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)

Ergot's derivatives are widely used to treat and prevent migraine and, associated with heparin, for the prevention of deep vein thrombosis. During a five-year period, 7 patients have been admitted in our hospital for severe vasospasm of one or several extremities due to ergot's derivatives. All patients presented with acute severe ischemia of the lower limb requiring iv infusion of vasodilator drugs. Ergotamine tartrate was the responsible drug in four patients and dihydroergotamine(DHE)-heparin in three patients. Intravenous administration of sodium nitroprusside (n = 6) relieved vasospasm in all but one of the patients within hours to days and no amputation was required. Ankle or great toe to arm systolic pressure index was normalized in the majority of the patients after treatment. A sympathectomy was performed in two patients which did not improve the clinical course. Distal necrosis developed in two patients (DHE-heparin). It is concluded that incidence of severe ergotism is less than 0.5/100,000/year in Geneva. This contrasts with the high prevalence (15%) of subclinical ergotism reported by others. No amputation was required in this series in spite of severe and prolonged vasospasms. Subclinical ergotism most probably precedes for weeks the onset of severe vasospasm, which calls for close monitoring of patients taking ergot's derivatives.
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PMID:Severe iatrogenic ergotism: incidence and clinical importance. 190 11

A 59-year-old man developed dystonia and reflex sympathetic dystrophy after receiving high doses of ergotamine for migraine treatment. Ischemia is suggested as the precipitating factor.
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PMID:Dystonia and reflex sympathetic dystrophy induced by ergotamine. 158 44

Endothelial cells are not just a semipermeable membrane that forms a barrier between the blood and the vascular smooth muscles. This cell system is a highly active metabolic endocrine organ. It not only produces a number of important substances in vascular and neural homeostasis but also inactivates vasoactive substances such as serotonin and bradykinin. In addition, it produces endothelin-1 and angiotensin II; more importantly in the context of migraine, endothelial cells produce the vasodilators prostacyclin and EDRF-NO, both of which are local (paracrine) hormones. The physiologic function of endothelial cells is affected by aspirin, which prevents prostacyclin formation but has little effect on normal blood pressure. From this information, one can infer that endothelial cell production of prostacyclin does not play an important part in normal cardiovascular control. On the other hand, the administration of Ng-monomethyl-L-arginine causes immediate increases in blood pressure. Because the administration of this substance inhibits the release of EDRF-NO, it appears that this paracrine endothelial hormone actively dilates the normal circulation. It is of cardinal importance that damage or flow perturbations of cell membranes of the endothelial lining of blood vessels cause an increased production of prostaglandins. However, smooth muscle cells underlying the endothelial lining also synthesize prostacyclin. This mechanism is thought to be held in reserve to reinforce local production of prostacyclin and vasodilatation when cell damage to the endothelial lining occurs and EDRF-No is not produced. Many theories for the causation of migraine have been proposed, and some have been reviewed. Those holding sway tend to ignore inconsistencies and cite supporting evidence in favor of their pet explanation only. I therefore have no hesitation to show that the best explanation at present, based on the most recent cellular evidence, explains all features of migraine and the response of migraineurs to therapy. The endothelial cell is the most likely site of the primary abnormality (Fig. 1). Although under physiologic circumstances perivascular innervation and endothelial systems closely interact in the control of vascular tone during pathologic conditions such as ischemia, the dominant role in protecting the circulation is endothelium-mediated. The biology of headache is so diverse and our ignorance sufficiently pervasive that the investigation of endothelial cell function may solve the mystery of migraine. To match the postulated crucial role of the endothelial cell in the pathogenesis of migraine, another cell would have to be ubiquitously present throughout the vasculature and not just confined to the central nervous system.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Pathogenesis of migraine. 202 Feb 28

Many neurologic syndromes are named for literary characters. For example, the "Alice in Wonderland" syndrome of altered body perceptions, usually caused by migrainous ischemia, is so called because of the resemblance of its symptoms to the fluctuations in size and shape that plague the main character in Lewis Carroll's 1865 novel Alice in Wonderland. The medical symptoms of distorted body images match the literary description so precisely that illustrations from the original book depict them very accurately. Because Lewis Carroll suffered from classic migraine headaches, scholars have speculated that he may have experienced this syndrome himself.
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PMID:Literary neurologic syndromes. Alice in Wonderland. 203 89

DC shifts are known to occur in association with a number of physiologic phenomena including spreading depression, hypoxia, epilepsy, and hypercapnia and possibly in migraine, closed head injury, and ischemia. Magnetoencephalography (MEG) makes it possible to record these shifts by prolonged DC monitoring of brain activity and offers several advantages over DC EEG and DC electrocorticography. Among the advantages of MEG is its non-invasive nature and the lack of impedance changes at the electrode-tissue interface that produce baseline shifts in DC EEG. In DC MEG measurements, great care must be taken in dealing with a variety of artifactual signals. Environmental noise can be reduced by magnetic shielding and recognized by use of reference magnetometers. Patient-generated artifacts are numerous and can be recognized and limited by a variety of methods.
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PMID:Techniques for DC magnetoencephalography. 205 Aug 18

