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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We used perfusion weighted magnetic resonance imaging (MRI) to determine relative regional cerebral blood volume (rCBV) in regions of white matter hyperintensity (WMH) in 28 elderly stroke patients and 27 healthy comparison subjects, using T2-weighted fluid-attenuated inversion recovery (FLAIR) sequence MRI for anatomical localization and bolus gadolinium-DTPA tracking for perfusion weighted imaging. We found that WMHs had significantly lower rCBV than contralateral normal WMH, irrespective of size or group membership, and rCBV was significantly related to the size of the WMH. For the larger WMHs, there was a significant increase in rCBV from inner core to outer ring. The findings suggest hemodynamic perturbation in the microvasculature of hyperintense regions, which becomes greater as the size of the WMH increases. This is equally applicable to stroke patients and healthy older individuals.
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PMID:Cerebral blood volume in T2-weighted white matter hyperintensities using exogenous contrast based perfusion MRI. 1499 Jul 63

White matter hyperintensities (WMHs) are commonly seen on brain magnetic resonance imaging (MRI) scans of elderly individuals, but their functional significance remains controversial. We used perfusion-weighted MRI to determine the impact of WMHs on cortical regional cerebral blood volume (rCBV). We studied 24 elderly stroke patients and 27 control subjects with conventional MRI which included T2-weighted FLAIR coronal slices through whole brain and gadolinium-DTPA (0.2 mmol/kg)-based perfusion MRI (pMRI) with echo planar imaging. Volumes of WMHs, including deep WMHs and periventricular hyperintensities (PVHs), were computed by an automated method after excluding regions of infarction. Partial correlations between WMH and corresponding cortical rCBV were determined after correction for age and atrophy. The relative rCBV of gray matter was higher in control subjects and there was no significant hemispheric asymmetry. When both stroke and control groups were included, there were significant correlations among frontal cortical rCBV and frontal WMHs, temporal cortical rCBV with temporal WMHs, and cortical rCBV with both total deep WMHs and PVHs. Although the trends of correlation still existed when the two groups were analyzed separately, they were not significant. The correlations between cortical rCBV and WMHs in the same lobe were significant for subjects with more severe hyperintensities irrespective of the group. In conclusion, T2-weighted WMHs are associated with reduced rCBV in the cerebral cortex, particularly in individuals with extensive hyperintensities.
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PMID:Effect of white matter hyperintensities on cortical cerebral blood volume using perfusion MRI. 1505 May 60

Apoplexy due to infarction and/or hemorrhage is a frequent complication of pituitary adenoma, occurring either spontaneously or precipitated by several factors, among them pituitary function test with hypothalamic releasing hormones. The mechanism by which releasing hormones cause pituitary apoplexy is unclear. It has been proposed that increase in pituitary size and/or alterations in blood flow could be responsible. The aim of this study was to explore the effects of intravenous administration of hypothalamic releasing hormones on pituitary size and hemodynamics in healthy subjects. Gadolinium-DTPA-enhanced dynamic magnetic resonance imaging (MRI) was performed in eight healthy volunteers under basal conditions and 20 min after injection of releasing hormones. Mean upslopes of Gadolinium-DTPA enhancement curves showed good correlation between basal and stimulated conditions (R = 0.89) and were significantly steeper after stimulation (P = 0.017). In contrast, pituitary height, width and length did not differ significantly between basal and stimulated conditions. In conclusion, the pituitary does not swell in healthy subjects in response to stimulation with hypothalamic releasing hormones, whereas transfer of contrast agent to tissue (blood flow and/or vessel permeability) is enhanced.
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PMID:Dynamic contrast-enhanced MR imaging of the stimulated pituitary gland. 1511 25

Focal ischemia followed by reperfusion initiates a harmful P- and E-selectin-mediated recruitment of leukocytes in brain microvasculature. In this study, we tested whether a novel magnetic resonance (MR) contrast agent (Gd-DTPA-sLe(x) A), which is designed to bind to activated endothelium could be detected by MR imaging (MRI) in a focal stroke mouse model. MRIs (9.4T) of the brain were acquired 24 hours after transient middle cerebral artery occlusion. T1 maps were acquired repeatedly before and up to 1.5 hours after the intravenous injection of either Gd-DTPA or Gd-DTPA-sLe(x) A. Analysis of images included a pixel-by-pixel subtraction of T1 maps from the precontrast T1 maps and quantification of T1 within the ischemic area. After injection of Gd-DTPA-sLe(x) A, T1 decreased compared with precontrast levels, and an interhemispheric difference between the pre-post contrast T1 developed within the stroke lesion at a mean time of 52 minutes after injection (p < 0.05). Animals injected with Gd-DTPA did not exhibit changes in T1 signal intensity between regions of the ipsilateral and contralateral hemispheres, indicating that the reductions in T1 observed with Gd-DTPA-sLe(x) A were unrelated to blood-brain barrier breakdown. Fluorescent-labeled sLe(x) A administered intravenously was observed to bind to the endothelium of injured but not control brain. The study suggests that the contrast agent Gd-DTPA-sLe(x) A can be used to visualize early endothelial activation after transient focal ischemia in vivo with MRI.
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PMID:MR molecular imaging of early endothelial activation in focal ischemia. 1523 8

