Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In persons with anti-Lewis antibodies, erythrocyte agglutination might take place during breathing of odors from secretors of Lewis antigens. The agglutinates occlude capillary vessels, increasing resistance to blood flow. This might lead to the sudden death of adults, sudden infant death syndrome or to diseases accompanied by tissue ischemia, such as migraine, glaucoma, epilepsy, etc.
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PMID:Lewis antigens as a possible cause of sudden death of previously healthy adults and infants and of diseases and phenomena linked to tissue ischemia. 946 79

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

Benign paroxysmal vertigo of childhood is a clinical disorder that usually begins at age 4. The child's otoneurological examination is normal in the intercrisis and the brief episodes of true vertigo are typical. In this paper we describe six new cases that had a follow-up of at least one year after diagnosis. Only a few of the patients had demonstrated vasomotor migraine, but all the children had a family history of migraine, which supports the hypothesis that this disorder is a migraine equivalent. The pathogenesis may be related with a transitory vascular disturbance that produces ischemia of the vestibular nuclei and pathways, as occurs in other vascular territories during typical migraine. One longer-than-usual episode is reported. Otherwise, the evolution of this condition is favorable.
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PMID:[Benign paroxysmal vertigo in childhood]. 965 Mar 15

The most common initial symptom of aortic dissection is chest pain. Other initial symptoms include pain in the neck, throat, abdomen and lower back, syncope, paresis, and dyspnoea. Headache as the initial symptom of aortic dissection has not been described previously. A 61-year-old woman with a history of migraine and arterial hypertension developed continuous bifrontal headache. Two hours later, right-sided thoracic pain and a diastolic murmur were suggestive of aortic dissection that was confirmed by echocardiography and subsequent surgery. The dissection commenced in the ascending aorta and involved all cervical arteries until the base of the skull. Headache as the initial manifestation of aortic dissection was assumed due to either vessel distension or pericarotid plexus ischemia. Aortic dissection has to be considered as a rare differential diagnosis of frontal headache, especially in patients who develop aortic regurgitation or chest pain for the first time.
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PMID:Headache as the initial manifestation of acute aortic dissection type A. 982 52

The authors present two patients with acute arterial vasospasm of the lower extremities causing marked ischemia. One patient had a history of Raynaud's disease, the second had been taking Cafergot for migraine headaches. Both patients's were given a test dose of intra-arterial tolazoline (50 mg). The patient with Raynaud's disease demonstrated marked improvement diffusely and was successfully treated with overnight infusion of papaverine. The second patient, taking Cafergot, demonstrated no angiographic response to tolazoline. It was speculated that the arteries of this patient were thrombosed. The patient was successfully treated with urokinase and remained free of pain at the 15-month follow-up.
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PMID:Limb-threatening lower extremity ischemia successfully treated with intra-arterial infusion--case reports. 1008 3

Despite normal cerebral oxygenation and normal global cerebral metabolism, vasogenic edema develops in humans (and sheep) who become moderately ill with AMS/ HACE during 24 hr or more of hypoxic exposure. Hypoxic cerebral vasodilatation appears to be a necessary ingredient but does not per se explain the development of brain edema. In addition to mechanical factors, a number of biochemical mediators might play a role in altering the blood-brain barrier. Brain cell swelling (cytotoxic edema) likely has a role only in the later stages of HACE and not in AMS. The hypothesis that AMS is due to cerebral edema appears to be true for moderate-to-severe illness, but whether early AMS, especially the headache, is caused by edema is not known. Other mechanisms for the headache, perhaps similar to those of migraine, need to be explored. New data suggest that the brain swells on ascent to high altitudes regardless of AMS. Whether this is due to edema or engorgement with blood is not yet clear. The "tight fit" hypothesis proposes that individual anatomy of the craniospinal axis determines tolerance to mild brain edema and might help explain individual susceptibility; preliminary studies support this notion. Therapy for AMS and HACE is directed to reducing brain volume and stopping the BBB leak (i.e., oxygenation, diuretics, and steroids) before secondary ischemia develops. New therapies directed specifically toward the defect in BBB permeability are likely to be successful.
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PMID:The cerebral etiology of high-altitude cerebral edema and acute mountain sickness. 1044 58

