Articles: traumatic-brain-injuries.
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Animal models of traumatic brain injury (TBI) provide important tools for studying the pathobiology of brain trauma and for evaluating therapeutic or diagnostic targets. Incorporation of additional insults such as hemorrhagic shock (HS) and/or hypoxemia (HX) into these models more closely recreates clinical scenarios as TBI often occurs in conjunction with these systemic insults (i.e., polytrauma). ⋯ The physiological, histological, and behavioral aspects of this animal model have been characterized and have demonstrated exacerbating effects of systemic insults on penetrating TBI. As such, this model may facilitate the use of simultaneous assessments of multiple mechanisms and provide a platform for testing novel diagnostic and therapeutic targets.
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Brain injury : [BI] · Jan 2016
Reducing head computed tomography after mild traumatic brain injury: Screening value of clinical findings and S100B protein levels.
The present prospective study was performed to investigate whether primary clinical findings and serum S100B concentrations at 3 and 6 hours post-trauma can contribute to the selection of patients for an initial computed tomography (CT) scanning. ⋯ Serum S100B measurement along with clinical evaluation of patients with mild traumatic brain injury has promising screening value to support selection of patients for CT scanning.
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Brain injury : [BI] · Jan 2016
Comparison of pupillary dynamics to light in the mild traumatic brain injury (mTBI) and normal populations.
To determine if mTBI adversely affects the pupillary light reflex (PLR). ⋯ MTBI adversely affects the PLR. This suggests an impairment of the autonomic nervous system. The findings suggest the potential for quantitative pupillary dynamics to serve as an objective mTBI biomarker.
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Intrathecal baclofen (ITB) therapy is a proven, effective treatment for disabling cortical spasticity. We describe the first local series of five patients with acquired brain injury (ABI) who received ITB and were followed up for 63.8 months. ⋯ Our preliminary study showed encouraging long-term outcomes and safety for ITB therapy after ABI-related intractable spasticity. Individual ITB responses over time were variable, with gender differences. The outcomes experienced by our centre were comparable to those in the general ABI population, supporting the efficacy of ITB therapy for chronic disabling spasticity.
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Nociceptive and neuropathic pain occurs as part of the disease process after traumatic brain injury (TBI) in humans. Central and peripheral inflammation, a major secondary injury process initiated by the traumatic brain injury event, has been implicated in the potentiation of peripheral nociceptive pain. We hypothesized that the inflammatory response to diffuse traumatic brain injury potentiates persistent pain through prolonged immune dysregulation. ⋯ We conclude that traumatic brain injury increased the inflammatory pain associated with cutaneous inflammation by contributing to systemic immune dysregulation. Regulatory T cells are immune suppressors and failure of T cells to differentiate into regulatory T cells leads to unregulated cytokine production which may contribute to the potentiation of peripheral pain through the excitation of peripheral sensory neurons. In addition, regulatory T cells are identified as a potential target for therapeutic rebalancing of peripheral immune homeostasis to improve functional outcome and decrease the incidence of peripheral inflammatory pain following traumatic brain injury.