, Volume 62, Issue 2, pp 387–414 | Cite as


A Review of its Use in Migraine
  • Susan J. KeamEmail author
  • Karen L. Goa
  • David P. Figgitt
Adis New Drug Profile



Almotriptan is a selective serotonin 5-HT1b/1d receptor agonist (‘triptan’). Its efficacy and tolerability have been assessed in a number of randomised, controlled trials in over 4800 adults with moderate or severe attacks of migraine.

Oral almotriptan has a rapid onset of action (significant headache relief is observed 0.5 hours after administration of a 12.5mg dose) and efficacy is sustained in most patients who respond by 2 hours. The drug is significantly more effective than placebo as measured by a number of parameters including 2-hour headache response and pain-free response rates. Other symptoms of migraine, including nausea, photophobia and phonophobia, are also alleviated by almotriptan.

The efficacy of oral almotriptan appears to be maintained over repeated doses for multiple attacks of migraine treated over a long period (up to 1 year). High headache response rates were reported over all attacks without tachyphylaxis.

For the relief of single attacks of migraine, oral almotriptan 12.5mg had similar efficacy to oral sumatriptan 50mg. Patients given almotriptan report less concern with adverse effects than patients given sumatriptan. The lower incidence of chest pain following treatment with almotriptan than with sumatriptan may lead to a reduction in direct costs, with fewer patients requiring management of chest pain.

Almotriptan is well tolerated. Most adverse events were of mild or moderate intensity, transient, and generally resolved without intervention or the need for treatment withdrawal. The most common adverse events associated with oral almotriptan 12.5mg treatment were dizziness, paraesthesia, nausea, fatigue, headache, somnolence, skeletal pain, vomiting and chest symptoms. The incidence of adverse events did not differ from placebo and decreased in the longer term.

Almotriptan can be coadministered with drugs that share a common hepatic metabolic path; in addition, dosage reduction is required only in the presence of severe renal or hepatic impairment.

Conclusions: Almotriptan is an effective drug for the acute treatment of moderate or severe attacks of migraine in adults. An oral dose of almotriptan 12.5mg has shown greater efficacy than placebo; current data indicate that efficacy is similar to that of oral sumatriptan 50mg, and is maintained in the long term (≤ 1 year). Almotriptan has a good adverse event profile and a generally similar overall tolerability profile to sumatriptan; of note, almotriptan is associated with a significantly lower incidence of chest pain than sumatriptan. However, further clinical experience is required to clearly define the place of almotriptan among the other currently available triptans. Nevertheless, because triptans have an important place in various management regimens, and because the nature of individual patient response to triptans is idiosyncratic, almotriptan is likely to become a useful treatment option in the management of adults with moderate or severe migraine headaches.

Pharmacodynamic Properties

Almotriptan has a high and specific affinity for serotonin 5-HT1b/1d receptors, with similar affinity for both 5-HT receptor subtypes demonstrated by specific radioligand displacement assays. The concentration of almotriptan required to inhibit the binding of a ligand by 50% for cloned human 5-HT1b and 5-HT in1d receptors was 0.012 and 0.013 μmol/L, respectively. The drug also has a high affinity for 5-HT1f receptors, and a weak affinity for 5-HT1a and 5-HT7 receptors, but little or low affinity for a wide range of other receptors.

Drugs used in the acute treatment of migraine cause vasoconstriction of the cranial blood vessels and redistribution of cranial blood flow as one of their major effects. Almotriptan induced potent constriction in a number of isolated vascular preparations containing 5-HT1b/1d receptors. The concentration of almotriptan required to produce 50% of maximum contraction in human meningeal and temporal arteries was 0.03 and 0.7 μmol/L respectively. The maximum contraction of coronary and pulmonary arteries with almotriptan was significantly lower than with sumatriptan (p < 0.05), as was that of basilar artery tissue (p < 0.001).

Reduction in carotid arterial blood flow with almotriptan in animal models was caused through constriction of carotid arteriovenous anastomoses. Almotriptan also induced a significant increase in cerebral blood flow and a reduction in blood flow through extracerebral cranial vessels.

The inhibition of neurogenic inflammation is thought to be relevant in managing the pain of migraine headache. Various animal models have shown that almotriptan has the ability to inhibit both peripheral and central trigeminovascular activity, which prevents the release of vasoactive neuropeptides that cause vasodilation and inflammation of the blood vessel walls of the dura mater.

Single doses of oral almotriptan at the optimal therapeutic dose (12.5mg) had no statistically or clinically significant effects on blood pressure, heart rate or ECG parameters in young and elderly healthy volunteers. Although doses of almotriptan 25 and 50mg resulted in small increases in blood pressure, these changes were not clinically important.

