Ecological validity of executive function tests in moderate traumatic brain injury in Ghana

2016 ◽  
Vol 30 (sup1) ◽  
pp. 1517-1537 ◽  
Author(s):  
Samuel Adjorlolo
2013 ◽  
Author(s):  
Ellie Perniskie ◽  
Nic Ward ◽  
John Dalrymple-Alford ◽  
Joyce Alberts ◽  
Ashok Jansari ◽  
...  

2004 ◽  
Vol 19 (4) ◽  
pp. 341-348 ◽  
Author(s):  
Anne M. Moseley ◽  
Stephanie Lanzarone ◽  
Johanna M. Bosman ◽  
Mirjam A. van Loo ◽  
Rob A. de Bie ◽  
...  

2021 ◽  
Vol 22 (15) ◽  
pp. 8276
Author(s):  
Pen-Sen Huang ◽  
Ping-Yen Tsai ◽  
Ling-Yu Yang ◽  
Daniela Lecca ◽  
Weiming Luo ◽  
...  

Traumatic brain injury (TBI) is a leading cause of disability and mortality worldwide. It can instigate immediate cell death, followed by a time-dependent secondary injury that results from disproportionate microglial and astrocyte activation, excessive inflammation and oxidative stress in brain tissue, culminating in both short- and long-term cognitive dysfunction and behavioral deficits. Within the brain, the hippocampus is particularly vulnerable to a TBI. We studied a new pomalidomide (Pom) analog, namely, 3,6′-dithioPom (DP), and Pom as immunomodulatory imide drugs (IMiD) for mitigating TBI-induced hippocampal neurodegeneration, microgliosis, astrogliosis and behavioral impairments in a controlled cortical impact (CCI) model of TBI in rats. Both agents were administered as a single intravenous dose (0.5 mg/kg) at 5 h post injury so that the efficacies could be compared. Pom and DP significantly reduced the contusion volume evaluated at 24 h and 7 days post injury. Both agents ameliorated short-term memory deficits and anxiety behavior at 7 days after a TBI. The number of degenerating neurons in the CA1 and dentate gyrus (DG) regions of the hippocampus after a TBI was reduced by Pom and DP. DP, but not Pom, significantly attenuated the TBI-induced microgliosis and DP was more efficacious than Pom at attenuating the TBI-induced astrogliosis in CA1 and DG at 7D after a TBI. In summary, a single intravenous injection of Pom or DP, given 5 h post TBI, significantly reduced hippocampal neurodegeneration and prevented cognitive deficits with a concomitant attenuation of the neuroinflammation in the hippocampus.


Brain Injury ◽  
2006 ◽  
Vol 20 (5) ◽  
pp. 519-527 ◽  
Author(s):  
Stephen R. McCauley ◽  
Claudia Pedroza ◽  
Sharon A. Brown ◽  
Corwin Boake ◽  
Harvey S. Levin ◽  
...  

2014 ◽  
Vol 127 ◽  
pp. 97-100 ◽  
Author(s):  
Eiichi Suehiro ◽  
Hiroyasu Koizumi ◽  
Yuichi Fujiyama ◽  
Hiroshi Yoneda ◽  
Michiyasu Suzuki

2017 ◽  
Vol 23 (7) ◽  
pp. 529-538 ◽  
Author(s):  
Gabriel C. Araujo ◽  
Tanya N. Antonini ◽  
Vicki Anderson ◽  
Kathryn A. Vannatta ◽  
Christina G. Salley ◽  
...  

AbstractObjectives:This study examined whether children with distinct brain disorders show different profiles of strengths and weaknesses in executive functions, and differ from children without brain disorder.Methods:Participants were children with traumatic brain injury (N=82; 8–13 years of age), arterial ischemic stroke (N=36; 6–16 years of age), and brain tumor (N=74; 9–18 years of age), each with a corresponding matched comparison group consisting of children with orthopedic injury (N=61), asthma (N=15), and classmates without medical illness (N=68), respectively. Shifting, inhibition, and working memory were assessed, respectively, using three Test of Everyday Attention: Children’s Version (TEA-Ch) subtests: Creature Counting, Walk-Don’t-Walk, and Code Transmission. Comparison groups did not differ in TEA-Ch performance and were merged into a single control group. Profile analysis was used to examine group differences in TEA-Ch subtest scaled scores after controlling for maternal education and age.Results:As a whole, children with brain disorder performed more poorly than controls on measures of executive function. Relative to controls, the three brain injury groups showed significantly different profiles of executive functions. Importantly, post hoc tests revealed that performance on TEA-Ch subtests differed among the brain disorder groups.Conclusions:Results suggest that different childhood brain disorders result in distinct patterns of executive function deficits that differ from children without brain disorder. Implications for clinical practice and future research are discussed. (JINS, 2017,23, 529–538)


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