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

This review examines interactions in the mammalian central nervous system (CNS) between carnosine and the endogenous transition metals zinc and copper. Although the relationship between these substances may be applicable to other brain regions, the focus is on the olfactory system where these substances may have special significance. Carnosine is not only highly concentrated in the olfactory system, but it is also contained in neurons (in contrast to glia cells in most of the brain) and has many features of a neurotransmitter. Whereas the function of carnosine in the CNS is not well understood, we review evidence that suggests that it may act as both a neuromodulator and a neuroprotective agent. Although zinc and/or copper are found in many neuronal pathways in the brain, the concentrations of zinc and copper in the olfactory bulb (the target of afferent input from sensory neurons in the nose) are among the highest in the CNS. Included in the multitude of physiological roles that zinc and copper play in the CNS is modulation of neuronal excitability. However, zinc and copper also have been implicated in a variety of neurologic conditions including Alzheimer's disease, Parkinson's disease, stroke, and seizures. Here we review the modulatory effects that carnosine can have on zinc and copper's abilities to influence neuronal excitability and to exert neurotoxic effects in the olfactory system. Other aspects of carnosine in the CNS are reviewed elsewhere in this issue.
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PMID:Interactions between carnosine and zinc and copper: implications for neuromodulation and neuroprotection. 1095 Oct 99

Cerebral (brain) arteriovenous malformations (BAVMs) are a tangle of disorganized vessels that are a rare cause of hemorrhagic stroke in the general population. Although clinical presentation of hemorrhage may be related to the structure of BAVM vessels, there has been no systematic quantitative analysis of BAVM vessel morphology. Histological sections of excised BAVM lesions were prepared from patients who presented with hemorrhage (n = 14) and from patients with no history of hemorrhage (n = 22). Mean values of radius and wall thickness in each section were determined. BAVM radii were 422+/-136 microm (mean +/- SD), minimum wall thickness (thinnest portion of the wall) was 54+/-14 microm; and the minimum thickness/radius ratio was 0.23+/-0.07. Greater vessel wall thickness was associated with hemorrhagic presentation (OR= 1.1; p = 0.046) after adjusting for feeding artery pressure. Because BAVM vessels from patients presenting with hemorrhage had thicker vessel walls, the search for structural properties predisposing BAVM rupture should be expanded beyond the morphological properties analyzed here.
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PMID:Relationship of nidal vessel radius and wall thickness to brain arteriovenous malformation hemorrhage. 1211 22

Tracking a bolus of contrast agent traveling through the cerebral vasculature provides a measure of the blood flow velocity in the respective cerebral tissue. This principle has been the basis for the first approaches in functional magnetic resonance (MR) imaging and is of great value for investigating patients with vascular disease, especially stroke. While bolus measurements are a standard procedure in MR imaging, optical bolus tracking is as yet not established. Here we study optical absorption changes induced by a bolus of the dye indocyanine-green with near infrared spectroscopy in healthy volunteers. The aim is to assess the latency and shape of the change in absorption. Since application in the adult human critically depends on differentiation between extra- and intracerebral vascular compartments we focus on an approach for such a separation. To do this frequency-domain and multidistance measurements are analyzed by a Monte Carlo based model for photon transport in tissue. Based on measurements of both the photon's mean time of flight (phase) and the intensity, our results allow differentiation between an upper (skin and skull) and a lower layer (brain). The bolus in the deeper tissue layers has a peak of about 10 s width, while the change in absorption in the upper layers shows a much longer recovery time. This is in qualitative agreement with MR imaging results using a gadolinium bolus. This result is promising with respect to the potential of bedside monitoring of mean transit time (MTT) changes in patients with stroke or related vascular disease.
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PMID:Noninvasive monitoring of cerebral blood flow by a dye bolus method: separation of brain from skin and skull signals. 1217 98