Pharmacokinetic Properties

Oral almotriptan is absorbed moderately rapidly in healthy volunteers [maximum plasma concentrations (Cmax) were achieved between 1.4 and 3.8 hours with single doses of almotriptan 5 to 200mg]. After administration of a single dose of oral almotriptan 12.5mg, the Cmax of 29 to 50 μg/L was reached in a time of 2.2 to 2.5 hours. Absorption of oral almotriptan does not appear to be slowed during an acute attack of migraine. Area under the plasma concentration-time curve (AUC) and Cmax values show dose proportionality over the range of almotriptan 5 to 200mg; AUC after a single dose of oral almotriptan 12.5mg was 0.229 to 0.266 mg · h/L. Food had no significant effect on the oral absorption of almotriptan 25mg.

In healthy volunteers, the mean absolute bioavailability of oral almotriptan 25mg is approximately 70%; the relative bioavailability of almotriptan 5 to 200mg is approximately 80%.

Almotriptan is cleared by hepatic metabolism, with faecal and urinary excretion of its metabolites and renal excretion of the unchanged drug occurring in almost equal proportions. It has two major metabolites (a γ-aminobutyric acid and an indoleacetic acid derivative) and three minor metabolites (an N-demethyl, an alcohol and an N-oxide derivative, identified in vitro), all of which appear to be inactive. Almotriptan is primarily metabolised by monoamine oxidase A (MAO-A) and the cytochrome P450 (CYP) isoenzyme 3A subfamily, with some contribution by CYP2D6. Almotriptan is rapidly eliminated from the body. The mean plasma elimination half-life (t½) is about 3.1 to 4 hours, after a single 12.5mg oral dose. Approximately 40 to 50% of a dose of almotriptan is excreted unchanged in urine; renal clearance is about 75% of total body clearance.

Changes in the pharmacokinetics of almotriptan in patients with mild or moderate renal failure are reported not to be clinically important. The pharmacokinetics of almotriptan have not been studied in patients with hepatic impairment because researchers predict that the changes in pharmacokinetic parameters with hepatic impairment are unlikely to exceed those seen with patients who have severe renal impairment. However, patients with severe renal failure [creatinine clearance < 1.8 L/h (< 30 ml/min)] or hepatic failure are likely to have increased systemic exposure to almotriptan, resulting from a prolonged t½ and an increased mean AUC.

Although renal clearance of almotriptan is reduced in the elderly, dosage adjustments are not required. No statistically significant gender-related differences in the pharmacokinetics of almotriptan have been demonstrated.

Clinical Efficacy

The therapeutic efficacy of orally administered almotriptan has been evaluated in more than 4800 adults with moderate to severe attacks of migraine in randomised, controlled trials.

Almotriptan 12.5mg has a rapid onset of action, with significant headache relief reported at 0.5 hours (p < 0.05). A single dose of almotriptan is consistently significantly more effective than placebo in relieving single episodes of moderate or severe migraine headache as measured using a number of endpoints. Headache response rates at 2 hours (the primary efficacy parameter of most migraine trials) after administration of almotriptan 12.5mg ranged between 57 and 65% for single or first attacks of migraine, and were significantly greater than those seen with placebo (32 to 42%).

Pain-free response rates at 2 hours were also increased by almotriptan 12.5mg when compared with placebo (38 and 39 vs 11 and 16%), and efficacy was maintained for 24 hours in a high proportion of patients who responded at 2 hours. Of those who relapsed, the majority responded to a second dose of medication and remained pain free. Nausea, photophobia and phonophobia associated with migraine are significantly improved following almotriptan administration.

The efficacy of almotriptan appears to be maintained after repeated doses for multiple attacks of migraine over a period of up to 12 months with high headache response rates (76 and 84%) reported over all attacks in two noncomparative studies. Almotriptan also appears to be effective in treating mild or moderate migraine headaches, with early intervention reducing the need for rescue or relapse medication. Headache and pain-free response is consistent over time, with no tachyphylaxis to almotriptan treatment developing.

Almotriptan 12.5mg appears to have a similar efficacy to sumatriptan 50mg, the optimal oral dose for each drug. Similar headache response rates were seen at 2 hours (58 vs 57.3%), although almotriptan was less effective than sumatriptan at achieving a pain-free response at 2 hours (17.9 vs 24.6%; p = 0.005). There was no significant difference between the two drugs in alleviation of migraine-related symptoms, the need for rescue medication, or recurrence of moderate or severe headache. According to the results of a Migraine-Specific Quality of Life Questionnaire, adverse effects are of significantly less concern to patients treated with almotriptan when compared with sumatriptan.


Results of several large trials (n > 2000), and two long-term studies (n > 1300), indicate that almotriptan is well tolerated. Adverse events were mainly mild or moderate in intensity, transient, generally did not require intervention or treatment withdrawal and were less frequent with time.

The most common adverse events with almotriptan 12.5mg were dizziness (2.7%), paraesthesia (2.7%), nausea (1.9%), fatigue, headache, somnolence, skeletal pain and vomiting (all 1.6%). The incidence of these events did not differ significantly from that with placebo. When consecutive attacks of migraine were treated with almotriptan or placebo, the incidence of adverse events reported in both study groups decreased with each attack treated.

