scholarly journals Using computerized tomography perfusion to measure cerebral hemodynamics following treatment of traumatic brain injury in rabbits

Author(s):  
Kefei Chen ◽  
Feihu Dai ◽  
Guangxu Li ◽  
Jirong Dong ◽  
Yuhai Wang
2019 ◽  
Vol 161 (12) ◽  
pp. 2467-2478 ◽  
Author(s):  
Matias Lindfors ◽  
Caroline Lindblad ◽  
David W. Nelson ◽  
Bo-Michael Bellander ◽  
Jari Siironen ◽  
...  

Abstract Background The prognosis of penetrating traumatic brain injury (pTBI) is poor yet highly variable. Current computerized tomography (CT) severity scores are commonly not used for pTBI prognostication but may provide important clinical information in these cohorts. Methods All consecutive pTBI patients from two large neurotrauma databases (Helsinki 1999–2015, Stockholm 2005–2014) were included. Outcome measures were 6-month mortality and unfavorable outcome (Glasgow Outcome Scale 1–3). Admission head CT scans were assessed according to the following: Marshall CT classification, Rotterdam CT score, Stockholm CT score, and Helsinki CT score. The discrimination (area under the receiver operating curve, AUC) and explanatory variance (pseudo-R2) of the CT scores were assessed individually and in addition to a base model including age, motor response, and pupil responsiveness. Results Altogether, 75 patients were included. Overall 6-month mortality and unfavorable outcome were 45% and 61% for all patients, and 31% and 51% for actively treated patients. The CT scores’ AUCs and pseudo-R2s varied between 0.77–0.90 and 0.35–0.60 for mortality prediction and between 0.85–0.89 and 0.50–0.57 for unfavorable outcome prediction. The base model showed excellent performance for mortality (AUC 0.94, pseudo-R2 0.71) and unfavorable outcome (AUC 0.89, pseudo-R2 0.53) prediction. None of the CT scores increased the base model’s AUC (p > 0.05) yet increased its pseudo-R2 (0.09–0.15) for unfavorable outcome prediction. Conclusion Existing head CT scores demonstrate good-to-excellent performance in 6-month outcome prediction in pTBI patients. However, they do not add independent information to known outcome predictors, indicating that a unique score capturing the intracranial severity in pTBI may be warranted.


Brain Injury ◽  
2016 ◽  
Vol 30 (4) ◽  
pp. 441-451 ◽  
Author(s):  
Miguel Angel Prieto-Palomino ◽  
Emilio Curiel-Balsera ◽  
Maria Dolores Arias-Verdú ◽  
Monica Delange-Van Der Kroft ◽  
Alfonso Muñoz-López ◽  
...  

Neurosurgery ◽  
2011 ◽  
Vol 68 (3) ◽  
pp. 588-600 ◽  
Author(s):  
Charles S. Cox ◽  
James E. Baumgartner ◽  
Matthew T. Harting ◽  
Laura L. Worth ◽  
Peter A. Walker ◽  
...  

Abstract BACKGROUND: Severe traumatic brain injury (TBI) in children is associated with substantial long-term morbidity and mortality. Currently, there are no successful neuroprotective/neuroreparative treatments for TBI. Numerous preclinical studies suggest that bone marrow-derived mononuclear cells (BMMNCs), their derivative cells (marrow stromal cells), or similar cells (umbilical cord blood cells) offer neuroprotection. OBJECTIVE: To determine whether autologous BMMNCs are a safe treatment for severe TBI in children. METHODS: Ten children aged 5 to 14 years with a postresuscitation Glasgow Coma Scale of 5 to 8 were treated with 6 × 106 autologous BMMNCs/kg body weight delivered intravenously within 48 hours after TBI. To determine the safety of the procedure, systemic and cerebral hemodynamics were monitored during bone marrow harvest; infusion-related toxicity was determined by pediatric logistic organ dysfunction (PELOD) scores, hepatic enzymes, Murray lung injury scores, and renal function. Conventional magnetic resonance imaging (cMRI) data were obtained at 1 and 6 months postinjury, as were neuropsychological and functional outcome measures. RESULTS: All patients survived. There were no episodes of harvest-related depression of systemic or cerebral hemodynamics. There was no detectable infusion-related toxicity as determined by PELOD score, hepatic enzymes, Murray lung injury scores, or renal function. cMRI imaging comparing gray matter, white matter, and CSF volumes showed no reduction from 1 to 6 months postinjury. Dichotomized Glasgow Outcome Score at 6 months showed 70% with good outcomes and 30% with moderate to severe disability. CONCLUSION: Bone marrow harvest and intravenous mononuclear cell infusion as treatment for severe TBI in children is logistically feasible and safe.


PLoS Medicine ◽  
2017 ◽  
Vol 14 (8) ◽  
pp. e1002368 ◽  
Author(s):  
Eric Peter Thelin ◽  
David W. Nelson ◽  
Juho Vehviläinen ◽  
Harriet Nyström ◽  
Riku Kivisaari ◽  
...  

2009 ◽  
Vol 8 (1) ◽  
pp. 61-63
Author(s):  
D. V. Kolmakov

In this work, we have analyzed 2 774 case records of children after traumatic brain injury for the period of 2003 to 2007 (based on materials of the Tomsk Municipal Children’s Hospital No. 4). The age structure and causes of a traumatic brain injury have been analyzed. Most often complaints of children coming to the hospital are revealed, as well as typical changes in the cerebral hemodynamics (from the data of по данным rheoencephalography) and some parameters characterizing the neurological status of patients immediately after the injury and six months later. Based on the analysis of case records and health status questionnaires of children having traumatic brain injury up to six months later, it is shown that parents of patients in some cases do not adhere doctor’s recommendations after leaving the hospital. The therapy of traumatic brain injury in children requires successive treatment in hospital and at home and development of simple and acceptable rehabilitation schemes for children.


2020 ◽  
pp. 0271678X2096259
Author(s):  
Amreen Mughal ◽  
Adrian M Sackheim ◽  
Maria Sancho ◽  
Thomas A Longden ◽  
Sheila Russell ◽  
...  

Traumatic brain injury (TBI) acutely impairs dynamic regulation of local cerebral blood flow, but long-term (>72 h) effects on functional hyperemia are unknown. Functional hyperemia depends on capillary endothelial cell inward rectifier potassium channels (Kir2.1) responding to potassium (K+) released during neuronal activity to produce a regenerative, hyperpolarizing electrical signal that propagates from capillaries to dilate upstream penetrating arterioles. We hypothesized that TBI causes widespread disruption of electrical signaling from capillaries-to-arterioles through impairment of Kir2.1 channel function. We randomized mice to TBI or control groups and allowed them to recover for 4 to 7 days post-injury. We measured in vivo cerebral hemodynamics and arteriolar responses to local stimulation of capillaries with 10 mM K+ using multiphoton laser scanning microscopy through a cranial window under urethane and α-chloralose anesthesia. Capillary angio-architecture was not significantly affected following injury. However, K+-induced hyperemia was significantly impaired. Electrophysiology recordings in freshly isolated capillary endothelial cells revealed diminished Ba2+-sensitive Kir2.1 currents, consistent with a reduction in channel function. In pressurized cerebral arteries isolated from TBI mice, K+ failed to elicit the vasodilation seen in controls. We conclude that disruption of endothelial Kir2.1 channel function impairs capillary-to-arteriole electrical signaling, contributing to altered cerebral hemodynamics after TBI.


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