Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018681 (headache)
 56,091 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We retrospectively studied the long-term (2-year) outcome of 50 consecutive patients admitted to our inpatient headache program because of chronic daily headache (CDH) associated with the overuse of analgesics, ergotamine, or both. They had been detoxified, given repetitive intravenous dihydroergotamine (IV DHE) and prophylactic medications as part of the program, and had become headache-free on this regimen. At the time of admission, 37 of the 50 patients had transformed migraine (TM), 12 had new daily persistent headache (NDPH), and 1 had chronic tension-type headache; 29 of the patients with TM, 7 of those with NDPH, and the single patient with chronic tension-type headache had coexistent migraine. Substances abused, alone or in combination, included: caffeine in 39 patients (av. 441 mg/d), acetaminophen in 32 (av. 2187 mg/d), aspirin in 24 (av. 1807 mg/d), ibuprofen in 9 (av. 1156 mg/d), narcotics in 7 (av. 10.1 mg morphine equivalents/d) and ergotamine in 11 (av. 2.3 mg/d). Twenty patients were using preventive medication at the time of admission. Follow-up evaluations were performed at 3, 6, 12, and 24 months after discharge. Forty-three patients were analyzed at 3 months. Of these, 44% had an excellent or good result and 28% a fair result; 3 were overusing analgesics. At 24 months, 39 patients were analyzed: 59% had a good or excellent result and 28% a fair result; 5 were overusing analgesics, 4 of whom were doing poorly.(ABSTRACT TRUNCATED AT 250 WORDS)
Headache 1992 Oct
PMID:Chronic daily headache: long-term prognosis following inpatient treatment with repetitive IV DHE. 144 87

Neurogenic plasma extravasation, endothelial cell activation (increase in vesicle number and vacuole formation), platelet aggregation and adhesion, and mast cell degranulation occur selectively in post-capillary venules of the dura mater following electrical trigeminal ganglion stimulation, and are mediated by release of neuropeptides from perivascular unmyelinated C fibres. Pre-treatment with the antimigraine drugs dihydroergotamine and sumatriptan, two drugs that bind with high affinity to 5-HT1B/1D receptors, markedly attenuated plasma protein extravasation induced by electrical trigeminal ganglion stimulation. Trigeminal stimulation increased plasma calcitonin gene-related peptide levels in rat superior sagittal sinus. Pre-treatment with dihydroergotamine and, to a lesser extent, sumatriptan, attenuated this increase. Both drugs reduced morphological changes in post-capillary venules and mast cells within dura mater following electrical trigeminal ganglion stimulation. Plasma protein extravasation was selectively blocked in dura mater (but not in extracranial tissues) by pre-treatment with those receptor agonists showing a rank order of potency suggesting a 3-HT1B/1D interaction (5-CT greater than 5-BT greater than DHE greater than sumatriptan greater than 8-OH-DPAT). Pre-treatment with 5-HT2 and 5-HT3 antagonists was not effective. Taken together, these data are consistent with the interpretation that putative 5-HT-1B/1D receptors located on sensory fibres are coupled to inhibition of peptide release and blockade of neurogenic inflammation. An important therapeutic action of ergot alkaloids and sumatriptan in migraine headaches is so defined.
Cephalalgia 1991 Sep
PMID:Evidence for 5-HT1B/1D receptors mediating the antimigraine effect of sumatriptan and dihydroergotamine. 166 Mar 51

In a two year period, 47 patients with migraine were hospitalized for the management of severe headache; 18 had acute migraine (duration less than 72 hours), 17 had status migrainosus (duration by definition more than 72 hours), and 12 had chronic daily headaches qualitatively of a migraine type. Treatment in all comprised cessation of all previous medication, plus one of the following: intravenous DHE, intravenous lidocaine, a combination of lidocaine + DHE, or subcutaneous sumatriptan. Improvement from DHE, lidocaine, or both was slow and often incomplete. Sumatriptan was not used in patients with chronic daily headaches; in the 8 cases of acute migraine or status migrainosus in which it was used, improvement was rapid and complete in seven.
Headache 1991 Nov
PMID:The hospital management of severe migrainous headache. 166 91

Ketorolac IM was compared to DHE and metoclopramide IV in migraine patients whose regular abortive medication had failed and who presented to a headache clinic for acute treatment. Pain scale ratings and ratings of ability to function were recorded before and after injection. Ketorolac provided moderate relief in headache in six of nine patients compared to eight of nine given DHE and metoclopramide. The average improvement in patients receiving DHE and metoclopramide was greater in pain (p = .031) and disability scores (p = .057), than in those patients given ketorolac.
Headache 1991 Sep
PMID:Ketorolac versus DHE and metoclopramide in the treatment of migraine headaches. 196 56

