P&T News: November 1998

Pharmacologic Management Of Migraines: Intranasal Treatment Options

Brian McAfee, Pharm.D.
Peer Review Status: Internally Peer Reviewed by Sue Barcellos, M.D., Assistant Professor, Director of the Headache Clinic, Department of Neurology


Migraine is a common medical condition characterized by episodic, pulsating, unilateral headaches of moderate to severe intensity (inhibits or prohibits daily activity) that are aggravated by simple activity. Additional symptoms include nausea, with or without vomiting, and photophobia with phonophobia. Criteria for the diagnosis of migraine have been developed by the International Headache Society (see Table 1).1 It is estimated that as many as 23 million Americans suffer from migraines;2 the prevalence may exceed 10% of the U.S. population, and the condition is three to four times more likely to occur in women than in men.3

Migraines significantly affect the patient's quality of life, decrease worker productivity, and utilize significant healthcare resources. In addition to direct costs for medications, office visits, emergency room visits, healthcare provider services, and other medical treatment costs, the indirect costs of migraines have a tremendous economic impact. In 1992, the indirect costs associated with migraines were estimated to be between $1.4 and $17.2 billion per year. 4

The management of migraines has concentrated on preventing attacks, and when they do occur, effectively aborting the attacks. Abortive agents have focused on action at the serotonin 5-HT1B and 5-HT1D receptors. This article focuses on two newer treatment options for the management of migraines: surnatriptan nasal spray and dihydroergotamine nasal spray.

Sumatriptan Nasal Spray
Approved for marketing in September 1997, surnatriptan nasal spray (Imitrex[R] - Glaxo Wellcome) is indicated for the acute treatment of migraine attacks with or without aura in adults.5 Injectable and oral formulations of sumatriptan were previously marketed for these indications. Sumatriptan is believed to provide migraine relief by binding to 5-HT1D receptors; activation of the 5-HT1D, receptors on sensory nerve endings in the trigeminal system results in the inhibition of pro- inflammatory neuropeptide release, which is postulated to lead to the clinical symptoms of migraine. Activation of the 5-HT1B receptor is involved in vasoconstriction.

Pharmacokinetic Properties
The time required to reach maximum serum concentration (tmax) following intranasal administration of sumatriptan is not specified in the manufacturer's labeling information; however, the International Intranasal Surnatriptan Study Group reported tmax was 48 minutes, 1 hour, and 1.8 hours for the 10 mg, 20 mg, and 40 mg doses, respectively.6 The median time to peak serum concentrations in healthy adults after a single 20 mg intranasal dose was 1 hour (range 0.08 to 4.00 hours).7 This is less than one-half of the time required for the oral tablet, but not nearly as fast as the subcutaneous injection. During a migraine attack the reported tmax for the oral tablets is approximately 2.5 hours,8 while for the subcutaneous injection formulation the time is reduced to approximately 12 minutes (range of 5 to 20 minutes).9

Table 1. International Headache Society Diagnostic Criteria for Migraine1

Migraine without Aura

1. Headache attacks lasting 4 to 72 hours (untreated or successfully treated)
2. Headache has at least two of the following characteristics:
  • Unilateral location
  • Pulsating quality
  • Moderate-to-severe intensity (inhibits or prohibits daily activities)
  • Aggravation by walking stairs or similar routine physical activity
3. At least one of the following symptoms during the headache:
  • Nausea and/or vomiting
  • Photophobia and/or phonophobia
4. A minimum of five attacks fulfilling criteria 1,2, and 3 above
5. History, physical examination, and, where appropriate, diagnostic tests exclude a secondary cause

