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At least 19 recordsLinked to original sources
PubMed1999

The impact of ergotamine-induced headache and ergotamine withdrawal on information processing.

Ergotamine abuse and subsequent ergotamine-induced headache is a common problem in the pharmacological treatment of migraine and other headache types; often, withdrawal therapy is necessary. This study investigated whether ergotamine abuse affects information processing and whether withdrawal therapy can lead to an improvement of information processing. We designed a standardized neurophysiological retrospective (ergotamine abuse) and prospective (ergotamine withdrawal) study in a supraregional headache outpatient clinic. Seventy-one patients abusing ergotamine derivatives with subsequent daily headache were enrolled and compared to 36 migraine patients without ergotamine intake and 36 healthy subjects. Information processing was evaluated by latencies and amplitudes of visually evoked event-related potentials (ERP) before and after ergotamine withdrawal therapy. P3 latency of the ERP was significantly increased in ergotamine abuse (442 +/- 45 ms) versus migraine (415 +/- 40 ms) and healthy subjects (410 +/- 33 ms), there was no difference between ergotamine tartrate and dihydroergotamine abuse. The migraine specific loss of habituation in information processing as measured by P3 latency could not be observed in migraine patients with ergotamine abuse. After successful withdrawal therapy in 36 patients, the abnormally prolonged P3 latency was significantly shortened (452 +/- 47 ms versus 433 +/- 30 ms; P < 0.004). Our findings imply that information processing is impaired by ergotamine abuse and can be improved but not normalized after withdrawal therapy. Furthermore, our data provide strong evidence that ergotamine, besides its peripheral effects, has a central mode of action.

Adrenergic alpha-Agonists↗
PubMed1984

Ergotamine toxicity and serum concentrations of ergotamine in migraine patients.

Twenty-five migraine patients (9 males and 16 females) aged 22-71 who had used between 7 and 60 mg ergotamine tartrate per week for 1.5-30 y volunteered to participate in the study. Side-effects attributable to ergotamine were wide ranging and included daily headache and pain in the limbs. Wide variation in sensitivity to the drug was observed and side-effects were not always proportional to the dose of ergotamine. Random serum ergotamine concentrations were estimated in all patients and 10 of them volunteered to take a 2 mg oral challenge of ergotamine tartrate. Ergotamine was not detected in 44% of the random estimations even though all patients exhibited clinical signs of ergotamine tartrate overdose. The remaining 56% estimations all showed low drug concentrations. After the 2 mg oral challenge of ergotamine in the 10 patients, significantly higher concentrations, but still within therapeutic range, were detected in the sera when compared with mean concentrations achieved after the same oral dose of the drug in healthy, non-migrainous subjects.

Adult↗
PubMed1982

Ergotamine abuse: results of ergotamine discontinuation, with special reference to the plasma concentrations.

Twenty-three patients suffering from continuous headache linked with habitual daily use of ergotamine tartrate were studied. Their headaches were classified clinically, and possible side effects of ergotamine medication, plasma levels of ergotamine, and occurrence of withdrawal symptoms after discontinuation of drug abuse were recorded. Seventeen of the patients were clinically diagnosed as suffering from "ergotamine headache", and seven of them complained of coldness in the extremities. Plasma ergotamine levels were measured by using a radioimmunoassay. In almost half of the patients the 1 h plasma levels after the daily dose were below the detection limit of the procedure (0.12 ng/ml). The duration and severity of the withdrawal symptoms did not correlate with the doses and plasma levels of ergotamine. In only 4 of the 21 patients who were followed up for 3 to 6 months did headache symptoms not improve after ergotamine withdrawal. The results indicate that even small (0.5-1.0 mg/day) doses of ergotamine tartrate taken regularly may cause continuous headache symptoms and withdrawal symptoms after discontinuation.

Adult↗
PubMed1980

Mild analgesics as an alternative to ergotamine in migraine. A comparative trial with acetylsalicylic acid, ergotamine tartrate, and a dextropropoxyphene compound.

