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Query: UMLS:C0018681 (headache)
 56,091 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We measured the cerebral blood flow (CBF) of 16 patients by the xenon-133 intracarotid method before and after the intramuscular injection of ergotamine tartrate. The regional and hemispheric CBF was unaltered, even in 3 migraneurs in who ergotamine relieved the headache. Ergotamine tartrate in therapeutic doses has no effect on the cerebral circulation.
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PMID:Ergotamine and cerebral blood flow. 74 94

Serial cerebral blood flow studies performed by the intra-carotid 133Xenon method were fortuitously determined during the course of a cluster headache in a 32 year old man. The initial study was performed about 10 min after the headache began and showed values at the upper limit of normal. Twenty min after the headache started a second procedure showed that the autoregulatory response on hyperventilation was normal. Ergotamine tartrate was given intra-muscularly 23 min after the headache began and there was partial relief. A third cerebral blood flow estimation showed abnormally high values. The probable reasons for this are discussed.
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PMID:Cerebral blood flow changes in cluster headache. 97 57

Regional cerebral blood flow studies during a typical prodromal phase of a migraine attack in a young woman showed a global decrease of cerebral blood flow in the carotid artery territory. These studies were repeated during the subsequent headache phase of the same attack and hemispheric blood flow increased considerably. Ergotamine tartrate was then administered intramuscularly which brought definite relief of symptoms but no change in cerebral blood flow. Carotid angiography performed immediately afterwards showed retrograde filling of the proximal portion of the basilar artery, which suggested that the brain stem was the site of hyper-perfusion. These findings illustrate certain features underlying both the pathophysiology of migraine itself and its response to ergotamine preparations.
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PMID:Changes in cerebral blood flow during a migraine attack. 118 54

Pharmacotherapy is the mainstay for patients with persistent headaches. When simple analgesics can no longer be used, combination analgesics are prescribed. Symptomatic medications also include antiemetics, ergot derivatives, corticosteroids, neuroleptics, and narcotics. Nonsteroidal anti-inflammatory drugs are commonly used both symptomatically and prophylactically, and are the treatment of choice for menstrual migraine. Exertional migraine, benign orgasmic cephalalgia, chronic paroxysmal hemicrania, cough headache, and "ice-pick" headache are treated with indomethacin. Ergotamine tartrate is often recommended when simple or combination analgesics do not relieve headaches. Dihydroergotamine (DHE) is effective for treating intractable headache; because it has fewer side effects than ergotamine, it is tolerated by patients unable to tolerate other ergotamine preparations. DHE is administered IM and, for occasional use, patients can be taught self-injection. Repetitive IV DHE therapy for chronic severe headaches requires hospitalization; most patients become headache-free within 3 days. Patients who refuse hospitalization, do not respond to the drug, or are not suitable candidates for DHE therapy may receive a short course of a corticosteroid, a neuroleptic or, rarely, a narcotic. For frequent headaches, prophylactic treatment usually begins with a tricyclic antidepressant or a beta blocker.
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PMID:Symptomatic and prophylactic treatment of migraine and tension-type headache. 155 87

Ergotamine tartrate and methysergide are widely used headache treatments with important vasoconstrictive properties. We report a 31-year-old man with cluster headaches who developed severe, prolonged myocardial ischemia following combination therapy with ergotamine tartrate and methysergide. We reviewed the cardiovascular complications of each agent alone and in combination. Given the pharmacologic similarity of these agents, we propose that they may have additive or synergistic cardiac toxicity, at least in vulnerable individuals. We recommend caution when these agents are used together.
Headache 1991 Jul
PMID:Myocardial ischemia related to ergot alkaloids: a case report and literature review. 177 59

The main treatment of the acute migraine attack remains sleep, sedation, an anti-nauseant and analgesics, and in some patients 1 or 2 mg of ergotamine tartrate. Drugs containing large amounts of caffeine should not be used. Absorption of drugs may be impaired in a migraine attack. Metoclopramide is probably the anti-emetic of choice because it is an effective anti-nauseant and promotes normal gastrointestinal activity. Domperidone has a similar action but is said not to go through the blood-brain barrier, so is less likely to cause extrapyramidal reactions. All drugs, including analgesics such as aspirin and paracetamol, are best given in a soluble or effervescent form. Where vomiting occurs early in the attack, suppositories may be indicated. Ergotamine tartrate is necessary in about one third of attacks and is best given by suppository or by inhalation. Doses higher than 2 mg per attack or 6 mg in one week may cause toxic symptoms, the early signs of which are headache, nausea, vomiting and a feeling of not being very well. The non-drug treatments of an acute attack include pressing on the temporal artery, hot and cold compresses and relaxation.
Cephalalgia 1983 Mar
PMID:Treatment of the acute migraine attack--current status. 640 72

