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74 Parenteral administration is

associated with bruising, redness, and discomfort at the injection site.

75 Due to the

risk of vasoconstriction associated with triptan use, special attention is required for

patients with cardiovascular disease or risk factors. Although the rate of adverse

cardiovascular events has been low,

76 sumatriptan should not be used in patients with

uncontrolled hypertension, peripheral or cerebral vascular disease, Wolff-ParkinsonWhite syndrome or arrhythmias associated with other cardiac accessory conduction

pathway disorders, coronary artery disease, previous myocardial infarction,

Prinzmetal angina, or coronary vasospasm. The provocation of coronary artery spasm

secondary to sumatriptan administration has been demonstrated in those with variant

angina, an effect likely mediated via the 1B receptor subtype.

77 A baseline

electrocardiogram is recommended for patients with potential cardiac risk prior to

triptan administration, and such an intervention may be considered for those patients

without cardiovascular risk factors experiencing chest tightness following triptan

administration.

78

Initial dosing should occur under medical supervision for patients

that possess cardiac risk factors but are deemed appropriate treatment candidates.

Drug Interactions

Drug interaction potential associated with sumatriptan centers on the modulation of

serotonergic activity, the risk of serotonin syndrome, and the potential for additive

vasoconstrictive properties. Serotonin syndrome potential exists with the

concomitant use of sumatriptan and ergot derivatives, selective serotonin reuptake

inhibitors (SSRIs), lithium, and/or monoamine oxidase inhibitors (MAOIs).

79 A 2006

Food and Drug Administration advisory further underscored the need for caution and

consideration of risk versus benefit with combination use of triptans used in

combination with SSRIs and serotonin norepinephrine reuptake inhibitors (SNRIs).

80

The medication profile for L.P. includes venlafaxine, an SNRI, for the management

of GAD; however, this does not exclude the possibility of using triptans to manage

her migraines. The clinician should evaluate the entire regimen to ensure optimal

management of all indications, and if the addition of a triptan is deemed appropriate,

L.P. should be educated on the potential for interaction and the clinical implications

of the combination. Because L.P. has attempted treatment with conventional

analgesics, she would be a candidate for initiating sumatriptan.

Table 58-1

Dosing and Comparative Pharmacokinetic Parameters of Triptans

Pharmacokinetic Parameters of Triptans in Healthy Volunteers and in Patients With Migraine

a

,

214-227

Drug

Dose and

Route of

Administration

↓ Tmax

(hours)

↓ Cmax

(mcg/L)

Bioavailability

(%)

↓ t1/2

(hours)

↓ AUC

(mcg/L/hour)

↓ Plasma

Protein

Binding

(%)

Almotriptan ↓ 12.5–25 mg

orally

1–3 – ≈70 3–4 — ≈35

Eletriptan ↓ 20–40 mg

orally

2 – ≈50 ≈4 — ≈85

Frovatriptan ↓ 2.5 mg orally 3 4.2/7

b 29.6 25.7 94 ≈15

↓ 40 mg orally 5 24.7/53.4

b 17.5 29.7 881

Naratriptan ↓ 2.5 mg orally 2 12.6 74 5.5 98 ≈28

Rizatriptan ↓ 5–10 mg orally 1–1.5,

3.2

c

– 45 2–3 — 14

Sumatriptan ↓ 6 mg

subcutaneously

0.17 72 96 2 90 14–21

↓ 100 mg orally 1.5 54 14 2 158 —

↓ 20 mg

intranasal

1.5 13 15.8 1.8 48 —

↓ 6.5 mg/4 hours

transdermal

1.1 22 – 3.1 110 14–21

Zolmitriptan ↓ 2.5 mg orally 1.5, 3

c 3.3/3.8

b 39 2.3/2.6

b 18/21

b ≈25

↓ 5 mg orally 1.5, 3

c 10 46 3 42

↓ 5 mg intranasal 3 3.93

d 102

e ≈3 22.4

d

aAUC, area under the curve; Cmax

, maximal drug concentration; Tmax

, time to maximal drug concentration; t1/2

= terminal half-life.

bValue for men and women, respectively.

cOrally disintegrating tablets.

dValues based on 2.5-mg dose.

eCompared with oral tablet.

Source: Facts & Comparisons. eAnswers. http://online.factsandcomparisons.com/MonoDisp.aspx?

monoID=fandc-hcp10008#fandc-hcp10008.b11. Accessed June 16, 2015.

p. 1238

p. 1239

CASE 58-1, QUESTION 8: During her annual physical examination, L.P. reports success in managing her

migraines with sumatriptan but notes that two doses are often required for resolution of symptoms. She inquires

as to whether another triptan would be more effective. How do second-generation triptans compare with

sumatriptan? Is an alternative triptan appropriate for L.P.?

