Chronic traumatic encephalopathy (CTE) is a neuropathologically defined disease reportedly linked to a history of repetitive brain trauma. As such, retired collision sport athletes are likely at heightened risk for developing CTE. Researchers have described distinct pathological features of CTE as well a wide range of clinical symptom presentations, recently termed traumatic encephalopathy syndrome (TES). These clinical symptoms are highly variable, non-specific to individuals described as having CTE pathology in case reports, and are often associated with many other factors. This review describes the cognitive, emotional, and behavioral changes associated with 1) developmental and demographic factors, 2) neurodevelopmental disorders, 3) normal aging, 4) adjusting to retirement, 5) drug and alcohol abuse, 6) surgeries and anesthesia, and 7) sleep difficulties, as well as the relationship between these factors and risk for developing dementia-related neurodegenerative disease. We discuss why some professional athletes may be particularly susceptible to many of these effects and the importance of choosing appropriate controls groups when designing research protocols. We conclude that these factors should be considered as modifiers predominantly of the clinical outcomes associated with repetitive brain trauma within a broader biopsychosocial framework when interpreting and attributing symptom development, though also note potential effects on neuropathological outcomes. Importantly, this could have significant treatment implications for improving quality of life.
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http://dx.doi.org/10.1007/s11065-016-9327-z | DOI Listing |
Intensive Care Med
January 2025
Global Health Research Group in Acquired Brain and Spine Injuries, Cambridge, UK.
Background: Invasive systems are commonly used for monitoring intracranial pressure (ICP) in traumatic brain injury (TBI) and are considered the gold standard. The availability of invasive ICP monitoring is heterogeneous, and in low- and middle-income settings, these systems are not routinely employed due to high cost or limited accessibility. The aim of this consensus was to develop recommendations to guide monitoring and ICP-driven therapies in TBI using non-invasive ICP (nICP) systems.
View Article and Find Full Text PDFEmerg Med Australas
February 2025
National Trauma Research Institute, Alfred Health, Melbourne, Victoria, Australia.
Objectives: To establish the determinants of death in hospital for patients with moderate to severe traumatic brain injury (TBI) in Australia.
Design, Setting, Participants: Retrospective analysis of Australia New Zealand Trauma Registry (ANZTR) data. Cases were included if they presented to a participating hospital between 1 July 2015 and 30 June 2020 and had an Abbreviated Injury Severity (AIS) score - head greater than 2.
Eur J Neurosci
January 2025
Department of Anesthesiology & Critical Care, Medical Center-University of Freiburg, Freiburg, Germany.
Traumatic brain injury is one of the most common cerebral incidences worldwide. Repetitive mild traumatic brain injuries occurring, for example, in athletes or victims of abuse, can cause chronic neurodegeneration due to neuroinflammation, in which the crosstalk between reactive astrocytes and activated microglia is crucial for modulating neuronal damage. The inducible enzyme heme oxygenase-1 and its product carbon monoxide are known to be ascribed neuroprotective and anti-inflammatory properties.
View Article and Find Full Text PDFMicrographia, characterised by small handwriting, is often linked to Parkinson's disease, but also resulted to injured brain lesions. The left-handed women in her 20s developed 'fast micrographia' after a traumatic brain injury from a traffic accident, showing bilateral subdural haematomas and frontal lobe contusions, but she had no paralysis and extrapyramidal symptoms. Neuropsychological tests showed reduced processing speed and memory deficits, aligning with frontal lobe damage.
View Article and Find Full Text PDFJ Neurotrauma
January 2025
Morehouse School of Medicine, Atlanta, Georgia, USA.
Traumatic brain injury (TBI) has long been a leading cause of death and disability, yet research has failed to successfully translate findings from the pre-clinical, animal setting into the clinic. One factor that contributes significantly to this struggle is the heterogeneity observed in the clinical setting where patients present with injuries of varying types, severities, and comorbidities. Modeling this highly varied population in the laboratory remains challenging.
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