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PubMed2002

An introduction to migraine: from ancient treatment to functional pharmacology and antimigraine therapy.

Migraine treatment has evolved from the realms of the supernatural into the scientific arena, but it seems still controversial whether migraine is primarily a vascular or a neurological dysfunction. Irrespective of this controversy, the levels of serotonin (5-hydroxytryptamine; 5-HT), a vasoconstrictor and a central neurotransmitter, seem to decrease during migraine (with associated carotid vasodilatation) whereas an i.v. infusion of 5-HT can abort migraine. In fact, 5-HT as well as ergotamine, dihydroergotamine and other antimigraine agents invariably produce vasoconstriction in the external carotid circulation. The last decade has witnessed the advent of sumatriptan and second generation triptans (e.g. zolmitriptan, rizatriptan, naratriptan), which belong to a new class of drugs, now known as 5-HT1B/1D/1F receptor agonists. Compared to sumatriptan, the second-generation triptans have a higher oral bioavailability and longer plasma half-life. In line with the vascular and neurogenic theories of migraine, all triptans produce selective carotid vasoconstriction (via 5-HT1B receptors) and presynaptic inhibition of the trigeminovascular inflammatory responses implicated in migraine (via 5-HT1D/5-ht1F receptors). Moreover, selective agonists at 5-HT1D (PNU-142633) and 5-ht1F (LY344864) receptors inhibit the trigeminovascular system without producing vasoconstriction. Nevertheless, PNU-142633 proved to be ineffective in the acute treatment of migraine, whilst LY344864 did show some efficacy when used in doses which interact with 5-HT1B receptors. Finally, although the triptans are effective antimigraine agents producing selective cranial vasoconstriction, efforts are being made to develop other effective antimigraine alternatives acting via the direct blockade of vasodilator mechanisms (e.g. antagonists at CGRP receptors, antagonists at 5-HT7 receptors, inhibitors of nitric oxide biosynthesis, etc). These alternatives will hopefully lead to fewer side-effects.

Animals↗

PubMed1992

The pathophysiology of migraine: a tentative synthesis.

It is proposed that the migraine attack is explicable by an interaction between the brain and the cranial circulation in subjects with unstable vascular and pain-control mechanisms. While peptides are undoubtedly involved in vasodilatation, there is strong evidence that 5-HT plays an important part in the genesis of migraine. Whether the place of 5-HT lies in central pain-control pathways, in the serotonergic project to the cerebral cortex, in a direct action on the cranial blood vessels or in its action at all three sites remains uncertain. It seems probable that the primary action of sumatriptan or ergotamine in terminating migraine headache is exerted on the cerebral and extracranial circulation whereas medications employed in prophylaxis may act centrally.

Brain Stem↗

PubMed2004

[Treatment and prophylaxis of an acute migraine attack].

The treatment of migraine takes into consideration the intensity of the headache and the accompanying symptoms. The goal is to reduce the headache intensity, to relieve nausea and vomiting and to restore the ability to function in the daily routine. For drug treatment, there are now highly effective serotonin agonists available in addition to the older ergotamine preparations. A problem with all migraine analgesics is that in long lasting migraine attacks, the headache can recur as the pharmacological effect of the medication wears off. Through nonmedicinal and medicinal prophylactic measures, the frequency and intensity of the migraine attacks can be reduced. Keeping a headache diary for documentation is essential.

Acupuncture Therapy↗

PubMedDate not supplied

[Transient global amnesia following the use of ergots in the treatment of migraine].

INTRODUCTION: Transient global amnesia (TGA) is defined as a selective, or almost selective, deficit of the memory that appears suddenly and lasts less than 24 hours. The aetiopathogenesis of this syndrome remains unknown and different theories have been put forward about its epileptic or ischemic origin, or the relationship that exists with the neuronal depression that is produced in migraine. A number of triggering factors have been described, including the taking of distinct pharmaceutical preparations. CASE REPORT: We report the cases of two patients with a history of migraines who suffered TGA after taking ergotamine and dihydroergotamine, respectively, to treat an attack of migraine. CONCLUSIONS: Given the vasoconstriction effect of these drugs, it was concluded that in both cases the main factor that triggered the TGA was the ingestion of ergots.

Aged↗

PubMed1992

[Vasospastic angina with angiographically normal coronary vessels of iatrogenic origin. Apropos of 2 cases].

Two cases of angina pectoris, induced by methylergometrine (Methergin) and by an association of ergotamine tartrate (Gynergene) and methysergide (Desernil) respectively, are reported. In both patients, angiography revealed spontaneous spasm in a coronary system free from any significant atheromatous stenosis. In the second case, a test administration of i.v. Methergin, administered during calcium-channel antagonist treatment a few days after the "guilty" drugs had been stopped was found to be negative. The outcome was favorable in both cases: the angina disappeared and the base-line and exercise ECG returned to normal. The hypothesis of coronary spasm induced by the treatment was adopted in both cases. In this context, the major iatrogenic etiologies of vasospastic angina are recalled, together with the prophylactic and therapeutic measures they call for.

Adult↗

PubMedDate not supplied

Severe facial ischaemia caused by ergotism.

