Journal of neurotrauma
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Journal of neurotrauma · Jul 2023
Lifetime Traumatic Brain Injury and Cognitive Domain Deficits in Late Life: The PROTECT-TBI Cohort Study.
Traumatic brain injury (TBI) causes cognitive impairment but it remains contested regarding which cognitive domains are most affected. Further, moderate-severe TBI is known to be deleterious, but studies of mild TBI (mTBI) show a greater mix of negative and positive findings. This study examines the longer-term cognitive effects of TBI severity and number of mTBIs in later life. ⋯ The most sensitive cognitive domains are attention and executive function, with approximately double the effect compared with processing speed and working memory. Post-TBI cognitive rehabilitation should be targeted appropriately to domain-specific effects. Significant long-term cognitive deficits were associated with three or more lifetime mTBIs, a critical consideration when counseling individuals post-TBI about continuing high-risk activities.
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Journal of neurotrauma · Jul 2023
Observational StudyWithdrawal of life sustaining therapies in children with severe traumatic brain injury.
Neuroprognostication in severe traumatic brain injury (sTBI) is challenging and occurs in critical care settings to determine withdrawal of life-sustaining therapies (WLST). However, formal pediatric sTBI neuroprognostication guidelines are lacking, brain death criteria vary, and dilemmas regarding WLST persist, which lead to institutional differences. We studied WLST practice and outcome in pediatric sTBI to provide insight into WLST-associated factors and survivor recovery trajectory ≥1 year post-sTBI. ⋯ Median survivor PCPC score improved from 4 to 2 with no vegetative patients 1 year post-sTBI. Our findings show the WLST decision process was multi-disciplinary and guided by specific clinical features at presentation, clinical course, and (serial) neurological diagnostic modalities, of which the testing combination was determined by case-to-case variation. This stresses the need for international guidelines to provide accurate neuroprognostication within an appropriate timeframe whereby overall survivor outcome data provides valuable context and guidance in the acute phase decision process.
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Journal of neurotrauma · Jul 2023
Use of support vector machines approach via ComBat harmonized diffusion tensor imaging for the diagnosis and prognosis of mild traumatic brain injury: a CENTER-TBI study.
The prediction of functional outcome after mild traumatic brain injury (mTBI) is challenging. Conventional magnetic resonance imaging (MRI) does not do a good job of explaining the variance in outcome, as many patients with incomplete recovery will have normal-appearing clinical neuroimaging. More advanced quantitative techniques such as diffusion MRI (dMRI), can detect microstructural changes not otherwise visible, and so may offer a way to improve outcome prediction. ⋯ Similar to the analysis between mTBI patients and controls, the three-category-harmonized ComBat FA and MD maps voxelwise approach yields statistically significant prediction scores between mTBI patients with complete and those with incomplete recovery (71.8% specificity, 66.2% F1-score and 0.71 AUC, p < 0.05), which provided a modest increase in the classification score (accuracy: 66.4%) compared with the classification based on age and sex only and ROI-wise approaches (accuracy: 61.4% and 64.7%, respectively). This study showed that ComBat harmonized FA and MD may provide additional information for diagnosis and prognosis of mTBI in a multi-modal machine learning approach. These findings demonstrate that dMRI may assist in the early detection of patients at risk of incomplete recovery from mTBI.
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Journal of neurotrauma · Jul 2023
History of traumatic brain injury in relation to cognitive functioning, memory complaints and brain structure in mid-life.
In this study, we investigated history of traumatic brain injury with loss of consciousness in relation to cognitive functioning, subjective memory complaints, and brain structure in mid-life. This study included 2005 participants (mean age: 47.6 years, standard deviation: 5.0, women: 65%) from the Origins of Alzheimer's Disease Across the Life Course (ORACLE) study between 2017 and 2020. History of traumatic brain injury was defined as at least one lifetime self-reported brain injury with loss of consciousness. ⋯ Additionally, the association was stronger in those with >30 min loss of consciousness (OR: 3.57; 95% CI: 1.48, 8.59) than in those with <30 min loss of consciousness (OR: 1.85; 95% CI: 1.25, 2.74), when compared with those without history of traumatic brain injury. Lastly, we found no associations between history of traumatic brain injury and any of the structural brain MRI outcomes. In conclusion, our study suggests that at least one lifetime traumatic brain injury with loss of consciousness in mid-life is associated with long-term subjective memory complaints, but not with cognitive functioning or brain structure.
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Journal of neurotrauma · Jul 2023
ADAM17 aggravates the inflammatory response by modulating microglia polarization through the TGF-β1/Smad pathway following experimental traumatic brain injury.
Microglia-mediated neuroinflammatory responses play important roles in secondary neurological injury after traumatic brain injury (TBI). The TGF-β pathway participates in the regulation of M1/M2 phenotype transformation of microglia. TGF-β can activate the Smad pathway by binding to TGF-βRs, which is regulated by the cleavage function of A disintegrin and metalloproteinase 17 (ADAM17). ⋯ The neuroprotective effect of ADAM17 inhibition was related to a shift from the M1 microglial phenotype to the M2 microglial phenotype, thus reducing TBI-induced neuroinflammation. ADAM17 inhibition increased expression of TGF-βRs on the microglia membrane, promoted formation of TGF-β1/TGF-βRII complexes, and induced intranuclear translocation of Smads, which activated the TGF-β/Smad pathway. In conclusion, our study suggested that ADAM17 inhibition regulated microglia M1/M2 phenotype polarization through the TGF-β1/Smad pathway and influenced the neuroinflammatory response after TBI.