Articles: traumatic-brain-injuries.
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The objective of this review was to evaluate the potential of tauroursodeoxycholic acid (TUDCA) for neuroprotection in traumatic brain injury (TBI) patients in the neurocritical care setting. Specifically, we surveyed preclinical studies describing the neuroprotective and systemic effects of TUDCA, and the potential therapeutic application of TUDCA. Preclinical studies have provided promising data supporting its use in neurological disease characterized by apoptosis-induced neuronal loss. ⋯ Additionally, preliminary data support the use of pharmacological therapies that reduce apoptosis and inflammation associated with TBI. The anti-apoptotic and anti-inflammatory mechanisms of TUDCA could prove promising in the treatment of TBI. Currently, there are no published data supporting improvement in clinical outcomes of TBI by treatment with TUDCA, but future studies should be considered.
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With regard to persistent posttraumatic headache, there is legitimate concern that duration of symptoms may have an impact on the efficacy of future treatment attempts. Without neuropathologic confirmation, a clinical diagnosis of chronic traumatic encephalopathy cannot be made with a high degree of confidence. Sport-related headaches are challenging in a return-to-play context, because it is often unclear whether an athlete has an exacerbation of a primary headache disorder, has new-onset headache unrelated to trauma, or is in the recovery phase after concussion. Regular physical exercise may prove beneficial to multiple neurologic disease states.
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In patients with traumatic brain injury (TBI), multicenter randomized controlled trials have assessed decompressive craniectomy (DC) exclusively as treatment for refractory elevation of intracranial pressure (ICP). DC reliably lowers ICP but does not necessarily improve outcomes. However, some patients undergo DC as treatment for impending or established transtentorial herniation, irrespective of ICP. ⋯ DC is most often performed for clinical and radiographic evidence of herniation, rather than for refractory ICP elevation. Results of previously completed randomized trials do not directly apply to a large proportion of patients undergoing DC in practice.
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Severe traumatic brain injury (TBI) damages the frontal lobes and connecting networks, which impairs executive functions, including the ability to self-regulate. Despite significant disabling effects, there are few treatment options in the chronic phase after injury. ⋯ DBS, deep brain stimulationIC, internal capsuleMPAI-4, Mayo-Portland Adaptability Inventory-4NAcc, nucleus accumbensTBI, traumatic brain injury.
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Journal of critical care · Aug 2016
Safety of peripheral administration of phenylephrine in a neurologic intensive care unit: A pilot study.
Integral to the management of the neurocritically injured patient are the prevention and treatment of hypotension, maintenance of cerebral perfusion pressure, and occasionally blood pressure augmentation. When adequate volume resuscitation fails to meet perfusion needs, vasopressors are often used to restore end-organ perfusion. This has historically necessitated central venous access given well-documented incidence of extravasation injuries associated with peripheral administration of vasopressors. ⋯ We were able to administer peripheral phenylephrine, up to a dose of 2 μg/(kg min), for an average of 14.29hours (1-54.3) in 20 patients with only 1 possible minor complication and no major complications. This was achieved by adding additional safety measures in our computerized physician order entry system and additional nurse-driven safety protocols. Thus, with careful monitoring and safety precautions, peripheral administration of phenylephrine at an optimized concentration appears to have an acceptable safety profile for use in the neurocritical care unit up to a mean infusion time of 14hours.