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We describe the case report of a migraine sufferer who developed ergotamine-induced headache and subsequently replaced ergotamine with daily sumatriptan (100 mg p.o.). The features of the headache were unchanged except for the presence of superimposed migraine-like headaches that occurred every 24 h.
Two patients (a woman aged 39, a man aged 46 years) had developed severe distal rectal stenoses after 20 years of anti-migraine treatment with ergotamine-containing suppositories. The woman required several bougie and laser treatments. In the man a megacolon had developed due to increasing, finally complete, rectal stenosis and this required a double colostomy (transverse colon) as an emergency. Ergotamine-containing suppositories are widely used in the treatment of migraine, but they should not be administered for prolonged periods.
Ergot alkaloids (EA) such as the ergopeptine alkaloid ergotamine (ET) are adrenergic, dopaminergic, and serotonergic agents. The objective of this experiment was to investigate regional brain neurotransmitter alterations caused by EA. Male BALB/c mice were treated s.c. daily with ergotamine tartrate for 10 d at 0 (saline), 0.4, 2, 10, or 50 mg/kg body weight. Twenty-four hours after the last treatment, animals were sacrificed and brains dissected. Regional concentrations of norepinephrine (NE), dopamine (DA), serotonin (5-HT), and metabolites 3-methoxy-4-hydroxyphenylethylene glycol (MHPG), dihydroxyphenylacetic acid (DOPAC), homovanillic acid (HVA), and 5-hydroxyindole-3-acetic acid (5-HIAA) were measured by high-performance liquid chromatography (HPLC). Moreover, selected organ weights and plasma prolactin (PRL) were determined. Dopamine concentration was significantly reduced by ET at all doses in the striatal and hypothalamic regions. A reduction of the DA metabolite HVA occurred in striatum at only the highest dose, whereas in the hypothalamus both HVA and DOPAC were markedly reduced. Concentrations of NE, MHPG, 5-HT, and 5-HIAA were not affected by treatment in these regions. In the cerebellum, MHPG was significantly elevated at the 50 mg/kg dose. No effect of treatment was observed in the cerebrum, medulla, and midbrain. Further, no treatment-related differences in plasma PRL and organ weights other than a significant liver weight decrease at intermediate doses were found. Therefore, the effects of ET were predominantly upon DA metabolism in the corpus striatum and hypothalamus. The reductions in DA, HVA, and DOPAC indicate decreased DA synthesis.
A 43-year-old woman with symptoms and signs of congestive heart failure and intermittent claudication was found to have moderately severe mitral stenosis and regurgitation, as well as severe bilateral upper and lower extremity arterial occlusive disease. She had a history of migraine headaches and had abused ergotamine tartrate (Cafergot) chronically for more than 20 years. Only rare instances of valvular heart disease have been associated with chronic ergotamine toxicity, with the majority of previously reported cases based on auscultatory findings alone.
A case of tongue necrosis in a patient with temporal arteritis who was taking ergotamine is described, and the role of ergotamine tartrate in provoking the tongue necrosis is considered. The literature on this unusual complication is critically reviewed, and the value of a carotid angiography in assessing the tongue ischaemia is exemplified.
BACKGROUND: Symptomatic postural hypotension in diabetes is uncommon. When it does occur, it can prove debilitating and difficult to treat. We report here the therapeutic challenges encountered in managing a patient with severe postural hypotension secondary to diabetes-related autonomic neuropathy. CASE REPORT: A 69-year-old gentleman with a 23-year history of Type 1 diabetes mellitus and multiple microvascular complications was admitted with symptoms of severe postural hypotension. Cardiovascular autonomic testing confirmed the presence of severe autonomic neuropathy. He failed to respond to non-pharmacological measures, fludrocortisone, midodrine, octreotide, erythropoietin and increased caffeine intake. Eventually he was commenced on half a Cafergot suppository (giving him a dose of ergotamine 1 mg and caffeine 50 mg) which resulted in dramatic clinical improvement. CONCLUSION: Ergotamine may be considered in refractory cases of postural hypotension.
The case of a 65-year-old male migraine patient with spontaneous internal carotid artery dissection is presented. He had been abusing ergotamine compounds for several years on at least 15 days per month. A possible association between arterial dissection and ergotamine abuse is discussed.
The effect of ergotamine and ergometrine on the venous compliance of the forearm has been studied in normal persons. Ergotamine tartrate (0.25 mg. intravenously) led to a fall in venous compliance amounting to 49% on average, while ergometrine maleate (0.25 mg. intravenously) caused a reduction of 41%; these changes were statistically significant. The potent veno-constrictor action of these ergot alkaloids appears to be a major component of the circulatory response to small doses and may be important in provoking the harmfull cardiovascular side-effects (such as angina and pulmonary oedema) that are sometimes observed in patients with pre-existing heart disease.
