Browsing by Subject "Traumatic brain injury (TBI)"

Now showing 1 - 8 of 8
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    An exploration of clinical dementia phenotypes among individuals with and without traumatic brain injury
    (Sage, 2013) Dams-O’Connor, K.; Spielman, L.; Hammond, F. M.; Sayed, N.; Culver, C.; Diaz-Arrastia, R.; Physical Medicine and Rehabilitation, School of Medicine
    Objective: To characterize the clinical profiles of individuals with dementia who do and do not report a history of TBI. Introduction: Some evidence suggests that a history of traumatic brain injury (TBI) is associated with an increased risk of dementia later in life. The clinical features of dementia associated with TBI have not been well investigated. While there is some evidence that TBI is associated with increased risk of Alzheimer's disease (AD), there are also indications that dementia associated with TBI has prominent behavioral, affective, and motor symptoms, making it distinct from AD. Methods: The current study involves secondary analysis of baseline data from the National Alzheimer's Coordinating Center (NACC) Uniform Data Set (UDS). Results: Individuals with dementia who reported a history of TBI had higher fluency and verbal memory scores and later onset of decline, but they are on more medications, had worse cardiovascular and cerebrovascular health, were more likely to have received medical attention for depression, and were more likely to have a gait disorder, falls, and motor slowness. Conclusion: These findings suggest that dementia among individuals with a history of TBI may represent a unique clinical phenotype that is distinct from known dementia subtypes.
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    Current advances in neurotrauma research: diagnosis, neuroprotection, and neurorepair
    (Wolters Kluwer, 2014) Chen, Jinhui; Shi, Riyi; Neurological Surgery, School of Medicine
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    Rapid neurological recovery with spontaneous resolution of acute subdural hematoma after severe head trauma: A case report of auto-decompression phenomena
    (Elsevier, 2025) Obeng-Gyasi, Barnabas; Chinthala, Anoop S.; Christodoulides, Alexei; Ordaz, Josue; Mao, Gordon; Neurological Surgery, School of Medicine
    Introduction: The spontaneous resolution of acute subdural hematoma (aSDH) represents an ill-defined but clinically significant phenomenon in traumatic brain injury (TBI). While surgical evacuation remains the standard of care for significant aSDH, rare cases of spontaneous resolution, termed auto-decompression in literature, suggest alternative pathways of hematoma clearance that warrant further investigation. Case presentation: We discuss the case of a 40-year-old male with background seizure disorder who fell off a ladder. His Glasgow Coma Score (GCS) at presentation was 5. Brain Computed Tomography (CT) scan revealed bilateral aSDH and multiple skull fractures. Within 24 h, his GCS quickly improved to 9 T. Repeat brain CT done 72 h post-trauma showed resolution of the aSDH following non-operative management. Discussion: Spontaneous resolution of bilateral aSDH with rapid neurological improvement is a rare but possible occurrence, often attributed to auto-decompression phenomenon in patients with severe head trauma and specific predisposing factors. Our discussion revolves around this patients presentation with polytrauma, complex skull fractures, history of craniotomy, and acute coagulopathy contributing to the spontaneous resolution of the hematoma. Given the complex nature of TBI and the unpredictable course of recovery, clinicians must remain vigilant in continuously reassessing neurological status. Conclusion: This case discusses the unpredictable nature of TBI and highlights the rapid and unexpected resolution of aSDH in a patient with complex neurosurgical history, coagulopathy, and polytrauma. The findings showcase the problems of polytraumatized patients and exemplify the importance of individualized care even when initial signs indicate poor prognosis.
