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

The cause of transient global amnesia (TGA) remains controversial. Focal cerebral ischemia, seizure, venous congestion, and migraine have all been proposed as underlying mechanisms. We describe a patient presenting with typical TGA who two days later developed a posterior circulation stroke due to basilar artery occlusion. He was treated successfully with intra-arterial thrombolytic therapy. Shortly thereafter, he had recurrent basilar artery thrombosis and jugular vein thrombosis, and was found to have a mucinous adenocarcinoma believed to be causing a hypercoagulable state. We believe this case supports the hypothesis that TGA can on occasion be caused by cerebral ischemia.
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PMID:Transient global amnesia heralding basilar artery thrombosis. 1631 Nov 49

Saline and indocyanine green dye were the first agents noted to produce a contrast effect when injected peripherally during M-mode echocardiographic imaging, although it was subsequently found that almost any type of injected solution would have this effect. These first-generation contrast agents were limited to opacification of right heart structures, and they prompted subsequent development of agents that traverse pulmonary circulation. Although opacification limited to right heart structures is considered a limitation of these first-generation agents, this is an advantage when attempting to identify the presence of right-to-left shunt. First-generation air contrast is considered the gold standard for identification of patent foramen ovale (PFO). However, PFO investigators have used varying criteria to define abnormal contrast studies. There are also multiple mechanisms by which saline contrast studies may produce both false-positive and false-negative results for presence of PFO. There is mounting experimental evidence that PFO is associated with cerebral ischemia and migraine headache, with a resulting evolution of devices for percutaneous closure of these shunts. Echocardiographic physicians must be aware of potential pitfalls of the air contrast technique to avoid exposing patients to unnecessary risk of closure devices, and missing the potential benefit of shunt closure in appropriately selected patients.
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PMID:A critical review of patent foramen ovale detection using saline contrast echocardiography: when bubbles lie. 1645 28

In this hospital case series study we enrolled 394 consecutive ischemic stroke patients aged 14-47 years, all of whom were submitted to a diagnostic protocol. We evaluated the incidence of cerebral ischemia in young adults, as well as the risk factors and the etiopathogenesis of this pathology. Modified diagnostic criteria adopted from the TOAST and Baltimore-Washington Cooperative Young Stroke Study were used for the etiologic classification. The crude annual incidence rate was 8.8/100,000 (95% CI 7.7-9.9), which is in keeping with the rates reported in comparable registries. Risk factors were distributed as follows: smoking in 56% of patients, hypertension in 23%, dyslipidemia in 15%, migraine in 26%, and diabetes mellitus in 2%. Oral contraceptives were being taken by 38% of the women enrolled. The etiology of stroke in the patients was as follows: cardioembolism in 34%, atherothrombosis in 12%, non-atherosclerotic vasculopathies in 14% (including arterial dissection in 12%), other determined causes in 13%, lacunar stroke in 2.5%, migraine in 1%, and undetermined causes in 24%. Despite its biased sampling frame, this large hospital case series, in which risk factor distribution and etiopathogenesis were investigated, stresses the need for an adequate diagnostic approach in young ischemic patients.
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PMID:A case series of young stroke in Rome. 1649 45

The identification of comorbid disorders in migraineurs is important since it may impose therapeutic challenges and limit treatment options. Moreover, the study of comorbidity might lead to improve our knowledge about causes and consequences of migraine. Comorbid neuropathologies in migraine may involve mood disorders (depression, mania, anxiety, panic attacks), epilepsy, essential tremor, stroke, and white matter abnormalities. Particularly, a complex bidirectional relation exists between migraine and stroke, including migraine as a risk factor for cerebral ischemia, migraine caused by cerebral ischemia, migraine as a cause of stroke, migraine mimicking cerebral ischemia, migraine and cerebral ischemia sharing a common cause, and migraine associated with subclinical vascular brain lesions.
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PMID:Comorbid neuropathologies in migraine. 1676 30

Current treatment protocols using reperfusion therapy for acute ischemic stroke rely on non-contrast computed tomography (NCCT), with most indications including the absence of acute hemorrhage or large volume of infarction in the presence of clinical signs and symptoms. This predictably results in a significant incidence of the administration of reperfusion therapy to patients with "stroke mimics," such as migraine headache or Todd's paralysis after a seizure. Diffusion-weighted imaging (DWI) is a technique based on magnetic resonance imaging (MRI) that may be more sensitive and specific for acute cerebral ischemia than NCCT. In addition, data for techniques such as perfusion-weighted imaging can be acquired with minimal additional time required. This may allow better risk assessment of a clinical response to reperfusion therapy vs. the possibility of hemorrhagic complications. This article describes a methodical review of studies comparing the sensitivity, specificity, positive predictive value, and negative predictive value of DWI vs. NCCT in the evaluation of acute ischemic stroke. Data from studies meeting our screening criteria are combined to produce overall values for each.
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PMID:Diffusion-weighted magnetic resonance imaging versus computed tomography in the diagnosis of acute ischemic stroke. 1698 60

The association between migraine and stroke is complex and bidirectional. Epidemiological studies suggest that migraine may be a risk factor for stroke; magnetic resonance studies suggest that white matter abnormalities may be more frequent in migraine patients than in controls; and stroke may occur during the course of a migraine with aura (MA) attack (migrainous stroke). However, the relationship between migraine, aura and stroke is complex and mechanisms other than a direct cause/effect relationship are possible. Migraine aura may be the consequence, rather than the cause of cerebral ischaemia. Furthermore both MA and stroke may be secondary to a third underlying condition. In this review we analyse data regarding the relationship between migraine and stroke considering 3 aspects: (1) migraine as a risk factor for stroke, (2) migraine as a cause of stroke and (3) migraine and cerebral ischaemia sharing a common cause.
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PMID:Migraine and cerebrovascular disease. 1750 64