Second-Generation Triptans

Second-generation triptans include almotriptan, eletriptan, frovatriptan, rizatriptan,

naratriptan, and zolmitriptan. All triptans have demonstrated superiority to placebo in

terms of efficacy.

62

,

81 These agents differ based on the pharmacokinetic profile and

the capacity for headache recurrence.

60

,

82 Among the class, zolmitriptan, rizatriptan,

eletriptan, and almotriptan are associated with a faster onset and higher likelihood of

recurrence compared with naratriptan and frovatriptan, both of which have a slower

onset of action with a lower risk of recurrence.

60

,

82 Naratriptan, in particular, is

metabolized by multiple isozymes, without strong enzymatic inhibition or induction

potential, creating less potential for CYP-induced interactions

83 whereas frovatriptan

is subject to a dual metabolic path via CYP1A2 and renal excretion.

62 Relative to

sumatriptan, oral bioavailability of second-generation agents is increased.

83

Meta-analyses have offered insight into triptan comparisons. For headache

response at 2 hours, eletriptan 80 mg and rizatriptan 10 mg elicited higher response

rates with sumatriptan 100 mg as the reference whereas eletriptan 20 mg, frovatriptan

2.5 mg, and naratriptan 2.5 mg were inferior to sumatriptan.

83

In assessing sustained

freedom from pain, greater efficacy has been observed with rizatriptan 10 mg,

eletriptan 80 mg, and almotriptan 12.5 mg.

83 The opposite effect in this efficacy

endpoint for almotriptan 12.5 mg has been observed in a parallel-group investigation

with sumatriptan 50 mg as a reference.

84 Further comparisons of 74 randomized trials

found that among the triptans, eletriptan was associated with the greatest potential of

producing a pain-free state at 2 hours and at 24 hours.

85 Favorable efficacy was

further observed for rizatriptan (2 hours) and zolmitriptan (24 hours).

85 Comparisons

between rizatriptan and frovatriptan have yielded similar pain-free outcomes at 2

hours and have favored frovatriptan for pain-free status at 4 hours.

86 More recently, a

therapeutic endpoint of the combination of freedom from pain with no incidence of

adverse outcomes has been used in studies involving migraines.

87–90 Using this

endpoint as a primary measure of comparison between zolmitriptan (2.5 mg) and

almotriptan (12.5 mg) in a multicenter European trial, both treatments were deemed

equally efficacious.

87

Drug Interactions

Striking the balance between theoretic drug interaction risk for triptans and what is

observed in clinical practice presents a challenge, especially because it relates to the

risk of serotonin syndrome.

80

,

91

,

92 For L.P., potential drug interactions exist between

triptans and venlafaxine (SNRI) and levonorgestrel/ethinyl estradiol (oral

contraceptive). Attributed to metabolism via CYP1A2, a slight increase in

frovatriptan AUC has been observed with oral contraceptive administration.

93

Prospective investigations assessing the combination of paroxetine and rizatriptan

91

and fluoxetine and zolmitriptan

91

found no instances of serotonin syndrome. These

studies lie in contrast to reports of symptoms of serotonin syndrome with the

combination of triptans and SSRIs or SNRIs.

41 The administration of a triptan should

not be excluded based on L.P.’s medication profile; however, educating her on the

potential for the interaction is warranted.

Increases in rizatriptan and zolmitriptan exposure have been observed secondary

to MAO inhibition.

92

Inhibition of CYP3A4 has facilitated increases in eletriptan

92

and almotriptan.

92

,

94

L.P. can be considered an appropriate candidate for triptan prescribing. Although

associated migraine symptoms are reported, the rapidity of onset for such symptoms

(e.g., nausea, vomiting) is less clear and should be a point of discussion with the

patient. Such information is important for the optimal formulation selection. A

nonoral formulation may be recommended in the context of early-onset vomiting.

Although a loss of efficacy is associated with triptan discontinuation,

95

the timeline

for triptan use prior to discontinuation has spanned years.

95 Evidence for replacing

one triptan with another is mixed. If treatment with one triptan results in suboptimal

efficacy, an alternative triptan may be prescribed.

82 However, recent evidence

evaluating the impact of such change does not suggest substantial benefit.

