scholarly journals Chronic Cognitive and Cerebrovascular Function Following Mild Traumatic Brain Injury in Rats

2022 ◽  
Author(s):  
Daniel R. Griffiths ◽  
L. Matthew Law ◽  
Conor Young ◽  
Alberto Fuentes ◽  
Seth Truran ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Smooth Muscle ◽  
Object Recognition ◽  
Brain Injury ◽  
Angiotensin Ii ◽  
Cognitive Dysfunction ◽  
Mild Tbi ◽  
Novel Object ◽  
Cerebrovascular Function

Severe traumatic brain injury results in cognitive dysfunction in part due to vascular perturbations. In contrast, the long-term vasculo-cognitive pathophysiology of mild TBI (mTBI) remains unknown. We evaluated mTBI effects on chronic cognitive and cerebrovascular function and assessed their interrelationships. Sprague-Dawley rats received midline fluid percussion injury (N=20) or sham (N=21). Cognitive function was assessed (3- and 6-month novel object recognition (NOR), novel object location (NOL) and temporal order object recognition (TOR)). 6-month cerebral blood flow (CBF) and blood volume (CBV) using contrast MRI and ex vivo pial artery endothelial and smooth muscle-dependent function were measured. mTBI rats showed impaired NOR, with similar (non-significant) trends in NOL/TOR. Regional CBF and CBV were similar in sham and mTBI. NOR correlated with CBF in lateral hippocampus, medial hippocampus and primary somatosensory barrel cortex while inversely correlating with arterial smooth muscle-dependent dilation. 6-month baseline endothelial and smooth muscle-dependent arterial function were similar among mTBI and sham, but post-angiotensin II stimulation, mTBI showed no change in smooth muscle-dependent dilation from baseline response, unlike the reduction in sham. mTBI led to chronic cognitive dysfunction and altered angiotensin II-stimulated smooth muscle-dependent vasoreactivity, a paradigm that could advance understanding of the long-term sequelae of human mild TBI.

scholarly journals Repetitive Mild Traumatic Brain Injury in Rats Impairs Cognition, Enhances Prefrontal Cortex Neuronal Activity, and Reduces Pre-synaptic Mitochondrial Function

2021 ◽  
Vol 15 ◽  
Author(s):  
Yin Feng ◽  
Keguo Li ◽  
Elizabeth Roth ◽  
Dongman Chao ◽  
Christina M. Mecca ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Prefrontal Cortex ◽  
Object Recognition ◽  
Brain Injury ◽  
Neuronal Activity ◽  
Home Cage ◽  
Novel Object Recognition ◽  
Novel Object ◽  
Closed Head

A major hurdle preventing effective interventions for patients with mild traumatic brain injury (mTBI) is the lack of known mechanisms for the long-term cognitive impairment that follows mTBI. The closed head impact model of repeated engineered rotational acceleration (rCHIMERA), a non-surgical animal model of repeated mTBI (rmTBI), mimics key features of rmTBI in humans. Using the rCHIMERA in rats, this study was designed to characterize rmTBI-induced behavioral disruption, underlying electrophysiological changes in the medial prefrontal cortex (mPFC), and associated mitochondrial dysfunction. Rats received 6 closed-head impacts over 2 days at 2 Joules of energy. Behavioral testing included automated analysis of behavior in open field and home-cage environments, rotarod test for motor skills, novel object recognition, and fear conditioning. Following rmTBI, rats spent less time grooming and less time in the center of the open field arena. Rats in their home cage had reduced inactivity time 1 week after mTBI and increased exploration time 1 month after injury. Impaired associative fear learning and memory in fear conditioning test, and reduced short-term memory in novel object recognition test were found 4 weeks after rmTBI. Single-unit in vivo recordings showed increased neuronal activity in the mPFC after rmTBI, partially attributable to neuronal disinhibition from reduced inhibitory synaptic transmission, possibly secondary to impaired mitochondrial function. These findings help validate this rat rmTBI model as replicating clinical features, and point to impaired mitochondrial functions after injury as causing imbalanced synaptic transmission and consequent impaired long-term cognitive dysfunction.

