scholarly journals Decreased Fractional Anisotropy Evaluated Using Tract-Based Spatial Statistics and Correlated with Cognitive Dysfunction in Patients with Mild Traumatic Brain Injury in the Chronic Stage

2012 ◽  
Vol 33 (11) ◽  
pp. 2117-2122 ◽  
Author(s):  
T. Wada ◽  
Y. Asano ◽  
J. Shinoda
Brain Injury ◽  
2008 ◽  
Vol 22 (2) ◽  
pp. 115-122 ◽  
Author(s):  
Laura Miles ◽  
Robert I. Grossman ◽  
Glyn Johnson ◽  
James S. Babb ◽  
Leonard Diller ◽  
...  

2020 ◽  
Author(s):  
Xiaoyan Jia ◽  
Xuebin Chang ◽  
Lijun Bai ◽  
Yulin Wang ◽  
Debo Dong ◽  
...  

AbstractThe mild traumatic brain injury (mTBI) results in traumatic axonal injury, which damages the long-distance white matter (WM) connections and thus disrupts the functional connectome of large-scale brain networks that support cognitive function. Patterns of WM structural damage following mTBI were well documented using diffusion tensor imaging, however, the functional organization of WM and its association with grey matter functional networks (GM-FNs) and cognitive assessments remains unknown. The present study adopted resting-state functional magnetic resonance imaging to explore WM functional properties in mTBI patients (113 acute patients, 56 chronic patients, 47 healthy controls (HCs)). Eleven large-scale WM functional networks (WM-FNs) were constructed by the k-means clustering algorithm which carried out in voxel-wise WM functional connectivity (FC). Compared to HCs, acute mTBI patients showed enhanced FC between inferior fronto-occipital fasciculus (IFOF) WM-FN and primary sensorimotor WM-FNs, and cortical primary sensorimotor GM-FNs. And FC between IFOF WM-FN and anterior cerebellar GM-FN was positively correlated with information processing speed. Moreover, all of these WM-FNs abnormalities were returned to the normal level at the chronic stage. Our findings suggest the compensatory mechanism of cognitive deficits in the acute stage and its involvement in facilitating recovery from cognitive deficits in the chronic stage. The convergent damage of the IFOF network highlighted its key role in our understanding of the pathophysiology mechanism of mTBI patients and thus might be regarded as a biomarker in the acute stage and a potential indicator of treatment effect.


2021 ◽  
Vol 15 ◽  
Author(s):  
Suna Huang ◽  
Su Li ◽  
Hua Feng ◽  
Yujie Chen

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.


Neurology ◽  
2014 ◽  
Vol 83 (6) ◽  
pp. 494-501 ◽  
Author(s):  
I. D. Croall ◽  
C. J. A. Cowie ◽  
J. He ◽  
A. Peel ◽  
J. Wood ◽  
...  

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