96

,

97

CASE 58-1, QUESTION 9: L.P. has noted that for some migraine episodes, nausea and vomiting has been

severe, and asks about the use of DHE and antiemetics. What is the role of ergot alkaloids and/or antiemetics in

migraine management?

ERGOT ALKALOIDS

Relative to triptans, ergot alkaloids function as receptor agonists with strong affinity

at 5-HT1A, 5-HT1B, and 5-HT1D.

98

In addition, these agents express activity at 5-

HT1F

, as well as alpha and dopaminergic receptors.

98

,

99 This pharmacologic profile

differs from that of the triptans because the latter exhibit no affinity for dopaminergic

or α-receptors.

98 Actions of ergot alkaloids are multifaceted, blocking neuropeptide

release, stimulating the ventroposteromedial thalamus, and blocking transmission of

afferent signals in trigeminal circuit.

98 Although ergot alkaloids have demonstrated

benefit in managing migraine,

82

,

100

,

101

the more targeted pharmacologic profile of the

triptans has gained preference.

Intranasal administration of dihydroergotamine has yielded significant

improvements in both pain reduction and functional status in comparison with

placebo.

102 A 2-mg DHE dose achieved headache resolution at 4 hours post

administration for 70% of subjects, compared with 28% in the placebo group.

102 This

level of efficacy at the 4-hour time point for DHE has been further substantiated in

comparison with sumatriptan.

103 Subcutaneous administration of 1 mg DHE or 6 mg

sumatriptan resulted in comparable headache resolution.

103 Functional capacity at 1

hour as well as the proportion of patients achieving pain relief at 2 hours

postadministration favored sumatriptan.

103 Adverse outcomes of nausea, vomiting,

and injection-site pain were more prominent for those administering DHE, whereas

incidence of chest pain was more common in the sumatriptan-treated group.

103 Orally

inhaled DHE represents a newer, noninvasive delivery (TEMPO inhaler, MAP

Pharmaceuticals) system.

104

,

105 Superiority to placebo has been demonstrated in the

FREEDOM-301 Study across endpoints of pain relief and freedom from auditory

sensitivity, light sensitivity, and nausea.

104 Associated adverse effects included

product taste and nausea, 6% and 4%, respectively.

104 This delivery system is not yet

commercially available.

Peripheral and cerebrovascular disease, renal and hepatic disease, sepsis, and

cardiac disease qualify as contraindications to the use of ergot alkaloids.

98

,

100

Further, with the potential to induce uterine contraction and distribute into breast

milk, use is contraindicated during pregnancy and lactation.

98

,

106

In patients with a

history of hypertension, it is important to determine whether blood pressure is

appropriately controlled before considering the use of these agents in migraine due to

the potential for arterial constriction peripherally.

107 Compared with ergotamine,

DHE exerts a more variable effect on blood pressure.

107

Adverse Effects

Nausea is the most prominent adverse outcome with ergot alkaloids.

107 The effect is

dose-related and is linked with 5-HT2 and

p. 1239

p. 1240

5-HT3

receptor activation.

60

Intranasal DHE and orally inhaled DHE have been

associated with prolonged nasal congestion

60 and altered taste.

104 Parenteral

administration has been associated with lightheadedness and leg cramping.

107

Antiemetics

In most patients, triptan agents provide effective relief of migraine-associated

nausea. Therefore, specific antiemetic therapy usually is not required. However, as

mentioned previously, persistent nausea is more common in patients who use

ergotamine for acute migraine therapy. In these patients, and in triptan-treated

patients who experience incomplete nausea relief, adjunctive antiemetic therapy

should be considered. Results from a more recent comparative trial

(prochlorperazine IV 10 mg vs. metoclopramide IV 20 mg) found similar efficacy in

managing nausea.

108 Efficacy of metoclopramide has been demonstrated at the lower

end of the dosing scale (10 mg), but higher doses (20–40 mg) were not associated

with improved outcomes.

109

CASE 58-1, QUESTION 10: In addition to triptans and ergot derivatives, what other abortive agents are

available for outpatient treatment of acute migraine?

NONSTEROIDAL ANTI-INFLAMMATORY DRUGS AND COMBINATION

ANALGESICS

Many NSAIDs and combination analgesics containing caffeine have been shown to

be effective for the acute treatment of migraine headache.

110

,

111 Significant clinical

benefit in double-blind, placebo-controlled trials has been shown for aspirin,

ibuprofen, naproxen sodium, and combination analgesics containing acetaminophen,

aspirin, and caffeine.

