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Query: UMLS:C0917798 (cerebral ischemia)
 17,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The incidence, prognosis and causes of strokes associated with pregnancy or puerperium are poorly known, and we do not know whether and to what extent they differ from those of the general female population of childbearing age. Based on early and mostly hospital-based studies, it has been claimed that pregnancy increases the likelihood of cerebral infarction to about 13 times the rate expected outside of pregnancy. However, because of methodological weaknesses, these estimates must be regarded with caution. In a recent study in Ile de France, the incidence of arterial ischemic strokes associated with pregnancy or early puerperium was 4.3 per 100,000 deliveries (95% confidence interval, 2.4 to 7.1), a rate not much different from that for all women of childbearing age. Ischemic strokes related to various etiologies have been reported in pregnancy and the puerperium. Their relative frequency is poorly known because there are no recent large series of pregnancy-related ischemic strokes benefiting from detailed investigation with modern imaging techniques. Most of the known causes of ischemic stroke in the young been reported during pregnancy. In most of these conditions, it is uncertain whether pregnancy is coincidental or plays a role in the occurrence of stroke. Among pregnancy-specific causes, eclampsia may be associated with focal neurological deficits of sudden onset, consistent with a clinical diagnosis of stroke. However, the precise pathogenesis of these stroke-like focal deficits remains poorly understood. Except for some women who have persisting neurological deficits and neuroradiological abnormalities suggesting brain infarction, the reversibility of the neurological clinical signs and neuroradiological lesions within a few days or weeks in most cases argues against the existence of true cerebral ischemic necrosis. The two other pregnancy-specific causes-choriocarcinoma and amniotic fluid embolism-are rarely responsible for focal cerebral ischemia. Other diseases such as peripartum cardiomyopathy and postpartum cerebral angiopathy were initially considered as pregnancy-specific causes but subsequently reported outside of pregnancy. In a significant number of patients, the cause of the stroke remains undetermined, despite an extensive etiological workup. Whether hypercoagulable state and vessel wall changes associated with pregnancy may play a role in the occurrence of these otherwise unexplained ischemic strokes remains unknown. Too frequently, the stroke is considered at the first attempt as a complication of pregnancy and another underlying etiology may be missed. Therefore, evaluation of arterial ischemic stroke in pregnancy should proceed as in the non-pregnant state. There are no follow-up studies that consider the risk of recurrent stroke in future pregnancies. No data are available on the risk associated with use of oral contraception in a woman who had ischemic stroke during pregnancy. The frequency of cerebral venous thrombosis associated with pregnancy and the puerperium is not precisely known. Indeed, epidemiologic studies have been difficult to perform because cerebral venous thrombosis may have a misleading presentation and a definite diagnosis requires angiography, MRI or autopsy. The incidence of cerebral venous thrombosis has been estimated at 10 to 20 per 100000 deliveries in occidental countries, whereas rates of 200 to 500 per 100,000 deliveries have been reported in India. The pregnant and puerperal state accounts for 5 to 20% of all cerebral venous thrombosis in occidental countries; this proportion may reach 60% in developing countries. Labor and delivery are characteristically normal in occidental countries. The occurrence of cerebral venous thrombosis is clearly linked to the puerperial state, suggesting a direct role of the puerperial state.(ABSTRACT TRUNCATED)
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PMID:[Cerebrovascular diseases in pregnancy and puerperium]. 894 39

We report CT and MRI findings in a girl with late-onset ornithine transcarbamylase deficiency, who presented with progressive somnolence. Both imaging methods showed signs of an acute cerebral ischaemia with new defects on follow-up. Despite an unusual clinical presentation, laboratory studies led to the diagnosis of this rare inherited metabolic defect.
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PMID:CT and MRI in a girl with late-onset ornithine transcarbamylase deficiency: case report. 895 9

Cervical artery dissection (CAD) accounts for up to one fifth of ischemic strokes occurring before 45 years. Their increasing recognition is probably due to an increased clinical awareness of this condition in patients with painful ischemic events. The internal carotid artery is the most commonly affected vessel. Cerebral ischemia is the most serious consequence of a CAD. It may be due to hemodynamic factors or emboli. The enlargement of the artery may lead to a direct compression of the lower cranial nerves. CAD typically occurs in young adults with a mean age of 40 years with a male:female ratio of 1.5. After exclusion of traumatic cases, the average annual incidence rate of CAD is 2.6 per 100,000, but the reported incidence figures in the literature are likely to be an underestimation of the incidence of CAD. A spontaneous dissection is assumed when no or only minor trauma preceded the onset. However, the differentiation between spontaneous and traumatic dissections is artificial because of a continuum between both forms. The pathogenesis of dissections remains unknown in most cases. However, traumas and primary diseases of the arterial wall are the main predisposing factors. The clinical presentation of spontaneous dissections of the internal carotid artery includes cerebral ischemia, cervical or cranial pain, Horner's syndrome and cranial nerve palsy; CAD may also be silent. Brainstem ischemic deficits and occipital pain are the most common findings in vertebral artery dissections, but these features may be biased because the most benign and the most severe cases may escape detection. The favorable natural history of CAD emphasizes the need for a noninvasive approach to the detection, monitoring and follow-up. This noninvasive approach can be obtained by means of CT scan, MRI, magnetic resonance angiography and ultrasonography, although angiography remains the gold standard for the diagnosis of arterial dissections. Follow-up studies suggest a fairly good overall prognosis in adults and in children. In many centers, CAD are treated by heparin at the acute stage, although the benefit of such a potentially dangerous treatment has never been proven by a randomized trial.
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PMID:Cervical artery dissections. 901 25

