scholarly journals Differential Progression of Magnetization Transfer Imaging Changes Depending on Severity of Cerebral Hypoxic-Ischemic Injury

2008 ◽  
Vol 28 (9) ◽  
pp. 1613-1623 ◽  
Author(s):  
Ursula I Tuor ◽  
Shuzhen Meng ◽  
Min Qiao ◽  
Nicole B Webster ◽  
Shauna M Crowley ◽  
...  
Keyword(s):  
White Matter ◽  
Magnetization Transfer ◽  
Ischemic Injury ◽  
Subcortical White Matter ◽  
Cerebral Injury ◽  
Magnetization Transfer Ratio ◽  
Magnetization Transfer Imaging ◽  
Cerebral Hypoxia ◽  
Hypoxia Ischemia ◽  
Hypoxic Ischemic Injury

We hypothesized that magnetic resonance magnetization transfer (MT) imaging would be sensitive for detecting cerebral ischemic injury in white matter of neonatal brain. We compared the progression of changes in T2 and the MT ratio (MTR) after cerebral hypoxic-ischemic insults of differing severity in neonatal rats. Magnetization transfer imaging parameters were first optimized, and then MTR and T2 maps were acquired at various times after a mild (rather selective white matter) or substantial insult produced by unilateral cerebral hypoxia—ischemia. Depending on insult severity, time after insult, and region (e.g., subcortical white matter or cortex), cerebral hypoxia—ischemia produced reductions in MTR and an increase in T2. The exception was acutely at 1 to 5 h at which time points MTR was reduced ipsilaterally in white matter, whereas T2 was not affected significantly. Progression of imaging changes differed in rats grouped according to whether gross damage was present after chronic recovery. Behavioral changes were generally associated with chronic reductions in MTR and gross brain damage. Magnetization transfer imaging was capable of early detection of hypoxic-ischemic injury and particularly sensitive for identifying the progression of cerebral injury in white matter. Magnetization transfer ratio has potential for assisting with early diagnosis and treatment assessment for infants affected by perinatal hypoxia—ischemia.

scholarly journals Perivascular nitric oxide and superoxide in neonatal cerebral hypoxia-ischemia

2008 ◽  
Vol 295 (4) ◽  
pp. H1809-H1814 ◽  
Author(s):  
Roderic H. Fabian ◽  
J. Regino Perez-Polo ◽  
Thomas A. Kent
Keyword(s):  
Nitric Oxide ◽  
Fluorescent Dyes ◽  
Ischemic Injury ◽  
Cerebral Hypoxia ◽  
Doppler Flowmetry ◽  
Ischemic Brain ◽  
Isoflurane Anesthesia ◽  
Enos Uncoupling ◽  
Hypoxia Ischemia ◽  
Hypoxic Ischemic Injury

Decreased cerebral blood flow (CBF) has been observed following the resuscitation from neonatal hypoxic-ischemic injury, but its mechanism is not known. We address the hypothesis that reduced CBF is due to a change in nitric oxide (NO) and superoxide anion O2− balance secondary to endothelial NO synthase (eNOS) uncoupling with vascular injury. Wistar rats (7 day old) were subjected to cerebral hypoxia-ischemia by unilateral carotid occlusion under isoflurane anesthesia followed by hypoxia with hyperoxic or normoxic resuscitation. Expired CO2 was determined during the period of hyperoxic or normoxic resuscitation. Laser-Doppler flowmetry was used with isoflurane anesthesia to monitor CBF, and cerebral perivascular NO and O2− were determined using fluorescent dyes with fluorescence microscopy. The effect of tetrahydrobiopterin supplementation on each of these measurements and the effect of apocynin and Nω-nitro-l-arginine methyl ester (l-NAME) administration on NO and O2− were determined. As a result, CBF in the ischemic cortex declined following the onset of resuscitation with 100% O2 (hyperoxic resuscitation) but not room air (normoxic resuscitation). Expired CO2 was decreased at the onset of resuscitation, but recovery was the same in normoxic and hyperoxic resuscitated groups. Perivascular NO-induced fluorescence intensity declined, and O2−-induced fluorescence increased in the ischemic cortex after hyperoxic resuscitation up to 24 h postischemia. l-NAME treatment reduced O2− relative to the nonischemic cortex. Apocynin treatment increased NO and reduced O2− relative to the nonischemic cortex. The administration of tetrahydrobiopterin following the injury increased perivascular NO, reduced perivascular O2−, and increased CBF during hyperoxic resuscitation. These results demonstrate that reduced CBF follows hyperoxic resuscitation but not normoxic resuscitation after neonatal hypoxic-ischemic injury, accompanied by a reduction in perivascular production of NO and an increase in O2−. The finding that tetrahydrobiopterin, apocynin, and l-NAME normalized radical production suggests that the uncoupling of perivascular NOS, probably eNOS, due to acquired relative tetrahydrobiopterin deficiency occurs after neonatal hypoxic-ischemic brain injury. It appears that both NOS uncoupling and the activation of NADPH oxidase participate in the changes of reactive oxygen concentrations seen in cerebral hypoxic-ischemic injury.