The effect of ergotamine tartrate was compared with that of acetylsalicylic acid and a dextropropoxyphene compound (Doleron novum) on 525 acute migraine attacks in a double-blind crossover study of 25 adult female patients. Ergotamine tartrate and the dextropropoxyphene compound were equally effective and significantly superior to acetylsalicylic acid in preventing the attacks entirely. If the attacks were only partially prevented, the dextropropoxyphene compound was significantly superior to acetylsalicylic acid in making the attacks shorter and milder, while ergotamine tartrate did not differ significantly from acetylsalicylic acid or the dextropropoxyphene compound. The incidence of nausea and vomiting was lowest during treatment with the dextropropoxyphene compound. In the patients' overall preference, the dextropropoxyphene compound and ergotamine tartrate were significantly superior to acetyl-salicylic acid. In acute migraine the combination of dextropropoxyphene, a centrally acting analgesic, with acetylsalicylic acid and phenazone gives an alternative to ergotamine tartrate that is equally effective and causes less nausea and vomiting.

Adult↗
PubMed1984

Ergotaminism after a single dose of ergotamine tartrate.

A 32-year-old female developed classical signs and symptoms of ergotaminism after taking a single rectal suppository of ergotamine tartrate. Her symptoms gradually resolved with minimal therapy over the next week. Ergotaminism is the most frequent form of ergotism and should be considered in all patients with vascular insufficiency who are taking ergotamine-containing drugs.

Adult↗
PubMed1993

Dopamine D2-receptor imaging with 123I-iodobenzamide SPECT in migraine patients abusing ergotamine: does ergotamine cross the blood brain barrier?

Two migraine patients were studied by in vivo SPECT using the dopamine D2-receptor specific radioligand 123I-3-iodo-6-methoxybenzamide (123I-IBZM) during ergotamine abuse and after withdrawal. Results were compared with 15 healthy controls. Striatum/cerebellum and striatum/occipital cortex ratios of count rate density were calculated as a semiquantitative measurement for striatal dopamine D2-receptor binding potential. No differences were found in striatal uptake of 123I-IBZM between healthy controls and the patients when on or off ergotamine. Preliminary evidence suggests that ergotamine may not occupy striatal dopamine D2-receptors to a large extent and thus may not cross the blood brain barrier in large quantities.

Benzamides↗
PubMed2000

Ergotamine alters plasma concentrations of glucagon, insulin, cortisol, and triiodothyronine in cows.

Bovine plasma was assayed to determine whether ergotamine, an ergopeptide isolated from endophytic tall fescue, affected cortisol, triiodothyronine, insulin, and glucagon concentrations. In Exp. 1, four heifers received an i.v. bolus injection of ergotamine tartrate (19 microg/kg BW) or saline vehicle in a simple crossover design 2 d after induced luteolysis. Oxytocin (100 USP units) was i.v. administered 4 h after ergotamine or saline. Treatment x time affected (P < .01) respiration rates and plasma concentrations of cortisol, triiodothyronine, insulin, and glucagon. Respiration rates were elevated (P < .01) 2 to 7 h after ergotamine, but they were unchanged after saline. Plasma cortisol concentrations were increased (P < .01) 1 to 3 h after ergotamine but not after saline. Plasma triiodothyronine was elevated 2 h after ergotamine, but it was unchanged in response to saline. Insulin decreased (P < .01) and glucagon increased (P < .01) during the 1st h after ergotamine, but not in response to saline. A second increase (P < .01) of glucagon was observed 3 h after ergotamine. In Exp. 2, six cows were treated with an i.v. bolus injection of ergotamine (20 microg/kg BW) or saline in a simple crossover design 10 d after receiving a s.c. ear implant containing norgestomet. Oxytocin (100 USP units) was i.v. administered 4 h after ergotamine or saline. Treatment x time affected (P < .001) respiration rates, cortisol, insulin, and glucagon and tended to influence (P = .12) triiodothyronine concentrations. Respiration rates were elevated (P < .01) 1 to 7 h after ergotamine but were unaltered by saline. Plasma cortisol was elevated (P < .01) 1 to 5 h after ergotamine, but not in response to saline. Plasma triiodothyronine was elevated (P < .01) 1 to 2 h after ergotamine, but not after saline. Insulin was decreased (P < .01) and glucagon increased (P < .01) within 1 h after ergotamine treatment, but they were not altered by saline. A second increase (P < .01) of glucagon occurred by 4 h after ergotamine. In Exp. 1 and 2, glucagon increased (P < .01) 1 h after oxytocin in saline and ergotamine cows. Results indicate that ergotamine can alter plasma concentrations of hormones that mediate nutrient metabolism and thermoregulation in cattle.