scholarly journals Alteration of FDG uptake by performing novel object recognition task in a rat model of Traumatic Brain Injury

NeuroImage ◽  
2019 ◽  
Vol 188 ◽  
pp. 419-426
Author(s):  
Shalini Jaiswal ◽  
Nicole Hockenbury ◽  
Hongna Pan ◽  
Andrew Knutsen ◽  
Bernard J. Dardzinski ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Object Recognition ◽  
Brain Injury ◽  
Rat Model ◽  
Recognition Task ◽  
Novel Object Recognition ◽  
Novel Object ◽  
Fdg Uptake ◽  
Object Recognition Task ◽  
Novel Object Recognition Task

scholarly journals AN ANALYSIS OF TRAUMATIC BRAIN INJURY [TBI] IN TERMS OF 3-MONTH GLASGOW OUTCOME SCORE [GOS] AT A TERTIARY CARE CENTRE

2021 ◽  
pp. 13-15
Author(s):  
Shrikant Govindrao Palekar ◽  
Kailash K Mogal ◽  
Vedanti Rajesh Patil ◽  
I Vijay Sundar
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Clinical Features ◽  
Tertiary Care ◽  
Glasgow Outcome Score ◽  
Tertiary Care Centre ◽  
Mild Tbi ◽  
Outcome Score ◽  
Severe Tbi

INTRODUCTION - Traumatic brain injury [TBI] most affects the working population and their earning capacity. The various sub categories of TBI in terms of clinical features,Glasgow coma scale [GCS] and radiology are well defined.We have attempted an analysis in terms of long term Glasgow outcome score [GOS] and tried to correlate with the various factors of TBI. MATERIALS AND METHODS – All patients of TBI over 12 years and below 60 years and those without other major trauma were included over a period of about two years. The clinical features, presentation GCS, treatment given, and outcomes were assessed.The three month GOS was scored for all patients and was used to analyse the the initial data in its light. RESULTS – A total of 200 patients were eligible for the study and were included. Of these 159 were males and 41 were females.The average age was 37.16 years.There was a relatively higher proportion of mild TBI and greater prevalence of fractures and EDH [extradural hematoma].On analyzing with three month GOS we found that 90.4 % of the patients with mild TBI had a three month GOS of 5 whereas only 31.9% of patients with moderate or severe TBI had a three month GOS of 5. CONCLUSION – The long term GOS is most representative of the extent to which the patient has been able to return to their pre TBI lives. In our study the three month GOS co related well with the initial GCS. Further prospective data can elaborate more on the effect of other clinical features and radiology on long term GOS

scholarly journals Iron Metabolism Disorders for Cognitive Dysfunction After Mild Traumatic Brain Injury

2021 ◽  
Vol 15 ◽  
Author(s):  
Suna Huang ◽  
Su Li ◽  
Hua Feng ◽  
Yujie Chen
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Cognitive Dysfunction ◽  
Mild Traumatic Brain Injury ◽  
Neurological Diseases ◽  
Nerve Fibers ◽  
Iron Deposition ◽  
Neural Cells ◽  
Initial Symptoms

Traumatic brain injury (TBI) is one of the most harmful forms of acute brain injury and predicted to be one of the three major neurological diseases that cause neurological disabilities by 2030. A series of secondary injury cascades often cause cognitive dysfunction of TBI patients leading to poor prognosis. However, there are still no effective intervention measures, which drive us to explore new therapeutic targets. In this process, the most part of mild traumatic brain injury (mTBI) is ignored because its initial symptoms seemed not serious. Unfortunately, the ignored mTBI accounts for 80% of the total TBI, and a large part of the patients have long-term cognitive dysfunction. Iron deposition has been observed in mTBI patients and accompanies the whole pathological process. Iron accumulation may affect long-term cognitive dysfunction from three pathways: local injury, iron deposition induces tau phosphorylation, the formation of neurofibrillary tangles; neural cells death; and neural network damage, iron deposition leads to axonal injury by utilizing the iron sensibility of oligodendrocytes. Thus, iron overload and metabolism dysfunction was thought to play a pivotal role in mTBI pathophysiology. Cerebrospinal fluid-contacting neurons (CSF-cNs) located in the ependyma have bidirectional communication function between cerebral–spinal fluid and brain parenchyma, and may participate in the pathway of iron-induced cognitive dysfunction through projected nerve fibers and transmitted factor, such as 5-hydroxytryptamine, etc. The present review provides an overview of the metabolism and function of iron in mTBI, and to seek a potential new treatment target for mTBI with a novel perspective through combined iron and CSF-cNs.

