Long-Term Deficits Following Cerebral Hypoxia–Ischemia in Four-Week-Old Rats: Correspondence between Behavioral, Histological, and Magnetic Resonance Imaging Assessments

Tuor, Ursula I.; Hudzik, Thomas J.; Malisza, Krisztina L.; Sydserff, S G; Kozłowski, Piotr; Bigio, Marc R. Del

doi:10.1006/exnr.2000.7565

Cited by 21 publications

(14 citation statements)

References 33 publications

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“…Brain activity slowly recovered but was still significantly suppressed up to 1 day after 10 minutes of cardiac arrest, despite normal CO 2 responsiveness and recovery of the tissue water ADC. Changes in limb stimulation-induced brain activation patterns have also been reported after unilateral MCA occlusion (Reese et al, 2000), unilateral CCA occlusion plus 30 minutes hypoxia (Tuor et al, 2001), and photothrombotic lesioning of the sensorimotor cortex in rats (Abo et al, 2001). Loss of brain activation responses in the forelimb region of the sensorimotor cortex after focal cerebral ischemia in rats occurred despite relatively mild tissue and perfusion impairment and normal cerebrovascular reactivity (Dijkhuizen et al, 2001b;Reese et al, 2000).…”

Section: Functional Magnetic Resonance Imagingmentioning

confidence: 83%

Magnetic Resonance Imaging in Experimental Models of Brain Disorders

Dijkhuizen

Nicolay

2003

J Cereb Blood Flow Metab

127

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Summary:This review gives an overview of the application of magnetic resonance imaging (MRI) in experimental models of brain disorders. MRI is a noninvasive and versatile imaging modality that allows longitudinal and three-dimensional assessment of tissue morphology, metabolism, physiology, and function. MRI can be sensitized to proton density, T 1 , T 2 , susceptibility contrast, magnetization transfer, diffusion, perfusion, and flow. The combination of different MRI approaches (e.g., diffusion-weighted MRI, perfusion MRI, functional MRI, cellspecific MRI, and molecular MRI) allows in vivo multiparametric assessment of the pathophysiology, recovery mechanisms, and treatment strategies in experimental models of stroke, brain tumors, multiple sclerosis, neurodegenerative diseases, traumatic brain injury, epilepsy, and other brain disorders. This report reviews established MRI methods as well as promising developments in MRI research that have advanced and continue to improve our understanding of neurologic diseases and that are believed to contribute to the development of recovery improving strategies.

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Section: Functional Magnetic Resonance Imagingmentioning

confidence: 83%

Magnetic Resonance Imaging in Experimental Models of Brain Disorders

Dijkhuizen

Nicolay

2003

J Cereb Blood Flow Metab

127

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“…70,71 Further, even transient hypoperfusion may produce prolonged changes in cortical thickness as evidenced by decreased cortical thickness and less fMRI activation in rats at 4 months after a single episode of hypoxia-ischemia. 72 Future studies that simultaneously measure cortical thickness and perfusion at an early stage after mTBI may shed light on this relationship.…”

Section: Early Cortical Thinning In Mtbi Survivors After Mvcsmentioning

confidence: 99%

Early Cortical Thickness Change after Mild Traumatic Brain Injury following Motor Vehicle Collision

Wang

Xie

Cotton

et al. 2015

Journal of Neurotrauma

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In a motor vehicle collision (MVC), survivors often receive mild traumatic brain injuries (mTBI). Although there have been some reports of early white matter changes after an mTBI, much less is known about early cortical structural changes. To investigate early cortical changes within a few days after an MVC, we compared cortical thickness of mTBI survivors with nonmTBI survivors, then reexamined cortical thickness in the same survivors 3 months later. MVC survivors were categorized as mTBI or non-mTBI based on concussive symptoms documented in emergency departments (EDs). Cortical thickness was measured from MRI images using FreeSurfer within a few days and again at 3 months after MVC. Post-traumatic stress symptoms and physical conditions were also assessed. Compared with the non-mTBI group (n = 23), the mTBI group (n = 21) had thicker cortex in the left rostral middle frontal (rMFG) and right precuneus gyri, but thinner cortex in the left posterior middle temporal gyrus at 7.2 -3.1 days after MVC. After 3 months, cortical thickness had decreased in left rMFG in the mTBI group but not in the non-mTBI group. The cortical thickness of the right precuneus region in the initial scans was positively correlated with acute traumatic stress symptoms for all survivors and with the number of reduced activity days for mTBI survivors who completed the follow-up. The preliminary results suggest that alterations in cortical thickness may occur at an early stage of mTBI and that frontal cortex structure may change dynamically over the initial 3 months after mTBI.

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“…Much focus has been placed upon the Olg precursors because they are more vulnerable to HI and glutamate toxicity than mature Olgs [8,10]. The axon (and neuron) as the primary source of injury has received less attention 37]. Our data cannot resolve this issue but we note that 1 month after the insult neurons still undergo extensive degeneration.…”

Section: Discussionmentioning

confidence: 69%

“…Other than their characterization at the macro level as being calcified, the cell types present in these human cysts has not been documented at either the ultrastructural or immunocytochemical level. Similarly, MRI studies after HI in neonatal rats and mice have been performed [22,37] but no ultrastructural descriptions of the focal zone have apparently been performed. In most of the neonatal rats that underwent 1.5 h of hypoxia, we found cores of tissue that were GFAP -and surrounded by a densely stained GFAP gliotic scar [24].…”

Section: Discussionmentioning

confidence: 99%

Plasticity of Neurons and Glia Following Neonatal Hypoxic-Ischemic Brain Injury in Rats

et al. 2006

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Periventricular white matter injury in premature infants is linked to chronic neurological dysfunction. Periventricular white matter injury is caused by many mechanisms including hypoxia-ischemia (HI). Animal models of HI in the neonatal rodent brain can replicate some important features of periventricular white matter injury. Most rodent studies have focused upon early cellular and tissue events following unilateral neonatal HI that is elicited by unilateral carotid artery ligation and followed by timed exposure to moderate hypoxia. Milder hypoxic-ischemic insults elicit preferential white matter injury. Little information is available about long-term cellular effects of unilateral HI. One month after unilateral neonatal hypoxia ischemia, we show that all the components for structural reorganization of the brain are present in moderately injured rats. These components in the injured side include extensive influx of neurites, axonal and dendritic growth cones, abundant immature synapses, and myelination of many small axons. Surprisingly, this neural recovery is often found in and adjacent to cysts that have the ultrastructural features of bone extracellular matrix. In contrast, brains with severe hypoxia ischemia one month after injury still undergo massive neuronal degeneration. While massive destruction of neurons and glia are striking events shortly after brain HI, neural cells re-express their intrinsic properties and attempt an anatomical recovery long after injury.

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Long-Term Deficits Following Cerebral Hypoxia–Ischemia in Four-Week-Old Rats: Correspondence between Behavioral, Histological, and Magnetic Resonance Imaging Assessments

Cited by 21 publications

References 33 publications

Magnetic Resonance Imaging in Experimental Models of Brain Disorders

Magnetic Resonance Imaging in Experimental Models of Brain Disorders

Early Cortical Thickness Change after Mild Traumatic Brain Injury following Motor Vehicle Collision

Plasticity of Neurons and Glia Following Neonatal Hypoxic-Ischemic Brain Injury in Rats

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