Transitory hearing impairment has been well documented in humans during basilar migraine attacks. Ischemia induced by activation of central nervous system adrenoreceptors by cAMP is one of the mechanisms that has been implicated, as well as calcium metabolism alterations. Propranolol-HCl has proven to be an effective treatment. Massive local adrenaline release is regarded as the primum movens mechanism triggering the liberation of other beta-receptor activators resulting in sterile edema and exudate. This exudate can be visualized (via ophthalmoscope) and is viewed as pathognomonic of a migraine attack. We investigated both the action of adrenaline and Propranolol-HCl on brainstem auditory potentials in 3 groups of young rats. The first group was perfused intra-arterially with adrenaline. The second group received the same treatment plus a prophylactic daily dose of Propranolol-HCl. The third group served as the control and received Propranolol-HCl, but was perfused with a Ringer solution. Alterations in blood flow and hearing sensitivity (BERA) following perfusion occurred in the first group only. Propranolol seems to exhibit a protective action during experimental attempts to induce migraine-like attacks in rats.
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PMID:Hearing fluctuation during migraine attacks. Activity of propranolol-HCl in rats. 206 10

Ergotamine tartrate and caffeine has been widely prescribed for the prevention and treatment of migraine headaches. Rarely the ergotamine can cause symptoms of peripheral vascular insufficiency, often concerning the lower extremities. A case report of bilateral severe ischemia to the upper limbs, caused by a chronic assumption of ergotamine tartrate is presented.
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PMID:Spasm of arm arteries due to ergotamine tartrate. A case report. 207 75

Drugs containing ergotamine are commonly used in the treatment of migraine. Hypersensitivity to these drugs may be triggered off even with intake of recommended doses, inducing peripheral ischemia. Contributing factors to ergotism are concurrent fever, liver disease and drugs such as erythromycin or propranolol. We present a case history and different methods of treatment.
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PMID:[Ergotamine induced ischemia]. 212 Jul 88

The CBF studies performed so far during attacks of migraine, may be interpreted as favouring "the vascular theory." This applies to migraine with aura as well as to migraine without aura. Migraine without aura may be due to mild focal CBF reduction--too mild to be detected by the available CBF techniques (i.e. 20% or less) and too mild to produce ischemia and aura phenomena. Migraine with aura may be due to focal CBF reduction severe enough to produce ischemia (i.e. 50% or more) and therefore also aura phenomena. The phenomenon termed "spreading oligemia" typically seen in CBF studies during migraine with aura, may be an artifact reflecting a gradual decrease of CBF in an area of constant size. The typical "march" of the aura symptoms may reflect differences in the ischemic threshold of various neurones leading to dysfunction of more and more neurones as the blood flow gradually decreases. It is concluded that migraine with and without aura may be due to the same disease process--the only difference being the intensity of vasospasm and CBF reduction.
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PMID:Migraine with and without aura: the same disease due to cerebral vasospasm of different intensity. A hypothesis based on CBF studies during migraine. 209 26

To better understand and treat painful conditions, one needs to identify the cause, discover the source, and develop knowledge of peripheral and central pain transmission; headaches are no exception. The development of appropriate animal models is important. Accordingly, we have reviewed the anatomy, neurochemistry, electrophysiology, and pharmacology of the trigeminovascular system in experimental animals and emphasized whenever possible the relevance of this final common pathway to migraine, cluster, and other headache syndromes in humans. For example, based on recent anatomic dissections, the pericarotid cavernous sinus plexus was suggested as an important focus to investigate cluster headache pathophysiology. This plexus is an anatomic point of convergence for the nerves giving rise to the signs of sympathetic and parasympathetic activity and sensory symptoms that develop in cluster patients. As in other nociceptive systems, trigeminovascular axons assume at least two important roles. One concerns the transmission of nociceptive information. Electrophysiologic evidence supports the trigeminal nucleus caudalis as an important site for the convergence of visceral (vessel) and somatic (forehead) inputs to mediate the referral of vascular pain to superficial tissues. A second important role concerns the initiation of local increases in blood flow and enhanced protein permeability (sterile inflammation) via the axonal release of vasoactive neuropeptides. Plasma extravasation develops within the dura mater following trigeminal stimulation. Extravasation can be blocked by the administration of ergot alkaloids or sumatriptan, a new serotonin-like agonist, and a prejunctional (neuronal) mechanism of action for these drugs (such as blockade of release) was suggested based on experimental evidence. Whether vasoconstriction also relates to the therapeutic efficacy remains to be determined. As in other organ systems, real or threatened tissue injury provides an important stimulus for depolarizing sensory fibers. The stimulus may come from external conditions such as reduced blood flow or hypoglycemia. The brain may also possess intrinsic neuronal mechanisms by which nociceptors may be synthesized (e.g., glutamate-induced neurotoxicity, seizures). Molecules of relevance include bradykinin, prostaglandins, leukotrienes, and potassium. Experimental evidence was presented demonstrating that the trigeminal nerve mediates hyperemia within cortical gray matter by axon-reflex like mechanisms. An important role for this nerve was established during the hyperemic period of recirculation after ischemia or during severe hypertension above the limits of autoregulation.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Basic mechanisms in vascular headache. 217 82


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