scholarly journals Lobar Distribution of Changes in Gray Matter and White Matter in Memory Clinic Patients: Detected Using Magnetization Transfer Imaging

2007 ◽  
Vol 28 (10) ◽  
pp. 1938-1942 ◽  
Author(s):  
A.C.G.M. van Es ◽  
W.M. van der Flier ◽  
F. Admiraal Behloul ◽  
H. Olofsen ◽  
E.L.E.M. Bollen ◽  
...  
Keyword(s):  
White Matter ◽  
Gray Matter ◽  
Magnetization Transfer ◽  
Magnetization Transfer Imaging ◽  
Memory Clinic

Characterization of white matter damage in animal models of multiple sclerosis by magnetization transfer ratio and quantitative mapping of the apparent bound proton fraction f*

2009 ◽  
Vol 15 (1) ◽  
pp. 16-27 ◽  
Author(s):  
M Rausch ◽  
PS Tofts ◽  
P Lervik ◽  
AR Walmsley ◽  
A Mir ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
White Matter ◽  
Animal Models ◽  
Tissue Damage ◽  
Magnetization Transfer ◽  
Transverse Relaxation Time ◽  
Magnetization Transfer Ratio ◽  
White Matter Damage ◽  
Transfer Ratio ◽  
Quantitative Mapping

Quantitative magnetization transfer magnetic resonance imaging (qMT-MRI) can be used to improve detection of white matter tissue damage in multiple sclerosis (MS) and animal models thereof. To study the correlation between MT parameters and tissue damage, the magnetization transfer ratio (MTR), the parameter f* (closely related to the bound proton fraction) and the bound proton transverse relaxation time T2B of lesions in a model of focal experimental autoimmune encephalomyelitis (EAE) were measured on a 7T animal scanner and data were compared with histological markers indicative for demyelination, axonal density, and tissue damage. A clear spatial correspondence was observed between reduced values of MTR and demyelination in this animal model. We observed two different levels of MTR and f* reduction for these lesions. One was characterized by a pronounced demyelination and the other corresponded to a more severe loss of the cellular matrix. Changes in f* were generally more pronounced than those of MTR in areas of demyelination. Moreover, a reduction of f* was already observed for tissue where MTR was virtually normal. No changes in T2B were observed for the lesions. We conclude that MTR and qMT mapping are efficient and reliable readouts for studying demyelination in animal models of MS, and that the analysis of regional f* might be even superior to the analysis of MTR values. Therefore, quantitative mapping of f* from human brains might also improve the detection of white matter damage in MS.

scholarly journals Calcium Accumulation during the Evolution of Hypoxic—Ischemic Brain Damage in the Immature Rat