With recent developments in current density imaging (CDI), it is feasible to utilize this new technique in brain imaging applications. Since CDI's ability to measure changes in current density depends on a concomitant activity-dependent change in the conductivity of the brain tissue, we have examined the changes in complex conductivity during spreading depression (SD) in rodent neocortex using a coaxial probe. SD was chosen because it is often referred to as an animal model of cerebral ischemia and migraine with aura. The conductivity measurements revealed a change with short latency (30-60 s) followed by a change with a longer latency (200-300 s). This change in conductivity with short latency has not been reported before, and we conjecture that it may be the priming or triggering mechanism prior to the main SD episode. A 20% change in conductivity during SD is sufficiently large to be measured by CDI. Therefore, the ability to measure changes in the conductivity, as opposed to metabolic changes, makes CDI a viable approach to the study of ischemia and migraine with aura.
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PMID:Changes in the complex permittivity during spreading depression in rat cortex. 1058 18

Migraine, a common disorder of uncertain pathogenesis, is linked to ischemia in a variety of ways. In some cases the relationship is coincidental. In others, migraine may be causally related to stroke, although the mechanism of migrainous stroke, if not due to arterial dissection, is unclear. In young women, additional risk factors for stroke such as cigarette smoking, use of combined oral contraceptives and anticardiolipin antibody immunoreactivity may potentiate migraine, especially migraine with aura, as a stroke risk factor. The complexity of the relationship is highlighted in certain genetic conditions such as cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy and mitochondrial encephalopathy with lactic acidosis and stroke in which migraine and stroke are both prominent clinical features.
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PMID:The relationship of migraine and stroke. 1065 84

Spreading depression is a fascinating phenomenon that can be provoked by chemical, electrical or mechanical stimuli of the cortex. Spreading depression-like transient depolarizations are observed in the peri-infarct tissue after focal ischemia. The reduction in electrical activity and a negative direct current potential shift propagating over the cortex with a rate of 2-5 mm/minute are the physiological hallmarks. It is thought that spreading depression and peri-infarct depolarizations might play a role in the pathogenesis of migraine and stroke. However, these events have never been detected in humans. This paper reviews the physiological characteristics of spreading depression and peri-infarct depolarizations and discusses their potential role in migraine and stroke.
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PMID:["Spreading depression" and peri-infarct depolarizations. Relevant pathological events in migraine and stroke?]. 1070 8

The aim of the study was to analyze cerebrovascular hypoplasia in childhood and its clinical manifestations in a clinical population of 205 children aged 3 to 14 years. Cerebrovascular hypoplasias were diagnosed using angiography (n=63), magnetic resonance angiography, and transcranial Doppler ultrasonography. Hypoplasias were localized in the internal carotid artery in 41.9% of patients, in the middle cerebral artery in 54.1%, the anterior cerebral artery in 1.0%, and in the vertebro-basilar system in 3.0%. Clinical manifestations included transient ischemic attacks (21% of patients), cerebral infarcts (17%), progressive unilateral cerebral hemisphere atrophy (1.0%), focal and secondary generalized epileptic seizures (56.1%), and migraine-like headache (4.9%). Hypoplasias of the internal carotid artery and middle cerebral artery manifested as focal and secondary generalized epileptic seizures, transient ischemic attacks, cerebral infarcts, migraine-like headache, and progressive unilateral cerebral hemisphere atrophy, in descending order of frequency. Hypoplasias in the anterior cerebral artery or the basilar artery caused cerebral infarcts, and hypoplasias in the vertebral arteries caused transient ischemic attacks. This article discusses the pathophysiology of ischemia in the territory of the hypoplastic cerebral artery in childhood, as well as possibilities for noninvasive neuroimaging for diagnosis of cerebrovascular hypoplasias.
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PMID:Clinical manifestations of cerebrovascular hypoplasias in childhood. 1075 72


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