Articles: traumatic-brain-injuries.
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This 3-year prospective study examined the association between red blood cell transfusion (RBCT) and 1-year neurocognitive and disability levels in 309 patients with traumatic brain injury (TBI) admitted to the neurological intensive care unit (NICU). ⋯ Our results strongly suggest an independent association between RBCT and unfavorable long-term functional outcomes of patients with TBI.
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Journal of neurosurgery · Jun 2016
Neuron-derived orphan receptor 1 transduces survival signals in neuronal cells in response to hypoxia-induced apoptotic insults.
OBJECT Hypoxia can induce cell death or trigger adaptive mechanisms to guarantee cell survival. Neuron-derived orphan receptor 1 (NOR-1) works as an early-response protein in response to a variety of environmental stresses. In this study, the authors evaluated the roles of NOR-1 in hypoxia-induced neuronal insults. ⋯ After reducing cIAP2 translation, OGD-induced cell death was reduced. Sequentially, application of NOR-1 small interfering RNA to neuro-2a cells significantly inhibited OGD-induced cIAP2 mRNA expression and concurrently alleviated hypoxia-induced alterations in cell viability, caspase-3 activation, DNA damage, and cell apoptosis. CONCLUSIONS This study shows that NOR-1 can transduce survival signals in neuronal cells responsible for hypoxiainduced apoptotic insults through activation of a CREB/cIAP2-dependent mechanism.
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Journal of neurotrauma · Jun 2016
Using post-traumatic amnesia to predict outcome following traumatic brain injury.
Duration of post-traumatic amnesia (PTA) has emerged as a strong measure of injury severity after traumatic brain injury (TBI). Despite the growing international adoption of this measure, there remains a lack of consistency in the way in which PTA duration is used to classify severity of injury. This study aimed to establish the classification of PTA that would best predict functional or productivity outcomes. ⋯ This finding indicates that the greatest accuracy in prognosis is likely to be achieved using PTA as a continuous variable. This enables the probability of productive outcomes to be estimated with far greater precision than that possible using a classification system. Categorizing PTA to classify severity of injury may be reducing the precision with which clinicians can plan the treatment of patients after TBI.
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Journal of neurotrauma · Jun 2016
Neuroprotective effects of the glutamate transporter activator, MS-153, following traumatic brain injury in the adult rat.
Traumatic brain injury (TBI) in humans and in animals leads to an acute and sustained increase in tissue glutamate concentrations within the brain, triggering glutamate-mediated excitotoxicity. Excitatory amino acid transporters (EAATs) are responsible for maintaining extracellular central nervous system glutamate concentrations below neurotoxic levels. Our results demonstrate that as early as 5 min and up to 2 h following brain trauma in brain-injured rats, the activity (Vmax) of EAAT2 in the cortex and the hippocampus was significantly decreased, compared with sham-injured animals. ⋯ Administration of (R)-(-)-5-methyl-1-nicotinoyl-2-pyrazoline (MS-153), a GLT-1 activator, beginning immediately after injury and continuing for 24 h, significantly decreased neurodegeneration, loss of microtubule-associated protein 2 and NeuN (+) immunoreactivities, and attenuated calpain activation in both the cortex and the hippocampus at 24 h after the injury; the reduction in neurodegeneration remained evident up to 14 days post-injury. In synaptosomal uptake assays, MS-153 up-regulated GLT-1 activity in the naïve rat brain but did not reverse the reduced activity of GLT-1 in traumatically-injured brains. This study demonstrates that administration of MS-153 in the acute post-traumatic period provides acute and long-term neuroprotection for TBI and suggests that the neuroprotective effects of MS-153 are related to mechanisms other than GLT-1 activation, such as the inhibition of voltage-gated calcium channels.
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Patients with traumatic brain injury (TBI) may develop pituitary dysfunction. Although, there is now increasing awareness of and investigations into such post-traumatic hypopituitarism (PTHP), the exact prevalence and incidence remain uncertain. Here, we aim to identify the incidence of PTHP in a selected population of TBI patients deemed at risk of PTHP at a regional neurosurgical centre in the UK. ⋯ In comparison, in cross-sectional late cohort, 21.3% (10/47) of the patients developed dysfunction in at least one of their pituitary axes at 6 months or more post-TBI, with hypogonadotrophic hypogonadism being the most common. Twenty-two patients from these two cohorts had their growth hormone assessment at 12 months or more post-TBI and 9.1% (2/22) were found to have growth hormone deficiency. Our results suggest that PTHP is a common condition amongst sufferers of TBI, and appropriate measures should be taken to detect and manage it.