Migraine with Aura

1. A minimum of three of the following characteristics:
  • One or more fully reversible aura symptoms indicating focal cerebral cortical and/or brain stem dysfunction
  • At least one aura symptom develops gradually over more than 4 minutes OR, two or more symptoms occur in succession
  • No single aura symptom lasts more than 1 hour (if more than 1 hour, then diagnosis or migraine with prolonged aura). If more than 1 aura symptom is present, accepted duration is proportionally increased
  • Headache follows aura with a free interval of less than 1 hour (it may begin before or simultaneously with the aura)
2. A minimum of two attacks fulfilling criterion 1 above
3. History, physical examination, and, where appropriate, diagnostic tests exclude a secondary cause
4. One or more aura symptoms of the following types:
  • Homonymous visual disturbances
  • Unilateral paraesthesia and/or numbness
  • Unilateral weakness
  • Aphasia or unclassified speech difficulty

The onset of migraine relief for each of the sumatriptan formulations is difficult to compare because the published clinical trials assessed symptom relief using different time intervals. The subcutaneous route was measured in 10-minute intervals, the intranasal route measured in 30-minute intervals, and the oral route was measured in hourly intervals. The manufacturer provides information regarding onset of relief for the injectable and oral routes, stating that the onset of relief begins as early as 10 minutes following a 6 mg subcutaneous injection and in 1 to 1.5 hours following a 25 mg, 50 mg or 100 mg oral dose. However, data are not provided for the intranasal route. When the Finnish group compared intranasal sumatriptan to placebo, there was a larger number of patients who responded to intranasal sumatriptan as early as 30 minutes after administration (p = 0.29), but the difference did not reach statistical significance until 60 minutes (p = 0.004).10 Results of two published intranasal sumatriptan studies11 conducted in the United States reported that the 20 mg dose was more effective than placebo at relieving headache beginning 15 minutes post-dose in one study and 60 minutes post-dose in the second study (p less than 0.05).

The International Intranasal Surnatriptan Study Group reported that the 100 mg oral and 6 mg subcutaneous doses give comparable efficacy to intranasal sumatriptan 20 mg doses, but produce mean peak levels (Cmax) of 54 and 72 ng/ml, respectively.6 These levels are roughly four to six times higher than those seen with intranasal sumatriptan (12 ng/ml); therefore, the Study Group concluded that "no linear association was found between the observed headache severity grades and any of the pharmacokinetic parameters (i.e., Cmax, tmax)." This apparent lack of a dose-response relationship for sumatriptan is in agreement with information found in the prescribing information for the oral and injectable formulations.8, 9

Clinical Efficacy
The Finnish Sumatriptan Group and the Cardiovascular Clinical Research Group published the first randomized, doubleblind, placebo-controlled clinical trial of intranasal sumatriptan.10 The study was conducted in six hospitals in Finland and included 74 patients between 18 to 60 years of age who met the International Headache Society criteria for moderate and severe migraine attack. The active treatment group received two doses of surnatriptan 20 mg/0.1 ml intranasally, given 15 minutes apart, following the onset of a single migraine attack. The researchers found that 64% and 75% of sumatriptan patients, versus 30% and 32% of placebo patients, experienced improvement in headache severity 60 minutes and 120 minutes after treatment, respectively. The requirement for rescue medication 120 minutes after the first dose was 32% in the sumatriptan group and 84% in the placebo group. The incidence of nausea (17% vs. 43%; p=0.014) and photophobia (28% vs. 57%; p=0.013) was significantly lower in the sumatriptan group; however, the incidence of vomiting was lower (0 % vs. 11 %; p more than 0. 05), this was not found to be different from placebo. The investigators contacted the patients by telephone 24 hours after treatment and found that the number of patients reporting migraine recurrence after sumatriptan was the same as the placebo group (29% vs.20%;p=0.417).

Many of the researchers involved with the Finnish group expanded the study in an attempt to determine both the optimum dosage and the effects of one nostril (n=245) versus two nostril (n=210) administration. The researchers used placebo or a 1 mg, 5 mg, 10 mg, 20 mg or 40 mg single dose of sumatriptan in one nostril or as a divided dose via both nostrils. Headache improvement was significantly better at 120 minutes with doses of 10 mg to 40 mg in each of the nostril administration groups when compared to placebo (p less than 0.05). The largest response rate was achieved with the 20 ing dose (78 % and 74 % for the one and two nostril administrations, respectively).