Diffusion weighted magnetic resonance imaging has evolved from an esoteric laboratory experiment to a critical aspect of routine clinical care of the patient presenting with symptoms suspicious of acute ischemic stroke. The purpose of this article is to review the basis of diffusion weighted imaging (DWI), to consider its application in acute stroke and to recognize potential pitfalls and stroke mimics that might be encountered. Included in the discussion are comments on the elimination of 'T2 shine through' phenomena as well as construction of pixel-by-pixel maps of the apparent diffusion coefficient (ADC). Furthermore, discussion of techniques such as parallel imaging (using SENSE) and PROPELLER sequences will be introduced as methods potentially allowing DWI to be utilized in areas usually associated with prohibitive susceptibility artifact (e.g. the base of the brain). Finally, the concept of interventional therapeutic approaches to salvaging ischemic tissue is introduced, both in terms of the ischemic penumbra (defined by a diffusion/perfusion mismatch) and also in terms of the potential reversibility of the diffusion-weighted hyperintensity, associated with the lesion core.
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PMID:Diffusion weighted magnetic resonance imaging in stroke. 1259 2

Fibrinolytic activity in the acute stroke was examined by monitoring the level of plasminogen activator inhibitor-1 (PAI-1), as one of the indicators of fibrinolytic activity. Given the role of PAI-1 in the processes of atherogenesis and thrombogenesis, plasma PAI-1 level was measured in 59 patients (up to 50 years of age) with atherothrombotic stroke (verified by computed tomography scanning or magnetic resonance imaging of brain) in the period from 12 to 24 hours (I analysis) and 30 days after the onset of stroke (II analysis); then, it was correlated with plasma PAI-1 level in the control group (57 healthy subjects), which was 2.86 +/- 0.70 U/ml. It was found that PAI-1 level was significantly higher in the acute stroke (I analysis: PAI-1 = 4.10 +/- 1.40 U/ml, p < 0.001; II analysis: PAI-1 = 3.64 +/- 0.90 U/ml, p < 0.001), while fibrinolytic activity was lower, especially on the first day from the stroke that was not completely increased even after 30 days. There was no difference in PAI-1 levels between the subgroups of patients with infarction and lacunar cerebral ischemia (p > 0.05), as well as between females and males (p > 0.05). Along with significantly increased fibrinogen level (4.65 +/- 1 g/l, in the controls--2.83 +/- 0.64 g/l, p < 0.001), significantly higher triglycerides (2.04 +/- 0.76 mmol/l, in the controls--1.38 +/- 0.54 mmol/l, p < 0.001) and lipoproteins(a) (0.405 +/- 0.29 g/l, in the controls--0.172 +/- 0.14 g/l, p < 0.001) were found, correlating with higher plasma PAI-1 level in these patients. The increased plasma level of PAI-1 pointed to possibility of decreased fibrinolytic activity in pathogenesis of ischemic stroke, as well as, risk of reinsult, which had been the greatest after the onset of stroke and declined gradually within several weeks.
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PMID:[Plasminogen activator inhibitor-1 in the evolution of stroke]. 1549 83

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

Imaging of stroke has evolved with the development of stroke units and the CE approval of intravenous thrombolysis in the first three hours after stroke onset. The goal of imaging in the acute phase of stroke is: to make the diagnosis of stroke; to rule out other diagnosis (above all hemorrhagic strokes); to precise the location of the arterial occlusion; to assess the level of hypoperfusion; to evaluate the viability and reversibility of brain lesions; to understand the origin of the stroke by evaluating cervical arteries. Constraints of imaging in the acute phase of stroke are: the need to be performed as fast as possible to not delay IV thrombolysis (time is brain); machines must be available 24 hours a day, 7 days a week as close as possible to the stroke unit. The aim of imaging are: in routine practice to evaluate the likely benefits (provided by penumbra imaging) and risks of IV thrombolysis; in term of "evidence based medicine" to better evaluate new specific stroke therapies in randomized studies (IV thrombolysis between 3 to 4 hours, use of anti GpIIbIIIa, intra-arterial mechanical or chemical thrombolysis...). Magnetic resonance imaging is considered the goal standard of stroke imaging allowing to evaluate in a "one stop shopping" the level of arterial occlusion, hypoperfusion and brain viability. However, stroke management is a regional issue and performing MR in extreme emergency is almost impossible in all stroke units outside or even within university hospitals 24 hours a day. CT-perfusion and CT angiography are therefore an accurate alternative tool for acute stroke imaging. Multislice CT is indeed available in almost all stroke units. The examination is very time-saving and clinically relevant to make the decision for IV thrombolysis.
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PMID:[Imaging of cerebral ischemia within first hours: computed tomography (CT)]. 1622 5