The adverse events profile of almotriptan and sumatriptan in doses demonstrating equivalent efficacy was similar, the only significant difference being a lower occurrence of chest pain after administration of almotriptan. The frequency of treatment-emergent adverse events in patients given oral almotriptan 12.5mg (n = 591) or oral sumatriptan 50mg (n = 582) was similar (15.2 vs 19.4%), with the most common adverse events in the almotriptan group being nausea (2.2 vs 3.4%), dizziness (2.0 vs 1.7%), headache (1.4 vs 1.5%) and somnolence (1.4 vs 1.9%). Patients treated with oral almotriptan 12.5mg (n = 184) or placebo (n = 99) reported fewer adverse events than the group treated with almotriptan 25mg (n= 191) [10.9 and 10.1%, respectively, vs 20.9%; p< 0.05 for both comparisons]. The incidence of adverse events reported after oral sumatriptan 100mg treatment (23.7%, n = 194) was similar to that with almotriptan 25mg, and significantly greater (p < 0.05) than that with almotriptan 12.5mg or placebo.

The good tolerability of almotriptan appears to persist, and the incidence of adverse events may decrease in the longer term. Over a 1-year period, the most frequent adverse events were vomiting (2.1%), nausea (1.4%), dizziness (1.6%), somnolence (1.7%), fatigue (1.4%) and chest symptoms (1.6%). Very few patients (60 out of 1347 patients) withdrew from long-term clinical trials as a result of adverse events; <1% of withdrawals from the 1-year trial were considered to be because of almotriptan. Almotriptan has not been associated with any clinically significant changes in clinical chemistry, haematology or urinalysis.

Overall, almotriptan was associated with a low incidence of adverse events relating to the cardiovascular system. When oral almotriptan 12.5mg was compared with sumatriptan 50mg (n = 1173), the incidence of chest-related adverse events (including vasodilation, palpitations, tachycardia and abnormal cardiac rhythm) with both treatments was low (<2.5%); chest pain was experienced significantly less often with almotriptan than with sumatriptan (0.3 vs 2.2%; p = 0.004). In a large double-blind study (n = 908), one patient developed transient symptomatic coronary ischaemia after a third dose of almotriptan 6.25mg. Significant risk factors, including a strong family history of heart disease and unsupervised use of oral contraceptives, were thought to have contributed to the event. In a 1-year study (n = 762), nine significant cardiovascular events were reported, including a conduction abnormality, palpitations, tachycardia and hypertension. 31 incidents of chest symptoms were reported in 12 patients; 20 were considered to be almotriptan related. Patients given single doses of almotriptan 5 to 150mg (n = 169) and 12.5mg (n = 591) show no clinically significant changes in ECG parameters or vital signs.

Pharmacoeconomic Studies: Compared with sumatriptan, direct cost savings are more likely when migraine headache is treated with almotriptan because of a lower incidence of chest-related symptoms and the associated costs of investigating them. A retrospective, population-based study using a computer-based model estimated that if patients had been treated with oral almotriptan 12.5mg instead of oral sumatriptan 25 and 50mg, direct annual medical cost savings for managing chest pain would have been $US 11.22 per patient, from the perspective of a health plan with one million covered lives (data reported as an abstract) [estimates based on costs for investigation of chest pain between 1996 and 1998; incidence of chest pain taken from a large (n = 1173) comparative study]. Analysis of data from a large (n = 1173) study using computer-based models (reported as abstracts) indicate that there is potential to reduce the likely direct, annual medical costs of managing chest pain, if patients are treated with oral almotriptan 12.5mg instead of oral sumatriptan 50mg.

Drug Interactions

Coadministration of a single oral dose of almotriptan 12.5mg with various other agents that are commonly used in the prevention of migraine (propranolol, verapamil), with antidepressants (moclobemide, fluoxetine) and with the potent CYP3A4 inhibitor ketoconazole, does not result in any clinically significant drug reactions. Administration of almotriptan with MAO-A or CYP3A4 inhibitors reduces clearance of the drug, but this is not considered clinically significant.

Dosage and Administration

Oral almotriptan is recommended for the acute treatment of migraine with or without aura in adults. According to the manufacturer’s prescribing information, the suggested initial dose of almotriptan tablets in the US is either 6.25 or 12.5mg. The recommended initial dose in the UK and Europe is 12.5mg. For headache recurrence, the dose may be repeated after 2 hours, but should not exceed two doses within a 24-hour period. Treatment should be limited to a maximum of four migraine headaches in any 30-day period.

In patients with severe renal impairment and, in the US, in patients with severe hepatic impairment the recommended initial dose of oral almotriptan is 6.25mg, with a maximum total daily dose of 12.5mg within a 24-hour period; in the UK and Europe treatment with almotriptan is contraindicated in patients with severe hepatic impairment. Almotriptan is contraindicated in patients with ischaemic heart disease, coronary artery vasospasm, any other significant underlying cardiovascular disease, or uncontrolled hypertension. Almotriptan is not recommended for use in patients under the age of 18 years as efficacy and tolerability have not been established in this patient group.