Do Mild Traumatic Brain Injury Severity Sub-classification Systems Help to Identify People Who Go on to Experience Long-Term Symptoms?

2017 ◽  
Vol 19 (2) ◽  
pp. 119-132
Author(s):  
Alice Theadom ◽  
Suzanne Barker-Collo ◽  
Andrea Greenwood ◽  
Priya Parmar ◽  
Kelly Jones ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Mild Traumatic Brain Injury ◽  
Classification System ◽  
Injury Severity ◽  
Contextual Factors ◽  
Classification Systems ◽  
Post Injury ◽  
Mild Tbi

Objective: To identify the systems available to sub-classify mild traumatic brain injury (TBI) and to determine their utility in predicting 1-year outcome.Methods: A systematic review to identify mild-TBI sub-classification systems was conducted until March 2016. The identified systems were applied to a cohort ofN= 290 adults who had experienced a mild-TBI, and who had been assessed for post-concussion symptoms 1-year post injury. ANOVAs and regression models were used to determine whether each sub-classification system could distinguish between outcomes and to explore their contribution to explaining variance in post-concussion symptoms 1-year post injury.Results: Nineteen sub-classification systems for mild-TBI met the inclusion criteria for this review. The Saal (1991) classification system significantly differentiated the experience of post-concussion symptoms in our cohort 1-year post injury (F= 2.39,p= 0.05). However, the findings did not remain significant following correction for multiple comparisons and inclusion of socio-demographic and contextual factors in the regression model.Conclusions: Current sub-classification systems fail to explain much of the variance in post-concussion symptoms 1 year following mild-TBI. Further research is needed to identify the factors (including socio-demographic and contextual factors) to determine, who may be at risk of developing persistent post-concussion symptoms.

Traumatic Brain Injury: A Trauma Surgeon's Perspective

2012 ◽  
Vol 22 (3) ◽  
pp. 82-89
Author(s):  
Oscar D. Guillamondegui
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Multidisciplinary Approach ◽  
Trauma Team ◽  
The United States ◽  
Long Term Outcomes ◽  
Term Care ◽  
Injured Brain ◽  
The Moment

Traumatic brain injury (TBI) is a serious epidemic in the United States. It affects patients of all ages, race, and socioeconomic status (SES). The current care of these patients typically manifests after sequelae have been identified after discharge from the hospital, long after the inciting event. The purpose of this article is to introduce the concept of identification and management of the TBI patient from the moment of injury through long-term care as a multidisciplinary approach. By promoting an awareness of the issues that develop around the acutely injured brain and linking them to long-term outcomes, the trauma team can initiate care early to alter the effect on the patient, family, and community. Hopefully, by describing the care afforded at a trauma center and by a multidisciplinary team, we can bring a better understanding to the armamentarium of methods utilized to treat the difficult population of TBI patients.

Prosodic Impairment Associated With Traumatic Brain Injury

2009 ◽  
Vol 19 (3) ◽  
pp. 97-102
Author(s):  
Billy Irwin
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Detailed Analysis ◽  
Acoustic Characteristics ◽  
Individual Variations

Abstract Purpose: This article discusses impaired prosody production subsequent to traumatic brain injury (TBI). Prosody may affect naturalness and intelligibility of speech significantly, often for the long term, and TBI may result in a variety of impairments. Method: Intonation, rate, and stress production are discussed in terms of the perceptual, physiological, and acoustic characteristics associated with TBI. Results and Conclusions: All aspects of prosodic production are susceptible to the effects of damage resulting from TBI. There are commonly associated prosodic impairments; however, individual variations in specific aspects of prosody require detailed analysis.

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