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

Vasoactive factors produced and released by the endothelium exert a powerful influence on vascular tone in the cerebral circulation. Impaired endothelium-dependent responses, such as decreased production of endothelium-derived relaxing factors, and/or release of endothelium-derived contractile factors may give rise to different pathophysiological conditions. Among the endothelium-derived contractile factors the endothelins have recently received particular attention. Endothelin-1 is the major isoform in the endothelin family, which also includes endothelin-2 and endothelin-3. Endothelin-1 is synthesized within the endothelium of cerebral vessels, whereas both endothelin-1 and endothelin-3 in addition have been identified in neurons and glia. Recent electrophysiological work has suggested a neuromodulatory role for these peptides, but at present the general interest is mainly focused on their vasoactive role. Physiological stimuli such as hypoxia, anoxia, and hemodynamic shear stress will stimulate the endothelial endothelin production. In the brain, at least two types of specific subreceptors have been cloned; ETA receptors, exclusively associated with blood vessels and ETB receptors also found on glial, epithelial, and ependymal cells. The endothelins seem so far to be the most potent vasoconstrictors yet identified. The circulating plasma levels of immunoreactive endothelin are low. Since more than 80% of the total amount released from endothelial cells seems to be secreted towards the underlying smooth muscle, endothelins have been ascribed a local vasoregulatory role. Endothelins are believed to be involved in several of our most common cerebrovascular diseases and the present review comments on their possible pathophysiological role in subarachnoid haemorrhage, cerebral ischemia, and migraine.
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PMID:Endothelins: a role in cerebrovascular disease? 795 53

This article addresses contraceptive issues for teenagers; women in the perimenopausal, postpartum, and postabortion periods; women with hematological disorders (e.g., acquired hemolytic anemia); women suffering from migraine; women with diabetes; and women with epilepsy. Specifically, it discusses how women's contraceptive needs change as they age. For example, the ideal method for perimenopausal women, who generally do not want to risk pregnancy, is male or female sterilization. The article also informs the reader what methods are most appropriate at the different periods of one's life and for various conditions. For example, since teens tend to be sexually active, the double Dutch method--condom plus combined oral contraceptive (COC) is a good practice for them. The low-dose lipid-friendly COC provides good cycle control for teens. Women with transient cerebral ischemia-related focal membrane, crescendo migraine, and focal migraine occurring for the first time after using COCs and currently use ergotamine therapy should absolutely not use COCs. The article also has tables which are helpful for practitioners. Table 1 lists the criteria for prescribing a medical contraceptive to teens without parental knowledge and consent. Table 2 explains either what contraceptives are or are not safe and effective for women with hemolytic disorders. For example, the IUD is contraindicated for women with immune thrombocytopenia purpura and thrombocythemia. A sidebar provides the reader a clinical focus.
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PMID:Contraceptive dilemmas. 807 39

The clinical use of calcium antagonists (Ca-antagonists) in neurological diseases focuses on 2 main therapeutic fields: (a) For the therapy of migraine flunarizine is the first choice therapy and nimodipine is a second line treatment. With verapamil cluster headache can be treated successfully, flunarizine shows less impressive clinical efficacy. The therapy with flunarizine may be restricted due to the incidence of extrapyramidal disturbances and depressions as known side effects. (b) The therapy of clinical conditions after subarachnoidal bleeding with nimodipine is well established. In the therapy of acute cerebral ischemia the therapeutic efficacy of nimodipine administered orally is not therapeutically proved until now; the intravenous administration of nimodipine offers the risk of acute hypotensive reactions. At present the usefulness of the administration of ca-antagonists in the so-called cerebrovascular insufficiency or dementia and various others cerebral disorders with vertigo could not be demonstrated.
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PMID:[Calcium channel blockers in therapy of neurologic diseases]. 813 34

Because there is uncertainty about the role of atherogenic and nonatherogenic risk factors for cerebral ischemia in the young, we carried out a multicenter, hospital-based, case-control study. 333 patients (15-44 years) with focal cerebral ischemia (transient ischemic attack or stroke within 8 weeks of admission) were eligible. 25 patients were excluded, according to the protocol. 308 cases were matched by age and gender to one hospital and one population control. Independent risk was shown by logistic conditional regression for migraine with aura [odds ratio (OR) = 14.8], smoking (OR = 3.7), alcohol (OR = 2.8), serum triglycerides (OR = 1.6), arrhythmias (OR = 9.5), mitral stenosis (OR = 56), coronary heart disease (OR = 4.3) and carotid stenosis or occlusion (OR = 41). Serum HDL-cholesterol had a relative protective effect (OR = 0.8). These data confirm the role of atherosclerosis and cardiac diseases as well as migraine with aura and alcohol consumption in the pathophysiology of cerebral ischemia in the young. More thorough prevention programs may contribute to earlier detection and control of all of these risk factors, but further investigations in patients with as yet unidentified risk factors are warranted because the above-mentioned factors do not account for the total risk of ischemic stroke in the young.
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PMID:Focal cerebral ischemia in young adults: a collaborative case-control study. The National Research Council Study Group. 823 6