Animal Feed↗
PubMed2001

Effect of an acute ergotamine challenge on reproductive hormones in follicular phase heifers and progestin-treated cows.

The objective of this research was to determine if ergotamine, an ergopeptine alkaloid isolated from Neotyphodium-infected grasses and associated with toxicoses in livestock, altered plasma concentrations of reproductive hormones in follicular phase heifers and in cows given a progestin implant. In Experiment 1, blood was sampled for 8h from four cycling heifers 2 days after synchronized luteolysis. Heifers were treated with ergotamine tartrate (19microg/kg) i.v. or saline vehicle in a simple cross-over design after 1h of pre-treatment blood sampling. Heifers received oxytocin (100USP units) i.v. 4h after ergotamine or saline treatment. Ergotamine reduced (P<0.01) prolactin concentrations from 1 to 4h post-treatment and increased (P<0.01) 13,14-dihydro-15-keto prostaglandin F2alpha (PGFM) concentrations from 2 to 5h post-treatment. A PGFM response to oxytocin was not detected. In Experiment 2, blood was sampled for 8h from six cycling cows 10 days after receiving a s.c. norgestomet implant. Cows were treated i.v. with ergotamine (20microg/kg) or saline in a simple cross-over design after 1h of pre-treatment blood sampling. Cows received gonadorelin (GnRH, 100microg) i.v. 1h after ergotamine or saline. Cows received oxytocin (100USP units) i.v. 4h after ergotamine or saline treatment. Ergotamine reduced (P<0.01) serum prolactin concentrations by 120min after treatment, with prolactin returning to pre-treatment concentrations by 200min after treatment. Saline-treated cows had lower (P<0.01) prolactin by 280min after treatment. Ergotamine-treated cows had higher (P<0.01) PGFM concentrations compared to saline-treated cows 120-240min after treatments, but the groups exhibited similar increases in PGFM after oxytocin. Plasma LH and FSH concentrations increased to peaks 100-120min after GnRH for both groups. However, the LH response to GnRH was greater (P<0.01) for ergotamine-treated cows. In summary, ergotamine lowered prolactin and elevated PGFM concentrations in follicular phase heifers and cows on norgestomet therapy. Ergotamine increased the LH response to exogenous GnRH in cows with norgestomet implants. These data highlight the potential of ergopeptine alkaloids to affect reproduction through altered endocrine function.

Animals↗
PubMed2003

Effect of ergotamine on plasma metabolite and insulin-like growth factor-1 concentrations in cows.

Bovine plasma was assayed to determine if ergotamine affected plasma metabolite and insulin-like growth factor-1 (IGF-1) concentrations. In Experiment 1, four cows received a single bolus intravenous injection of ergotamine tartrate (19 microg/kg body wt.) or saline vehicle in a crossover design 2 days after prostaglandin-induced luteolysis. Treatmentxtime affected plasma glucose, triglyceride, total cholesterol and IGF-1 concentrations. Glucose and cholesterol were increased after ergotamine. Triglycerides were elevated within 1 h after ergotamine, but were decreased 3 h after ergotamine treatment. Plasma IGF-1 decreased in response to ergotamine. Blood constituents were unchanged after treatment with saline. In Experiment 2, six cows received a single bolus intravenous injection of ergotamine (20 microg/kg body wt.) or saline vehicle in a crossover design 10 days after receiving norgestomet (6 mg) via subcutaneous ear implant. Treatmentxtime affected glucose, triglycerides, total cholesterol and IGF-1 concentrations. Glucose and cholesterol were increased after ergotamine. Triglycerides were elevated 1 h after ergotamine and decreased 3-7 h after ergotamine. Plasma IGF-1 decreased after ergotamine treatment. Blood constituents were unresponsive to the saline vehicle. Results indicated ergotamine altered plasma metabolite and IGF-1 concentrations in cows.

