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PubMed2001

Dexamethasone decreases migraine recurrence observed after treatment with a triptan combined with a nonsteroidal anti-inflammatory drug.

BACKGROUND AND OBJECTIVES: Triptans are effective drugs for the acute treatment of migraine. However, 30-40% of the patients commonly present recurrence before 24 hours therefore requiring another dose. Nonsteroidal anti-inflammatory drugs (NSAID) such as tolfenamic acid and naproxen sodium combined with sumatriptan have demonstrated efficacy in reducing recurrence observed with the single use of this drug. Steroids also have been suggested to treat refractory migraine and status migranosus. The aim of this study was to evaluate whether patients presenting frequent recurrence with the combination triptan plus NSAID, would decrease it with the association of dexamethasone. METHOD: Twenty three patients, 17 women and 6 men with migraine according to IHS criteria were prospectively studied. All patients presented frequent recurrence (> or= 60%, mean recurrence rate 74,8%) with the single use of sumatritpan 100 mg or zolmitriptan 2,5 mg or rizatriptan 10mg in at least 5 consecutive attacks, and didn't present a reduction of the recurrence rate superior than 20% with the combination of tolfenamic acid 200 mg or rofecoxib 25 mg in at least 5 other consecutive attacks (mean recurrence rate 60%). The patients had to treat 6 consecutive moderate or severe migraine attacks with their usual combination plus 4 mg of dexamathasone with a maximum of twice a week, and fill out a diary reporting headache parameters. RESULTS: Twenty patients, 16 women and 4 men completed the study. Of those who completed the study, 11 took rizatriptan plus rofecoxib, 4 rizatriptan plus tolfenamic acid, 3 zolmitriptan plus rofecoxib, 1 zolmitriptan plus tolfenamic acid and 1 patient took sumatriptan plus tolfenamic acid, having the 20 patients taken as a third medication, a single tablet of 4 mg of dexamethasone. All patients took oral formulations and none presented vomiting after that. Among all 20 patients, one female and one male patient presented recurrence in 3 out of the 6 attacks (50%) while the remaining 18 patients revealed recurrence in 1 or 2 treated attacks (mean 23,4%) (p<0,001). CONCLUSION: We concluded that the judicious use of oral dexamethasone might be useful for a limited population of migraine patients still presenting recurrence with the combination of a triptan and a NSAID. Case-control studies and studies with a randomized double-blind design are necessary to confirm these observations.

Adolescent↗
PubMedDate not supplied

Meta-analysis of oral triptan therapy for migraine: number needed to treat and relative cost to achieve relief within 2 hours.

OBJECTIVE: To determine the cost-effectiveness of the 5-HT1B/1D agonists, or triptans, in the acute treatment of migraine. METHODS: To determine the cost-effectiveness of the triptans, a meta-analysis was conducted of the efficacy data from 27 oral triptan trials, using the endpoint of "pain-free" status within 2 hours after initial dosing as the indicator of efficacy. Efficacy data were used to determine the number needed to treat (NNT) to achieve pain-free status in 1 patient within 2 hours postdose and then applied the per-dose costs for each triptan to the NNT values. RESULTS: Rizatriptan 10 mg and almotriptan 12.5 mg were the most cost-effective of the triptans, costing $48.34 and $48.57 US dollars, respectively, to achieve pain-free status in 1 patient within 2 hours postdose. Frovatriptan 2.5 mg was the most costly, with a cost-effective ratio of $162.49 US dollars. All other triptans fell between these extremes: zolmitriptan 5 mg ($65.18 US dollars), sumatriptan 100 mg ($70.83 US dollars), sumatriptan 50 mg ($75.67 US dollars), zolmitriptan 2.5 mg ($78.74 US dollars), and naratriptan 2.5 mg ($141.43 US dollars), in decreasing order of cost-effectiveness. CONCLUSION: Using an NNT analysis, the least-costly drugs to achieve migraine cure within 2 hours are rizatriptan 10 mg and almotriptan 12.5 mg. From a population health perspective, the lower acquisition cost of almotriptan 12.5 mg allows for effective treatment of more patients than rizatriptan 10 mg for no additional medication cost.