Ryan et al reported the results of two identical, randomized, placebo-controlled, multicenter studies (n=409 and n=436).11 They evaluated the efficacy and tolerability of 10 mg and 20 mg doses of intranasal sumatriptan in the acute treatment of moderate and severe migraine as diagnosed according to the International Headache Society criteria. Two hours after dosing, headache relief was experienced by 62 % to 63 % of patients in the 20 mg group, 43% to 54% in the 10 ing group, and 29% to 35% of the placebo-treated patients (p less than 0.05 sumatriptan 10 mg or 20 mg vs. placebo in study 1 and 20 mg in study 2). The percentage of patients with recurrent headache requiring a second dose was 32% in the sumatriptan 20 ing groups, 43% to 46% in the sumatriptan 10 ing group, and 34% to 55% of patients receiving placebo. These recurrence rates were not significantly different from placebo.

Overall, the response to single intranasal administrations of 5 mg, 10 mg, or 20 mg doses was more effective than placebo for the treatment of acute migraine.6,1-12 The response rate for sumatriptan nasal spray ranges from 43% to 78% of patients, (i.e., experiencing mild to no pain at 120 minutes post-dose). The 20 mg dose is consistently effective at relieving migraine symptoms, and single doses greater than 20 mg do not result in added benefit. These efficacy rates are comparable to oral 100 mg sumatriptan with a response rate of 50% to 67% at 120 minutes post-dose. 13,11 Controlled studies have demonstrated that 6 mg of sumatriptan administered subcutaneously provides rapid and effective relief of migraine in a higher percentage of patients (70% to 77% at 60 minutes post-dose and 81% to 87% response at 120 minutes).13,15 All three formulations of sumatriptan have a recurrence rate that ranges from 34% to 43%; this may be associated with the short half-life (2 hours) of sumatriptan relative to the usual 4 to 72 hour duration of a migraine attack. 13-15 Therefore, the need for repeat doses does not differ among the formulations.

Safety Issues
Bad, bitter or unpleasant taste was the most frequently reported adverse event and was experienced by 17% to 38% sumatriptan patients10,11 The frequency of taste disturbance was found to increase with larger doses.6 Approximately 5% of patients reported nose irritation or a burning sensation, and this was noted to be severe in 1% of the cases. The manufacturer describes the symptoms as transient and states that 60% of these symptoms resolved in less than 2 hours. Nose and throat discomfort is reported at approximately the same rate as placebo (0.9%) for the 5 mg dose, but increases to 1.8% and 2.4% for the 10 mg and 20 mg doses, respectively.5 Other minor transient adverse events reported were dizziness (2%), drowsiness (1%) and nausea (6%). Patients often experience atypical sensations/paresthesias after administration of sumatriptan; therefore, the recommendation is that all patients, independent of risk, receive the first dose under physician supervision. Overall, the adverse event profile of intranasal sumatriptan is similar to that observed with the oral and subcutaneous routes.

Sumatriptan nasal spray carries the same contraindications and warnings as the oral and injectable formulations. The most serious adverse effect is coronary vasospasm. after sumatriptan use, and deaths due to myocardial infarction and cardiac arrest have been reported. Due to the potential for fatal cardiac events, use of all formulations of sumatriptan (i.e., oral, injectable, and nasal spray) is contraindicated in the conditions depicted in Table 2.

Table 2. Contraindications to the Use of Sumatriptan5,8,9
  • Ischemic heart disease (coronary artery disease)
    • Angina pectoris
    • History of myocardial infarction
    • Documented silent ischemia
  • Coronary artery vasospasin
    • Prinzmetal's variant angina
    • Used within 24 hours of ergotamine-type medications
    • MAO-Inhibitor use
    • Hemiplegic or basilar migraine
    • Uncontrolled hypertension
    • Other 5-HT1, agonist use within 24 hours

The prescribing information also includes boldface warnings that sumatriptan nasal spray should only be used where a clear diagnosis of migraine has been established. The manufacturer strongly recommends that sumatriptan not be given to patients with risk factors for coronary artery disease. Patients who have the risk factors for coronary artery disease (Table 3) should have a cardiovascular assessment prior to the use of sumatriptan.

