Ergotamine, Dihydroergotamine: Current Uses and Problems

P. Tfelt-Hansen

Disclosures

Curr Med Res Opin. 2001;17(1s) 

In This Article

Summary and Introduction

In randomized clinical trials oral ergotamine was found superior to placebo but inferior to oral sumatriptan 100mg. In contrast, rectal ergotamine was found to have higher efficacy (73% headache relief) than rectal sumatriptan (63% headache relief). Intranasal dihydroergotamine (DHE) was found superior to placebo but less effective than subcutaneous and intranasal sumatriptan.

In general, the use of the more specific drugs, the triptans, causing less adverse events and being more effective, is preferable to the use of the ergotamine in the acute treatment of migraine. If ergotamine is to be used the rectal route is preferable. The rectal dose of ergotamine should be tailored to the individual patient.

The intranasal dose of DHE , between 1 and 2 mg, should also be tailored to the individual patient. In order to avoid drug-induced headache ergotamine and DHE should not be used daily.

In the Middle Ages grain contaminated with ergot (Claviceps purpurea) caused epidemics of gangrene known as 'St. Anthony's Fire'[1]. Ergotamine, one of the ergot alkaloids mainly responsible for this effect, was isolated from ergot in 1918 and introduced in migraine therapy in 1926 as a sympatholytic drug[2]. In 1938, Graham andWolff concluded that the efficacy of ergotamine was probably due to vasoconstriction of the extracranial vasculature[3]. Soon afterwards, in 1945, dihydroergotamine was introduced in migraine therapy as a more potent sympatholytic agent than ergotamine[2]. The vasoconstrictor activity of these ergot alkaloids is the most likely mode of action in migraine pain, although other possible mechanisms for the beneficial effect of ergot alkaloids have been suggested, including an effect on neurogenic inflammation[4,5] and an action on central serotonergic neurones[6].

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