As the reduction in clearance of almotriptan when coadministered with MAO or CYP3A4 inhibitors is not clinically significant, dosage reduction is not required. Like other triptans, almotriptan should not be administered within 24 hours of ergot derivatives, and care should be taken when almotriptan is prescribed with selective serotonin reuptake inhibitors. The UK and European manufacturer’s prescribing information recommends that coadministration with lithium should be avoided.


Migraine Sumatriptan Almotriptan Cefditoren Oral Sumatriptan 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.


Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.


  1. 1.
    Stewart WF, Lipton RB, Celentano DD, et al. Prevalence of migraine headache in the United States: relation to age, income, race and other sociodemographic factors. JAMA 1992; 267(1): 64–9PubMedCrossRefGoogle Scholar
  2. 2.
    Lipton RB, Stewart WF. Acute migraine therapy: do doctors understand what patients with migraine want from therapy? Headache 1999; 39 Suppl. 2: S20–6CrossRefGoogle Scholar
  3. 3.
    Dahlöf C, Linde M. One-year prevalence of migraine in Sweden: a population-based study in adults. Cephalalgia 2001; 21: 664–71PubMedCrossRefGoogle Scholar
  4. 4.
    Headache Classification Committee of the International Headache Society. Classification and diagnostic criteria for headache disorders, cranial neuralgias and facial pain. Cephalalgia 1988; 8 Suppl. 7: 1–96Google Scholar
  5. 5.
    Silberstein SD, Lipton RB. Overview of diagnosis and treatment of migraine. Neurology 1994 Oct; 44 Suppl. 7: S6–16PubMedGoogle Scholar
  6. 6.
    Rasmussen BK, Olesen J. Migraine with aura and migraine without aura: an epidemiological study. Cephalalgia 1992; 12: 221–8PubMedCrossRefGoogle Scholar
  7. 7.
    Mounstephen AH, Harrison RK. A study of migraine and its effects in a working population. Occup Med 1995; 45(6): 311–7CrossRefGoogle Scholar
  8. 8.
    Stewart WF, Lipton RB, Simon D. Work-related disability: results from the American migraine study. Cephalalgia 1996; 16: 231–8PubMedCrossRefGoogle Scholar
  9. 9.
    Silberstein SD, Lipton RB. Headache epidemiology: emphasis on migraine. Neurol Clin 1996 May; 14(2): 421–34PubMedCrossRefGoogle Scholar
  10. 10.
    Kosinski M, Harris Garber W, Diamond M, et al. HIT6 scores discriminate among headache sufferers differing in headache-associated workplace productivity loss [abstract]. JNS 2001; 187 Suppl. 1: 13Google Scholar
  11. 11.
    Warshaw LJ, Burton WN, Schneider WJ. Role of the workplace in migraine disease management. Dis Manage Health Outcomes 2001; 9(2): 99–115CrossRefGoogle Scholar
  12. 12.
    Hargreaves RJ, Shepheard SL. Pathophysiology of migraine: new insights. Can J Neurol Sci 1999; 26 Suppl. 3: S12–19PubMedGoogle Scholar
  13. 13.
    Lance JW, Anthony M. The effect of serotonin on cranial vessels and its significance in migraine. Proc Aust Assoc Neurol 1968; 5(3): 639–42PubMedGoogle Scholar
  14. 14.
    Curran DA, Hinterberger H, Lance JW. Total plasma serotonin, 5-hydroxyindoleacetic acid and p-hydroxy-m-methoxy-mandelic acid excretion in normal and migrainous subjects. Brain 1965 Dec; 88(5): 997–1010PubMedCrossRefGoogle Scholar
  15. 15.
    Lance JW, Anthony M, Hinterberger H. Serotonin and migraine. Trans Am Neurol Assoc 1967; 92: 128–31PubMedGoogle Scholar
  16. 16.
    Pascual J. Nuevas perspectivas en el tratamiento de la migrãna. Neurologia 1999; 14 Suppl. 6: 26–35PubMedGoogle Scholar
  17. 17.
    Amirall Prodesfarma. Product monograph. 2000 JulGoogle Scholar
  18. 18.
    Bou J, Domènech T, Puig J, et al. Pharmacological characterization of almotriptan: an indolic 5-HT receptor agonist for the treatment of migraine. Eur J Pharmacol 2000 Dec 20; 410(1): 33–41PubMedCrossRefGoogle Scholar
  19. 19.
    McHarg AD, Napier CM, Stewart M, et al. The functional activity of eletriptan and other 5-HT1b/1d agonists at the human recombinant 5-HT1b and 5-HT1d receptors [abstract]. Headache 1999 May; 39: 369–70Google Scholar