Table 3. Risk Factors for Coronary Artery Disease 5,8,9
  • Postmenopausal women
  • Obesity
  • Smoking
  • Males over 40
  • Strong family history of coronary artery disease
  • Hypercholesterolemia
  • Hypertension
  • Diabetes

If a patient has one cardiovascular risk factor, the prescriber should be alerted to verify other possible risk factors; if a patient has two or more risk factors, the manufacturer strongly recommends that first dose should be given in the presence of a physician.

In vitro studies suggest that sumatriptan is mainly metabolized by monoamine oxidase isoenzyme A. Concurrent administration of monoamine oxidase-A inhibitors (MAOI) and sumatriptan results in a two-fold increase in plasma concentrations of sumatriptan when administered subcutaneously, and a seven-fold increase after oral administration; therefore, the use of sumatriptan is contraindicated within 2 weeks of discontinuation of MAOI therapy.5 Constituents of the herbal product St. John's wort are believed to inhibit monoarnine oxidase and/or serotonin reuptake;16 therefore, until its pharmacologic mechanism of action is better defined, concomitant use with sumatriptan should be avoided. Due to the risk of vasoconstriction or marked increases in blood pressure, sumatriptan should not be used within 24 hours of administration of ergotamine and ergot-type medications (dihydroergotamine or methysergide). The selective serotonin reuptake inhibitors (SSRI) have been rarely reported to cause weakness, hyperreflexia, and incoordination when given with sumatriptan. While concomitant use is not contraindicated, caution should be exercised.5

Dosage Range
Sumatriptan (Imitrex[R]) nasal spray is available in 5 mg and 20 mg unit dose nasal spray devices.5 The lowest effective dose should be used to decrease the potential for adverse drug reactions. The spray is to be administered to one nostril only. If the headache returns, the dose may be repeated once after 2 hours with a maximum dose of 40 mg in a 24-hour period.

Place in Therapy
Many patients with acute migraine suffer from nausea and vomiting which may complicate treatment with oral agents. While subcutaneous administration is an alternative, aversion to injection or the inability to self-administer may make the injectable product unacceptable for some patients. For these patients, intranasal surnatriptan is an effective and well tolerated treatment for acute migraine. Based upon the data presented, sumatriptan nasal spray appears to have a response rate and onset of action that is less than the subcutaneous route, but it appears to have an onset that may be slightly faster than the oral route, with comparable efficacy.


Dihydroergotamine Nasal Spray

Dihydroergotamine (DHE) nasal spray (Migranal[R] - Novartis) is indicated for the acute treatment of migraine headaches with or without aura.17 It is not intended for prophylactic therapy or for the treatment of hemiplegic or basilar migraine. Dihydroergotarnine is a 5-HT1Da, and 5-HT1DB agonist and it binds to serotonin 5-HT1A, 5-HT1C receptors, noradrenaline a2A,a2B,a1, and dopamine D2L receptors. Activation of the 5-HT1B receptors on intracranial blood vessels leads to vasoconstriction and the inhibition of pro-inflammatory neuropeptide release.17 Previously, dihydroergotamine was only available as the 1 mg/ml parenteral preparation D.H.E.45[R].

Pharmacokinetic Properties
Humbert et al studied the pharmacokinetic properties of DHE nasal spray versus intramuscular (IM) DHE in healthy volunteers.18 Following a 1 mg intranasal dose, the mean time required to reach maximum serum concentration (tmax) was 55.8 minutes and the mean peak serum concentration (Cmax) was 1.02 ng/ml; results were 22.8 minutes (tmax) and 4.44 ng/ml (Cmax) with the IM route. The 1 ing IV administration of DHE results in peak plasma levels more than 10 ng/ml in 1 to 2 minutes.19