Administration, Oral↗
PubMed2001

When should triptans be taken during a migraine attack?

The common strategy to treat a migraine attack as soon as it begins, made for classical acute antimigraine treatments such as ergotamine and analgesics, has not been transposed to the triptans. The recommendation to delay triptan intake until headache intensity is at least moderate is merely a habit generated by the protocol used in triptan trials and a nonvalidated attempt to reduce costs. It is also favoured by the few studies suggesting that sumatriptan is less effective when given early in an attack, especially during the aura phase. Recent retrospective analyses of small numbers of 'protocol violators' in controlled trials of sumatriptan suggest that the drug is more efficient when taken while the headache is mild. Pain-free responses and therapeutic gains over aspirin (acetylsalicylic acid)-metoclopramide or ergotamine-caffeine combinations were increased under these conditions. The available circumstantial evidence is reviewed and discussed. Before any conclusion can be drawn and recommendation made, results are awaited from randomised controlled trials specifically addressing whether or not triptans are more efficient in mild headache. Meanwhile, there seems to be no medical reason to withhold treatment of a mild headache with a triptan as long as triptan intake does not exceed 1 or 2 doses per week. Most mild headaches in patients with migraine appear indeed to be mild migraine attacks, even when the headache characteristics are those of tension-type headache.

Humans↗
PubMed2003

Migraine: pathophysiology, pharmacology, treatment and future trends.

Migraine treatment has evolved 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, the 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↗
PubMedDate not supplied

Pharmacological characterisation of [35S]-GTPgammaS binding to Chinese hamster ovary cell membranes stably expressing cloned human 5-HT1D receptor subtypes.

[35S]-GTPgammaS binding has been used to study the function of cloned human 5-HT1D receptor subtypes stably expressed in chinese hamster ovary (CHO) cells. 5-HT stimulated [35S]-GTPgammaS binding to membranes from cells expressing 5-HT1Dalpha or 5-HT1Dbeta receptors. In membranes containing 5-HT1Dbeta receptors, 5-CT and sumatriptan stimulated binding to a similar extent as 5-HT while yohimbine, metergoline and 8-OHDPAT were partial agonists. The order of potency for agonists was 5-CT > 5-HT > metergoline > sumatriptan > yohimbine > 8-OHDPAT. The stimulation of binding by 5-HT in membranes containing 5-HT1Dbeta receptors was potently antagonised by methiothepin (pA2 8.9 +/- 0.1). The overall pharmacological profile for the human 5-HT1Dbeta receptor, defined using [35S]-GTPgammaS binding, agreed well with that reported for inhibition of forskolin-stimulated adenylyl cyclase. In addition, methiothepin and ketanserin inhibited basal [35S]-GTPgammaS binding to membranes containing 5-HT1Dalpha or 5-HT1Dbeta receptors, suggesting that these compounds show negative efficacy at 5-HT1D receptor subtypes. The data show that [35S]-GTPgammaS binding is a suitable method for studying the interaction between cloned human 5-HT1D receptors and G-proteins.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1999

[Anti-migraine treatment: present and future].

This is a review of major new findings in migraine therapy during the last 2-3 years. As for acute treatment, large population studies have underscored both the advantages and the shortcomings of sumatriptan. Its subcutaneous form is by far superior to the other galenic forms, which may not be clearly better than adequately used NSAIDs. If one considers total headache relief at 1 hour (gain over placebo) for second generation oral triptans, elitriptan 80 mg seems superior to the others, but it is probably endowed with more CNS adverse effects; eletriptan 40 mg and rizatriptan 10 mg are slightly superior to sumatriptan 50 mg, zolmitriptan 2.5 mg or naratriptan 2.5 mg. It has been shown, including in humans, that the less hydrophilic triptans can act on central receptors. Efficacity in acute treatment was also demonstrated for an association of lysine acetylsalicylate-metoclopramide, for ibuprofen, for ketoprofen and for intranasal xylocaïne. In migraine prophylaxis a significant breakthrough came from riboflavin 400 mg, which has an outstanding efficacy-side effect profile.

