Articles: traumatic-brain-injuries.
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Wien. Klin. Wochenschr. · Oct 2023
Red blood cell distribution width and Charlson comorbidity index help to identify frail polytraumatized patients : Experiences from a level I trauma center.
Little is known about the potential impact of the red blood cell distribution width (RDW) and pre-existing comorbidities on the late-phase survival of polytraumatized patients. ⋯ Even younger elderly polytraumatized patients (> 55 years of age) showed significant higher RDW values and higher CCI scores. In addition to the presence of severe TBI and age > 55 years, RDW value > 13.75% on admission and CCI score > 2 might help to identify the "younger" frail polytraumatized patient at risk.
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Journal of neurotrauma · Oct 2023
A morphologically individualized deep learning brain injury model.
The brain injury modeling community has recommended improving model subject specificity and simulation efficiency. Here, we extend an instantaneous (< 1 sec) convolutional neural network (CNN) brain model based on the anisotropic Worcester Head Injury Model (WHIM) V1.0 to account for strain differences due to individual morphological variations. Linear scaling factors relative to the generic WHIM along the three anatomical axes are used as additional CNN inputs. ⋯ This tool could be especially useful for youths and females due to their anticipated greater morphological differences relative to the generic model, even without the need for individual neuroimages. It has potential for a wide range of applications for injury mitigation purposes and the design of head protective gears. The voxelized strains also allow for convenient data sharing and promote collaboration among research groups.
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Journal of neurotrauma · Oct 2023
Inherent Susceptibility to Acquired Epilepsy in Selectively-Bred Rats Influences the Acute Response to Traumatic Brain Injury.
Traumatic brain injury (TBI) often causes seizures associated with a neuroinflammatory response and neurodegeneration. TBI responses may be influenced by differences between individuals at a genetic level, yet this concept remains understudied. Here, we asked whether inherent differences in one's vulnerability to acquired epilepsy would determine acute physiological and neuroinflammatory responses acutely after experimental TBI, by comparing selectively bred "seizure-prone" (FAST) rats with "seizure-resistant" (SLOW) rats, as well as control parental strains (Long Evans and Wistar rats). ⋯ SLOW rat strains) determines acute responses after experimental TBI. Differences in the neuropathological response to TBI between commonly used control rat strains is also a novel finding, and an important consideration for future study design. Our results support further investigation into whether genetic predisposition to acute seizures predicts the chronic outcomes after TBI, including the development of post-traumatic epilepsy.
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Eur J Trauma Emerg Surg · Oct 2023
Early administration of high dose enoxaparin after traumatic brain injury.
Early enoxaparin 30 mg BID administration at 24 h post-injury has been demonstrated in patients with traumatic brain injury (TBI). However this dose can also yield subtherapeutic anti-Xa levels in 30-50% of trauma patients, suggesting that larger doses may be required for adequate prophylaxis against venous thromboembolism (VTE). The safety of enoxaparin 40 mg BID in trauma patients has previously been shown - however, these studies have largely excluded TBI patients. Therefore, we sought to demonstrate the safety of early enoxaparin 40 mg BID in a low-risk group of TBI patients. ⋯ Prior studies have demonstrated that enoxaparin 40 mg BID dosing is superior to traditional VTE prophylaxis in trauma patients. However, TBI patients are often excluded from this dosing due to concern for progression. Our study showed no clinical decline in mental status in a small cohort of low-risk TBI patients who received enoxaparin 40 mg BID.
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Effect of voluntary exercise on endogenous pain control systems and post-traumatic headache in mice.
Traumatic brain injury (TBI) can cause acute and chronic pain along with motor, cognitive, and emotional problems. Although the mechanisms are poorly understood, previous studies suggest disruptions in endogenous pain modulation may be involved. Voluntary exercise after a TBI has been shown to reduce some consequences of injury including cognitive impairment. ⋯ PERSPECTIVE: This article evaluates the effects of exercise on pain-related behaviors in a preclinical model of traumatic brain injury (TBI). The findings show that exercise reduces nociceptive sensitization, loss of diffuse noxious inhibitory control, memory deficits, and spinal nociception-related gene expression after TBI. Exercise may reduce or prevent pain after TBI.