We sought to identify magnetic resonance imaging (MRI) parameters that can identify as well as predict disruption of the blood-brain barrier (BBB) after embolic stroke in the rat. Rats subjected to embolic stroke with (n=13) and without (n=13) rt-PA treatment were followed with MRI using quantitative permeability-related parameters, consisting of: transfer constant (K(i)) of Gd- DTPA, the distribution volume (V(p)) of the mobile protons, and the inverse of the apparent forward transfer rate for magnetization transfer (k(inv)), as well as the apparent diffusion coefficient of water (ADC(w)), T2, and cerebral cerebral blood flow (CBF). Tissue progressing to fibrin leakage resulting from BBB disruption and adjacent tissue were then analyzed to identify MRI markers that characterize BBB disruption. Animals were killed after final MRI measurements at 24 h after induction of embolic stroke and cerebral tissues were perfused and stained to detect fibrin leakage. K(i), V(p), and k(inv) were the most sensitive early (2 to 3 h) indices of the cerebral tissue that progresses to fibrin leakage. Cerebral blood flow was not significantly different between ischemic tissue with a compromised and an intact BBB. Our data indicate that compromise of the BBB can be sensitively predicted using a select set of MR parameters.
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PMID:Quantitative evaluation of BBB permeability after embolic stroke in rat using MRI. 1571 59

Using MRI, we investigated dynamic changes of brain angiogenesis after neural progenitor cell transplantation in the living adult rat subjected to embolic stroke. Neural progenitor cells isolated from the subventricular zone (SVZ) of the adult rat were labeled by superparamagnetic particles and intracisternally transplanted into the adult rat 48 h after stroke (n = 8). Before and after the transplantation, an array of MRI parameters were measured, including high resolution 3D MRI and quantitative T1, T1sat (T1 in the presence of an off-resonance irradiation of the macromolecules of brain), T2, the inverse of the apparent forward transfer rate for magnetization transfer (kinv), cerebral blood flow (CBF), cerebral blood volume (CBV), and blood-to-brain transfer constant (Ki) of Gd-DTPA. The von Willerbrand factor (vWF) immunoreactive images of coronal sections obtained at 6 weeks after cell transplantation were used to analyze vWF immunoreactive vessels. MRI measurements revealed that grafted neural progenitor cells selectively migrated towards the ischemic boundary regions. In the ischemic boundary regions, angiogenesis confirmed by an increase in vascular density and the appearance of large thin wall mother vessels was coincident with increases of CBF and CBV (CBF, P < 0.01; CBV, P < 0.01) at 6 weeks after treatment, and coincident with transient increases of K(i) with a peak at 2 to 3 weeks after cell therapy. Relative T1, T1sat, T2, and kinv decreased in the ischemic boundary regions with angiogenesis compared to that in the non-angiogenic ischemic region (T1, P < 0.01 at 6 weeks; T1sat, P < 0.05 at 2 to 6 weeks; T2, P < 0.05 at 3 to 6 weeks; kinvP < 0.05 at 6 weeks). Of these methods, Ki appear to be the most useful MR measurements which identify and predict the location and area of angiogenesis. CBF, CBV, T1sat, T1, T2, and kinv provide complementary information to characterize ischemic tissue with and without angiogenesis. Our data suggest that select MRI parameters can identify the cerebral tissue destined to undergo angiogenesis after treatment of embolic stroke with cell therapy.
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PMID:Investigation of neural progenitor cell induced angiogenesis after embolic stroke in rat using MRI. 1611 79

Pathologic changes in brain tissue during and after stroke may lead to injury of the blood-brain barrier (BBB) and subsequent hemorrhagic transformation (HT). In a rat model of HT, the apparent diffusion coefficient of water, cerebral blood flow, relaxation times, T(1) and T(2), and magnetization transfer (MT) related parameters (T(1sat), K(for) and the MT ratio) were repetitively measured during 3 h of focal ischemia and 2 h of reperfusion (n = 8). Areas of BBB opening were identified by sequential assay of the transcapillary influx of Gd-diethylenetriaminepentaacetic acid (Gd-DTPA) by MRI and (14)C-alpha-aminoisobutyric acid (AIB) by quantitative autoradiography. Ischemia-injured regions of interest were identified from the MRI data and divided into those with and without BBB opening. Of the several MRI parameters measured, the T(1sat) in the caudate-putamen and preoptic area during ischemia and the first 2 h of reperfusion correlated best with the regional pattern of BBB opening observed thereafter. These data suggest that an ipsilateral/contralateral T(1sat) ratio > 1.6 demarcates leakage of small molecules such as Gd-DTPA and AIB across the BBB. As to clinical relevance, the quantitation of MT parameters in acute stroke may enable the early detection of areas of BBB opening and potential HT.
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PMID:Acute blood-brain barrier opening in experimentally induced focal cerebral ischemia is preferentially identified by quantitative magnetization transfer imaging. 1614 16