Adrenergic alpha-Agonists↗
PubMed2001

Patterns of ergotamine and sumatriptan use in the Netherlands from 1991 to 1997.

The objective of this study was to assess usage patterns of ergotamine and sumatriptan over a period of 6 years, primarily to evaluate the impact that sumatriptan has had on the prescription of ergotamine. This study used ergotamine and sumatriptan prescription data representing inhabitants of eight cities in the Netherlands and covering the period of 1991-1997. The yearly incidence of new users between 1991 and 1997 was estimated for both drugs as well as for the drug of first choice to be prescribed to patients initiating specific abortive migraine treatment with either ergotamine or sumatriptan. Intra-individual ergotamine and sumatriptan usage patterns, characterized by single (incidental), continuous (rate of retention) or switch use, were examined for five patient cohorts, each for a follow-up period of 1 year. During the year of sumatriptan introduction (1991-1992), the overall incidence of new use for both drugs was highest (5.4 per 1000 inhabitants). Hereafter, a substantial reduction of more than 50% was observed. From 1992 to 1996, the yearly incidence of ergotamine first-time use was significantly higher than that of sumatriptan and up to 1996 ergotamine was more than twice as likely than sumatriptan to be prescribed to patients initiating specific abortive treatment. Hereafter, sumatriptan was as likely as ergotamine to be prescribed as the drug of first choice, which coincided with the full reimbursement of sumatriptan tablets. Overall, neurologists were more likely than general practitioners (GPs), to prescribe sumatriptan as the drug of first choice. Approximately half of the total study population were identified as single-time users. This phenomonen occurred more frequently in the ergotamine cohorts. The sumatriptan cohorts displayed a slight yet significant stronger retention rate compared with the ergotamine cohorts. The overall impact of sumatriptan on ergotamine use in The Netherlands was marginal, predominantly due to GP's adherence to migraine treatment guidelines and reimbursement policies concerning sumatriptan tablets. Overall, incidental use was relatively high and may reflect the reported difficulties in diagnosing migraine, lack of patient-doctor consultation, or that anticipated benefits of the drug were not achieved. Further study is required to clarify these issues.

Adolescent↗
PubMed1998

Effect of ergotamine on serotonin-mediated responses in the rodent and human brain.

In the rat dorsal hippocampus and dorsal raphe nucleus, the microiontophoretic application of ergotamine and 5-HT suppressed the firing activity of CA3 pyramidal neurons and 5-HT neurons, an effect antagonized by selective 5-HT1A receptor antagonists. Co-application of ergotamine prevented the inhibitory action of 5-HT on the firing activity of CA3 pyramidal neurons but not of 5-HT neurons, indicating that ergotamine acted as a partial 5-HT1A receptor agonist in the dorsal hippocampus and as a full agonist at 5-HT1A autoreceptors. Ergotamine decreased, in a concentration-dependent manner, the electrically evoked release of [3H]5-HT in preloaded rat and guinea pig hypothalamus slices; this effect was prevented by the nonselective 5-HT receptor antagonist methiothepin but not by the selective 5-HT1B/1D receptor antagonist GR 127935 or the alpha 2-adrenoceptor antagonist idazoxan. Although body temperature in humans remained unchanged following inhaled ergotamine, in the rat, subcutaneously injected ergotamine produced a hypothermia that was prevented by a pretreatment with the 5-HT1A/1B receptor/beta-adrenoceptor antagonist pindolol. Finally in humans, ergotamine did not alter prolactin or adrenocorticotropic hormone levels, but increased growth hormone level, which was prevented by pindolol. Cortisol level was increased in humans by ergotamine, but this enhancement was unaltered by pindolol. In conclusion, the present results suggest that ergotamine acted in the rat brain as a 5-HT1A receptor agonist and as an agonist of terminal 5-HT autoreceptor of a yet undefined subtype. In humans, ergotamine also displayed some 5-HT1A receptor activity but, probably because of lack of receptor selectivity, it did not present the same profile as other 5-HT1A receptor agonists.

Analgesics, Non-Narcotic↗
PubMed2002

The effect of rizatriptan, ergotamine, and their combination on human peripheral arteries: a double-blind, placebo-controlled, crossover study in normal subjects.

