Articles: traumatic-brain-injuries.
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Review Comparative Study
A systematic review of levetiracetam versus phenytoin in the prevention of late post-traumatic seizures and survey of UK neurosurgical prescribing practice of antiepileptic medication in acute traumatic brain injury.
Guidelines recommend 1 week of prophylactic phenytoin for post-traumatic seizures (PTS). Levetiracetam is gaining popularity as an alternative with a superior side-effect profile and may be suitable for extended use. We performed a systematic review comparing the efficacy of levetiracetam and phenytoin in reducing the incidence of late PTS. The secondary objectives were to compare their effects on the Extended Glasgow Outcome Scale (GOS-E) and length of stay. We also aimed to survey current prophylaxis prescribing practices. ⋯ While our review found no evidence of a difference in late seizure incidence, there is evidence of improved long-term outcomes with levetiracetam. Neither study used an extended course of levetiracetam or continuous electroencephalography. Further research which accounts for these factors is required for the development of guidelines which take levetiracetam into account. Our survey showed a lack of awareness of the potential harms of extended phenytoin use and a move towards levetiracetam.
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In recent years, several randomized controlled trials evaluating pharmaceutical treatments for traumatic brain injury (TBI) have failed to demonstrate efficacy over placebo, with both active and placebo arms improving at comparable rates. These findings could be viewed in opposing ways, suggesting on the one hand failure of the tested outcome, but on the other, representing evidence of robust placebo effects in TBI. ⋯ We then extrapolate from the literature to explore whether something inherent in TBI makes it particularly responsive to placebos. Viewed as such here, placebos may indeed represent a powerful and effective treatment for a variety of post-TBI complaints.
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Critical care medicine · Jun 2018
Revisited: A Systematic Review of Therapeutic Hypothermia for Adult Patients Following Traumatic Brain Injury.
Therapeutic hypothermia has been of topical interest for many years and with the publication of two international, multicenter randomized controlled trials, the evidence base now needs updating. The aim of this systematic review of randomized controlled trials is to assess the efficacy of therapeutic hypothermia in adult traumatic brain injury focusing on mortality, poor outcomes, and new pneumonia. ⋯ Overall, this review is in-keeping with the conclusions published by the most recent randomized controlled trials. High-quality studies show no significant difference in mortality, poor outcomes, or new pneumonia. In addition, this review shows a place for fever control in the management of traumatic brain injury.
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Melatonin (MEL) is a hormone that is produced in the brain and is known to bind to MEL-specific receptors on neuronal membranes in several brain regions. MEL's documented neuroprotective properties, low toxicity, and ability to cross the blood-brain-barrier have led to its evaluation for patients with traumatic brain injury (TBI), a condition for which there are currently no Food and Drug Administration (FDA)-approved therapies. The purpose of this manuscript is to summarize the evidence surrounding the use of melatonin after TBI, as well as identify existing gaps and future directions. ⋯ Notably, available evidence is largely based on data from adult male rats and, to a lesser extent, mice. Few studies collected data beyond a few days of the initial injury, necessitating additional longer-term studies. Other future directions include diversification of samples to include female animals, pediatric and geriatric animals, and transgenic strains.
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Acta neuropathologica · May 2018
Review Case ReportsEvidence of amyloid-β cerebral amyloid angiopathy transmission through neurosurgery.
Amyloid-β (Aβ) is a peptide deposited in the brain parenchyma in Alzheimer's disease and in cerebral blood vessels, causing cerebral amyloid angiopathy (CAA). Aβ pathology is transmissible experimentally in animals and through medical procedures in humans, such as contaminated growth hormone or dura mater transplantation in the context of iatrogenic prion disease. ⋯ In addition, we identified in the literature four patients with a history of neurosurgical intervention and subsequent development of CAA. These findings raise the possibility that Aβ pathology may be transmissible, as prion disease is, through neurosurgical procedures.