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)

Five patients, all women in their 50s and all with a documented history of migraine headaches, had ischemic chest pains investigated. Four patients had angina primarily occurring at rest, with documented ischemic electrocardiographic changes during pain in all five. Three subjects sustained myocardial infarction, one shortly after taking ergotamine tartrate for an acute attack of migraine. Subsequent coronary angiography in all five subjects revealed no evidence of atherosclerotic coronary artery disease, suggestive of spasm as the cause of ischemia. In subjects with known migraine, the occurrence of chest pain may represent coronary artery spasm, and should be investigated with concurrent electrocardiographs, as these two clinical entities may be related as part of a generalised vasospastic disorder. The use of ergot preparations should be contraindicated in such patients, as exacerbation of chest pain and frank myocardial infarction may result. These chest pains responded favourably to calcium channel blockers.
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PMID:A possible relationship between migraine and coronary artery spasm. 346 72

Acute ischemia of the brain induces a cascade of biochemical and physiological events. The final consequences depend on the fact whether ischemia is of transient or permanent, total or partial nature. Alteration of extracellular potassium concentration, intracellular calcium and potassium concentration, development of cytotoxic and vasogenic edema, postischemic hyperfusion and no-reflow phenomenon are important factors which decide about the final fate of functional capacity. CO2 reactivity, autoregulation and hemorheology must be considered when therapeutic approaches are used to influence basic flow during ischemic condition. At present there exists no therapy which has been fully accepted and is able to guarantee benefit to the hypoperfused tissue. Since the calcium metabolism is altered by ischemic processes, substances which act on this metabolism might be of value in the treatment of ischemia and its consequences. However, their beneficial effect on cerebral infarction has not been proven yet. In subarachnoid hemorrhage and migraine calcium antagonists are used to prevent and treat ischemia. In epilepsia calcium overload blockers have been tried by one group with promising results.
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PMID:Is there a need for alternative approaches in the therapy of cerebrovascular disorders? 375 10

A retrospective study was conducted on a young adults population affected by permanent symptoms of cerebral focal ischemia. Within 6 years, 24 patients between the ages of twenty and fifty were admitted to the Neurological and Medical department of our Hospital because of cerebral ischemic stroke. In 7 (29.2%) there was a previous history of common or classic migraine. No patients suffered headache at the time of neurologic deficit onset. In the other 17 patients in the study, 6 (25%) had valvular heart disease, 2 (8.3%) had signs suggestive of vasculitis, 2 (8.3%) had a story of head and neck injury, and in the remaining 7 (29.2%) patients no discernible etiology was demonstrated. Our data confirm the hypothesis that migraine may be considered an etiologic factor for persistent cerebral ischemia in young adults.
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PMID:[Hemicrania and cerebral ischemia in young adults]. 377 93

Treatment of migraine with ergot alkaloids may produce systemic vasospasm in patients, especially as a result of automedication and overconsumption but also due to individual hypersensitivity. Peripheral vasoconstriction may lead to gangrene of the extremities, necessitating amputation. Various treatments have been tried against ischemic complications during ergotism with varied and unpredictable results. We report two recent cases of severe acute peripheral ischemia due to ergotamine abuse successfully treated with continuous systemic sodium nitroprusside infusion. The doses used during intraarterial injection are well below those known to be toxic. Consequently, the adverse effects of cyanide toxicity can be avoided. We think that intraarterial infusion of sodium nitroprusside, associated with forced diuresis and the administration of hydroxycobalamin, constitutes the treatment of choice of extreme peripheral ischemia of ergotism.
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PMID:Intraarterial sodium nitroprusside infusion in the treatment of severe ergotism. 380 6

This study investigates whether the cerebral blood flow reduction occurring in attacks of classic migraine is sufficient to cause neurologic deficits. Regional cerebral blood flow measured with the xenon 133 intracarotid injection technique was analyzed in 11 patients in whom a low-flow area developed during attacks of classic migraine. When measured with this technique, regional cerebral blood flow in focal low-flow areas will be overestimated because of the effect of scattered radiation (Compton scatter) on the recordings. In this study, this effect was particularly taken into account when evaluating the degree of blood flow reduction. During attacks of classic migraine, cerebral blood flow reductions averaging 52% were observed focally in the 11 patients. Cerebral blood flow levels known to be insufficient for normal cortical function (less than 16 to 23 mL/100 g/min) were measured in seven patients during the attacks. This was probably also the case in the remaining four patients, but the effect of scattered radiation made a reliable evaluation of blood flow impossible. It is concluded that the blood flow reduction that occurs during attacks of classic migraine is sufficient to cause ischemia and neurologic deficits. Hence, this study suggests a vascular origin of the prodromal neurologic deficits that may accompany attacks of classic migraine.
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PMID:Ischemia may be the primary cause of the neurologic deficits in classic migraine. 230 80

