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PubMed1999

Cluster Headache.

The care of patients with cluster headache has at least two goals: 1) immediately abolishing an ongoing attack and 2) stopping or shortening a bout (a cluster period). The fierceness and the relative brevity of the attacks dictate the use of a fast-acting agent. There are probably three agents fulfilling these criteria: sumatriptan (by subcutaneous injection), oxygen (inhaled through a face mask), and ergotamines (by injection or, perhaps, sublingual tablets). An abundance of data from controlled studies as well as recent clinical experience probably favors sumatriptan as the most effective alternative, the most significant drawback being its high cost. Oxygen inhalation is free of side effects and may be effective but is inconvenient to use. Ergotamines in tablet form act less rapidly, and there are more contraindications to their use. In short-term prophylaxis, however, ergotamine may still be a drug of choice if the timing of the attacks allows planned use of the drug shortly before the attack. If the timing is more irregular, steroids may at least temporarily break a cycle (eg, prednisolone, 60 or 80 mg/d, gradually tapered to zero in 3 to 4 weeks). If more long-lasting prophylaxis is needed or expected, lithium carbonate, 900 mg/d, or verapamil, 360 mg/d, both have reasonable response rates. As for chronic cluster headache, lithium probably will still be the drug of choice. For a very limited group of patients with chronic cluster headache, surgery may be a last resort. The best surgical options are probably radiofrequency rhizotomy or microvascular decompression of the trigeminal nerve.

Journal Article↗
PubMed1998

Characterization of 5-HT receptors mediating constriction of porcine carotid arteriovenous anastomoses; involvement of 5-HT1B/1D and novel receptors.

1. It was previously shown that porcine cranial arteriovenous anastomoses (AVAs) constrict to 5-hydroxytryptamine (5-HT), ergotamine, dihydroergotamine, as well as sumatriptan and that sumatriptan acts exclusively via 5-HT1B/1D receptors. The present study was devoted to establish the contribution of 5-HT1B/1D receptors in the constriction of AVAs elicited by 5-HT (in presence of 0.5 mg kg(-1) ketanserin), ergotamine and dihydroergotamine in anaesthetized pigs. 2. Intracarotid infusion of 5-HT (2 microg kg(-1) min(-1)) and intravenous doses of ergotamine (2.5-20 microg kg(-1)) and dihydroergotamine (3-100 microg kg(-1)) reduced AVA and increased nutrient blood flows and vascular conductances. The vasodilator response to 5-HT, observed mainly in the skin and ear, was much more prominent than that of the ergot alkaloids. 3. Treatment with the 5-HT1B/1D receptor antagonist GR127935 (0.5 mg kg(-1), i.v.) significantly attenuated both ergot-induced AVA constriction and arteriolar dilatation, whereas GR127935 only slightly affected the carotid vascular effects of 5-HT. 4. The results suggest that 5-HT constricts carotid AVAs primarily via receptors, which seem to differ from those (5-HT1B/1D) stimulated by sumatriptan. The ergot alkaloids produce AVA constriction for a substantial part via 5-HT1B/1D receptors, but also stimulate unidentified receptors. Both these non-5-HT1B/1D receptors may be targets for the development of novel antimigraine drugs. 5. The moderate vasodilator response to the ergot derivatives seems to be mediated, at least in part, by 5-HT1B/1D receptors, whereas the arteriolar dilatation caused by 5-HT may be mediated by other, possibly 5-HT7 receptors.

Animals↗
PubMed1979

Alpha- and beta-adrenergic stimulation of arachidonic acid metabolism in cells in culture.

Madin-Darby canine kidney cells (MDCK) synthesize prostaglandin (PG) F(2alpha), PGI(2) (measured as 6-keto-PGE(1alpha)), PGE(2), PGD(2), and thromboxane A(2) (measured as thromboxane B(2)). When incubated in the presence of norepinephrine (6 muM), the syntheses of these arachidonic acid metabolites are stimulated 3-fold. Norepinephrine's effect can be antagonized by the addition of alpha-adrenergic receptor blocking agents (phenoxybenzamine>phentolamine>yohimbine>dibenamine>tolazoline) but not by the beta-adrenergic blocking drug propranolol. Norepinephrine's stimulation is also inhibited by low concentrations of dihydroergotamine, bromocryptine, ergocryptine, and ergotamine. The stimulation of PG synthesis by norepinephrine is reversible, continues during the 24 hr of incubation, and requires the presence of norepinephrine at the receptor site but it is not blocked by the addition of colchicine, cytochalasin B, or cycloheximide. Neither phenoxybenzamine nor ergotamine at concentrations that block norepinephrine's stimulation of PG biosynthesis suppresses the increase in PG synthesis induced by exogenous arachidonic acid, suggesting that the alpha-adrenergic regulation is not occurring primarily at the cyclooxygenase step in the metabolism of arachidonic acid. In mouse lymphoma cells (WEHI-5), low concentrations of isoproterenol or norepinephrine stimulate the synthesis of thromboxane, an effect that can be blocked by the addition of propranolol but not by relatively high concentrations of phenoxybenzamine or ergotamine. Taken together, these results suggest that alpha-adrenergic receptor stimulation promotes the deacylation of phospholipids by MDCK cells whereas beta-adrenergic mechanisms lead to activation of similar pathways in WEHI-5 cells.

