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

The authors analysed clinically 108 patients (61 males and 47 females), aged below 50 years treated at the department of neurology, because of acute cerebral ischaemia. Attention is called to risk factors such as arterial hypertension, heart disease, atherosclerosis, obesity and diabetes which may be the cause of earlier development of ischaemic changes in the central nervous system. In the analysed group in 18 cases cerebral thrombosis, in 23 cases embolism, in 31 cerebral circulatory failure were diagnosed. In 36 cases the cause could not have been established.
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PMID:[Acute cerebral ischemic disease in patients under the age of 50]. 88 1

It is sometimes very difficult to diagnose dissecting aortic aneurysms (DAA), particularly in its early stage, due to manifold signs and symptoms. The purpose of this study is to clarify the reasons for such erroneous diagnoses. A total of 41 patients with DAA were referred to our hospitals for further examination and/or surgery from April 1986 to August 1989. In 18 of these patients, the diagnostic possibility of an underlying DAA was overlooked by the referring physicians. Among these 18 patients, 2 were mistakenly diagnosed as uncomplicated myocardial infarction (MI), one as pneumonia, 2 as cerebral infarction, 6 as acute abdominal disease, one as cholelithiasis, 5 as thrombosis of the lower extremities, and one as malignant metastasis to the pericardium. The following is the detail: In 2 cases thought to be uncomplicated MI, an expanding dissecting ascending aorta had crushed the lumen of the left coronary artery, causing MI, in turn, wasting clinical treatment and consuming precious time. In one case, enlargement of the descending aorta on the chest radiography was overlooked and the patient's symptoms were mistakenly attributed to pneumonia. In 2 cases in which symptoms of cerebral ischemia were thought to be attributed to cerebral thrombosis, the real cause turned out to be occlusion of the brachiocephalic artery following aortic dissection. Among 6 cases which were initially considered to have only acute abdominal disease, 3 presented with symptoms and signs of ileus, and their exploratory laparotomies yielded no positive findings.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The pitfalls in the clinical diagnosis of dissecting aortic aneurysm]. 133 5

A drug surveillance study was conducted, aimed at evaluating the efficacy and safety of nicardipine in outpatients with cerebrovascular diseases and at assessing the changes in nonfocal symptoms in the treated patients. The 3,150 outpatients (mean age, 68.9 years) were being treated by general practitioners and neurologists in Barcelona, Spain. Cerebral embolism was diagnosed in 4.0%, cerebral thrombosis in 13.0%, transitory ischemic attack in 28.0%, and chronic cerebral ischemia in 55.0%. The daily dose of nicardipine ranged from 20 to 180 mg; 87.7% of the patients received 60 mg of nicardipine daily. Concomitant medications were being taken by 89.1% of the patients. Treatment was evaluated in 2,913 patients. After 60 days of treatment, marked improvement was noted in 31.0% of the patients, moderate improvement in 39.0%, slight improvement in 20.0%, and no change in 10.0%. Marked or moderate improvement was noted in 69.6% of the patients who received nicardipine alone and in 66.9% of the patients who received concomitant medications. Clinically significant drops in blood pressure during treatment were found in the hypertensive patients. Side effects were reported by 14.5% of all patients and by 4.6% of the patients who received nicardipine alone. It is concluded that the daily administration of nicardipine is safe and effective in outpatients with cerebrovascular disorders.
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PMID:Nicardipine in the treatment of outpatients with cerebrovascular disorders. 193 2

