Search results for "Traumatic Brain Injury"

showing 10 items of 121 documents

Caspase-dependent cell death involved in brain damage after acute subdural hematoma in rats

2006

Abstract Traumatic brain injury is associated with acute subdural hematoma (ASDH) that worsens outcome. Although early removal of blood can reduce mortality, patients still die or remain disabled after surgery and additional treatments are needed. The blood mass and extravasated blood induce pathomechanisms such as high intracranial pressure (ICP), ischemia, apoptosis and inflammation which lead to acute as well as delayed cell death. Only little is known about the basis of delayed cell death in this type of injury. Thus, the purpose of the study was to investigate to which extent caspase-dependent intracellular processes are involved in the lesion development after ASDH in rats. A volume o…

Brain InfarctionMalePathologymedicine.medical_specialtyTraumatic brain injuryIschemiaApoptosisBrain damageNeuroprotectionAmino Acid Chloromethyl KetonesBrain IschemiaRats Sprague-DawleyLesionIn Situ Nick-End LabelingmedicineAnimalsHematoma Subdural AcuteEnzyme InhibitorsSubdural spaceMolecular BiologyIntracranial pressurebusiness.industryVascular diseaseGeneral Neurosciencemedicine.diseaseRatsDisease Models AnimalBloodNeuroprotective AgentsTreatment Outcomemedicine.anatomical_structureBrain InjuriesCaspasesAnesthesiaNeurology (clinical)Intracranial Hypertensionmedicine.symptombusinessSignal TransductionDevelopmental BiologyBrain Research
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Plasma Hyperosmolality Prolongs QTc Interval and Increases Risk for Atrial Fibrillation in Traumatic Brain Injury Patients

2020

Introduction: Hyperosmotic therapy with mannitol is frequently used for treatment cerebral edema, and 320 mOsm/kg H2O has been recommended as a high limit for therapeutic plasma osmolality. However, plasma hyperosmolality may impair cardiac function, increasing the risk of cardiac events. The aim of this study was to analyze the relation between changes in plasma osmolality and electrocardiographic variables and cardiac arrhythmia in patients treated for isolated traumatic brain injury (iTBI). Methods: Adult iTBI patients requiring mannitol infusion following cerebral edema, and with a Glasgow Coma Score below 8, were included. Plasma osmolality was measured with Osmometr 800 CLG. Spatial Q…

Cardiac function curvemedicine.medical_specialtyTraumatic brain injuryosmolar gapelectrocardiographylcsh:Medicine030204 cardiovascular system & hematologyQT intervalArticleCerebral edema03 medical and health sciences0302 clinical medicineInternal medicinemedicine030212 general & internal medicinecardiovascular diseasesbusiness.industrytraumatic brain injurylcsh:RGlasgow Coma ScaleCardiac arrhythmiaAtrial fibrillationGeneral Medicinemedicine.diseaseplasma osmolalityPlasma osmolalitycardiac arrhythmiasCardiologycardiovascular systembusinessJournal of Clinical Medicine
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Ketamine in acute phase of severe traumatic brain injury “an old drug for new uses?”

2021

AbstractMaintaining an adequate level of sedation and analgesia plays a key role in the management of traumatic brain injury (TBI). To date, it is unclear which drug or combination of drugs is most effective in achieving these goals. Ketamine is an agent with attractive pharmacological and pharmacokinetics characteristics. Current evidence shows that ketamine does not increase and may instead decrease intracranial pressure, and its safety profile makes it a reliable tool in the prehospital environment. In this point of view, we discuss different aspects of the use of ketamine in the acute phase of TBI, with its potential benefits and pitfalls.

DrugSecondary insultmedicine.medical_specialtyTime FactorsIntracranial PressureTraumatic brain injurySedationmedia_common.quotation_subjectCritical Care and Intensive Care MedicineNeuroprotectionCooperative sedation03 medical and health sciencesViewpointTraumatic brain injury0302 clinical medicinePharmacokineticsBrain Injuries TraumaticmedicineHumansHypnotics and SedativesKetamineIntensive care medicineIntracranial pressuremedia_commonAnesthetics DissociativeAgitationbusiness.industrylcsh:Medical emergencies. Critical care. Intensive care. First aid030208 emergency & critical care medicinelcsh:RC86-88.9medicine.diseaseNeuroprotectionSafety profileSedationKetaminemedicine.symptombusiness030217 neurology & neurosurgerymedicine.drugCritical Care
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Corrigendum to “Neuromuscular electrophysiological disorders and muscle atrophy in mechanically-ventilated traumatic brain injury patients: New insig…

2019

Electrophysiologybusiness.industryTraumatic brain injuryAnesthesiaMedicineObservational studymedicine.symptomCritical Care and Intensive Care Medicinebusinessmedicine.diseaseMuscle atrophyJournal of Critical Care
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Lactate and glucose as energy substrates and their role in traumatic brain injury and therapy

2009

Traumatic brain injury is a leading cause of disability and mortality worldwide, but no new pharmacological treatments are clinically available. A key pathophysiological development in the understanding of traumatic brain injury is the energy crisis derived from decreased cerebral blood flow, increased energy demand and mitochondrial dysfunction. Although still controversial, new findings suggest that brain cells try to cope in these conditions by metabolizing lactate as an energy substrate ‘on-demand’ in lieu of glucose. Experimental and clinical data suggest that lactate, at least when exogenously administered, is transported from astrocytes to neurons for neuronal utilization, essential…

Energy demandTraumatic brain injuryMetabolismPharmacologyBiologymedicine.diseasePathophysiologyNeurologyCerebral blood flowBiochemistrymedicineTreatment strategyGlycolysisNeurology (clinical)Future Neurology
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Nitric Oxide/Cyclic Guanosine Monophosphate Signaling via Guanylyl Cyclase Isoform 1 Mediates Early Changes in Synaptic Transmission and Brain Edema …