Adrenergic alpha-Antagonists↗
PubMed1989

Migraine headache. Its diagnosis and treatment.

Many theories exist on the pathogenesis of migraine. However, the clinical picture of migraine is agreed on universally as a familial disorder characterized by recurrent attacks of headache that are variable in intensity, frequency, and duration. The attacks are usually unilateral and often associated with anorexia, nausea, and vomiting. Migraine therapy is complex and difficult, focusing on abortive and prophylactic regimens. General therapeutic measures, including diet and establishing schedules for meals and sleeping, may benefit many migraineurs. A variety of medications, including ergotamine, propranolol, the calcium channel blockers, antidepressants, and nonsteroidal anti-inflammatory drugs (NSAIDs) have been beneficial in the prophylactic treatment of migraine. Ergotamine is the drug of choice in the abortive treatment, although other agents, such as the NSAIDs, have been used successfully. Inpatient therapy in a specialized unit for headache patients may be indicated for the recidivist patient, the patient habituated to analgesics or ergotamine, or the patient with the mixed headache syndrome, i.e., migraine occurring with coexistent muscle contraction headaches.

Humans↗
PubMed1997

Cognitive processing in primary headache: a study on event-related potentials.

BACKGROUND: There is experimental evidence for loss of cognitive habituation in migraine but not in other types of headache and not by visual event-related potentials (ERP). OBJECTIVE: Determining the latencies (msec) and amplitudes (microV) of ERP components and the differences of these values in a two-trial analysis representing the amount of cognitive habituation. PARTICIPANTS: Two hundred thirty-three patients with a headache diagnosis according to the criteria of the International Headache Society: migraine without aura (N = 77); migraine with aura (N = 31); cluster headache during period (N = 26); cluster headache during interval (N = 11); chronic paroxysmal hemicrania (N = 8); episodic tension-type headache (N = 33); ergotamine-induced headache (N = 47). Thirty age-matched healthy subjects served as a control group. METHODS: ERPs were evoked by a visual oddball paradigm consisting of 2 x 200 flashes of light (85% white light; 15% red light). Evaluation of ERP components was done separately for the first 200 and the second 200 stimuli as well as for the entire series of stimuli. RESULTS: We found an acceleration of the P3 latency during the second trial in migraine with and without aura, but not in the other headache types, and not in healthy controls. Ergotamine and sumatriptan abolished this loss of habituation in migraine patients. Increased ERP latencies as compared with healthy controls were present in patients with cluster headache, tension-type headache, ergotamine-induced headache, and migraine with aura, but not in migraine without aura. CONCLUSION: There is a loss of cognitive habituation in migraine, which may serve as a specific but not sensitive diagnostic tool. The pathophysiologies of migraine and cluster headache have a specific modifying property on cognitive processing reflected by a loss of cognitive habituation or an increased cognitive processing time. These effects can, in part, be counterbalanced by antimigraine medication.

Adolescent↗
PubMed2001

Clinically significant drug interactions with agents specific for migraine attacks.

