Cognitive Deficits and Inflammatory Response Resulting from Mild-to-Moderate Traumatic Brain Injury in Rats Are Exacerbated by Repeated Pre-Exposure to an Innate Stress Stimulus

2017 ◽  
Vol 34 (8) ◽  
pp. 1645-1657 ◽  
Author(s):  
Michaël Ogier ◽  
Amor Belmeguenai ◽  
Thomas Lieutaud ◽  
Béatrice Georges ◽  
Sandrine Bouvard ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Inflammatory Response ◽  
Cognitive Deficits ◽  
Moderate Traumatic Brain Injury

scholarly journals Importance of Posttraumatic Hypothermia and Hyperthermia on the Inflammatory Response after Fluid Percussion Brain Injury: Biochemical and Immunocytochemical Studies

2000 ◽  
Vol 20 (3) ◽  
pp. 531-542 ◽  
Author(s):  
Katina Chatzipanteli ◽  
Ofelia F. Alonso ◽  
Susan Kraydieh ◽  
W. Dalton Dietrich
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Inflammatory Response ◽  
Cortical Region ◽  
Myeloperoxidase Activity ◽  
Fluid Percussion ◽  
Moderate Traumatic Brain Injury ◽  
Activity Temperature ◽  
Series Of Experiments ◽  
Subcortical Regions

The purpose of this study was to investigate: 1) the temporal and regional profile of polymorphonuclear leukocyte (PMNL) infiltration after moderate traumatic brain injury using the parasagittal fluid percussion model and 2) the effects of posttraumatic hypothermia (30°C) and hyperthermia (39°C) on the acute and subacute inflammatory response. We hypothesized that posttraumatic hypothermia would reduce the degree of PMNL accumulation whereas hyperthermia would exacerbate this response to injury. In the first series of experiments we quantitated the temporal profile of altered myeloperoxidase activity under normothermic (37°C) conditions (n = 20). The rats were allowed to survive for 3 hours, 24 hours, 3 days, or 7 days after trauma, and brains were dissected into cortical and subcortical regions ipsilateral and contralateral to injury. Additional animals were perfused and fixed for the immunocytochemical visualization of myeloperoxidase (n = 15). In the second series of experiments, rats (n = 25) were killed 3 hours or 3 days after the 3-hour monitoring period of normothermia (36.5°C), hypothermia (30°C), or hyperthemia (39°C) (n = 4 to 5 per group), and myeloperoxidase activity was again quantitated. In normothermic rats, the enzymatic activity of myeloperoxidase was significantly increased ( P < 0.05) at 3 hours within the anterior cortical segment (213.97 ± 56.2 versus control 65.5 ± 52.3 U/g of wet tissue; mean ± SD) and posterior (injured) cortical and subcortical segments compared to shamoperated rats (305.76 ± 27.8 and 258.67 ± 101.4 U/g of wet tissue versus control 62.8 ± 24.8 and 37.28 ± 35.6 U/g of wet tissue; P < 0.0001, P < 0.05, respectively). At 24 hours and 7-days after trauma only the posterior cortical region ( P < 0.005, P < 0.05, respectively) exhibited increased myeloperoxidase activity. However, 3 days after trauma, myeloperoxidase activity was also significantly increased within the anterior cortical segment ( P < 0.05) and in posterior cortical and subcortical regions compared to sham-operated cortex ( P < 0.0001, P < 0.05, respectively). Immunocytochemical analysis of myeloperoxidase reactivity at 3 hours, 24 hours, 3- and 7-days demonstrated large numbers of immunoreactive leukocytes within and associated with blood vessels, damaged tissues, and subarachnoid spaces. Posttraumatic hypothermia and hyperthermia had significant effects on myeloperoxidase activity at both 3 hours and 3 days after traumatic brain injury. Posttraumatic hypothermia reduced myeloperoxidase activity in the injured and noninjured cortical and subcortical segments compared to normothermic values ( P < 0.05). In contrast, posttraumatic hyperthermia significantly elevated myeloperoxidase activity in the posterior cortical region compared to normothermic values at both 3 hours and 3 days (473.5 ± 258.4 and 100.11 ± 27.58 U/g of wet tissue, respectively, P < 0.05 versus controls). These results indicate that posttraumatic hypothermia decreases early and more prolonged myeloperoxidase activation whereas hyperthermia increases myeloperoxidase activity. Temperature-dependent alterations in PMNL accumulation appear to be a potential mechanism by which posttraumatic temperature manipulations may influence traumatic outcome.