Acute myocardial infarction is most commonly initiated by fissuring of an atheromatous plaque. Through such fissures the blood is exposed to thrombogenic constituents of the intima, causing thrombotic obstruction of the coronary artery. Why plaque fissuring occurs is not known. Our investigation is to establish which types of plaque undergo fissuring by relating their mechanical with their cellular and biochemical properties; and to quantify the distribution of fissures. Results so far indicate that fissures occur predominantly in plaques with lipid pools in one segment of intima, and that the commonest single site of fissuring is that of maximal stress concentration as predicted by computer modelling. The results also suggest that arterial spasm at the immediate site of fissuring is not involved, as more than half the fissures occur at sites where there is no residual medial smooth muscle. Obstructive coronary thrombosis is initiated in most cases by plaque fissure with local haemorrhage which induces intravascular platelet aggregation. Recent observations with novel techniques have provided evidence that platelet aggregation in vivo is initiated by ADP and potentiated by thromboxane A2 and thrombin, with actual contribution of exposed collagen still undetermined. These observations provide an explanation for the limited effectiveness of any simple platelet-inhibiting drug, including Aspirin, by itself whenever arterial, eg. coronary or cerebral thrombosis is initiated by haemorrhages into atheromatous plaques. On the other hand, Aspirin is significantly effective when myocardial infarction follows unstable angina and when strokes follow transient episodes of cerebral ischaemia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Coronary thrombosis: pathogenesis and prevention. 210 21

Treatment with the calcium entry blocker nimodipine is recommended as effective therapy for cerebral ischemia due to cerebral vasospasm or cerebral thrombosis. On the other hand, treatment with induced hypertension is a widely accepted measure to reverse ischemic deficits caused by vasospasm. Thus, a combination of the two regimens--nimodipine and induced hypertension--may have real benefits for cerebral ischemia. But it is possible that the benefit of one is abolished by adverse effects of the other, or that a combination of both may not be as effective as the use of only one therapy. In order to investigate these problems, the effects of nimodipine and induced hypertension on cerebral vessel, cerebral blood flow, cerebral edema and cerebral infarction using a one hour middle-cerebral-artery occlusion model in cats. Twenty-one anesthetized cats were divided into a control group, the nimodipine-treated group, and the nimodipine-and-induced-hypertension group. There were seven cats in each group. Occlusion of the middle cerebral artery (MCA) was continued for one hour in each animal. Induced hypertension was a little higher than resting values, and it was continued for only one hour during MCA occlusion, brought on by instillation of dopamine. Cerebral pial arteries dilated much more prominently during and after the occlusion of MCA in the nimodipine-and-induced-hypertension group than other groups. Although cerebral blood flow in the nimodipine group, and the nimodipine-and-induced-hypertension group increased more in the non-ischemic hemisphere, the most remarkable increase was seen around the infarcted cortex in the control group.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Effect of calcium antagonist nimodipine and induced hypertension on cerebral vessel reactivities, cerebral blood flow, cerebral edema and infarction in cats with one hour middle-cerebral-artery occlusion]. 238 17

Of 171 patients evaluated prospectively and consecutively for cerebral ischemia, 26 (15%) developed symptoms while hospitalized. Cerebral ischemia complicated operative procedures in 12 patients, unsuccessful cardioversion in one and coronary angiography in another. Twelve patients had apparent cerebral embolism and 14 patients had cerebral thrombosis as a mechanism of their symptoms. Hospitalized patients who suffered cerebral ischemia had one or more of the following: risk factors for stroke including cardiac source of embolus, previous stroke, diagnostic or therapeutic procedures for vascular disease, or chronic hypertension complicated by acute hypotension.
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PMID:Mechanism of in-hospital cerebral ischemia. 371 40

One hundred and one patients below 45 years and showing objective signs of cerebral ischemia were studied retrospectively for pathogenic factors. Twelve were below 15 years; the male to female ratio was 1:1. Factors known as predisposing (heart disease, hypertension, hyperlipemia, diabetes mellitus or infectious diseases) and other possible factors (e.g. trauma, abuse) were found in 41 patients. Among women using contraceptive pills there might be an increased risk of development of cerebral thrombosis, but the material was not large enough to warrant statistical analysis. In 64 patients one or more abnormal coagulation values were found, the most frequent being a deficient vessel wall fibrinolysis, which was noted in 38%. We therefore consider it worthwhile to investigate the fibrinolytic defence mechanism of the vessel wall in patients with cerebral thrombosis, since it is possible to treat this condition with specific fibrinolytic stimulating agents.
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PMID:Coagulation studies in children and young adults with cerebral ischemic episodes. 732 67

