Articles: traumatic-brain-injuries.
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After traumatic brain injury (TBI), neurons surviving the initial insult can undergo chronic (secondary) degeneration via poorly understood mechanisms, resulting in long-term cognitive impairment. Although a neuroinflammatory response is promptly activated after TBI, it is unknown whether it has a significant role in chronic phases of TBI (>1 year after injury). Using a closed-head injury model of TBI in mice, we showed by MRI scans that TBI caused substantial degeneration at the lesion site within a few weeks and these did not expand significantly thereafter. However, chronic alterations in neurons were observed, with reduced dendritic spine density lasting >1 year after injury. In parallel, we found a long-lasting inflammatory response throughout the entire brain. Deletion of one allele of CX3CR1, a chemokine receptor, limited infiltration of peripheral immune cells and largely prevented the chronic degeneration of the injured brain and provided a better functional recovery in female, but not male, mice. Therefore, targeting persistent neuroinflammation presents a new therapeutic option to reduce chronic neurodegeneration. ⋯ Traumatic brain injury (TBI) often causes chronic neurological problems including epilepsy, neuropsychiatric disorders, and dementia through unknown mechanisms. Our study demonstrates that inflammatory cells invading the brain lead to secondary brain damage. Sex-specific amelioration of chronic neuroinflammation rescues the brain degeneration and results in improved motor functions. Therefore, this study pinpoints an effective therapeutic approach to preventing secondary complications after TBI.
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To examine the prognostic discrimination and prediction of initial intracranial pressure (ICP) in patients with traumatic brain injury (TBI) undergoing decompressive craniectomy (DC). ⋯ For TBI patients undergoing DC, the initial ICP value provides great prognostic discrimination and is an independent predictor of unfavorable outcomes and mortality. We suggest that the initial ICP be included as a prognosticator in the overall assessment of prognosis of head-injured patients after DC.
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Patients with severe traumatic brain injury (TBI) are at risk of the development of acute respiratory distress syndrome (ARDS). TBI and ARDS pathophysiologic mechanisms are known to independently involve significant inflammatory responses. The literature on the association between plasma inflammatory cytokines and ARDS in patients with TBI is sparse. ⋯ Plasma markers of IL-6, IL-8, and IL-10 are associated with ARDS in patients with severe TBI.
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Our objective was to apply the technique of measuring diameters of optic nerve sheath (ONSD) for the intracranial pressure assessment for the cases with traumatic head injury without hemorrhage. In a retrospective study, CT data of 720 adult patients were collected and analyzed. ONSDs were measured at the point where the ophthalmic artery crosses the optic nerve (anatomical landmark) together with the eyeball transverse diameter (ETD). ⋯ ONSD/ETD ratio was 0.28±0.05 against 0.19±0.02 in healthy adults (p=0.02). We did not find correlation between ONSD/ETD ratio with initial Glasgow Coma Scale score but there was an inverse correlation between ONSD/ETD ratio and the Glasgow Outcome Score (r=-0.64). We conclude that in majority of cases with traumatic head injury without hemorrhage the ONSD is significantly enlarged indicating elevated intracranial pressure even if CT scans are negative.
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Intracranial bleeding and inflammatory reactions are common consequences of traumatic brain injury (TBI). Neutrophil gelatinase-associated lipocalin (NGAL), an iron-handling and acute phase protein, may participate in the pathogenesis of TBI. Therefore, we hypothesize that NGAL may be of high diagnostic and therapeutic relevance in the prognosis of TBI. ⋯ NGAL may be a novel biomarker reflecting TBI severity, which increased obviously and negatively correlated with GCS, TS, and RTS scores; additionally, this characteristic of NGAL may be helpful in guiding clinical TBI therapeutic strategies.