An attempt was made to determine the plasma ergotamine concentrations in nine male patients with cluster headache 15-600 min after oral therapeutic doses of ergotamine tartrate (Cafergot). Some of the patients were studied twice. Five patients received a constant dose of 2-4 mg daily for at least seven days. Four patients were given 1 mg five times on one day and three patients a single oral dose of 2 mg. Ergotamine was determined by means of high performance liquid chromatography with fluorescence detection--a new highly sensitive, specific method, the detection limit of which is less than 100 pg/ml for ergotamine. Ergotamine tartrate was not discovered in any of the plasma samples. In one patient ergotamine could not be detected in the cerebrospinal fluid one hour after a single oral dose of 2 mg. The oral biological availability is less than 1%, which is the maximal available fraction of unchanged ergotamine after oral administration. A clinical benefit was observed in several of our patients. These effects of the drug may be because of active metabolites being formed and/or to high affinity of ergotamine to cranial vessels.
Cephalalgia 1981 Dec
PMID:Low biological availability of ergotamine tartrate after oral dosing in cluster headache. 681 61

The ergot alkaloids are a family of chemical entities that have many pharmacologic effects. Their diversity results from their interaction with multiple receptors, their variable receptor affinity and intrinsic activity, and their variable organ-specific receptor access. Ergotamine tartrate (ET) was one of the first ergot alkaloids to be isolated. Dihydroergotamine (DHE) is synthesized by reducing an unsaturated bond in ergotamine (E); this modification results in a changed pharmacologic profile. Dihydroergotamine exhibits greater alpha-adrenergic antagonist activity and much less potent arterial vasoconstriction and emetic potential. Both E and DHE are 5-HT1A, 5-HT1B, 5-HT1D, and 5-HT1F receptor agonists. The vasoconstrictor activities of these ergot compounds have long been believed to be the basis of their clinical effects, but recent evidence suggests that their antimigraine action may result in part from their inhibitory effects on neurogenic inflammation and neuronal transmission and not from vasoconstriction. Improvements in assay methodology have provided more accurate determination of the pharmacokinetics of E and DHE. The long duration of action appears to result from active metabolites and tight tissue binding. Intranasal (IN) administration of DHE delivers adequate plasma concentrations of the drug without the need for parenteral administration and should further expand its role in migraine pharmacotherapy.
Headache 1997
PMID:The pharmacology of ergotamine and dihydroergotamine. 900 70

Ergotamine tartrate (ET) and dihydroergotamine (DHE) are effective therapies for migraine and cluster headache. Optimal management with these agents must take several factors into account, including headache type and severity, associated symptoms, side effect potential, choice of dosage forms, and appropriate dosing. Oral ET is most appropriate for slowly evolving migraine without early onset nausea and/or vomiting, or for treatment of cluster headaches. Delivery of ET via rectal suppository (available only in combination with caffeine) is the most effective form, especially for patients with severe, rapid onset migraine accompanied by nausea and/or vomiting. Dihydroergotamine offers numerous benefits compared to ET, including a lower incidence of nausea and vomiting and headache recurrence, and a lack of rebound headache. Dihydroergotamine can be administered at any time during a migraine attack, including the aura. Intravenous administration provides rapid peak plasma levels and is the most effective form when a rapid effect is desired or for patients with intractable severe headache (status migrainosus, transformed migraine, rebound headache) and cluster headache. Intramuscular administration is effective for moderate to severe migraine with or without nausea and vomiting in the clinic. Intranasal delivery of DHE has shown significant promise for effective and convenient therapy in acute migraine and may be especially useful in the presence of nausea and/or vomiting. When used appropriately, DHE and ET provide clinicians with highly effective therapeutic options in a range of useful dosage forms for patients with migraine or cluster headaches.
Headache 1997
PMID:Dosing and administration of ergotamine tartrate and dihydroergotamine. 900 71

Ergotamine tartrate (ET) and dihydroergotamine mesylate (DHE) have been widely and effectively used in the treatment of migraine for many decades, although few randomized, controlled clinical trials have been conducted with these compounds. To compare their safety profiles, the world literature on the two agents was surveyed. The results are summarized, along with a critical analysis of the strengths and limitations of the various sources of safety data (in vitro research, animal studies, Phase I and II studies, controlled clinical trials, and postmarketing surveillance). Significant pharmacologic and safety differences exist between ET and DHE. Dihydroergotamine mesylate is a less potent arterial vasoconstrictor than ET, although nearly equipotent as a venoconstrictor. It is a more potent alpha-adrenergic antagonist, but is much less emetic, has less effect on the uterus, and is not associated with rebound headache. Adverse effects associated with ET (which are often due to excessive dosage and/or chronic usage) include nausea, acroparesthesia, ischemia, habituation and overuse headache, and, rarely, overt ergotism. Reports of serious adverse effects following recommended doses of DHE are rare. As with most antimigraine drugs, the most frequent adverse effect with intravenous (i.v.) DHE is nausea; however, following intramuscular (i.m.) or intranasal (IN) administration, the incidence of nausea is low and concomitant administration of an antiemetic is not needed. In patients without contraindications, both DHE and ET are safe and effective when used in recommended doses. Nearly 50 years of clinical experience without major safety problems allows a high level of confidence in their clinical use.
Headache 1997
PMID:Ergotamine tartrate and dihydroergotamine mesylate: safety profiles. 900 72


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