Diffusion-weighted MRI has been used to investigate therapeutic intervention with MK-801 in an animal model of permanent focal cerebral ischaemia. The animals were imaged continuously for 4 h and again at 24 h following occlusion of the middle cerebral artery (MCA) allowing the development of the ischaemic lesion to be monitored continuously in the same animals. An increased DWI signal, seen as a region of hyperintensity, was detected 1 h after MCA-occlusion in the lateral cortex and caudate nucleus in both control and MK-801 (administered at a dose of 3 mg/kg i.p. 5 min post-ischaemia) treated animals. However, the volume of hemispheric and cortical hyperintensity was smaller in the MK-801-treated animals. The area of hyperintensity progressively increased in the control group over the 4 h imaging time and there was also an increase in the area of hyperintensity between 4 and 24 h. At these time points the area of hyperintensity encompassed the dorsolateral cortex and caudate nucleus. MK-801 treated animals also demonstrated some progressive increase in the area of hyperintensity between 1 and 3 h, but no significant increase in the area of hyperintensity was seen after this time. The hyperintense regions at 4 and 24 h were restricted to the so-called 'core areas' of the lesion in MK-801-treated animals. Thus, using DWI the tissue 'at risk' following ischaemia could be identified and the protective effect of therapeutic intervention demonstrated.
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PMID:The protective effect of MK-801 on infarct development over a period of 24 h as assessed by diffusion-weighted magnetic resonance imaging. 907 2

We assessed the temporal and spatial correlation between perfusion deficits and tissue damage in the first hours of focal cerebral ischemia in the rat. Repetitive dynamic susceptibility contrast-enhanced ('bolus track') and diffusion-weighted (DW) MRI, performed from ca. 0.5 up to 6 h after intraluminal middle cerebral artery occlusion (MCA-O), allowed the determination of the time course of various hemodynamic parameters and ischemic tissue damage in specific brain regions. In addition, blood oxygenation level dependent (BOLD) MRI combined with a respiratory challenge provided complementary information on brain hemodynamics. Within the territory of reduced blood flow, the degree of the hemodynamic disturbances was heterogeneous. Interestingly, the spatial pattern of perfusion deficiencies remained essentially the same from ca. 0.5 to 6 h post-MCA-O. However, the area and the extent of ischemic tissue damage, as expressed by reductions in the apparent diffusion coefficient (ADC) of tissue water, tended to progress with increasing occlusion time. Different ADC profiles correlated with different degrees of hemodynamic disturbances. In the ischemic core, which showed severely compromized perfusion, the ADC dropped significantly within 1 h. In perifocal areas, ADC reductions were delayed and less pronounced. Data from the bolus track and BOLD MRI experiments revealed the existence of residual flow, particularly in perifocal regions. Our data point to a time-dependent change in the relationship between ADC reductions and hemodynamic alterations and, therefore, agree with the concept of a progressively increasing perfusion threshold for ischemic tissue damage as a function of time of ischemia.
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PMID:Regional assessment of tissue oxygenation and the temporal evolution of hemodynamic parameters and water diffusion during acute focal ischemia in rat brain. 909 41

Diffusion-weighted imaging (DWI) detects small changes in water diffusion that occur in ischemic brain. This study evaluated the clinical usefulness of a phase-navigated spin-echo DWI sequence compared with T2-weighted magnetic resonance imaging (T2W MRI) in patients with cerebral ischemia and assessed apparent diffusion coefficient (ADC) and T2-weighted imaging (T2WI) changes over time. ADC values and T2 ratios of image intensity were measured from the region of ischemia and from the corresponding contralateral brain region. The clinical histories of patients with DWI scans obtained over the course of 1 year were reviewed to ascertain whether DWI aided in clinical diagnosis or management. Of 103 scans obtained a mean of 10.4 days after symptom onset, DWI detected six lesions not seen on T2WI and discriminated two new infarcts from old lesions. DWI was most useful within 48 hours of the ictus. The evolution of ADC values and T2 ratios was evaluated in 26 cases with known symptom onset times. ADC values were low at less than 1 week after stroke onset and became elevated at chronic time points. T2 ratios were near normal acutely, increasing thereafter. DWI was superior to T2W MRI in detecting acute stroke, whereas both techniques assisted in determining lesion age.
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PMID:Clinical utility of diffusion-weighted magnetic resonance imaging in the assessment of ischemic stroke. 915 15

