scholarly journals Regional Differences in Susceptibility to Hypoxic-Ischemic Injury in the Preterm Brain: Exploring the Spectrum from White Matter Loss to Selective Grey Matter Injury in a Rat Model

2012 ◽  
Vol 2012 ◽  
pp. 1-11 ◽  
Author(s):  
D. B. Selip ◽  
L. L. Jantzie ◽  
M. Chang ◽  
M. C. Jackson ◽  
E. C. Fitzgerald ◽  
...  
Keyword(s):  
Brain Injury ◽  
White Matter ◽  
Rat Model ◽  
Grey Matter ◽  
Very Low Birth Weight ◽  
Neuronal Degeneration ◽  
Periventricular Leukomalacia ◽  
White Matter Injury ◽  
Injury Patterns ◽  
Grey Matter Injury

Models of premature brain injury have largely focused on the white matter injury thought to underlie periventricular leukomalacia (PVL). However, with increased survival of very low birth weight infants, injury patterns involving grey matter are now recognized. We aimed to determine how grey matter lesions relate to hypoxic-ischemic- (HI) mediated white matter injury by modifying our rat model of PVL. Following HI, microglial infiltration, astrocytosis, and neuronal and axonal degeneration increased in a region-specific manner dependent on the severity of myelin loss in pericallosal white matter. The spectrum of injury ranged from mild, where diffuse white matter abnormalities were dominant and were associated with mild axonal injury and local microglial activation, to severe HI injury characterized by focal MBP loss, widespread neuronal degeneration, axonal damage, and gliosis throughout the neocortex, caudate putamen, and thalamus. In sum, selective regional white matter loss occurs in the preterm rat concomitantly with a clinically relevant spectrum of grey matter injury. These data demonstrate an interspecies similarity of brain injury patterns and further substantiates the reliable use of this model for the study of preterm brain injury.

scholarly journals Diffusion Tensor Imaging Reveals White Matter Injury in a Rat Model of Repetitive Blast-Induced Traumatic Brain Injury

2014 ◽  
Vol 31 (10) ◽  
pp. 938-950 ◽  
Author(s):  
Evan Calabrese ◽  
Fu Du ◽  
Robert H. Garman ◽  
G. Allan Johnson ◽  
Cory Riccio ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Diffusion Tensor Imaging ◽  
Brain Injury ◽  
White Matter ◽  
Rat Model ◽  
Diffusion Tensor ◽  
White Matter Injury

scholarly journals NMDA Receptor Blockade with Memantine Attenuates White Matter Injury in a Rat Model of Periventricular Leukomalacia

2008 ◽  
Vol 28 (26) ◽  
pp. 6670-6678 ◽  
Author(s):  
S. M. Manning ◽  
D. M. Talos ◽  
C. Zhou ◽  
D. B. Selip ◽  
H.-K. Park ◽  
...  
Keyword(s):  
White Matter ◽  
Nmda Receptor ◽  
Rat Model ◽  
Periventricular Leukomalacia ◽  
White Matter Injury ◽  
Receptor Blockade ◽  
Nmda Receptor Blockade

scholarly journals GPR18 Agonist Resolvin D2 Reduces the Early Brain Injury in A Rat Model of Subarachnoid Hemorrhage by Multi-Mechanisms of Protection

2021 ◽  
Author(s):  
Tongyu Zhang ◽  
Gang Zuo ◽  
Hongqi Zhang
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Brain Injury ◽  
White Matter ◽  
Western Blot ◽  
Rat Model ◽  
Time Course ◽  
Early Brain Injury ◽  
Brain Regions ◽  
White Matter Injury ◽  
Tnf Α

Abstract Background Early brain injury (EBI) is the early phase of secondary complications resulted in poor prognosis of subarachnoid hemorrhage (SAH). GPR18 is a G protein-coupled receptor which has been reported for neuroprotection in ischemia. In this study, we aimed to use resolvin D2 (RvD2) as an agonist to investigate the roles of GPR18 in different brain regions during EBI. Methods Location and time course of GPR18 after SAH were measured with immunofluorescence and western blot in endovascular perforation rat model. RvD2 was given one hour intranasally post-SAH, and SAH grades, neurobehavior and brain water content tests were performed after 24 hours. TUNEL and DHE staining were measured 24 hours post-SAH in cortex. Immunofluorescence, western blot and immunohistochemistry of proteins related to EBI in different brain regions were also performed. Results We found GPR18 mainly located in meninges, hypothalamus, cortex and white matter. And GPR18 expression increased in meninges and hypothalamus after EBI, however, it decreased in cortex and white matter. RvD2 could improve neurological scores and brain edema. Mast cell degranulation was attenuated, Chymase and Typtase expression decreased after RvD2 administration in meninges. RvD2 attenuated inflammation with increase of POMC, IL-10 and decrease of NPY, TNF-α in hypothalamus. In cortex, RvD2 alleviated oxidative stress and apoptosis, protected blood-brain barrier. RvD2 also ameliorated white matter injury by MBP elevation and APP depression. Conclusions Current results emphasized the importance of GPR18 in the whole brain during EBI. Upregulation of GPR18 with RvD2 may improve neurological functions with multi-mechanisms in different brain regions.