  20. 20.
    Bou J, Gras J, Cortijo J, et al. Vascular effects of the new anti-migraine agent almotriptan on human cranial and peripheral arteries. Cephalalgia 2001; 21: 804–12PubMedCrossRefGoogle Scholar
  21. 21.
    Gras J, Bou J, Llenas J, et al. Functional profile of almotriptan in animal models predictive of antimigraine activity. Eur J Pharmacol 2000 Dec 20; 410(1): 43–51PubMedCrossRefGoogle Scholar
  22. 22.
    Gras J, Cardelus I, Llenas J, et al. Cardiovascular safety profile of almotriptan, a new indolic derivative for the treatment of migraine. Eur J Pharmacol 2000 Dec 20; 410(1): 53–9PubMedCrossRefGoogle Scholar
  23. 23.
    Boyce M, Dunn K, Warrington S. Hemodynamic and electrocardiographic effects of almotriptan in healthy volunteers. J Cardiovasc Pharmacol 2001 Mar; 37(3): 280–9PubMedCrossRefGoogle Scholar
  24. 24.
    Jansat JM, Warrington S, Cabarrocas X, et al. Oral pharmacokinetics of the new antimigraine agent almotriptan in young and elderly healthy volunteers. Eur J Pharm Sci 1999 May; 8: XXIVGoogle Scholar
  25. 25.
    Cabarrocas X. Efficacy of oral almotriptan, a novel 5-HT1b/d agonist in migraine [poster]. Almotriptan Oral Study Group. Eighth Congress of the International Headache Society; 1997 Jun 10; AmsterdamGoogle Scholar
  26. 26.
    Garcia E, Cabarrocas X, Jansat JM, et al. A clinical trial to determine the lack of food interaction on the bioavailability of almotriptan, a new 5-HT1b/1d agonist, in healthy volunteers [abstract]. Headache 1998; 38: 381Google Scholar
  27. 27.
    Bou J, Domènech T, Gras J, et al. Pharmacological profile of almotriptan, a novel antimigraine agent [poster]. Eighth Congress of the International Headache Society; 1997 Jun 10; AmsterdamGoogle Scholar
  28. 28.
    Cabarrocas X, Fernandez FJ, Popescu G, et al. The pharmacokinetics and tolerability of almotriptan in renal impairment [abstract]. Headache 1999 May; 39: 346Google Scholar
  29. 29.
    Cabarrocas X, Salvà M. Pharmacokinetic and metabolic data on almotriptan, a new antimigraine drug [abstract]. Cephalalgia 1997; 17: 421Google Scholar
  30. 30.
    Cabarrocas X, Salvà M. Pharmacokinetic and metabolic data on almotriptan, a new antimigraine drug [poster]. Eighth Congress of the International Headache Society; 1997 Jun 10; AmsterdamGoogle Scholar
  31. 31.
    Fernandez FJ, Jansat JM, Cabarrocas X, et al. Absolute bioavailability of oral and subcutaneous almotriptan [abstract]. Cephalalgia 1999 May; 19: 363Google Scholar
  32. 32.
    Cabarrocas X, Jansat JM, Ferrer P, et al. Pharmacokinetics of oral almotriptan during and outside a migraine attack [abstract]. Cephalalgia 2000; 20: 417Google Scholar
  33. 33.
    Pharmacia Corporation. Axert™ (almotriptan malate) tablets: Professional information brochure. 2001 MayGoogle Scholar
  34. 34.
    Salvà M, Palacios JM, Martínez-Tobed A. Metabolism of the novel anti-migraine compound almotriptan (LAS 31416) in humans [abstract]. 6th European International Society for the Study of Xenobiotics (ISSX) Meeting 1997: Gothenberg, Sweden, 174Google Scholar
  35. 35.
    Palacios JM. Almotriptan: clinical profile. Migraine, Current Status and Developments Conference; London [conference presentation]. 1998Google Scholar
  36. 36.
    Palacios JM, Rabasseda X, Castañer J. Almotriptan.Antimigraine 5-HT[in1d/1b agonist. Drugs Future 1999; 24(4): 367–74CrossRefGoogle Scholar
  37. 37.
    Fleishaker JC, Ryan KK, Jansat JM, et al. Effect of MAO-A inhibition on the pharmacokinetics of almotriptan, an antimigraine agent in humans. Br J Clin Pharmacol 2001 May; 51(5): 437–41PubMedCrossRefGoogle Scholar
  38. 38.
    Fleishaker JC, Sisson TA, Carel BJ, et al. Lack of pharmacokinetic interaction between the antimigraine compound, almotriptan, and propranolol in healthy volunteers. Cephalalgia 2001 Feb; 21(1): 61–5PubMedCrossRefGoogle Scholar
  39. 39.
