Articles: traumatic-brain-injuries.
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Journal of neurotrauma · Nov 2015
Clusters of low FDG uptake voxels in combat veterans with traumatic brain injury and post-traumatic stress disorder.
Individuals with mild traumatic brain injury (TBI) show diminished metabolic activity when studied with positron emission tomography (PET) with (18)F-fluorodeoxyglucose (FDG). Since blast injury may not be localized in the same specific anatomical areas in every patient or may be diffuse, significance probability mapping may be vulnerable to false-negative detection of abnormalities. To address this problem, we used an anatomically independent measure to assess PET scans: increased numbers of contiguous voxels that are 2 standard deviations below values found in an uninjured control group. ⋯ Patients with mild TBI alone and patients with TBI+PTSD had larger clusters of low uptake voxels, and cluster size significantly differentiated the mild TBI groups from combat controls. Clusters were more irregular in shape in patients, and patients also had a larger number of low-activity voxels throughout the brain. In mild TBI and TBI+PTSD patients, but not healthy subjects, cluster volume was significantly correlated with verbal learning during FDG uptake.
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World J Crit Care Med · Nov 2015
Therapeutic temperature modulation is associated with pulmonary complications in patients with severe traumatic brain injury.
To examine complications associated with the use of therapeutic temperature modulation (mild hypothermia and normothermia) in patients with severe traumatic brain injury (TBI). ⋯ Exposure to TTM is associated with an increase in pulmonary complications. These findings support more attention to these complications in studies of TTM in TBI patients.
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Minerva anestesiologica · Nov 2015
Review Meta AnalysisCerebral vasospasm after traumatic brain injury: an update.
Post-traumatic vasospasm (PTV) remains a poorly understood entity. Using a systematic review approach, we examined the incidence, mechanisms, risk factors, impact on outcome and potential therapies of PTV. ⋯ Mechanical stretching, inflammation, calcium dysregulation, endotelin, contractile proteins, products of cerebral metabolism and cortical spreading depolarization have been involved in PTV pathophysiology. PTV occurs in up to 30-40% of the patients after severe traumatic brain injury. Usually, PTV starts within the first 3 days following head trauma and may last 5 to 10 days. Young age, low Glasgow Coma Score at admission and subarachnoid hemorrhage have been identified as risk factors of PTV. Suspected on transcranial Doppler, PTV diagnosis is best confirmed by angiography, CT angiography or MR angiography, and perfusion and ischaemic consequences by perfusion CT or MRI. Early PTV is associated with poor outcome. No PTV prevention strategy has proved efficient up to now. Regarding PTV treatment, only nimodipine and intra-arterial papaverine have been studied up to now. Treatment with milrinone has been described in a few cases reports and may represent a new therapeutic option.
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Journal of neurosurgery · Nov 2015
Case ReportsMassive cerebral swelling immediately after cranioplasty, a fatal and unpredictable complication: report of 4 cases.
Cranioplasty after decompressive craniectomy (DC) is associated with increased morbidity, but the reported mortality rate is low. Recently, some authors have reported a rare unexplained complication of sudden death in association with massive cerebral edema immediately after cranioplasty. The author reports on 4 patients who underwent cranioplasty after DC between January 2005 and August 2010 at his department and died because of massive cerebral edema immediately after uneventful surgery and anesthesia. ⋯ A MEDLINE search showed 8 similar cases that were reported previously. Fatal cerebral swelling after uneventful cranioplasty is a distinct clinical entity, although it is unpredictable. It is postulated that a negative pressure difference from the elimination of atmospheric pressure that had been chronically applied on the injured sinking brain in combination with the negative pressure applied by the closed subgaleal suction drain may lead to a massive brain shift toward the cranioplasty site and initiate a fatal vasomotor reaction.
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Epilepsy & behavior : E&B · Nov 2015
ReviewThe enigma of the latent period in the development of symptomatic acquired epilepsy - Traditional view versus new concepts.
A widely accepted hypothesis holds that there is a seizure-free, pre-epileptic state, termed the "latent period", between a brain insult, such as traumatic brain injury or stroke, and the onset of symptomatic epilepsy, during which a cascade of structural, molecular, and functional alterations gradually mediates the process of epileptogenesis. This review, based on recent data from both animal models and patients with different types of brain injury, proposes that epileptogenesis and often subclinical epilepsy can start immediately after brain injury without any appreciable latent period. ⋯ Knowing whether a latent period exists or not is important for our understanding of epileptogenesis and for the discovery and the trial design of antiepileptogenic agents. The development of antiepileptogenic treatments to prevent epilepsy in patients at risk from a brain insult is a major unmet clinical need.