Administration, Oral↗
PubMed1999

5-Hydroxytryptamine(1A) receptor activation enhances norepinephrine release from nerves in the rabbit saphenous vein.

Although serotonergic receptor agonists are known to modulate release of central serotonin, less is known about the ability of serotonin to alter neurotransmission in peripheral adrenergic nerves. The present study used field stimulation (40V, 0.7 ms duration, 1-16 Hz) to contract the rabbit saphenous vein, an effect that was abolished in the presence of tetrodotoxin and prazosin (10(-6) M), consistent with stimulation of neuronal norepinephrine release. Furthermore, the field-stimulated contraction was not altered by the 5-hydroxytryptamine (5-HT)(1B/1D) receptor antagonist GR127935 (10(-6) M), but was markedly inhibited by the 5-HT(1A) receptor antagonist WAY 100635 (10(-6) M). GR127935 (10(-8) M) inhibited contraction to sumatriptan, documenting that the concentration used was sufficient to block 5-HT(1B/1D-like) vascular receptors in this tissue. Likewise, WAY 100635 (10(-6) M) inhibited contraction to the 5-HT(1A) receptor agonists (+/-)-8-hydroxydipropylaminotetralin hydrobromide (8-OH-DPAT) and LY238729, without altering contraction to norepinephrine or sumatriptan. Furthermore, both 8-OH-DPAT and LY228729 enhanced the contractile response to field stimulation (1. 0-8.0 Hz) and activated norepinephrine release in the absence of field stimulation. Contractile responses of the rabbit saphenous vein to both 5-HT(1A) receptor agonists were markedly inhibited by prazosin and dextrally shifted by WAY 100635, supporting the idea that the 5-HT(1A) receptor agonists were activating presynaptic 5-HT(1A) receptors to enhance norepinephrine release even in the absence of field stimulation. Thus, in the rabbit saphenous vein, 5-HT(1A) but not 5-HT(1B/1D) receptors enhanced neurotransmitter release from adrenergic nerves. These observations suggested that serotonergic nerves or other cell types in the saphenous vein are activated by field stimulation to release serotonin, which in turn activates presynaptic 5-HT(1A) receptors on adrenergic neurons to effect norepinephrine release. To support this hypothesis, serotonin levels were measured in the saphenous vein and were increased after pargyline pretreatment (30 mg/kg s.c.), decreased after dl-p-chlorophenylalanine methyl ester pretreatment (300 mg/kg s.c.), and unaltered after pretreatment with 6-hydroxydopamine hydrobromide (100 mg/kg s.c.). Thus, we provide strong evidence for the 1) presence of serotonin and its direct synthesis independent of adrenergic nerves and 2) a novel excitatory effect of presynaptic 5-HT(1A) receptor activation on adrenergic nerves in a peripheral blood vessel.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1999

Triptans. A support to the central link between serotonin and acetylcholine in migraine.

Recently synthesized triptans, sumatriptan derivatives, display aborting migraine activity at doses and with plasmatic maximum peak dramatically lower (20-40 times) than sumatriptan, the 5-HT like agonist, which is the original molecule. That triptans easily cross blood-brain barrier strongly supports the central theory of migraine. We recently discovered the anti-migraine prophylactic action of centrally acting anti-cholinesterase agents, that seems a further support to the central theory of migraine. Indeed, acetylcholine is an important analgesia neurotransmitter and is intertwined with 5-HT central pathways.

Acetylcholine↗
PubMed2000

The physiology and the pathophysiology of the gastric accommodation reflex in man.