2021

Traumatic brain injury (TBI) often induces structural damage, disruption of the blood-brain barrier (BBB), neurodegeneration, and dysfunctions of surviving neuronal networks. Nitric oxide (NO) signaling has been suggested to affect brain functions after TBI. The NO exhibits most of its biological effects by activation of the primary targets-guanylyl cyclases (NO-GCs), which exists in two isoforms (NO-GC1 and NO-GC2), and the subsequently produced cyclic guanosine monophosphate (cGMP). However, the specific function of the NO-NO-GCs-cGMP pathway in the context of brain injury is not fully understood. To investigate the specific role of the isoform NO-GC1 early after brain injuries, we perfor…

Gene isoform030506 rehabilitationTraumatic brain injuryBrain EdemaReceptors Cell SurfaceNeurotransmissionBlood–brain barrierNitric OxideSynaptic TransmissionNitric oxide03 medical and health scienceschemistry.chemical_compoundMice0302 clinical medicineBrain Injuries TraumaticmedicinePremovement neuronal activityAnimalsCyclic guanosine monophosphateCyclic GMPMice KnockoutNeurodegenerationSomatosensory Cortexmedicine.diseaseIsoenzymesmedicine.anatomical_structurenervous systemchemistryGuanylate CyclaseNeurology (clinical)0305 other medical scienceNeuroscience030217 neurology & neurosurgerySignal TransductionJournal of neurotrauma
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Validation of brain extracellular glycerol as an indicator of cellular membrane damage due to free radical activity after traumatic brain injury.

2008

Following severe traumatic brain injury (TBI), increasing oxygen delivery to the brain has been advocated as a useful strategy to reverse mitochondrial dysfunction and improve neurological outcome. However, this might also promote overproduction of free radicals, responsible for lipid peroxidation and hence brain cell damage. Therefore, a method for monitoring this potential adverse effect in humans is desirable. Glycerol, an end product of phospholipid breakdown, easily detectable in the human brain by means of microdialysis, might represent a reliable indicator of free radical-induced cell membrane damage. Brain microdialysates were collected from 24 adult male Sprague-Dawley rats over a …

GlycerolMaleCellular membraneMicrodialysisFree RadicalsTraumatic brain injuryMicrodialysisPharmacologyAntioxidantsHead traumaCyclic N-OxidesRats Sprague-Dawleychemistry.chemical_compoundmedicineExtracellularGlycerolAnimalsbusiness.industryCell MembraneBrainExtracellular FluidMetabolismmedicine.diseaseRatsnervous systemchemistryAnesthesiaBrain InjuriesOxygen deliverySpin LabelsNeurology (clinical)businessJournal of neurotrauma
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The Increased Mortality Rate with Lower Incidence of Traumatic Brain Injury during the COVID-19 Pandemic: A National Study

2022

Background: the COVID-19 pandemic with the following lockdown strategies have affected virtually all aspects of everyday life. Health services all over the world faced the crisis on an unprecedented scale, hampering timely care delivery. The present study was designed to assess the impact of the COVID-19 outbreak on the incidence and treatment of traumatic brain injuries in Poland. Methods: the data on hospital admissions with traumatic brain injuries as the primary diagnosis were extracted from the National Health Fund of Poland. For the purpose of this study, the search was limited to four relevant diagnosis-related groups. The overall in-house mortality was calculated. Results: there wer…

Health Information Managementtraumatic brain injury; head trauma; COVID-19; mortality; lockdownLeadership and ManagementHealth PolicyHealth InformaticsHealthcare
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Pathophysiology of traumatic brain injury.

2007

The knowledge of the pathophysiology after traumatic head injury is necessary for adequate and patient-oriented treatment. As the primary insult, which represents the direct mechanical damage, cannot be therapeutically influenced, target of the treatment is the limitation of the secondary damage (delayed non-mechanical damage). It is influenced by changes in cerebral blood flow (hypo- and hyperperfusion), impairment of cerebrovascular autoregulation, cerebral metabolic dysfunction and inadequate cerebral oxygenation. Furthermore, excitotoxic cell damage and inflammation may lead to apoptotic and necrotic cell death. Understanding the multidimensional cascade of secondary brain injury offers…

InflammationNecrosisTraumatic brain injurybusiness.industryInflammationVasospasmBrain Edemamedicine.disease_causemedicine.diseaseBioinformaticsPathophysiologyOxidative StressAnesthesiology and Pain MedicineOxygen ConsumptionCerebral blood flowAnesthesiaBrain InjuriesCerebrovascular CirculationmedicineHumansmedicine.symptombusinessCell damageOxidative stressBritish journal of anaesthesia
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Extubation in neurocritical care patients: the ENIO international prospective study

2022

Purpose: Neurocritical care patients receive prolonged invasive mechanical ventilation (IMV), but there is poor specific information in this high-risk population about the liberation strategies of invasive mechanical ventilation. Methods: ENIO (NCT03400904) is an international, prospective observational study, in 73 intensive care units (ICUs) in 18 countries from 2018 to 2020. Neurocritical care patients with a Glasgow Coma Score (GCS) ≤ 12, receiving IMV ≥ 24 h, undergoing extubation attempt or tracheostomy were included. The primary endpoint was extubation failure by day 5. An extubation success prediction score was created, with 2/3 of patients randomly allocated to the training cohort …

Intensive Care UnitsTracheostomyTraumatic brain injuryExtubationAirway ExtubationHumansProspective StudiesBrain injuryCritical Care and Intensive Care MedicineIntra-cranial haemorrhageRespiration Artificial
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