Mental fatigue and impaired information processing after mild and moderate traumatic brain injury

Brain Injury ◽  
2009 ◽  
Vol 23 (13-14) ◽  
pp. 1027-1040 ◽  
Author(s):  
Birgitta Johansson ◽  
Peter Berglund ◽  
Lars Rönnbäck
Keyword(s):  
Traumatic Brain Injury ◽  
Information Processing ◽  
Brain Injury ◽  
Mental Fatigue ◽  
Moderate Traumatic Brain Injury

scholarly journals Cognitive deficits in patients with mild to moderate traumatic brain injury

2010 ◽  
Vol 68 (6) ◽  
pp. 862-868 ◽  
Author(s):  
Eliane Correa Miotto ◽  
Fernanda Zanetti Cinalli ◽  
Valéria Trunkl Serrao ◽  
Glaucia Guerra Benute ◽  
Mara Cristina Souza Lucia ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Information Processing ◽  
Brain Injury ◽  
Cognitive Deficits ◽  
Processing Speed ◽  
Visual Memory ◽  
Memory Recall ◽  
Information Processing Speed ◽  
Mild Tbi ◽  
Moderate Traumatic Brain Injury

Traumatic brain injury (TBI) is one of the most frequent causes of brain damage. Cognitive deficits reported in the literature after moderate to severe TBI include memory, language, executive functions, attention and information processing speed impairments. However, systematic studies on patients with mild TBI are scarce although neuropsychological changes are present. OBJECTIVE: To investigate the cognitive functioning of patients with mild to moderate TBI. METHOD: We evaluated 12 patients with mild to moderate TBI using a comprehensive protocol (PN01) of neuropsychological tests. RESULTS: There were significant deficits of episodic memory including immediate and delayed verbal memory recall, verbal recognition, immediate and delayed visual memory recall, naming, verbal fluency and information processing speed. CONCLUSION: These results emphasize the importance of comprehensive neuropsychological assessments even in cases of mild TBI in order to identify impaired and preserved functions providing adequate managing including rehabilitation programs for each case.

scholarly journals 3,6′-Dithiopomalidomide Ameliorates Hippocampal Neurodegeneration, Microgliosis and Astrogliosis and Improves Cognitive Behaviors in Rats with a Moderate Traumatic Brain Injury

2021 ◽  
Vol 22 (15) ◽  
pp. 8276
Author(s):  
Pen-Sen Huang ◽  
Ping-Yen Tsai ◽  
Ling-Yu Yang ◽  
Daniela Lecca ◽  
Weiming Luo ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Short Term Memory ◽  
Post Injury ◽  
Behavioral Deficits ◽  
Cognitive Behaviors ◽  
Moderate Traumatic Brain Injury ◽  
Short And Long Term ◽  
Behavioral Impairments ◽  
Hippocampal Neurodegeneration

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.

Confirmatory factor structure of the Center for Epidemiologic Studies-Depression scale (CES-D) in mild-to-moderate traumatic brain injury

Brain Injury ◽  
2006 ◽  
Vol 20 (5) ◽  
pp. 519-527 ◽  
Author(s):  
Stephen R. McCauley ◽  
Claudia Pedroza ◽  
Sharon A. Brown ◽  
Corwin Boake ◽  
Harvey S. Levin ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Factor Structure ◽  
Depression Scale ◽  
Epidemiologic Studies ◽  
Moderate Traumatic Brain Injury ◽  
Confirmatory Factor

Predictors of deterioration indicating a requirement for surgery in mild to moderate traumatic brain injury

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

Critical Care Resource Utilization and Outcomes of Children With Moderate Traumatic Brain Injury

2017 ◽  
Vol 18 (12) ◽  
pp. 1166-1174 ◽  
Author(s):  
Theerada Chandee ◽  
Vivian H. Lyons ◽  
Monica S. Vavilala ◽  
Vijay Krishnamoorthy ◽  
Nophanan Chaikittisilpa ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Critical Care ◽  
Brain Injury ◽  
Resource Utilization ◽  
Moderate Traumatic Brain Injury ◽  
Critical Care Resource

scholarly journals Enhancement of Neurogenesis and Memory by a Neurotrophic Peptide in Mild to Moderate Traumatic Brain Injury

Neurosurgery ◽  
2014 ◽  
Vol 76 (2) ◽  
pp. 201-215 ◽  
Author(s):  
Muhammad Omar Chohan ◽  
Olga Bragina ◽  
Syed Faraz Kazim ◽  
Gloria Statom ◽  
Narjes Baazaoui ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Dentate Gyrus ◽  
Parietal Cortex ◽  
Saline Solution ◽  
Neuronal Loss ◽  
Synaptic Density ◽  
Moderate Traumatic Brain Injury ◽  
Long Term Treatment ◽  
Newborn Neurons

ABSTRACT BACKGROUND: Traumatic brain injury (TBI) is a risk factor for Alzheimer disease (AD), a neurocognitive disorder with similar cellular abnormalities. We recently discovered a small molecule (Peptide 6) corresponding to an active region of human ciliary neurotrophic factor, with neurogenic and neurotrophic properties in mouse models of AD and Down syndrome. OBJECTIVE: To describe hippocampal abnormalities in a mouse model of mild to moderate TBI and their reversal by Peptide 6. METHODS: TBI was induced in adult C57Bl6 mice using controlled cortical impact with 1.5 mm of cortical penetration. The animals were treated with 50 nmol/d of Peptide 6 or saline solution for 30 days. Dentate gyrus neurogenesis, dendritic and synaptic density, and AD biomarkers were quantitatively analyzed, and behavioral tests were performed. RESULTS: Ipsilateral neuronal loss in CA1 and the parietal cortex and increase in Alzheimer-type hyperphosphorylated tau and A-β were seen in TBI mice. Compared with saline solution, Peptide 6 treatment increased the number of newborn neurons, but not uncommitted progenitor cells, in dentate gyrus by 80%. Peptide 6 treatment also reversed TBI-induced dendritic and synaptic density loss while increasing activity in tri-synaptic hippocampal circuitry, ultimately leading to improvement in memory recall on behavioral testing. CONCLUSION: Long-term treatment with Peptide 6 enhances the pool of newborn neurons in the dentate gyrus, prevents neuronal loss in CA1 and parietal cortex, preserves the dendritic and synaptic architecture in the hippocampus, and improves performance on a hippocampus-dependent memory task in TBI mice. These findings necessitate further inquiry into the therapeutic potential of small molecules based on neurotrophic factors.

Reconstruction of Identity After Brain Injury

2000 ◽  
Vol 1 (1) ◽  
pp. 12-28 ◽  
Author(s):  
Mark Ylvisaker ◽  
Timothy Feeney
Keyword(s):  
Traumatic Brain Injury ◽  
Information Processing ◽  
Brain Injury ◽  
Personal Identity ◽  
Positive Sense ◽  
Potential Contributor ◽  
Behavioural Adjustment ◽  
The Impact ◽  
Instructive Case ◽  
Processing Framework

AbstractFollowing severe traumatic brain injury, difficulty with behavioural adjustment and community reintegration is common. A potential contributor to this difficulty is a sense of personal identity that is inconsistent with the restrictions on activity and need for effortful compensation imposed by persistent impairment. We summarise an information processing framework within which the impact of schematic mental models of self is explained and present intervention procedures designed to help individuals with traumatic brain injury reconstruct an organised and positive sense of personal identity. We conclude the paper with three instructive case illustrations.

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