Articles: traumatic-brain-injuries.
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Journal of neurotrauma · Sep 2022
Multimodal Biomarkers of Repetitive Head Impacts and Traumatic Encephalopathy Syndrome: A Clinico-Pathological Case Series.
Traumatic encephalopathy syndrome (TES) criteria were developed to aid diagnosis of chronic traumatic encephalopathy (CTE) pathology during life. Interpreting clinical and biomarker findings in patients with TES during life necessitates autopsy-based determination of the neuropathological profile. We report a clinicopathological series of nine patients with previous repetitive head impacts (RHI) classified retrospectively using the recent TES research framework (100% male and white/Caucasian, age at death 49-84) who completed antemortem neuropsychological evaluations, T1-weighted magnetic resonance imaging, diffusion tensor imaging (n = 6), (18)F-fluorodeoxyglucose-positron emission tomography (n = 5), and plasma measurement of neurofilament light (NfL), glial fibrillary acidic protein (GFAP), and total tau (n = 8). ⋯ Memory and executive function decline, limbic system brain changes (atrophy, decreased white matter integrity, hypometabolism), and plasma biomarker alterations are common in RHI and TES but may reflect multiple neuropathologies. In particular, the neuropathological differential for patients with RHI or TES presenting with medial temporal atrophy and memory loss should include limbic TDP-43. Researchers and clinicians should be cautious in attributing cognitive, neuroimaging, or other biomarker changes solely to CTE tau pathology based on previous RHI or a TES diagnosis alone.
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Observational Study
Health care implications of the COVID-19 pandemic for patients with severe traumatic brain injury - A nationwide, observational cohort study.
Containment measures during the coronavirus disease of 2019 (COVID-19) pandemic have resulted in a substantial reduction in treatment of injury. The effect of the COVID-19 pandemic on the epidemiology and mortality of severe traumatic brain injury on a national, population-based level is unknown. ⋯ The containment and lockdown measures during the COVID-19 pandemic in Norway did not affect the number of patients or mortality of patients with severe traumatic brain injury.
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Journal of neurotrauma · Sep 2022
Fluvoxamine confers neuroprotection via inhibiting infiltration of peripheral leukocytes and M1 polarization of microglia/macrophages in a mouse model of traumatic brain injury.
Neuroinflammation is an important mediator of secondary injury pathogenesis that exerts dual beneficial and detrimental effects on pathophysiology of the central nervous system (CNS) after traumatic brain injury (TBI). Fluvoxamine is a serotonin selective reuptake inhibitor (SSRI) and has been reported to have the anti-inflammatory properties. However, the mechanisms and therapeutic effects of fluvoxamine in neuroinflammation after TBI have not be defined. ⋯ Fluvoxamine treatment promoted microglial/macrophage phenotypic transformation from pro-inflammatory M1-phenotype to anti-inflammatory M2-phenotype in in vivo and in vitro experiments. In addition, fluvoxamine treatment attenuated neuronal apoptosis, blood-brain barrier (BBB) disruption, cerebrovascular damage, and post-traumatic edema formation, thereby improving neurological function of mice subjected to TBI. These findings support the clinical evaluation of fluvoxamine as a neuroprotective therapy for TBI.