    Fleishaker JC, Sisson TA, Carel BJ, et al. Pharmacokinetic interaction between verapamil and almotriptan in healthy volunteers. Clin Pharmacol Ther 2000 May; 67(5): 498–503PubMedCrossRefGoogle Scholar
  40. 40.
    Fleishaker JC, Herman BD, Azie NE, et al. Effect of ketoconazole on the clearance of the antimigraine compound, almotriptan, in humans [abstract]. Clin Pharmacol Ther 2001 Feb; 69 Suppl.: 25Google Scholar
  41. 41.
    Fleishaker JC, Ryan KK, Carel BJ, et al. Evaluation of the potential pharmacokinetic interaction between almotriptan and fluoxetine in healthy volunteers. J Clin Pharmacol 2001 Feb; 41(2): 217–23PubMedCrossRefGoogle Scholar
  42. 42.
    Dahlöf C, Tfelt-Hansen P, Massiou H, et al. Dose-finding, placebo-controlled study of oral almotriptan in the acute treatment of migraine. Neurology 2001 Nov 27; 57: 1811–7PubMedCrossRefGoogle Scholar
  43. 43.
    Pascual J, Falk RM, Piessens F, et al. Consistent efficacy and tolerability of almotriptan in the acute treatment of multiple migraine attacks: results of a large, randomized, double-blind, placebo-controlled study. Cephalalgia 2000 Jul; 20(6): 588–96PubMedCrossRefGoogle Scholar
  44. 44.
    Cabarrocas X, Zayas JM, Suris M. Equivalent efficacy of oral almotriptan, a new 5-HT1b/1d agonist, compared with sumatriptan 100 mg [abstract]. Headache 1998; 38: 377–8Google Scholar
  45. 45.
    Spierings ELH, Gomez-Mancilla B, Grosz DE, et al. Oral almotriptan vs oral sumatriptan in the abortive treatment of migraine: a double-blind, randomized, parallel-group, optimum-dose comparison. Arch Neurol 2001 Jun; 58(6): 944–50PubMedCrossRefGoogle Scholar
  46. 46.
    Gomez-Mancilla B, Mathew NT, Smith TR, et al. A 6-month open-label study of orally administered almotriptan in migraine patients [abstract]. Neurology 2000 Apr 11; 54 Suppl. 3: 269Google Scholar
  47. 47.
    Pascual J, Falk R, Docekal R, et al. Tolerability and efficacy of almotriptan in the long-term treatment of migraine. Eur Neurol 2001; 45(4): 206–13PubMedCrossRefGoogle Scholar
  48. 48.
    Colman SS, Brod MI, Krishnamurthy A, et al. Treatment satisfaction, functional status, and health-related quality of life of migraine patients treated with almotriptan or sumatriptan. Clin Ther 2001 Jan; 23(1): 127–45PubMedCrossRefGoogle Scholar
  49. 49.
    Anon. Section Ib.Migraine and other headache syndromes: description and diagnostic criteria. Cephalalgia 1997 Oct; 17 Suppl. 19: 7–38Google Scholar
  50. 50.
    Anon. Guidelines for controlled trials of drugs in migraine.First edition. Cephalalgia 1991; 11: 1–12Google Scholar
  51. 51.
    International Headache Society Clinical Trials Subcommittee. Guidelines for controlled trials of drugs in migraine: second edition. Cephalalgia 2000; 20: 765–86CrossRefGoogle Scholar
  52. 52.
    Robert M, Cabarrocas X, Fernandez FJ, et al. Efficacy and tolerability of oral almotriptan in the treatment of migraine [abstract]. Cephalalgia 1998; 18: 406Google Scholar
  53. 53.
    Pfaffenrath V, Cunin G, Sjonell G, et al. Efficacy and safety of sumatriptan tablets (25 mg, 50 mg, and 100 mg) in the acute treatment of migraine: defining the optimum doses of oral sumatriptan. Headache 1998 Mar; 38: 184–90PubMedCrossRefGoogle Scholar
  54. 54.
    Pascual J, Lainez JM, Leira R, et al. Beneficial effects of early intervention with almotriptan during long-term treatment of migraine [abstract]. Cephalalgia 2001; 21: 428CrossRefGoogle Scholar
  55. 55.
    Cabarrocas X, Zayas JM. Advantageous tolerability of almotriptan 12.5 mg compared with sumatriptan 100 mg [abstract]. Almotriptan Comparative Study Group. Headache 1999 May; 39: 347Google Scholar
  56. 56.
    Houghton LA, Foster JM, Whorwell PJ, et al. Is chest pain after sumatritpan oesophageal in origin? Lancet 1994 Oct 8; 344(8928): 985–6PubMedCrossRefGoogle Scholar
  57. 57.
    Boska MD, Welch KMA, Schultz L, et al. Effect of the anti-migraine drug sumatriptan on muscle energy metabolism: relationship to side-effects. Cephalalgia 2000; 20(1): 39–44PubMedCrossRefGoogle Scholar
  58. 58.