Summarizing the previous sections, we have demonstrated that the gastric accommodation reflex in man involves the release of serotonin and the activation of a nitrergic motor neuron. We observed that almost half of the patients with functional dyspepsia have an impaired accommodation reflex, and this is associated with early satiety and weight loss. Drug-induced inhibition of the accommodation reflex is able to induce early satiety in healthy subjects. Administration of the anti-migraine drug sumatriptan, an agonist at 5-HT1P receptors on gastric myenteric neurons, causes a relaxation of the proximal stomach in man through a nitrergic pathway. Pretreatment with sumatriptan is able to restore impaired accommodation and to improve early satiety in patients with functional dyspepsia. We conclude from these data that fundus-relaxing drugs may have a therapeutic potential in functional dyspepsia, and we hypothesize that fundus-contracting drugs may have therapeutic potential in the treatment of obesity.

Adaptation, Physiological↗
PubMed2000

[Effect of migraine medications on monocyte chemotaxis] .

Monocytes play an important role in humoral as well as in cell-mediated immunity. In the present study, the influences of the anti-migraine preparations metoprolol, propranolol, metoclopramide, acetylsalicylic acid, dihydro-ergotamine and sumatriptan on monocyte chemotaxis were examined in vitro. First, mononuclear cells were isolated by centrifugation from venous blood samples obtained from 10 healthy male volunteers. Chemotaxis was determined using a microchemotaxis chamber. While metoprolol, metoclopramide, dihydroergotamine and sumatriptan did not influence monocyte chemotaxis, high doses of propranolol and acetylsalicylic acid caused a significant (p < or = 0.001) inhibition of this important cellular function. Therefore, it is quite possible that both drugs produce adverse immunological effects in vivo in cases of high dosage or obstruction of elimination.

Adult↗
PubMed2000

[Clinical pharmacology of triptans].

The 5HTI receptor antagonists currently used for the treatment of migraine headache all belong to the "triptan" group of drugs and have a chemical formula derived from serotonin. This structural similarity explains in part the MAO-A metabolism of certain triptan drugs used in human medicine. Chemical substitutions explain the variable role of different cytochrome P450 isoenzymes and differences in terms of drug interactions. Beyond the analysis of clinical trials, the pharmacologist must examine the epidemiological data on triptans. Prescription studies show an erroneously frequent use of sumatriptan for non-migraine headache. A low percentage of patients consume a large proportion of the sumatriptan prescribed and could be considered as "drug abusers". Epidemiological observation provides better knowledge of adverse effects and a better statistical definition of risk. The high cost of triptans, compared with older drugs, suggests the need to examine the pharmacoeconomical aspects of the question. Much more costly than ergot derivatives, triptans have a favorable cost-benefit and cost-usefulness ratio as is demonstrated by the reduction in loss of productivity, improved quality of life, and cost effectiveness studies.

Diagnosis, Differential↗
PubMed2000

[Treatment of cluster headache].

Management of cluster headache has greatly changed in recent years although most of the drugs used have not received approval for this indications. Subcutaneous injections of sumatriptan has been found to be remarkable effective for acute episodes. This drug continues to exhibit efficacy for long periods of use up to several months and has no serious adverse effects if used according to recommendations. Nasal administration of oxygen (not approved for this indication in France) continues to be an adjuvant treatment for patients with a contraindication for sumatriptan or for those with more than two acute episodes per day. Other treatments are under debate. Prophylactic first intention verapamil (not approved in France for this indication) could be useful. Lithium (not approved in France for this indication) could also be helpful, particularly for certain clinical forms. Other options are discussed.

Cluster Headache↗
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 trigemino-vascular system and migraine.

Neurogenic inflammation has been proposed as a possible pathogenetic mechanism for migraine and cluster headache. Antidromic stimulation of trigeminal fibers causes plasma protein extravasation, mast cell activation and degranulation, vacuolation and increase in endothelial vesicle number within post capillary venules in rat dura mater. The antimigraine drugs sumatriptan and dihydroergotamine block the development of plasma extravasation and ultrastructural changes, as well as plasma calcitonin gene-related peptide (CGRP) increase in the superior sagittal sinus following electrical trigeminal ganglion stimulation. Sumatriptan and dihydroergotamine bind with high affinity to the 5-HT1D/1B receptors, thus suggesting that their neurogenic antiinflammatory activity is mediated by activation of 5-HT autoreceptors present on sensory fibers innervating blood vessels in dura mater.