1988 ◽  
Vol 8 (6) ◽  
pp. 834-842 ◽  
Author(s):  
Dagmar T. Stein ◽  
Robert C. Vannucci
Keyword(s):  
Brain Damage ◽  
Cerebral Hemisphere ◽  
Ischemic Injury ◽  
Calcium Flux ◽  
Variable Degree ◽  
Ischemic Brain Damage ◽  
Ischemic Brain ◽  
Calcium Accumulation ◽  
Hypoxia Ischemia ◽  
Hypoxic Ischemic Injury

An excessive accumulation of calcium in neuronal and other tissues has been postulated to represent a “final common pathway” for cell death arising from hypoxia-ischemia. To clarify the role of altered calcium flux into and distribution within the perinatal brain undergoing hypoxic-ischemic injury, 7-day postnatal rats underwent unilateral common carotid artery ligation followed by 3 h of hypoxia with 8% oxygen. This insult is known to produce brain damage confined to the cerebral hemisphere ipsilateral to the arterial occlusion in >90% of the animals. Either before or after hypoxia-ischemia, the animals received a subcutaneous injection of [45Ca]Cl2, and their brains were subjected to 45Ca autoradiography at 0–1, 5, 24, and 72 h, 7 or 15 days thereafter. During hypoxia-ischemia, calcium flux into the ipsilateral cerebral hemisphere was prominent in 13 of 14 rat pups, especially in neocortex, hippocampus, striatum, and thalamus. Calcium accumulation also occurred to a variable degree (6 of 14 animals) in the contralateral cerebral hemisphere. During recovery, radioactivity in the contralateral cerebral hemisphere was no longer apparent, whereas in the ipsilateral hemisphere, the extent of calcium accumulation was mild in four of six at 1 h, moderate in three of six at 5 h, moderate to intense in six of seven and six of seven at 24 and 72 h, respectively, and intense in three of three and two of two animals at 7 and 15 days, respectively. As during hypoxia-ischemia, the distribution of the radioactivity was most prominent in those structures that are known to be vulnerable to hypoxic-ischemic injury. Thus, hypoxia-ischemia is associated with enhanced calcium uptake into the immature brain, which does not dissipate but rather progressively accumulates for up to 15 days of recovery. The findings implicate a disruption of intracellular calcium homeostasis as a major factor in the evolution of perinatal hypoxic-ischemic brain damage.

Surface-in pathology in multiple sclerosis: a new view on pathogenesis?

Brain ◽  
2021 ◽  
Author(s):  
Matteo Pardini ◽  
J William L Brown ◽  
Roberta Magliozzi ◽  
Richard Reynolds ◽  
Declan T Chard
Keyword(s):  
Multiple Sclerosis ◽  
White Matter ◽  
Grey Matter ◽  
Magnetization Transfer ◽  
Neuronal Loss ◽  
Magnetization Transfer Ratio ◽  
Supporting Evidence ◽  
Transfer Ratio ◽  
Meningeal Inflammation

Abstract While multiple sclerosis can affect any part of the CNS, it does not do so evenly. In white matter it has long been recognized that lesions tend to occur around the ventricles, and grey matter lesions mainly accrue in the outermost (subpial) cortex. In cortical grey matter, neuronal loss is greater in the outermost layers. This cortical gradient has been replicated in vivo with magnetization transfer ratio and similar gradients in grey and white matter magnetization transfer ratio are seen around the ventricles, with the most severe abnormalities abutting the ventricular surface. The cause of these gradients remains uncertain, though soluble factors released from meningeal inflammation into the CSF has the most supporting evidence. In this Update, we review this ‘surface-in’ spatial distribution of multiple sclerosis abnormalities and consider the implications for understanding pathogenic mechanisms and treatments designed to slow or stop them.

Abstract WP90: Activate Protein C Analog Protects Ischemic Injury of Subcortical White Matter in Mice

Stroke ◽  
2018 ◽  
Vol 49 (Suppl_1) ◽  
Author(s):  
Yaoming Wang ◽  
Zhen Zhao ◽  
Axel Montagne ◽  
John H Griffin ◽  
Berislav Zlokovic
Keyword(s):  
White Matter ◽  
Protein C ◽  
Ischemic Injury ◽  
Subcortical White Matter
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