47

,

111

,

112 Ketoprofen doses of 75 or 150 mg have demonstrated

efficacy relative to placebo in reducing migraine severity.

113

CASE 58-1, QUESTION 11: L.P. reports that her migraines have been successfully managed with

naratriptan 2.5 to 5 mg/episode, with most episodes resolving with the lower dose. Naratriptan was selected on

the basis of a lower likelihood of recurrence. L.P. has been experiencing a severe migraine for the past few

days and has been unsuccessful in treating the episode with naratriptan. She has now sought treatment at a

nearby hospital and has been diagnosed with status migrainosus. What is the most appropriate approach to

managing status migrainosus in L.P.?

Intractable Migraine

Status migrainosus, or intractable migraine, is characterized by an extended duration

of headache, exceeding 72 hours.

5 The typical management strategy usually requires

hydration and parenteral therapy with ergot derivatives, sumatriptan, or opioid

analgesics.

DIHYDROERGOTAMINE

Dihydroergotamine has demonstrated efficacy in treating intractable migraine by

either intermittent or continuous administration.

114 The successful resolution of

symptoms by DHE avoids the need for administration of corticosteroids and opioids

for the same purpose. Adjunctive antiemetics should be administered for

nausea.

114

,

115

SUMATRIPTAN

Sumatriptan 6 mg subcutaneously is also effective for the treatment of established

migraine.

41

If the first injection does not provide relief at 1 hour, a second injection

may be administered. Sumatriptan should not be administered within 24 hours of

ergot alkaloids because of the potential for prolonged vasospastic reactions.

PROCHLORPERAZINE

Prochlorperazine has established efficacy in managing migraine-related nausea, with

intravenous administration being effective during intractable migraine.

47

,

114

,

116

In

randomized, controlled trials, prochlorperazine 10 mg IV was more effective than

placebo, IV metoclopramide, IV ketorolac, and IV valproate for the treatment of

acute migraine in the ED.

116

CORTICOSTEROIDS

Parenteral dexamethasone may be administered in cases of intractable migraine.

114

Among a subset of patients experiencing migraine symptoms beyond 72 hours, a

greater percentage of patients achieved pain-free status following parenteral

dexamethasone administration, relative to placebo.

117 Further, lower headache

recurrence has been observed in patients receiving dexamethasone after standard

abortive treatment.

118

L.P. may be treated with DHE, sumatriptan, prochlorperazine, or metoclopramide

due to demonstrated efficacy and tolerability in comparison with other treatment

options.

119

CASE 58-1, QUESTION 12: During a return visit to her PCP, L.P. has reported that most migraine episodes

have been successfully managed with naratriptan. Although effective, she expresses concern related to episode

frequency noting that in some instances, she is using naratriptan 3 times weekly. Her PCP is considering

prophylactic management and wants to prescribe propranolol. Is propranolol an appropriate option for L.P.?

Prophylactic Therapy

CRITERIA FOR USE

The relevance for initiating prophylactic therapy for migraine is not simply defined

by one common feature among patients. Rather, the impact of migraine for an

individual patient needs to be assessed. Estimates pertaining to prevalence suggest

that only a small percentage (around 5%) receive prophylactic management.

120

Targeted outcomes for prophylactic therapy includes a reduction in both migraine

frequency and severity, enhancing response to acute management strategies, and a

general improvement in daily function.

120 As previous criteria have addressed the

frequency of migraine episodes (two or more episodes monthly) as a principle

consideration,

120

further guidance on suitability for such treatment should also

address disability associated with the episodes, track record of failure with acute

treatments or the overuse of acute treatments, adverse effects precipitated by acute

treatments, or a more pathologically complex migraine (e.g., basilar or hemiplegic

episodes, prolonged auras).

120

,

121 Optimizing prophylactic treatment may likely

require a 2- to 3-month window. This becomes an important consideration to convey

to patients with a focus on maintaining adherence. Medications utilized in

prophylactic migraine management generally fall into the categories of

antihypertensives, antidepressants, or anticonvulsants. A fourth category comprised

of nonprescription treatments is considered as well. The evaluation of evidence

associated with prophylactic treatments is often challenging due to the lack of studies

with comparisons between agents or with crossover design.

An evidence-based guideline for prophylactic treatment of migraine has been

created by the US Headache Consortium, published through the American Academy

of Neurology.

120 Further evidence has been provided via a combined panel of the

American Academy of Neurology and the American Headache Society.