We reviewed our experience with 54 cluster headache patients (23 episodic, 31 chronic) admitted to our headache center 64 tines over the past five years and treated with repetitive intravenous dihydroergotamine (IV DHE). DHE therapy was initiated on admission and prophylactic medication regimens were started or adjusted. All 54 patients had complete relief of their cluster headache, usually within two days. Most (82.8%) had no side effects. The average length of hospitalization was 6.7 days. At the three month followup, 92.9% of the episodic cluster patients were headache-free and 7.1% had a 50-74% improvement; at six months, all were headache-free. Of the chronic cluster patients, 44.4% were headache-free at three months and 52.8% had at least 50% improvement. At six months, 75% were headache-free and 22.2% were at least 75% improved, probably as a result of continued prophylactic medication. Repetitive IV DHE safely, rapidly, and effectively controls cluster headache.
Headache 1991 Sep
PMID:The treatment of cluster headache with repetitive intravenous dihydroergotamine. 196 57

DHE is effective in the treatment of acute and chronic migraine. The side effects most commonly observed are abdominal discomfort, muscle pain, diarrhea and anxiety. DHE is a dehydrogenated amino acid ergot alkaloid and, as such, causes only limited vasoconstriction; indeed, its overall effects include peripheral vasodilation. The literature is replete with reports of clinical vasospasm and claudication occurring with therapeutic doses of ergotamine. There has not been any previous description of claudication caused by DHE. This paper describes pulselessness in two patients during relatively short courses of DHE. Treatment consisted of calcium channel blockers and discontinuation of DHE. Recovery was complete.
Headache 1991 Apr
PMID:Claudication: an unusual side effect of DHE administration. 205 May 18

The efficacy of the combination of dihydroergotamine (10 mg) with acetylsalicylic acid (80 mg) (DHE + ASA) in the prophylaxis of migraine was studied in a double-blind, placebo-controlled crossover trial (8 weeks twice). Of 45 patients who entered the study, 38 completed it. The number of attacks was significantly (p = 0.003) reduced during active treatment (11.5 +/- 6.2) compared with placebo (16.6 +/- 9.9). The mean duration, the mean severity, and the mean score for symptomatic acute medication of attacks did not differ significantly. The overall assessment made by the patients themselves was in favor of DHE + ASA (p = 0.001). These results indicate a moderately beneficial effect of the dihydroergotamine/low-dose acetylsalicylic acid combination in migraine prophylaxis.
Cephalalgia 1988 Sep
PMID:Combined low-dose acetylsalicylic acid and dihydroergotamine in migraine prophylaxis. A double-blind, placebo-controlled crossover study. 319 98

With the combined pharmacokinetic-pharmacodynamic approach, the bioavailability and venoconstrictor effects of two DHE formulations (programmed release capsules and oral solution) have been compared after acute oral dose administrations in the healthy volunteer subjects. The bioavailability of DHE from programmed release capsules has been significantly greater than that shown by the oral solution. DHE capsules formulation has seemed to provide appropriate plasma concentrations for at least 10 h after administration. That may well account for its efficacy in the treatment of morning migraine.
Cephalalgia 1983 Aug
PMID:On the treatment of migraine. Pharmacokinetic-pharmacodynamic relationships for a programmed release formulation of dihydroergotamine administered orally in the human. 661 96

The authors evaluated the efficacy of a DHE methanesulphonate for migraine attacks and its tolerability on liver, gallbladder and cardiovascular system functions. Twenty-eight patients affected by migraine were studied. They were withdrawn from preventive therapy for at least one month and treated for three months. The drug showed a good efficacy with a statistical significant reduction of severity and duration of attacks. No variation of the biochemical and morphological parameters of liver, gallbladder and cardiovascular function were found throughout the treatment.
Cephalalgia 1983 Aug
PMID:DHE retard for prophylactic therapy of migraine: efficacy and tolerability. 661 1

Using the computerized venotest, it is possible to evaluate both the venospastic activity of the vasoactive monoamines (NA,5-HT, DA) and the effects of the relative agonistic and antagonistic drugs. The ergot-derivatives are 5-HT and NA agonists at low doses, and are 5-HT antagonists at high doses. Dihydroergotamine timed release (DHE-TR) administered orally is capable at 12 hours following the last administration of producing a significant increase of 5-HT and NA venospasm. It is hypothesized that 12 hours after the last administration of DHE-TR, hematic concentrations, corresponding to clinical and therapeutic levels, capable of potentiating the monoamine venospasm still exists.
Cephalalgia 1983 Aug
PMID:Clinical pharmacological aspects of dihydroergotamine timed release: activity on monoamine venospasm. 661 2


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