Journal of neurotrauma
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Journal of neurotrauma · Jan 2007
Effects of crystalloid-colloid solutions on traumatic brain injury.
The purpose of this study was to compare the effects of crystalloid and crystalloid-colloid solutions administered at different times after isolated traumatic brain injury. Male Sprague-Dawley rats were randomized to receive one of three intravenous treatments (4 mL/kg body weight) at 10 min or 6 h after moderate traumatic brain injury. Treatments included hypertonic saline, hypertonic albumin, and normal albumin. ⋯ The presence of colloid in the infusion solutions was associated with an improvement in tissue damage and edema following isolated head injury while hypertonic saline alone, when given immediately after injury, worsened tissue damage and edema. When hypertonic saline was administered at 6 h after injury, tissue damage and edema were not worsened. In conclusion, the presence of colloid in solutions used to treat traumatic brain injury and the timing of treatment have a significant impact on tissue damage and edema.
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Journal of neurotrauma · Jan 2007
Hybrid outcome prediction model for severe traumatic brain injury.
Numerous studies addressing different methods of head injury prognostication have been published. Unfortunately, these studies often incorporate different head injury prognostication models and study populations, thus making direct comparison difficult, if not impossible. Furthermore, newer artificial intelligence tools such as machine learning methods have evolved in the field of data analysis, alongside more traditional methods of analysis. ⋯ Consistently high outcome prediction accuracy was seen with logistic regression and decision tree. Combining both logistic regression and decision tree models, a hybrid prediction model was then developed. This hybrid model would more accurately predict the 6-month post-severe head injury outcome using baseline admission parameters.
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Journal of neurotrauma · Jan 2007
Coagulation abnormalities associated with severe isolated traumatic brain injury: cerebral arterio-venous differences in coagulation and inflammatory markers.
Although coagulopathy is known to be the major contributor to a poor outcome of traumatic brain injury (TBI), the mechanisms that trigger coagulation abnormalities have not been studied in detail. We undertook a prospective observational study at a neurosurgical ICU (NICU) in a university hospital. We examined 11 patients with severe isolated TBI, at admittance to the hospital and during the next 3 days. ⋯ C5b-9 levels were moderately increased in blood samples, 270 +/- 114 microg/L, versus controls, 184 +/- 39 (p < 0.05). We conclude that activation of the coagulation system takes place during the passage of blood through the damaged brain, and is already evident hours after the trauma. IL-6 and activation of the complement system (C5b-9) co-vary with hemostatic parameters in TBI patients.
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Journal of neurotrauma · Jan 2007
Basic science; repetitive mild non-contusive brain trauma in immature rats exacerbates traumatic axonal injury and axonal calpain activation: a preliminary report.
Infants who experience inflicted brain injury (shaken-impact syndrome) present with subdural hematoma, brain atrophy, and ventriculomegaly, pathologic features that are suggestive of multiple incidences of brain trauma. To develop a clinically relevant model of inflicted brain injury in infants, the skulls of anesthetized 11-day-old rat pups were subjected to one, two, or three successive mild impacts. While skull fractures were not observed, a single impact to the intact skull resulted in petechial hemorrhages in the subcortical white matter, and double or triple impacts led to hemorrhagic tissue tears at 1 day postinjury. ⋯ Calpain activation was observed in axons in subcortical white matter tracts in all brain-injured animals at 1 day and increased with the number of impacts. Despite these pathologic alterations, neither one nor two impacts led to acquisition deficits on the Morris water maze. While indicative of the graded nature of the pathologic response, these data suggest that repetitive mild brain injury in the immature rat results in pathologic features similar to those following inflicted brain injuries in infants.