Blood Proteins↗
PubMed2003

[Pitfall in migraine treatment].

Migraine is a very common disorder. In Japan, an estimated 8.4% of population experience migraine, but most of them go undiagnosed and undertreated. Recent advances in basic and applied clinical neuroscience have led to the development of sumatriptan, a new class of selective serotonin (5-hydroxytryptamine (5-HT)) receptor agonists that activate 5-HT 1B/1D receptors. Following sumatriptan several other triptans were produced. They have three main mechanism of action: cranial vasoconstriction, peripheral trigeminal inhibition, and inhibition of transmission through second order neurons of the trigeminocervical complex. Even in our country, we can now use three kinds of triptans, which are very effective medicine against acute migraine with a well-developed scientific rationale. Despite the higher price, triptans were preferred over ergots in most patients. Recently Limmroth et al reported a prospective study for medication overuse headache (MOH) in 98 patients. The mean critical duration until onset of MOH was shortest for triptans (1.7 years), longer for ergots (2.7 years), and longest for analgesics (4.8 years). The mean critical monthly intake frequencies was lowest for triptans (18 single doses per month), higher for ergots (37), and highest for analgesics (114). We should keep in mind that overuse of triptans leads to MOH faster and with lower dosages compared with ergots and analgesics.

Contraindications↗
PubMed2005

[Particular features of the impact of certain vegetotropic drugs on the excitability of cholinergic structures, contractile myocardial function and electromotive stomach activity].

The study examined particular features of the impact of propranolol (obsidan), bretylium tosylate (ornid), sumatriptan (imigran) and morphine on the excitability of cholinergic structures, contractile myocardial function and electromotive stomach activity. It was shown that ornid and obsidan reduce the contractile myocardial function, and a drug of selection can be ornid. Introduction of morphine reduced the excitability threshold of myocardial cholinergic structures. Sumatriptan is a 5-HT 1,2-serotonin blocker.

Animals↗
PubMed1994

Migraine: a pharmacologic review with newer options and delivery modalities.

The management of migraine usually centers on two approaches: preventive and abortive therapy. Preventive therapy, designed to reduce the frequency, duration, and intensity of attacks, can be accomplished through a wide variety of medications. The most commonly used are beta-blockers, but calcium channel blockers, antidepressants, anticonvulsants, and nonsteroidal anti-inflammatory agents have all been used with success. Agents used in abortive migraine therapy treat the intensity and duration of pain, as well as the associated symptoms. New treatment options have been developed, including such newly approved medications as sumatriptan. Sumatriptan is a very effective agent that has joined the ranks of other effective abortive migraine treatments, such as ergotamine, dihydroergotamine, and nonsteroidal anti-inflammatory agents, as well as narcotic analgesics. New delivery systems, such as the nasal-spray formulation of butorphanol, allow for a route of administration previously unavailable to migraine sufferers. These new and developing treatment modalities will give physicians a wider choice of outpatient therapy options.

Administration, Intranasal↗
PubMed1993

Recent advances in migraine management.

Migraine periodically disables millions of Americans and thus has a significant economic impact on society. Successful treatment of migraine requires that the physician understand the pathophysiology underlying migraine and educate the migraineur in the management of this chronic pain syndrome. Recent advances in the receptor biochemistry of serotonin have given important insight into the mechanisms of migraine pain and treatment. An understanding of these mechanisms has resulted in treatment strategies that address the mechanism of headache control rather than just symptom control. Advances in pharmacologic therapy include a newly developed highly selective serotonin agonist called sumatriptan, which appears to be a promising addition to the armamentarium of abortive migraine treatments. Further data correlating the role of daily analgesics and ergotamines in transforming episodic migraine into chronic daily headache represent another significant advance in migraine management. Clinical trials of sumatriptan are reviewed, and the role of daily analgesic and ergotamine use is discussed in relation to advances in migraine pathophysiology and available demographic data on migraine.

Analgesics↗