Patel ◽  
Andrew D. Greenhalgh
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Mild Traumatic Brain Injury ◽  
Immune Cell ◽  
Chronic Traumatic Encephalopathy ◽  
Anxiety And Depression ◽  
Mild Tbi ◽  
Patient Health ◽  
History Of ◽  
The Impact

Mild traumatic brain injury (mild TBI), often referred to as concussion, is the most common form of TBI and affects millions of people each year. A history of mild TBI increases the risk of developing emotional and neurocognitive disorders later in life that can impact on day to day living. These include anxiety and depression, as well as neurodegenerative conditions such as chronic traumatic encephalopathy (CTE) and Alzheimer's disease (AD). Actions of brain resident or peripherally recruited immune cells are proposed to be key regulators across these diseases and mood disorders. Here, we will assess the impact of mild TBI on brain and patient health, and evaluate the recent evidence for immune cell involvement in its pathogenesis.

Organic Eating Disorders of Morbid Hunger & Hyperphagia After Traumatic Brain Injury (TBI): Presentation and Prevalence

2009 ◽  
Vol 24 (S1) ◽  
pp. 1-1 ◽  
Author(s):  
R. Faruqui ◽  
A. Rowell
Keyword(s):  
Traumatic Brain Injury ◽  
Eating Disorders ◽  
Brain Injury ◽  
Head Injury ◽  
Case Reports ◽  
Tertiary Care ◽  
Case Series ◽  
List Type ◽  
Type Number ◽  
Life Threatening

Background:Morbid Hunger or persistent Hyperphagia are rare conditions after TBI and can pose life threatening health risks to the patient, risks of aggression towards professional and family carers managing this behaviour, and the ability to function in social settings.Method:1.Systematic search of Medline, Embase, PsychInfo, CINAHL, DARE, Cochrane Database of Systematic Reviews, and Cochrane Clinical Trials Register, using terms Eating Disorders, Organic Eating Disorders, Binge Eating, Anorexia Nervosa, Hyperphagia, Morbid Hunger, Satiety, Hypothalamus, Pituitary Glands, Traumatic Brain Injury, and Acquired Brain Injury.2.Diagnostic review of currently admitted hospital patients at a tertiary care brain injury rehabilitation centre in order to establish point prevalence.3.Review of Dietetic records to establish clinical presentation and management principles.Results:Systematic review identified case reports and case series of these disorders, providing description of three distinct traumatic presentations:a. Persistent Hyperphagia after head injury.b. Serious food seeking behaviour and overeating after surgery for neoplasm resulting in pituitary/ hypothalamic injury.c. Head Injury variant of Kleine Levine Syndrome presenting with Hyperphagia, Hypersomnolence, and Hypersexuality.Diagnostic review of 88 admitted patients identified 2 (3%) patients presenting with this condition.Review of dietetic records confirmed the persistent and serious nature of this presentation and identified a high need for environmental and cue exposure control in management of this condition.Conclusions:Organic eating disorders are rare but potentially life threatening conditions, requiring formal cataloguing and recognition in diagnostic classifications to facilitate systematic study of pathophysiology and relevant management strategies.

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