T2 and diffusion weighted MRI, as well as 31P and 1H MRS were performed in kaolin-induced hydrocephalic rats. Extracellular white matter edema was detected in the early stages of progressive hydrocephalus. Phosphocreatine (PCr)/inorganic phosphate (Pi) ratios in hydrocephalic animals were decreased compared to controls, and lactate was detected during the acute and chronic stages of hydrocephalus. These MR spectroscopic results are indicative of a compromised energy metabolism and suggest the occurrence of cerebral ischemia in experimental hydrocephalus.
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PMID:Cerebral ischemia and white matter edema in experimental hydrocephalus: a combined in vivo MRI and MRS study. 920 Jul 61

MR spectroscopy(MRS) is a powerful method to evaluate brain metabolism directly and non-invasively. We developed 3D-CSI method as a multi-voxel MRS. It has some advantages or single-voxel MRS; 1) spectra in many voxels can be acquired simultaneously 2) Mapping of metabolites can be acquired 3) A small size voxel can be obtained. It make it possible to evaluate the change of NAA in wide area. In case of cerebral ischemia, we found the tendency that NAA decreases in fatal damage area and is normal in recoverable damage area. Therefore, we suppose that NAA could be a indicator of viability of neuron. It is necessary to coordinate the data from MRI/ MRS and PET/SPECT for analyzing the pathophysiology of cerebral ischemia.
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PMID:[Evaluation of cerebral ischemia with metabolic image by using 3D-CSI--comparing with SPECT and PET]. 923 23

Determination of tissue perfusion rates by MRI bolus tracking methods relies on the central volume principle which states that tissue blood flow is given by the tissue blood volume divided by the mean tracer transit time (MTT). Accurate determination of the MTT requires knowledge of the arterial input function which in MRI experiments is usually not known, especially when using small animals. The problem of unknown arterial input can be circumvented in animal experiments by directly injecting the contrast agent into a feeding artery of the tissue of interest. In the present article the passage of magnetite nanoparticles through the rat cerebral cortex is analyzed after injection into the internal carotid artery. The results are discussed in the framework of linear system theory using a one-compartment model for brain tissue and by using the well characterized gamma-variate function to describe the tissue concentration profile of the contrast agent. The results obtained from the intra-arterial tracer administration experiments are then compared with the commonly used intra-venous injection of the contrast agent in order to estimate the contribution of the peripheral circulation to the MTT values in the latter case. The experiments were analyzed using a two-compartment model and the gamma-variate function. As an application perfusion rates in normal and ischemic cerebral cortex of hypertensive rats were estimated in a model of focal cerebral ischemia. The results indicate that peripheral circulation has a significant influence on the MTT values and thus on the perfusion rates, which cannot be neglected.
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PMID:Analysis of tracer transit in rat brain after carotid artery and femoral vein administrations using linear system theory. 925 99

We developed a new model of embolic cerebral ischemia in the rat which provides a reproducible and predictable infarct volume within the territory supplied by the middle cerebral artery (MCA). The MCA was occluded by an embolus in Wistar rats (n = 71). An additional three non-embolized rats were used as a control. Cerebral blood flow (CBF) was measured by means of laser Doppler flowmetry (LDF) and perfusion weighted imaging (PWI) before and after embolization. The evolution of the lesion was monitored by diffusion weighted imaging (DWI). Cerebral vascular perfusion patterns were examined using laser scanning confocal microscopy. Infarct volumes were measured on hematoxylin and eosin (H&E) stained coronal sections. The lodgment of the clot at the origin of the MCA and the ischemic cell damage were examined using light microscopy. Regional CBF in the ipsilateral parietal cortex decreased to 43 +/- 4.1% (P < 0.05) of preischemic levels (n = 10). Confocal microscopic examination revealed a reduction of cerebral plasma perfusion in the ipsilateral MCA territory (n = 6). MRI measurements showed a reduction in CBF and a hyperintensity DWI encompassing the territory supplied by the MCA (n = 4). An embolus was found in all rats at 24 h after embolization. The infarct volume as a percentage of the contralateral hemisphere was 32.5 +/- 3.31% at 24 h (n = 20), 33.0 +/- 3.6% at 48 h (n = 13), and 34.5 +/- 4.74% at 168 h (n = 12) after embolization. This model of embolic focal cerebral ischemia results in ischemic cell damage and provides a reproducible and predictable infarct volume. This model is relevant to thromboembolic stroke in humans and may be useful in documenting the safety and efficacy of fibrinolytic intervention and in investigating therapies complementary to antithrombotic therapy.
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PMID:A rat model of focal embolic cerebral ischemia. 935 90


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