122 Migraine

prophylaxis is an area for which the off-label use of medications is a particularly

common practical consideration. Only a select number of agents have been approved

by the Food and Drug Administration (FDA) for migraine prophylaxis in the

p. 1240

p. 1241

US, including propranolol, timolol, topiramate, valproic acid or divalproex

sodium, and botulinum toxin A (onabotulinumtoxinA). The approval of botulinum

toxin is within the context of treating chronic migraine. Although triptans are not

FDA-approved for migraine prophylaxis, select agents (frovatriptan, naratriptan, and

zolmitriptan) are considered off-label for migraine prophylaxis during menstruation.

PROPRANOLOL

Evidence supports propranolol safety and efficacy in migraine prophylaxis.

120–123

Various mechanisms for efficacy may be considered, including the modulation of

central catecholamines

124 and interaction with serotonin receptors.

124

,

125 Propranolol

has also demonstrated a suppressive effect on cortical spreading depression in

animal models.

124

,

126

In a small study of migraine patients, propranolol has decreased

cerebrovascular reactivity, mediated by action on vascular tone.

127 For L.P., the

prescribing of propranolol for migraine prophylaxis could be considered, as there

are no contraindications within her profile that would prevent use. A limiting

variable to continued use may be the adverse effect profile, including lethargy,

fatigue, and sleep disruption.

122

,

128 As an alternative to propranolol, metoprolol could

be considered similarly appropriate for L.P. Comparisons with aspirin

122

,

129 or

propranolol

120 suggest that metoprolol would be appropriately effective. Metoprolol

has been further compared with nebivolol.

130 While similarly effective in

prophylactic migraine management, better tolerability and ease of titration were

associated with nebivolol.

130

Dosing

Initial dosing for propranolol for prophylaxis of migraine headaches is 20 mg by

mouth 2 or 3 times a day with gradual titration (weekly intervals) according to

patient tolerability to 80 to 160 mg/day in two to four divided doses.

121 Once the

daily dosage of propranolol required to control headaches is established, patient

adherence may be improved by changing to a long-acting oral dosage form (e.g.,

Inderal LA).

Migraine with Aura

CASE 58-2

QUESTION 1: V.M. is a 24-year-old female, reporting to her primary care provider with a 3-month history of

“throbbing” headaches. Although V.M. has reported experiencing tension headaches “on and off” in the past,

the character of these recent headaches has been different, accompanied by early-onset, severe, nausea and

vomiting, and preceded by “flashes of light” and a unilateral facial “numbness.” The “numbness” and visual

flashes have typically resolved after 30 minutes with headaches developing soon after. She has taken naproxen

or ibuprofen for treating recent episodes, but neither has proven effective. The MIDAS score was 11. Medical

history includes hypothyroidism, treated with levothyroxine 100 mcg by mouth daily, and a past history of tension

headache. Her medication profile also includes an oral contraceptive, norgestimate/ethinyl estradiol, for the past

5 years. She describes herself as an “occasional smoker” and denies a history of alcohol use or illicit

substances. Which information is consistent with the diagnosis of migraine with aura in V.M.?

Although both the “throbbing” character of the headache and associated

gastrointestinal (GI) symptoms are consistent with migraine, it is the presence of both

the visual (light flashes) and sensory (numbness) disturbances correlate with the

diagnosis of migraine with aura. Relevant information for confirming this diagnosis

would be a minimum of two episodes, the accompaniment of an aura symptom, the

duration and unilateral nature of the aura, and the evolution of the headache following

the aura.

5

Propagating glial and neuronal depolarization, characterized as cortical spreading

depression, has been implicated in aura.

20

,

131

It is suggested that the pathologic basis

for aura involves gap junction modulation at the neuronal level of the

trigeminovascular circuitry.

20 Aura has been associated with migraine in

approximately one-third of patients

131 and visual phenomena are typically the most

prevalent aura features.

131

It is important to note that visual effects are substantially

varied and can include flashing lights, waving lines, or areas of localized blindness

(scotoma).

132 Further, a “visual snow” effect has been described in the literature,

bearing resemblance to television static.

133 Although visual phenomena are most

prevalent, sensory disturbances (e.g., numbness, pins, and needles sensation) may

also comprise an aura.

5

In the case of V.M., the aura includes both visual and sensory

disturbance, and coupled with the report of additional symptoms (e.g., throbbing

headache, n/v), a diagnosis of migraine with aura is appropriate. The temporal

relationship between the aura and evolution of the migraine is one of further

consideration. Although V.M. reports the evolution of the migraine following the

aura, there is evidence to support classical migraine symptoms occurring during the

aura phase.

134

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