Clinical Efficacy
Several large, placebo-controlled, clinical trials have demonstrated the efficacy of DHE nasal spray in the treatment of acute migraine attacks.20-22 In one of the larger randomized, double-blind, placebo-controlled trial, 310 patients between 18 to 65 years of age were evaluated for safety and efficacy of DHE nasal spray for the treatment of migraines.21 The patients were required to have a diagnosis of migraine with or without aura as defined by the International Headache Society criteria. They were randomized to one of three groups: DHE 2 mg, DHE 3 mg, or placebo. At the onset of a moderate to severe headache, the patients administered one spray into each nostril every 15 minutes for a total of 6 sprays. The patient's self assessments revealed that pain intensity was significantly less in the 2 mg DHE group, starting at 30 minutes after administration and continuing through 4 hours, when compared to placebo. The 3 mg DHE group demonstrated a response that was significantly greater than placebo from 2 to 4 hours. Approximately 27% of patients experienced no pain or mild pain at 30 minutes post-dose in the 2 ing DHE group (p less than 0.01), compared to approximately 10% in the 3 mg and 8% in the placebo group. The 3 mg DHE dose did not become significantly different from placebo until the 2-hour point (p less than 0. 0 1). Seventy percent of patients treated with DHE responded by the 4-hour point, compared to 25% treated with placebo. The 2 mg patients reported a mean improvement in severity of nausea that was significantly greater than placebo beginning 30 minutes after treatment (p less than 0.05) and less photophobia. at 2 hours (p less than 0.05). In the discussion, the authors report significantly fewer headache recurrences 24 hours post treatment with DHE; however, percentages were not provided.

There are currently no published trials that compare DHE nasal spray and sumatriptan nasal spray. While a trial by Touchon et al23 compared 6 mg subcutaneous (SQ) doses of sumatriptan versus two sprays of 0.5 mg DHE in each nostril (1 mg total), this dose is lower than the manufacturer's labeling, which recommends a 2 mg dose of DHE. Headache relief was faster with SQ sumatriptan, but more patients reported headache recurrence with SQ surnatriptan (31%) than with DHE nasal spray (17%). Furthermore, the study assessed and reported responses up to 2 hours after dosing which may have been too short to see the full effect of DHE nasal spray.

Safety Issues
The most common side effects reported by the manufacturer for DHE nasal spray include rhinitis (26%), nausea (10%), altered sense of taste (8%), application site reaction (6%), dizziness and vomiting (4%).17 The manufacturer describes the local irritation as predominantly mild to moderate in severity, with 70% resolving within 4 hours after application. DHE nasal spray has the ability to cause coronary artery vasospasm and should not be used in patients with risk factors for ischernic heart disease or infarction. Significant elevations in blood pressure have also been reported with DHE administration; therefore, it should not be given to patients with uncontrolled hypertension. The concomitant use of DHE with 5-HT1 agonists, ergotamine, or ergot-type medications may result in additive or synergistic elevations in blood pressure and should be avoided. Contraindications for DHE nasal spray are listed in Table 4.

Table 4. Contraindications to the Use of Dihydroergotamine Nasal Spray17
  • Ischemic heart disease (coronary artery disease)
    • Angina pectoris
    • History of myocardial infarction
    • Documented silent ischemia
  • Coronary artery vasospasm.
    • Prinzmetal's variant angina
  • Severe renal or hepatic impairment
  • Concomitant use of peripheral or central vasoconstrictors
  • Used within 24 hours of ergotamine-type medication
  • Other 5-HT1B agonist use within 24 hours
  • Hemiplegic or basilar migraine
  • Uncontrolled hypertension
  • Peripheral artery disease
  • Following vascular surgery
  • Pregnant women or nursing mothers

The prescribing information also includes prominent warnings that DHE nasal spray should only be used where a clear diagnosis of migraine has been established. The manufacturer strongly recommends that DHE nasal spray should not be given to patients with risk factors for coronary artery disease (Table 3). If a patient has one cardiovascular risk factor, the prescriber should be alerted to verify other possible risk factors, and if a patient has two or more risk factors, the first dose should be given in the presence of a physician. DHE is a substrate as well as an inhibitor of the cytochrome P450 3A4 enzyme system. Macrolide antibiotics (e.g., erythromycin) which are also known inhibitors of CYP3A4 cause increased blood levels of DHE and increased peripheral vasoconstriction;17 if possible, this drug combination should be avoided.