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    Regeneration Through in vivo Cell Fate Reprogramming for Neural Repair
    (Frontiers Media, 2020-04-24) Tai, Wenjiao; Xu, Xiao-Ming; Zhang, Chun-Li; Neurological Surgery, School of Medicine
    The adult mammalian central nervous system (CNS) has very limited regenerative capacity upon neural injuries or under degenerative conditions. In recent years, however, significant progress has been made on in vivo cell fate reprogramming for neural regeneration. Resident glial cells can be reprogrammed into neuronal progenitors and mature neurons in the CNS of adult mammals. In this review article, we briefly summarize the current knowledge on innate adult neurogenesis under pathological conditions and then focus on induced neurogenesis through cell fate reprogramming. We discuss how the reprogramming process can be regulated and raise critical issues requiring careful considerations to move the field forward. With emerging evidence, we envision that fate reprogramming-based regenerative medicine will have a great potential for treating neurological conditions such as brain injury, spinal cord injury (SCI), Alzheimer's disease (AD), Parkinson's disease (PD), and retinopathy.
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    Time to Command-Following and Outcomes After Traumatic Brain Injury
    (American Medical Association, 2024-12-02) Snider, Samuel B.; Deng, Hansen; Hammond, Flora M.; Kowalski, Robert G.; Walker, William C.; Zafonte, Ross D.; Okonkwo, David O.; Giacino, Joseph T.; Puccio, Ava M.; Bodien, Yelena G.; Physical Medicine and Rehabilitation, School of Medicine
    This cohort study examines the association of time to command-following with death or dependency at 1 year among individuals with moderate-severe traumatic brain injury (TBI).
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    Traumatic brain injury and Alzheimer’s Disease biomarkers: A systematic review of findings from amyloid and tau positron emission tomography (PET)
    (medRxiv, 2023-12-01) Dybing, Kaitlyn M.; Vetter, Cecelia J.; Dempsey, Desarae A.; Chaudhuri, Soumilee; Saykin, Andrew J.; Risacher, Shannon L.; Radiology and Imaging Sciences, School of Medicine
    Traumatic brain injury (TBI) has been discussed as a risk factor for Alzheimer's disease (AD) due to its association with dementia risk and earlier cognitive symptom onset. However, the mechanisms behind this relationship are unclear. Some studies have suggested TBI may increase pathological protein deposition in an AD-like pattern; others have failed to find such associations. This review covers literature that uses positron emission tomography (PET) of amyloid-β and/or tau to examine subjects with history of TBI who are at risk for AD due to advanced age. A comprehensive literature search was conducted on January 9, 2023, and 24 resulting citations met inclusion criteria. Common methodological concerns included small samples, limited clinical detail about subjects' TBI, recall bias due to reliance on self-reported TBI, and an inability to establish causation. For both amyloid and tau, results were widespread but inconsistent. The regions which showed the most compelling evidence for increased amyloid deposition were the cingulate gyrus, cuneus/precuneus, and parietal lobe. Evidence for increased tau was strongest in the medial temporal lobe, entorhinal cortex, precuneus, and frontal, temporal, parietal, and occipital lobes. However, conflicting findings across most regions of interest in both amyloid- and tau-PET studies indicate the critical need for future work in expanded samples and with greater clinical detail to offer a clearer picture of the relationship between TBI and protein deposition in older subjects at risk for AD.