The drugs which provide specific relief from migraine attacks, the ergopeptides (ergotamine and dihydroergotamine) and the various 'triptans' (notably sumatriptan), are often prescribed for persons already taking various migraine preventative agents, and sometimes drugs for other indications. As a result, migraine-specific drugs may become involved in drug-drug interactions. The migraine-specific drugs all act as agonists at certain subclasses of serotonin (5-hydroxytryptamine; 5-HT) receptor, particularly those of the 5-HT1D subtype, and produce vasoconstriction through these receptor-mediated mechanisms. The oral bioavailabilities of these drugs, particularly those of the ergopeptides, are often incomplete, due to extensive presystemic metabolism. As a result, if migraine-specific agents are coadministered with drugs with vasoconstrictive properties, or with drugs which inhibit the metabolism of the migraine-specific agents, there is a risk of interactions occurring which produce manifestations of excessive vasoconstriction. This can also occur through pharmacodynamic mechanisms, as when ergopeptides or triptans are coadministered with methysergide or propranolol (although a pharmacokinetic element may apply in relation to the latter interaction), or if one migraine-specific agent is used shortly after another. When ergopeptide metabolism is inhibited by the presence of macrolide antibacterials, particularly troleandomycin and erythromycin, the resultant interaction can produce ergotism, sometimes leading to gangrene. Similar pharmacokinetic mechanisms, with their vasoconstrictive consequences, probably apply to combination of the ergopeptides with HIV protease inhibitors (indinavir and ritonavir), heparin, cyclosporin or tacrolimus. Inhibition of triptan metabolism by monoamine oxidase A inhibitors, e.g. moclobemide, may raise circulating triptan concentrations, although this does not yet seem to have led to reported clinical problems. Caffeine may cause increased plasma ergotamine concentrations through an as yet inadequately defined pharmacokinetic interaction. However, a direct antimigraine effect of caffeine may contribute to the claimed increased efficacy of ergotamine-caffeine combinations in relieving migraine attacks. Serotonin syndromes have been reported as probable pharmacodynamic consequences of the use of ergots or triptans in persons taking serotonin reuptake inhibitors. There have been two reports of involuntary movement disorders when sumatriptan has been used by patients already taking loxapine. Nearly all the clinically important interactions between the ergopeptide antimigraine agents and currently marketed drugs are likely to have already come to notice. In contrast, new interactions involving the triptans are likely to be recognised as additional members of this family of drugs, with their different patterns of metabolism and pharmacokinetics, are marketed.

Drug Interactions↗
PubMed1992

Symptomatic and prophylactic treatment of migraine and tension-type headache.

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.

Analgesics↗
PubMed1989

[The rabbit thermo-regulatory system. Effects of high dose of sodium fluoride].

The mechanism of sodium fluoride (NaF) induced hypothermia was investigated on relations between the monoamine synthesis and metabolism in the rabbit brain. Five male rabbits per a group, weighing about 2.5kg and having rectal temperatures of 38.4 to 39.3 degrees C, were used in this experiment. The rectal temperature measurements were made by means of an electric thermometer for 5 hours at intervals of 15 or 30 minutes. Through this experiment, animals were housed in a room kept at 22 to 23 degrees C. The following drugs were used in this experiment: NaF (40 mg/kg i.v.), barbital sodium (0.1 g/kg s.c.), hexamethonium bromide (C6, 10 mg/kg i.v.), ergotamine tartrate (30 mg/kg s.c.), phenoxybenzamine hydrochloride (15 mg/kg i.v.), propranolol hydrochloride (5 mg/kg s.c.), pindolol (0.3 mg/kg s.c.), atropine sulfate (30 mg/kg s.c.), 2, 4-dinitrophenol (DNP, 20 mg/kg i.v.), l-DOPA (20 mg/kg i.v.), 5-HTP (20 mg/kg i.v.) Results 1. Intravenous injection of 30 mg/kg of NaF induced a drop of 0.66 degrees C in rectal temperature. 2. Pretreatment with 0.1 mg/kg of barbital sodium or 10 mg/kg of C6 prominently inhibited the NaF-induced hypothermia. 3. The alpha-blockade caused by ergotamine tartrate and phenoxybenzamine or the beta blockade by propranolol hydrochloride and pindolol resulted in an approximate 50% inhibition of maximum drop in body temperature induced by NaF administration. Both alpha- and beta-blockades caused by ergotamine tartrate and propranolol or by phenoxybenzamine and pindolol, however, made a remarkable inhibition of the NaF effect. Cholinergic blockade brought on by atropine sulfate, on the other hand, had no effect against NaF-induced hypothermia. 4. Bilateral splanchnicotomy completely inhibited drops in rectal temperature. 5. Intravenous injection of NaF 40 mg/kg failed to counteract the rise of rectal temperature caused by DNP 20 mg/kg. 6. Pretreatment with l-DOPA made a prominent inhibition of NaF-induced hypothermia. The inhibiting effects of 5-HTP, however, were slight. 7. Administration of NaF made a significant decrease in norepinephrine levels in the rabbit hypothalamus, but had no effect on 5-HT levels.

Animals↗
PubMed1986

Effects of cyclopiazonic acid on the contractility of organs with smooth muscles, and on frog ventricles.