    Maasen VanDenBrink A, Reekers M, Bax WA, et al. Coronary side-effect potential of current and prospective antimigraine drugs. Circulation 1998; 98: 25–30CrossRefGoogle Scholar
  59. 59.
    Wang JT, Barr CE, Torigoe Y, et al. Cost savings in migraine associated with less chest pain on new triptan therapy [abstract and poster]. Value Health 2001; 4(2): 160CrossRefGoogle Scholar
  60. 60.
    Danish Neurological Society, Danish Headache Society. Guidelines for the management of headache. Cephalalgia 1998; 18: 9–22CrossRefGoogle Scholar
  61. 61.
    Mannix LK, Adelman JU, Goldfarb SD, et al. An economic decision model for chest symptom events associated with triptan use in migraine [abstract]. Cephalalgia 2001; 21: 341Google Scholar
  62. 62.
    Rothermich EA, Levaux HP, Colman SS, et al. Economic analysis of acute migraine: results from a controlled comparison of almotriptan and sumatriptan [abstract]. Cephalalgia 2001; 21: 341Google Scholar
  63. 63.
    Almogran® 12.5mg film-coated tablet: European summary of product characteristics. 2001 Jul 13Google Scholar
  64. 64.
    Bartleson JD. Treatment of migraine headaches. Mayo Clin Proc 1999; 74: 702–8PubMedCrossRefGoogle Scholar
  65. 65.
    Steiner TJ, MacGregor EA, Davies PTG. Management guidelines: guidelines for all doctors in the diagnosis and management of migraine and tension-type headache. British Association for the Study of Headache (BASH) [online]. Available from URL: [Accessed 2001 Aug 14]
  66. 66.
    Goadsby PJ, Olesen J. Diagnosis and management of migraine. BrMedJ 1996; 312: 1279–83Google Scholar
  67. 67.
    Goldberg MR, Sciberras D, De Smet M, et al. Influence of β-adrenoreceptor antagonists on the pharmacokinetics of rizatriptan, a 5-HT1b/1d agonist: differential effects of propranolol, nadolol and metoprolol. Br J Clin Pharmacol 2001; 52: 69–76PubMedCrossRefGoogle Scholar
  68. 68.
    Diener H-C, Brune K, Gerber WD, et al. Therapie der migräneattacke und migräneprophylaxe: Empfehlungen der Deutschen Migräne- und Kopfschmerzgesellschaft (DMKG). Akt Neurol 2000; 27: 273–82CrossRefGoogle Scholar
  69. 69.
    Smith MA, Ross MB. Oral 5-HTi receptor agonists for migraine: comparative considerations. Formulary 1999 Apr; 34: 324–38Google Scholar
  70. 70.
    Meyler WJ. Side effects of ergotamine. Cephalalgia 1996; 16: 5–10PubMedCrossRefGoogle Scholar
  71. 71.
    Williams P, Dowson AJ, Rapoport AM, et al. The cost effectiveness of stratified care in the management of migraine. Pharmacoeconomics 2001; 19(8): 819–29PubMedCrossRefGoogle Scholar
  72. 72.
    Sheftell FD, Fox AW. Acute migraine treatment outcome measures: a clinician’s view. Cephalalgia 2000; 20 Suppl. 2: 14–24PubMedCrossRefGoogle Scholar
  73. 73.
    Pauwels PJ, John GW. Present and future of 5-HT receptor agonists as antimigraine drugs. Clin Neuropharmacol 1999 May 30; 22: 123–36PubMedGoogle Scholar
  74. 74.
    Goadsby PJ. The scientific basis of medication choice in symptomatic migraine treatment. Can J Neurol Sci 1999; 26 Suppl. 3: 20–6Google Scholar
  75. 75.
    Goadsby PJ. Serotonin 5-HT1b/1d receptor agonists in migraine: comparative pharmacology and its therapeutic implications. CNS Drugs 1998 Oct; 10(4): 271–86CrossRefGoogle Scholar
  76. 76.
    Mathew NT. Serotonin 1d (5-HT1d) agonists and other agents in acute migraine. Neurol Clin 1997; 15: 61–83PubMedCrossRefGoogle Scholar
  77. 77.
    Spencer CM, Gunasekara NS, Hills C. Zolmitriptan: a review of its use in migraine. Drugs 1999 Aug; 58: 347–74PubMedCrossRefGoogle Scholar
  78. 78.
    Dooley M, Faulds D. Rizatriptan: a review of its efficacy in the management of migraine. Drugs 1999 Oct; 58: 699–723PubMedCrossRefGoogle Scholar
  79. 79.
    Bardsley-Elliot A, Noble S. Eletriptan. CNS Drugs 1999 Oct; 12: 325–33CrossRefGoogle Scholar
  80. 80.
    Visser WH, de Vriend RHM, Jaspers NMWH, et al. Sumatriptan in a clinical practice: a 2-year review of 453 migraine patients. Neurology 1996; 47: 46–51PubMedCrossRefGoogle Scholar
  81. 81.