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.

In search of the ‘self’: Holistic rehabilitation in restoring cognition and recovering the ‘self’ following traumatic brain injury: A case report

2021 ◽  
pp. 1-12
Author(s):  
Meenakshi Banerjee ◽  
Shantala Hegde ◽  
T Harish ◽  
Girish B. Kulkarni ◽  
Narasinga Rao
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Cognitive Deficits ◽  
Emotional Regulation ◽  
Anterograde Amnesia ◽  
Depression Score ◽  
The Self ◽  
Future Research ◽  
Post Injury ◽  
Moderate Traumatic Brain Injury

BACKGROUND: Following mild-moderate traumatic brain injury (TBI), an individual experiences a range of emotional changes. It is often difficult for the patient to reconcile with their post-injury persona, and the memory of pre-injury personhood is particularly painful. Insight into one’s cognitive deficits subsequent to injury can lead to an existential crisis and a sense of loss, including loss of self. OBJECTIVE: Restoration of cognitive functions and reconciliation with loss of pre-traumatic personhood employing a holistic method of neuropsychological rehabilitation in a patient suffering from TBI. METHODS: Ms. K.S, a 25-year-old girl, presented with emotional disturbances following TBI. She reported both retrograde and anterograde amnesia. A multidimensional holistic rehabilitation was planned. Treatment addressed cognitive deficits through the basic functions approach. Cognitive behavioural methods for emotional regulation like diary writing helped reduce irritability and anger outbursts. Use of social media created new modes of memory activation and interactions. Compensatory strategies were used to recover lost skills, music based attention training helped foster an individualised approach to the sense of one’s body and self. RESULTS: As a result of these differing strategies, changes were reflected in neuro-psychological tests, depression score and the patient’s self-evaluation. This helped generate a coherent self-narrative. CONCLUSION: Treatment challenges in such cases are increased due to patient’s actual deficits caused by neuronal/biochemical changes. Innovative and multi-pronged rehabilitation strategies which involve everyday activities provided an answer to some of these problems. This method of rehabilitation may provide an optimistic context for future research.

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.

scholarly journals Influence of Glutamine on Intestinal Inflammatory Response, Mucosa Structure Alterations and Apoptosis following Traumatic Brain Injury in Rats

2007 ◽  
Vol 35 (5) ◽  
pp. 644-656 ◽  
Author(s):  
D Feng ◽  
W Xu ◽  
G Chen ◽  
C Hang ◽  
H Gao ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Inflammatory Response ◽  
Intestinal Inflammation ◽  
Glutamine Supplementation ◽  
Intercellular Adhesion Molecule ◽  
Intercellular Adhesion Molecule 1 ◽  
Tissue Samples ◽  
Weight Drop ◽  
Factor Α

Traumatic brain injury (TBI) can induce a persistent inflammatory response, histopathological changes and apoptosis in the intestine. Glutamine has been shown to reduce bacterial translocation and maintain intestine mucosal integrity, but its effects on the inflammatory response, structural alterations and apoptosis in intestinal mucosa following TBI have not been previously investigated. Using the weight-drop method, a right parietal cortical contusion was induced in rats and, for the next 5 days, they were fed either chow alone or chow mixed with glutamine. Intestinal tissue samples were then removed for analysis. Following TBI, glutamine supplementation was found to: decrease intestinal concentrations of interleukin (IL) −1β, tumour necrosis factor-α (TNF-α) and IL-6; downregulate intercellular adhesion molecule-1 (ICAM-1) expression; attenuate TBI-induced damage to the intestine structure; and reduce apoptosis. These results suggest that post-TBI glutamine administration could suppress intestinal inflammation, protect intestinal mucosal structure and reduce mucosal apoptosis.

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
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