Journal of neurotrauma
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Journal of neurotrauma · Dec 2020
Observational StudyPoint-of-Care Platform Blood Biomarker Testing of GFAP versus S100B for Prediction of Traumatic Brain Injuries: a TRACK-TBI study.
Glial fibrillary acidic protein (GFAP) is cleared by the Food and Drug Administration (FDA) to determine need for head computed tomography (CT) within 12 h after mild traumatic brain injury (TBI) (Glasgow Coma Score [GCS] 13-15); S100 calcium-binding protein B (S100B) serves this function in Europe. This phase 1 biomarker cohort analysis of the multi-center, observational Transforming Research and Clinical Knowledge in Traumatic Brain Injury (TRACK-TBI) study compares GFAP's diagnostic performance, measured on a rapid point-of-care platform, against protein S100B to predict intracranial abnormalities on CT within 24 h post-injury across the spectrum of TBI (GCS 3-15). Head CT scan performed in TBI subjects and blood was collected for all consenting subjects presenting to 18 United States level 1 trauma centers. ⋯ Receiver operating characteristic curves were generated for prediction of intracranial injury on admission CT scan; area under the curve (AUC) for GFAP was significantly higher than for S100B in the same cohort (GFAP AUC - 0.85, 95% confidence interval [CI] 0.83-0.87; S100B AUC - 0.67, 95% CI 0.64-0.70; p 0.001). GFAP, measured on a point-of-care platform prototype assay, has high discriminative ability to predict intracranial abnormalities on CT scan in patients with TBI across the full injury spectrum of GCS 3-15 through 24 h post-injury. GFAP substantially outperforms S100B.
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Journal of neurotrauma · Dec 2020
Obstructive Sleep Apnea Risk is Associated with Cognitive Impairment After Controlling for mild TBI history: A Chronic Effects of Neurotrauma Consortium Study.
The contribution of sleep disturbance to persistent cognitive symptoms following a mild traumatic brain injury (mTBI) remains unclear. Obstructive sleep apnea (OSA) is very common, yet its relationship between risk factors for developing OSA and cognitive performance in those with history of mTBI has not been investigated. The current study examined OSA risk levels and its association with cognitive performance in 391 combat-exposed, post-911 veterans and service members (median age = 37 years) enrolled in the Chronic Effects of Neurotrauma Consortium (CENC) prospective multi-center study. ⋯ After adjustment for TBI status and demographic variables, increased OSA risk was significantly associated with worse performance on measures of complex processing speed and executive functioning (Wechsler Adult Intelligence Scale Fourth Edition Coding, Trail Making Test, part B) and greater symptom burden (Neurobehavioral Symptom Inventory). Thus, OSA, a modifiable behavioral health factor, likely contributes to cognitive performance following mTBI. Accordingly, OSA serves as a potential point of intervention to improve clinical and cognitive outcomes after injury.
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Journal of neurotrauma · Dec 2020
The Utility Of The Modified Frailty Index In Outcome Prediction For Elderly Patients With Acute Traumatic Subdural Haematoma.
This study aimed to evaluate the utility of the 11-variable modified Frailty Index (mFI) in prognosticating elderly patients with traumatic acute subdural hematomas (aSDHs). A state-service level 1 trauma center registry was interrogated to investigate consecutive patients ≥65 years of age presenting with traumatic aSDH, with or without major extracranial injury, between January 2013 and December 2017. mFI on admission, demographics, and admission details, including Glasgow Coma Scale (GCS) and pupillary status and radiological findings, were retrospectively retrieved from institutional records. Clinical outcome data were retrieved from medical records and the Victorian State Trauma Registry (VSTR). ⋯ Multi-variate analysis showed that greater mFI score of ≥3/11 variables (≥0.27) suggested a significantly higher risk of 30-day mortality (p = 0.009) and unfavorable outcome (p < 0.001). We conclude that increasing frailty, as measured by the mFI, was associated with significantly higher risk of 30-day mortality and 6-month unfavorable outcome in elderly patients presenting with aSDH to a level 1 neurotrauma center. Assessment of mFI in elderly patients with aSDH may be a useful determinant of outcome for this rapidly growing population.
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Journal of neurotrauma · Dec 2020
Sodium cromoglycate decreases sensorimotor impairment and hippocampal alterations induced by severe traumatic brain injury in rats.
Severe traumatic brain injury (TBI) results in significant functional disturbances in the hippocampus. Studies support that sodium cromoglycate (CG) induces neuroprotective effects. This study focused on investigating the effects of post-TBI subchronic administration of CG on hippocampal hyperexcitability and damage as well as on sensorimotor impairment in rats. ⋯ The TBI+CG group presented hippocampal volume reduction (12.7%, p = 0.94) and damage (0.10 ± 0.03 mm3, p > 0.99) similar to the TBI+SS group. However, their hippocampal neuronal preservation was similar to that of the Sham+SS group. These results indicate that CG represents an appropriate and novel pharmacological strategy to reduce the long-term sensorimotor impairment and hippocampal damage and hyperexcitability that result as consequences of severe TBI.
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Journal of neurotrauma · Dec 2020
Early increase in cortical T2 relaxation is a prognostic biomarker for the evolution of severe cortical damage, but not for epileptogenesis, after experimental traumatic brain injury.
Prognostic biomarkers for post-injury outcome are necessary for the development of neuroprotective and antiepileptogenic treatments for traumatic brain injury (TBI). We hypothesized that T2 relaxation magnetic resonance imaging (MRI) predicts the progression of perilesional cortical pathology and epileptogenesis. The EPITARGET animal cohort used for MRI analysis included 120 adult male Sprague-Dawley rats with TBI induced by lateral fluid-percussion injury and 24 sham-operated controls. ⋯ Logistic regression analysis, however, showed that the different severities of T2 lesion volumes at days 2, 7, and 21 post-TBI did not explain the development of epilepsy (χ2(18,95) = 18.4; p = 0.427). In addition, the location of the T2 abnormality within the cortex did not correlate with epileptogenesis. A single measurement of T2 relaxation MRI in the acute post-TBI phase is useful for identifying post-TBI subjects at highest risk of developing large cortical lesions, and thus, in the greatest need of neuroprotective therapies after TBI, but not the development of post-traumatic epilepsy.