Dosage Range
Dihydroergotamine (Migranal[R]) nasal spray is available in 4 mg/1 ml amber glass ampuls and a single-use nasal spray applicator. After squeezing the applicator four times to prime it, 0.5 mg (one spray) is administered to each nostril and repeated in 15 minutes, for a total dose of 2 mg (four sprays).17 Doses greater than 2 mg for a single administration have not shown any additional benefit. The safety of doses greater than 3 mg in 24 hours and 4 mg in a 7-day period has not been determined.

Place in Therapy
While the parenteral formulation of DHE requires a visit to the physician's office or emergency room for administration, the nasal formulation can be self-administered by the patient at home. The onset is slower than sumatriptan nasal spray, but there is less headache recurrence with DHE administration. This longer duration of action may be a better choice for patients who experience migraines with an extended duration.

Conclusion
Careful patient selection should be exercised when considering treatment with either surnatriptan nasal spray or DHE nasal spray. The prescribing information for both agents includes recommendations that the agents should only be used where a clear diagnosis of migraine has been established (see Table 1). Due to their ability to cause coronary artery vasospasm and the potential for fatal cardiac adverse events, both agents carry contraindications for use in patients with ischemic heart disease or uncontrolled hypertension. Furthermore, the manufacturers strongly recommend that the agents not be given to patients with risk factors for ischemic heart disease.

Drug interactions should also be considered when prescribing these agents. The concomitant use of sumatriptan or DHE with either 5-HT1 agonists, ergotamine, or ergot-type agents may result in additive or synergistic elevations in blood pressure and/or vasoconstriction and therefore should be avoided.

Both medications have been proven to be effective for the treatment of acute migraine. Although there are currently no published clinical trials directly comparing surnatriptan nasal spray and DHE nasal spray, placebo-controlled trials have indicated that the onset of action of surnatriptan nasal spray is quicker than DHE nasal spray; however, there appears to be a higher rate of headache recurrence with surnatriptan nasal spray.

Many patients with acute migraine suffer from nausea and vomiting which may complicate treatment with oral therapy. While subcutaneous injection with surnatriptan is an alternative, aversion to injections or the inability to self-administer injections may make the injectable product unacceptable for some patients. For these patients, intranasal administration offers an effective and generally well-tolerated alternative.

References

1. Cephalalgia 1988;8(Suppl 7):1-96.
2. JAMA. 1992;267:64-9.
3. Cephalalgia 1991;11(Suppl 11):87-8.
4. Pharmacoeconomics 1992;2:67-76.
5. Glaxo Wellcome. Imitrex[R] nasal spray package insert. Research Triangle Park, NC:1997.
6. J Neurol 1994;241:463-9.
7. Cephalalgia 1997; 17:541-50.
8. Glaxo Wellcome. Imitrex[R] oral tablets package insert. Research Triangle Park, NC: 1997.
9. Glaxo Wellcome. Imitrex' subcutaneous injection package insert. Research Triangle Park, NC: 1997.
10. Eur Neurol 1991; 31:332-8.
11. Neurology 1997;49:1225-30.
12. Arch Fam Med 1998;7:234-40.
13. JAMA 1991;265:2831-5.
14. Eur Neurol 1991;31:306-13.
15. Drugs 1992; 43(5): 776-98.
16. Arch Intern Med 1998; 158:2000-11.
17. Novartis Pharmaceuticals Corporation. Migranal[R] nasal spray package insert. East Hanover, NJ: 1997.
18. Clin Pharmacol Ther. 1991;60:265-75.
19. Headache 1997;37(Suppl 1):S15-S25.
20. Neurology 1994;44:447-53.
21. Arch Neurol. 1996;53:1285-91.
22. Headache 1995;35:177-84.
23. Neurology 1996;47:361-5

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