A case of ergotamine induced severe face ischaemia mimicking acute arteritis is presented. The unique clinical picture was due to bilateral involvement of both external carotid arteries. No case of ergotism with such a localization has been previously described in the literature.

Arteritis↗

PubMed1991

Links between headache mechanisms and new medications.

A milestone in migraine (M) treatment was the discovery of the dramatic analgesic action of a nonanalgesic drug, ergotamine. The second step consisted in the identification of the prophylactic power of serotonin antagonists, particularly methysergide, in support of the serotonin theory of M. A growing number of drugs has widened the therapeutic resources in this area and at the same time has raised more and more complex and fascinating pathogenetic questions. According to the personal theory, pain in idiopathic headaches (IH) is the clinical expression of an automatism of transmission of painful signals along the neuroaxial sensory pathways. This automatism is in turn linked to a fault in the suprespinal pain modulating systems. This is a similar, but obviously not identical, situation to that of automatic pain transmission in organic deafferentation. As animal experiments have shown, the activation of the afferents may cause the retrograde (antidromic) release of substance P (SP) (and of the neurokinins related to it). This substance is devoid of algogenic capacity but endowed with a high capillary permeabilizing power, with consequent neurogenic edema (NGE) due to plasma overflow. The heavy and lasting edema provoked in both the forearm and the hand by injection of both SP and releasing histamine 48/80 b.w. into the humeral artery, is by no means painful, unlike that induced by injection into the superficial temporal artery (moderate urent pain), probably because of the greater sensitivity of the vascular structures of the head. It may be postulated that the repeated episodes of NGE may lead to a "sterile" phlogosis (neurogenic inflammation) which is capable of increasing and prolonging the pain in the periphery.(ABSTRACT TRUNCATED AT 250 WORDS)

Cluster Headache↗

PubMed1990

Modern pharmacotherapy of migraine.

Rectal ergotamine and naproxen are the major candidates for the ad hoc treatment of migraine attacks; for particularly dramatic episodes, intravenous DHE with prochlorperazine is the author's preference. For long-term stabilization, after simpler measures fail, valproate appears to be a major addition to migraine therapy.

Analgesics↗

PubMed1990

Drug-induced headache.

Headache induced by medications used for nonheadache conditions, and more importantly, headache perpetuated by symptomatic medications used for primary headache disorders are discussed in detail in this article. The clinical features and mechanisms of drug-induced headaches are reviewed. Ergotamine and analgesic rebound phenomena are described. Management strategies for drug-induced headaches are outlined.

Analgesics↗

PubMed1990

[Ergotism--a rare cause of acute ischemia of the extremities].

Clinical ergotism as seen today results almost exclusively from the excessive intake of ergotamine tartrate in the treatment of migraine headache. Vasospasm of peripheral arteries is the leading clinical picture. Beside formation of collaterals and secondary thrombosis, vasospasm is one of the specific findings in angiography. Early diagnosis and withdrawal of the medication makes complete restitution possible. In all other cases intraarterial or intravenous infusion of sodium nitroprusside or nitroglycerin has turned out to be the most effective therapy. Balloon dilatation or operative intervention are an alternative therapy in those cases, where amputation of the limb seems to be necessary.

Acute Disease↗

PubMed1989

Effect of beraprost sodium on peripheral circulation insufficiency in rats and rabbits.

Beraprost sodium (sodium (+/-)-(1R*,2R*,3aS*,8bS*)-2,3,3a,8b-tetrahydro-2- hydroxy-1-[(E)-(3S*)-3-hydroxy-4-methyl-1-octen-6-ynyl]-1H- cyclopenta[b]benzofuran-5-butyrate, TRK-100) is a chemically and biologically stable epoprostenol analogue which possesses both potent antiplatelet and peripheral vasodilating actions. Its effect on obstruction of the peripheral artery was studied in three different models: 1. acute thrombosis induced by electrical-stimulation of the femoral artery in rabbits, 2. occlusion induced by intra-arterial injection of sodium laurate in rats and 3. tail gangrene induced by subcutaneous injections of both ergotamine and epinephrine in rats. Oral administration of beraprost sodium resulted in suppression of thrombus formation in the acute thrombosis model, marked improvement of macroscopic and histological observations in the laurate-occlusion model and inhibition of tail gangrene extension. In contrast, ticlopidine improved thrombus formation in the acute thrombosis model and slightly improved histological observation in the laurate-occlusion model, but not in the tail gangrene model. Cilostazol suppressed lesions in the acute thrombosis model, but not in the tail gangrene model. These findings suggest that beraprost sodium may be very useful clinically for the therapy of peripheral circulation insufficiency diseases such as Buerger's disease and Raynaud's disease.

Acute Disease↗

PubMed1989

[The neurons that determine the passive defense reaction in the pteropod mollusk Clione limacina].