A retrospective case control study was carried out in order to assess the risk of developing cerebral thromboembolism with the use of low-dose oral contraceptives (OC). The subjects were all the 794 women in Denmark aged 15-44 who had suffered a cerebral thromboembolic attack (CTA) during the period of January 1, 1985 and December 31, 1989, and an age-matched randomly selected control population of 1588 women. CTA included occlusion of precerebral arteria, cerebral thrombosis, cerebral embolism, transitory cerebral ischaemia, and the unspecified group apoplexia cerebri. 590 of 692 cases (85.1%) and 1396 of 1584 controls were provided, among whom 1197 reported use/non-use of OC. Among 320 cases, 116 (36.3%) were OC users at the time of the CTA vs. 191 users (16.0%) among 1197 controls, corresponding to a crude odds ratio (OR) of 3.00. After multivariate analysis including confounder control for age, smoking habits, years of schooling and the trend in use of different types of OC during the period 1985-1990, OC use with 50 mcg estrogen implied an OR for CTA of 2.9 (1.6-5.4), 30-40 mcg estrogen OC an OR of 1.8 (1.1-2.9), and pure progestogen minipills an OR of 0.9 (0.4-2.4), which was not significantly different from the risk of never users. The OR did not change significantly with duration of OC use or with increasing age. 63.6% of cases smoked compared to 48.8% of controls. After correction for age, OC use and the duration of education, smoking suggested an OR for CTA of 1.5-1.6 (1.1-2.4) (p 0.001). A 50% increased risk of developing CTA among cigarette smokers (after appropriate confounder control) was independent of OC status and age. Low-dose OC use suggests an increased risk of developing CTA. Combination or sequential OCs with 30-40 mcg estrogen represent a one-third reduced risk compared to preparations with 50 mcg estrogen. Minipills containing pure progestogen do not pose an increased risk of CTA.
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PMID:[Oral contraceptives and cerebral thromboembolism. A Danish case-control study]. 823 74

Single photon emission computed tomography (SPECT) using 123I-Iomanzenil (IMZ), a tracer which binds specifically to central-type benzodiazepine receptors, was performed in patients with cerebrovascular diseases (CVD) to determine the clinical signicigance of IMZ SPECT studies in evaluating the pathophysiology of CVD. IMZ SPECT images obtained three hours after administration of the tracer were compared with the images of cerebral blood flow (CBF) studies in 206 cases. In regions with decreased CBF, the uptake of IMZ was relatively preserved in patients with cerebral thrombosis in comparison with cerebral embolism, and in those with perforator branch infarction in comparison with cortical infarction. The uptake of IMZ decreased as a function of both the severity of the decrease in the CBF and the duration of illness in regions with a significantly decreased perfusion reserve. These results suggest that decreased IMZ binding in ischemic stroke reflects the neuronal damage caused by the cerebral ischemia. On the other hand, in patients with intracerebral hemorrhage, the cortical uptake of IMZ was relatively well-preserved in regions with decreased CBF, and the decrease in the uptake of IMZ was more profound as a function of the decrease in the CBF, especially in cases of putaminal hemorrhage. These results also suggest that the decreased cortical CBF is a remote effect caused by a neuronal disconnection, and neuronal damage may occur in regions with severely impaired CBF.
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PMID:[A phase 3 clinical trial of 123I-iomazenil, a new central-type benzodiazepine receptor imaging agent (Part 4)--Report on clinical usefulness in diagnosis of cerebrovascular diseases]. 862 66

This paper will examine how cerebral perfusion deficits in cocaine abusers may be a target for pharmacotherapy. The review covers five areas: (1) cerebral ischemia and neuropsychological impairment in cocaine abusers, (2) neuroimaging evidence for cerebral perfusion defects in cocaine abusers, (3) mechanisms for cocaine induced cerebral thrombosis, (4) neurotoxicity from cerebral ischemia and excitatory amino acids, (5) glutamate antagonists as potential treatment agents for cocaine induced neurotoxicity. Several pharmacotherapies are suggested including antiplatelet agents and excitatory amino acid (EAA) antagonists such as lamotrigine. Clinical trials in cocaine abusers with cerebral perfusion defects are indicated and EAA antagonists hold promise as they are developed for stroke treatment.
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PMID:Pharmacotherapy of cerebral ischemia in cocaine dependence. 954 50


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