Articles: traumatic-brain-injuries.
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Review Case Reports
Treatment of Penetrating Nonmissile Traumatic Brain Injury. Case Series and Review of the Literature.
Penetrating traumatic brain injuries (TBIs), with the exception of gunshot wounds, are relatively rare occurrences and affect all ages. Clinical presentation varies depending on the mechanism of the injury. Prompt surgical treatment is often indicated and is influenced by patient clinical examination, anatomic trajectory, and the penetrating object's size, shape, and velocity. ⋯ Surgery in penetrating TBI is the treatment of choice. Our cases demonstrate how certain principles applied to individual patient scenarios may optimize clinical results. Severity of the injury and operative approach are among the most important considerations to achieve the best patient outcomes.
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J Head Trauma Rehabil · Jul 2016
Persistent Hypogonadotropic Hypogonadism in Men After Severe Traumatic Brain Injury: Temporal Hormone Profiles and Outcome Prediction.
To (1) examine relationships between persistent hypogonadotropic hypogonadism (PHH) and long-term outcomes after severe traumatic brain injury (TBI); and (2) determine whether subacute testosterone levels can predict PHH. ⋯ PHH status in men predicts poor outcome after severe TBI, and PHH can accurately be predicted at 12 to 16 weeks.
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Sodium butyrate (SB) has been widely used to treat cerebral diseases. The aim of the present study is to examine the neuroprotective effects of SB on early TBI in mice and to explore the underlying mechanisms of these effects. TBI was induced using a modified weight-drop method. ⋯ Moreover, SB reversed the decrease in occludin and ZO-1 expression induced by TBI. These findings suggest that SB might attenuate neurological deficits, brain oedema, neuronal change and BBB damage, as well as increase occludin and ZO-1 expression in the brain to protect against TBI. The protective effect of SB may be correlated with restoring the BBB following its impairment.
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Epilepsy & behavior : E&B · Jul 2016
Epileptogenesis after traumatic brain injury in Plaur-deficient mice.
Binding of the extracellular matrix proteinase urokinase-type plasminogen activator (uPA) to its receptor, uPAR, regulates tissue remodeling during development and after injury in different organs, including the brain. Accordingly, mutations in the Plaur gene, which encodes uPAR, have been linked to language deficits, autism, and epilepsy, both in mouse and human. Whether uPAR deficiency modulates epileptogenesis and comorbidogenesis after brain injury, however, is unknown. ⋯ Both the Wt-CCI and uPAR-CCI groups showed increased seizure susceptibility in the PTZ test (p<0.05), impaired recovery of motor function (p<0.001), and neurodegeneration in the hippocampus and cortex (p<0.05) compared with the corresponding sham-operated controls. Motor recovery and emotional learning showed a genotype effect, being more impaired in uPAR-CCI than in Wt-CCI mice (p<0.05). The findings of the present study indicate that uPAR deficiency does not increase susceptibility to epileptogenesis after CCI injury but has an unfavorable comorbidity-modifying effect after TBI.
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Journal of neurotrauma · Jul 2016
Time Course and Size of Blood-Brain Barrier Opening in a Mouse Model of Blast-Induced Traumatic Brain Injury.
An increasing number of studies have reported blood-brain barrier (BBB) dysfunction after blast-induced traumatic brain injury (bTBI). Despite this evidence, there is limited quantitative understanding of the extent of BBB opening and the time course of damage after blast injury. In addition, many studies do not report kinematic parameters of head motion, making it difficult to separate contributions of primary and tertiary blast-loading. ⋯ Exposure to blast with 272 ± 6 kPa peak overpressure, 0.69 ± 0.01 ms duration, and 65 ± 1 kPa*ms impulse resulted in significant acute extravasation of NaFl, 3 kDa dextran, and EB. However, there was no significant acute extravasation of 70 kDa or 500 kDa dextrans, and minimal to no extravasation of NaFl, dextrans, or EB 1 day after exposure. This study presents a detailed analysis of the time course and pore size of BBB opening after bTBI, supported by a characterization of kinematic parameters associated with blast-induced head motion.