AIMS: To compare the peripheral vasoconstrictor effects of ergotamine, rizatriptan, and their combination, in normal subjects. METHODS: This was a double-blind, four-way, crossover study. Sixteen young male volunteers, selected as responders to the vasoconstrictor effect of 0.5 mg ergotamine i.v., were administered 10 mg oral rizatriptan, 0.25 mg i.v. ergotamine, 10 mg oral rizatriptan+0.25 mg i.v. ergotamine, and placebo. The vasoconstrictor effect on peripheral arteries was measured with strain gauge plethysmography up to 8 h after dosing. The 8 h assessment period was divided into two 4 h intervals to assess the immediate (0-4 h) vs sustained effect (4-8 h) of treatment. RESULTS: For the 0-4 h interval, the decreases in peripheral systolic blood pressure gradients were: placebo (-1 mmHg [95% CI: -3, 1])<rizatriptan (-5 mmHg [95% CI: -7, -3])<ergotamine (-15 mmHg [95% CI: -16, -13])=rizatriptan+ergotamine (-15 mmHg [95% CI: -17, -13]). For the 4-8 h interval, the decreases were: placebo (-5 mmHg [95% CI: -8, -3])=rizatriptan (-8 mmHg [95% CI: -11, -5])<ergotamine (-26 mmHg [95% CI: -29, -24])=rizatriptan+ergotamine (-28 mmHg [95% CI: -31, -26]). CONCLUSIONS: In normal subjects, rizatriptan 10 mg orally had only a small transient vasoconstrictor effect on peripheral arteries compared with the sustained and more pronounced effect of 0.25 mg i.v. ergotamine. Furthermore, rizatriptan exerted no additional effect on ergotamine-induced constriction of peripheral arteries when the two drugs were given in combination.

Adult↗
PubMed1986

Comparison of pharmacodynamic effects and plasma levels of oral and rectal ergotamine.

Plasma levels and the vasoconstrictive effect of 1 mg ergotamine tartrate given as tablets or suppositories were compared. In a crossover study, eight male volunteers received tablets or suppositories containing ergotamine in a drug combination (Anervan) and, as a control, suppositories without ergotamine. Blood sampling and measurement of toe-arm systolic gradients with a strain-gauge technique were done for up to 6 h and again after 24 h and 48 h. Only 29 of 160 blood samples contained detectable (greater than 0.1 ng/ml) amounts of ergotamine, and kinetic comparison could not be performed. Only ergotamine-containing suppositories caused a significant (p less than 0.008) decrease in toe-arm systolic gradient which was significantly different (p less than 0.003) from the effects of ergotamine tablets and control suppositories. Rectal ergotamine is thus more biologically active, for the factor used, than oral ergotamine. We suggest that a rectal dose of 1 mg ergotamine tartrate should be tried as the initial dose in the treatment of migraine attacks.

Administration, Oral↗
PubMed1975

Analysis of ergotamine - 5-HT interaction on the isolated rat stomach preparation.

The effect of ergotamine on the isolated rat stomach and its influence on the response to ACh and 5-HT were investigated. The log dose-response curve of ergotamine was bell-shaped. Extension of the incubation time of ergotamine resulted in a parallel shift to the left of the curve. The response to ergotamine was inhibited by methyserigide and piperoxan. Incubation with ergotamine resulted in a decrease of the pD2-value of 5-HT together with a marked suppression of the maximum of the 5-HT curve. The response to ACh was affected in accordance with the prediction of an action of ACh and ergotamine on different receptors. The prolonged receptor stimulation by 5-HT or ACh resulted in a decrease of the apparent affinity towards their receptors. Incubation with ACh resulted in a parallel shift to the right of the 5-HT curve. However no inconsistency with the theoretical prediction of an action on separate receptors was observed with the ACh curve in the presence of 5-HT. It is concluded that ergotamine is a partial agonist on the D-tryptamine receptors of tbe isolated rat stomach. The marked decrease of the maximum of the 5-HT curve by ergotamine is probably caused by the slowly reversible character of its antagonism. The parallel shift to the left of the ergotamine curve with the extension of the incubation time and the persistence of its antagonism both are probably caused by a slow diffusion into and from the biophase.

Acetylcholine↗