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    Traumatic brain injury and cognitive resilience in the Framingham Heart Study
    (Wiley, 2025-01-09) Hwang, Phillip H.; Durape, Shruti; Price, Eden; Gurnani, Ashita S.; Ang, Ting Fang Alvin; Devine, Sherral A.; Choi, Seo-Eun; Lee, Michael L.; Scollard, Phoebe; Gibbons, Laura E.; Mukherjee, Shubhabrata; Trittschuh, Emily H.; Sherva, Richard; Dumitrescu, Logan C.; Hohman, Timothy J.; Saykin, Andrew J.; Crane, Paul K.; Tripodis, Yorghos; Alosco, Michael L.; Katz, Douglas I.; Dams-O'Connor, Kristen; Au, Rhoda; Farrer, Lindsay A.; Mez, Jesse; Radiology and Imaging Sciences, School of Medicine
    Background: Some evidence supports an association between traumatic brain injury (TBI) and greater risk of dementia, but the role of cognitive resilience in this association is poorly understood. Method: 2,050 participants from the Framingham Heart Study Offspring cohort who were aged ≥60 year and had a plasma total tau (t‐tau) measure at Exam 8 (2005‐2008), and a neuropsychological (NP) exam visit within five years were included. Plasma t‐tau was measured using the Simoa assay (Quanterix). NP factor scores were previously derived for memory, language, and executive function using confirmatory factor analysis. Information on TBIs was collected by comprehensive review of medical records, health history updates, exams, and self‐report. TBI occurrence and severity were operationalized using modified ACRM & VA/DoD criteria, respectively. Cognitive resilience was operationalized using a residual approach by regressing each NP factor score on the plasma t‐tau measure, adjusting for age at Exam 8, sex, education, time from blood draw, and APOE ε4 genotype. The adjusted residuals were then regressed on history of TBI (yes versus no), and severity of TBI (moderate‐to‐severe versus mild versus none). Result: The sample was, on average, 67 years of age at Exam 8, 54% female, and college educated. No differences were observed in plasma t‐tau levels between those with and without TBI. Having a history of TBI was significantly associated with a reduction in resilience in executive function (β: ‐0.110; 95% CI: ‐0.175, ‐0.044; p: 0.001) as compared to not having a history of TBI. No significant associations were observed between history of TBI and resilience in memory or language. Greater TBI severity was significantly associated with worse resilience in executive function in a dose‐response manner (Ptrend: <0.001), with the association being strongest in the moderate‐to‐severe TBI group (β: ‐0.209; 95% CI: ‐0.340, ‐0.078; p: 0.002) followed by the mild TBI group (β: ‐0.082; 95% CI: ‐0.155, ‐0.010; p: 0.026). Conclusion: Having a TBI was associated with worse resilience to neurodegeneration in executive function, and most strongly among individuals with moderate‐to‐severe TBI. These results suggest that having a TBI may increase vulnerability to late‐life executive dysfunction after accounting for a primary neurodegenerative disease process.
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    TRAUMATIC BRAIN INJURY LEADS TO ABERRANT MIGRATION OF ADULT-BORN NEURONS IN THE HIPPOCAMPUS
    (Office of the Vice Chancellor for Research, 2012-04-13) Ibrahim, Sara; Gao, Xiang; Chen, Jinhui
    Traumatic brain injury (TBI) is the leading cause of death in children and young adults, leading to substantial cognitive impairment, motor dysfunction and epilepsy. There is no effective treatment for these dis-orders. The discovery of neural stem/progenitor cells (NSCs) in the adult brain raises a potentially promising strategy for repairing CNS in-jury.Our previous study showed that TBI promotes NSC proliferation in an attempt to initiate innate repair and/or plasticity mechanisms. However, the spontaneously post-traumatic recovery of hippocampal-related cognitive and memory functions is very limited. Better under-standing of neurogenesis following TBI may provide additional inter-vention to further enhance neurogenesis for successfully repairing the damaged brain following TBI. Although newborn neurons generated from NSCs are continuously added to the brain throughout our life, they must migrate from their birthplace to their appropriate destina-tion to develop into mature neurons. When we tracked the migration of newly generated neurons in the adult hippocampus after TBI, we found that a large percentage of immature neurons migrate pass their normal stopping site at the inner granular cell layer, and misplace in the outer granular cell layer of the hippocampal dentate gyrus. The aberrant migration of adult-born neurons in the hippocampus occurs 3 days after TBI, and lasts for 10 weeks, resulting in a great number of newly generated neurons misplaced in the outer granular layer in the hippocampus. The newborn neurons at the displaced position will not be able to make correct connections with their appropriate targets, and may even make wrong connections with inappropriate nearby tar-gets in the pre-existing neural network. Abnormal migration can cause several diseases including epilepsy. These results suggest that stimu-lation of endogenous adult neural stem cells following TBI might offer new avenues for cell-based therapy. Additional intervention is required to further enhance successful neurogenesis for repairing the damaged brain.