    Visser WH, Jaspers NMWH, de Vriend RHM, et al. Chest symptoms after sumatriptan: a two-year clinical practice review in 735 consecutive migraine patients. Cephalalgia 1996; 16: 554–9PubMedCrossRefGoogle Scholar
  82. 82.
    Gunasekara NS, Wiseman LR. Naratriptan. CNS Drugs 1997; 8(5): 402–8CrossRefGoogle Scholar
  83. 83.
    Perry CM, Markham A. Sumatriptan: an updated review of its use in migraine. Drugs 1998; 55: 889–922PubMedCrossRefGoogle Scholar
  84. 84.
    van Haarst AD, van Gerven JMA, Cohen AF, et al. The effects of moclobemide on the pharmacokinetics of the 5-HT1b/1d agonist rizatritpan in healthy volunteers. Br J Clin Pharmacol 1999; 48: 190–6PubMedCrossRefGoogle Scholar
  85. 85.
    Tepper SJ. Safety and rational use of the triptans. Med Clin North Am 2001 Jul; 85(4): 959–70PubMedCrossRefGoogle Scholar
  86. 86.
    Lipton RB. Methodologic issues in acute migraine clinical trials. Neurology 2000; 55 Suppl. 2: 3–7Google Scholar
  87. 87.
    Jhee SS, Salazar DE, Ford NF, et al. Monitoring of acute migraine attacks: placebo response and safety data. Headache 1998;38(l): S35–8CrossRefGoogle Scholar
  88. 88.
    Goadsby PJ. The pharmacology of headache. Prog Neurobiol 2000; 62(5): 509–25PubMedCrossRefGoogle Scholar
  89. 89.
    Goadsby PJ. A triptan too far? J Neurol Neurosurg Psychiatry 1998; 64: 143–7PubMedCrossRefGoogle Scholar
  90. 90.
    Gruffyd-Jones K, Kies B, Middleton A, et al. Zolmitriptan versus sumatriptan for the acute oral treatment of migraine: a randomized, double-blind, international study. Eur J Neurol 2001 May; 8(3): 237–45PubMedCrossRefGoogle Scholar
  91. 91.
    Goldstein J, Ryan R, Jiang K, et al. Crossover comparison of rizatritptan 5 mg and 10 mg versus sumatriptan 25 mg and 50 mg in migraine. Headache 1998; 38(10): 737–47PubMedCrossRefGoogle Scholar
  92. 92.
    Pitman V, Forster E, Jackson NJ. Comparison of the efficacy of oral eletritpan and oral sumatritpan for the acute treatment of migraine: combined analysis across three clinical trials [abstract]. Headache 1999; 39: 374Google Scholar
  93. 93.
    Göbel H, Boswell D, Winter P, et al. A comparison of the efficacy, safety and tolerability of naratriptan and sumatriptan [abstract]. Cephalalgia 1997; 17: 426Google Scholar
  94. 94.
    Ferrari MD, Roon KI, Lipton RB, et al. Oral triptans (serotonin 5-HT1b/1d agonists) in acute migraine treatment: a meta-analysis of 53 trials. Lancet 2001 Nov 17; 358: 1668–75PubMedCrossRefGoogle Scholar
  95. 95.
    Dahlöf CGH, Mathew N. Cardiovascular safety of 5HT1b/1d agonists: is there a cause for concern? Cephalalgia 1998; 15: 539–45CrossRefGoogle Scholar
  96. 96.
    Saper JR. What matters is not the differences between triptans, but the differences between patients. Arch Neurol 2001 Sep; 58: 1481–2PubMedCrossRefGoogle Scholar
  97. 97.
    Jhee SS, Shiovitz T, Crawford AW, et al. Pharmacokinetics and pharmacodynamics of the triptan antimigraine agent: a comparative review. Clin Pharmacokinet 2001; 40(3): 189–205PubMedCrossRefGoogle Scholar
  98. 98.
    Goadsby PJ. Migraine treatment and mistreatment: primum non nocere. Med J Aust 2000; 172(9): 412–3PubMedGoogle Scholar
  99. 99.
    Weaver M, Patrick DL, Markson LE, et al. Issues in the measurement of satisfaction with treatment. Am J Manag Care 1997; 3(4): 579–94PubMedGoogle Scholar
  100. 100.
    Dahlöf C. How to assess patient preference of migraine treatments. Cephalalgia 1999; 19 Suppl. 24: 2–6PubMedGoogle Scholar
  101. 101.
    Spierings EL. Optimum-dose determination of the triptans [abstract]. Headache 2000 May; 40: 433–4Google Scholar
  102. 102.
    Dahlöf C. Assessing patient preference in migraine treatment. Cephalalgia 2001; 21: 791–5PubMedGoogle Scholar

Copyright information

© Adis International Limited 2002

Authors and Affiliations

  • Susan J. Keam
    • 1
    Email author
  • Karen L. Goa
    • 1
  • David P. Figgitt
    • 1
  1. 1.Adis International LimitedMairangi Bay, AucklandNew Zealand

Personalised recommendations