scholarly journals Brain Magnetic Resonance Imaging Pattern in Cerebral Palsy

2021 ◽  
Author(s):  
Prastiya Indra Gunawan ◽  
Riza Noviandi ◽  
Sunny Mariana Samosir
Keyword(s):  
Magnetic Resonance Imaging ◽  
Cerebral Palsy ◽  
White Matter ◽  
Magnetic Resonance ◽  
Disease Severity ◽  
Grey Matter ◽  
White Matter Injury ◽  
Control Group ◽  
Resonance Imaging ◽  
Grey Matter Injury

Abstract Background Cerebral palsy (CP) leads to a common static motor neurological disease in children that can be demonstrated with varied neuroimaging findings. Magnetic Resonance Imaging (MRI) has a vital role of determining the presence of brain injury and its extent, with any possibility of determining pathogenic pattern and disease severity. The objective of the study is to evaluate the neuroimaging findings in CP and their correlation to disease severity. Method The research was case-control study, consecutive and complete records of all patients who had a clinical diagnosis of CP and performed a head MRI between 2018 and 2019 were enrolled in this study. Cases group were children diagnosed as severe CP with The Gross Motor Function Classification System (GMFCS) IV-V. Control group were children confirmed as CP with GMFCS I-III. Brain imaging was examined by MRI, in which the abnormalities were classified into grey matter or white matter injury, focal vascular disorder and brain malformation. Kruskal-Wallis statistical analysis was applied to identify the correlation. Results Almost 60 cases were reviewed. White matter injury, malformation and focal vascular insult were not correlated significantly to CP severity (OR = 0.73; 95% CI = 0.2-2.2; p = 0.78 and OR = 0.61; 95% CI = 0.2-1.9; p = 0.57 and OR = 2.034; 95% CI = 0.51-0.76; p = 0.63, respectively). Grey matter injury was more frequent discovered in severe CP (50%) and increased the risk of CP severity (OR = 9; 95% CI = 2.2 – 36; p = 0.002). Conclusion Grey matter injury is considered the most frequent abnormalities of Brain MRI in CP and it could increase the risk of severity.

scholarly journals Chloride cotransporter NKCC1 inhibitor bumetanide protects against white matter injury in a rodent model of periventricular leukomalacia

2015 ◽  
Vol 77 (4) ◽  
pp. 554-562 ◽  
Author(s):  
Lauren L. Jantzie ◽  
Melody Y. Hu ◽  
Hyun-Kyung Park ◽  
Michele C. Jackson ◽  
Jenny Yu ◽  
...  
Keyword(s):  
White Matter ◽  
Periventricular Leukomalacia ◽  
Rodent Model ◽  
White Matter Injury

scholarly journals White Matter Injury in Early Brain Injury after Subarachnoid Hemorrhage

2018 ◽  
Vol 28 (1) ◽  
pp. 26-35 ◽  
Author(s):  
Jinwei Pang ◽  
Jianhua Peng ◽  
Ping Yang ◽  
Li Kuai ◽  
Ligang Chen ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Brain Injury ◽  
White Matter ◽  
Early Brain Injury ◽  
Therapeutic Strategies ◽  
White Matter Injury ◽  
High Morbidity ◽  
Normal Brain ◽  
Neurological Outcomes ◽  
Multiple Substrates

Subarachnoid hemorrhage (SAH) is a major cause of high morbidity, disability, and mortality in the field of neurovascular disease. Most previous SAH studies have focused on improving cerebral blood flow, reducing cerebral vasospasm, reducing neuronal calcium overload, and other treatments. While these studies showed exciting findings in basic science, therapeutic strategies based on the findings have not significantly improved neurological outcomes in patients with SAH. Currently, the only drug proven to effectively reduce the neurological defects of SAH patients is nimodipine. Current advances in imaging technologies in the field of stroke have confirmed that white matter injury (WMI) plays an important role in the prognosis of types of stroke, and suggests that WMI protection is essential for functional recovery and poststroke rehabilitation. However, WMI injury in relation to SAH has remained obscure until recently. An increasing number of studies suggest that the current limitations for SAH treatment are probably linked to overlooked WMI in previous studies that focused only on neurons and gray matter. In this review, we discuss the biology and functions of white matter in the normal brain, and discuss the potential pathophysiology and mechanisms of early brain injury after SAH. Our review demonstrates that WMI encompasses multiple substrates, and, therefore, more than one pharmacological approach is necessary to preserve WMI and prevent neurobehavioral impairment after SAH. Strategies targeting both neuronal injury and WMI may potentially provide a novel future for SAH knowledge and treatment.

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