Several mechanisms are currently thought to contribute to migraine pathogenesis, including interictal neuronal hyperexcitability, cortical spreading depression underlying the symptom of aura, and trigeminal nerve activation at a peripheral and central level. However, these mechanistic concepts incompletely explain migraine susceptibility in individual patients and do not fully account for the well documented association between migraine and ischemic cerebrovascular disease, including increased risk of both clinical stroke and subclinical brain lesions in migraine patients. The circle of Willis is a major source of collateral blood flow supply in the human brain, and developmental morphologic variants of the circle of Willis are extremely frequent. Altered cerebral blood flow (CBF) has been demonstrated in regions supplied by variant circle of Willis vessels. Our central hypothesis is that circle of Willis anomalies correlate with alterations in cerebral hemodynamics and contribute to migraine susceptibility and ischemic complications of migraine. Dysregulation of CBF may allow relative ischemia to develop in the setting of increased metabolic demand related to neuronal hyperexcitability, may trigger cortical spreading depression, and may predispose individuals with migraine to ischemic lesions and stroke. Identification of structural alterations in the cerebral vasculature in migraine patients would have several important pathophysiological and clinical implications. First, it would provide a developmental mechanism for migraine susceptibility that may lead to further insights into genetic predisposition to migraine. Second, it would expand understanding of potential mechanisms underlying migraine aura and linking migraine with both clinical and subclinical cerebral infarction. Third, it could help to identify the subpopulation of patients at risk of progressive cerebral ischemia so as to target preventative therapies appropriately. Fourth, it would suggest a role for further diagnostic evaluation to determine migraine mechanism in individual patients, analogous to the current paradigm in ischemic stroke in which determination of stroke mechanism is critical to therapeutic decision-making.
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PMID:Migraine and circle of Willis anomalies. 1822 67

This perspective discusses cortical spreading depression (CSD) phenomena and their translational significance for human migraine aura and the peri-infarct events following cerebral ischemia and injury. They begin with interstitial K(+) release and accumulation following neuronal stimulation, and a buffering astrocytic K(+) influx and remote liberation propagating waves of neuronal hyperexcitability and depression. Diffusion-weighted echoplanar MRI demonstrates CSD features in gyrencephalic brains recapitulating human migraine aura, spatial and temporal features of single primary events and multiple secondary events, their stimulus dependence, pharmacological properties, and their relationship to blood oxygenation level-dependent signals and late cerebrovascular changes. The article finally explores prospects for physiological studies of CSD gaining fuller insights both into mechanisms underlying the pathology of the corresponding human condition and possible approaches to management.
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PMID:Translational imaging studies of cortical spreading depression in experimental models for migraine aura. 1845 33

Numerous epidemiologic observations reporting high prevalence of migraine among young individuals with stroke as well as dysfunction of cerebral arteries during migraine attacks prompt speculation on the existence of a comorbidity between the two disorders. The recent finding of silent infarct-like brain lesions in migraineurs reinforced this hypothesis and raised questions on whether migraine may be a progressive disorder rather than simply an episodic disorder. Stroke can occur during the course of migraine attacks with aura, supporting the assumption of a causal relation between the two diseases. Migraine may accentuate other existing risk factors for stroke, and both jointly increase the risk of cerebral ischemia outside of migraine attacks. In this regard, the role of migraine might be that of predisposing condition for cerebral ischemia. Migraine and ischemic stroke may be the end phenotype of common pathogenic mechanisms. Evidence of a migraine-stroke relation in cases of specific disorders, such as CADASIL (cerebral autosomal-dominant arteriopathy with subcortical infarcts and leukoencephalopathy) and MELAS (mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes), strongly supports this concept. Finally, acute focal cerebral ischemia can trigger migraine attacks, and, thus, migraine may be the consequence of stroke. In this paper, we will review contemporary epidemiologic studies, discuss potential mechanisms of migraine-induced stroke and comorbid ischemic stroke, and pose new research questions.
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PMID:Migraine and ischemic stroke: a debated question. 1846 Oct 80

The antiphospholipid syndrome (APS) is defined by the presence of antiphospholipid antibodies (aPL), associated with thrombosis or recurrent spontaneous abortions. APS can occur alone or secondary to other conditions, especially associated to inflammatory systemic autoimmune diseases. Among the neurological manifestations associated with aPL, only ischemic stroke is recognized by the actual classification criteria for APS. Other neurological manifestations have been, however, repeatedly reported in case studies of APS patients. Headache, and especially migraine, was commonly reported in APS patients and is one of the classical features described by Hughes as related to aPL, but studies failed to confirm this association. We studied retrospectively the association between headache syndromes and aPL in 428 patients with inflammatory connective tissue diseases admitted in the Neurology and Internal Medicine Departments of Colentina Hospital-Bucharest. We found that migraine alone, not headache of all types, is significantly associated with aPL in patients with systemic immune disease. We studied the presence of cerebral ischemia in patients with headache and aPL. In SLE patients, headache (all types) is significantly associated with positive titers of aPL, and cerebral ischemic lesions are significantly encountered. Even if both migraine and aPL are conditions with high frequency in patients with immune systemic disease and their association may be coincidental, the presence of ischemic lesions in patients showing this association suggests the need to define a sub-group at risk, for whom headache can be a marker and anticoagulants can be discussed.
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PMID:Antiphospholipid antibodies and migraine: a retrospective study of 428 patients with inflammatory connective tissue diseases. 1876 11


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