Object: Traumatic parenchymal mass lesions are common sequelae of traumatic brain injuries (TBIs). They occur in up to 8.2% of all TBI cases and 13%-35% of severe TBI cases, and they account for up to 20% of surgical intracranial lesions. Controversy exists concerning the association between radiological and clinical evolution of brain contusions. The aim of this study was to identify predictors of unfavorable outcome, analyze the evolution of brain contusions, and evaluate specific indications for surgery.
Methods: In a retrospective, multicenter study, patients with brain contusions were identified in separate patient cohorts from 11 hospitals over a 4-year period (2008-2011). Data on clinical parameters and course of the contusion were collected. Radiological parameters were registered by using CT images taken at the time of hospital admission and at subsequent follow-up times. Patients who underwent surgical procedures were identified. Outcomes were evaluated 6 months after trauma by using the Glasgow Outcome Scale-Extended.
Results: Multivariate analysis revealed the following reliable predictors of unfavorable outcome: 1) increased patient age, 2) lower Glasgow Coma Scale score at first evaluation, 3) clinical deterioration in the first hours after trauma, and 4) onset or increase of midline shift on follow-up CT images. Further multivariate analysis identified the following as statistically significant predictors of clinical deterioration during the first hours after trauma: 1) onset of or increase in midline shift on follow-up CT images (p < 0.001) and 2) increased effacement of basal cisterns on follow-up CT images (p < 0.001).
Conclusions: In TBI patients with cerebral contusion, the onset of clinical deterioration is predictably associated with the onset or increase of midline shift and worsened status of basal cisterns but not with hematoma or edema volume increase. A combination of clinical deterioration and increased midline shift/basal cistern compression is the most reasonable indicator for surgery.
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http://dx.doi.org/10.3171/2013.12.JNS131090 | DOI Listing |
Neurol Res
January 2025
Department of Physiology, Faculty of Medicine, Izmir Democracy University, Izmır, Turkey.
Objective: Within the scope of this research, the long-term effects of experimental blunt head trauma on immature rats and MK-801 administered acutely after trauma on the brain tissue will be examined. In addition, the impact of trauma and MK-801 on Nestin and CD133, which are essential stem cells, will be evaluated by immunohistochemical and ELISA methods.
Methods: In this study, the contusion trauma model was used.
Biomolecules
January 2025
Department of Surgery, University of South Florida Morsani College of Medicine, Tampa, FL 33612, USA.
Traumatic brain injury (TBI) is an inflammatory disease causing neurodegeneration. One of the consequences of inflammation is an elevated blood level of fibrinogen (Fg). Earlier we found that extravasated Fg induced an increased expression of neuronal nuclear factor kappa B (NF-κB) p65.
View Article and Find Full Text PDFHealthcare (Basel)
January 2025
Faculty of Medicine, "Titu Maiorescu" University of Medicine, 031593 Bucharest, Romania.
Background: The ongoing military conflict in Ukraine has had a devastating impact on children's health, exposing them to a range of illnesses. The aim of this study was to analyze the most common medical conditions among Ukrainian children since the beginning of the conflict, with a focus on identifying and understanding these problems in a wartime setting.
Method: To assess the health status of affected children, we collected data from 422 pediatric patients who presented to the emergency department.
J Neuroinflammation
January 2025
Spinal Cord and Brain Injury Research Center, Department of Physiology, College of Medicine, University of Kentucky, Lexington Kentucky, USA.
Objective: Therapeutic translation is challenging in spinal cord injury (SCI) and large animal models with high clinical relevance may accelerate therapeutic development. Pigs have important anatomical and physiological similarities to humans. Intraspinal inflammation mediates SCI pathophysiology.
View Article and Find Full Text PDFSci Rep
January 2025
Laboratorio de Neuroinflamacion i2-06, Hospital Nacional de Paraplejicos, Finca La Peraleda s/n, Toledo, 45071, Spain.
Spinal cord injury (SCI) causes abnormal liver function, the development of metabolic dysfunction-associated steatotic liver disease features and metabolic impairment in patients. Experimental models also demonstrate acute and chronic changes in the liver that may, in turn, affect SCI recovery. These changes have collectively been proposed to contribute to the development of a SCI-induced metabolic dysfunction-associated steatohepatitis (MASH).
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