Platelet aggregation responses to 5-hydroxytryptamine (5-HT) were measured in plasma from migrainous subjects taking either methysergide maleate or ergotamine tartrate and were found to be reduced. Blood 5-HT levels of subjects free of headache were not affected by these drugs. The results support the hypothesis that methysergide and ergotamine act by occupying 5-HT uptake sites in vessel walls, leaving 5-HT molecules available to occupy receptors concerned with vasoconstriction.
Arterial complications following ergotamine therapy have been well recognized since the beginning of this century. Venous complications, however, have only rarely been reported. A 48 year old Nigerian woman developed extra-hepatic portal hypertension coincident with a chronic overdosage of ergotamine. The literature elucidating the possible mechanisms involved is reviewed.
22 migraine patients with a history of chronic ergotamine abuse were compared with 12 patients with a similar intake of dihydroergotamine. The study of somatosensory-evoked potentials showed that 50% of the patients with a history of ergotamine abuse had increased central conduction times after stimulation of the tibial nerve. Corticomotoneuronal latencies obtained by noninvasive electrical stimulation of the motor cortex were normal in 5 patients. The functional sensory deficits were not related to clinical impairment and were more frequently observed in patients with a comparatively high mean daily and cumulative intake.
An elderly patient with a history of chronic migraine was hospitalized with systolic hypertension and significant mental status changes, including increasing confusion, combative behavior, and remarkably detailed auditory hallucinations of several weeks' duration. Daily increased consumption of a product containing ergotamine 1 mg and caffeine 100 mg coincided with both onset and increasing severity of symptoms. To our knowledge, this is the first case reported in the contemporary literature of severe mental status changes and hallucination possibly due to ergotamine-caffeine.
After a brief review on the orthostatic disturbances in the regulation of blood circulation the author stresses upon the treatment of the orthostatic hypotonia with dihydrated ergotamine derivatives (Dihydergot retard). A favourable effect was obtained in 59 patients (84.3%) out of the treated 45 patients with secondary orthostatic hypotonia and 25 patients with primary hypotonia. The treatment of orthostatic hypotonia with dihydrated ergotamine derivatives was emphazised to be pathogenetically grounded, because tones the venous system (system of low pressure) and eliminates the developed contraregulatory sympathicotonia. Its combination with low doses of sympathominetics improves even more the effect.
Ergotamine tartrate and methysergide maleate each significantly altered serotonin (5-HT) metabolism in the rat brain. Whole brain levels of 5-HT were markedly reduced in a dose-related manner, with peak activity observed 30 minutes after I.P. administration and persisting through four hours after dosing. In addition, turnover rate of 5-HT was significantly increased. Pentylenetetrazol (PTZ)-induced convulsions were not inhibited by either ergotamine or methysergide but each drug interacted with PTZ to induce lethality, which is suggestive evidence of central 5-HT antagonist activity. Moreover, regional distribution of 5-HT in the rat brain was altered by these drugs in such a way to suggest that neihter was a "universally acting" central 5-HT antagonist.
A 37-year-old patient had migraine without aura over a six year period. He developed tolerance and dependency to ergotamine tartrate defined as the irresistible and dependable use of the drug. This is contingent upon a self-sustaining, rhythmic headache/medication cycle. The diagnosis of this entity is clinical and is supported by the typical and expected evolution of the migraine in response to the sudden interruption of ergotamine tartrate use.
Ergotamine is used to abort or prevent migraine. The most common adverse reactions are nausea, vomiting, myalgia, diarrhea or mouth dryness, and the contraindications are peripheral vascular disease because of its vasospastic effect, and liver disease because the drug is metabolized in this organ. Its effects on the heart are less frequent and less well known. We report two patients on long-term ergotamine treatment who developed valvular disorders.
Perianal ulcerations caused by suppositories application is an exceptional situation. We describe a 64 years old female with recurrent painless perianal ulcerations evoluting from 14 months. She medicates herself daily, since 8 to 10 years, with ergotamine tartarate suppositories, for the treatment of migraine. The diagnosis of ulcerated cutaneous drug reaction induced by ergotamine tartarate was confirmed by the complete healing of the lesions after stopping this medication and by their recurrence after the reintroduction of the treatment. These ulcerations are probably due to vasospasm of regional arterioles.
We report a case of a 28-year-old woman with C5 quadriplegia, unresponsive to conservative treatment for orthostatic hypotension. Ergotamine, daily combined with fludrocortisone, successfully prevented symptomatic hypotension. In this report, neural, renal, and hormonal blood pressure regulatory mechanisms are described. Experiences obtained from this case and the existing literature suggest that (1) in persons with quadriplegia, plasma catecholamine levels show little increase with sitting, indicating an inability to activate baroreceptor and chemoreceptor reflexes, (2) elevated plasma aldosterone and renin levels indicate a renal compensatory response to decreased renal perfusion secondary to low plasma volume and/or chronic hypotension, and (3) the net effect of ergotamine and fludrocortisone is probably a combination of plasma volume expansion and direct peripheral vasoconstriction.