Thrombolytic therapy with rtPA increases the risk of hemorrhagic transformation (HT) after cerebral ischemia. We employed contrast enhancement MRI with Gd-DTPA to detect HT in a rat model of embolic stroke treated with rtPA and a glycoprotein IIb/IIIa receptor antagonist, 7E3 F(ab')2, at 4 h after embolic stroke. Male Wistar rats were subjected to embolic stroke and treated with the combination of rtPA and 7E3 F(ab')2 (n=12) or with saline (n=10) at 4 h after onset of stroke. MRI studies were performed immediately and at 24 h after embolization using a 7-T system. Histological measurements were obtained at 48 h. With Gd-DTPA, T1WI images and permeability related MRI parameters (the blood-to-brain transfer constant, Ki, and the distribution volume of mobile protons, Vp) of 15 out of 18 animals showed hyperintensity regions in gross or microscopic HT areas at 24 h, confirmed histologically at 48 h post stroke. Contrast enhancement MRI detected six of seven (86%) animals with gross HT and nine of eleven (82%) animals with microscopic HT at 24 h after ischemia. Two of eighteen animals with HT, had MRI indices of hemorrhage at 3 h post stroke. However, compared to HT data measured histologically at 48 h in embolic stroke rats, the enhanced areas by Gd-DTPA at 24 h were larger, and the patterns (time, intensity and region) did not directly correlate to the subtypes of HT, i.e., gross or microscopic hemorrhage. Contrast enhancement MRI using Gd-DTPA provides a method to detect gross and microscopic HT after stroke in rats.
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PMID:Detection of BBB disruption and hemorrhage by Gd-DTPA enhanced MRI after embolic stroke in rat. 1695 Feb 36

The objective of this article is to illustrate both the potential and the limitations of molecular imaging in stroke research. By molecular imaging we mean the visual representation of biological processes at the cellular and molecular level. The use of molecular imaging for stroke diagnosis is still at a very preliminary stage and many of these procedures have only been tested in animals. In rats, stroke therapy using stem cells can be monitored by magnetic resonance imaging (MRI), green fluorescent protein (GFP) or luciferase (LUC) imaging. The migration of macrophages, which take up intravenously administered iron-based contrast agents and then migrate to the area of infarction, can already be observed in stroke patients. With MRI, the new agent Gd-DTPA-sLexA that binds to E- and P-selectin can specifically visualize selectin-mediated early endothelial activation after transient focal ischemia "in vivo". Decreased glial fibrillary acidic protein (GFAP) gene expression can be imaged in vivo by scintigraphy 24 hours after cerebral ischemia using a peptide nucleic acid antisense conjugate labeled with 111In and that hybridizes to the rat GFAP mRNA. Technetium-99m hydrazine nicotinamide-labeled HYNIC-annexin V SPECT can not only detect sites of neuronal injury in stroke patients but also can monitor the effects of neuroprotective therapy with a monoclonal antibody raised against FasLigand (FasL) in rats. Finally, information about cell metabolism in the infarct region can be gained using certain intracellular tracers [e.g. 18F-fluoromisonidazole (FMISO)]. Imaging benzodiazepine receptors with 11C-flumazenil (FMZ) can distinguish between irreversibly damaged and viable penumbra tissue early after stroke.
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PMID:Future contrast agents for molecular imaging in stroke. 1762 9

Thrombus (blood clot) is implicated in a number of life threatening diseases, e.g., heart attack, stroke, pulmonary embolism. EP-2104R is an MRI contrast agent designed to detect thrombus by binding to the protein fibrin, present in all thrombi. EP-2104R comprises an 11 amino acid peptide derivatized with 2 GdDOTA-like moieties at both the C- and N-terminus of the peptide (4 Gd in total). EP-2104R was synthesized by a mixture of solid phase and solution techniques. The La(III) analogue was characterized by and 1D and 2D NMR spectroscopy and was found to have the expected structure. EP-2104R was found to be significantly more inert to Gd(III) loss than commercial contrast agents. At the most extreme conditions tested (pH 3, 60 degrees C, 96 hrs), less than 10% of Gd was removed from EP-2104R by a challenge with a DTPA based ligand, while the commercial contrast agents equilibrated within minutes to hours. EP-2104R binds equally to two sites on human fibrin (Kd = 1.7 +/- 0.5 microM) and has a similar affinity to mouse, rat, rabbit, pig, and dog fibrin. EP-2104R has excellent specificity for fibrin over fibrinogen (over 100-fold) and for fibrin over serum albumin (over 1000-fold). The relaxivity of EP-2104R bound to fibrin at 37 degrees C and 1.4 T was 71.4 mM(-1) s(-1) per molecule of EP-2104R (17.4 per Gd), about 25 times higher than that of GdDOTA measured under the same conditions. Strong fibrin binding, fibrin selectivity, and high molecular relaxivity enable EP-2104R to detect blood clots in vivo.
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PMID:EP-2104R: a fibrin-specific gadolinium-Based MRI contrast agent for detection of thrombus. 1839 3


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