The mycotoxins cyclopiazonic acid (CPA) and ergotamine, and the neurotransmitter serotonin all have the beta-aminoethylindole moiety in common. These compounds enhanced the peristaltic movements of the jejunum, ileum and estrous uterus and produced broncho-constriction in vitro. Atropine and cyproheptadine were able to counter the CPA-induced peristaltic movements of the ileum and jejunum. L-epinephrine was able to stop the contractions induced by CPA on both estrous and pregnant rat uteri. Unlike chlorpromazine, CPA did not block the inotropic effects of dopamine, epinephrine and serotonin in vas deferens. This indicated that the previously reported toxic effects of CPA (hypothermia, catalepsy, hypokinesia, tremor) which resembled the effects of anti-psychotic drugs (chlorpromazine, reserpine) probably were not due to the blocking of the neurotransmitter-receptors. In contrast to ergotamine, which decreased the inotropic effects of serotonin on the uterus, CPA had no anti-serotonin effects. The uterotonic effect of CPA (similar to that of ergotamine) suggested that CPA also might have an adverse effect on the reproductive function of humans and animals consuming CPA-contaminated foods.

Animals↗
PubMed1994

[Migraine--summary of diagnostic and therapeutic strategies].

The International Headache Society 1988 has boosted the research on and therapy of migraine by classifying the headache and operationalizing the diagnostic criteria in the recent years. The prevalence of migraine (12% in the western industrial countries) and its genetic causes are now undoubted. Numerous short-term or long-term triggers, like for instance the female hormone constellation from puberty to menopause, or prolonged stress, contribute considerably to the severity and frequency of the illness. Due to the central role of serotonin in the pathomechanism of the migraine headache and intensive research on the part of the pharmaceutical industry it was possible to develop a new, efficient drug for the treatment of migraine attacks: sumatriptan, a 5HT1-agonist. The efficiency of prophylactics has been defined and covered. For about one third of the migraine patients a long-term therapy, which is continuously adapted, is necessary, because they suffer simultaneously from a tension-type headache and a continual headache due to an abuse of pain-killers or ergotamin (analgesic or ergotamin headache), and from accompanying anxiety syndromes, depression and cervical syndromes. Only in this way can the abuse of pain-killers or ergotamin be prevented or cut back, the fear of the next attack reduced, and the ability to work maintained as well as the quality of life improved. The strategies of the therapy of migraine attacks and their prophylaxis are summed up.

Humans↗
PubMed2004

Fragmentation patterns of selected ergot alkaloids by electrospray ionization tandem quadrupole mass spectrometry.

Tall fescue toxicosis and other maladies in livestock result from the ingestion of vasoconstrictive ergot alkaloids produced by fungal endophytes associated symbiotically with the grass. In order to facilitate future analyses of grass extracts considered responsible for outbreak of related livestock diseases, we examined the electrospray ionization mass spectra of specific ergot alkaloids under conditions that permit protonation. Our purposes were both to record the spectra with interpretation of mechanisms of fragmentation and to derive commonalities that would allow the prediction of mass spectra of related compounds for which standards were not readily available. With [M + H](+) values in parentheses, water-insoluble lysergic acid peptide ergot derivatives ergovaline (m/z 534), ergotamine (m/z 582), ergocornine (m/z 562), ergocryptine (m/z 576) and ergocrystine (m/z 610) exhibited a consistent loss of water (-18 u) from the C-12' alpha-hydroxy functionality. Of this group, ergovaline and ergotamine generated an m/z 320 fragment deriving from cleavage of ring E amide and ether functions with retention of the peptide ring system methyl group. Ergocornine, ergocryptine and ergocrystine similarly formed an m/z 348 fragment with retention of isopropyl. These assignments were supported by the lack of similar fragments from the water-soluble ergot ergonovine, which lacks a peptide ring system. Clavine-type ergot alkaloids lysergic acid and lysergol lack any substituents beyond simple ones directly on the C-8 position and, similarly to ergonovine, lack significant fragments at m/z 268, 251 and 225 shared by the peptide ergot alkaloids.

Animal Feed↗
PubMed1984

Pain relief by somatostatin in attacks of cluster headache.

The pain relieving effect of somatostatin treatment during 72 attacks of cluster headache in 8 male patients was compared to treatment with ergotamine or placebo in a double-blind study. Infusion of somatostatin (25 micrograms/min for 20 min i.v.) reduced the maximal pain intensity and the duration of pain significantly compared to placebo treatment, and to a degree comparable to ergotamine tartrate treatment (250 micrograms i.m.). The results obtained provide new information concerning the possible mechanism of cluster headache attacks and suggest a new therapeutic approach.