Pd13 neurons have been identified in pedal ganglia. They are always excited with a short latency following tactile stimulation of the head. Then the passive-defensive reaction is arisen. Activation of neuron Pd13 induces inhibition of the whole locomotor generator. A number of neurons (P1 2, 3, 4 and 5) excited only after strong tactile stimulation have been identified in pleural ganglia. Activation of a certain pleural neuron induces inhibition of the whole locomotor generator. Inhibitory pleural neurons have synaptic contact with Pd13 neurons. Each spike in the pleural neuron is followed by one EPSP in Pd13 neuron. These relations are able to potentiation, soon changed by habituation. So, after strong tactile stimulation of the head, excitation of pleural neurons increases the activity of Pd13 neuron. Cerucal and ergotamine block the inhibition effect from Pd13 and pleural neurons on motoneurons, which testifies to the dopaminergic nature.

Animals↗

PubMed1985

Alpha- and beta-adrenergic receptor blockers and the effects of noradrenaline on heat production and body temperature.

Noradrenaline (NA) administered systemically or into the lateral cerebral ventricle (ICV) in appropriate doses increased heat production and colonic temperature in 1-12 day-old guinea pigs. The effect of systemically applied NA could be blocked by systemically applied beta-adrenergic receptor blockers, while beta-blockers administered centrally or alpha-adrenergic blockers injected systemically or centrally had no effect on the action of systemically applied NA. Accordingly, the effect of systemically applied NA was mediated by peripheral beta-adrenergic receptors. The effect of centrally applied NA was blocked by alpha-adrenergic receptor antagonists applied into the lateral cerebral ventricle and attenuated by systemically applied phentolamine, but not by phenoxybenzamine or ergotamine. Beta-adrenergic receptor blocking agents applied either ICV or systemically had no effect on the action of centrally applied NA. It is concluded that ICV applied NA acts through central alpha-adrenergic receptors.

Adrenergic alpha-Antagonists↗

PubMed1988

Migraine.

Recent advances in migraine therapy include the recognition of analgesic or ergotamine abuse as a cause of chronic daily migraine, the introduction of effective non-narcotic drugs such as chlorpromazine, dihydroergotamine and corticosteroids for the treatment of intractable migraine attacks, the increased number of beta-blockers now recognized as effective prophylactic agents and the introduction of calcium-channel blockers for prophylaxis. There is a sufficient variety of antimigraine drugs, and therapy should be successful for most sufferers.

Acute Disease↗

PubMed1978

[The pathogenesis and treatment of migraine (author's transl)].

191 migraine patients reported previous allergic diseases, tendency to vertigo and collapse, attacks of tachycardia, blood coagulation disorders, surgically treated cysts and fibromas and inflammatory diseases of various organs significantly more frequently than a control group similar in age, sex and social standing (N equal to 150). 140 patients reported retrospectively on the efficacy and side effects of different drugs. Ergotamine preparations showed a significantly better effect than others. The shorter the untreated attack, the more effective the preparations appeared to be. The younger the patients the better the effect of Dihydergot for interval treatment of migraine. Acupuncture was not successful. 16% of the patients abused their drugs.

Adult↗

PubMed1986

Proteinases of various Claviceps purpurea strains.

Extra- and intracellular proteinases from various Claviceps purpurea strains grown in submerged culture have been studied. A maximum level of intracellular proteinases was observed on the 6th day of culture growth, whereas extracellular activity continued to increase throughout the culture growth. Proteinases were purified and characterized. The ergotamine strain secreted one aspartic and two serine proteinases, whereas from the disrupted mycelium only the aspartic proteinase could be isolated. The ergocornine strain secreted the aspartic proteinase in two forms and the ergocristine strain produced an aspartic and a serine proteinase.

Claviceps↗

PubMedDate not supplied

[The present treatment of headaches (author's transl)].

Considered from the point of view of clinical practice, the treatment of chronic headache may be either symptomatic and etiological or physiopathological. Progress in symptomatic treatment depends first on the reasonable and graduated use of pure analgesics, looking out for the toxic side effects of the usual drugs and then the fairly definite efficacy of certain psychotropic drugs. The discovery of an etiology gives a specific dimension to the treatment: either anti-cerebral oedema drugs with above all tetracosactide, a diagnostic test of cerebral tumours, or antidepressor or tranquillizer drugs, depending on the variety of disturbance to be corrected. An attack of migraine always benefits from ergotamine used occasionally and in limited dosage (not more than 6 mg daily or 10 mg per week). For the basic treatment the drugs act mainly peripherally and fairly regularly in the following order: methysergide, beta-blockaders, pizotifene, cyproheptadine, oxetorone. Other drugs have a central effect, Tiapridal, MAO inhibitors which are too often neglected, and clonazepam which is not very easy to use.

Adrenergic beta-Antagonists↗

PubMed1986

[Cluster headache].

59 patients with cluster headache are discussed. Treatment can be divided into treatment of the acute attack, and prophylactic treatment. The acute attack can be interrupted in most cases by ergotamine, either sublingually or in the form of suppositories. A number of patients respond to the inhalation of pure oxygen. Most patients with the episodic type of cluster headache do well on prophylactic treatment with methysergide. If they prove refractory to this drug, treatment with lithium salts can be instituted. Most patients with the chronic type of cluster headache respond favourably to lithium therapy.

Adolescent↗