Adult marrow-derived Mesenchymal Stem Cells (MSCs) are capable of dividing and their progeny are further capable of differentiating into one of several mesenchymal phenotypes such as osteoblasts, chondrocytes, myocytes, marrow stromal cells, tendon-ligament fibroblasts, and adipocytes. In addition, these MSCs secrete a variety of cytokines and growth factors that have both paracrine and autocrine activities. These secreted bioactive factors suppress the local immune system, inhibit fibrosis (scar formation) and apoptosis, enhance angiogenesis, and stimulate mitosis and differentiation of tissue-intrinsic reparative or stem cells. These effects, which are referred to as trophic effects, are distinct from the direct differentiation of MSCs into repair tissue. Several studies which tested the use of MSCs in models of infarct (injured heart), stroke (brain), or meniscus regeneration models are reviewed within the context of MSC-mediated trophic effects in tissue repair.
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PMID:Mesenchymal stem cells as trophic mediators. 1661 57

The hypertension is one of chronic vascular diseases, which often implicates multiple tissues causing stroke, cardiac hypertrophy, and renal failure. A growing body of evidence suggests that inflammatory mechanisms are important participants in the pathophysiology of hypertension. In this study, the inflammatory status of these tissues (kidney, liver, heart, and brain) in spontaneously hypertensive rats (SHR) was analyzed and its molecular mechanism was explored. The tissues were dissected from SHR and age-matched control Wistar-Kyoto (WKY) rats to investigate the abundance of inflammation-related mediators (IL-1beta, TNFalpha, ICAM-1, iNOS, C/EBPdelta and PPARgamma). mRNA levels were determined by reverse transcription-polymerase chain reaction and protein expression was evaluated by Western blot. To evaluate the oxidative stress of tissues, carbonyl protein content and total antioxidant capacity of tissues were detected by spectrophotometry and ferric reduction ability power (FRAP) method. The results suggest that: (1) Expressions of inflammation-related mediators (IL-1beta, TNFalpha, ICAM-1, iNOS, C/EBPdelta and PPARgamma) in SHR were higher compared with those in WKY rats except no evident increase of IL-1beta mRNA in liver and brain in SHR. (2) Tissues in SHR contained obviously increased carbonyl protein (nmol/mg protein) compared to that in WKY rats (8.93+/-1.08 vs 2.27+/-0.43 for kidney, 2.23+/-0.23 vs 0.17+/-0.02 for heart, 13.42+/-1.10 vs 5.72+/-1.01 for brain, respectively, P<0.05). However, no evident difference in the amount of carbonyl protein in liver was detected between SHR and WKY rats. (3) Total antioxidant capacities of kidney, liver, heart and brain were markedly lower in SHR than that in WKY rats (P<0.05). Thus, the present data reveal a higher inflammatory status in the important tissues in SHR and indicate that inflammation might play a potential role in pathogenesis of hypertension and secondary organ complications.
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PMID:Inflammation of different tissues in spontaneously hypertensive rats. 1690 31

Although the number of fish species that have been studied for both hypoxia/anoxia tolerance and ammonia tolerance are few, there appears to be a correlation between the ability to survive these two insults. After establishing this correlation with examples from the literature, and after examining the role Peter Lutz played in catalyzing this convergent interest in two variables, this article explores potential mechanisms underpinning this correlation. We draw especially on the larger body of information for two human diseases with the same effected organ (brain), namely stroke and hepatic encephalopathy. While several dissimilarities exist between the responses of vertebrates to anoxia and hyperammonemia, one consistent observation in both conditions is an overactivation of NMDA receptors or glutamate neurotoxicity. We propose a glutamate excitotoxicity hypothesis to explain the correlation between ammonia and hypoxia resistance in fish. Furthermore, we suggest several experimental paths to test this hypothesis.
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PMID:Piscine insights into comparisons of anoxia tolerance, ammonia toxicity, stroke and hepatic encephalopathy. 1704 1


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