Adult↗
PubMed1986

Anorectal ergotism: another cause of solitary rectal ulcers.

Anorectal ulceration was observed in 6 patients who excessively used suppositories containing ergotamine tartrate. The mucosal lesions of the rectum resembled those observed in the "solitary rectal ulcer syndrome." However, characteristic features of ergotamine-induced ulcers are absence of a mucosal prolapse, lack of a history of constipation, and rapid healing after discontinuation of the drug. Furthermore, the rectal lesion may be associated with anal ulceration, which occasionally presents as the only clinical manifestation of "anorectal ergotism."

Adult↗
PubMed1983

Treatment of the acute migraine attack--current status.

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.

Acetaminophen↗
PubMed1984

Reversible cerebral arteriopathy associated with the administration of ergot derivatives.

Three cases of intracranial arteriopathy associated with the administration of ergot derivatives are reported. In the first case, excessive doses of dihydroergotamine and of ergotamine tartrate seemed to be the cause, but simultaneous treatment with an antibiotic and the existence of a cytomegalovirus infection could have favoured the arteriopathic process. The second patient also received excessive doses of these two drugs, but in addition she was taking oestrogen and progesteron containing contraceptives. In the third case, an intravenous injection of methylergometrine in a dose of 0.2 mg seemed to have initiated the arteriopathy. Arteriograms were comparable in all three cases, with segmental stenosis of several cerebral arteries, whereas internal carotid and vertebral arteries remained normal. In the first case a control cerebral arteriography was normal one month later. These findings suggest that widespread cerebral arteriopathy can appear in subjects who chronically abuse ergotamine tartrate.

Adult↗
PubMed1982

Lower extremity ischemia due to combined drug therapy for migraine.

Three days after initiation of migraine headache therapy with ergotamine tartrate and propranolol, severe acute arterial insufficiency of the lower extremities developed in a 48-year-old woman who had been in general good health. Angiography revealed hypoplastic aortoiliac arteries, with tubular narrowing of the leg arteries. Lower extremity blood pressures rapidly returned to normal with a single intraarterial injection of 25 mg of tolazoline. Cases of peripheral ischemia due to either ergotamine or propranolol have been reported. Combined use of these two drugs may enhance the risk of acute arterial compromise.

Drug Therapy, Combination↗
PubMed1979

Ergotism in a patient with a portosystemic shunt.

A case of ergotism is described in a patient with Banti's syndrome in whom a porto-systemic shunt had been made three times. She was admitted to hospital with severe ischaemia of the extremities after having taken a single oral dose of 1 mg ergotamine tartrate. Her condition improved rapidly after 2 to 3 days and the circulation was normal after one week. The possible mechanism of ergotism in this patient is discussed. Although the plasma concentration of ergotamine was not measured, the likeliest explanation was that the serious side effects were related to the altered pharmacokinetics and loss of first-pass metabolism of the drug due to the venous bypass of the liver.

Adult↗
PubMed1989

The effects of transmitters on the affinity of the insoluble fraction of ox brain for Na+ and K+.

The insoluble fraction of ox-brain, which had previously been shown to have a non-linear affinity for Na+ and K+, was prepared. Acetylcholine (1 x 10(-8) mol/l and 1 x 10(-7) mol/l) reduced the affinity of the fraction for Na+ and K+ to zero, while at 1 x 10(-6) mol/l, the affinity for the cations was almost as high as in the absence of the transmitter; the affinities for Na+ and K+ were particularly high, when the supernatant concentrations of these ions exceeded 80-100 mM. Addition of eserine (3 x 10(-5) mol/l) considerably modified the response of the fraction to acetylcholine (1 x 10(-5) mol/l). Atropine (1 x 10(-8) mol/l) in the absence or presence of acetylcholine (1 x 10(-5), or 1 x 10(-4) mol/l) reduced the affinity of the fraction for Na+ and K+ to zero. Epinephrine (3 x 10(-10) mol/l) lowered the affinity for Na+ and K+, while ergotamine itself (1 x 10(-5) mol/l) reduced it to zero. The addition of both epinephrine and ergotamine at the latter concentrations restored the affinity of the fractions for Na+ and K+ to what it had been in the absence of the transmitter or antagonist, previously reported. Norepinephrine (3 x 10(-10) mol/l), or ouabain (1 x 10(-7) mol/l) reduced the affinity of the fraction for Na+ and K+ to zero. Thus, the transmitters and antagonists altered the affinity of the insoluble fraction for Na+ and K+ non-linearity, dependent upon their concentrations, the concentrations of the cations, and the interaction of transmitter and antagonist.

Acetylcholine↗