Articles: traumatic-brain-injuries.
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Neurorehabil Neural Repair · Nov 2013
Neuroprotective, neuroplastic, and neurobehavioral effects of daily treatment with levetiracetam in experimental traumatic brain injury.
Prophylactic treatment with antiepileptic drugs (AEDs) has been recommended to prevent early seizure onset in patients with traumatic brain injury (TBI). However, the potential neuroprotective and/or detrimental effects of prophylactic AED treatment on behavioral and cognitive function after TBI are not well studied. ⋯ These results suggest that daily LEV treatment has beneficial effects on histological, molecular, and behavioral elements of neurological recovery after TBI, in part, via modulation of neuroinflammatory and excitatory pathways.
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Arch Phys Med Rehabil · Nov 2013
Long-term disability and survival in traumatic brain injury: results from the National Institute on Disability and Rehabilitation Research Model Systems.
To document long-term survival in 1-year survivors of traumatic brain injury (TBI); to compare the use of the Disability Rating Scale (DRS) and FIM as factors in the estimation of survival probabilities; and to investigate the effect of time since injury and secular trends in mortality. ⋯ Long-term survival prognosis in TBI depends on age, sex, and disability. FIM and DRS are useful prognostic measures with comparable statistical performance. Age- and disability-specific mortality rates in TBI have not declined over the last 20 years. A survival prognosis calculator is available online (http://www.LifeExpectancy.org/tbims.shtml).
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Neurobiol Learn Mem · Nov 2013
Non-spatial pre-training in the water maze as a clinically relevant model for evaluating learning and memory in experimental TBI.
Explicit and implicit learning and memory networks exist where each network can facilitate or inhibit cognition. Clinical evidence suggests that implicit networks are relatively preserved after traumatic brain injury (TBI). Non-spatial pre-training (NSPT) in the Morris Water Maze (MWM) provides the necessary behavioral components to complete the task, while limiting the formation of spatial maps. ⋯ Place learning differences between CCI/NSPT and sham/NSPT rats more accurately reflect spatial deficits in our CCI model compared to untrained controls. These data suggest NSPT as a clinically relevant construct for evaluating potential neurorestorative and neuroprotective therapies. These findings also support development of non-spatial cognitive training paradigms for evaluating rehabilitation relevant combination therapies.
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The p75 neurotrophin receptor (p75(NTR)) influences the proliferation, survival, and differentiation of neuronal precursors and its expression is induced in injured brain, where it regulates cell survival. Here, we test the hypotheses that pharmacologic modulation of p75(NTR) signaling will promote neural progenitor survival and proliferation, and improve outcomes of traumatic brain injury (TBI). LM11A-31, an orally available, blood-brain barrier-permeant small-molecule p75(NTR) signaling modulator, significantly increased proliferation and survival, and decreased JNK phosphorylation, in hippocampal neural stem/progenitor cells in culture expressing wild-type p75(NTR), but had no effect on cells expressing a mutant neurotrophin-unresponsive form of the receptor. ⋯ In vivo, intranasal administration of LM11A-31 decreased postinjury hippocampal and cortical neuronal death, neural progenitor cell death, gliogenesis, and microglial activation, and enhanced long-term hippocampal neurogenesis and reversed spatial memory impairments. LM11A-31 diminished the postinjury increase of SOX2-expressing early progenitor cells, but protected and increased the proliferation of endogenous polysialylated-neural cell adhesion molecule positive intermediate progenitors, and restored the long-term production of mature granule neurons. These findings suggest that modulation of p75(NTR) actions using small molecules such as LM11A-31 may constitute a potent therapeutic strategy for TBI.