Articles: traumatic-brain-injuries.
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Ann Fr Anesth Reanim · Jul 2013
ReviewUpdate on prehospital emergency care of severe trauma patients.
The prognosis of severe trauma patients is determined by the ability of a healthcare system to provide high intensity therapeutic treatment on the field and to transport patients as quickly as possible to the structure best suited to their condition. Direct admission to a specialized center ("trauma center") reduces the mortality of the most severe trauma at 30 days and one year. Triage in a non-specialized hospital is a major risk of loss of chance and should be avoided whenever possible. ⋯ However, it does not help predict the need for urgent resuscitation procedures. Hemodynamic management is central to the care of hemorrhagic shock and severe head trauma. Transport helicopter with a physician on board has an important role to allow direct admission to a specialized center in geographical areas that are difficult to access.
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Frontiers in neurology · Jan 2013
ReviewRole of intravenous levetiracetam in seizure prophylaxis of severe traumatic brain injury patients.
Traumatic brain injury (TBI) can cause seizures and the development of epilepsy. The incidence of seizures varies from 21% in patients with severe brain injuries to 50% in patients with war-related penetrating TBI. In the acute and sub-acute periods following injury, seizures can lead to increased intracranial pressure and cerebral edema, further complicating TBI management. ⋯ Phenytoin is the most widely prescribed anticonvulsant in these patients. Intravenous levetiracetam, made available in 2006, is now being considered as a viable option in acute care settings if phenytoin is unavailable or not feasible due to side-effects. We discuss current data regarding the role of intravenous levetiracetam in seizure prophylaxis of severe TBI patients and the need for future studies.
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DAI is a leading cause of the patient's death or lasting vegetable state following severe TBI, and up to now the detailed mechanism of axonal injury after head trauma is still unclear. Inflammatory responses have been proved to be an important mechanism of neural injury after TBI. However, most of these studies are concerned with focal cerebral injury following head trauma. ⋯ From the studies reviewed, immune response cells would become reactive around the sites of axonal injury after DAI. Besides, the concentrations of several important inflammatory factors, such as IL-1 family, IL-6 and TNF-ɑ, increased after DAI as well, which implies the participation of inflammatory responses. It can be concluded that inflammatory responses probably participate in the neural injury in DAI, but at present the study of inflammatory responses following DAI is still limited and the clear effects of inflammatory response on axonal injury remain to be more explored.
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Review Historical Article
Guanfacine for the treatment of cognitive disorders: a century of discoveries at Yale.
The prefrontal cortex (PFC) is among the most evolved brain regions, contributing to our highest order cognitive abilities. It regulates behavior, thought, and emotion using working memory. Many cognitive disorders involve impairments of the PFC. ⋯ Recent research has found that the noradrenergic α2A agonist guanfacine can improve PFC function by strengthening PFC network connections via inhibition of cAMP-potassium channel signaling in postsynaptic spines. Guanfacine is now being used to treat a variety of PFC cognitive disorders, including Tourette's Syndrome and Attention Deficit Hyperactivity Disorder (ADHD). This article reviews the history of Yale discoveries on the neurobiology of PFC working memory function and the identification of guanfacine for treating cognitive disorders.
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World J Crit Care Med · Feb 2012
ReviewContemporary view on neuromonitoring following severe traumatic brain injury.
Evolving brain damage following traumatic brain injury (TBI) is strongly influenced by complex pathophysiologic cascades including local as well as systemic influences. To successfully prevent secondary progression of the primary damage we must actively search and identify secondary insults e.g. hypoxia, hypotension, uncontrolled hyperventilation, anemia, and hypoglycemia, which are known to aggravate existing brain damage. For this, we must rely on specific cerebral monitoring. ⋯ This, in turn, will support our therapeutic decision-making and also allow a more individualized and flexible treatment concept for each patient. For this, however, we need to learn to integrate several dimensions with their own possible treatment options into a complete picture. The present review summarizes the current understanding of extended neuromonitoring to guide therapeutic interventions with the aim of improving intensive care treatment following severe TBI, which is the basis for ameliorated outcome.