Neuroplasticity for spontaneous functional recovery after neonatal hypoxic ischemic brain injury in rats observed by functional MRI and diffusion tensor imaging

NeuroImage ◽  
2016 ◽  
Vol 126 ◽  
pp. 140-150 ◽  
Author(s):  
Won-Beom Jung ◽  
Geun Ho Im ◽  
Julius Juhyun Chung ◽  
So-Yoon Ahn ◽  
Tae Yeon Jeon ◽  
...  
2012 ◽  
Vol 528 (1) ◽  
pp. 16-21 ◽  
Author(s):  
Ah Young Lee ◽  
Dong-Gu Shin ◽  
Jong-Seon Park ◽  
Geu Ru Hong ◽  
Pyung-Hun Chang ◽  
...  

2021 ◽  
Author(s):  
SungHO Jang ◽  
YOUSUNG SEO

Abstract Objectives We investigated the relationship between cingulum injury and impaired consciousness in patients with hypoxic-ischemic brain injury (HI-BI) by using diffusion tensor tractography (DTT). Methods We recruited 29 patients with HI-BI and 25 normal control subjects. The patients were classified as intact consciousness (group A, 13 patients) or impaired consciousness (group B, 16 patients). The DTT parameters of fractional anisotropy (FA) and tract volume (TV) were estimated for both cinguli. Glasgow Coma Scale (GCS) and Coma Recovery Scale-Revised (CRS-R) scores were also evaluated. Results The FA and TV values of the cinguli in groups A and B were lower than those of the control group (p < 0.05), and the FA and TV values of group B were lower than those of group A (p < 0.05). The FA and TV values of the cinguli in group A were not significantly correlated with GCS and CRS-R scores (p > 0.05); however, regarding the group B, the FA correlations with GCS (r = 0.457, p < 0.05) and CRS-R (r = 0.494, p < 0.05) and those of TV with GCS (r = 0.500, p < 0.05) and CRS-R (r = 0.491, p < 0.05) were moderately positive. Conclusions We found a significant relationship between injury of the cingulum and impaired consciousness in patients with HI-BI. Our results suggest that an injured cingulum could be an appropriate target for neurointervention or neurorehabilitation in patients with impaired consciousness following HI-BI.


2008 ◽  
Vol 28 (7) ◽  
pp. 1294-1306 ◽  
Author(s):  
Joshua D Koch ◽  
Darryl K Miles ◽  
Jennifer A Gilley ◽  
Cui-Ping Yang ◽  
Steven G Kernie

Patterns of hypoxic-ischemic brain injury in infants and children suggest vulnerability in regions of white matter development, and injured patients develop defects in myelination resulting in cerebral palsy and motor deficits. Reperfusion exacerbates the oxidative stress that occurs after such injuries and may impair recovery. Resuscitation after hypoxic-ischemic injury is routinely performed using 100% oxygen, and this practice may increase the oxidative stress that occurs during reperfusion and further damage an already compromised brain. We show that brief exposure (30 mins) to 100% oxygen during reperfusion worsens the histologic injury in young mice after unilateral brain hypoxia—ischemia, causes an accumulation of the oxidative metabolite nitrotyrosine, and depletes preoligodendrocyte glial progenitors present in the cortex. This damage can be reversed with administration of the antioxidant ebselen, a glutathione peroxidase mimetic. Moreover, mice recovered in 100% oxygen have a more disrupted pattern of myelination and develop a static motor deficit that mimics cerebral palsy and manifests itself by significantly worse performance on wire hang and rotorod motor testing. We conclude that exposure to 100% oxygen during reperfusion after hypoxic-ischemic brain injury increases secondary neural injury, depletes developing glial progenitors, interferes with myelination, and ultimately impairs functional recovery.


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