According to classic theory, a migraine attack is initiated by cerebrovascular spasm followed by extracranial vasodilatation. Results of recent studies support this theory and suggest that cerebral blood flow during the initial phase of migraine symptoms is, in fact, decreased and this decrease probably leads to ischemia and hypoxia. Cellular hypoxia, in turn, can cause an increase in the flow of calcium from the extracellular fluid to the intracellular space, resulting in calcium overload and cellular dysfunction. Because calcium-channel blockers selectively inhibit the intracellular influx of calcium ions, investigators have begun evaluating the efficacy of these agents for migraine prophylaxis. Nimodipine, a calcium-channel blocker that exhibits selective effects on cerebral vessels, seems to offer protection against the cerebral ischemia and hypoxia presumed to be operative during migraine attacks. In a double-blind, placebo-controlled study, nimodipine decreased the frequency and duration of migraine attacks by at least half in 69% of patients treated with this agent. Comparable reductions in migraine frequency and duration were attained in 58, 51, 41 and 52% of patients treated with methysergide maleate, pizotifen, clonidine hydrochloride and propranolol, respectively. The piperazine derivative flunarizine also has calcium-channel blocking properties. This agent prevents vasospasm in cerebral arteries and protects against cerebral hypoxia. Results of double-blind studies of migraine prophylaxis with flunarizine demonstrate the beneficial effects of this agent, particularly in younger patients. Flunarizine proved to be superior to pizotifen in decreasing the severity of migraine attacks and comparable to pizotifen in decreasing their frequency.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Calcium-channel blockers in the treatment of migraine. 388 6

The clinical picture and investigation of 26 patients (16 males and 10 females) with diagnosis of transient global amnesia (TGA) are reported. Age ranged from 51 to 78 years at the time of TGA, which occurred mor often between 60 and 70 year-old people. Three patients presented more than one episode (3, 4 and 5). Precipitating factors were identified in 8 cases (emotional stress in 7 and physical exercise in 1). Risk factors for cerebrovascular disease were found in 13 cases, mainly hypertension (9 cases) and diabetes (3 cases). EEG was normal in 20 cases and disclosed diffuse delta waves in 2, temporal delta waves in 1 and temporal theta waves in another patient. CAT scan showed no abnormalities in 3 cases and ischemia in the vertebro-basilar system in another 2. Brain angiography was normal in 1 case and showed abnormalities in the vertebro-basilar system arteries in 3. During the follow-up period, which ranged from 1 to 84 months, no neurologic deterioration was seen. The role of risk factors for vascular diseases, epilepsy and migraine in the development of TGA is discussed.
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PMID:[Transient global amnesia: study of 26 cases]. 401 36

One hypothesized cause of low-tension glaucoma is chronic or intermittent ischemia of the optic nerve. Since the optic nerve and brain are both parts of the central nervous system and share a common blood supply, the authors wondered if patients with low-tension glaucoma might also have clinical or radiographic evidence of cerebral atrophy. In this study, 27 patients with low-tension glaucoma were examined using neurobehavioral testing, electroencephalography, computerized tomographic scan, neurological history, and physical examination. In only a small number of patients were these tests abnormal. However, 12 of the 27 patients gave a history of common or classic migraine. This unexpected finding raises the possibility that migraine-related ischemia might be the pathogenic mechanism in some cases of low-tension glaucoma.
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PMID:The neurologic evaluation of patients with low-tension glaucoma. 401

The effect of 30 min voluntary toothclenching was studied in 48 patients with common migraine, randomized in two groups. Group 1 performed low-level tension at 5% and group 2, high-level tension at 30% of the individual maximum, as judged by surface EMG from the temporal muscle. Pericranial muscle tenderness was evaluated by manual palpation and a four-point verbal scale. Headache, nausea, and soreness of the chewing muscles were scored on visual analogue scales. Although surface EMG, soreness, blood pressure, heart rate and difficulty in completing the toothclenching session all showed that group 2 patients were subjected to significantly higher levels of muscle tension than group 1 patients, headache developed equally often in both groups (63%). Headache was even more pronounced in group 1 (n.s.). Five patients in group 1 and none in group 2 developed an attack of migraine during the following 24 h. Pericranial muscle tenderness was unaffected by the experimental procedure. There was no significant correlation between headache intensity and pericranial muscle tenderness. Muscle ischemia, muscle "fatigue", and strain on muscle insertions are thus unlikely to cause attacks of common migraine.
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PMID:Experimental toothclenching in common migraine. 408 79

Clinical ergotism as seen today results almost exclusively from the excessive intake of ergotamine tartrate in the treatment of migraine headache. Although both gangrenous and convulsive symptoms are seen in naturally occurring ergotism resulting from the ingestion of fungus infected rye, only gangrenous ergotism has been reported following the excessive ingestion of ergotamine tartrate. The symptoms of both iatrogenic and naturally occurring ergotism appear to result from regional ischemia caused by ergot induced vasospasm. This report discribes experiences in the diagnosis and management of two patients with unusual manifestations of iatrogenic ergotism. One patient presented with ischemia of all extremities and bilateral foot drop probably due to ischemic damage to the common peroneal nerves, a finding not previously described in ergot intoxication. The foot drop totally resolved in several months following the discontinuation of ergot. A second patient presented with unilateral leg ischemia and transient monocular blindness, both of which resolved after discontinuation of ergot. Both patients displayed typical angiographic findings of ergotism. There is no convincing evidence that any treatment other than discontinuation of ergotamine is of benefit in the treatment of iatrogenic ergotism.
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PMID:Ergot intoxication: historical review and description of unusual clinical manifestations. 437 16


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