Eleven cases of migraine with and without aura were investigated with positron emission tomography (PET). Regional cerebral blood flow (rCBF), oxygen metabolism (rCMRO2) and oxygen extraction (rOER) were measured during baseline (n = 11), aura (n = 6), headache (n = 10) and after treatment with sumatriptan (n = 4). Data were analysed using an ROI-based approach from 26 different anatomically defined regions, and also an exploratory approach whereby all subjects were normalized to a stereotactic brain atlas; t-maps were constructed by depicting significant changes between states. The exploratory approach revealed a region corresponding to the primary visual cortex with significant reductions in rCBF (23.1%) and rCMRO2 (22.5%), but no change in rOER during the headache phase compared to baseline. These data suggest that cerebral ischemia was not the primary cause of the attacks in these cases.
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PMID:Regional cerebral blood flow and oxygen metabolism during migraine with and without aura. 960 15

Prevailing hypotheses for the mechanisms of migraine are reviewed. Models of aura mechanisms include transient cerebral ischemia and spreading depression. Models of headache involve trigeminovascular and brainstem mechanisms. The ability to trigger an attack may depend on a threshold of brain excitability. Mitochondrial disorder, magnesium deficiency, and abnormality of presynaptic calcium channels may be responsible for neuronal hyperexcitability between attacks. It remains to be determined whether cortical or brainstem centers generate the attack.
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PMID:Pathogenesis of migraine. 947 13

There is uncertainty about the etiology of transient global amnesia and none of the pathogenetic hypotheses proposed so far, i.e. transient ischemia, epileptic discharge and spreading depression of cortical electrical activity, is completely satisfactory. Using water suppressed proton magnetic resonance spectroscopy we studied one patient during a typical episode of transient global amnesia and 2 weeks thereafter in order to investigate the metabolic changes in the hippocampal region. In both hippocampi, spectra of N-acetyl-aspartate, creatine-phosphocreatine, compounds containing choline and lactate failed to show changes consistent with cerebral ischemia, both in the acute phase and in the follow-up. Spreading depression in response to emotional stress seems a likely explanation in this patient, who suffered from migraine in the past.
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PMID:Proton magnetic resonance spectroscopy during transient global amnesia. 955 91

Transient global amnesia (TGA) is an acute amnestic syndrome without neurological symptoms and remitting spontaneously. Though cerebral ischemia, epilepsy, and migraine have been implicated in some cases, non of these factors could be proven responsible for most, and etiology remains unclear. Of special interest is the induction of TGA by psychological and emotional stress in about 14-29% of all cases, which is illustrated by the clinical example of a 72-year-old women who suffered an attack of TGA after discovering a burglary in her home. Psychopathological and pathogenetic aspects are discussed in the context of recent neurobiological memory research. This suggests that TGA involves transient dysfunction of a specific memory subsystem associated with hippocampal structures. Neural network modelling explains the syndrome of TGA on a pathogenetic basis allowing for heterogeneous etiology and even for psychogenic release. Thus TGA serves as a model for pathogenetic explanation in the neuro-psychiatric borderland.
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PMID:[Transitory global amnesia--psychogenic origin of organic disease? Psychopathologic basis and pathogenetic considerations]. 958 75

Anticardiolipin antibodies (aCL) are a risk factor for cerebral ischemia. In migraine, the association is controversial, with widely varying results in different small series. The controversy in part may be due to the inherent difficulty in distinguishing the transient focal neurologic events (TFNE) of migraine from TIA. To assess the frequency of aCL in migraine, we prospectively evaluated consecutive adults under 60 years of age with migraine without aura and with recent TFNE (<24-hour duration) clinically suggestive of either migraine with aura or TIA. We concomitantly enrolled persons with no CNS disease. Each person was interviewed and had blood drawn for solid-phase ELISA with IgG and IgM aCL isotyping. Neuroradiologic studies were reviewed. Patients with TFNE were followed every 6 months for the duration of the 3-year study. The frequency of aCL positivity (IgG >20, IgG >40, IgM >7.5) for the 645 patients with TFNE (8.8, 3.1, 4.2%), the 518 persons in the TFNE subgroup with migraine with aura (8.9, 3.3, 4.1%), the 497 persons with migraine without aura (7.0, 2.0, 3.6%), and the 366 control subjects (9.3, 3.6, 3.9%) did not differ significantly between groups. In TFNE patients with elevated aCL titer, the association was positive with diabetes mellitus, TFNE duration <15 minutes, and diplopia and was negative with hemiparesis, tinnitus, and family history of stroke. Findings on imaging consistent with cerebral ischemia were more frequent in aCL-positive persons. The short-term risk of stroke was uniformly low. In young persons, aCL is not associated with migraine or with TFNE, although diabetes mellitus, negative family history of stroke, and brief duration of symptoms (including diplopia) may predict immunoreactivity. Imaging studies suggest an ischemic etiology of TFNE in this cohort.
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PMID:Role of anticardiolipin antibodies in young persons with migraine and transient focal neurologic events: a prospective study. 1010 49

When young patients suffer a stroke the etiology often differs from that found in the elderly. One of the risk factors for stroke in young people could possibly be migraine. The first author to describe what was probably a migrainous cerebral infarction was Wepfer, in 1727. In recent years, cases of stroke in migraineurs have been frequently reported. Extensive cohort studies and smaller, well-conducted case-control studies seem to confirm that migraine is a risk factor for stroke. However, the risk is only moderately increased, perhaps doubled. Among women under the age of 45, the correlation is greater with a threefold increased risk of stroke in a migraineur; it is even greater in patients suffering attacks of migraine with aura. Pure migrainous infarctions are probably rare and reports are perhaps exaggerated in the literature. Cerebral ischaemia may lead to symptomatic migraine attacks. Overall, the absolute risk of stroke is small enough to validate the opinion that migraine is a benign condition.
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PMID:[Migraine and stroke]. 963 61


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