Articles: traumatic-brain-injuries.
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Depending on severity, traumatic brain injury (TBI) induces immediate neuropathological effects that in the mildest form may be transient but as severity increases results in neural damage and degeneration. The first phase of neural degeneration is explainable by the primary acute and secondary neuropathological effects initiated by the injury; however, neuroimaging studies demonstrate a prolonged period of pathological changes that progressively occur even during the chronic phase. ⋯ Neuroimaging quantification in TBI demonstrates degenerative effects from brain injury over time. An adverse synergistic influence of TBI with aging may predispose the brain injured individual for the development of neuropsychiatric and neurodegenerative disorders long after surviving the brain injury.
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Traumatic brain injury (TBI) survivors often suffer from long-lasting cognitive impairment that stems from hippocampal injury. Systemic administration of insulin-like growth factor-1 (IGF-1), a polypeptide growth factor known to play vital roles in neuronal survival, has been shown to attenuate posttraumatic cognitive and motor dysfunction. However, its neuroprotective effects in TBI have not been examined. ⋯ IGF-1 overexpression stimulated Akt phosphorylation and reduced acute (1 and 3d) hippocampal neurodegeneration, culminating in greater neuron survival at 10d after CCI injury. Hippocampal neuroprotection achieved by IGF-1 overexpression was accompanied by improved motor and cognitive function in brain-injured mice. These data provide strong support for the therapeutic efficacy of increased brain levels of IGF-1 in the setting of TBI.
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Traumatic brain injury (TBI) occurs in an estimated 80% of all pediatric trauma patients and is the leading cause of death and disability in the pediatric population. Decompressive craniectomy is a procedure used to decrease intracranial pressure by allowing the brain room to swell and therefore increase cerebral perfusion to the brain. ⋯ This study supports the current literature that decompressive craniectomy is no longer an intervention used as a last resort but an effective first line treatment to be considered.
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Int J Circumpolar Health · Jan 2013
Abusive head trauma among children in Alaska: a population-based assessment.
Serious physical abuse resulting in a traumatic brain injury (TBI) has been implicated as an underreported cause of infant mortality. Nearly 80% of all abusive head trauma (AHT) occurs among children <2 years of age, with infants experiencing an incidence nearly 8 times that of 2-year olds. ⋯ In Alaska, applying the CDC PAHT definition to the multi-source database enabled us to capture 49% more AHT cases than any of the individual database used in this analysis alone.
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Frontiers in neurology · Jan 2013
Amyloid-β Peptides and Tau Protein as Biomarkers in Cerebrospinal and Interstitial Fluid Following Traumatic Brain Injury: A Review of Experimental and Clinical Studies.
Traumatic brain injury (TBI) survivors frequently suffer from life-long deficits in cognitive functions and a reduced quality of life. Axonal injury, observed in many severe TBI patients, results in accumulation of amyloid precursor protein (APP). Post-injury enzymatic cleavage of APP can generate amyloid-β (Aβ) peptides, a hallmark finding in Alzheimer's disease (AD). ⋯ The heterogeneity of animal models, clinical cohorts, analytical techniques, and the complexity of TBI in the available studies make the clinical value of tau and Aβ as biomarkers uncertain at present. Additionally, the link between early post-injury changes in tau and Aβ peptides and the future risk of developing AD remains unclear. Future studies using methods such as rapid biomarker sampling combined with enhanced analytical techniques and/or novel pharmacological tools could provide additional information on the importance of Aβ peptides and tau protein in both the acute pathophysiology and long-term consequences of TBI.